WOMEN’S - noblogs.org...years to treat the kind of women’s health problems that I was seeing every day, ranging from irregular periods and menstrual cramps to hot ﬂashes. As

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AAlternative TTherapies aand IIntegrative

Medicine ffor TTotal HHealth aand WWellness

New York Chicago San Francisco Lisbon London Madrid Mexico CityMilan New Delhi San Juan Seoul Singapore Sydney Toronto

TORI HUDSON, N.D.

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C O N T E N T S

Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix

Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xi

Contributors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xvii

1 Abnormal Uterine Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

2 Amenorrhea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

3 Cervical Dysplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

4 Contraception . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51

5 Cystitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

6 Endometriosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75

7 Fibrocystic Breasts. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89

8 Genital Herpes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99

9 Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109

10 Infertililty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155

11 Interstitial Cystitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167

12 Menopause . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175

13 Menstrual Cramps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225

14 Osteoporosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237

15 Pelvic Inflammatory Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267

16 Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275

17 Premenstrual Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301

18 Sexually Transmitted Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 317

19 Uterine Fibroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327

20 Vaginitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341

Appendix A: General Exercise Program . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359

Appendix B: Body Mass Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 365

Appendix C: Hormone Replacement Therapy Prescriptions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 367

Appendix D: Procedures and Practices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373

Appendix E: Recommended Screening Tests and Immunizations . . . . . . . . . . . . . . . . . . . . . . . . . 375

Resources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 481

vii

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F O R E W O R D

ix

I’ve long been a fan of the work of Dr. ToriHudson, the foremost national leader in natur-

opathic and botanical medicine specifically forwomen. And unbeknownst to her, Dr. Hudsonhas been a guiding light for me in using botanicaland naturopathic approaches to women’s healthproblems for many years. Long before herbal medicine enjoyed its current mainstream accept-ance, my patients who were interested in naturalapproaches to their gynecologic problems broughtme copies of Dr. Hudson’s articles and even thetext that she wrote for her students to fill in theinformation gap about gynecology and naturalmedicines that existed in the naturopathic trainingprogram where she teaches. In this text, entitledGynecology and Naturopathic Medicine: A Treat-ment Manual, Dr. Hudson set down natural treat-ment protocols that she had used effectively foryears to treat the kind of women’s health problemsthat I was seeing every day, ranging from irregularperiods and menstrual cramps to hot flashes. As a conventionally trained allopathic gynecologist, Iwas gratified to learn about and help my patientsapply some of Dr. Hudson’s gentle, natural, andplant-based approaches. They were an excellentcomplement to the standard gynecologic care Iwas already practicing.

So when Dr. Hudson called and told meabout her new book, I was delighted. Here in onevolume is everything a woman needs to know tobegin applying gentle, natural, naturopathic

solutions to her health problems on her own,along with guidance about when she needs toseek professional help. Many of these solutionsare available at your local natural food store.Some are even available in your own kitchen.Many naturopathic approaches stand alone as a viable, safe, and effective treatment option.Others can be used in an integrative approachalong with conventional medicine. Some womenand situations will require the most conventionalof medical treatments. Dr. Hudson’s book helpsto sort through these options. In general, thenaturopathic treatments outlined in this bookoffer safer and gentler solutions to many women’shealth problems that can be applied to helprebalance the body and restore it to health longbefore more serious conditions develop.

Women have used the healing power of plantssince the beginning of time. Now Dr. Hudsonbrings her years of scientific and clinical expertiseto the field of natural, plant-based healing andhelps make it safer and more effective for womenthan ever before. This is a book that should be inevery woman’s health library and every alternativepractitioner’s library, and it is a resource for thenew breed of conventional practitioners open to amore integrative health-care system.

—Christiane Northrup, M.D., author ofWomen’s Bodies, Women’s Wisdom andThe Wisdom of Menopause

Copyright © 2008 by Tori Hudson. Click here for terms of use.


A C K N O W L E D G M E N T S

xi

Throughout the course of writing the origi-nal book, and now the second edition, I

have had overwhelming moments of gratitudefor all the people that have helped.

I have reflected on those who helped me withthe first edition: Norman Goldfind, the originalpublisher. Dr. Susanna Reid, who worked withme from almost the very beginning when she wasstill a student at the National College of Naturo-pathic Medicine. If it were not for her, I wouldnot have learned to use a computer. Thanks toher weekly tutoring, I finally achieved at least afunctional level of competence. Susanna was crit-ically involved in the research of information forthe first edition of the book and in planning itsorganization and format. I also want to thank Dr.Sandoval Melin for his expertise in the area ofexercise. Sandoval has elevated the role of exercisetherapeutics in the first edition of the book andis responsible for its inclusion.

I would also like to thank my editor of thesecond edition, Deborah Brody. She graciouslyaccommodated my need for additional time anddistinctly improved the feel and readability ofeach chapter.

Dr. Elizabeth Newhall generously gave of hertime and expertise as an obstetrician and gyne-cologist for the first edition. If it were not for hergenerous sharing of her conventional medicalknowledge over the last 14 years, my expertise inwomen’s health would not have been complete.

I am fortunate to have a very talented andsupportive sister, Karen Hudson. Not manywomen have the good fortune to have a sisterthat knows everything they do not know. Beingin business together at our clinic, A Woman’sTime, is the perfect blend of what we each dobest. Our joint commitment of delivering health-care options to women is our work and our play.

My family has been very supportive through-out my entire career. My mother, Pat Lawrence, has provided me with lifelong love, support, andtrust and has always made it clear that I am worthyand special. She’s also the one that keeps me intouch with what the media are communicatingabout alternative medicine. Not everyone has her own clipping service from all the popular mag-azines and regular updates on what’s happening on “Oprah,” “20/20,” and the rest. Her husband,Dick, who has now passed on, was my special proj-ect man. All the things I haven’t had time for—hanging the Christmas lights, cleaning the gutters,staining the deck—what a guy! My real father, KenGuenther, made it possible for me to go back toschool and receive an education in naturopathicmedicine, and I thank him for providing the sup-port and resources that allowed me to pursue acareer as a naturopathic physician. My stepdad,Jack Hudson, who passed away at too young anage, gave me the gift of learning and doing all thethings normally reserved for boys. My niece, Jana,delights me with her spirit and resilience.

Sometimes I cannot believe my good fortuneto have Doug Stapf in my life—trusted businesspartner at Vitanica, easygoing Texan friend,fellow basketball fan, the most excellent of menone could hope to know and work with.

Having become a naturopathic physician in1984, I am honored to be an alumna and facultymember of the National College of NaturopathicMedicine (NCNM) these last 24 years. TheNational College of Naturopathic Medicine isthe oldest college of naturopathic medicine inthe United States, and the expertise and experi-ence of its faculty in the field of natural medicineare exceeded by no other college in the country. Ihonor the faculty, administration, and employeesof NCNM for their commitment and vision.


My naturopathic colleagues as a whole, andparticularly the members of the American Association of Naturopathic Physicians, are anincredible community of individuals with anextraordinary commitment to living on thisplanet in a respectful, mindful way and healingthe humans of this planet in gentle ways that uti-lize the medicines of Mother Nature.

I could not have succeeded in the generationand manifestation of two important projects (theInstitute of Women’s Health and Integrative Medicine and the Naturopathic Education andResidency Consortium) without the years of sup-port, trust, and guidance from three individualsand companies: Wally Simons, R.Ph., of Women’sInternational Pharmacy; David Shefrin, N.D., ofBezwecken; and Sharon McFarland of Transitionsfor Health/Emerita.

Several other people have lent their profes-sional, business, academic, and personal supportand extended themselves in various ways: MichaelMurray, N.D., of Natural Factors; Don West,R.Ph., of Lloyd Center Pharmacy; Rick Liva, N.D.,and Jackie Germain, N.D., of Vital Nutrients;Ronnie Boyer, M.D., of The Center for Educationand Development in Homeopathy; Riley Liv-ingston; David Hanning of Biogenesis; Jon Thore-son and Nigel Plummer, Ph.D., of Pharmax; KyleBliffert of Nordic Naturals; Ken Koenig, D.C., ofWise Woman Herbals; Michael Schaeffer of Well-ness Naturals; Steve Wickham of Metametrix;Brehan Griswold of Emerson Ecologics; and ShaneMcCamey of Boiron.

I have a special place in my heart for the dailyprivilege I have in working with my associates atA Woman’s Time. This group of women practi-tioners are extraordinary in their work and trulyan incredible pleasure to work with. I am grate-ful for their camaraderie and collaboration in allthat we do together: Barbara McDonald, N.D.,L.Ac.; Stephanie Kaplan, N.D.; Leigh Kochan,N.D., L.Ac.; Wendy Vannoy, N.D.; Moira Fitz-patrick, Ph.D., N.D.; Michelle Rogers, N.D.;

Karen Hudson, M.P., H.C.; Theresa Baisley,LMT; and Mari Greenly, L.Ac.

I would also like to thank our clinic staff, aformidable group of fine women who extendtheir skill, compassion, ethics, and care ofpatients and coworkers on a daily basis: Tamara,Kim, Whitney, Susan, Renee, and Audra.

In order to practice an integrative medicineapproach, I have had the guidance and support ofmany conventional practitioners in the Portlandcommunity. I can’t possibly list them all, but hereis an important beginning list: Mike McClung,M.D.; Trish Burford, M.D.; Nathalie Johnson,M.D.; Jane Harrison-Hohner, N.P.; KatherineHill, N.P.; Nina Davis, M.D.; Renee Edwards,M.D.; Kim Surianno, M.D.; Sandra Emmons,M.D.; Lisa McCluskey, M.D.; Michael Lewis,M.D.; Kim Suriano, M.D.; Brenda Kehoe, M.D.;Sally Holtzman, M.D.; Pillippa Ribbink, M.D.;Liz Newhall, M.D.; Randi Ledbetter, M.D.; TomJohnson, M.D.; Paul Kucera, M.D.; RodneyPommier, M.D.; Jeff Jensen, M.D.; Laura Green-berg, M.D.; Dan Gruenberg, M.D.; KasraKaramlov, M.D.; Maureen Goldring, M.D.; Cyn-thia Ferrier, M.D.; Kip Kemple, M.D.; WesleyLewis, M.D.; and many more. I thank them fortheir open-mindedness and fierce commitment totheir patients and medicine.

When things are up and things are down, oreven just content, my trusted friend, playmate, and confident Dee Packard is one of those specialbeings the universe has brought into my life. Iconsider myself fortunate to have the lovingfriendship and committed support of EileenStretch, Cindy Phillips, Holly Lucille, NiralaJacobi, Kate Krider, Patti Kohler, Tracy Waters,Laurel Haroon, Steve Austin, Kathy Hitchcock,and Sidney Henry. I also thank my specialfriends Lupita and Jon McClanahan who teachand share with me the “beauty way” of theNavajo people. To K. C. Snellgrove, D.C., Ithank you for keeping my body going, despitelong hours at my desk, and I thank her able

xii A C K N O W L E D G M E N T S

coworker, Lucille Gouge, who always seems to fitme into the schedule for a treatment.

To Bette Joram, Ph.D., I thank you for yourintellect and remarkable insights, your contain-ment, your support, and your trustworthiness.

And to Ann Kafoury, L.P.C., I thank you foryour skill, your grace and compassion, your trustin me and trustworthy ways, and your commit-ment to me and my own healing.

I also want to thank all the women I havetreated over these last 24-plus years. I am a better

teacher, better physician, and better personbecause of you.

For those with whom I’ve played, worked,nourished, and loved, you have brought aboutmy evolution as a human being.

Finally, we all owe our gratitude to thewomen who seek safe, effective, respectful medi-cine and choices in their health care. You havechanged history on more than one occasion andprotected our humanness.

xiiiA C K N O W L E D G M E N T S


xv

The second edition of Women’s Encyclopediaof Natural Medicine would not have been

possible without the studious help of two col-leagues in particular: Leigh Kochan, N.D., L.Ac.,and Randi Ledbetter, M.D. Dr. Kochan is aformer resident and now an associate at our clinic,A Woman’s Time, in Portland, Oregon. She hasspent countless weeks and months assisting me incompiling the scientific literature of the last sevenyears, particularly for updated research in herbaland nutritional therapies. Her efforts have keptme from feeling overwhelmed and made thisdaunting project of updating the book a real possibility. Dr. Randi Ledbetter is a gynecologistpracticing in Portland, Oregon, at The Meno-pause Clinic. She has generously offered her gyne-cological expertise to me and other alternativepractitioners these past many years and now hasextended that to helping me to rewrite and updatethe sections on conventional medicine. I considerthese sections of the book vital in the education ofpatients and fellow practitioners.

My gratitude and appreciation for the contri-butions of Dr. Leigh Kochan and Dr. Randi Led-better are immense and will extend long into thefuture. Without their knowledge and assistance,this would have been a much longer and morearduous process.

The following additional practitioners havemade selected contributions in different sections of the book, reviewing, editing, and contributingtheir expertise:

Sandoval Melin, N.D., Ph.D. Exercise therapeutics

Elizabeth Newhall, M.D. Obstetrics, gynecology

Nina Davis, M.D. UrologyKatherine Hill, N.P. InfertilitySusanna Reid, Ph.D., N.D. First edition

research assistantJudy Fulop, N.D. First edition

research assistant,endometriosis

C O N T R I B U T O R S



I N T R O D U C T I O N

xvii

I’ve spent the last 28 years studying, practic-ing, teaching, and evolving as a naturopathic

physician. Two themes have been consistent: natural medicine and the health care of women.

Alternative medicine has come to be the popular term used to distinguish natural, nonin-vasive therapies from conventional medicine.Whether the terms alternative medicine, comple-mentary medicine, natural medicine, or holisticmedicine are used, they all reflect the transforma-tion that is occurring in health care: a focus ondisease prevention, the promotion of healthylifestyle habits, and the treatment of disease withnatural, nontoxic, and less invasive therapies. Atthe center of this transformation is a distinctsystem called naturopathic medicine.

The roots of naturopathic medicine are seen in the healing traditions of Egypt, India, China,Greece, Germany, South and Central America,Africa, and native North America. The Europeanhydrotherapy tradition had a strong influence onthe development of naturopathy, and by the endof the nineteenth century, Benedict Lust, a physi-cian trained in the water-cure methods of Europe,came to America and began using the term natur-opathy to describe an eclectic combination of nat-ural healing principles and methods.

The first college of naturopathic medicine in the United States opened in New York City in 1902. It taught a system of medicine that included nutritional therapy, natural dietetics,herbal medicine, homeopathy, manipulation, ex-ercise therapy, hydrotherapy, electrotherapy, andstress reduction techniques.

Naturopathic medicine grew and flourishedfrom the early 1900s until the mid-1930s. At thatpoint in history, the conventional medical profes-sion began to influence the health-care system inseveral ways. It abandoned some of its barbaric

bloodletting therapies and toxic mercury dosingand replaced them with more effective and lesstoxic treatments. With therapies more acceptableto the public, subsidies from wealthy foundations,the support of the developing pharmaceuticalindustry, and political savvy and legislation in itsfavor, conventional medicine was able to restrictthe use of unorthodox doctors, midwives, herbal-ists, and others and gain a virtual monopoly onthe health-care system.

Fortunately, alternative medicine and naturo-pathic medicine have seen a rebirth in the last 15to 20 years, and especially in the last 5. A publichungry for choices in their health care, an increased awareness about the role of diet andlifestyle in cancer and chronic disease, the aging ofthe baby boomer generation, and the failures ofcertain aspects of modern conventional medicineand the health insurance industry to deal withpeople and their health problems respectfully,carefully, fairly, and effectively have been responsi-ble for this resurgence. Conventional medicine hasbrought great insights, successes, and miracles ofwhat human intelligence can accomplish. Naturalmedicine has matured, particularly in the areas of scientific research, educational institutions,number of licensed practitioners, and profession-alism and is now poised to serve those who seek itsgentle ways.

Naturopathic medicine is its own distincthealing art and is best defined by its principlesand therapies. Simply put in modern terms,naturopathic physicians are primary health-careproviders, family physicians who specialize innatural medicine. The following seven principlesare the foundation for naturopathic medicine:

1. The healing power of nature (vis medica-trix naturae). The body has the inherent ability


xviii I N T R O D U C T I O N

to establish, maintain, and restore health. Thephysician’s role is to facilitate and augment thisprocess with the aid of natural, nontoxic thera-pies; to act to identify and remove obstacles tohealth and recovery; and to support the creationof a healthy internal and external environment.2. First, do no harm (primum no nocere).

Naturopathic physicians seek to do no harmwith medical treatment by employing safe,effective, less invasive, and natural therapies.3. Identify and treat the cause (tolle

causam). Naturopathic physicians are not onlytrained to investigate and diagnose diseases,they are also trained to view things more holisti-cally and look for an underlying cause, be itphysical, mental, or emotional. Symptoms areviewed as expressions of the body’s attempt toheal but are not the cause of disease. The physi-cian must evaluate fundamental underlyingcauses on all levels, using treatment thatincludes addressing the root cause rather thanjust suppressing symptoms.4. Treat the whole person. Health and disease

are conditions of the whole organism, involvinga complex interaction of physical, spiritual,mental, emotional, genetic, environmental, andsocial/cultural/economic factors. The physicianmust treat the whole person by taking all ofthese factors into account. Homeostasis andharmony of functions of all aspects of the indi-vidual are essential to recovery from disease,prevention of future health problems, andmaintenance of wellness.5. Physician as teacher (docere). The naturo-

pathic physician’s major role is to educate,empower, and motivate the patient to takeresponsibility for his or her own health. Thephysician educates about risk factors, hereditarysusceptibility, lifestyle habits, and preventivemeasures and makes recommendations on howto avoid or minimize future chronic healthproblems. A healthy attitude, diet, exercise, andother lifestyle habits serve as the cornerstone ofour recommendations.

6. Prevention is the best cure. The ultimategoal of naturopathic medicine is prevention.This is accomplished through education andpromotion of lifestyle habits and through natu-ral therapeutic recommendations. The emphasisis on building health rather than on fightingdisease.7. Establish health and wellness. The pri-

mary goals of naturopathic physicians are toestablish and maintain optimum health and topromote wellness. They strive to increase thepatient’s level of wellness, characterized by apositive emotional state, regardless of the levelof health or disease.

In addition to these seven principles, there aretwo principles that I believe are fundamental notonly to natural medicine, but to good medicinein general: the principle of resonance and theprinciple of choice. Let me explain. Resonance is basically an issue of compatibility. Whatapproach, what therapy, what herb, or what ofany substance is compatible with this particularpatient in this particular moment and set of lifecircumstances? The selection of the therapeuticapproach that is resonant with the individual isthe therapy that will create the most healingmomentum. Picture a child on a swing. Youstand behind the child pushing her forward soshe can achieve the most momentum, and herswinging becomes effortless. If you push her atthe right moment, your force is perfectly timedwith her body motion and the rhythm of theswing. The perfect timing sends her smoothlyand easily higher, and with the slightest effort shecan keep swinging forever. If you push her at thewrong moment, the swinging becomes jerky, sheloses speed and height, and the rhythm is dis-rupted. It then takes a great deal of effort toregain momentum. The perfect effortless swingcomes from the perfect timing and perfect force-fulness of the “push.” This is resonance. Theperson with the health problem is the child onthe swing. The person who pushes the swing is

xixI N T R O D U C T I O N

the physician and the therapy she uses. Any med-icine, natural or pharmaceutical, can be resonant.The art of medicine is to know when to use what,for whom, and for how long. I believe the mostprofound healing principle in the practice ofmedicine is the principle of resonance, notwhether the medicine is natural or synthetic, alter-native or conventional, or a naturopathic philoso-phy versus conventional allopathic philosophy.The healing method is the medicine that is rightfor that person. The true goal of a physician is to perceive what is resonant with that individual.

Dr. John Bastyr was considered by mostnaturopathic physicians to be the modern patri-arch of naturopathic medicine. A whole newgeneration of naturopaths looked to him fortheir wisdom as the holder of true naturopathicmedicine. The story goes, a young naturopathicmedical student asked Dr. Bastyr, “How are wesupposed to know what therapy to choose when there are so many different medicines andsystems to choose from?” Dr. Bastyr calmly andquickly responded, “Choose what works.”Another question was posed to Dr. Bastyr: “Howcan you tell an excellent physician from a goodphysician?” Dr. Bastyr’s answer: “The results.”

My second guiding principle is that of choice.Each patient chooses what is right for her. Thedoctor’s role is to educate about the health prob-lem, about the options, including their pros andcons, and to share resources. The goal is to providethe context in which the patient can make aninformed decision. The physician must be percep-tive and must listen, investigate, evaluate, educate,offer recommendations, and then create an envi-ronment where the individual can make a decisionfor herself. The individual seeking my help gets to choose. It may be black cohosh, or it may beestrogen. It may be a rigorous naturopathic health regimen, or it may be surgery. It may be an inte-grated combination, a “complementary” approachusing the best of two worlds. Choice is a powerfulforce—the force of individual responsibility,empowerment, and self-direction. Choice fosters

will, desire, discipline, and motivation. Freedomof choice occurs in an environment of equalityand respect between physician and patient.

These two principles, resonance and choice,are what motivates me toward the vision of anintegrative health-care model. I no longer believein a fractionated approach to health and healingwhere alternative medicine is on one side andconventional medicine is on the other. There is aspectrum of options that go from simple to com-plex, from the least intervention to the mostaggressive intervention, and from the most natu-ral therapy to the most synthetic or technologi-cal. We need all of it. Human intelligence hascreated incredible tools and techniques. Thephysician who is educated and aware of all theoptions and learns to understand how and whento best use all these choices on behalf of someonewho is ill and suffering is the true physician inmy book. An integrative model incorporates thenatural/naturopathic perspective and the con-ventional perspective and knows the strengthsand weaknesses of each in different circum-stances. When we can do something effectivelyand safely with nontoxic, natural medicines withfar fewer side effects, then what would stop us? Ifwe can’t, or it’s too risky to wait and find out,then let’s move up the ladder to more invasive,riskier medicines with more side effects that maywork better or be a more appropriate choicebecause the risk of the disease is greater than therisks of the treatment.

Naturopathic and other alternative medicinedisciplines have their strengths and their weak-nesses. Conventional medicine has its strengthsand its weaknesses. I encourage consumer andpractitioner alike to advocate for practitioners ofall disciplines to integrate their intelligence,experience, and energies to build cooperativeworking relationships with each other so thatthey can truly help people to choose what worksbest for them.

In addition to recommendations on lifestyle,diet, and exercise, naturopathic physicians utilize

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a vast array of therapeutic tools to promotehealth and treat illnesses. Naturopathic physi-cians are trained in what is called the eclectic tra-dition. They have a broad range of therapies andtend to use a selected mixture of these therapieswhen treating their patients. Naturopathic thera-pies include dietary and lifestyle changes, clinicalnutrition (nutritional supplementation), botanicalmedicine (herbs), homeopathy, Chinese medicineand acupuncture, hydrotherapy, manipulation,physical therapies, psychotherapy, and minor sur-gery. We also recognize the judicious use of pre-scription medications when the benefits exceedthe risks, integrated into a comprehensive naturo-pathic health-care plan. Some naturopathic physi-cians receive extra training and licensure topractice obstetrics and natural childbirth.

And now for the second consistent theme inmy life: the delivery of health care to women.Modern women are the first women in history toenjoy the luxury of anticipating that their lives willbe healthy, long, and self-directed. This awarenessof opportunities and choices is leading them todayto seek the benefits of natural medicine in ever-increasing numbers. More dominant and discrim-inating consumers of health care than men orchildren, and quicker to grasp the advantages of avitalistic, holistic healing art, their innate wisdomhas already led to many significant changes in conventional medicine in recent years. Womeninsisted on natural childbirth, and now it is thegoal of most pregnant women and available every-where. They have too long felt the restrictions ofpaternalistic conventional medicine with its uni-formity and lack of individualization of healingapproaches and are therefore more than ready toembrace the natural principle of treating the indi-vidual. Moreover, the success of natural treatmentsin relieving disease and suffering has done much topromote their popularity. The now well-recognizedneglect of women in allopathic conventionalresearch and the failure to prioritize women’shealth in general have left a profound gap in healthcare that alternative medicine is well poised to fill.

Women want safe, effective, affordable medi-cine. Women want to be educated about theirbodies and their health. Women want to makechoices in their health care that they have deter-mined are right for them. By philosophy, bydesign, and by commitment, alternative healingsystems have the package to offer women whatthey want.

Beginning with the AMA’s exclusion ofwomen in the late 1800s, orthodox medicine’slack of respect for women both as healers andpatients has been all too obvious. Today, signifi-cantly more empowered women have come toreject the dictums of orthodox medicine in greaternumbers. Women intuit the limitations of the biomechanical model to completely explain phys-iological processes. Despite the orthodox physi-cian’s uniform advocacy for menopausal hormonereplacement therapy (HRT) for all, only a frac-tion, less than 20 percent of women, comply; 90percent of the women who begin HRT stopwithin the first year of use. Partially a failure ofaccess, it is also a profound testimonial to theirlack of trust in conventional medicine’s safety, effi-cacy, and commitment to their well-being.

The creation of synthetic hormones in the1950s and 1960s was unquestionably revolution-ary for women in that it suddenly allowed per-sonal life autonomy through successful fertilitycontrol and the elimination of the hot flashes andmood swings of menopause. Women’s lives werechanged forever. However, with hormonescoming as they did on the heels of the “miraclemedicine era” in which antibiotics and vaccinesled the general public to believe medicine coulddo no wrong, the consequences of hormoneexcess and side effects were not anticipated orquickly recognized and dealt with. Up until2002, most conventional practitioners recom-mended a postmenopausal lifetime on HRT.This has recently changed, and the data havebegun to show that the risk of breast cancerincreases after five years of use. Consequently,many women distrust and fear hormonal medi-

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cine and their conventional physicians. Unfortu-nately, this fear and mistrust may lead to therefusal of a medicine that in some cases mayachieve more benefit than risk. Here’s where theintegrated wisdom and approach come in. Whileclearly not a panacea, hormones are not all badand have important uses for selected individuals.We can also use hormones in a form that mayenhance their benefits and minimize their risks,or use a combination of a reduced dose of hor-mones along with soy and herbal medicines tobring about the most benefit with the least risk.

Women today are insisting on participatingin their health-care decisions in a way conven-tional medicine is just beginning to recognize. I believe that the baby boomer menopausalwoman is having and will continue to have amore significant impact on our health-caremodel than any other previous group of health-care consumers. Menopausal women today rejectthe notion of a single therapeutic modality beingessential for all women undergoing a naturalprocess. They reject the notion of taking a drugfor the rest of their lives, especially if they haveother options, especially if they can do otherthings to help prevent osteoporosis and heart dis-ease, and especially if that drug increases theirrisk of a life-threatening disease.

Women are the biggest consumers of healthcare in America. A menopause supplement to OB-GYN, the journal of the American College of Ob-Gyn, states, “Focus groups, involvingwomen age 40 to 60, reveal that women knowmore about herbal medicines than about estro-gen.” That seems an impressive testimonial to thepower of alternative medicine in its alliance withthe natural wisdom of women to define their ownhealth-care standards. It is an invitation to alterna-tive medicine to continue to provide women withthe wider, healthier options they seek. Fifty per-cent of American women will be menopausal bythe year 2015, and they will provide alternativemedicine the greatest opportunity yet to serve ourcommunities.

In addition to practitioner-delivered naturalhealth care, natural medicine offers safe andeffective self-care options for many commonconditions such as vaginitis, PMS, fibrocysticbreasts, menstrual cramps, menopause symp-toms, bladder infections, and more, furtherexpanding women’s health-care autonomy.

I support the self-care approach to healing.Much of the practice of medicine is not particu-larly difficult or complex. Education andresources can provide a lot of very practical infor-mation. One of the things I’ve tried to do in thisbook is not only to provide some self-care treat-ments for common female disorders but also toprovide guidelines about when self-care is notappropriate. Health care is a team approach: thepatient, the practitioner, the therapies. The teamcan include both the alternative and the conven-tional practitioner—and, better still, those thattalk to each other on behalf of the patient.

Choice in doctors and medical approaches,involvement in the health-care process, healthylifestyles, and safer, nontoxic natural therapies arerecognized by today’s women as essential to healthand well-being. Women highly value the longertime spent in discussion with their alternativeprovider as well as the careful, complete, andrespectful collection of their history. They valueprocessing their options thoroughly and individu-ally. This unique quality of alternative health-caresystems is rare in conventional medicine and is oneof the chief reasons women seek alternative care.

Naturopathic physicians and other providersof alternative medicine must seek to verify the“scientific” truth of their medicines wheneverpossible—by research and by modifying themechanistic model when necessary to suit theirvitalistic philosophy. They must continue tostand by their tradition of resonance betweenpatient and therapy, ever seeking the resonancefor a particular woman with a particular problemat a particular time in her life.

Last, alternative medicine must recognize thatconventional medicine, while inadequate alone, is

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here to stay and offers important options and life-saving measures. Likewise, conventional medicinemust recognize that natural therapies are a funda-mental healing tradition of all cultures and thatmodern alternative medicine is also here to stay.The more practitioners make themselves aware ofthese options, the better they can guide women in

selecting from all options, both naturopathic andconventional. A combined, well-thought-out coop-erative and integrative approach is often the bestthat medicine has to offer. Our open-mindednesswill be rewarded manyfold by the improved healthof women and their increased satisfaction and trustin their health-care providers.




1

OVERVIEW

Changes in the amount of menstrual blood flow,duration, and pattern are among the mostcommon health concerns that women face.Although these changes cause a lot of anxiety forwomen and do warrant a medical evaluation,most cases of abnormal bleeding are due tobenign and easily addressed conditions. Whetheralternative or conventional treatments are usedfor intervention, prompt evaluation is highly recommended.

There are many causes of abnormal bleeding,but our main purpose in this chapter is to discussa benign hormonal cause of bleeding called dys-functional uterine bleeding (DUB), abnormaluterine bleeding without any demonstrableorganic cause. First, we need a little backgroundand overview on abnormal bleeding in general.

A wide variety of clinical disorders can mani-fest as abnormal bleeding from the vagina. Whatis considered abnormal bleeding depends on theage of the patient. The bleeding can take manyforms, including heavy and/or prolonged menses(menorrhagia), intermenstrual bleeding (metror-rhagia), frequent menses (polymenorrhea), infre-quent menses (oligomenorrhea), heavy andirregular intermenstrual bleeding (menometror-rhagia), or postmenopausal bleeding. Normalmenses are defined as vaginal bleeding that occursapproximately every 28 days (with a range of 21to 35 days) and lasts for 4 to 7 days. Abnormalbleeding is bleeding that occurs more frequentlythan every 21 days, less frequently than every 35days, lasts more than 7 days, is unusually heavy orlight, or occurs after menopause. In addition,vaginal bleeding is considered heavy if a womanloses more than 80 ml of blood per cycle (normalis 30 to 35 ml).

Benign Abnormal Bleeding

The causes of abnormal bleeding can be benign,premalignant, or malignant. Benign causes canbe further subdivided as either organic or hor-monal. Organic disorders are all benign causes of bleeding that are not hormonal. This mayinclude systemic health problems, abnormalpregnancy, foreign bodies, trauma, infections,and growths.

Systemic diseases that are associated withproblems in how the blood clots are called coag-ulopathies and can cause heavy vaginal bleeding.Heavy bleeding in a teenage girl may be causedby a coagulopathy called von Willebrand’s dis-ease. In fact, 20 percent of teenage girls withsevere menorrhagia have a significant coagulationproblem. A decrease in the number of bloodplatelets (thrombocytopenia) can also causeabnormal bleeding. Other systemic diseases, suchas hypothyroidism and severe liver diseases, canalso cause prolonged menses, heavy menses, orintermenstrual bleeding.

An abnormal pregnancy is the most commoncause of abnormal vaginal bleeding in womenwho are of reproductive age. Any type of mis-carriage can present with abnormal bleeding that is also often associated with cramping pains.Women with an ectopic pregnancy (a pregnancyin the fallopian tubes rather than the uterus) canpresent with abnormal bleeding, as can thosewith a molar pregnancy (an abnormality of theplacenta caused by a problem when the egg andsperm join together at fertilization).

Abnormal bleeding in children can be causedby foreign bodies that they may have placed intheir vaginas while playing. The most commonforeign body in women of reproductive age is an IUD, or intrauterine birth control device.

1A B N O R M A L U T E R I N E B L E E D I N G

C H A P T E R


2 W O M E N ’ S E N C Y C L O P E D I A O F N A T U R A L M E D I C I N E

Women with IUDs will tend to have heaviermenses and sometimes intermenstrual bleeding.

Trauma during intercourse can cause vaginalbleeding, for example in postmenopausal womenwho may have a dry vagina with thinning vaginaltissue. Just the friction of normal vaginal penetra-tion during sex may be traumatic to this sensitivetissue. Trauma may also be experienced in a violentsituation such as sexual abuse and rape. In childrenor adolescents, sexual abuse must be considered incases of traumatic vaginal bleeding. Traumaticbleeding may also occur after gynecological proce-dures such as biopsies and instrumentation.

Occasionally, a uterine infection calledchronic endometritis can present with abnormalvaginal bleeding or spotting. Other symptomsoften associated with this infection include avaginal discharge, fever, abdominal/pelvic pain,or lower back pain.

Of the most common causes of abnormalbleeding are growths known as myomas, morecommonly referred to as uterine fibroids. Thesetend to be more common in women over the ageof 30, particularly women in their 40s. Differentkinds of fibroids are discussed in Chapter 19, butsubmucous fibroids tend to be the most trouble-some in terms of heavy bleeding. Fortunately, theyrepresent only about 5 to 10 percent of all fibroids.

Endometrial polyps can also cause abnormalbleeding, but the bleeding is usually not heavy.Adenomyosis, a variant of endometriosis, mayresult in very heavy bleeding associated with men-strual cramping. Endometriosis itself can causeirregular changes in the menstrual cycle, but nottypically heavy menses. Finally, bleeding mayresult from cervical polyps or a simple inflamma-tion of the cervix called cervicitis. Cervical polypsand cervicitis tend to present with intermenstrualbleeding or spotting after intercourse.

Malignant Abnormal Bleeding

Now let us look at the premalignant and malig-nant causes of uterine bleeding. Vaginal canceraccounts for only 2 percent of malignancies of

the female genital tract. Eighty-five percent of the primary vaginal cancers are squamous cell(a particular cell type) carcinoma. The mostcommon symptoms of invasive squamous cellcancer include vaginal bleeding or foul-smellingdischarge. Pain is usually a late symptom.

The tragedy of another cancer, cervicalcancer, is that it is a preventable disease. It is pre-ceded by a prolonged precancerous state inalmost all cases and can be detected at its earlyprecancerous states by annual Pap smears. Theseearlier states of abnormal cells and cervical dys-plasias are easily treatable conditions. Cervicalcancer accounts for approximately 18 percent offemale genital cancer in the United States. Thepeak incidence of cervical cancer is from 35 to 39and 60 to 64 years of age. Vaginal bleeding aftervaginal sexual activity is the most commonsymptom occurring in cancer of the cervix. Inwomen with advanced disease, a foul-smellingdischarge may be present.

Endometrial hyperplasia is an increased growthof the lining of the uterus (endometrium) and asubsequent thickening. Most cases of endometrialhyperplasia revert to normal, either spontaneouslyor with hormonal treatment. Some may persist,and others can progress to endometrial cancer.Endometrial hyperplasia may occur in any agegroup but is most commonly seen in older women.Chronic lack of ovulation, as seen in the teenageyears, after menopause, and as a result of polycysticovary disease, is a condition where we may seeendometrial hyperplasia. Endometrial hyperplasiacan be simple or complex, and either atypical,which is precancerous, or without atypia. Thesedistinctions are very important when it comes totreatment and management and can best be madewith a procedure called an endometrial biopsy.Pelvic ultrasound has improved to the point whereit can detect thickening of the endometrium. Oncethickening is observed, a biopsy will probably berecommended to further evaluate the situation.

Some endometrial hyperplasias will progressto cancer of the endometrium, i.e., uterine


cancer. As in cervical dysplasia and cervicalcancer, endometrial hyperplasia is the precancer-ous state; its adequate treatment will prevent thedevelopment of endometrial cancer. Endometrialcancer is the most common malignancy of thefemale genital tract and accounts for approxi-mately 7 percent of all cancers in women. Theaverage age of patients with endometrial cancer is 59 years; the highest range for the incidence isage 50 to 59 years in postmenopausal women.The most common symptom associated withendometrial cancer is abnormal uterine bleeding.Typically, the bleeding is in the form of spotting,especially in postmenopausal women.

Dysfunctional Uterine Bleeding (DUB)

DUB can occur at any age but is most commonat either end of the reproductive age span. Oneuses the term DUB when other causes for abnor-mal bleeding have been excluded (fibroids,polyps, and endocrine or other disorders). Ado-lescents account for about 20 percent of DUBcases after the first menstrual cycle. These casesare due to the immature endocrine system, par-ticularly the immature function of the hypothal-amus. Perimenopausal women account forapproximately 50 percent of DUB cases due towaning ovarian function. As the ovary ages, itbecomes less efficient in completing the ovula-tory process. Initially there is a decrease in prog-esterone production, which causes shorter cycles.As the aging process progresses, ovulationbecomes less frequent, resulting in a variablelength of the menstrual cycle and a variation inthe duration of the flow. Eventually, the lack ofovulation puts women in an estrogen-dominantstate in the presence of too little progesteronebecause ovulation must occur in order to pro-duce progesterone. Women who are in a state ofchronic anovulation tend to have an excess ofestrogen in the body. This excess estrogen is whatdisrupts the normal pattern of menstruation.

The remaining 30 percent of cases of DUBoccur among women age 20 to 40, generally as a

result of polycystic ovarian syndrome, elevatedprolactin levels, emotional stress, obesity, weightloss due to anorexia, or athletic training.

The actual cause of DUB is not completelyclear. One theory is that the fluctuating estrogenlevels seen in chronic lack of ovulation can causeintermittent estrogen withdrawal bleeding.Another theory is that the continuous estrogenstimulation leads to a thickening of the endo-metrium, which needs more estrogen in order tomaintain itself. Eventually, the need for estrogensurpasses the production and breakthroughbleeding results. Another theory is that someareas of the endometrium outgrow their bloodsupply, and subsequent bleeding occurs becauseof the lack of progesterone.

There are also cases of DUB that are not dueto anovulation but rather occur even thoughthere is regular monthly ovulation. OvulatoryDUB is defined as heavy menses in women whoovulate and who do not have a coagulopathy orany uterine abnormality. The cause of this formof DUB is not clear.

DIAGNOSIS

The key to accurate diagnosis of abnormal bleed-ing is the woman’s medical history. Several perti-nent pieces of information will facilitate diagnosis:

• Previous menstrual patterns for the last threemonths

• The presence or absence of pain along withthe bleeding

• Heaviness of the flow (number of pads ortampons per day and how often they arechanged when saturated)

• Contraceptive methods, if any• Symptoms of pregnancy• Dates and histories of past pregnancies• Premenstrual symptoms• Recent abdominal, pelvic, or vaginal trauma• Clotting problems• Easy bruising or bleeding• Symptoms of systemic diseases


• History of taking estrogens without ade-quate progesterone/progestins

• History of sexually transmitted diseases• Past gynecologic history

A physical exam will involve visualizing thecervix, feeling the contour and size of the uterus,and general palpation of the pelvic area. Labora-tory testing may include:

• Pap smear• Thyroid function tests• Pregnancy test• Complete blood count to rule out anemia• Follicle-stimulating hormone

(FSH)/luteinizing hormone (LH)• Liver function tests• Prolactin levels• Adrenal function studies• Pelvic ultrasound to identify uterine fibroids

or measure endometrial thickness• Pelvic saline infusion sonohystogram• Testing for sexually transmitted diseases• Endometrial biopsy

An endometrial biopsy may be recommendedto test the tissue itself. This is a simple proceduredone in the practitioner’s office in which the clini-cian inserts a small narrow plastic instrumentcalled a pipelle into the uterine cavity to extract asmall sample of tissue. It only takes about 30 to 60seconds, but women can experience mild to signif-icant cramping during that time. A local anestheticis usually not required, and the cramping generallysubsides very quickly once the procedure is over.Endometrial pipelle biopsies can determine thepresence of endometrial hyperplasia, uterinecancer, infection (endometritis), a disrupted hor-monal effect, a lack of estrogen as is seen in post-menopausal women, or a uterine polyp.

If an endometrial biopsy is done at the righttime, it can also be used to verify ovulation. If thebiopsy shows that the endometrium has prolifer-ated, when the woman’s next bleeding episodeoccurs within 10 to 12 days, it generally indicates

a lack of ovulation. Tests such as saline infusionsonohysterography (SIS—an ultrasound proce-dure that gives a three-dimensional view so as notto miss any portion of the uterine cavity), hys-teroscopy (a procedure that involves dilating thecervix so that a small lighted scope can be insertedto visualize the intrauterine cavity), or a dilationand curettage (D&C) may be recommended inaddition to or instead of the pelvic ultrasound andthe pipelle biopsy in selected cases to improveaccuracy of the results.

KEY CONCEPTS

• Seek and utilize a health-care practitioner whowill distinguish DUB from benign, premalignant,and malignant causes. If benign, is the causeorganic or hormonal?

• Workup will include a medical history and mayinclude a physical exam and further laboratorytests, pelvic imaging, and/or endometrialbiopsy.

• Do not self-treat unless assured that the causeis DUB.

• Practitioners can often presume a diagnosis ofDUB temporarily and recommend a furtherworkup depending on response to the treatment.

PREVENTION

• Reduce stress.• Avoid taking any form of estrogen without ade-

quate progesterone or progestins.• Engage in healthy lifestyle habits.• Protect yourself against sexually transmitted

diseases.• Use well-tolerated forms of contraception.• Have regular medical visits, including an annual

physical exam.• Maintain optimal body weight.

OVERVIEW OF ALTERNATIVE TREATMENTS

The goals of alternative treatment for DUB are thesame as the goals of conventional treatment: con-


trol the bleeding, prevent and treat anemia, restorean acceptable menstrual pattern, and preventendometrial hyperplasia/endometrial cancer.

Repeated episodes of heavier and prolongedbleeding should be distinguished from acutehemorrhage. My general guidelines are as follows:If a woman is saturating a super tampon or heavypad every hour for six to eight hours or more shewill often need some form of prescription hor-mone intervention. Herbal/nutritional interven-tions can be tried, but if there is no change withintwo to four hours, then hormonal therapiesshould be utilized. Even heavier bleeding (i.e., sat-urating pads every half hour or less) will mostlikely require surgical intervention. Monitoringphysical symptoms, blood pressure, pulse, andhemoglobin and hematocrit levels will help todetermine management of these more semi-urgent and urgent cases. Use of high-dose oral bio-identical estrogens (estradiol) and bio-identicalprogesterone (oral micronized progesterone) maybe substituted in some cases of heavier semi-acutebleeding, although the net effect is the same aswhen using conventional hormones. In moststates, licensed naturopathic physicians can pre-scribe bio-identical hormones and conventionalhormones. They would approach these dramaticsituations with the same high degree of concernand astuteness as would a conventional practi-tioner and may integrate acute antihemorrhagicbotanicals or nutrients in combination with thehormonal therapies.

Less dramatic cases that still involve heavymenstrual flow will be best managed with bothan immediate plan for the semi-acute bleedingepisode, which should slow down within a fewhours to 48 hours, and a comprehensive planthat should bring results with no further episodesin one to four months. A comprehensive planmay include the use of soy and flax products toregulate the menstrual cycle, herbal extracts toaddress immediate bleeding episodes, nutrientssuch as bioflavonoids and bromelain for theirnatural anti-inflammatory effect, herbal extracts

for their ability to bring about ovulation andorderly stimulation of ovarian function, andherbs for their tonifying and astringent effects.

The concept of tissue tonification is a key fea-ture of the philosophy of herbal medicine. It isthought that gynecological conditions associatedwith bleeding may occur as a result of poor tissuetone of the mucous membranes, poor uterinetone, and a constitutional weakness of the tissuesthat presents as generalized lack of tissueintegrity, in this case the uterus. The astringents(herbs that slow the loss of body fluids, i.e., men-strual bleeding) are the herbs most likely to affecttissue tone, while the uterine tonics and theemmenagogues (herbs to promote menses) aremost likely to affect uterine tone. Traditionally,the ability of an astringent herb to stop bleedinghas been attributed to the tannin content of theplants. Uterine tone is related to the ability of theuterus to function as a smooth muscle. When theuterine tone is normal, there is a normalizationof menstrual flow. A hypertonic uterus can beassociated with a delayed menses and crampinguterine pains. A hypotonic uterus is frequentlyaccompanied by heavy bleeding and a feeling ofpelvic congestion.

Stress reduction has an underappreciated butsignificant influence on irregular menses andDUB. A disruption in the messages between thehypothalamus (which produces gonadotropin-releasing hormones) and the anterior pituitary(which releases FSH and LH, follicle-stimulatingand luteinizing hormones) brings about a mis-timing of the release of these hormones and asubsequent lack of ovulation and/or estrogen andprogesterone production by the ovaries. Thetiming of the release of these pituitary hormones,as well as of estrogen and progesterone, is whatdetermines a normal, regular menstrual cycle.This timing can be adversely affected by stress,and by the same token, the timing can beimproved by stress reduction. A third hormoneproduced by the pituitary, prolactin, also plays animportant role in the menstrual cycle. Increased


production of prolactin can inhibit the matura-tion of ovarian follicles and induce menstrualabnormalities and sterility. Prolactin release isoften stress related.

Nutrition

Consume a whole foods diet rich in whole grains,fruits, vegetables, legumes, quality cooking oils(canola and olive), nuts, and seeds. Emphasizefish high in omega-3 oils (salmon, tuna, sardines,halibut, mackerel, herring) and reduce saturatedanimal fats (beef, chicken, butter, cheese) to pro-mote the preferred prostaglandin pathways thatare discussed in Chapters 9 and 13 (in the discus-sions of heart disease and menstrual cramps).These preferred prostaglandins will reduceinflammation and may thereby help to reduceheavy and profuse menstrual flows.

Foods high in iron in particular should beincorporated into the general diet when heavyblood loss persists on a monthly basis. Refinedbreads and cereals are the single greatest nutri-tional contributor to iron-deficiency anemia.Although we do have iron “enriched” flour, it hasonly about one-third the iron content of wholewheat flour. Brewer’s yeast and wheat germ areboth excellent sources of iron, supplying about18 and 8 mg respectively per half cup. Blackstrapmolasses is not only one of the richest sources ofiron but also of many other minerals. It suppliesabout 9 mg of iron per tablespoon; dark unre-fined molasses contains 1.5 mg of iron per table-spoon, and sugar, none. Single foods high in ironprobably cannot surpass the amount found inliver and kidneys. However, I do not recommendthese because it is very difficult to get organicproducts, and these organs accumulate manymetabolic wastes. Apricots and eggs are alsorather high in iron. We often think of dark greenleafy vegetables as high in iron, but iron is diffi-cult to absorb in this form. Foods such as yogurtthat contain Lactobacillus acidophilus and sourfruits and citrus juices aid in the absorption ofiron because of their high vitamin C content.

Two foods stand out in their ability to regulatethe menstrual cycle: flaxseed and soy protein.Flaxseed contains a group of phytoestrogenscalled lignans that have been shown to haveweakly estrogenic and antiestrogenic properties.Two specific lignans, enterodiol and enterolac-tone, are absorbed after formation in the intes-tinal tract from plant precursors particularlyabundant in flaxseed.

The ingestion of flaxseed powder and its effecton the menstrual cycle was studied in 18 normallycycling women.1 Each woman consumed herusual omnivorous, low-fiber diet for three cyclesand her usual diet supplemented with 10 gramsper day of flaxseed for another three cycles. Allwomen were instructed to avoid soy foods. Thesecond and third flax cycles were compared to thesecond and third control diet cycles. Threenonovulatory cycles occurred among the 18women during the control diet (36 total cycles)compared to none during the 36 flaxseed cycles.The ovulatory flax cycles were consistently associ-ated with about one more day in the luteal phase(second half of the cycle) when compared to theovulatory non-flax cycles. Only one day longerbefore you bleed and a slight increase in thenumber of ovulations may not seem like much.However, over a period of months and years, thecumulative effect not only has implications forregulating the menstrual cycle but may also play apositive role in reducing the risk of breast andother hormonally dependent cancers.

The influence of a diet containing soy proteinon the length of the menstrual cycle in pre-menopausal women has also been studied.2 Sixtygrams of soy protein containing 45 mg ofisoflavones (a phytoestrogen compound found inhigh amounts in soy; see Table 1.1) was givendaily for one month in a study lasting ninemonths. A significant increase in the length ofthe follicular phase (first half of the menstrualcycle) by an average of 2.5 days and/or delayedmenstruation was observed in the six womenwho consumed the soy protein. Again, as with


flaxseed, soy protein has a role not only in con-tributing to the regularity and lengthening of themenstrual cycle, but adding 2.5 days per monthand lengthening the number of days from onemenses to another may in part contribute to alower incidence of breast cancer.3

Nutritional Supplements

Vitamin A. A deficiency of vitamin A maycontribute to menorrhagia in adult women. Vit-amin A deficiency impairs enzyme activity andhormone production in the ovaries of animals,4

and serum levels of vitamin A have been foundto be lower in women with menorrhagia than inhealthy women.5 In the latter study, vitamin Awas used as a treatment in 40 women who haddiagnosed menorrhagia as a result of a diversearray of causes. In the group who received60,000 IU of vitamin A for 35 days, menstrua-tion returned to normal in 23 women (57.5 per-cent) for a period of at least three months. Asignificant decrease in the amount of blood or areduction in the duration of the menses or bothwas obtained in 14 women (35 percent). Thevitamin A was ineffective in 3 of the 40 women(7.5 percent). The overall result with vitamin A

therapy showed that 92.5 percent of the 40 casesof menorrhagia were cured or alleviated.

It is important to understand that 60,000 IUof vitamin A given for long periods of time couldlead to vitamin A toxicity, but generally thiswould only occur if doses in excess of 50,000 IUwere used for several years. Smaller doses mayproduce toxicity symptoms if there are problemsin storage and transport of vitamin A. Theseproblems are generally found only in people withcirrhosis of the liver, hepatitis, or malnutritionand in children and adolescents. However, for aperiod of only one month, as in this study, vita-min A toxicity is of virtually no concern, and Iwould not hesitate to use it for this amount oftime, or up to three months. Using lower dosesof 25,000 IU for longer periods of time shouldbe considered in those cases where ongoing treat-ment is necessary to control menorrhagia.

Vitamin A

60,000 IU per day for 1–3 months10,000–25,000 IU ongoing, if necessary, but be aware

of potential increase in urinary calcium loss

Note: Vitamin E improves vitamin A storageand utilization, and zinc is required to mobilizevitamin A. A deficiency of zinc, vitamin C, pro-tein, or thyroid hormone may impair the conver-sion of carotenes to vitamin A. Provitamin Acarotenes such as beta-carotene require thesenutrients for their conversion to vitamin A.

B Complex. There may be a correlationbetween a nutritional deficiency of vitamin Bcomplex and menorrhagia and metrorrhagia. Ithas been shown that the liver loses its ability toinactivate estrogen in vitamin B-complex defi-ciency. We know that some cases of heavy mensesand intermenstrual bleeding are due to an excessof estrogen. Therefore, supplementing with acomplex of B vitamins may restore the propermetabolism of estrogen and thus have a role intreating DUB. A study done over 50 years ago

Table 1.1 Isoflavone Content of Soybeans

Serving IsoflavonesFood Size (mg)

Textured soy protein granules 1⁄4 cup 62

Nutlettes breakfast cereal 1⁄4 cup 61

Roasted soy nuts 1⁄4 cup 60

Tempeh 1⁄2 cup 35

Tofu, low-fat and regular 1⁄2 cup 35

Soy beverage powders (varies with manufacturer) 1–2 scoops 20–50

Regular soy milk 1 cup 30

Low-fat soy milk 1 cup 20

Roasted soy butter 2 tbsp 17


was undertaken to determine if the B-complexvitamins were effective in the treatment of thesemenstrual conditions. Although the study, donein the 1940s, was not up to today’s scientificstandards, a series of consecutive cases showedthat a B-complex preparation was effective in“prompt” improvement in both menorrhagia andmetrorrhagia.6 The B-complex preparations usedorally in the study were usually given in dailydoses providing 3 to 9 mg of thiamin, 4.5 to 9mg of riboflavin, and up to 60 mg of niacin.

Vitamin B-100 Complex

1–2 capsules daily of a B-100 combination

Vitamin K. Vitamin K deficiency is prettyrare, but its role in the manufacture of clotting fac-tors like prothrombin and clotting factors VII, IX,and X has obvious implications for women withheavy or prolonged menses.7 Even when the causeof the excessive bleeding is not a clotting disorder,it may be prudent to use vitamin K as part of acomprehensive treatment plan. Fat-soluble chloro-phyll is a good source of vitamin K and is found infresh green juices. Consider increasing the intakeof green leafy vegetables and/or supplementingwith 150 to 500 mcg per day of vitamin K.

Vitamin K

150–500 mcg per day

Vitamin C. Vitamin C helps to reduce heavybleeding by strengthening the capillaries. In atleast one study, vitamin C was able to reduceheavy bleeding in 87 percent of the women.8 Vit-amin C also is an important supplement forwomen who have acquired iron-deficiency anemiafrom menstrual blood loss. It helps to increase ironabsorption and can be used to prevent anemia aswell as to treat it.

Vitamin C

2,000–4,000 mg per day

Bioflavonoids. Like vitamin C, bioflavonoidshave demonstrated a significant ability to reduceheavy menstrual bleeding by strengthening thevessel walls of the capillaries in women with men-orrhagia.8 Bioflavonoids also can have an anti-estrogen effect on the uterus by occupying the estrogen receptor sites and thus limiting the estrogen-stimulating effect on the endometrium.This can help to reduce bleeding. Just as conven-tional medicine prescribes nonsteroidal anti-inflammatories to reduce heavy bleeding, alterna-tive medicine has natural anti-inflammatories suchas bioflavonoids that can be used for the same pur-pose. Foods high in bioflavonoids (and vitamin C)include grape skins, cherries, blackberries, blueber-ries, and the pulp and white rind of citrus fruits.

Bioflavonoids

1,000–2,000 mg per day

Botanicals

Chaste Tree (Vitex Agnus Castus). Chastetree is probably the best-known herb in all ofEurope for hormonal imbalances in women.Since at least the time of the Greeks, chaste treehas been used for the full scope of menstrual dis-orders: heavy menses, lack of ovulation, frequentand infrequent menses, irregular menses, and acomplete lack of menses. Chaste tree has beenrepeatedly studied in Germany. Although thefruit was used traditionally, it is the seeds that aremainly used for medicine in Europe and in thiscountry. Consequently, most of the testing hasbeen done on the seeds. Chaste tree acts on thehypothalamus and pituitary glands. It increasesLH production and mildly inhibits the release ofFSH. The result is a shift in the ratio of estrogento progesterone and consequently a “progesterone-like” effect.9 The ability of chaste tree to raiseprogesterone levels is an indirect effect and not adirect hormonal action.10 Chaste tree has alsobeen shown to inhibit prolactin release by thepituitary gland, particularly under stress.11


The first major study on chaste tree was pub-lished in 1954,12 proving the herb’s effectivenessfor patients with cystic hyperplasia (excessive pro-liferation of the endometrium). Although thiscondition is not technically DUB, it is impressivethat chaste tree was able to bring about enough ofa progesterone effect to reduce the hyperplasia. Ina separate study, 126 women with menstrual dis-orders took 15 drops of a chaste tree liquid extractthree times daily over several menstrual cycles.13 In33 women who had frequent menses (polymenor-rhea), the duration between periods lengthenedfrom an average of 20.1 days to 26.3 days. In 58patients with excessive bleeding (menorrhagia),the number of heavy bleeding days was decreased.

As mentioned earlier, chaste tree has an abilityto inhibit prolactin production. A double-blind,placebo-controlled study done in 2005 was able toexamine the effect of a chaste tree preparation on52 women with luteal phase defects due to elevated prolactin levels.14 The dose given was 20 mg chaste tree extract daily for three months.After three months of treatment, prolactin releasewas significantly reduced in those taking chastetree. The shortened luteal phase was normalized as was the decrease in progesterone production. In another study examining the pharmacology of vitex (another term for chaste tree), serum prolactin levels were reduced via vitex’s natural prolactin-suppressive compounds, namely diter-penes. These diterpenes have dopaminergic prop-erties and bind to the DA2-receptor protein,which, in turn, suppressed prolactin release.15

Chaste tree is the most important herb to nor-malize and regulate the menstrual cycle. Chastetree is not a fast-acting herb; do not hesitate to useit over a long period of time. In fact, results maynot be achieved until after four to six months. It isnot an herb to be relied on for immediate relief,and it will not be effective in reducing semi-acutebleeding episodes. Human and animal studieshave determined chaste tree to be safe for mostmenstruating women. It is not recommendedduring pregnancy, although this is not an absolute

contraindication, and women should not worry ifthey become pregnant while taking chaste tree forthe first trimester. Chaste tree is completely safeduring lactation, and there are no known interac-tions with other drugs, but theoretically, it mightinterfere with dopaminergic antagonists. Mini-mal, reversible side effects have included itching,occasional rash, nausea, headache, gastrointestinaldisturbance, menstrual disorders, acne, and possi-bly a lowered libido.16

Note: Aucubin and agnuside are differentmarker compounds found in chaste tree, used tostandardize the product to assure an effective dose.

Chaste Tree

30–60 drops liquid extract or 215 mg .6% aucubinstandardized extract or 175 mg .75% agnuside stan-dardized extract per day

Ginger (Zingiber Officinale). Ginger hasbeen shown to inhibit prostaglandin synthetase17

and cyclooxygenase-2 (COX-2)18 enzymes believedto be related to the altered prostaglandin-2 ratioassociated with excessive menstrual loss.19 Pro-staglandins are hormone-like substances, and anexcess of prostaglandin 2s can cause increased painand inflammation. The most potent constituentappears to be gingerol, the pungent ingredient inthe ginger. Inhibition of prostaglandin andleukotriene formation could explain ginger’s tradi-tional use as an anti-inflammatory agent, and anti-inflammatories are effective in reducing the flowfrom heavy and protracted menses.

Ginger

1–4 g dry powder per day for semi-acute blood loss orginger root extract (5%) gingerols 100 mg per day

Dietary Kelp or Bladderwrack (FucusVesiculosus). A very small study of three womendemonstrated that dietary kelp may be effective innormalizing DUB by decreasing 17 beta-estradiol(one of the estrogens the body naturally produces)and increasing progesterone. These pilot data sug-


gest that dietary bladderwrack may prolong thelength of the menstrual cycle and exert anti-estrogenic effects in premenopausal women.20

Traditional Astringent Herbs. Astringentherbs form a large category of tannin-containingplants that are used to reduce blood loss from the reproductive tract as well as from the bowel,stomach, respiratory tract, and skin. In the repro-ductive tract, the astringent herbs are used to correct uterine or cervical bleeding. The astrin-gents most effective in uterine blood loss areoften high in tannins, but other constituents alsoexplain their mechanism of action. The followingherbs are the major astringent and hemostaticherbs used in gynecological problems:

With Tannins• Yarrow (Achillea millefolium)• Ladies’ mantle (Alchemilla vulgaris)• Cranesbill (Geranium maculatum)• Beth root (Trillium erectum)• Greater periwinkle (Vinca major)

Cranesbill. This astringent herb, high intannic acid, was relied on by early American Indi-ans to treat diarrhea, dysentery, leukorrhea, andchronic menorrhagia, especially cases of prolongedbleeding. Cranesbill was used by early practition-ers of natural medicine (the eclectic physicians) toachieve prompt and predictable results in cases ofmenorrhagia without any unpleasant side effects.

Without Tannins• Horsetail (Equisetum arvense)• Goldenseal (Hydrastis canadensis)• Shepherd’s purse (Capsella bursa-pastoris)

Shepherd’s Purse. Shepherd’s purse is a mildastringent that contains saponins, choline, acetyl-choline, and tyramine, all likely to be helpful infemale reproductive health.21 Chemical analysisshows that it can coagulate blood.22 Its best use isin combination with other astringent and hemo-static herbs for uterine bleeding, particularly whenthere is extremely heavy flow. Shepherd’s purse is

a good choice for both semi-acute situations andchronic recurring episodes of DUB.

Uterine Tonics. In traditional herbal medi-cine, uterine tone determines the ease of menstrualflow. If the uterus is hypertonic, then it may be dif-ficult to initiate menses in a timely manner. If theuterus is hypotonic, there may be heavy bleeding.In either case, improving uterine tone will tend tonormalize and regulate menstrual bleeding. Twocategories of herbs are said to have the most effecton uterine tone and therefore bleeding.

Tonics That Regulate Uterine Tone. The fol-lowing are uterine tonics or amphoterics that reg-ulate tone (both reduce excess tone and increasetone in states of laxity):

• Dong quai (Angelica sinensis): potent antico-agulant and hemostatic effects via plateletaggregation23

• Blue cohosh (Caulophyllum thalictroides)• Helonias (Chamaelirium luteum)• Squaw vine (Mitchella repens)• Raspberry leaves (Rubus idaeus)• Life root (Senecio aureus)

Life root, also known as ragwort, is a time-honored “female regulator” that has been usedconsistently in traditional herbal medicine formenstrual cramps, menorrhagia, suppressed men-struation, and other disturbances of the reproduc-tive tract. It is a classic uterine tonic that has beenused to tonify a soft, less-than-firm uterus, includ-ing laxity of the uterine ligaments. It adds toneand structure to the nervous and muscular struc-tures of the reproductive female organs and regu-lates the quantity of the monthly flow.

Tonics That Stimulate Menstrual Flow. Thefollowing are uterine stimulants or emmenagogues(agents that stimulate menstrual flow) thatincrease tone or muscular activity and serve to ini-tiate the onset of menses:

• Squaw vine (Mitchella repens)• Yarrow (Achillea millefolium)


• Chaste tree (Vitex agnus castus)• Pennyroyal* (Mentha pulegium)• Mugwort (Artemisia vulgaris)• Blue cohosh (Caulophyllum thalictroides)

Blue cohosh is a perennial herb that grows all over the United States, and it is the root orrhizome that is used medicinally. The chemicalconstituents include alkaloids, saponins, phyto-sterols, and many minerals. As an emmenagoguethat promotes the onset of menstrual flow, itwould seem odd to use it as a treatment for men-orrhagia. Yet, traditionally, blue cohosh, whenused with other astringent herbs, acts as a uterinetonic and in fact helps to regulate the menses andthe amount of flow.

Astringent and uterine tonic herbs can beused in combination formulations and used forweeks to several months. Use as a tea, liquidextract, or powdered capsule.

Traditional Herbs for Semi-Acute and Acute Blood Loss• Cinnamon* (Cinnamomum verum)• Life root (Senecio aureus)• Canadian fleabane* (Erigeron canadensis)• Greater periwinkle (Vinca major)• Shepherd’s purse (Capsella bursa-pastoris)• Yarrow (Achillea millefolium)• Savin (Sabina officinalis)

Bio-Identical Hormones

Bio-identical hormones are made in a manufactur-ing laboratory and are derived from a compoundfound in either Mexican wild yam root or soy-beans. The diosgenin plant compound from Mex-ican wild yam or beta-sitosterol from soybeans isextracted from the plant and then used to make ahormone, in this case progesterone, that is bio-chemically identical to the progesterone in awoman’s body. Sometimes these are called naturalhormones, and other times they are called bio-identical hormones.

Natural Progesterone. Cyclic bio-identicalor natural progesterone that is given 12 days outof the month (usually day 15 of the cycle to day26) can be used to correct infrequent menses,heavy menses, and sometimes intermenstrualbleeding. This therapy substitutes for what thebody is not producing due to the lack of ovula-tion. A woman must ovulate in order to produceadequate levels of progesterone. Because naturalprogesterone is biochemically identical to human

Dosage for Botanicals

The herbs listed in the text with an asterisk (*) maybe toxic if given in inappropriate doses, so correctdosing is very important. Use a botanical reference toassure safe dosage.

Essential oil of cinnamon: 1–5 drops every 3–4hours

Other herbs: Do not exceed 20 drops every 2 hoursor 1 capsule every 4 hours if using a single herb.Several herbs may be used in combination, and inthese cases it is important to consult a referencebook or an herbal practitioner to know the doselimitations.

*May be toxic if given in inappropriate doses. See the dosageguidelines in this section.

Natural Bio-Identical Progesterone

A dose of 200 mg is thought to be adequate to regu-late abnormal bleeding. Natural progesterone is sev-eral times less potent than a progestin (a syntheticsubstance). Even 400 mg per day of oral micronizedprogesterone may not work as well as 10 mg ofmedroxyprogesterone acetate (Provera).

Oral dosage: 100–200 mg twice daily, given 7 to 12days per month for infrequent menses, menorrha-gia, and, occasionally, intermenstrual bleeding

Cream dosage: (product that contains at least 400mg progesterone per ounce) 1⁄4–1⁄2 tsp twice dailyfor 12 to 21 days per month for cases of mild men-orrhagia, infrequent menses, and, occasionally,intermenstrual bleeding

Sublingual tablets: 50–75 mg twice daily for 12 to21 days per month for cases of mild menorrhagia


progesterone, it is generally very well tolerated bywomen. One study found that while traditionalprogestin treatments such as norethindrone candecrease estradiol, follicle-stimulating hormone,luteinizing hormone, sex-hormone-bindingglobulin, and high-density lipoprotein choles-terol, bio-identical progesterone offers the hor-monal benefits without these side effects and is a

viable alternative therapy in premenopausalbleeding disorders.24 You may want to read muchmore on bio-identical hormones in Chapter 12.

The disadvantages to the natural hormoneinclude a short half-life (three to six hours) thatrequires giving it two to three times a day. Naturalprogesterone can be delivered by injection, sub-lingual tablets, rectal or vaginal suppositories, oral

Sample Treatment Plans for Abnormal Uterine Bleeding

See the Resources section for formulation sources.

Chronic Recurring Menorrhagia• Bioflavonoids: 1,000 mg twice per day• Vitamin A: 60,000 IU per day up to 3 months• Chaste tree (standardized extract): 175 mg per

day, or 1 tsp daily• Combination herbal product using astringents

and uterine tonics; sample herbal tincture:

Yarrow: 2 ozHelonias: 2 ozSquaw vine: 2 ozLife root: 2 oz1 tsp twice daily

• Consider natural progesterone cream, 1⁄4–1⁄2 tsptwice daily, days 15–26 (day 1 is the first dayof your menses)

Semi-Acute Menorrhagia

• Bioflavonoids: 1,000 mg 2–3 times daily• Combination herbal products using astringents

and uterine tonics; sample herbal tincture:

Yarrow: 2 ozGreater periwinkle: 2 ozShepherd’s purse: 2 ozLife root: 2 oz20–30 drops every 2–3 hours

If you choose to use one of the more toxicherbs, such as cinnamon or beth root, be surenot to exceed recommended doses.

• Essential oil of cinnamon: 1–5 drops every 3–4hours

• Oral micronized progesterone: 200–400 mg perday for 7–12 days, followed by a cyclic hor-mone product for 21 days on and 7 days off

• If there is no change in 24 to 48 hours, high-dose estrogens may be needed to stop theimmediate bleeding, followed by a proges-terone regimen.

Oligomenorrhea (Infrequent Menses)

• Chaste tree: .6–.75% standardized extract, one175–215 mg capsule daily; or liquid extract, 1tsp daily

• Combination herbal emmenagogue:

Squaw vine: 11⁄2 ozYarrow: 1 ozBlue cohosh: 1 ozPennyroyal: 1⁄2 oz20 drops every 2–3 hours

• Natural progesterone cream

Apply 1⁄4 tsp 1–2 times daily, days 7–14 of cycleApply 1⁄2 tsp 1–2 times daily, days 15–26

Polymenorrhea (Frequent Menses)

• Chaste tree: .6–.75% standardized extract, one 175–215 mg capsule daily; or liquidextract, 1 tsp daily

• Natural progesterone cream: 1⁄4–1⁄2 tsp twicedaily, 21 days on, 7 days off (during menstrualflow)

• Some cases may require higher doses of oralmicronized progesterone.

• Some cases may require a naturalestrogen/natural progesterone formulation thatrequires more individualized dosing.


capsules or tablets, and topical creams. Dosing isdependent on the delivery system and the charac-teristic bleeding problems. When treating womenwith DUB, the amount of progesterone givenmust be adequate to convert the endometrium forcomplete sloughing to avoid endometrial hyper-plasia. Continuous progesterone can be effectivein controlling menorrhagia.

Natural Estradiol. To control an acute bleed-ing episode, the use of natural estradiol should bejust as effective as one of the dosing regimens ofconjugated estrogens. These hormones are pre-scription items and should be administered by apractitioner qualified to use them. One high-doseregimen would be 2 mg of estradiol every fourhours for 24 hours, a single daily dose for 7 to 10days, followed by oral micronized progesterone,200 mg per day for 7 to 12 days.

CONVENTIONAL MEDICINE APPROACH

The goals of conventional treatment for abnor-mal uterine bleeding are to control bleeding, pre-vent endometrial hyperplasia or cancer, preventor treat anemia, and restore quality of life. Whenthe diagnosis is definitely DUB, it is preferable touse medical, not surgical, treatments.

To control an acute bleeding episode, 10 mg oforal conjugated estrogens (or the equivalent)administered daily as 2.5 mg four times per day areusually effective. If bleeding is not controlledwithin the first 24 hours, higher doses (20 mg) maybe effective. Once the bleeding has stopped, oralestrogen therapy is continued at the same dosagefor a total of 21 days; the addition of a progestin,such as medroxyprogesterone acetate (MPA), 10mg daily, should be added for the last 7 to 10 daysof those 21 days. Alternatively, 200 to 400 mgdaily of progesterone may be substituted for theMPA. At the end of 21 days, both hormones arestopped, at which time the patient should expect alight “withdrawal” bleed. At this time, a strategy forlong-term management should be developed.

Oral contraceptives containing estrogen andprogestin are also used to stop acute bleeding,although they may not be as effective as the highdoses of estrogen alone. Three tablets of an oralcontraceptive containing a progestin plus 35 mcgof estrogen taken every 24 hours (one tabletevery eight hours) will usually provide sufficientestrogen to stop acute bleeding while simultane-ously providing progestin. Treatment is contin-ued for at least one week after the bleeding stops.The practitioner can choose from a variety ofequally effective treatment regimens.

The treatment of choice for chronic, stableanovulatory bleeding is a progestogen medication.Use either MPA or norethindrone (NE) in dosesof 5 to 10 mg daily or oral micronized proges-terone (either compounded or Prometrium) 200to 400 mg daily for 14 days starting on day 14 ofthe menstrual cycle. The patient can stop the med-ications if she has begun menstruating before theend of her progestogen.

Nonsteroidal anti-inflammatory drugs(NSAIDs) are also used to reduce blood loss,especially in women who have DUB but still havenormal ovulation. When NSAIDs are taken duringthe episode of menorrhagia, the effect is a 20 to 50percent reduction in blood loss. The followinganti-inflammatories are usually given for the firstthree days of menses, or throughout the menstrualflow, and seem to have similar effects:

1. Ibuprofen: 600 mg every 6–8 hours2. Naproxen sodium: 550 mg every 6–8 hours3. Mefenamic acid: 500 mg first dose, then

250 mg every 8 hours4. Meclofenamate sodium: 100 mg every 8

hours5. Naproxen: 500 mg every 12 hours

NSAIDs may be used alone in some cases orcombined with an oral contraceptive or proges-togen. Other, more sophisticated medical regi-mens may be used to intervene, including GnRHagonists (Lupron), androgenic steroids (danazol),


or an antifibrinolytic agent. However, theseoptions have significant side effects, and their useis limited to women who fail to respond to othermethods of drug management and who do notwant surgery.

Progesterone-releasing IUDs (Mirena) aregaining interest because of their lack of systemicside effects, duration of action of five years, and 60 to 80 percent reduction in menstrual bloodflow. They also can suppress the growth of theendometrium in oligo-ovulatory patients, therebypreventing hyperplasia or uterine cancer.

There are basically three surgical options thatmay be considered in individual cases: dilationand curettage (D&C), endometrial ablation, orhysterectomy.

1. Dilation and curettage (D&C) can be bothdiagnostic and therapeutic. A D&C is thequickest way to stop bleeding; therefore, it is atreatment of choice in women with DUB whosuffer from anemia due to heavy menstrualblood loss or who are acutely unstable. Theproblem with a D&C is that it is only tempo-rary in most cases and does not cure the prob-lem the majority of the time. One advantage,though, is that it can give the doctor tissue fordiagnosis.2. Endometrial ablation is a procedure to

destroy the endometrial tissue. It is highly pop-ular because of the ease of treatment, the suc-cess, and the low incidence of complications.There are several types of ablations now: theoriginal roller ball or loop unipolar resection, abipolar electrical vaporization method, a bipolarelectrical mesh, a balloon filled with dextrosewater that is heated to 200 degrees Fahrenheit,free-flowing hot water, and a microwave andcryo probe technology as well. The methodused depends on practitioner preference andselect uterine characteristics. All ablationsrequire IV sedation or general anesthesia andmay not be well tolerated in an office setting

because of the pain of the procedure. Ablationtechnology continues to advance with the hopesof developing a procedure that can be done inthe office.3. Hysterectomy, surgical removal of the

uterus, should be reserved for the woman withother indications for hysterectomy such as uter-ine fibroids, uterine prolapse, or atypical hyper-plasia. When a hysterectomy is done forbleeding problems there is usually no need toremove the ovaries.

SEEING A LICENSED PRIMARYHEALTH-CARE PRACTITIONER(N.D. , M.D. , D.O. , N.P. , P.A. )

Changes in the pattern or amount of menstrualblood flow is one of the most common health con-cerns of women. Even though many of these casesare of no serious concern, a woman with abnormalbleeding distinctly different from her familiar his-tory should do the cautious thing and be seen bya licensed health-care practitioner such as a natur-opathic doctor (N.D.), medical doctor (M.D.),osteopathic doctor (D.O.), nurse-practitioner(N.P.), or physician’s assistant (P.A.). After a thor-ough medical history is taken, a physical exam and further laboratory testing and imaging may be requested not only to adequately diagnose thecause of the problem but also to determine ifexcessive blood loss has caused an anemic state.

The most worrisome situation is an acutebleeding episode. As stated earlier, bleeding thatmeets or exceeds saturation of a super tampon orheavy pad every hour for six to eight hours ormore requires medical intervention. Bleedingthat is even more severe will require immediatemedical attention to assess the need for a surgicalintervention and management of the dangers ofacute blood loss.

A licensed naturopathic physician may workin tandem with conventional medical colleaguesto cooperate on an integrated approach to opti-mize the patient outcome.

15

OVERVIEW

Traditionally, amenorrhea (absence of menstrualbleeding) has been classified as either primary orsecondary. Primary amenorrhea means that novaginal bleeding has ever occurred by the time ofexpected initial onset (usually age 16). Secondaryamenorrhea means that vaginal bleeding has pre-viously occurred but has now ceased—for threemonths in a woman with a history of regularcyclic bleeding or for six months in a womanwith a history of irregular periods. In the UnitedStates, females normally experience the onset oftheir first menstrual period between the ages of 9 and 18. It has been estimated that the prevalenceof amenorrhea in the general U.S. female popula-tion during the reproductive years is 1.8 to 3 percent, the prevalence in college-aged women is2.6 to 5 percent, and amenorrhea may be seen in20 percent of women reporting infertility.

Determining the cause of amenorrhea is one ofthe most challenging tasks in gynecology. Causesof amenorrhea can be organized into four classifi-cations: disorders of the vagina or uterus, disordersof the ovary, disorders of the anterior pituitarygland, and disorders of the central nervous system.The causes of primary amenorrhea are often verycomplex, and approximately 40 percent of all casesare due to a chromosomal defect. Absence of avagina is the second-most-common cause, fol-lowed by testicular feminization syndrome. Othercauses of primary and secondary amenorrhea areoften overlapping.

The majority of amenorrheic young womenhave very low levels of estrogen, and a minoritywill have subnormal, noncyclic estrogen levelswithout progesterone due to a lack of ovulation.This distinction is important in considering thelong-term implications of amenorrhea. Amenor-

rhea caused by low levels of estrogen, or hypo-estrogenic amenorrhea, is associated with loss ofbone mineral density and an increased risk laterin life of osteoporosis and fractures. Lipid levelsin the bloodstream are also negatively affected byprolonged hypoestrogenic states, and this is asso-ciated with an increased risk of cardiovasculardisease. Amenorrhea without ovulation is associ-ated with an increased risk of endometrial hyper-plasia and uterine cancer because of the lack ofprogesterone and the presence of what is called an “unopposed” estrogen state. Polycystic ovariansyndrome (PCOS) is an example of this type of amenorrhea. Characteristics of PCOS includeobesity, hirsutism (abnormal hair growth), acne,infertility, hypertension, and diabetes.

Evaluating and managing amenorrhea is bestaddressed with the medical knowledge of a quali-fied primary care practitioner. Sometimes a spe-cialist in endocrinology is necessary, to rule out orconsider an array of potential diseases and disor-ders of the hypothalamus, pituitary gland, ovaries,thyroid, and/or uterus.

THE NORMAL MENSTRUAL CYCLE

Normal menstruation results from a complex chainof events initiated in the central nervous system:

1. The hypothalamus secretes gonadotropin-releasing hormone (GnRH) that regulatespituitary function.

2. The anterior pituitary produces luteinizinghormone (LH) and follicle-stimulating hor-mone (FSH) that govern ovarian function.The main action of LH is to stimulate syn-thesis of androgens by the theca cells in theovary and progesterone synthesis by thecorpus luteum. LH also induces ovulation,

2A M E N O R R H E A C H A P T E R



which leaves behind the corpus luteum. Theprimary action of FSH is to stimulate thegranulosa cells in the ovary to produce estro-gen. Both the theca cells and the granulosacells are sources of androgens (such as testos-terone) and estrogen.

3. The ovaries respond to these gonadotropinsby synthesizing the steroid hormones estradioland progesterone that affect uterine function.

4. The uterus has a cavity capable of endome-trial thickening and shedding according tothe levels of ovarian hormones in the blood(estrogen and progesterone), and an outflowtract (vagina) to allow the emptying of men-strual flow.

Phases of the Menstrual Cycle

The menstrual cycle can best be broken intothree phases.

1. Menstrual phase (menstruation): days 1–5• Estrogen and progesterone withdrawn

before onset of menstrual flow• Shedding of endometrial lining

2. Proliferative (follicular) phase: days 6–14• Regrowth of endometrial tissue• Secretion of FSH by the pituitary gland• Development in ovary of a mature

graafian follicle containing a mature egg• Secretion of increasing amounts of estro-

gen by graafian follicle• Suppression of FSH when estrogen level

becomes high, leading to secretion of LHby pituitary gland

3. Secretory (luteal) phase: days 15–28• Rupture of graafian follicle releasing egg

(ovulation) starts the secretory phase• Movement of egg through fallopian tube

to uterus• Formation of corpus luteum at site of rup-

tured follicle• Production of progesterone by corpus

luteum• Stimulation by progesterone of endome-

trial cell growth• Significant decrease in progesterone level if

implantation does not occur; menstrualphase then begins again

Figure 2.1 Normal Menstrual Cycle

FSH &LHIU/L

20 500 10

18 9

16 400 8

14 7

12 300 6

10 5

8 200 4

6 3

4 100 2

2 4 6 8 10 12 14 16 18 20 22 24 26 28

2 1

0 0 0

Estradiolpg/nl

Estradiol

Progesterone17-OHPng/ml

FSH

LH Progesterone

OvulationMenses

17-OH Progesterone

17A M E N O R R H E A

DIAGNOSING AND EVALUATING AMENORRHEA

A good history is the most important part of themedical evaluation to diagnose amenorrhea. Thehistory will include evaluating for pregnancy, men-strual history, emotional stress, weight gain or loss, alcohol use or abuse, dietary habits, exercisehabits, medications, narcotics, drug abuse, acute orchronic illnesses, accidents or injuries, infertility,metabolic disease, immune system abnormalities,tuberculosis, hot flashes, breast discharge, head-aches, and family history.

A physical and pelvic exam will confirm themost likely causes as suggested by the history.During the pelvic exam, the practitioner willattempt to determine if there is an adequate estro-gen effect on the cervix and vagina, check for thesize of the ovaries, assure the normalcy of theuterus and vagina, and observe for the presence orabsence of secondary sex characteristics (such asbreasts and pubic hair). The thyroid gland will alsobe checked, and laboratory tests will be chosenselectively to document the suspected diagnosis.

Due to the complexity of amenorrhea and thediverse array of causes, it is impossible to address each potential cause in this chapter. The guiding

rule in the management of amenorrhea is to diag-nose before treating. The appropriate manage-ment depends not only on the diagnosis but alsoon the presenting problem. Each woman mustthen be treated according to the specific causativefactors involved. Consequently, in the discussionof alternative treatment, we will largely focus onfour of the most common causes of amenorrhea:

1. Hypergonadotropic hypogonadism. Thepituitary secretes elevated amounts of its hor-mones, but the ovary does not respond. Exam-ple: premature ovarian failure.2. Hyperprolactinemia. The pituitary secretes

too much prolactin. Examples: certain drugs,pituitary tumors, hypothyroid disease.3. Hypogonadotropic hypogonadism.

Reduced secretion of FSH and LH that resultsin failure of the ovarian follicle to develop and,

KEY CONCEPTS

• Successful management of amenorrhea dependson an accurate diagnosis.

• Amenorrhea is a symptom, not a diagnosis.• The absence of menses in itself has no deleteri-

ous effect on health, but it may be a presentingsymptom of an underlying disorder that requirestreatment.

• A licensed primary health-care practitioner isneeded to conduct a careful history, examina-tion, and indicated tests.

• The most common cause of secondary amenor-rhea is pregnancy.

• Prolonged amenorrhea that is hypoestrogenic(hypergonadotropic hypogonadism or hypogo-nadotropic hypogonadism) prior to menopause isa risk factor for osteoporosis.

PREVENTION

• Have adequate calories in the diet.• Include adequate levels of dietary fat.• Keep regular daily eating habits.• Avoid being underweight.• Avoid obesity.• Avoid excessive exercise.• Practice stress reduction and management.• Women with hypoestrogenic amenorrhea must be

vigilant about prevention of osteoporosis andcoronary artery disease.

• Women with anovulatory amenorrhea must bemonitored for endometrial thickening and thedevelopment of endometrial hyperplasia, a precancerous state, and endometrial cancer.

• Women who have been diagnosed with polycys-tic ovarian syndrome (PCOS), the normogo-nadotropic anovulation state, must not only betreated for current problems related to the PCOS,but they need assertive prevention for diseasesfor which they are at higher risk, including type 2 diabetes, high blood pressure, heart disease, endometrial cancer, and possibly breastcancer.


hence, a lack of secretion of estradiol by theovaries. Examples: psychological stress, weightloss, genetic diseases.4. Normogonadotropic anovulation. Normal

FSH and LH, but the cyclic nature of thepulsed secretions is disrupted. The ovarian folli-cles develop and estrogen is produced, but atsome stage the follicles do not fully mature.Thus, there is no ovulation but there is no signof estrogen deficiency; rather, there is a proges-terone deficiency. Example: polycystic ovarysyndrome.


A licensed alternative primary care practitionersuch as a naturopathic physician must first makean accurate diagnosis as to the cause of the amen-orrhea, utilizing a medical history, physical exam,and possible laboratory testing. Naturopathicphysicians often see patients who are on extremediets due to some other health concern; sometimesthese diets are inappropriate for that individualand are the cause of the amenorrhea. Insufficientcalories and insufficient dietary fat and cholesterolmay be the culprit in some of these cases. Otherhealth-conscious individuals may have becometoo thin with a combination of diet and exercise,and they may have acquired amenorrhea becausethey have too little body fat. It is unlikely thatoverexercise alone will cause amenorrhea; it usu-ally takes a combination of low body fat and heavyexercise to induce amenorrhea.

In other cases such as polycystic ovarian syn-drome (PCOS), about 50 to 60 percent of womenwill be overweight. In these cases, a 10 percentweight loss can lead to ovulation and also decreaseinsulin resistance. A diet lower in starchy carbs andhigher in healthy protein is an important strategyfor women with PCOS, whether they are over-weight or not.

A holistic approach to treatment requiresexploring the mental, spiritual, emotional, andphysical aspects of the patient integrated with a

meticulous medical approach employing mind-body-oriented perspectives. Specific dietarycounseling may be warranted, and practitionersmay find themselves in the unusual position ofadvocating an increase in cholesterol and otherfats in the diet and counseling patients to gainweight or exercise less. Because stress disrupts themenstrual cycle, it is also important to provideguidance about stress reduction.

The goal of a natural therapeutic treatmentplan for amenorrhea is to address the specificunderlying cause as would conventional medi-cine, while also taking a more constitutional andholistic approach to treatment. Even in caseswhere something specific such as an elevated pro-lactin level may be the cause, the practitionerwould want to address the mental and emotionalcomponent, support the digestion, provide toni-fying and nutritive support to the reproductivesystem in general, and more. This organ-specificas well as constitutional approach is a commontheme in many alternative medicine disciplines,and especially naturopathic medicine.

The natural therapies presented in this chap-ter deal with these four general states:

1. Premature ovarian failure (See Chapter 12for more in-depth information and treat-ment.)

2. Hyperprolactinemia3. Inadequate estrogen production4. Chronic lack of ovulation, including poly-

cystic ovary syndrome (PCOS)

Keep in mind that causes such as thyroid disor-ders, tumors, systemic diseases, genetic disorders,and others will require therapies to specificallyaddress those underlying problems, which arebeyond the scope of this book.

Nutrition

Both weight loss and obesity can be associatedwith amenorrhea. A range of weight-loss prob-lems are associated with amenorrhea, includingcrash diets, malnutrition, and life-threatening


anorexia nervosa. Anorexia nervosa occurs pri-marily in young white middle- to upper-classwomen under age 25, yet has also been known tooccur in young men and middle-aged women.The family situation of a young woman withanorexia is very often success-achievement-appearance oriented. The pattern usually startswith a diet to control weight and a fear of excessweight when in fact the weight being gained isdue to normal maturing. There is often a preoc-cupation with food that may manifest itself bylarge intakes of lettuce, raw vegetables, and otherlow-calorie foods. Other manifestations may bechaotic eating habits and eating times, radicaldiets, missed meals, and bingeing episodes.

Bulimia is a syndrome of episodic and secre-tive binge eating followed by self-induced vomit-ing, fasting, or the use of laxatives and diuretics.Bulimic behavior is frequently seen in about halfof women with anorexia nervosa. Body weight in“pure” bulimics fluctuates but does not fall to thelow levels seen in anorexics.

Teenagers with low body weight, amenorrhea,and overachievement (excellent grades and manyextracurricular activities) need astute evaluationfor an eating disorder. Psychological counseling,consistent support, and monitoring for calorieintake will be needed to break the established pat-terns. The earlier the recognition of the problem,the more successful the intervention. Familymembers, friends, and health-care practitionersshould pay particular attention to weight and dietin young women with amenorrhea.

Obese women exhibit several abnormalitiesin their hormone profile. Elevated serum concen-trations of androstenedione, testosterone, andDHEA-sulfate are associated more closely withthe pattern of fat distribution (abdominal vs.hips, in particular) than to the body fat mass.1

High levels of these hormones, called androgens,are known to be a cause of menstrual irregulari-ties including amenorrhea, hirsutism (abnormalbody hair growth), and other metabolic distur-bances. In addition, type 2 diabetes, elevated

insulin, and glucose intolerance, conditions thatoften co-occur with obesity and polycystic ovar-ian syndrome, are associated with amenorrheaand oligomenorrhea (infrequent menses).2, 3

Usually, oligomenorrhea and chronic anovula-tion caused by hormonal abnormalities is thecause of the menstrual irregularity in womenwith significant amounts of excess body fat.2 Areduction in body weight by reducing calories,increasing physical exercise, and possibly otherweight-management interventions will result inbeneficial changes in the hormonal profile,including a marked reduction of androgenic hor-mones and their effects.1 A reduction of weightby even as little as 5 to 10 percent can not onlyrestore regular menses, but also improve fertility.4

Some women may have low body weight but do not have an eating disorder or exercise-induced amenorrhea. This may be a metabolismissue, a hereditary factor, or a diet that is ex-tremely low in fat although not low in calories.Women who take in insufficient calories, such asstrict vegetarians who eat no animal products orothers with extreme diets, may have insufficientdietary fat and low cholesterol. Adequate choles-terol is needed to manufacture hormones. If nocholesterol is found in the diet and the liver isnot manufacturing adequate cholesterol, thesewomen may have amenorrhea due to insufficienthormone levels. Measuring the cholesterol levelcan be telling in such cases. If cholesterol is low(below 120), a change in vegetarian philosophywill probably be necessary so that some animalproducts can be included in the diet in order toraise the cholesterol levels.

Sometimes it is difficult to find the best nutri-tional program for one’s body type and lifestyle.In these cases, nutritional counseling and nutri-tional analysis with a qualified practitioner canbe very helpful. No one diet plan is right foreveryone. Not everyone needs to eat from all thefood groups, not everyone can be a vegetarian,and not everyone responds well to a high-proteinor high–complex carbohydrate diet.


In addition to proper food choices, anotherbasic general principle for good nutrition is reg-ularity. Just as going to bed and rising at regulartimes with a certain amount of sleep assures ade-quate energy and vitality, regular mealtimes andconsistency in eating habits lead to good diges-tion and absorption of nutrients necessary fornormal physiology.

Not all advice on nutritional habits forwomen with amenorrhea is related to dietary fat, calories, body weight, or eating disorders.Some nutritional guidance is relevant to the pre-vention of osteoporosis, a potential consequenceof amenorrhea. Please see Chapter 14 for moreinformation on preventing osteoporosis.

Supplements

Vitamin A and the Carotenes. Carotenemia,an abnormal elevation of plasma carotene levels,may result from an excessive ingestion of carotene-rich vegetables, anorexia, and impaired ability ofthe body to metabolize carotenes.5–7 Carotenemiahas been linked with menstrual dysfunction andamenorrhea in some women, generally in associa-tion with weight loss. In 1968, elevated carotenelevels were observed in 9 of 12 women withanorexia nervosa who did not ingest excessiveamounts of carotenes.8 An additional study alsofound that patients with amenorrhea and weightloss had carotenemia.9 Another group of re-searchers found elevated serum carotene levels inwomen with anorexia nervosa, but not in womenwith normal or abnormal menstrual function.7 Itis thought that mobilization of fat stores second-ary to weight loss might be responsible for hyper-carotenemia in women with anorexia nervosa.

In 1971, a small study examined six womenwith elevated serum carotene levels who hadexcessive intake of carrots or pumpkins.10 Theresearcher described what he called “goldenovaries” and noted that amenorrhea developed inthe two younger patients and irregular menstrualbleeding in the four older patients. For sometime it was thought that exercise-induced amen-

orrhea in long-distance runners was associatedwith hypercarotenemia, but that association wasdisproved, and no difference in carotene levelswas observed.11

I found no reference to amenorrhea or men-strual irregularities associated with taking carotenesupplements, and, as of this writing, I don’t believeamenorrhea has been reported as a side effect ofbeta-carotene ingestion. However, I will probablyencourage women who are experiencing signifi-cant weight loss and amenorrhea to eat lesseramounts of carotene foods for the time being. Iwould also be inclined to reduce their vitamin Aand carotene supplementation if they were onhigh doses for some other medical reason.

Calcium. One of the serious long-term con-sequences of amenorrhea due to premature ovar-ian failure or lower production of estrogen(hypothalamic amenorrhea) is a lower bone den-sity and an increased risk for osteoporosis andfractures later in life. Even when calcium intakeis the same between amenorrheic women andwomen who menstruate normally, there is adecrease in calcium absorption and an increase incalcium excretion in estrogen-deficient women.There is ample evidence that a lack of estrogenincreases the daily calcium requirement.12 As aresult, I recommend a higher-than-normal dailyintake (1,200 to 1,500 mg per day) of either cal-cium carbonate or calcium citrate to maintaincalcium balance in low-estrogen states in womenof reproductive age. (For more information onosteoporosis, please see Chapter 14.)

Calcium Carbonate or Calcium Citrate orCombination

1,200–1,500 mg per day

Additional Vitamins and Minerals. Manyother minerals and nutrients affect bone densityand are relevant to the prevention of osteoporo-sis in amenorrheic women. Magnesium, man-ganese, zinc, copper, boron, vitamin K, vitamin


D, and other nutrients determine bone health,each in their own way. In Chapter 14, I discussthis in detail.

Botanicals

Chaste Tree (Vitex Agnus Castus). Chastetree is probably the best-known herb in all ofEurope for hormonal imbalances in women. Sinceat least the time of the Greeks, chaste tree has beenused for the full scope of menstrual disorders,including amenorrhea. Chaste tree acts on thehypothalamus and pituitary glands by increasingLH production and mildly inhibiting the releaseof FSH. The result is a shift in the ratio of estro-gen to progesterone, in favor of progesterone.13

Chaste tree stimulates ovulation, which in turnproduces progesterone. Thus, chaste tree indi-rectly raises progesterone levels,14 an effectivetreatment for some cases of amenorrhea.

If we were to give progesterone hormone forseveral days, stop, and then a menses occurs, thisindicates an intact reproductive system that lackscyclicity and ovulation, or at least regular cyclicovulation. It suggests that the body is producingenough FSH to stimulate the ovaries and that theovaries can develop follicles. Furthermore, itindicates that follicular production of estrogen issufficient to cause the lining of the uterus (endo-metrium) to grow and that the sloughed endo-metrium is able to pass through the cervicalopening and the vagina. This tells us that theproblem most likely is a dysfunction in the hypo-thalamus or pituitary. The ability of chaste tree tomodulate the hypothalamus or pituitary thenmakes this herb an obvious choice.

The first major study on chaste tree was published in 1954.15 Subsequent studies havecontinued to prove its effectiveness. In a studypublished in 1990, 20 women with secondaryamenorrhea were admitted to a six-month studyusing chaste tree liquid extract at 40 dropsdaily.16 At the end of the six-month study, 10 outof the 15 women had menstrual cycles. Testingshowed that values for progesterone and LH

increased, and FSH values either did not changeor decreased slightly.

Chaste tree also inhibits prolactin release bythe pituitary gland, particularly when elevatedprolactin is caused by stress, by binding dopa-mine receptors and then inhibiting prolactinrelease in the pituitary.17, 18 Since elevated pro-lactin levels cause some cases of amenorrhea,chaste tree is also indicated for these cases. Adouble-blind, placebo-controlled study examinedthe effect of a chaste tree (vitex) preparation on 52women with luteal phase defects due to hyperpro-lactinemia (elevated prolactin levels).19 The dailydose of the extract was 20 mg, and the studylasted for three months. Prolactin release was sig-nificantly reduced in the vitex group. The shortluteal phase (second half of the cycle) was normal-ized, and the decreased progesterone productionwas normalized. No side effects were noted, andtwo women became pregnant.

When using chaste tree, don’t expect immedi-ate results. It’s not the same as giving proges-terone, even natural progesterone. Chaste tree ismore of a medium-range plan; usually it beginsto take effect after three or four months whengiven daily.

Chaste Tree

40 drops tincture or 175 mg .6% aucubin standardizedextract per day

Black Cohosh (Cimifuga Racemosa). Blackcohosh has become one of the most significantwomen’s herbs in all of botanical medicine. Alsoknown as snakeroot or rattleroot, this plantbelongs to the buttercup family and is indigenousto the eastern part of North America. The nativepeoples of Canada and America used black cohoshfor many different indications, such as uterinepains during menses and childbirth, rheumatism,rattlesnake bites, and general malaise. Blackcohosh was introduced to Western gynecology inthe middle of the eighteenth century in the treat-ment of menopausal symptoms.20


The exact mechanism of how black cohoshworks has yet to be elucidated. We attribute mostof its gynecological effects to its “estrogen-like”action, yet recent research has shown that blackcohosh does not contain phytoestrogens, nor doesit change hormone levels such as estradiol, LH,FSH or prolactin.21–23 The primary constituents inblack cohosh extract are glycosides, particularlythe triterpene glycosides, mainly cimicifugosideand actein, which are assumed to interfere withpituitary gland receptors and the hypothalamus.Other characteristic constituents are the flavo-noids, resins, volatile oils, fatty acids, tannins,alkaloids, cimicifugin, and salicylic acid. Althoughthe constituents in black cohosh may be able tobind to receptors in the pituitary or hypothala-mus, these constituents do not seem to be able to bind to receptors in target organs. Olderresearch showed the effects of a black cohoshpreparation on LH and FSH secretion in meno-pausal women. After a treatment of two months,LH (but not FSH) levels were significantlyreduced in the black cohosh–treated group.24

There have been many studies using blackcohosh preparations in menopausal women.These studies and the further use of this plant inmenopausal women will be discussed in muchdetail in Chapter 12. For women who have amen-orrhea due to hypoestrogenic states, a state similarto menopause, black cohosh will be important inrelieving some symptoms. Recent studies evenindicate that black cohosh may decrease risk fac-tors associated with menopause such as osteoporo-sis and cardiovascular disease and may even beeffective in preventing bone loss.25–27

Black Cohosh

40–80 mg standardized extract twice daily

Rhodiola. Rhodiola, also called golden root,has enjoyed centuries of use in Eastern Europe,Scandinavia, and Asia. Traditionally, this herbwas used in folk medicine to increase physicalendurance, work productivity, longevity, resist-

ance to high altitude sickness, fatigue, depres-sion, anemia, impotence, gastrointestinal ail-ments, infections, and disorders of the nervoussystem. The folklore surrounding rhodiola led tothe first investigations in its phytochemistry inthe early 1960s, when scientists identified adap-togenic compounds in its roots. These adapto-gens, believed to help the body adapt to stress bysupporting the adrenal glands and endocrinesystem, as well as the antioxidant and stimulatingcompounds that were later discovered in rhodi-ola, are responsible for its medicinal properties.

Animal studies looking at the effect of rhodi-ola on thyroid function, adrenal function, andovarian egg maturation have raised interest inrhodiola for endocrine problems in humans.Forty women suffering from amenorrhea (loss ofmenstrual cycles) were given 100 mg of rhodiolatwice daily for two weeks or an injection for 10days. Remarkably, normal menses were restoredin 25 women, 11 of whom became pregnant.28

Physicians have reported cases of women whohad failed to conceive with standard fertilitydrugs, who then became pregnant within severalmonths of beginning Rhodiola rosea extract. Fortreatment, look for extracts that are standardizedto contain 3 percent rosavin.

Rhodiola (3% Rosavin)

200 mg per day (or 100 mg twice daily)

Maca (Lepidium Peruvianum). Maca is aroot vegetable, in the same family as turnips andbroccoli, which grows at high elevations, native tothe high Andean plateaus of Peru. It has been usedtraditionally by native Peruvians as both a foodand medicine. It has historically been used for avariety of purposes, including hormone balancing,thyroid function, sexual function, PMS, meno-pause, and as a tonic for healthy aging.

A recent study proved maca’s effectiveness intreating women with amenorrhea due to hypo-estrogenic states, and especially premature ovarianfailure. In a study of 20 healthy menopausal


women in the early phase of their menopause,maca (2,000 mg per day) was given for up toeight months and was shown to lower follicle-stimulating hormone (FSH) (higher levels ofFSH are a measure of low estrogen productionfrom the ovaries) and increase luteinizing hor-mone (LH) (elevated LH is necessary to stimu-late ovulation), resulting in increases in bothestrogen levels and progesterone levels.29 Theseresults would seem to suggest that maca, depend-ing on the length of use, could act as a hormonaltoner and stimulate the production of estrogenand progesterone.

Maca

Four 500-mg capsules (2,000 mg) per day

Traditional Herbs

Uterine Stimulants. Uterine stimulants oremmenagogues increase tone or muscular activ-ity and serve to initiate the onset of menses andstimulate reproductive function. Most importantare the herbs that cause shedding of the endo-metrium and stimulate normal menstrual cyclesin the absence of pregnancy.

• Squaw vine/partridgeberry (Mitchella repens)• Yarrow (Achillea millefolium)• Chaste tree (Vitex agnus castus)• Pennyroyal* (Mentha pulegium)• Mugwort (Artemisia vulgaris)• Water pepper (Polygonum hydropiper)

Water Pepper.30 In a medical journal of 1846,Dr. Thomas Ogier, a surgeon and obstetrician,published an herbal approach for amenorrhea.31

He maintained that administering a tincture ofwater pepper successfully treated a case of obsti-nate amenorrhea. Exactly how the water pepperworks is not known.

Phytoestrogens. Phytoestrogens are by andlarge nonsteroidal hormone-like constituentsfound in over 300 medicinal and edible plants.With the currently available evidence, soybeansare probably the richest edible source of phyto-estrogens. Some plant compounds, such as lig-nans, found in flaxseed, are not phytoestrogensbut are converted to estrogens in the intestines.There are many herbs that contain phytoestrogencompounds and have a role in amenorrhea. Theysupport the reproductive cycle and relieve meno-pausal symptoms in women who are appropri-ately menopausal (see Chapter 12) as well aswomen who are amenorrheic and prematurelymenopausal. These herbs include:

• Alfalfa (Medicago sativa)• Dong quai (Angelica sinensis)• Flaxseed (Linum usitatissimum)• Ginseng (Panax ginseng)• Hops (Humulus lupulus)• Licorice (Glycyrrhiza glabra)• Red clover (Trifolium pratense)

Progesterone Precursors. Diosgenin andsarsasapogenin can be converted in the labora-tory to various hormones, including proges-terone, which in turn can be converted to adrenalsteroids and then to testosterone or estrogens.Even though diosgenin from plants is used bypharmaceutical companies to synthesize varioushormones, there is very little scientific informa-tion on diosgenin-containing plants and theirrelationship to human metabolism. A number ofherbs contain diosgenin or sarsasapogenin:

• Bloodroot (Sanguinaria canadensis)• Blue cohosh (Caulophyllum thalictroides)• Fenugreek (Trigonella foenumgraecum)• Sarsaparilla (Smilax officinalis)• Wild yam (Dioscorea spp)• Yucca (Yucca spp)

Special Herbal and Supplemental Consid-erations for Polycystic Ovarian Syndrome.For PCOS, include herbs that will increase

*Important caution: Do not use essential oil of pennyroyalinternally in any situation.


sex-hormone-binding globulin. This will bind upsome of the excess androgens secreted by theovarian follicles.

• Nettle root• Green tea• Soy• Flaxseed

Other herbs and nutrients can improve insulinsensitivity and PCOS:

• Chromium• Fenugreek powder• Vitamin C• Bitter melon

Licorice can lower serum testosterone in womenand saw palmetto can inhibit the conversion oftestosterone to dihydrotestosterone (a strongerform of testosterone). By inhibiting this conver-sion, we can maybe modestly decrease testosterone-induced hair loss and acne.

• Licorice• Saw palmetto

Bio-Identical Hormones

Bio-identical, also known as natural, proges-terone can be used for both diagnosis and treat-ment of amenorrhea. Progesterone-inducedmenses indicates that there are adequate estrogenlevels and that anatomical problems causingobstruction of the outflow of blood are not pres-ent. In these instances, the progesterone chal-lenge is an effective means of diagnosis.

The progesterone challenge test is consideredpositive if uterine bleeding (even a few days ofspotting) occurs and correlates with a serumestradiol level of 40 g/mL or higher. Onset ofmenstruation after intramuscular injection of150 mg of progesterone in oil suggests thatanovulation is the most likely explanation of theamenorrhea. Oral micronized progesterone(OMP) (also called oral natural progesterone)administered for seven days at 400 mg per day

will induce complete secretory changes in theendometrium and induce a menses in a womanwhose uterus has been adequately stimulated byestrogen. Lack of vaginal bleeding after the prog-esterone challenge suggests either inadequatepriming of the endometrial lining, absence of anendometrial cavity, or some kind of obstruction.

If no withdrawal bleeding occurs after theprogesterone challenge, then it is important to usea birth control pill—generally one that contains atleast 30 mcg of ethinyl estradiol, for 21 days. Atthe end of these 21 days, withdrawal bleedingshould occur within 14 days; even spotting is suf-ficient to count as withdrawal bleeding. Absence of uterine bleeding under these circumstancesindicates uterine end-organ failure that may resultfrom congenital malformation of the uterus andvagina or from distortion of the endometrial cavityby intrauterine adhesions due to tuberculousendometritis, also called Asherman’s syndrome. Ifbleeding does occur after the oral contraceptivepill, then the likely diagnosis is hypothalamicamenorrhea, after excluding a pituitary tumor.

The woman who is hypoestrogenic and is nota candidate for induction of ovulation requireshormone replacement therapy. In young women,especially those in their 20s and 30s, the bestapproach is most likely to take oral contracep-tives (OCs). Hormone replacement therapy,whether bio-identical hormones or conventionalhormone replacement, could potentially be usedin the usual doses for normal-aged menopausalwomen. However, these doses are considerablylower than the body’s normal level in a youngreproductive-aged woman and considerablylower than the dose of hormones in oral contra-ceptives. As these lower doses may not be ade-quate for bone protection at this young age, myrecommendation is to use a 20 to 30 mcg oralcontraceptive pill for women in their 20s and 30swho have hypothalamic amenorrhea or prema-ture ovarian failure. (Smokers older than 35 willneed to consider other options, most preferablyto stop smoking.)


Younger women who insist on using alterna-tive medicine need to fully understand their risksin premature states of insufficient hormone pro-duction. If the herbal, nutritional, and lifestyleinterventions are not sufficient to stimulate themenstrual cycle, they must understand that boneloss in amenorrheic women shows the same pat-tern over time as that seen in postmenopausalwomen.32 The loss is most rapid in the first fewyears, emphasizing the need for early treatment.

If bio-identical hormones are your choice asan alternative to OCs, then the following pre-scription, called bi-est (for bi-estrogen), would be considered a higher-than-average hormonereplacement dose for menopausal women: estriol2 mg/estradiol 0.5mg/progesterone 100 mg; onepill twice daily, for three weeks on and one weekoff. Beginning medication on the first of everymonth establishes an easily remembered routine.Some practitioners use a tri-estrogen formulationinstead of the bi-estrogen formulation. In thiscase, the formula would be estriol 2 mg/estradiol0.250 mg/estrone 0.250 mg/progesterone 100mg; one pill twice daily, for three weeks on andone week off.

Menstruation generally occurs within threedays after the last pills, the 28th day of eachmonth. Bleeding that occurs at any other timemay indicate that the body’s own function hasreturned. The natural hormone replacement pro-gram should then be discontinued and thepatient monitored for the return of ovulation.

Natural progesterone creams may be used inselected cases to help maintain a monthly cycle in women with anovulatory amenorrhea. Somewomen only need this monthly lower-dose hormone support during the second half of amonthly cycle. The typical dosing recommenda-tions are from one-quarter to one-half teaspoonapplied to the palms, inner forearms, and chesttwice daily from day 15 to day 26. This cycle canbe repeated. In the event that menstruation doesnot occur, it may be necessary to return to theestrogen/progesterone plan and/or herbal/nutri-

tional therapies that induce ovulation such aschaste tree extract.

Exercise

Amenorrhea in the female athlete is associatedwith reduced caloric intake and strenuous exer-cise, which leads to low estrogen and is associatedwith stress fractures, osteoporosis, and a potentialincrease in the risk of premature cardiovasculardisease.33

Most cross-sectional studies suggest thatfemale competitive athletes, whether runners34–39

or bodybuilders,40, 41 have increased incidence of menstrual cycle disturbance, shorter lutealphases, and amenorrhea than do sedentary con-trols. Because of subject self-selection and conse-quent oversampling, results of these studies mustbe interpreted with caution.42 Prospective studieshave found no hormonal changes in women fol-lowing one year of endurance training43 and, upto 1994, had not detected induction of second-ary amenorrhea by exercise alone.42

In her excellent review, Bonen states that sec-ondary amenorrhea “is difficult to induce by exer-cise alone.”42 She concludes that some of the factorsthought to be associated with exercise-inducedamenorrhea—type, duration, intensity of exercise,age of menarche, training before menarche, andtraining history—remain speculative and that, infact, little is known about the true incidence of secondary amenorrhea in athletic populations.

The higher incidence of secondary amenorrheadetected in competitive athletes appears related tometabolic factors. In weight lifters and body-builders, the appearance of luteal-phase distur-bances and oligo- or amenorrhea is directly relatedto drastic reduction in caloric intake prior to com-petition combined with increases in strenuousexercise. For example, Sandoval found that femalebodybuilders, examined for a period of 48 hoursbefore competition, achieved a degree of leannesssimilar to their male counterparts.44 Kleiner foundin female bodybuilders, competing at the 1988National Physique Committee’s Junior USA


Bodybuilding Championships, a 9.8 percent bodyfat (males, 6.0 percent).45 In a group of femalebodybuilders studied for one month pre- and post-competition, Walberg-Rankin detected a twofoldincrease in caloric intake and a tenfold increase infat intake postevent as compared to pre-event.41

Furthermore, these unhealthy practices are fol-lowed by college-age women who compete inbodybuilding events.46 In this context, it is not surprising that in Walberg’s study, 86 percent offemale competitive bodybuilders not on birth control pills reported menstrual dysfunction, andin Kleiner’s, 81 percent of female elite body-builders had contest-related amenorrhea for one ortwo months precontest.

The picture is similar for competitive femalerunners whose caloric intake is inadequate orfalls below the constant energy demanded bytheir sports. Time and again, menstrual cycle dis-turbances in these populations have been shownto be related to inadequate caloric intake com-bined with strenuous, abrupt increases in run-ning distances.34, 42, 47–49 Amenorrhea usually isnot seen in athletes with a high percentage ofbody fat.49 Since the cause of amenorrhea andother menstrual disturbances is linked to energydeficiency, there is no justification for fears thatexercise itself is unhealthy for women.50

As mentioned earlier, amenorrheic athletesshow dangerous reductions in mean trabecularbone density as compared to eumenorrheic coun-terparts (42 percent).51 Exercise may intensify these effects48 as well as low calorie intake itself. The effects of insufficient caloric intake on bonemineral density likely represents an estrogen-independent mechanism for bone loss; exercise-associated amenorrhea alters additional hormonesthat play an important role in modulating boneturnover and bone mineral density in thesewomen.52 A study of amenorrheic ballet dancerstreated with estrogen plus progesterone replace-ment demonstrated that there was no significantimprovement in bone mineral density even in thosethat resumed menses.53

The hypoestrogenic state that predisposespostmenopausal women to cardiovascular diseaseis similar to that of the amenorrheic athlete and,therefore, so is the cardiovascular risk. Specifi-cally, amenorrheic athletes have been shown tohave elevated LDL and total cholesterol,impaired endothelial function, and increasedlipid peroxidation.54, 55 Though this phenome-non warrants further study, present data suggeststhat the risk of premature cardiovascular diseasedeserves attention in monitoring and treatmentof these women.

Finally, as shown by Bonen, menstrual distur-bances are quite common in the general popula-tion of sedentary women. Different factors—weight change, starvation, crowding, travel, com-munal living, exercise, and severe stress of anykind—have been implicated in altered menstrualcyclicity.42 Ronkainen and colleagues foundincreased abnormalities in the menstrual cyclesof women during the short sunlight days of fall.56 Thus, amenorrhea appears to have multipleetiologic relationships. Inappropriate exercise isonly one of them.

Exercise Recommendations. If a woman hasdocumented secondary amenorrhea not due topregnancy, a careful history of eating and exercis-ing habits is critical. In addition, her body weightand percentage body fat should be ascertainedand compared to the normal ranges for her bodybuild and age. For those women with amenor-rhea due to hypoestrogenic states, a bone densit-ometry test, called a DEXA scan, particularly ofthe lumbar spine and proximal femur, is highlydesirable.

In cases where the history and tests recom-mended indicate inadequate calorie consump-tion, a bone mass density below normal range,and body fat less than 15 percent, the recom-mended course is as follows:

• Adapt diet to individual needs; particularlyemphasize protein, calcium, magnesium,vitamin D, zinc, copper, and chromium.57


• Reduce or stop intensive training, particu-larly running, until cycling resumes.

• Modify type of exercise. Instead of running,do moderate walking (30 minutes per day)and add a regular program of moderateweight lifting for 30 minutes, three timesper week.

• Avoid competition in sports, on the job, andelsewhere.

For those women who have PCOS and areoverweight, regular and preferably almost dailyaerobic exercise in the range of two and a half to

five hours per week is necessary to improveinsulin resistance and lose weight.


Successful management of amenorrhea depends onan accurate diagnosis. A careful history and exami-nation and simple laboratory investigations willmost likely yield a diagnosis that allows one to offerappropriate treatment in the majority of cases. Aphysical exam should assess the signs of secondarysexual characteristics (such as breast developmentand the presence or absence of normal or abnormal

Sample Treatment Plans for Amenorrhea


Premature Ovarian Failure

Diet: A whole foods diet using plenty of grains,beans (especially soybeans), fruits, vegetables(especially dark leafy greens), nuts and seeds(especially flaxseed), and fish (salmon, tuna, hal-ibut, sardines)

Exercise: Regular aerobic and weight-bearing exer-cise 30 to 60 minutes, 4 to 7 days per week;weight/strength training 2 days per week

Mineral supplementation: Calcium/magnesium/boron/vitamin D/other trace minerals and nutrients(see Chapter 14)

Consider oral contraceptives with 30 mcg ofethinyl estradiol: Estriol 2 mg/estradiol 0.5 mg/OMP 200 mg; 1 pill twice daily, 3 weeks on and 1week off

Consider bio-identical hormones: Estriol 2 mg/estradiol 0.5 mg/progesterone 100 mg; 1 pill twicedaily, 3 weeks on and 1 week off

Consider short-term trial (less than 6 months):

Black cohosh extract: standardized extract,40–80 mg twice daily

Maca: 2,000 mg per dayRhodiola: 3% rosavin, 200 mg per day

Polyglandular products: To stimulate the hypothala-mus/pituitary/ovarian feedback mechanisms, usebovine extracts of combinations of pituitary, thy-

roid, adrenal, and ovarian tissue. (Each woman isunique and requires an individualized approach.)

Hyperprolactinemia

Diet: A whole foods diet using plenty of grains,beans (especially soybeans), fruits, vegetables(especially dark leafy greens), nuts and seeds(especially flaxseed), and fish (salmon, tuna, hal-ibut, sardines)

Exercise: Moderate exercise 150 minutes per weekChaste tree extract: 40 drops or 175 mg .6% aucu-

bin standardized extract per day

Hypoestrogenic States (HypothalamicAmenorrhea)

These states are often associated with weight loss,psychological states, and anorexia nervosa.

Diet:

Increase calories, dietary protein, fat, and carbohydrates.

Consume regular meals using whole foods.Avoid extreme dieting.Increase soy foods and flaxseed.

Lifestyle:

Counseling (for eating disorders)Stress management counseling and practicesReduce exercise from excessive to moderate

(continued )


body hair). Pelvic ultrasound might be helpful indetermining whether the ovaries are enlarged withsmall, peripherally located follicular cysts indicativeof polycystic ovary syndrome (PCOS). Blood teststo measure FSH, LH, prolactin, estradiol, testos-terone, and thyroid function may be used to helpdetermine the diagnosis.

On the basis of this information, womenwith amenorrhea can be classified into the fourgroups mentioned earlier in this chapter, withtreatments as follows:

1. Hypergonadotropic hypogonadism. Hor-mone therapy with estrogen will induce second-ary sexual characteristics in girls with primaryamenorrhea. Estrogen in combination with cyclicprogestins will prevent osteoporosis, endometrialhyperplasia, or cancer. The hormone therapy

medications and regimens are discussed earlier inthis chapter and also in Chapter 12. Oral contra-ceptives may also be used and may even be anoptimal choice because of the higher dose ofestrogen for relieving symptoms, ease and cost, orcoverage for contraception in case the amenor-rhea is temporary and the women wants preg-nancy protection.2. Hyperprolactinemia. Treatment with dopa-

mine agonists (bromocriptine, cabergoline,quinagolide) leads to reduction in prolactinsecretion by the pituitary gland. When prolactinis elevated, a CT or MRI should be done to dis-tinguish between overactive pituitary produc-tion by a microadenoma versus an actual tumor(macroadenoma). The large tumor can be asso-ciated with headaches or vision changes andrequires surgical resection, but it is very rare.

Sample Treatment Plans for Amenorrhea (continued )

Mineral supplementation: Calcium/magnesium/boron/vitamin D/other trace minerals and nutrients(see Chapter 14)

Oral contraceptives with 30 mcg of ethinyl estradiol

Consider bio-identical hormones: Estriol 2 mg/estradiol 0.5 mg/OMP 100 mg (not 200 mg); 1 pilltwice daily, 3 weeks on and 1 week off

Consider short-term trial (less than 6 months):

Black cohosh extract: standardized extract,40–80 mg twice daily

Maca: 2,000 mg per dayRhodiola: 3% rosavin, 200 mg per day

Polyglandular products: To stimulate the hypothala-mus/pituitary/ovarian feedback mechanisms, usebovine extracts of combinations of pituitary, thy-roid, adrenal, and ovarian tissue. (Each woman isunique and requires an individualized approach.)

Chronic Anovulation Due to PCOS

Diet: Reduce carbohydrates (80 g per day) andincrease protein in the diet (60 mg or more perday). Diets such as the Zone Diet can be very help-

ful in this situation to reduce the hyperinsulinemiaand provide better weight management. Increasesoy foods and flaxseed. Emphasize whole grains,fruits, vegetables, nuts, seeds, fish (salmon,tuna, sardines, halibut), organic low-fat meats(chicken, turkey, beef, buffalo, elk, deer), low-fatdairy products, eggs, and beans.

Chaste tree extract: 40 drops or 175 mg .6% aucu-bin standardized extract per day

Rhodiola: 3% rosavin, 200 mg per dayGreen tea extract: 500 mg per dayNettles root: 600 mg per daySaw palmetto extract: 400 mg per daySoy isoflavones: 50–100 mg per dayFlaxseed: 1–2 tbsp per dayChromium: 500–1,000 mcg per dayFenugreek powder: 24 g per dayOral micronized natural progesterone: 200–400 mg

per day for 12 days per monthNatural progesterone cream (20 mg per 1⁄4 tsp):

1⁄4–1⁄2 tsp twice daily, days 16–25. Or 1⁄4 tsp 1 or2 times daily, days 7–14; 1⁄4–1⁄2 tsp twice daily,days 15–26


Once a tumor is excluded, medical therapy todecrease prolactin is mainly used to achievepregnancy, and it is not required in an asympto-matic patient who is not seeking fertility.3. Hypogonadotropic hypogonadism. In the

majority of women with this classification, noorganic disease can be identified in the hypothala-mus, anterior pituitary, or ovary. Management ofhypothalamic amenorrhea associated with weightloss must focus primarily on trying to correct theunderlying cause of the weight loss. Amenorrheafrom anorexia, bulimia, and exercise-inducedweight loss requires prompt diagnosis and treat-ment. Some women will require hospitalization ina controlled environment for their malnutrition.Dietary counseling, psychological counseling, andadvice about exercise could all help to correct theproblem and restore ovarian function.

If amenorrhea persists for more than 12months, then osteoporosis should be excludedwith bone density testing, or some form ofestrogen therapy should be considered to pre-vent bone loss. Women with hypothalamicamenorrhea who wish to become pregnant aretreated by administering GnRH medications ina pulsatile manner via a portable programmablepump that releases the medication every one totwo hours, simulating the body’s pulsatile secre-tions. Women with rare disorders such as thepituitary disease Sheehan’s syndrome are givenhormones FSH and LH.4. Chronic anovulation and polycystic ovary

syndrome. About 30 percent of women withsecondary amenorrhea have concentrations ofFSH, LH, and estrogen within the normalrange. Polycystic ovarian syndrome is acommon cause of this type of amenorrhea.Many women with this type of amenorrheaactually present with irregular menstrual pat-terns more often than amenorrhea. Thesewomen do not have estrogen deficiency, butrather experience problems related to continuedexposure to estrogen unopposed by proges-terone. The buildup of the uterine lining caused

by the continuous estrogen can cause endome-trial hyperplasia or cancer.

Polycystic ovary syndrome is associated withclinical symptoms such as obesity, hirsutism,anovulation, and irregular bleeding. The rangeof problems that women with polycystic ovarysyndrome have varies greatly from woman towoman. There are significant differences interms of the amount of acne, hair growth, men-strual irregularity, infertility, hypertension, anddiabetes. There is no current known treatmentfor the disease, so treatment by conventionalmedicine is aimed at individual patient goals andsymptom relief. Obviously, the health concernsof hypertension, hyperlipidemia, and diabetesneed to be addressed in terms of lifestyle changesand periodic monitoring of blood pressure,lipids, and blood sugar. For the woman who hasvery infrequent menses, the prevention of uter-ine hyperplasia or cancer is most important.However, most women with PCOS haveuncomfortable side effects that can be improved.

If a woman has very infrequent menstruation,she should either use birth control pills for regularmenstrual withdrawal or at least quarterly pro-gestogens that cause withdrawal bleeding. Theprogestogens that have been used include Proveraor Cycrin (medroxyprogesterone), 10 mg daily forseven days; Prometrium (oral micronized proges-terone) or compounded oral micronized proges-terone, 400 mg daily for seven days; Aygestin(norethindrone acetate), 5 mg daily for seven days;and Megace (megestrol), 20 mg daily for sevendays. Most of the progestogens have similar symp-toms of nausea, bloating, moodiness, and oily skinin varying degrees, but they are usually tolerablefor a few days or a week.

Hirsutism can be with treated topically withVaniqa, which reduces the transformation oftestosterone to dihydrotesterone at the hair folli-cle, reducing the growth, or at least the size andcolor, of the hair. This product needs to beapplied once to twice daily in the areas of hair


growth and works while it is being used. There isno permanent effect, so it has to be used daily.Also, electrolysis and laser hair removal are veryeffective permanent hair removal treatment.

Spironolactone, an antiandrogen medicationwith minimal side effects, can reduce acne andhair growth. The recommended does is 50 to 200mg once daily. There has been some concern ofvery rare cases of hyperkalemia (abnormally highpotassium levels) with this product, so patientsneed to be warned of cardiac arrhythmias andmuscle cramping.

Metformin, an insulin-receptor-improvingmedication used for diabetes, has been touted todecrease weight gain and stimulate ovulation inwomen with PCOS. However, many studieshave shown minimal effect on weight gain, and ithas significant side effects of nausea, vomiting,and diarrhea, as well as uncommon but seriousliver enzyme problems. Most practitioners useonly it for treatment of diabetes or as an adjunctin infertility. Metformin usage, along with clomi-phene and/or Pergonal, seems to improve ovaryreceptiveness and ovulation. Encouraging weightloss can help the situation tremendously, butwomen with polycystic ovary syndrome and obe-sity seem to be very resistant to standard weight-loss programs. It is possible to lose weight, butthey need to be persistent and have a good sup-port system, possibly even some help frombariatric medicine (obesity doctors).

The treatment that achieves the best symp-tom control is oral contraceptives. Oral contra-ceptives can reduce hair growth, reduce acne,cause regular menstrual sloughing, suppressluteinizing hormone (LH) and ovarian cyst pro-duction, and are very widely prescribed forwomen who also need contraception.

Antiestrogens such as clomiphene are some-times given to induce ovulation and may restorefertility in women seeking pregnancy. However,PCOS can be resistant to normal ovulationinduction and often requires the help of an infer-

tility specialist. Sometimes metformin is addedto help aid clomiphene in induction of ovula-tion, or the patient is given more intense ovula-tion induction medications such as Pergonal.

Probably the most important treatment ofpolycystic ovary syndrome is recognition of theproblem. When counseling the patient, the focusshould be on the management of her lifelongsymptoms. We need to inform women that thisdisease comes in all shades and that there will bedifferent treatment regimens for different womenrather than one treatment for all.


All women with amenorrhea should be evaluatedby a licensed primary care practitioner (naturo-pathic doctor, medical doctor, osteopathic doctor,nurse-practitioner, or physician’s assistant) becauseof the diverse array of potential diseases and disor-ders. Some of these conditions are rare, such asAsherman’s syndrome, Cushing’s disease, Sheehan’ssyndrome, and pituitary-secreting tumors. Othercauses are more common but can be complex, suchas malnutrition, anorexia nervosa, hyperthy-roidism, polycystic ovary syndrome, and pituitarydisorders. Other causes are rather straightforward;for example, hypothyroidism, strenuous exercise,pregnancy, and stress-related amenorrhea.

Fortunately, most women with amenorrheahave relatively simple problems that can be man-aged easily by primary care physicians, whetherthey are alternative medicine practitioners, con-ventional practitioners, or a team approach usingthe best choices of each. After an evaluation hasbeen done and a cause diagnosed, natural thera-pies can be administered as the primary therapyor integrated with the conventional treatment.Conventional treatments may be necessary inmany cases of amenorrhea, but dosing regimensmay be lower when natural therapies are used aspart of an integrated plan.

31

OVERVIEW

Over the past four decades, cervical cancer rateshave dropped dramatically in most developedcountries. This improvement in our health isattributable to the commonly available Papsmear, whereby early premalignant lesions can befound and treated, most often with fairly simpleoffice techniques. Cervical cancer presently ranksthird in cancer deaths of American women,although it remains the leading cause of deathfrom cancer among women in developing coun-tries who do not enjoy the same access to diagno-sis and early treatment.1 In the United States,approximately 9,710 cases of cervical cancer werediagnosed in 2006 and about 3,700 women diedfrom it. Worldwide, human papilloma infectioncauses almost 500,000 cases of cervical cancerand 280,000 deaths each year.

Squamous cell cervical cancer is virtuallyalways preceded by cervical dysplasia, which is100 percent treatable in its noninvasive stage.(Cervical cancer of the glandular cells, adenocar-cinoma, is more problematic and requires moreaggressive treatment.) Human papillomavirus(HPV) is the most common sexually transmittedinfection in the United States,2 and about 75percent of the U.S. adult population has beenexposed to HPV.3 Fortunately, the majority ofgenital HPV infections don’t cause any symp-toms and go away on their own. The others goon to cause abnormal cells, including cervicaldysplasia and/or cervical cancer.

Cervical cancer and dysplasia, genital warts,and condyloma are caused by the human papillo-mavirus, which is sexually transmitted. Virtually100 percent of cervical dysplasias and cervicalcancer is caused by HPV. This association isreflected in a simple rating system, in use since

1988, of low- and high-grade (precancerous)lesions or, more specifically, low-grade squamousintraepithelial lesions (SIL) and high-grade SIL,also referred to as LSIL and HSIL, respectively.In the new terminology, low-grade SIL replacesthe former terms mild dysplasia and CIN 1 (cer-vical intraepithelial neoplasia) and includeschanges of simple infection with the humanpapillomavirus. High-grade SIL includes moder-ate and severe dysplasia, formerly classified asCIN 2 and CIN 3. Both the newer and tradi-tional terms are used in this chapter and in themedical literature.

What exactly is dysplasia? The mucous mem-brane that covers the cervix changes in adolescencefrom more bumpy columnar cells, like those thatalso line the uterus, to squamous cells, like thosethat line the mouth, through a normal processcalled metaplasia. Squamous cells make up all ofour external body surfaces that are characteristi-cally smooth, like our skin, for example. Wherethese two types of cells meet is called the squamo-columnar junction—and it is here that our cellsare most susceptible to premalignant transforma-tion. The Pap smear samples cells from this area toexamine microscopically.

The very bottom layer of squamous cells arecalled basal cells. They are the largest and round-est with the biggest nuclei. As the cells progresstoward the surface, they become smaller, flatter,and ultimately lose their nuclei before they get tothe top. In mild dysplasia, the basal cell layer isthicker, up to one-third the total thickness of thetissue; in moderate dysplasia, they occupy thebottom and into the middle third; in severe dys-plasia, they extend to the top third. Carcinoma“in situ” is not an invasive malignancy, but ratherthe extension of the immature basal cells to the

3C E R V I C A L D Y S P L A S I A

C H A P T E R



very top of the tissue thickness. While it doescarry a higher risk of conversion to true cancer, ittoo is completely treatable.

The possibility of progression to cervicalcancer increases with the severity of the dysplasia.Mostly, though, it is a slow process, occurring overabout 10 to 15 years in most women who areuntreated. Currently, more than 100 HPV sub-types have been identified, numbered, and catego-rized. More than 30 types can infect the genitalarea. The progression of dysplasia to cancer variesaccording to which HPV subtype one is infectedwith. The low-risk types (6 and 11) are generallyassociated with external genital warts but do notcause cervical cancer. The most aggressive or high-risk types are HPV 16, 18, 26, 31, 33, 35,39, 45, 51, 51, 56, 58, 59, 66, 68, 73, and 82.These can transform susceptible tissue into cancerin about 18 months, but this is the exceptionrather than the norm, and dysplasia typically takesmore than 10 years to progress to cervical cancer.In the United States, HPV 16 accounts for morethan 50 to 60 percent of cervical cancer cases, fol-lowed by HPV 18 (10 to 12 percent) and HPV 31and 45 (4 to 5 percent each).

A recent study confirmed that lesions of thecervix persist longer and progress more quickly inwomen with the aforementioned oncogenic HPVtypes, known as the higher risk types, than inwomen with nononcogenic types or withoutHPV.4 However, it is important to remember thatmost women with the human papillomavirusnever get dysplasia at all. On the other hand, somewomen with normal Pap smears, but showinginflammation, may indeed harbor the oncogenicHPV types 16 and 18,5 suggesting women withchronic inflammation may benefit from high-riskHPV screening. Some estimate that as many as 70percent of women are or have been infected intheir lifetime. On the other hand, only about 10women per 100,000 get cervical cancer.

In addition to eliminating dysplasia throughtreatment, there can be a significant amount ofspontaneous regression of even the most severe

forms, thanks to our well-functioning immunesystems. Spontaneous regression of CIN 1 andCIN 2 has been documented to be as high as 50percent to 40 percent respectively, with numbersimproving the longer women are followed (usu-ally one to three years). Almost 70 percent reso-lution of HPV alone was observed.6

Other studies confirm this, and the majority ofuntreated mild dysplasias were shown to regress tonormal within two years. A critical review of theliterature on the natural history of CIN was doneover a span of over 40 years.7 The author con-cluded that approximately 60 percent of CIN 1regressed to normal, 30 percent persisted, 10 per-cent progressed to CIN 3 (a high-grade lesion),and only about 1 percent progressed to cervicalcancer. CIN 2 regressed in 40 percent of the cases,persisted in 40 percent, progressed to CIN 3 in 20percent, and progressed to cervical cancer in lessthan 5 percent of cases. CIN 3 regressed in 33 per-cent of the cases and progressed to cervical cancerin more than 12 percent.

A recent study demonstrates that the risk ofprogression from mild to severe dysplasia orfrank cervical cancer was only 1 percent per year,but the risk of progression from moderate dys-plasia was 16 percent within two years and 25percent within five years.8

Mild dysplasia is detected in about 1 percentof women visiting their private gynecologist andabout 14 percent of women who visited desig-nated sexually transmitted disease clinics.6

Besides HPV, other risks include early age at firstintercourse, giving birth before age 22, cigarettesmoking, low socioeconomic status, number oflifetime partners, and possibly, although not con-clusively, oral contraceptive use. Women withfive or fewer lifetime heterosexual partners hadhigher rates of regression of untreated CIN 1 andCIN 2 than did women with more than five part-ners, independent of barrier contraceptionmethod use (condoms or diaphragms).9 It is dif-ficult to separate out the effects of sexual activitywithout barrier protection from that conferred


by ingesting hormonal contraception. For what-ever reason, women who used these barrier meth-ods had less dysplasia. In fact, condom use wasassociated with higher rates of CIN regressionand clearance of cervical HPV infection inwomen as well as protection from genital wartsand invasive cervical cancer.10–12

Evaluation of an abnormal Pap smear result isdone by a method called colposcopy, which is alot like using binoculars to view the cervix. Thecolposcope magnifies the cervix, and white vine-gar is applied to make the abnormal areas showup. Tiny biopsies are taken of these areas, a fewmillimeters at most. These are examined by thepathologist and graded into mild, moderate, orsevere as described previously.

One of the most important points I am sureto explain to my clients is that cervical cancer isa sexually transmitted disease, greatly promotedby smoking, but one that usually grows slowlyover years from its precursor, dysplasia, and istreatable in all of its earliest forms.

Atypia

Another possible Pap smear result is atypia—whichis really a kind of fence-sitting cell. The cells are notchanged enough to warrant being labeled as abnor-mal, but they are not quite normal either. Usuallyatypia is either an early abnormal change or evi-dence of tissue repairing itself, for example follow-ing a birth or vaginal infection. These Pap tests areusually just repeated, but if atypia persists, thewoman should be evaluated.

Atypical Glandular Cells of UndeterminedSignificance (AGUS). AGUS may be the mostdifficult diagnostic challenge of all the Pap smearabnormalities. AGUS represents a significantlygreater risk of cervical cancer than atypical squa-mous cells of undetermined significance (ASC-US, discussed later in this chapter) or low-gradesquamous intraepithelial lesions. The good news isthat AGUS is not a common diagnosis and onlyrepresents 0.13 to 0.8 percent of all Pap smears.

Fortunately, there are benign changes thatresult in an AGUS Pap smear. These includechronic endocervicitis, microglandular hyperpla-sia of the endocervix, or ciliated cell metaplasia ofthe endocervix, which is often seen in womenwho have IUDs. Some women with AGUS havehigh-grade (precancerous) squamous cells. Thecomplicating problem is that AGUS cells mayalso come from the upper genital tract, such astubal or ovarian cells, or even metastasis from the pelvis.

Risk Factors for Cervical Dysplasia and Cervical Cancer

• Smoking. Women who smoke are about twice aslikely to develop cervical cancer.

• Human immunodeficiency virus (HIV) infection.Immunocompromise results in increased risk forHPV infections.

• Chlamydia infection. Recent or past positive testresults for chlamydia may lead to greater risk forcervical cancer.

• Poor nutrition. Diets low in fruits and vegetablesmay increase the risk for cervical cancer.

• Multiple heterosexual partners. Having three ormore partners in a lifetime increases risk of cervi-cal cancer.

• Obesity. Overweight women are more likely todevelop cervical cancer.

• Oral contraceptives. Although the research ismixed, long-term use of oral contraceptives mayincrease the risk of cervical cancer.

• Low socioeconomic status. Poor access to ade-quate health care, including Pap tests and treat-ment of precancerous lesions, leads to higher riskfor cervical cancer.

• Family history of cervical cancer. Recent studiessuggest that women with a mother or sister withcervical cancer are at higher risk for developingcervical cancer.

• First intercourse. Women at highest risk of test-ing positive for HPV are those in the first fewyears after first intercourse.

• Age. HPV risk prevalence declines with age.


When the report says AGUS “favor neopla-sia,” this is of great concern, because 50 to 100percent of patients with this test result have a significant cervical lesion. These could include ahigh-grade CIN, adenoma carcinoma in situ, oradenocarcinoma. Even though more than 50 per-cent of women with AGUS will be found to benormal, we cannot predict this, and a normalfollow-up Pap smear may be falsely normal, orwhat is called a false negative. Therefore, a prac-titioner must carefully evaluate AGUS.

Evaluation may include colposcopy, biopsy,endocervical curettage and endometrial biopsy,in some cases dilation and curettage or hys-teroscopy, and in some cases a conization. Ifthere is adenomacarcinoma in situ on biopsy, acervical conization is recommended. Cervicalconization for any woman with AGUS “favorneoplasia,” adenocarcinoma in situ, or adenocar-cinoma is recommended for most women. Ifthere is frank invasion detected by biopsy, moreextensive surgery is recommended.

A Note About New Technologies

Most women are familiar with the Pap smear. Cellsare scraped from the cervix and placed on a slide forexamination in a laboratory. There is now a newliquid-based technique in which the cervical cellscollected by scraping the cervix are placed in liquid.In the laboratory much of the mucus, blood, andinflammatory cells are removed from the cellsample. Liquid-based methods are more expensivethan conventional Pap tests but have a higher sensi-tivity for detection of lower-grade squamous celllesions and can be used to test for HPV types inwomen with atypical squamous cells of undeter-mined significance (ASC-US) Pap results. The FDAhas approved two liquid-based cytology methods:the Sure-Path system and the ThinPrep Pap test.

Reporting of Abnormal Pap Results

About 5 to 10 percent of Pap tests performed in the United States each year are abnormal.Abnormal cells include the following:

• ASC-US: atypical squamous cells of unde-termined significance. This is considered amild abnormality. ASC-US is often thentested for HPV types.

• ASC-H: atypical squamous cells, cannot ruleout high-grade (precancerous) lesions.Women with ASC-H are at greater risk forCIN 2 or CIN 3. For this reason, andbecause detection of high-risk types of HPVis much more common with ASC-H, therecommendation is that these women getcolposcopy and biopsies.

• LSIL: low-grade squamous intraepitheliallesion—early changes in the size, shape, andnumber of abnormal cells. Lesion refers toan area of abnormal tissue, and intraepithe-lial means that the abnormal cells are pres-ent in the surface layer of cells, not thedeeper glandular layer. This is considered amild abnormality. Colposcopy and biopsiesare recommended.

• HSIL: high-grade squamous intraepitheliallesions. There may be a few, or there may bemany. This is obviously more severe andserious and has a higher likelihood of pro-gressing to cervical cancer. Colposcopy andbiopsies are recommended.

• ASC-US and ASC-H: HPV testing is recommended.

• LSIL and HSIL: These are generally nottested for HPV typing, as it does not alterthe course of treatment.

If the results of the Pap smear are ASC-H,LSIL, or HSIL, the clinician should perform orrecommend a colposcopy and biopsies. This is theonly certain way to evaluate the abnormal cells anddetermine the appropriate course of treatment.


Cervical dysplasia is an excellent example of whatpreventive medicine can accomplish because, inalmost all cases, it is a preventable disease. Through


lifestyle habits, dietary factors, nutritional supple-mentation, and regular Pap smears, most cases ofcervical dysplasia and its consequence, cervicalcancer, could be avoided.

Natural medicine perspectives on cervical dys-plasia are consistent with conventional medicine’sunderstanding that the human papillomaviruscauses virtually all cases and that this virus is sexu-ally transmitted. Many cofactors serve as cocar-cinogens in the development of cervical dysplasia,including smoking, nutrient deficiencies, immunedeficiency, and possibly oral contraceptives. Wherenatural medicine diverges in its approach is inadvising patients what they can do about thesecofactors. In addition, there are nutrients that canbe used in supplement form both to prevent theprogression of cervical dysplasia to cervical cancerand to reverse some cases of dysplasia.

Recommendations for Pap Smear Testing

• For women up to age 29: annual Pap with con-ventional smear, or every two years usingliquid-based smear

• For women 30 years and older: if three consec-utive normal Paps, may go to every two tothree years unless history of DES or HIV orimmunocompromised

Note: Despite these recommendations, consider thatall women should have annual Paps; this is to ensurethat they also get an annual exam. Begin Pap smeartesting approximately three years after onset of vagi-nal intercourse, no later than 21 years of age.

• Stop screening: for women 70 years or olderwho have had three or more consecutivenormal Paps after age 60

• Women with ASC-US and ASC-H can receiveHPV testing to determine low-risk or high-riskHPV subtypes

• Women with ASC-H, LSIL, and HSIL should geta colposcopy and biopsies

KEY CONCEPTS

• Cervical dysplasia is a sexually transmitted dis-ease transmitted through skin-to-skin contact.Condoms do not fully protect because HPVextends onto skin beyond the condom, but theymay impart some protection and may enhancepossibility of regression of low-grade lesions tonormal.

• The human papillomavirus (HPV) causes virtuallyall cases of cervical dysplasia, although mostwomen exposed to HPV actually never get dysplasia.

• Cervical dysplasia is classified as either low-gradeor high-grade and, if left untreated or if the bodyis not able to reverse it on its own, can progressto cervical cancer, especially if a person isinfected with the oncogenic strains of HPV.

• Cervical cancer of squamous cells is a preventabledisease.

• Pap smears are screening tests, not diagnostictests.

PREVENTION

• Annual Pap smears are the single most impor-tant factor in preventing cervical cancer and indetecting earlier grades of cervical dysplasia.

• The use of condoms during intercourse is a sig-nificant tool in preventing exposure to HPV,reducing the risk of chlamydia and HIV, andreducing the risk of cervical dysplasia.

• Reduce sexual risk factors: multiple partners,sexual exposure to men who have genital warts,sexual exposure to men sexually exposed towomen with genital warts or cervical dysplasia,and intercourse prior to age 18.

• Avoid smoking.• Eat a healthy whole foods diet rich in green,

yellow, orange vegetables and lignans.• Use folic acid supplementation if using oral

contraceptives.• HIV-positive women and women who are

immunosuppressed because of kidney dialysis orimmunosuppressive medications are at higherrisk for cervical dysplasia and cervical cancerand need more frequent screening.

• Consider contraceptive options other than oralcontraceptives.


Cervical dysplasia is both a local problem in-volving the cervical tissue immunity and healthand a systemic problem involving generalimmune health and resistance to viral exposure.The overriding goals of natural treatments are toreduce exposure to the human papillomavirus,reduce cofactors, correct nutrient insufficiencies,improve local immune response, strengthen gen-eral immune health, and prevent the progressionto cervical cancer.

NUTRITION

Cervical cancer has been studied in relationship to many dietary factors. In general, diets high in vitamin C, carotenoids, vitamin E, selenium,and other substances found in fruits and vegetableshave been found to be protective in at least somestudies.13–17 A recent study found that higher levelsof vegetable consumption were associated with a54 percent decrease in risk of HPV persistence.Also, a 56 percent reduction in the persistence ofthe virus was observed in women with the highestplasma cis-lycopene concentrations comparedwith women with the lowest plasma cis-lycopeneconcentrations. These results suggest that veg-etable consumption and circulating cis-lycopenemay be protective against HPV persistence.18

Another report revealed that the risk of chronicHPV infection was lower among women reportinghigher intake of the following foods: carotenessuch as beta-cryptoxanthin (found in eggs, yellowand orange fruits and vegetables), lutein and zeax-anthin (eggs, dark green vegetables), vitamin C,and, specifically, papaya.19

In the treatment sections of this chapter, Iemphasize a vegetarian diet, one that is high infruits and vegetables, especially yellow-orange oneslike carrots, yellow squash, cantaloupe, peaches,and corn. In China, consumption of both animalfoods (including meat, eggs, and fish) and greenvegetables was significantly correlated with a lowerdeath rate from cervical cancer.20 One studyamong white women showed that risk of cervicaldysplasia and cervical cancer was not affected by

increased consumption of vegetables, yellow-orange vegetables, fruits, or legumes.21 Nonethe-less, there is enough evidence to support a diet richin beneficial vegetables.

Phytoestrogens may also play a role in loweringpremalignancies of the cervix. A recent studydemonstrated that plasma levels of equol andenterodiol, two isoflavonoids, were positively asso-ciated with a lower cervical dysplasia risk, and inaddition found a nonsignificant positive associa-tion with enterolactone, a lignan. Consistent withthese results, dietary sources of lignans, includinggarlic, onions, grapefruit, seeds, seaweed, and taro,were positively associated with lowered CIN risk.22

Indole-3-carbinol, found in cruciferous veg-etables such as broccoli, cabbage, brussels sprouts,cauliflower, and kale, has the potential to preventand treat several cancers. Eating these foods altersestrogen metabolism in such a way as to reducethe carcinogenic metabolites of estrogen metabo-lism. Women with CIN 1 or 2 have altered estro-gen metabolism and have higher 16-alphahydroxyestrone, a potent carcinogen, and fewer 2-hydroxyestrogen metabolites than women with noabnormal cells of the cervix.23


Carotenes. Carotenes include beta-carotene,alpha-carotene, cryptoxanthin, gamma-carotene,zeaxanthin, lutein, and lycopene. Studies haveshown that beta-carotene deficiency in the cervi-cal cells plays an etiologic role in the develop-ment of cervical dysplasia.24 In addition, asignificant decrease in plasma beta-carotenelevels is found in women with either cervical dys-plasia or cancer of the cervix.25

It has been suspected that carotenes likelycopene, found in tomatoes, are more responsi-ble for an improvement in dysplasia than is beta-carotene or the other carotenes.26 In fact, recentstudies have found that high serum levels oflycopene and alpha-carotene are associated with adecreased risk of cervical dysplasia,27 and increas-ing serum levels of lycopene alone was found to


increase clearance of oncogenic HPV infectionsby over 50 percent.28, 29

My own research study investigating naturaltreatment methods for cervical atypia, cervical dysplasias, and carcinoma in situ of the cervix used beta-carotene supplementation as one part ofa multifactorial supplementation and local treat-ment protocol. I found a high success rate using this combination protocol. Most of the women weregiven supplements of 150,000 units of mixed natu-ral carotenes daily for a minimum of three months.Of 43 women studied, 38 patients returned tonormal, 3 patients had partial improvement, 2 stayed the same, and none of the patients pro-gressed to a worse state of dysplasia during thecourse of the natural treatment protocol.30, 31

The full treatment protocols for each degree ofdysplasia are described in the treatment plans inthis chapter. Overall, my approach has been to rec-ommend increased sources of carotenes in the dietas well as supplementation. There are potentialconcerns about using beta-carotene by itself, espe-cially in women who are at higher risk for lungcancer. As a precaution, I avoid beta-carotene sup-plementation in women at high risk for lungcancer (smokers), and for everyone else, I only rec-ommend products that have mixed carotenes andnatural carotenes. Careful label reading is essential.If the label doesn’t say “natural,” then the producthas synthetic beta-carotene.

Do not be alarmed if your skin turns an orangetint when supplementing with high amounts ofcarotenes. It is merely a pigment and is not a signof liver toxicity. Carotenes are not toxic.

Carotenes

Mixed, natural carotenes, 75,000 IU twice daily25,000–50,000 IU for prevention (see treatment plans)

Vitamin A. Studies have shown that dietaryvitamin A protects against cervical cancer. Womenwith lower serum levels and dietary intakes of totalvitamin A are significantly more likely to have dysplasia or carcinoma in situ than women with a

higher intake of these nutrients.32–34 Anotherstudy showed that the rate of progression fromdysplasia to cervical cancer was nearly five timeshigher in women with lower serum retinol levelsthan those with higher serum retinol levels35 andthat diets rich in vitamin A and high-retinol foodsmay reduce risk of in-situ and invasive cervicalcancer.36 In addition, in vitro studies confirm thatvitamin A and its analogues inhibit the prolifera-tion of HPV infection through apoptosis (celldeath) and inhibition of cell growth rates. Suchtherapy is promising in decreasing the progressionof early cervical lesions to cancer.37–39

Topical vitamin A is an important form of treat-ment as well. In one study of 301 women, topicalvitamin A (retinoic acid) increased the completeregression rate of moderate dysplasia from 27 per-cent in the placebo group to 43 percent in the treat-ment group. Women with severe dysplasia failed torespond.40 An earlier, well-known study on topicalvitamin A and dysplasia on the exocervix (externalsurface of the cervix) at the University of Arizonahad comparable results, eliminating the disease in10 of the 20 women. Five of the 10 had mild dys-plasia, and 5 had moderate dysplasia.41 Too fewpatients had severe dysplasia to evaluate. This find-ing was replicated recently in a study of three differ-ent doses of topical retinoic acid in women withCIN 1 and 2.42 In my own research, vitamin A sup-positories were applied topically as part of a multi-factorial systemic and local treatment plan. (Theprotocol is described later in this chapter.)

Vitamin E. Low levels of serum vitamin Ehave been associated with an increased risk of allstages of CIN and cervical cancer and high levelsassociated with a decreased risk.43–46 Low levels ofvitamin E combined with deficient levels of vita-min A have been associated with an increased riskof oncogenic HPV infection.47 One study demon-strated a greater than 50 percent inhibition of proliferation of HPV-infected cells in vitro.48 Inaddition, vitamin E is a potent antioxidant and,therefore, may mitigate the oxidative damage asso-


ciated with cervical dysplasia and cancer.49 In arecent study, women with CIN or cervical cancerwere found to have low levels of vitamin E andother antioxidants—like glutathione, vitamin C,and CoQ10—were found to be low, while mark-ers of lipid peroxidation were found to be high,both corresponding to severity of disease stage.50–52

Vitamin E can help in the treatment of cervi-cal cancer as well by improving the efficacy ofradiation therapy and enhancing tumor responseand chromosomal damage of cancer cells whileconcurrently protecting normal cells.53

Vitamin C. The possible role of vitamin C inpreventing cervical dysplasia is of special interestbecause vitamin C is involved in collagen synthe-sis, detoxifies chemical carcinogens, interferes withthe formation of chemical carcinogens, and mod-ulates the immune system. It has been demon-strated in more than one study that there is asignificant decrease in vitamin C intake as well asplasma levels of vitamin C in patients with cervi-cal dysplasia.54, 55 Vitamin C supplementation hasnot been studied by itself as a treatment for cervi-cal dysplasia. It was a part of the comprehensivetreatment protocol in my research study.

Vitamin C

2,000–6,000 mg per day1,000–2,000 mg per day for prevention (see treatment

plans)

Folic Acid. There have been several studiesusing folic acid supplementation in women withmild and moderate cervical dysplasia, with con-flicting results. In one study, women with mild ormoderate dysplasia received 10 mg daily of folicacid supplementation or placebo for threemonths. All of these women had used oral con-traceptives for at least six months and continuedto do so. The results showed significant improve-ment or normalization of Pap smears and biop-sies at the end of the treatment period.56

In patients with folic acid deficiency, changesin the cells of the cervix (called megaloblastic

abnormalities) and low blood levels of folic acidhave been associated with a moderately increasedrisk of invasive cervical cancer.57, 58 Deficiency hasbeen observed more often in women who aretaking oral contraceptives. In another study,women taking 10 mg of folic acid daily for threeweeks (while continuing oral contraceptives)showed a striking reversion of the megaloblasticchanges toward the normal,59 with a regression-to-normal rate of 20 percent in this study and 100percent in another.60 Folic acid supplementationmay be effective in preventing dysplasia from pro-gressing as well. Theoretically, folic acid may actby decreasing homocysteine, which, when ele-vated, has been associated with an increased risk of cervical cancer.61, 62 It should be noted that arecent study demonstrated the difficulty of gettingadequate folate via diet and, therefore, additionalsupplementation is warranted.63

When doses as high as 10 mg of folic acid perday are given, two points must be kept in mind.The first is that most retail natural foods storeshave folic acid available only in capsules up to800 mcg (less than 1 mg, which is equal to 1,000mcg). Higher doses of folic acid are available onlyby prescription from your medical doctor orlicensed alternative practitioner. A prescriptionliquid form is available for which one drop isequal to 5 mg, which is very cost effective. Thesecond issue is that high doses of folic acid canmask a vitamin B12 anemia. To avoid this, takeeither a multiple vitamin-mineral, B-complex, orB12 supplement along with the daily folic acid.

Folic Acid

2.5–10 mg per day800–2,400 mcg per day for prevention (see treatment

plans)

B Vitamins. B vitamins, specifically ribo-flavin, thiamine, and B12, have an inverse corre-lation with risk for CIN, leading someresearchers to promote the protective role theymay play in cervical cancer, reducing the risk by


as much as 50 to 90 percent for the upper limitsof intake.64 Women with the highest levels ofserum B12 were less likely to have a persistentinfection.65 Serum B12 levels should be evaluatedand deficiency corrected. As with folic acid, B12

may act by decreasing homocysteine, which,when elevated, has been associated with anincreased risk of cervical cancer.66, 67

Vitamin B12

1,000 mcg per day

Botanicals

Green Tea. One of the most exciting advancesin the treatment of cervical dysplasia is theresearch that has been published on green tea. Inboth laboratory and clinical studies, constituentsof green tea, namely polyphenol E (poly E) andepigallocatechin-3-gallate (EGCG), have beeneffective against HPV-infected cervical cells andlesions. The mechanisms involved appear to beapoptosis, cell cycle arrest, modification of geneexpression, and antitumor effects.68, 69 A clinicalstudy confirms these findings in patients throughthe use of either topical application via a poly Eointment and/or oral ingestion via a poly E or anEGCG capsule. All treatment groups improvedcompared to placebo (50 to 75 percent versus 10percent), but the topical treatment groupsimproved the most significantly compared to oralalone (75 percent versus 50 to 60 percent).70

Green Tea

Green tea extract (95% polyphenols, 80% catechins,55% EGCG, 10% caffeine): 300 mg per day orally

Green tea suppositories: insert one twice weekly (seetreatment plans)

Indole-3-Carbinol/Diindolylmethane (DIM).Indole-3-carbinol (I3C) is a phytochemical foundin cruciferous vegetables, including cabbage, broc-coli, Brussels sprouts, cauliflower, and kale. I3C isconverted in the stomach to a variety of com-

pounds including diindolylmethane (DIM). It hasbeen suggested that I3C can act in several ways toprevent abnormal cell growth and prevent tumorprogression. Recent studies indicate that I3C hasthe ability to prevent and maybe even treat somecommon cancers, especially those that are estrogenrelated,71 by altering the pathway of estrogenmetabolism.72–74

Women with CIN 2 and 3 have altered estro-gen metabolism; higher 16-alpha hydroxyestrone,a potent carcinogen; and fewer 2-hydroxyestrogenmetabolites than normal.75 One therapeutic goal of treatment, then, is to increase the 2-hydroxylation of estrogen and decrease the 16alpha-hydroxylation. In one double-blind, placebo-controlled study of 30 women with CIN 2 orCIN 3,76 4 of 8 patients in the 200 mg group and4 of 9 in the 400 mg group had complete regres-sion of their CIN compared to none of theplacebo group. A laboratory study of human cer-vical cancer cells determined that I3C and DIMcould induce apoptosis (cell death) of human cer-vical cancer cells and HPV-16-infected cervicalcells of mice.77 It appears DIM is preferred overI3C due to increased bioavailability and the factthat it increases the protective 2-hydroxyestrogenwithout increasing another harmful metabolite,the 4-hydroxyestrogens.

Diindolylmethane (DIM)

200–400 mg per day

Additional Botanicals. Traditional herbalmedicine includes the use of many plants for systemic immune support. No plants (exceptgreen tea) have been studied by themselves inrelationship to the human papillomavirus andcervical dysplasia that I am aware of, althoughmany plants are known both to act as immunemodulators and to be antiviral in their activity.

This concept of immune support is animportant part of preventive medicine as well asin reversing and preventing the progression ofcervical dysplasia. Since up to 80 percent of the


U.S. sexually active adult population carries thehuman papillomavirus and less than 5 percenthave a visible lesion or abnormal Pap smears, it iscommon sense that most people’s bodies have theability to prevent the virus from causing an actualdiseased state. Specifically, their immune systemsare doing a better job at keeping them healthy.This is true for women both systemically and inthe vagina. There is local immune tissue in thecervical epithelium, and the immune status ofthis tissue is in part responsible for resistance tothe virus.

This is the background logic for both systemicimmune support and local immune support. Aspart of the research protocol, you will see the use

of a systemic botanical formula including thuja,echinacea, ligusticum, and goldenseal. You willalso notice herbal suppositories containing manytraditional herbs for immune support, antiviralactivity, and squamous cell repair. These includemyrrh, echinacea, usnea, goldenseal, marshmallowroot, geranium, and yarrow.

Recent evidence supports the use of cur-cumin in the prevention of cervical cancer due toits ability to inhibit lipid peroxidation and down-regulate HPV virus.78–80

Curcumin

350–500 mg once to twice daily

Criteria and Guidelines for Treatment Selection

Note: Not all of the treatments described in thischapter are appropriate for self-care. Some, such asthe escharotic treatment, need to be administeredby a licensed health-care practitioner trained inwomen’s health. In addition, not all cases of cervi-cal dysplasia are appropriate for the natural treat-ment protocols. Licensed practitioners familiar withdiagnosing and treating cervical dysplasias shouldbe consulted to assist in making appropriate andsafe decisions. For practitioners reading this book,the following criteria may be helpful in determiningthe appropriate treatment:

Criteria for Naturopathic Protocol

1. ASC-US.2. ASC-US with documented HPV.3. ASC-H: endocervical curettage is negative or

positive with a satisfactory colposcopy.4. Low-grade squamous intraepithelial neoplasia:

endocervical curettage is negative with a satis-factory colposcopy.

5. High-grade squamous intraepithelial neoplasia:endocervical curettage is negative with a satis-factory colposcopy.

6. ASC-H: endocervical curettage is positive with asatisfactory colposcopy, but the patient is at lowrisk for more serious disease or has low-risk HPVtyping, or at the discretion of the practitioner.

7. Low-grade squamous intraepithelial neoplasia:endocervical curettage is positive with a satis-factory colposcopy, but the patient is at low riskfor more serious disease or has low-risk HPVtyping, or at the discretion of the practitioner.

8. High-grade squamous intraepithelial neoplasia:endocervical curettage is positive with a satis-factory colposcopy, but the patient is at lowrisk, or at the discretion of the practitioner andconsidered carefully after colposcopy, biopsies,and careful follow-up.

9. It is possible to treat carcinoma in situ in selected cases, but this is definitely a judgmentcall and should be considered very carefully aftercolposcopy, biopsies, and careful follow-up.

Referrals for Colposcopy with Biopsies

1. ASC-US if HPV DNA testing is positive for high-risk HPV; if no HPV testing is done, then repeatthe Pap twice at 4 to 6 month intervals. If HPVtyping is negative for high-risk types, thenrepeat Pap in 12 months.

2. ASC-H.3. Low-grade squamous intraepithelial lesions.4. High-grade squamous intraepithelial lesions.5. AGUS (atypical glandular cells of undetermined

significance); need endometrial biopsy as well.6. Adenocarcinoma in situ (AIS): need endometrial

biopsy as well.(continued )


Criteria and Guidelines for Treatment Selection (continued )

7. Pap smear diagnosis of microinvasion or frankinvasion.

8. Endometrial cells present in a postmenopausalwoman even if the cells are benign; also needs anendometrial biopsy.

9. A patient that may not follow through with therecommended follow-up Pap smear after an abnor-mal Pap result.

10. Visible unknown cervical lesion, regardless of thePap smear test result.

11. Initial exam of a DES daughter.12. Unexplained or persistent cervical bleeding.13. Vulvar condyloma with abnormal Pap smear test

result.14. To be used for follow-up after treatment plan is

completed, especially in high-grade squamousintraepithelial lesions.

Referrals for Conization or LEEP

1. Pap smear results that are more than one grade ofdysplasia different than that seen on colposcopyor reported on in the biopsy.

2. Biopsy squamous intraepithelial lesions with threeto four quadrants involved.

3. Unsatisfactory colposcopy with any degree ofsquamous intraepithelial lesions on biopsy.

4. The patient may not be a good candidate for moreongoing treatments and the closer follow-uprequired by alternative treatments.

5. No improvement in pathology using the initialnaturopathic plan or repeated alternate plan.

6. If AGUS on Pap smear and no detection of diseaseon colposcopy, biopsies, and endocervical curettage.

7. If AIS on Pap smear and no detection of diseaseon colposcopy, biopsies, and endocervical curettage

Practitioner and patient discretions:

8. Positive endocervical curettage with any degreeof squamous intraepithelial lesions. A moreassertive approach is recommended.

9. High-risk patients: the last Pap test was morethan one year previous, a history of genitalwarts, a history of cervical dysplasia, smokers,multiple sexual partners with lack of safe sexpractices. In these cases, a more proactive andassertive approach is recommended.

Referrals for Probable Hysterectomy

1. Microinvasive cervical cancer.2. Frank invasive cervical cancer.3. Adenocarcinoma.

Toxicity studies prove its safety up to 8,000mg per day by mouth for up to three months aswell as its efficacy in chemoprevention in cancer,including cervical cancer.

The Escharotic Treatment. The escharotictreatment is a topical caustic treatment of thecervix used to remove abnormal cells. It involvesthe use of zinc chloride mixed with a botanical,Sanguinaria canadensis (bloodroot). I have usedthe escharotic treatment for more than 24 years,and at one time I conducted a small study usingit as a treatment along with suppositories andherbal/nutritional supplementation in sevenwomen with carcinoma in situ of the cervix.30

After one year, four of the women remained dis-ease free, one woman improved to atypia andthen reverted to mild dysplasia, and two womenhad partial improvement. In a follow-up study,

similar protocols were used including theescharotic treatment with some of the moresevere cases. I discussed this in more detail in thesection of this chapter on carotenes. Indicationsand directions for use of the escharotic treatmentare given later in this chapter.

Botanical Formula I

Red clover: 1 ozDandelion root: 11⁄2 ozLicorice root: 1 ozGoldenseal: 1⁄2 oz

Botanical Formula II

Thuja: 1 ozEchinacea: 11⁄2 ozGoldenseal root: 1⁄2 ozLigusticum: 1 oz


LIFESTYLE HABITS

Sexuality

Early age at first intercourse (before age 18) withunprotected sex and/or multiple heterosexualpartners with unprotected sex are associated withan increased risk of cervical dysplasia and cervicalcancer. As nearly all cases of cervical dysplasia

involve HPV, women can best protect themselvesby using condoms during intercourse. Even if amale partner does not have visible genital warts,he can have nonvisible genital warts and can alsocarry the virus.

If the partner is female, it is more difficult tocontract the virus and cervical dysplasia, but notimpossible. Avoiding genital-to-genital contact

See the Resources section for information on the con-tents of and resources for the suppositories and otherproducts included in these treatment plans.

Initial Naturopathic Plan

Topical

Week 1: vitamin A suppository nightly for 6 nightsWeek 2: herbal vaginal suppository nightly for 6

nightsWeek 3: vitamin A suppository nightly for 6 nightsWeek 4: herbal vaginal suppository nightly for 6

nightsWeek 5–12: green tea suppository 2 nights per week

Systemic

Folic acid: 10 mg dailyVitamin C: 6 g dailyBeta-carotene: 150,000 IU dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyBotanical Formula I: 1⁄2 tsp, twice daily

Use systemic treatment for 3 months until follow-up.

Constitutional

Vegetarian diet for 3 months until follow-up

Alternative Naturopathic Plan

Topical

Week 1: vitamin A suppository nightly for 6 nights,Vag Pack suppository 1 night per week

Week 2: herbal vaginal suppository nightly for 6nights, Vag Pack suppository 1 night per week

Week 3: vitamin A suppository nightly for 6 nights,Vag Pack suppository 1 night per week

Week 4: herbal vaginal suppository nightly for 6nights, Vag Pack suppository 1 night per week

Weeks 5–12: green tea suppository twice per week

Systemic

Vitamin C: 6 g dailyBeta-carotene: 150,000 IU dailyFolic acid: 10 mg dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyBotanical Formula I: 1⁄2 tsp twice daily


Constitutional


Additional Therapies to Consider

Zinc: 30 mg dailyVitamin E: 400 IU dailySelenium: 400 mcg dailyGreen tea suppository: twice per weekDIM: 200 mg daily

Comments: A follow-up Pap smear in 3 to 6 monthsthat is still abnormal warrants colposcopy and biopsies.

Maintenance Plan for 3 Months (After Normal Pap Smear)

Vitamin C: 2 g dailyBeta-carotene: 150,000 IU dailyFolic acid: 2.5 mg dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyVegetarian diet

Sample Treatment Plan for ASC-US


Sample Treatment for Mild Dysplasia (CIN 1, Low-Grade SIL)



Topical

Week 1: vitamin A (Vital-A) suppository nightly for 6nights, Vag Pack suppository for 1 night

Week 2: herbal vaginal suppository nightly for 6nights, Vag Pack suppository for 1 night

Week 3: vitamin A suppository nightly for 6 nights,Vag Pack suppository for 1 night

Week 4: herbal vaginal suppository (Herbal-C) nightlyfor 6 nights, Vag Pack suppository for 1 night


Systemic

Vitamin C: 6 g dailyBeta-carotene: 150,000 IU dailyFolic acid: 10 mg dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyBotanical Formula I: 1⁄2 tsp twice daily


Constitutional


Alternate Naturopathic Plan

Topical

Escharotic treatment (described later in this chapter)twice per week for 3 weeks

After the last escharotic treatment:


nightsWeek 3: vitamin A suppository (Vital-A) nightly for 6

nightsWeek 4: herbal vaginal suppository nightly for 6

nightsWeeks 5–12: green tea suppository twice per week

Systemic

Vitamin C: 6 g dailyBeta-carotene: 200,000 IU dailyFolic acid: 10 mg dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyBotanical Formula I: 1⁄2 tsp twice dailySelenium: 400 mcg daily


Constitutional



Zinc: 30 mg dailyVitamin E: 800 IU dailySelenium: 400 mcg dailyDIM: 200–400 mg daily

Maintenance Plan for 6–12 Months


or practicing safer sex if the partner has knowngenital warts may be advisable. It is consideredvery low risk for the virus alone to be transmittedbetween women, although it is theoretically pos-sible. Both heterosexual and homosexual womenask about the risk of transmitting or contractingthe virus through oral sex. Again, this is theoret-

ically possible, and there are conditions when theHPV virus may lodge in the larynx and oralcavity. However, these cases are extremely rare,and so it is left to each person to make that judg-ment on her own. If one of the partners isimmunocompromised (HIV-positive, a trans-plant patient, or has chronic hepatitis), then she


is more vulnerable to contracting HPV, and pre-cautions are definitely warranted.

Smoking

Probably the single most important cofactor in the development of cervical dysplasia and cervical

cancer is smoking. Smokers have a two- to threefoldincrease in the incidence of cervical dysplasia.81

Some studies indicate that the incidence comparedto nonsmokers is even greater than that. Nicotine isactually concentrated in the glands of the cervix,where it then acts as a carcinogenic compound.

Sample Treatment for Moderate Dysplasia (CIN 2, High-Grade SIL)



Topical

Week 1: vitamin A suppository nightly for 6 nights,2 Vag Pack suppositories for 1 night

Week 2: herbal vaginal suppository nightly for 6nights, 2 Vag Pack suppositories for 1 night






Systemic

Vitamin C: 6 g dailyBeta-carotene: 200,000 IU dailyFolic acid: 10 mg daily for 3 monthsSelenium: 400 mcg dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyCarotene: 150,000 IU dailyBotanical Formula II: 1⁄2 tsp twice daily


Constitutional



Topical

Escharotic treatment twice per week for 4 weeks


Week 1: vitamin A suppository nightly for 6 nightsWeek 2: papilloma suppository nightly for 6 nightsWeek 3: vitamin A suppository nightly for 6 nightsWeek 4: papilloma suppository nightly for 6 nightsWeeks 5–12: green tea suppository twice per week

Systemic

Folic acid: 10 mg dailyVitamin C: 6 g dailyMultiple vitamin/mineral: follow label directionsBeta-carotene: 150,000 IU dailyGreen tea capsules: 1 capsule dailyBotanical Formula I: 1⁄2 tsp twice daily


Constitutional



Zinc: 30 mg dailyVitamin E: 800 IU dailySelenium: 400 mcg dailyDIM: 200–400 mg daily

Maintenance Plan for 1 Year



Sample Treatment for Severe Dysplasia (CIN 3, High-Grade SIL)



Topical






Systemic

Folic acid: 10 mg dailyVitamin C: 6 g dailyBeta-carotene: 150,000 IU dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyBotanical Formula II: 1⁄2 tsp twice daily


Constitutional



Topical



Week 1: vitamin A suppository nightly for 6 nightsWeek 2: papilloma suppository nightly for 6 nightsWeek 3: vitamin A suppository nightly for 6 nights

Week 4: papilloma suppository nightly for 6 nightsWeeks 5–12: green tea suppository twice per week

Systemic

Vitamin C: 6 g dailyBeta-carotene: 200,000 IU dailyFolic acid: 10 mg dailySelenium: 400 mcg dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyDIM: 200–400 mg dailyBotanical Formula II: 1⁄2 tsp twice daily


Constitutional



Zinc: 30 mg dailyVitamin E: 800 IU dailySelenium: 400 mcg dailyPyridoxine: 50 mg 3 times daily


Vitamin C: 3 g dailyBeta-carotene: 150,000 IU dailyFolic acid: 2.5 mg dailyVitamin E: 400 IU dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyBotanical Formula II: alternate 1 month on,

1 month offVegetarian diet

Smoking may also alter immune functionand affects the levels and distribution of ascorbicacid. Ascorbic acid in the cells of the cervix andthe vagina and plasma levels of ascorbic acid arereduced in smokers.82

Oral Contraceptives

Earlier studies suggested that oral contraceptive(OC) use increased the risk of cervical neoplasia,both invasive and precancerous cervical dysplasias.83

Recently, however, studies that are controlled for


sexual history have been reassuring. In addition, noform of hormonal contraception, be it oral or injec-tion, was found to be associated with an increasedrisk for developing dysplasia.84 While hormonalcontraception is not implicated in HPV-related dys-plasia, condoms should still be used concurrently.

Three large, well-controlled studies looked atinvasive cervical cancer and OC use and did notfind statistically significant associations comparedwith women who never used OCs.85–87 There wasno overall change in risk of invasive cervicalcancer. However, one of the three studies did find

Sample Treatment for Carcinoma In Situ (CIN 3, High-Grade SIL)



Topical






Systemic

Folic acid: 10 mg dailyVitamin C: 6 g dailyBeta-carotene: 180,000 IU dailySelenium: 400 mcg dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyBotanical Formula II: 1⁄2 tsp twice daily


Constitutional



Topical



Week 1: vitamin A suppository nightly for 6 nightsWeek 2: papilloma suppository nightly for 6 nights

Week 3: vitamin A suppository nightly for 6 nightsWeek 4: papilloma suppository nightly for 6 nightsWeeks 5–12: green tea suppository twice per week

Systemic

Vitamin C: 10 g dailyBeta-carotene: 200,000 IU dailyFolic acid: 10 mg dailySelenium: 400 mcg dailyMultiple vitamin/mineral: follow label directionsGreen tea capsules: 1 capsule dailyDIM: 200–400 mg dailyBotanical Formula II: 1⁄2 tsp 3–4 times a day


Constitutional



Zinc: 30 mg dailyVitamin E: 800 IU dailySelenium: 400 mcg dailyPyridoxine: 50 mg 3 times a dayLomatium isolate: 5 drops twice dailyAlternating sitz baths twice weekly for 4 weeks dur-

ing suppository routine


Vitamin C: 3 g dailyBeta-carotene: 150,000 IU dailyFolic acid: 2.5 mg dailyMultiple vitamin/mineral: follow label directionsVitamin E: 400 IU dailyBotanical Formula I: alternate 1 month on,

1 month offVegetarian diet


a modestly increased risk in long-term OC users.85

The other two studies failed to find a significantlyincreased risk of invasive cervical cancer even withlong-term OC use. The definition of long-termuse is not always consistent, but some define it asmore than five years of use. Two other recent stud-ies assessed OC use and risk of cervical dysplasia,and neither of these found any statistically signifi-cant associations.88, 89

One disturbing finding with OC use is anassociation with an increase in the incidence of arare cancer of the cervix called adenocarcinoma, avariant of squamous cervical cancer. The incidenceof this disease has increased over the past severaldecades, while the incidence of invasive squamouscervical cancer has decreased since the pill wasintroduced. Two recent studies86, 90 found a modestbut statistically significant increased risk of inva-sive cervical adenocarcinoma in OC users withover 12 years of use. However, it is important toremember that the cause of cervical cancer is thesexually transmitted human papillomavirus.

PSYCHOLOGICAL FACTORS

The association between psychosocial factors andcervical dysplasia has been the subject of severalinvestigations. Significant life stressors werefound to be correlated, including low coping

style, pessimism, a high degree of social alien-ation, high anxiety states, and feeling threat-ened.91, 92 Life stressors with negative impact overthe previous six months showed a direct, positiveassociation with level of dysplasia, while copingstyle showed a less prominent effect.


The degree of aggression used to combat simplehuman papillomavirus waxes and wanes throughthe years and from provider to provider. WhileHPV can be dormant for decades, recurrence isalways possible. Some practitioners recommendobservation alone through the acute viral phaseof cervical infection in low-risk patients. We haveseen this work at least as often as not. Many doc-tors give patients the option, considering theirlifestyle, other risk factors, prior history, andimmune system status.

Most everyone in the conventional medicalcommunity agrees on how to manage moderateand severe dysplasia: remove it. There is someongoing controversy about the treatment of milddysplasia. Since recent studies have shown that 70to 80 percent of mild dysplasia will revert tonormal tissue before one year, there is an equallycompelling recommendation to just repeat the Papsmear in one year and avoid further treatmentunless the condition progresses. If it is still milddysplasia at 12 months, then repeat the colposcopyand biopsies to exclude more significant lesions. Inother words, mild dysplasia can be observed evenlonger, as long as close follow-up occurs.

When treatment is needed, the proceduresgenerally used are cryotherapy; a conization witha scalpel or laser; laser ablation; or loop electro-surgical excision procedure, referred to as LEEP.All of them remove the dysplastic cells and allownew cells to replace the old. They all workupward of 90 percent of the time when used cor-rectly. Cryotherapy is reserved for mild dysplasia(CIN 1), because of the lesser depth of penetra-tion. The other procedures are recommended for

Sample Treatment Plan AfterLEEP, Conization, or Cryotherapy

Wait for 3 weeks after the procedure (described laterin this chapter), and then begin the following plan.See the Resources section for information on the con-tents of and resources for the suppositories and otherproducts used.

Week 1: vitamin A suppository nightly for 6 nightsWeek 2: herbal suppository nightly for 6 nightsWeek 3: vitamin A suppository nightly for 6 nightsWeek 4: herbal suppository nightly for 6 nights

Systemic and constitutional treatment plans are thesame as is described for the degree of lesion in theother corresponding treatment plans.


moderate and severe dysplasias (CIN 2, CIN 3).Tissue destruction beyond the dysplastic lesionsoccurs in all of these procedures to varyingdegrees to help prevent recurrences. Recurrencesare usually due to new infection, reactivation ofthe virus because of immune system changes, or

inadequate prior treatment with residual cellsthat then persist and regrow.

Cryotherapy is the oldest and cheapest of theseprocedures and is a simple office procedure per-formed with a blunt probe applied to the cervixand tubing that supplies concentrated nitrous

Cervical Escharotic Treatment

The escharotic treatment is especially indicated formoderate dysplasia and severe dysplasia, both high-grade lesions, but only when there is a satisfactorycolposcopy performed by a clinician. In addition, theuse of the escharotic treatment, rather than a LEEP orconization, needs to fall within the guidelines as out-lined in the criteria for naturopathic protocol. Pleasealso read the section in this chapter clarifying whena conization or LEEP is a more appropriate treatment.

The escharotic treatment is best done twice aweek with two full days between treatments. The zincchloride (ZnCl) solution will have to be made by acompounding pharmacist, by prescription.

Instructions for the Practitioner

Before beginning the treatment, you will need thefollowing items:

• 1 cup distilled water• A cup containing 2 powdered bromelain cap-

sules or tablets. Remove the powder from thecapsules or crush the tablets to powder.

• 1⁄4 tsp ZnCl2 solution (90 g ZnCl/60 ml sterlizedwater) mixed in a bottle with 3⁄4 tsp sanguinariatincture

• 1⁄3 cup calendula succus

1. Insert speculum and visualize the cervix.2. Blot the cervix dry with large cotton swab or

cotton ball on the end of a ring forceps.3. Dip a large cotton swab into the distilled water

and then squeeze out the water. Place the dampswab into the bromelain and thickly cover theface of the cervix with the powder, repeating asneeded to cover the cervix completely. Applythe powder in the endocervical canal usingsmall, dampened cotton tip applicators (use anew applicator each time).

4. Leave the bromelain on the cervix and in theendocervical canal for 15 minutes. Place a GYNlamp facing the vagina to provide gentle heatduring this portion of the treatment.

5. Now remove the bromelain by placing a largecotton swab in the calendula succus and thenapplying it to the cervix, thus washing off thebromelain. Repeat with a small cotton tip appli-cator to the endocervical canal. Be liberal;repeat washing two to four times. Take a drylarge swab and absorb the washings that havepooled in the vagina.

6. Now soak a large swab in the ZnCl2/sanguinariamixture that you prepared earlier. Apply this tothe cervix once. Repeat this procedure with asmall cotton tip applicator inserted in the endo-cervical canal. Leave on for one minute. If thiscauses pain, wash the cervix with a smallamount of distilled water. Avoid contact of theZnCl2/sanguinaria mixture with the vaginal wall.

7. Wash off the ZnCl2/sanguinaria mixture withswabs of calendula succus. Wash the endocervi-cal canal as well with a cotton tip applicator.Absorb the liquid that has pooled in the vaginawith a dry cotton swab.

8. Insert two Vag Pack suppositories. Instruct thepatient to leave the suppositories in place for24 hours, using a sanitary napkin as needed forleakage.

9. After the last escharotic treatment, use the fol-lowing treatment plan:

Week 1: vitamin A suppository nightly for 6nights

Week 2: herbal vaginal suppository nightly for 6nights, or in cases with HPV, use condylomasuppository

Week 3: vitamin A suppository nightly for 6nights

Week 4: herbal vaginal or papilloma suppositorynightly for 6 nights


oxide to cause the probe to get very cold. Tissuepenetration is several millimeters. This proceduretakes approximately two to three minutes and isassociated with cramping at the time, whichresolves quickly and is rarely present for more thana day. The devitalized tissue is sloughed as a waterydischarge over the next 10 to 14 days. The cervixis usually well healed within a month.

Conization is employed primarily for endo-cervical dysplasia. A cold-knife procedure is per-formed in the operating room under anesthesiaand employs a scalpel to remove a cone-shapedpiece of cervix and cervical canal. Conization hasthe advantage of more clearly evaluating the mar-gins, because there is no thermal artifact. Laserablation of the transformation zone can be per-formed in the operating room or the office andallows for precise management of lesions butdoes not provide tissue for pathology. Laserconization obtains tissue similar to the cold-knifecone procedure, with some thermal destructionat the margins, and is significantly more expen-sive than LEEP.

The most common current treatment ofendocervical or cervical dysplasia of moderate-to-severe degree is a LEEP procedure, which isgenerally performed in the office with cervicalanesthetic and is usually well tolerated and verycost effective. LEEP can be used to remove theendocervical canal and/or the transformationzone. It also has thermal degradation at the mar-gins. When LEEP or laser is used, the tissuebeyond the cut margin is heated and destroyedfor another 1 to 2 mm of penetration. Even whenthe dysplasia is seen all the way to the margin ofthe biopsy, there is still usually complete treat-ment of the lesion because the heat destructionpenetrates into the tissue beyond the surgical site.

Women treated by LEEP are more likely toconvert to HPV-negative status within one to twoyears after the procedure and do so significantlysooner than those who are merely watched with-out treatment. The LEEP can reduce cervicalmucus and can occasionally cause a stenosis of the

opening to the cervix. The advantage of LEEP isthat it can be done in the office, is well tolerated,and is minimally expensive.

These techniques are all relatively safe andeffective for preventing future cervical cancer.However, their effects on future fertility and preg-nancy outcomes are unclear. Some say that doneproperly, none of these procedures affects fertility,sexuality, or pregnancy. There is no adequate datafrom randomized controlled trials to evaluatethese potential effects. In one analysis of 27 obser-vational trials comparing the fertility and preg-nancy of women who underwent ablation orexcision of CIN lesions to women who were nottreated with these therapies, LEEP and cold-knifeconizations were both associated with significantlyincreased risk for preterm delivery. LEEP was asso-ciated with an increased risk for preterm ruptureof membranes, and the cold-knife cone was asso-ciated with an increased risk for cesarean section.The laser cone and the laser ablation had no asso-ciation with any significant change for any of theoutcomes. None of the treatments had any signif-icant association with perinatal mortality, compli-cation for the infant, or fertility.

Follow-up recommendations may vary depend-ing on your overall case history and your practi-tioner’s perspective. Some patients treated with anyof these conventional treatments are advised tohave three-month Pap smears for the first year andsix-month Pap smears for the next year. Others willhave the recommendation of annual Pap smearsfollowing the conventional treatment.

Prevention: The HPV Vaccine

The newest approach to conventional medicaltreatment of dysplasia is prevention. After a clini-cal trial done in 2002 initially showed that anHPV-16 vaccine reduced the incidence of bothHPV-16 infection and HPV-16 cervical dyspla-sia,93 continued research has lead to the reality ofan HPV vaccine to reduce the incidence of cervi-cal cancer. The FDA approved a quadrivalent vac-cine in June 2006. It vaccinates women against


strains 6 and 11, which cause venereal warts, and16 and 18, which are the most common strainsfound in cervical cancer. The intended recipientsof this vaccine will be pubertal girls who have notyet had intercourse. However, the vaccine has beenrecommended up to age 26, because it will alsohelp prevent venereal warts in women who arecurrently sexually active.

In one study young women without historiesof HPV infection or abnormal Pap smears whowere given the type 16 and 18 vaccine were sig-nificantly less likely to develop HPV type 16 or18 infections or abnormal cervical cells duringthe two-plus years of follow-up.94 In anotherstudy, the 6, 11, 16, and 18 vaccine decreased theincidence of infection by 90 percent in youngwomen compared to placebo.95


Accurate and adequate diagnosis and evaluationis the key to knowing which is the most appro-priate treatment for your case. Colposcopy (mag-nification) and cervical biopsies are the specificdiagnostic methods for evaluation. Pap smears

are not diagnostic; they are screening tests. Whenyour licensed practitioner (naturopathic doctor,medical doctor, osteopathic doctor, nurse-practitioner, or physician’s assistant) recommendsthat you need a colposcopy and biopsy, this isgood advice. They are not recommending treat-ment; they are recommending accurate diagnosis.

Decisions regarding treatments such as aLEEP, cone biopsy, or cryotherapy versus one ofthe natural treatment protocols require a medicalhistory, Pap smear report, colposcopy report,biopsy/pathology report, and a working knowl-edge of the advantages and disadvantages of eachof the treatments. If your conventional practi-tioner is not aware of the research on the naturaltreatment protocols or is biased without knowl-edge, then he or she may not be the most appro-priate person to help you make the rightdecision. Likewise, if your alternative practi-tioner is not aware of the clinical indications forthe conventional treatments as distinguishedfrom the clinical indications for the safety andefficacy of the alternative treatment plan or isbiased without knowledge, then he or she toomay not be the most appropriate person to helpyou make the right decision.

51

OVERVIEW

Around the same time suffragettes were securingthe right to vote, other women, most notablyMargaret Sanger, desperately sought to providewomen a means of “family limitation,”1 latercalled birth control. The political struggle tolegitimize contraception and bring it into themedical arena was long and fierce. Sanger wasjailed on obscenity charges more than once andfinally fled the country rather than face a trial sheultimately won years later. Any public discussionof reproduction was judged obscene under theprevailing Comstock Law. Although women fre-quently died in childbirth or struggled to feedfamilies of six to ten or more, they were forbid-den information concerning fertility regulationthat was literally lifesaving. Although diaphragmsand condoms gradually became more readilyavailable (the first diaphragms in use in Americawere smuggled from Europe through Canada bySanger and her husband), it was not until theSupreme Court decision Griswald v. Connecticutin 1966 that married women’s rights to accessbirth control became assured.

While we modern women lament the absenceof a perfect fertility control option, the mere factthat the birthrate has fallen so drastically these past50 years illustrates both women’s desire to havefewer children and the efficacy of the combinedmethods in achieving that goal. Nevertheless, evenwith the current availability of contraception, fully57 percent of American pregnancies today areunintended.2 Perhaps our difficulty with the issuerelates to our prudish roots. Safe, effective birthcontrol does exist, although failures, whetherhuman or methodological, occur with each. Thebest we can do is choose wisely and minimizehuman error. In addition to natural family plan-

ning or fertility awareness methods (oftendescribed as the rhythm method), there are threegeneral categories—hormonal contraception, bar-rier contraception and the intrauterine devices,and abortion—that complete the list of birth con-trol methods. Sterilization, the most commonmethod of fertility control, is a safe surgical proce-dure for either men or women. This method isused by about 20 percent3 of couples; yet it, too,has a failure rate of about 1 in 400.

4C O N T R A C E P T I O N C H A P T E R

KEY CONCEPTS

• Consult your health-care practitioner to deter-mine the effectiveness, health benefits, andhealth risks of each contraceptive method.

• Consult your health-care practitioner about cau-tions and contraindications for each method.

• Smokers older than 35 should not use hormonalcontraceptive methods.

• The choice of contraception method is based onbenefits, risks, effectiveness, cost, side effects,ease of use, and personal choice.

• The key to the contraceptive benefit is properuse and compliance with the chosen method.

• Pregnancy itself carries considerable healthrisks. These must also be considered whenchoosing a method of contraception.

• Regular annual health exams are required forusers of hormonal contraception.

• Report any side effects that you think arerelated to your method of contraception to yourhealth-care practitioner.

FERTILITY AWARENESS

Many couples successfully rely on this drug-freeand device-free method that depends on identi-fying a woman’s fertile periods and abstainingfrom intercourse during those times. However, to



achieve the lowest failure rates of 1 to 10 percentrequires relatively long periods of abstinence eachmonth—at least 10 and up to 20 days—depend-ing on cycle length and predictability. The average pregnancy rate with most who use thismethod is 20 percent, clearly less than the 85percent rate experienced with no method at all.More pregnancies result from taking chancesduring fertile times than from difficulty deci-phering the methods.4 These methods work bestwhen women have a predictable cycle length.Ovulation is then predicted most accurately, andintercourse is restricted for the least amount oftime. Barrier methods can be combined with thecalendar method pretty effectively during therestricted time, but spermicide can obscure thecervical mucus method. All variations of thismethod assume that an ovulated egg can be fer-tilized for up to 24 hours and that sperm can sur-vive in the female reproductive tract for aboutthree but possibly up to seven days.4 Amazingly,one might become pregnant up to a week afterthe last intercourse! So much for romanticallyplanning conception location or dating a preg-nancy simply from the timing of sex.

Combining all the methods somewhat prob-ably works the best; for example, many womenare quite good at predicting when they ovulatefrom a variety of symptoms (such as pelvic painor mittelschmerz), but this is only something younotice after the fact. To successfully avoid preg-nancy, you have to be able to predict ovulationabout five to seven days in advance or else avoidexposure completely during the first half of thecycle. Obviously noncoital activities are permissi-ble at all times; this method does not requireactual abstinence, just avoidance of intercourse.

Calendar Methods

Rhythm, the oldest of birth control schemes,relies on a woman having a regular 28-day cycle,with ovulation occurring on day 14—exactlymidcycle. Intercourse must be avoided for at leastthree days before and three days after ovula-

tion—days 11 through 17 at least, and optimallyseven days before and at least four days after. If awoman’s cycle is not this regular, another calendar method is useful that takes into accountcycle variance. First gather information aboutcycle length over enough time to figure out howwide the range is. You must know the longest andthe shortest cycle length you experience—day 1being the first day of menses and the last daybeing the one just before menses resumes. Sub-tract 20 from the shortest cycle to get the firstfertile day (day 4 in a 24-day cycle). Subtract 10from the longest cycle (day 22 in a 32-day cycle)to get the last fertile day. Thus, a woman withcycles ranging from 25 to 30 days avoids inter-course days 5 through 20 (25 � 20 � 5 and 30 � 10 � 20). (Read through this paragraph twoor three times to make sure you understand it.)

Cervical Mucus

This method uses the recognition of “fertilemucus” to predict ovulation. It depends on thephysiological fact of the presence of slippery thinmucus at the cervical orifice around ovulation.You can easily learn to discern fertile mucus byexperimenting with egg white, which resemblesfertile mucus. Use your index finger to gathermucus from as close to the uterine opening aspossible. Fertile mucus stretches between thumband index fingers as they are separated, just likeraw egg white, without breaking in the middle.Nonfertile mucus is tackier and breaks aparteasily at short distances between the fingers.Experiment with an egg white, then try room-temperature butter—you will see the difference.Imagine the sperm swimming easily betweenlong slippery parallel strands of mucus aroundovulation, which is thought to ease transport intothe uterus and may also modify the sperm so thatit is capable of fertilizing the egg. Ovulation usu-ally occurs in the middle or toward the end of thefertile mucus time; thus it is best to determineyour length of fertility in advance a few cyclesbefore relying on this method. Obviously semen,

53C O N T R A C E P T I O N

spermicides, vaginal creams, or lubricants canadulterate the mucus and make this assessmentunreliable. Experiment.

Basal Body Temperature

Basal body temperature is measured by takingone’s temperature the very first thing in themorning before getting out of bed and before anyactivity at all. Wake up, reach over, take the tem-perature, record. Plotting these numbers dailyover a few months will show a nice pattern ofovulation. The temperature may drop a bit (usu-ally around half a degree) just before ovulation,and then goes up about a degree from there (nowhalf a degree over baseline) just after ovulation.Release of the egg probably occurs the day beforethe elevation,3 which persists until menses. Ele-vation longer than the expected 12 to 14 daysusually indicates pregnancy. A digital thermome-ter will help you demonstrate this rise more accu-rately, but you can use any thermometer if youare willing to precisely plot the points.

BARRIER METHODS

Barrier methods include anything that imposes a barrier between egg and sperm and includecondoms, diaphragm, cervical cap, and any ofthe spermicides. Only the condom physicallyprevents sperm from reaching the egg. Thediaphragm and the previously available cervicalcap are both methods of holding spermicideagainst the cervix; they don’t really keep the eggfrom meeting sperm. The new FemCap doescover the cervix but doesn’t hold the spermicideagainst the cervix. Rather, it contains a groovefacing the vaginal opening to store and deliverspermicide or any microbicide. Without spermi-cide, these methods are not highly effective.Most condoms are impregnated with spermicidethese days, because of the presumed protectionnonoxynol-9 provides against sexually transmit-ted diseases. Nonoxynol-9 kills gonorrhea,herpes, trichomonas, syphilis, and HIV in vitro,4

which may or may not translate into reduced

transmission of these diseases between humans.Because some organisms, such as HIV, are intra-cellular, they may not get exposed to the spermi-cide during sexual intercourse, and thereforeprotection may be compromised. In fact,nonoxynol-9 is rather irritating to some, and theirritation may result in vaginal mucosa (thelining of the vagina) that is more susceptible tothe AIDS virus. It is safe to use nonoxynol-9unless it irritates you; in that case, don’t.

Condoms should obviously be used with anynew sexual partner to protect against many, butnot all, sexually transmitted diseases. Alone as amethod of birth control, they can be reasonablyeffective. If used consistently and properly, fail-ure rates are reputed to be as low as 3 percent,although actual use failure rates are closer to 10to 14 percent. Using condoms with an intravagi-nal spermicide provides about 96 percent safetyfrom pregnancy with typical use. This combina-tion is the best over-the-counter method.

Healthy noninfected couples that choosecondoms may prefer the comfort of lambskincondoms; the pores of these condoms are too big to protect well against viral-size organisms,but they do just fine in keeping out sperm. Con-doms, a very old tried-and-true method, areenjoying a surge in popularity.

Caps and diaphragms work similarly; bothcover the cervix and hold spermicide eitheragainst the cervix or facing the entrance to thevagina. The suction-based cervical cap is cur-rently not available in the United States due to abusiness decision by the European manufacturer.This had nothing to do with safety or effective-ness. What is now available, perhaps the newestmethod of birth control, is the FemCap. TheFemCap is made of nonallergenic, latex-freematerial and is designed to cover the cervix. Ithas a groove facing the vaginal opening thatstores and delivers spermicide. It is available byprescription only but does not require a technicalfitting session and measurement by the health-care provider. A FemCap must be applied before


arousal and should be kept in place for at least six hours after the last intercourse. A backupmethod is recommended while you are learningto use it. FemCaps have the advantage of beingable to be left in with ongoing efficacy for as long as 48 hours. A FemCap comes with aninstructional video. (Information is available atwww.femcap.com.)

A diaphragm is a latex shield that covers thecervix. Diaphragms come in several sizes, and thecorrect size must be determined as part of a pelvicexam by a health-care practitioner. Spermicidemust be placed in the diaphragm, which is thenplaced up against the cervix. The diaphragm mustbe left in for at least six hours after intercourse,and any additional intercourse during that sixhours must be preceded by the addition of anapplicator of spermicide. Diaphragms with sper-micide have an effectiveness rate of approximately94 percent.

The contraceptive sponge was originallyintroduced in 1983 and remained on the marketuntil January 1995. It was taken off the marketbecause the manufacturer chose not to modern-ize the manufacturing and hygiene standards. In2005, the Today sponge returned to the market-place with a new manufacturer. The sponge is aconvenient, disposable, one-size-fits-all vaginalcontraceptive that can be purchased over thecounter at most drugstores. It is used with a sper-micide and offers an 82 to 92 percent effective-ness rate.

INTRAUTERINE DEVICES

Intrauterine devices are in a contraceptive class allby themselves, and they may arguably be the leastinvasive and highest efficacy form of birth control.Rumors persist that Cleopatra had a gold ring inher uterus that prevented pregnancy and allowed ahealthy, active love life. And the camel drivers inthe same era are said to have put small rocks intheir camels’ uteruses to prevent pregnancy on thelong roads they traveled. These may just be goodstories, but for those women who are good candi-

dates, IUDs are simple, cheap, highly effective,reversible, and have a minimal impact on underly-ing physiological processes.

Modern IUDs became popular with theintroduction of the Lippes Loop in the early1960s, when as many as 10 percent of womenwho used contraceptives chose this method. Thefailure rate was about 2 percent, although theexpulsion rate (coming out with the menstrualflow) was reported to be as high as 12 to 20 per-cent.3 Lippes Loops are still available and in usearound the world, although not available in theUnited States.

IUDs are used much more commonly inEurope than in the United States, largely becauseof the persistent fear American women andproviders still harbor from the Dalkon Shielddebacle during the 1970s. Unfortunately, thisdevice traumatized the cervix on insertion, andthe string was made of a material that was a perfect conduit for bacteria to ascend into theuterus. An infection called pelvic inflammatorydisease (PID) increased dramatically in DalkonShield users, essentially due to the prevalence ofsexually transmitted diseases that ascended intothe uterus and/or fallopian tubes; many womenacquired serious infections and in many, infertil-ity resulted. Yet the company did not recall thedevice for 10 years—at least 5 years after theproblems were known. The reputation of theIUD was tarnished forever, and a good contra-ceptive method is all but lost to women whomight well benefit from it today.

There are presently very few IUDs in theUnited States because manufacturers don’t want totake a chance on a device that has become sounpopular. Copper was added to IUDs to increaseeffectiveness in the 1980s, which allowed smallerand better-tolerated devices to be used. The Para-gard copper T fails less than 1 percent of the time4 and lasts for at least 10 years. Fertility isunchanged over baseline in women who do notcontract sexually transmitted diseases. The devicecomes in only one size, and so is better tolerated in

www.femcap.com


a uterus that has carried a pregnancy. It can be putin during nursing for excellent carefree contracep-tion that will not interfere with lactation. Themechanism of action is now fairly well docu-mented as a inflammatory response in the uterinecavity. It is not felt to be an abortifacient (a sub-stance that induces abortion).

IUDS can make menstrual flow heavier andwith more cramping. For those women with mod-erate or light menses, however, it is a method that requires no mess or loss of spontaneity, andIUDs can be used for years without loss of efficacy.Even at a cost of $600 to $700, this is a minimalexpense if used over a 10-year period.

Women who are in monogamous relation-ships, have given birth, and are not at risk for sexually transmitted infections are perfect candi-dates for IUD use, if their periods are normal.Again, though, IUDs can increase the amount ofthe menstrual flow and increase cramping. Theexception is the newer IUD called Mirena. Itcontains a progestin (Levonorgestrel) on thestem, which shrinks the endometrium anddecreases menstrual flow and cramping. It canreduce the normal flow by 80 percent and causesa lack of menses in 15 percent of patients. TheMirena lasts 5 years, and the progestin staysactive inside the uterus. It is thought that in themajority of women and in the majority of thetime, the progestin is confined to the uteruswithout systemic absorption. However, clinicianswill report cases of patients who appear to havehad systemic progestin side effects from theMirena. The Mirena is an important option incontraception—a method that provides 99 per-cent protection and decreases menstrual pain andheavy flows.

Insertion of an IUD must be done in a prac-titioner’s office. Most women report nothingmore than light cramping. STI testing forchlamydia and gonorrhea should precede inser-tion. Infections caused by the insertion itself arerare and may occur approximately 1 percent ofthe time, within 30 days of insertion. An antibi-

otic can be utilized to prevent infection. If youdo become pregnant, the IUD should beremoved. Pregnancies will be interrupted by theIUD, and a miscarriage can occur about half thetime. If desired, ultrasound can be used to iden-tify the IUD before removal to minimize disrup-tion of a wanted pregnancy.

BIRTH CONTROL PILLS (BCPS)

Never has there been a more perfect love/haterelationship than that between women and hormonal contraception or birth control pills(BCPs), also called oral contraceptives (OCs). In1951, Margaret Sanger is credited with convinc-ing Gregory Pincus (who ultimately synthesizedthe first oral contraceptive) that his research infertilization could be used to create an oral contraceptive. Available for the first time in the1960s, oral contraceptives were truly a revolu-tionary medical option for women. Womenreadily embraced the option of having fewer children, and the dramatically lower birthratethat resulted has persisted, undoubtedly due tothe pill’s continued widespread use. Women’smaternal burden was lifted for the first time inhistory. That’s the good news.

Unfortunately, the hormonal content of earlybirth control pills—estrogen and progesterone—was much higher than today’s pills, and morewomen smoked then. Both factors affected whatis always the course of any new medicine—thedownside became obvious only with mass use. Itsoon became apparent that cardiovascular dis-ease, including heart attacks, strokes, blood clots,and pulmonary emboli, was more frequent inwomen who used birth control pills. But eventhough “more frequent,” these diseases are stillexceedingly rare in the healthy population ofyoung women who are the usual pill takers. It isalso true that these risks are dose related and havefallen measurably as the estrogen and progestincontent of pills has fallen 4 and 10 times respec-tively since their initial use. The FDA-approvedpackage insert states the following:


The information contained in this packageinsert is principally based on studies carriedout in patients who used oral contraceptiveswith formulations containing 0.05 mg [50mcg] or higher of estrogen. The effects oflong-term use with lower-dose formulationsof both estrogens and progestogens remainto be determined.

The birth control pills in common use todayhave 20 to 35 mcg of estrogen, and only one ortwo formulations containing 50 mcg are evenavailable. Moreover, the studies documentingthese higher risks in the earlier days did not con-trol for other risk factors such as smoking, highblood pressure, obesity, and so forth—all knownto independently increase a woman’s risk of car-diovascular disease. I like the way the late Dr.Felicia Stewart, who dedicated much of her lifeand career to designing research and policies thatmake safe, effective contraception and abortionaccessible to women, describes pill risk:4

If you were to draw a line 215 meters high(the height of a 70-story building) to repre-sent 100,000 young nonsmoking pill users,and then draw a line beside it to representthe number of pill users in the United Stateswho die each year from complications relat-ed to higher-dose pills, that second linewould be about 0.5 centimeters high [aboutone-fifth of an inch]. In comparison, theline representing the number of U.S.women who would die of pregnancy-relatedproblems would be just under 2.5 centime-ters high [about an inch]. A line represent-ing maternal mortality in developing coun-tries would be 25 centimeters to 1.5 meterstall [10 inches to just under five feet].

Risks attendant to birth control use must bemeasured against the risk of the pregnancies theyprevent. We are fortunate to live in the time ofthe lowest maternal mortality ever—and still therisk of oral contraception we all worry about is

one-fifth that of pregnancy. If we can manage toavoid pregnancy in other ways, presumably theyare safer than the pills.

There are some significant health benefitsattributable to the pill—for example, an 80 per-cent reduction in ovarian cancer and a 50 percentreduction in uterine cancer with about a decadeof use.3 Assessing an individual’s risk/benefitratio requires individualization based on healthstatus, family history, and so forth. If one’s risk ofcardiovascular disease doubles with use (it does),that sounds worrisome. But if doubling one’s riskmeans going from a risk of 1 in 10,000 to 2 in10,000, that doesn’t sound so bad. This is justanother way of looking at the same fact. Inciden-tally, this risk is not even close to the risk we takedriving our car to work or school.

Smokers older than 35, however, should notuse the birth control pill. Most other women athigher risk of heart disease, like those with dia-betes, hypertension, or elevated cholesterol,should consider other options as well—but evenin these conditions, pills are usually safer than anundesired pregnancy. Blood pressure needs to befollowed in all pill takers, and, if elevated signifi-cantly by use, another birth control method mustbe chosen.

Breast Cancer and the Pill

Much attention has been given to the relation-ship between the pill and breast cancer, andslowly some answers emerge. The Centers forDisease Control (CDC) conducted a study in the1980s called the “Cancer and Steroid HormoneStudy” that looked at nearly 5,000 cases of breastcancer and 5,000 healthy control women andconcluded that there was no increased risk ofbreast cancer in women who had used the pill.3

Another significant study evaluated a pooledanalysis from 54 studies involving 53,297women with breast cancer and over 100,000controls and concluded that there is a slight butmeasurable increase in the relative risk of breastcancer for current BCP users that declines


shortly after stopping the pill and disappearswithin 10 years.5 By age 50, there is no differencein the risk of breast cancer in women who haveever used oral contraceptives versus those whohave never used them. Also, the increase in riskduring use (1.24 relative risk) translates differ-ently in a 20-year-old woman versus a 40-year-old woman. If the risk of breast cancer at 20 is 1in 5,000 (or less), then a relative risk of 1.24increases it to 1 in 4,000. However, if a womanis 40 and the risk of breast cancer is about 1 in250, a relative risk of 1.24 increases her risk to 1in 200. Thus, the increase is clearly more signifi-cant in an older woman. In this age group, of1,000 40-year-old women who take the pill, onewill contract breast cancer as a consequence.Only about 15 percent of breast cancers occur inwomen younger than age 45,6 which is whenmost of us take oral contraceptives.

A very recent meta-analysis that revisited oralcontraceptives and the risk of breast cancer, pub-lished in October 2006, concluded that oral con-traceptives do increase the risk of premenopausalbreast cancer.7 Thirty-four case-control studies oforal contraceptives and premenopausal breastcancer during or after 1980 were identified. Analy-sis of the data from these studies showed that therisk of breast cancer was slightly increased for bothnulliparous (having never given birth) and parous(having birthed one or more times) women. Innulliparous women, the longer duration of use ofthe pill did not significantly affect risk. In parouswomen, the increased risk was more substantialwhen the oral contraceptives were used before thefirst-full term pregnancy. The risk was highest inparous women who had used the pill for four ormore years before their first full-term pregnancy.There are many limitations of this kind of reviewbecause there are so many variables, including race,possible recall bias, difference in the age of firstusing the pill, and poor information on when thepills were last used. Taking oral contraceptivesmust be decided based ultimately on the benefitscompared to the risks for each woman.

The cancers in former users are generally of aless advanced stage than the cancers of nonusers,and benign breast disease (cysts, fibrosis, breastpain, swelling) is generally improved by BCP use.Overall, there appears to be no evidence of anysignificant increase in the lifetime risk of gettingbreast cancer among women who have used oralcontraceptives.

Before deciding for or against BCPs, consideryour risk for breast cancer (although mostwomen who get breast cancer are not at risk, andmost at risk don’t get it),6 whether pregnancyposes a risk, and any other health risks and ben-efits related to BCP use.

Other Health Benefits of Birth Control Pills

Several years ago, the FDA began to require that,in addition to risks, pill manufacturers list bene-fits, because they are so significant. Some womenactually take birth control pills for the healthbenefits they offer. Oral contraceptives protectfrom uterine and ovarian cancers in the generalpopulation, but we aren’t sure yet about those infamilies with a higher incidence. They protectfrom pregnancy nearly 100 percent of the time,although even with perfect use, there is stillabout 1 pregnancy in 1,000 women per year, andwith common human error, a 2 percent failurerate is more accurate. As a bonus, they reduceheavy, painful periods in everyone.

About 80 to 90 percent of functional ovariancysts (those related to ovulation, the mostcommon type) are eliminated in women whotake birth control pills.4 Those who suffer fromendometriosis can frequently reduce their ongo-ing pain by suppressing the disease with oral contraceptives. Women with polycystic ovarysyndrome and abnormal male pattern hairgrowth can decrease hair growth with oral con-traceptives because they measurably reduce themale hormones known as androgens in thesewomen. Interestingly, because of the thickeningin cervical mucus that birth control pills induce,


it is less likely that women who take them willget pelvic inflammatory disease if they areunlucky enough to get gonorrhea or chlamydiain the cervix. Fertility is spared in this way.

Several recent studies have shown that a seven-day hormone-free interval causes more of a rise infollicle-stimulating hormone (FSH), which causesovulation. Continuous daily regimens or shorterdrug-free intervals (three or four days only) pre-vent ovulation. Suppression of ovulation reducesthe cyclic symptoms some women have on thetypical 21 days on and 7 days off pill regimens.There is also less breakthrough bleeding and adecrease in pregnancy rates with these shortertime-off regimens. More and more women areusing their birth control daily, or for three monthsat a time. Many oral contraceptives are beingrepackaged with only three or four days of hor-mone-free pills, and we will likely see more of thisin the future.

Nutritional Supplements for Pill Users

Apart from their hormonal effect, the hormones in birth control pills have been shown to affectmetabolic and nutritional factors. Women on oral contraceptives may want to take nutritional sup-plementation to adjust for some of the biochemi-cal alterations caused by the pill. Women on BCPshave a higher requirement for folate,8 and this maybe especially true for women who have had cervi-cal dysplasia (precancerous abnormal cells of thecervix). The frequent ingestion of the steroidsfound in BCPs have been shown to depress levelsof riboflavin, pyridoxine, vitamin B12, ascorbicacid, and zinc.9 Hormones can also affect breasttenderness, increase risk of blood clots, and inducean array of side effects in some women, and theyare metabolized in the liver. Providing selectivenutritional support, supporting breast health, andenhancing hormonal metabolism and detoxifica-tion pathways may optimize the experience ofusing hormonal contraception.

Riboflavin deficiency may occur with longperiods of oral contraceptive (OC) use.9 It may

be that OCs interfere with gastrointestinalabsorption or with metabolism or binding. Thereseems to be general consensus in the literaturethat consumption of oral contraceptives con-tributes to pyridoxine (vitamin B6 deficiency).9 Ithas been estimated that the majority of womenon OCs for longer than six months manifestabnormal tryptophan metabolism. Vitamin B6

can normalize tryptophan metabolism.Although not consistent, some research has

shown that OCs disturb folate metabolism.Anemia, the gastrointestinal and genital tracts,bone and heart health, and mental function areall affected by folic acid deficiencies. For thisreason, folate is an important nutrient to supple-ment for women taking the pill. Oral contracep-tion users have also been reported to havereduced levels of vitamin B12.9 This may berelated to malabsorption, increased renal excre-tion, and enhanced tissue acidity. A woman mayor may not acquire an anemia associated with aB12 deficiency, but long-term use of the pill maylead to this, or at least may compromise nervefunction, mood, mental function, and the healthof the digestive system. Carotenoids are alsoincluded in this formula to protect the cervix.Oral contraceptives have shown mixed results inincreasing abnormal changes in the cervix thatcan lead to cervical cancer. Beta-carotene defi-ciency in the cervical cells may be a cofactor inthe development of cervical dysplasia,10 anddecreases in plasma beta-carotene levels is foundin women with either cervical dysplasia or cancerof the cervix.11

Reduced levels of ascorbic acid have also beenobserved in those who take oral contraceptives.9

It is possible that the steroids of oral contracep-tives increase the breakdown of ascorbic acid,decrease absorption, and/or change tissue distri-bution. Limited research in animals has shownthat oral contraceptives lower blood levels of vita-min E.9 Vitamin E is the premier antioxidant forlipids, protects structures against toxic com-pounds, and is important in immune function.


Most investigations have shown a reduction inplasma zinc levels following the administrationof OCs.9 Decreased absorption, increased uri-nary excretion, and a decrease in albumin, animportant carrier of zinc, may account for this.Zinc is essential to good health and is involved inmany enzyme and body functions. Immunefunction; wound healing; the nervous system;maintenance of vision, taste, and smell; and skinhealth are dependent on adequate levels of zinc.Zinc competes with copper for absorption, there-fore adding a small amount of copper is also sug-gested to avoid any problems.

Borage seed oil is high in gamma linolenicacid (GLA), which is important in maintainingpain-free breasts. GLA decreases abnormal sensi-tivity of breast tissue to normal hormone levels.The proposed mechanism of GLA’s action is thatit normalizes the balance of fatty acids containedwithin the cell membranes. The steroid receptorsin the breasts then have a reduced affinity forestrogen, dramatically reducing breast sensitivity.

Oral contraceptives can increase the risk ofblood clots, although this risk has been consider-ably reduced since the lower-dose pills havebecome the norm. However, these concerns stilldeserve our attention. Bromelain has a very favor-able effect on inflammation of a vein. In research,bromelain has been shown to reduce all the symp-toms of inflammation in those who had developedacute thrombophlebitis.12 Garlic preparationshave been shown to promote fibrinolysis, whichcan offer benefit in prevention of strokes and otherclotting events.13, 14 Excessive clumping togetherof platelets is linked to heart disease and strokes.Garlic and its volatile oils can inhibit plateletaggregation and thereby improve circulation.15

Finally, women taking hormonal contracep-tives can experience changes in vaginal pH, whichcan lead to changes in the balance of organisms inthe vagina. Lactobacillus species are fundamentalto maintaining a healthy ecological vaginal envi-ronment, which helps to prevent yeast and vaginalinfections. It may be possible to favorably alter this

vaginal ecology by taking lactobacillus in the formof a nutritional supplement.

Additional considerations may include liversupport to aid in the metabolism of the steroids.There are many options here, including alipotropic supplement and herbs such as dande-lion root, burdock root, and milk thistle.

Little information is available about anyinteractions between botanicals and birth controlpills. For now, my only real caution is with Saint-John’s-wort. A few case reports, as well as twocontrolled clinical trials, indicate that Saint-John’s-wort can cause breakthrough bleeding andinterferes with the metabolism of the hormonesin the pill. These observations lead me to thinkthat the effectiveness of oral contraceptives maybe reduced when taken in conjunction withSaint-John’s-wort.16–18 Other speculations havebeen made about the possibility of other herbsand nutrients interfering with the effectiveness ofbirth control pills. However, hypotheses aboutchaste tree, indole-3-carbinole, soy, dong quai,and others have no documentation to supportthese concerns.

Side Effects

Many women prefer not to take birth controlpills because they see them as an unnatural formof birth control. Others are concerned, rightly so,about some of the issues that have been raisedhere, but some women just plain don’t feel goodon them. Some women have bloating, breast ten-derness or pain, headaches, mood swings, depres-sion, weight gain, nausea, lowered libido, andbreakthrough bleeding. Other women may expe-rience significant, more serious side effects suchas complete hair loss, blood clots, high bloodpressure, heart attack, and elevated liver enzymes.

There are many kinds of birth control pillstoday, and fortunately they are significantly lowerin dose and cause far fewer side effects than in thepast. The pills vary in their estrogen and progestindosages and contain different kinds of estrogensand progestins. A woman may tolerate one pill


poorly and another very well. If you struggle withfeeling good on “the pill,” you should work with ahealth-care provider who knows the products well.Many side effects come from the progestin, andthere are currently six different progestins found invarious birth control pills. Merely switching to apill with a different progestin can result in feelingnormal while on the pill. There are pills with dif-ferent estrogen doses as well.

Overall, women need to assess how they feelon oral hormonal contraceptives. Some womenare moody, some are less so. Some women lovethe regularity of their periods and their reducedpain; others feel nauseous and bloated. Some lovethat their acne improves; others fret about breastcancer. Some women feel great and have lowrisks for most diseases; for them, the hormonescan fit into a healthy life.

The pill is not a natural form of birth control,but for some women the benefits outweigh thedownside. If you do choose to use birth controlpills, remember that one of the advantages to barrier methods of contraception (diaphragm,FemCap, condoms) is the reduced incidence of sexually transmitted infections (STIs), especiallypelvic inflammatory disease. Oral contraceptivesdo not significantly protect against most STIs.Condoms are the best method of contraceptionthat also offers a “safer sex” method. Diaphragmsand caps do not provide for safer sex, but theymay help stop sexually transmitted infectionsfrom ascending into the uterus and pelvic region.These are important considerations when choos-ing your method of contraception.

Emergency Contraception

Emergency contraception refers to using birthcontrol pill hormones to prevent pregnancy afterintercourse has occurred. The only emergencycontraceptive pill (ECP) that is currently avail-able is a progestin-only pill called Plan B. Twopills, taken 12 hours apart, reduce the risk ofpregnancy by 75 percent if initiated within 72hours after unprotected intercourse. The effect

appears to result primarily from an inhibition ordelay of ovulation and does not disrupt analready established pregnancy.

It is also possible to use more pills of a birthcontrol pill that you might already have on handfor emergency contraception.

OTHER FORMS OF HORMONAL CONTRACEPTION

There are other hormonal contraceptive optionsavailable, in addition to the familiar estrogen/progestin pills. There are progestin-only hormonepreparations—pills, injections, and implants.These options can have many of the same nui-sance side effects of combination pills—weightgain, irritability, and depression. Progestin-onlybirth control pills are used by women who arebreast-feeding or who have a contraindication toestrogen, such as hypertension. The injection(Depo-Provera) and the new implant (Implanon)have a lower failure rate because compliance is notrequired on a daily basis—only once every threemonths for the Depo-Provera shot and every three

Emergency Contraception

Take 4 of one of the following pills within 72 hoursafter unprotected sex, and take 4 more pills 12 hourslater:

CryselleLevlenLevoraLo/Ovral

Another option: take 5 of one of the following pillswithin 72 hours after unprotected sex and take 5more pills 12 hours later:

AlesseAvianeLessinaLevliteLow-OgestrelNordettePortiaSeasonale


years for the Implanon. Both work by suppressingovulation to an extent, neither as completely as thecombination birth control pill, but this mecha-nism is augmented by even thicker cervical mucusthat impedes the sperm at the cervix. They aren’tas good for cyst suppression because of the incom-plete suppression of ovulation. Implanon boaststhe lowest systemic hormone dose of any hor-monal method because it is released at such asteady low dose by the implant. As a consequence,menses are irregular in up to 40 percent ofwomen. This tends to improve over time and istolerated better by some than others.

Depo-Provera, on the other hand, suppressesmenses entirely by one year of use, and it can take5 to 18 months for fertility to return. There is con-cern that inadequate estrogen will be available forbone density protection as a consequence of theestrogen suppression. There is reversible bone lossover time on Depo-Provera, and the FDA hasrequired the company to do a prospective study ofbone density in users. Because both the shot andthe implant cannot be immediately reversed oncethey start, I encourage women to try the pill first,unless they can’t remember to take a daily pill orcan’t tolerate the estrogen. There is also a vaginalring, Nuvaring, that contains both estrogen andprogestin and lasts three weeks, which is popularwith women who forget their daily pill.

Transdermal combined estrogen/progestincan be delivered in a contraceptive patch and isavailable as Ortho Evra. It was approved by theFDA in 2002 and delivers 20 mcg of ethinylestradiol and 150 mcg of norelgestromin, anactive metabolite of norgestimate. The regimen isto apply a patch once weekly for three consecu-tive weeks, followed by a patch-free week. It hasa side effect profile similar to the oral contracep-tives, although recent concerns have been raisedabout higher blood levels of estrogen in womenon the patch than on the birth control pill. Thenewer estrogen patch is associated with about 60percent higher blood levels of estrogen than theequivalent version in an oral pill. This increase in

estrogen levels can expose women to a higher riskof clotting. Clearly, this issue needs to be dis-cussed with your health-care practitioner.

STERILIZATION

Sterilization for men and women is still a widelyused form of birth control. For men, this is a vasec-tomy. For women, there is now an alternative to atubal ligation, called Essure. Tiny springs areinserted into the openings of the fallopian tubesfrom the cavity of the uterus, so no surgery is done.It can be provided in an outpatient setting. Adoctor uses a speculum, dilates the cervix, inserts aflexible fiber optic scope to see inside the uterus,then threads the springs into the tubes.

You must have a tubal dye x-ray test threemonths after insertion to check that tissue grewinto the springs and blocked the tubes, indicat-ing a successful sterilization.

ABORTION

Unfortunately, all methods of birth control canfail. Humans make mistakes. Women have sexagainst their wills. For all these reasons and more,abortion will always be with us, and it bears amention in a discussion of fertility control.Women practiced abortion long before they prac-ticed birth control, because that’s what was avail-able to them. The last measurable drop inmaternal mortality in the United States occurredwith the legalization of abortion in 1973. Abor-tion has never been safer, with mortality at 0.25deaths per 100,000 women—about 20 times saferthan childbirth.19 Unfortunately, the politicalfracas around abortion—and the real risk to work-ers and patients of clinic violence—has madeaccess to abortion more rather than less difficult inrecent times. We must recall that the battle forbirth control was nearly as emotional; perhapssomeday we will see this struggle resolved as well.

In the interim, if you choose an abortion, con-sult your regular provider first. Gynecologists andfamily doctors need to realize how many women(1.5 million per year) in all walks of life need this


service and how judged they feel—most obviouslyby “pro-life” practitioners, but also by their pro-choice doctors who send them across town to aclinic just because it’s easier for that doctor. If yourgynecologist won’t help, go to one of the wonder-ful women-run and supported clinics that providethe service out of love and respect for women.Their doctors are very experienced, with extremelylow complication rates. Emergency contraceptioncan be obtained at most clinics as well, althoughemergency contraception is now available over thecounter for women over the age of 18.

Rather than a surgical abortion, medical abor-tion with a drug called mifepristone (Ru-486) is agood option for early pregnancies, and it offers amethod of abortion that aligns much more natu-rally with our bodies. The medical abortion is justlike a miscarriage. There is more bleeding andcramping than a period, but it occurs within a 4-to 24-hour period, and 98 percent of the timeavoids surgery altogether. The infection rate islower, and the chance of significant uterine injury,already miniscule, is further lowered. Manywomen are quite pleased with this method.

Summary of Contraceptive Choices

Birth Control Pills

Advantages

Continuous contraceptive protection when taken correctly

ReversibleOther possible health benefits

Disadvantages

Has to be taken dailyIncreases the risk of blood clots, heart attack, and

stroke, especially in smokers over age 35Side effects such as nausea, weight gain, headaches

Effectiveness

99 percent or greater

Depo-Provera Injections

Advantages

Continuous contraceptive protection for up to 5years

ReversibleDon’t need to remember to take a daily pill or use a

device

Disadvantages

Requires a visit to a practitioner for quarterly injections

Delayed fertility after stopping the injections

Side effects such as weight change, irregular bleeding

Effectiveness


Tubal Ligation

Advantages

Continuous contraceptive protection

Disadvantages

PermanentA surgical procedure

Effectiveness


Essure

Advantages

Continuous contraceptive protectionInsertion through vagina and uterus; no surgery is

needed

Disadvantages

Permanent

Effectiveness


(continued )


Summary of Contraceptive Choices (continued )

Intrauterine Device (Copper IUD)

Advantages

Continuous contraceptive protection for up to 10 yearsDon’t need to remember to take a daily pill or use a

deviceReversible

Disadvantages

May be expelled by the uterus; may perforate theuterus

Increases the risk for PIDMay cause heavier bleeding and menstrual cramps

Effectiveness

97 to 99 percent

Intrauterine Device (Progestin IUD)

Advantages

Continuous contraceptive protection for at least 5years

Don’t need to remember to take a daily pill or use adevice

May decrease menstrual cramps and heavy bleedingReversible

Disadvantages

May be expelled by the uterus; may perforate theuterus

Increases the risk for PID

Effectiveness

97 to 99 percent

Condom (Alone)

Advantages

Easily obtainedInexpensiveBest method for protection against STIsBetter results when used with a spermicide

Disadvantages

May reduce sexual sensationLess sexual spontaneity

Condoms may breakMale partner must agree

Effectiveness

88 to 98 percent

Diaphragm (with Spermicide)

Advantages

Insert up to 6 hours before intercourseNoninvasive methodInexpensive

Disadvantages

Must leave in for at least 8 hours after intercourseMust reapply spermicide for repeat intercourseDiscomfortMust be able to insert by oneselfIncreases the risk of urinary tract infections

Effectiveness

82 to 94 percent

FemCap

Advantages

Insertion before sexual arousalEasy fittingsInexpensive

Disadvantages

Must leave in for 6 to 8 hours after intercourseVaginal odor and dischargeMay be uncomfortable to insert

Effectiveness

82 to 94 percent

Spermicide (Alone)

Advantages

Easy to obtain and useGood results when used with cervical caps, condoms,

or diaphragmsInexpensive

(continued )


Summary of Contraceptive Choices (continued )

Disadvantages

Must be inserted within half hour prior to intercourse

Reapplication necessary for repeated intercourseMay be messy

Allergies in some peopleMay increase the risk of urinary tract infections,

especially with diaphragms

Effectiveness

79 to 97 percent

65

OVERVIEW

Ten to twenty percent of all women have somekind of urinary discomfort or infection at leastonce a year. Acute uncomplicated cystitis (infec-tion of the bladder) and recurrent cystitis are twoimportant categories of urinary tract infectionsin adults. Distinguishing between uncomplicatedand complicated urinary tract infections (UTIs)is important because they may require differentevaluation tests and procedures, as well as differenttypes and duration of treatment plans. A compli-cated infection is associated with a condition thatincreases the risk of urinary tract infections or isassociated with an increased likelihood of treat-ment failure such as HIV, diabetes, or having acatheter. An uncomplicated infection is one thatlasts less than one week, is unaccompanied by afever, and presents itself in low-risk individuals,such as nonpregnant, otherwise healthy women.

Symptoms of uncomplicated cystitis includepainful and frequent urination, the urge to uri-nate even though the bladder may be nearlyempty, and pressure and pain in the pelvic area.Acute cystitis is generally uncomplicated but maybe complicated if the individual has a catheter oralso has a stone in the bladder. It is not alwayspossibly to classify someone as having a compli-cated or uncomplicated UTI based on urinarytract symptoms alone. However, there are factorsthat suggest the presence of a complicated UTIin women. These include:

• Being elderly or young• Having a hospital-acquired infection• Pregnancy• Having a urinary catheter• Having had a recent procedure involving

urinary tract instrumentation

• Recent use of antibiotics• Symptoms that have lasted longer than

seven days• Diabetes• Immunosuppression (HIV, immunosuppres-

sive medications)

Simple, short-duration therapies may not beappropriate for these situations.

It is reassuring that most of the acute UTIs thatoccur are uncomplicated. Health-care practitionerscan generally assume that a premenopausal, sexu-ally active woman who is not pregnant, has notbeen recently treated with antibiotics, and doesnot have a history of a genitourinary tract abnor-mality has uncomplicated cystitis if she presentswith dysuria (painful or difficult urination), fre-quent urination, or urgency. It is even likely thatmost postmenopausal women who do not have agenitourinary tract abnormality have uncompli-cated UTIs.

A narrow spectrum of microbes are responsiblefor the infections in young women with acuteuncomplicated cystitis: Escherichia coli (80 per-cent), Staphylococcus saprophyticus (5 to 15 per-cent), and occasionally Klebsiella species, Proteusmirabilis, or other microorganisms. Bacteriuria(bacteria in the urine) is more common in womenwho are sexually active, and certain forms of con-traception are associated with urinary tract infec-tions. Sexual intercourse, diaphragm use withspermicide, spermicides used alone, oral contracep-tives, delayed postcoital urination, and a history ofa recent urinary tract infection all increase the riskof initial and recurrent infection. Sexual inter-course is the strongest risk factor for UTIs, inde-pendent of contraception influences. As many as30 percent of women with cystitis symptoms mayhave subclinical upper urinary tract involvement.

5C Y S T I T I S C H A P T E R



Young women who present with acute painwith urination or difficult urination usually haveeither acute cystitis or acute urethritis due toChlamydia trachomatis, Neisseria gonorrhoeae, orherpes simplex virus. Vaginitis due to candida ortrichomonas can also involve dysuria. These prob-lems can usually be differentiated on the basis ofsymptoms, physical exam, and urinalysis. A urineculture and vaginal cultures may also be needed.

Pregnancy is also a risk factor for UTI. TheAmerican College of Obstetricians and Gynecolo-gists (ACOG) recommends that all pregnantwomen be screened for bacteriuria, even withoutsymptoms. However, not all major authorities rec-ommend this. Screening involves an initial urineculture in all women who are pregnant. If a preg-nant woman has classic symptoms of an acute anduncomplicated cystitis and no previous history ofbacteria in the urine without symptoms, some cli-nicians would go ahead and treat for cystitis, whileothers would do a urine culture before treating.

Recurrent infections, defined as more thanthree infections in six months or six to seveninfections in a year, occur in about 20 percent ofyoung women that have experienced a previousepisode of cystitis. Over 90 percent of recur-rences in young women are episodes of reinfec-tion from exogenous sources that typically occurmonths apart. Recurrences due to a persistentfocus of infection in the urinary tract or toanatomical or functional abnormalities are lesscommon. Cases of recurrent cystitis should becultured and documented at least once. Somewomen may need not only treatment but alsocontinuous prophylaxis (preventive measures) orpostcoital prophylaxis.

Postmenopausal women may also have fre-quent reinfections, which are often due to resid-ual urine retention after voiding or to a lack ofestrogen, which can cause marked changes in thevaginal and bladder microflora, including loss oflactobacilli and increased colonization by E. coli.Vaginal estrogen treatments are a key in restoringnormal vaginal and bladder flora.

Diagnosis of a bladder infection can be basedon symptoms and physical exam alone, a urinedipstick, urinalysis, and/or a urine culture. Basingthe diagnosis on symptoms alone is consideredreliable when the episodes are infrequent or occurless than three times per year. The urine dipsticktest is a simple test performed in the practitioner’soffice that uses a dipstick of the urine to test forleukocyte esterase with or without urinary nitriteand pyuria (the presence of pus in the urine).There are problems with the sensitivity and speci-ficity of the test, and it may be incorrectly negativeif bladder bacteria have not had enough time to produce a sufficient amount of nitrite to bedetectable. The accuracy of the test is also alteredif the individual is eating a vegetable-free diet or isusing a diuretic. The nitrite tests on the urine dipare frequently negative, even in the presence oftwo bacteria, S. saprophyticus and Enterococcusspecies. The leukocyte esterase test is more accu-rate than the nitrite test.

The urinalysis is a macroscopic and micro-scopic analysis of urine performed at the practi-tioner’s office or the lab. The urine is examined forcolor and cloudiness, then examined under themicroscope for white blood cells, red blood cells,epithelial cells (looking especially for an increasednumber or some sloughing down from the kid-neys), bacteria, yeast, and crystals. The urine dip-stick test is also done in a complete urinalysis.

A urine culture is often done after a history andphysical exam suggests something other than anacute, uncomplicated UTI. If a recent UTI has justbeen treated and now the symptoms are recurring,a culture would identify the possibility of a resist-ant pathogen. Worrisome symptoms such as fever,malaise, and back pain over the kidney regionsuggest that the infection may have ascended theurinary tract and warrant a urine culture.

Other diagnostic evaluations of UTI such as acystourethroscopy, ultrasound, or intravenouspyelogram should be considered in women whohave recurrent UTIs. Even though these moresophisticated studies should be considered, it is also

67C Y S T I T I S

important to realize that some women may reportsymptoms that may sound like an infection, butare actually symptoms from an overactive bladder,interstitial cystitis, or a pelvic-floor problem such asa cystocele or uterine prolapse. Keep in mind thatsome recurrent UTIs are caused by anatomic fac-tors such as a shorter urethra-to-anus length orbirth defects in the urinary tract.


For most bladder infections, a natural approach isusually very effective and the infection resolvesquickly without recurrence or complications. Theprimary goals of a natural therapeutics approachare to:

• Enhance the individual’s internal defensesagainst the infection by providing immunesupport

• Restore vaginal and bladder microflora,enhancing the flow of urine

• Promote a proper pH by acidifying the urine• Prevent bacteria from adhering to the blad-

der lining

Simple goals, such as increasing the urinaryflow, are easily accomplished by increasing the

quantity of liquids. Water and herbal teas relatedto the treatment goals are the most logicalchoices. Sixty-four ounces of liquids per day isthe common recommendation. Urinating afterintercourse is also an important bladder hygienepractice that can prevent recurring UTIs.

The lactobacilli species are an especially effec-tive means of alternative treatment for a couple ofreasons. For one, they defend against E. coli, whichcauses the majority of urinary infections. A healthyvaginal ecology is dominated by lactobacillispecies,1 bacteria that defend against both UTIsand infectious vaginitis. Studies have shown thatwomen who have recurrent UTIs have a prepon-derance of uropathogens on the introitus and inthe vagina.2 Lactobacilli adhere to the uroepithelialcells and inhibit the adherence of pathogenicorganisms such as E. coli to the cells, thereby pre-venting proliferation. In addition, the H2O2-producing lactobacilli that are most commonlyfound in the normal bladder flora (Lactobacilluscrispatus and Lactobacillus jensenii ) can help tokeep the bladder in its preferred acidic state.3

Nutrition

Since most UTIs are caused by E. coli, and thisresides predominantly in the gastrointestinal tract,

KEY CONCEPTS

• UTIs are most commonly caused by the organismE. coli.

• UTIs are most common in young heterosexuallyactive women.

• Sexual intercourse is the strongest risk factor fora UTI.

• Spermicides, diaphragms, and hormonal contra-ception all increase the risk for UTIs.

• Pregnant women and postmenopausal womenare also at risk for UTIs due to the effect of hormones on the flora of the vagina, urethra,and bladder.

• Common diagnostic tests include the urine dipstick and the urine culture.

PREVENTION

• Increase fluid intake.• Urinate when you have the urge.• Maintain bathroom hygiene.• Wear cotton undergarments.• Urinate after intercourse.• Consider a different contraceptive method if you

are getting recurring UTIs.• Drink fresh juices, especially berry juices includ-

ing cranberry and blueberry.• Eat fermented milk products containing probi-

otic bacteria.• Reduce dietary bladder irritants such as alcohol,

chocolate, citrus fruits, coffee, black tea, toma-toes, vinegar, and sugar.


it seems reasonable that the risk for infectionmight be altered by dietary influences and diges-tive health. In fact, the risk for infection changeswith dietary modifications.4 The dietary andlifestyle habits of 139 women university studentswith a diagnosis of an acute UTI were comparedwith those of 185 age-matched women with noUTIs in the last five years. It was found that fre-quent consumption of fresh juices, especially berryjuices, and fermented milk products containingprobiotics was associated with a decreased risk of recurring UTIs. Consuming fermented milkproducts three or more times per week was betterthan less than one time per week. In this samestudy, frequency of intercourse was associated withincreased risk of UTI as well.

Common probiotic-containing fermentedmilk products include lactobacillus acidophilusand kefir. Increasing garlic and onions in the dietmay also be helpful due to their antimicrobialactivity. They have been shown to inhibit thegrowth of E. coli, Proteus, Klebsiella pneumonia,Staphylococcus, and Streptococcus.5–7

Other logical dietary considerations forwomen with recurring infections are to avoidexcess sugar consumption, assess and avoid foodallergens, and eat a diet that promotes healthydigestive function, including complex carbohy-drates, high fiber, fermented dairy products, andhealthy oils such as olive oil, nuts, and seeds.

Large amounts of fluids are highly recom-mended for preventing UTIs, as they literallyflush out the urinary tract and dilute the concen-tration of disease-causing bacteria. Drink approxi-mately 64 ounces (two liters) per day, including16 ounces (500 ml) of unsweetened cranberryjuice (see section on cranberry) and 8 ounces ofblueberry juice (250 ml) daily.


Cranberry. No natural approach to cystitiswould be complete without mention of cran-berry. Women have used cranberry juice as ahome remedy for decades. Several studies have

shown that cranberries and cranberry juice areeffective in women with active urinary tractinfections.8–9 In a large randomized, controlledstudy, 300 ml (10 ounces) of cranberry juice wasgiven to 153 elderly women with confirmed bac-teruria.10 The level of bacteria in the urine andthe frequency of recurring infections was dramat-ically decreased. In another study, 500 ml per day (17 ounces) of cranberry juice was shown tobe helpful in 73 percent of the individuals withactive UTIs.11 In an older study, 16 ounces ofcranberry juice daily was effective in 73 percentof individuals with an active infection.

This effectiveness is commonly attributed tocranberry juice’s hippuric acid content, antibac-terial effect, and acidity. However, studies haveshown that components in cranberry juicereduce the ability of E. coli to adhere to the liningof the bladder and urethra.12–15

Often, women prefer cranberry extractsinstead of cranberry juice as unsweetened cran-berry juice is unpalatable and sweetened cranberryis more challenging to the immune system. Cran-berry extracts are available in capsule form andhave been studied for prevention of UTIs. Cran-berry extracts were compared with cranberry juicein a one-year randomized, controlled trial in 150sexually active women of diverse ages.16 One tabletwas given twice daily to women in one group, and250 ml of cranberry juice was given three timesper day to the other group. Both decreased thenumber of individuals who had at least one infec-tion per year. Antibiotics were also used less inboth the extract and the juice group, comparedwith the placebo group.

Cranberry extracts are less expensive thancranberry juice. Another advantage of theextracts is the concern that the oxalates in cran-berry juice could contribute to kidney stone formation. While logical, no studies have yetdemonstrated an increase in kidney stones afterdrinking cranberry juice.

Cranberry extracts can also be found innumerous combination herbal/nutritional for-

69C Y S T I T I S

mulations along with uva-ursi, pipsissewa,Oregon grape root, marshmallow root, buchu,vitamin C, and others. Cranberry is safe for preg-nant and lactating women.

Cranberry Extract

Acute infections: 400 mg 3 times daily or moreChronic, recurring infections: 400 mg 1–2 times

daily

Lactobacilli. Probiotics, especially lacto-bacilli, are commonly used by alternativeproviders to prevent UTIs. Lactobacilli speciespredominate the vaginal and urinary tracts ofhealthy premenopausal women. Women whohave recurring UTIs have an imbalance of theirflora, and if we restored the flora, we could go along way to prevent the infection-causing organ-isms from dominating.

A recent review was done of all studies on therole of lactobacilli and UTIs in 2006.17 From the studies that are available, probiotics appear to be beneficial for preventing recurrent UTIs inwomen. The Lactobacillus rhamnosus and reuteri(previously called L. fermentum) strains were foundto be the most effective.

The hydrogen peroxide–producing lactobacilliare critical in maintaining acidity and inhibitingpathogenic bacteria from adhering to both thevaginal and bladder walls. In addition to consum-ing fermented dairy products with lactobacilli,vaginal suppositories and oral supplementation are good means of administering lactobacilli. In asmall study, women with recurrent urinary tractinfections were treated with Lactobacillus caseispecies topically and via suppository twice

weekly.18 Each patient had infection-free periodsranging from four weeks to six months.

Lactobacilli species are safe for pregnant andlactating women.

Vitamin C. The beneficial effects and functionsof vitamin C are numerous and critical to optimalhealth. Vitamin C is involved in the manufactureof collagen, the main protein substance in the body,which results in its role in wound repair, connectivetissue structures, vascular wall integrity, skin elastic-ity, healthy gums, and more. It is also critical toimmune function, the absorption and utilization ofother nutrients, and the manufacture of numeroushormones and nerve conduction substances, and itis an antioxidant. As early as the 1960s, ascorbicacid (vitamin C) was shown to be an effectiveurinary acidifying agent,19 a successful means oftreating urethra and bladder infections.

While some of these functions help maintainnormal tissue health of the bladder and urethra,vitamin C has some additional effects when itcomes to treating UTIs. During a UTI, nitratesare often generated by bacteria in the urine.Acidifying nitrite forms nitric oxide along withother reactive nitrogen oxides that are toxic to ahost of organisms, including cystitis-causing bac-teria. A study examining the effects of ascorbicacid on nitrite in the urine and bacterial growthfound that acidifying the urine, even mildly, gen-erated large amounts of nitrous oxide, which wasincreased by larger amounts of ascorbic acid. Asa result, the growth of three common bladderpathogens, E. coli, Pseudomonas aeruginosa, andStaphylococcus saprophyticus were significantlyinhibited.20 These results provide a good ration-

Lactobacilli Species

Acute infections: 24 billion organisms or more perday for active treatment

Chronic, recurring infections: 8–16 billion organismsper day

Prevention: 2–8 billion organisms daily

Vitamin C

Acute infections: 500–2,000 mg every 2 hours for 2days, then 500–2,000 mg 3 times daily for 5–10days

Chronic, recurring infections: 1,000–3,000 mg dailyPrevention: 500–1,000 mg daily


ale for the beneficial effects of vitamin C for bothprevention and treatment of UTIs.

Vitamin C is likely safe for pregnant and lactat-ing women in controlled amounts: up to 2,000 mgper day in women over age 19 and up to 1,800 mgper day for women 14 to 18.

D-Mannose. D-mannose is a naturally occur-ring simple sugar contained in cranberry juice thatis helpful in treatment of UTIs. D-mannose adheresto the bladder epithelium, interfering with the abil-ity of the E. coli to adhere21 and cause infection. Itis likely safe for pregnant and lactating women.

Mannose Powder

Acute infections: 1⁄2–1 tsp 3 times dailyChronic, recurring infections: 1 tsp or more dailyPrevention: 1⁄2–1 tsp daily

Botanicals

Uva-Ursi (Arctostaphylos Uva-Ursi ). Oneof the most useful herbs for bladder infection is uva-ursi (Arctostaphylos uva-ursi ), also knownas bearberry or upland cranberry. Uva-ursi hasantiseptic, antibacterial, and astringent properties,largely due to its arbutin content. Uva-ursi is espe-cially active against E. coli and has diuretic proper-ties. Uva-ursi has also been used with recurrentbladder infections and was proven effective in adouble-blind study of 57 women.22 After one year,5 out of 27 women in the placebo group had arecurrence of cystitis, while none of 30 womenhad a recurrence in the uva-ursi group.

Historically, many herbalists have taught that herbs with arbutin work best in an alkalineenvironment. That would appear to present aproblem given that acidifying the urine is a funda-mental concept in the successful treatment ofUTIs. This potential issue has not been a factor inthe great success I’ve witnessed in treating UTIs byacidifying the urine with vitamin C while simulta-neously using uva-ursi and other botanicals.

Because of its potential irritating and inflam-matory effects on the urinary tract mucous mem-

branes, uva-ursi is best used in combination withother botanicals. It is not safe for use by pregnantwomen and unknown whether or not it is safefor lactating women.

Uva-Ursi

Acute infections: 1–11⁄2 tsp tincture or 300 mg driedherb capsule every 3 hours for 2 days, then 1–11⁄2tsp 3 times daily for 7 days

Chronic, recurring infections: best not to use morethan 5 or 6 times per year; use in combination withsoothing botanicals such as marshmallow

Prevention: best not to use daily for long term

Pipsissewa (Chimaphila umbellata). Pipsis-sewa, a native plant of the Pacific Northwest andalso known as chimaphila, bitter wintergreen, orground holly, is a traditional remedy for urinaryinfections. As with uva-ursi, its antiseptic/mildlyantimicrobial effects are attributed to its arbutincontent. It has mildly diuretic, astringent, and anti-spasmodic properties as well, all important mecha-nisms in treating UTIs. Due to its arbutin content,this herb is best used for shorter-term use, or occa-sional use (up to four or five times per year), as foruva-ursi. It is unknown whether or not pipsissewais safe for pregnant and lactating women.

Pipsissewa

Dried root: 1–2 g per dayTincture: 1–11⁄2 tsp per day

Best used in combination with other botanicals, forboth acute and chronic recurring infections

Goldenseal (Hydrastis Canadensis) andOregon Grape Root (Berberis Aquifolium).Goldenseal and Oregon grape root are two of themost important herbs for bladder infections due totheir antimicrobial properties. Berberine, an alka-loid constituent found in the rhizome and root ofthese plants, has demonstrated antibacterial activ-ity against E. coli species, Klebsiella species, Staphy-lococcus, and Pseudomonas species.23, 24 Berberine iseffective against many bacteria and is also able to

71C Y S T I T I S

fight infections by inhibiting the bacteria fromadhering to the host cell.25 It is unsafe for pregnantwomen and best not used by lactating women.

Goldenseal

Freeze-dried root: 500–1,000 mgDried root: 1–2 g per dayTincture: 1–11⁄2 tsp per day

Additional Botanicals. Other botanicalshave been traditionally used for bladder infec-tions with positive effect. The water-solublemucilage herbs are known to be soothing to theirritated uroepithelium and reduce inflamma-tion. These include corn silk for its soothing and

cooling effect on the urinary tract; marshmallowroot due to its content of mucilage, which canform a protective layer on the lining of the blad-der; and even plantain leaf with its high percent-age of mucilage and allantoin.

Additional antimicrobial herbs for the bladderinclude bucchu, myrrh, propolis, and juniper berry.Numerous immune stimulants may be helpful,including echinacea, osha, and wild indigo root.Bladder tonics stimulate the flow of blood andnutrients to the urinary tract and may be usefuladjunct herbs. These herbs include nettle leaves,goldenrod, kava, and horsetail. Dandelion leaf,bucchu, and parsley root have diuretic effects andincrease the flow of urine to help flush the bacteria.

Sample Treatment Plans

See the Resources section for sources of herbal products.

Acute UTI

• Cranberry juice: 16 oz daily• Increase water: 8 or more 8-oz glasses daily• Vitamin C: 2,000 mg every 2 hours for 2 days,

then 2 g 3 times daily for 7–10 days• Combination herbal product such as cranberry,

Oregon grape root, bucchu, uva-ursi, pipsissewa,marshmallow root: 2 capsules every 2 hours for 2days, then 2 capsules 3 times daily for 5–10days

• D-mannose: 1⁄2–1 tsp 3 times daily for 5–10days

Chronic, Recurring UTI (3- to 6-Month Plan)

Premenopausal Women

• Urinate upon urge and after intercourse.• Use condoms for intercourse.• Increase fluids.• Take the following supplements:

Combination herbal product: 1–2 capsules dailyCranberry extract: 400 mg twice dailyCranberry juice: 8–16 oz daily

Oral probiotics: 8–16 billion organisms dailyMannose: 1⁄2–1 tsp daily; more if needed

Postmenopausal Women

• Urinate upon urge and after intercourse.• Use condoms for intercourse.• Increase fluids.• Take the following supplements:

Combination herbal product: 1–2 capsulesdaily

Cranberry extract: 400 mg twice dailyCranberry juice: 8–16 oz dailyOral probiotics: 8–16 billion organisms per dayMannose: 1⁄2–1 tsp daily; more if neededIntravaginal estriol (1 mg/g): insert 1 g twice

daily for 2 weeks, then twice weekly asmaintenance dose; or estriol suppositories (1 mg): insert 1 daily for 2 weeks, thentwice weekly as maintenance dose

• Consider oral hormone therapy.

With these prevention and treatment strategies, itwill rarely be necessary to use antibiotics foracute, chronic, or recurring UTIs. Please consultwith your practitioners about use of these productsin pregnancy and lactation or if you are taking medications.


Intravaginal Estriol. In postmenopausalwomen, other influences are important to con-sider for chronic recurring UTIs. Lower estrogenstates result in fewer lactobacilli in the vagina andbladder. Fortunately, vaginal estrogens are a very safe and effective solution. Intravaginalestriol effectively treats recurring UTIs in post-menopausal women26 by restoring the normalvaginal flora and reducing the risk of vaginal E.coli colonization. Other, more commerciallyavailable vaginal estrogens are also used for thissame purpose.

Intravaginal Estriol

For chronic, recurring infections and for prevention:intravaginal compounded estriol: 1 mg/g, insert 1 g twice daily, long term

This is a prescription item. Discuss the issue of usinga progestational agent with your licensed primarycare practitioner, although most women will not needsuch an agent when using this low dose of vaginalestriol.

CONVENTIONAL MEDICAL APPROACH

The diagnosis of UTI in conventional practice is the same as that for alternative medicine. Conventional treatment, however, relies prima-rily on antibiotic therapy. For uncomplicated urinary tract infections, especially those follow-ing sexual intercourse, culture and sensitivitytesting are not mandatory, and any antibioticexcept penicillin will likely be effective. (Mostgram-negative bacterial isolates are resistant topenicillin.) The most commonly used agents arenitrofurantoin macrocrystals (100 mg twice aday), trimepthoprim-sulfamethoxazole double-strength (twice a day), or a fluoroquinolone suchas ciprofloxacin (500 mg twice a day).

Cephalexin (500 mg three or four times a day)is another reasonable choice, but the dosing sched-ule may be onerous for most patients. The currentrecommendation is for three days of oral therapy. If

three days of therapy does not result in resolutionof symptoms, a culture is recommended and theantibiotic changed pending sensitivities. Mostpractitioners, in such a circumstance, will treat fora longer period, usually seven days.

Recurrent uncomplicated urinary tract infec-tions, particularly in young, sexually activewomen, may require what is called prophylactic(prevention) therapy to allow the bladder’sdepleted defenses to regenerate. This involveseither a single dose of antibiotic daily, a singledose of antibiotic following intercourse, or oneor two doses of antibiotic at the onset of earlysymptoms prior to a full-blown UTI.

Women who have structural or functionalurinary tract abnormalities or who are immuno-compromised develop complicated UTIs andrequire more aggressive evaluation and treat-ment. The workup will depend on the nature ofthe symptoms and the clinical situation.

Generally, complicated infections are treatedfor 7 to 21 days. A “test-of-cure” culture should bedone approximately 5 to 7 days after completingtherapy. In rare cases, when the response to theantibiotic does not occur, surgery may be requiredto drain or remove the focus of infection.

Conventional medicine has also borrowedfreely from the naturopathic community, com-monly employing prophylactic regimens of cran-berry preparations and acidophilus. Blueberriesalso have abundant proanthocyanidins and are,therefore, recommended as well. Current litera-ture discourages the use of vitamin C, as it hasnot proven to be of benefit. In the postmeno-pausal population, topical estrogen therapy hasalso been shown to prevent infection.

Due to the prevalence of UTI amongwomen, there is a great impetus to develop new,non-antimicrobial preventative therapies. Themost promising current work involves vaccinesdelivered transvaginally. Multiple applications ofthe vaccine are required to confer resistance toinfection. In the recent past, bacteriophages,viruses that invade bacteria, were developed by

73C Y S T I T I S

the Russians to treat resistant pathogens. Thistechnology was brought to the United States andtested briefly, but further development wastabled because the bacteria rapidly became resist-ant to the treatment. Scientists therefore con-tinue to seek more ideal means of preventing anderadicating infection. In the meantime, we are barely able to keep one step ahead of the bacteria.


There are some definite situations as to when a licensed practitioner should be consulted. Cer-tainly, this list includes women with urinary symp-toms who are pregnant, have catheters, have had symptoms for longer than seven days, are immunocompromised (immunosuppressive drugs,HIV), or have chronic kidney disease or diabetes.

Women who have recurring infections shouldprobably be evaluated for underlying causes as wellas more sophisticated treatments. In addition, ifyou have symptoms of a bladder infection, plus afever, this warrants a practitioner visit right away, asit may indicate that the infection has traveled tothe kidneys. Blood in the urine is another signwhen one should see a practitioner.

It is important to keep in mind that sexuallytransmitted infections due to chlamydia, gonor-rhea, or herpes simplex cause similar symptomsto bladder infections, as do yeast or bacterialvaginal infections. Making an accurate diagnosisis a key to successful treatment. A thorough his-tory, physical, and laboratory test are the mainways a practitioner can diagnose UTIs. Whetherit’s alternative or conventional treatment, self-care should be limited to simple, uncomplicated,acute bladder infections that occur only once ortwice per year.


75

OVERVIEW

Endometriosis, one of the most common yetmisunderstood diseases, affects 10 to 15 percentof menstruating women between the ages of 24 and 40 years. In some cases, symptoms begin with the onset of menstruation. In others,symptoms begin later and progressively becomeworse until menopause. The triad of symptomsincludes dysmenorrhea (pain with menses), dys-pareunia (pain with vaginal intercourse), andinfertility. Acute pain occurs before menses andcan last for a day or two during menses orthroughout the month. This pain can be a life-disrupting experience, affecting a woman’s socialrelationships, work, school, and well-being. Forsome women, vomiting, diarrhea, and faintingcan occur along with intense labor-like pains.Other pain is described as chronic bearing-downpain and pressure on the lower back and pelvis,sometimes radiating down the legs. Other lesscommon complaints include pain with urinationand bowel movements and bleeding from thenose, bladder, and/or bowels. Endometriomas,enlarged areas of ectopic endometrial involve-ment on the ovaries, are found in two out ofthree patients with endometriosis.1

Early research as to the source of infertilityinitially led to the concept that endometriosiswas a “working woman’s disease.” Women whodelayed pregnancy until later in life and werefound to have endometriosis were told to “justget pregnant.” Current research does not supportthis concept. However, research as to alteredimmune action within the pelvic cavity and thepossibility of antibody reactions to sperm hasprompted recognition of an immunological basisfor endometriosis. Other studies suggest thatinfertility is a cause of endometriosis, due to

the unruptured follicle, rather than a result.2

Whether endometriosis causes infertility or infer-tility causes endometriosis, tubal scarring, adhe-sions, and unruptured follicles are common withwomen having endometriosis and infertilityproblems.

The main risk factor for endometriosis isheredity. The likelihood for a woman who has afirst-degree relative with severe endometriosishaving endometriosis is six times higher thanthat for relatives of women without the disease.3

Women with menstrual cycles that are shorter intime between cycles and longer in length havebeen found to be at higher risk for endometri-osis.4 Increased or altered estrogen levels, lack ofexercise from early age, a high-fat diet, and use ofintrauterine devices have also been found to berisk factors. Even natural red hair color wasfound in one study to be a factor in the develop-ment of endometriosis.5

Baboons who developed endometriosis in cap-tivity were found to have higher stress levels and adecreased ability to react to stress compared tothose in the wild, suggesting a stress factor.6 Indi-viduals who exercised consistently from an earlyage reported a decreased risk for endometriosis,while those who began an exercise program lateron experienced less painful periods. Although notall women with endometriosis have a childhoodhistory of abuse, a greater number of individualswith adhesions and/or endometriosis havereported abuse in their history.7 Additional possi-ble risk factors include prenatal exposure to highlevels of estrogen and pelvic contamination withmenstrual products, although these issues arelargely theory and research is needed.

Physical examination reveals one or more ofthe following: tenderness of the pelvic area

6E N D O M E T R I O S I S C H A P T E R



and/or cul-de-sac (a deep pouch anterior to therectum, separating the uterus from the largeintestine); enlarged or tender ovaries; a uterusthat tips backward and lacks mobility; fixedpelvic structures; and adhesions. Endometrialtissue can be found on surgical scar tissue, in thevagina, and on the cervix. Physical examinationduring the first or second day of menses high-lights tender areas in the septum between therectum and vagina, most likely correlated withdeeply infiltrating endometriosis.8

An ultrasound study can determine the con-sistency of the endometriomas (areas of cysticendometriosis within the ovary). Evidence ofendometriosis other than on the ovaries cannotbe seen on the ultrasound. Although magneticresonance imaging (MRI) can detect endometri-omas, cost prevents widespread use. A blood testcalled a CA-125 can have positive results inendometriosis. The problem is that a high CA-125 cannot completely differentiate endometri-osis from uterine fibroids, cancerous growths,and normal tissue. High levels of CA-125 havebeen found in stages III and IV of endometriosis,which are the diagnoses for more advanced endo-metriosis.9 The CA-125 test may, however, helpin monitoring treatment and progression onceendometriosis has been confirmed. However, thistest is not used by many practitioners.

Definitive diagnosis of endometriosis can onlybe accomplished with a biopsy using either of thefollowing two surgical procedures. A laparoscopyis a surgical procedure in which the surgeon insertsa scope through one of two very small pelvic inci-sions. More invasive, a laparotomy consists ofmajor pelvic and/or abdominal surgery.

Endometrial implants or lesions are known tohave similarities to uterine tissue—featuringendometrial glands, endometrial stroma, andhemorrhage into adjacent tissue. Growth of thistissue may be stimulated by estrogen. Therapeu-tic treatment aimed at manipulating the body’sown level of hormones as in menopause or preg-nancy has had a positive effect. In some individ-

uals, the implants have their own cycle, with anebb and flow that differ from the estrogen bind-ing during the menstrual cycle.10

Although the most commonly accepted theo-ries of origin today vary and sometimes seemcontradictory, they all have their place in holisticapproaches to the treatment of endometriosis.The predominant theory first proposed by Dr.John Albertson Sampson in 1927 is the theory ofretrograde flow—that during menses, bloodflows backward and becomes seeds of implants inthe pelvic cavity.11 This theory and researchshowing that over 90 percent of menstruatingwomen without endometriosis have retrogradeflow have raised questions as to the biochemicaland immunological differences causing implan-tation within the pelvic environment.12 Endome-trial implants from women with endometriosiscompared with normal women have been foundto be biochemically different.13 Other studiessuggest that cells may only implant in womenwith altered cell immunity.14 As implants arefound in the nose, lungs, and other organs farfrom the uterus, transportation through lym-phatic channels and blood vessels has been sug-gested. Still other researchers believe the implantsto be of embryological origin, pieces of the uterusleft behind during development, which, whenactivated, secrete a chemical causing the nearbycapillaries to bleed.15 Research on baboons withendometriosis suggests activation by environ-mental toxins that mimic estrogens.16

Whether implants are caused by retrogradeflow, decreased immune function, genetic fac-tors, environmental influences, or embryologicaldevelopment or are stimulated by high estrogenlevels from the environment or within the body,the worsening of symptoms prompts individualsto seek medical help. There is not necessarily acorrelation between pain and the extent of thedisease. Women with fixed ovaries and largeendometriomas may only report mild discom-fort, while those with visibly smaller lesions mayreport severe and chronic pain. Upon surgery,

77E N D O M E T R I O S I S

these lesions are found to extend more deeply;they are possibly more influenced by circulatingestrogens.17 Research has found that the severityof symptoms is correlated with the depth of thelesions rather than the number of lesions.18

The abnormalities found in women withendometriosis and the conditions that may pre-dispose them to it are complex. Some discussion,however, will help guide us toward more effectivemanagement and a better understanding of treat-ment options.

Genetic Factors

Groupings of endometriosis within families hasbeen found in clinical studies,3, 19 populations-based studies,20 and even studies of twins.21–23

Several analyses of the locations on the genes thatare shared by siblings indicate abnormalities indetoxification enzymes. This would lead to sus-ceptibilities to environmental exposures to sub-stances that could then lead to the increase in thedisease. Other insights have included that thegenes involved are associated with tumor sup-pressor genes. If these tumor suppressor genes areaffected, there is susceptibility to abnormal tissuegrowth, such as the endometriosis. Aberrantlyexpressed genes can also occur during the time ofimplantation, which may be an explanation forsome of the cases of endometriosis-associatedinfertility. Other genetic errors may occur inmultistep fashion involving both the develop-ment and the progression of the disease.24

Environmental Factors

Information about environmental influences onendometriosis in humans has been gleaned byobserving the negative effects of environmentalexposures to rhesus monkeys. Radiation exposureand dioxin exposure have lead to higher fre-quency of developing endometriosis in mon-keys.25, 26 It would seem plausible to extend thisconsideration to environmental effects onwomen, especially when it was reported that thehighest dioxin pollution in the world was in

Belgium, which also has the highest incidence ofsevere endometriosis.27 In two studies since,however, one in Belgium found no significantlyincreased risk with dioxins or polychlorinatedbiphenyls,28 and in Italy, no significantly in-creased risk of endometriosis was seen in womenwho had high levels of dioxin in their blood.29

Currently, there is no epidemiological studydefinitively linking any one class of chemicals tothe risk of endometriosis, although there appearsto be some suggestion of a link with estrogen-likecompounds in the environment30 called xeno-estrogens, which can disrupt estrogen and estro-gen metabolism. Substances that have beenshown to have estrogenic effects in the bodyinclude polychlorinated biphenyls (PCBs), weedkillers, substances that line cans, plastics, deter-gents, and household cleaners.31

Despite this lack of identification of a defini-tive link between chemical exposures and endo-metriosis, we do know that women are exposedto a multitude of chemicals in utero, in child-hood, peripubertally (the time around theappearance of secondary sex characteristics suchas pubic hair), and as adults. We can identifychemicals in cosmetics, nail polish, plastics,household cleaners, dry cleaning, and foods. Asurvey by the Centers for Disease Control andPrevention (the National Report on HumanExposure to Environmental Chemicals) is cur-rently underway, which monitors 145 chemicalsin 2,500 people in the United States.32

I would assert that the roles of toxic chemicalsin reproductive health should not be underesti-mated, and that scientific investigations that“suggest a correlation” should be motivationenough to reduce the toxic exposure to chemicalestrogen-like compounds that disrupt our ownbodies’ hormone-receptive tissues.

The Immune Connection

Increasingly, we are finding evidence that a lackof proper surveillance by the immune system inthe pelvic area is the cause of endometriosis, and


alterations in other aspects of the immune systemare involved in the progression of the disease.33

In studies on the immunological functions ofbaboons with spontaneous (noninduced) endo-metriosis, researchers have found a correlationbetween suppressed immunity and a highernumber and greater area of lesions.34 Both typesof immunity, cell mediated and humoral, havebeen implicated in endometriosis, with immuno-logical defects present even in the mildest formsof the disease.35 Macrophages (a kind of whiteblood cell) that scavenge other microbes, debris,and aberrant tissue are found in greater numbersin the early stages of endometriosis.36 Thisincrease in macrophage activity may correlatewith decreased fertility and possible reaction tosperm perceived by the woman’s body as for-eign.37 In the peritoneal fluid (fluid aspiratedfrom the area behind the membrane lining theabdominopelvic wall) of women with severeendometriosis, natural killer cell activity has beenfound to be suppressed.38, 39 Natural killer cellsrelease cell toxins and thus help keep tumor andother abnormal cells in check. By a decrease innatural killer cells, the immune defense againstthe growth of tissue is decreased. Interestingly,studies suggest a correlation between high estra-diol levels and decreased killer cell activity.40

Humoral immunity is the component of theimmune system that produces antibodies, morespecifically immunoglobulins, which are pro-duced by B lymphocytes. These immunoglobu-lins provide protection to the body by theirattachment to foreign substances called antigens.Patients with endometriosis have been found tohave high levels of immunoglobulins IgG andIgM when compared with normal controls.41

Higher than normal amounts of immunoglobu-lins cause destruction of the body’s own tissue, asseen in autoimmune conditions. Evidence ofhigh levels of autoantibodies against ovarian andendometrial cells is consistent with the finding ofindividuals who have both endometriosis andautoimmune diseases.42, 43

Numerous changes in the makeup of the peritoneal fluid are also evident in women withendometriosis. Immune cells that mediate theinflammatory reaction such as cytokines, macro-phages, T lymphocytes, and tumor necrosis factorshave all been found to be increased in concentra-tion in the peritoneal fluid in women with endo-metriosis,44–46 and their increase correlates withthe severity of the disease. Growth factors, angio-genic factors (increasing blood supply to areas ofendometriosis tissue), and lipid peroxidation inthe peritoneal fluid may stimulate the endometrialcell growth. Targeting these proinflammatorycompounds and blocking their action with antiox-idants and other compounds provide a goodrationale for new treatment strategies, both con-ventional and with natural compounds.

As mentioned earlier, irregular cycles arecommon among women with endometriosis.Anovulatory cycles (lack of ovulation), premen-strual spotting (very light bleeding before theonset of the menstrual flow), luteal phase defects(abnormal length of the second half of the men-strual cycle), and salivary progesterone secretionare altered in women with endometriosis.47 Sincehigher estrogen levels are implicated in endome-triosis, it is not surprising that heavy smokershave a decreased risk for endometriosis if theybegan smoking earlier in life, as smoking isknown to decrease estrogen levels.48 In addition,an increased body fat placement indicative ofincreased estrogen levels was also found to becorrelated with a higher incidence of endometri-osis.49 Since estrogens are known to stimulateendometrial implants, women on hormonereplacement therapy have been known to experi-ence a recurrence of endometriosis.50

The Role of the Liver and the Gut in Hormone Metabolism

The liver has the enormous task of breaking downestrogen and secreting metabolites through thebile into the large intestine. Whether hormonesare produced naturally within the body, are pro-


vided through medication, or enter the body assubstances from the environment that mimicestrogen, optimal functioning of the liver is imper-ative in maintaining a healthy balance.51 Inappro-priate breakdown of estrogen can result in localliver damage, continual recycling of estrogens, andalterations in immune function. Since the liver isinvolved in breaking down 80 to 90 percent of thehormones in the body, it follows that optimal liverfunction can be of benefit in treatment.

The large intestine, which contains differenttypes of microflora or gut organisms, has a uniquerole in the excretion and recycling of estrogen. Theliver inactivates estrogen by attaching a bondbetween glucuronic acid and the estrogen moleculeand excreting this substance with the bile. Some“unfriendly” bacteria in the large intestine, how-ever, secrete an enzyme called beta-glucaronidasethat breaks down these bonds, releasing a strongestrogen that is then recycled back through thebody. In order to produce this enzyme, these bac-teria feed on fat taken in by the body. However,the balance can be restored by greater numbers of the “friendly” bacteria that feed on fiber and crowd out the “unfriendly” bacteria. With abalance of the “friendly” bacteria in the largeintestine, a higher amount of inactivated estrogenmetabolites leave the body through the largeintestine, preventing their reactivation and move-ment back through the body.52

Endometriosis is a complex disease with avariety of interconnecting influences. Enhancingthe immune system, the endocrine system, andthe liver’s detoxification of hormones; reducingand blocking proinflammatory chemicals pro-duced by the body; and providing optimal healthin the large intestine represent innovative andeffective approaches to the treatment of endome-triosis. Considering the long-term consequencesof endometriosis—pain, disability, and disrup-tion in personal, family, and work activities—innovative approaches that treat the whole bodyand remove the cause promise a light at the endof the tunnel.


While analgesics, anti-inflammatories and estrogen-blockers temporarily relieve symptoms, the needfor a long-term definitive treatment that involvesremoval of the cause is imperative. A systemicapproach to treatment that takes into considera-tion a multifaceted cause with long-term andacute symptomatic relief is the goal of alternativetherapy. While late-stage endometriosis may only be addressed by radical surgery, early treat-ment, in the form of stimulation of the body’sinherent ability to heal through enhancing theimmune system, restoring proper inflammatoryresponses, balancing hormones, and aiding in the

KEY CONCEPTS

• A gynecological checkup is imperative with anytype of pelvic pain to rule out any pelvic orabdominal abnormality.

• Provide symptom relief for acute pain.• Provide removal of cause (endocrine, immune,

environmental, liver).• Create a plan for treatment of the chronic

problem.• Optimize nutritional intake and avoid environ-

mental toxins.

PREVENTION

• Eat nutritious whole foods. Include foods knownto reduce inflammation such as fish, curries, andgarlic and high amounts of fruits and vegeta-bles, whole grains, and legumes. Reduce redmeat, especially grain-fed meat.

• Get regular exercise.• Avoid pesticides, chemicals, solvents, and heavy

metals.• Eat organic foods.• Drink purified water.• Maintain good digestion and regular bowel

habits.• Avoid alcohol.


liver’s ability to break down environmental andnaturally occurring estrogen, is worthy of consid-eration.

Certain foods and supplements aid in enhanc-ing the body’s ability to mount a natural immuneresponse. Optimal liver function involves enhanc-ing the liver’s ability to detoxify hormones, excessmedicines, and toxins through two main phases,called phase I and phase II detoxification. Individ-uals who have decreased function of the first path-way continue to recycle hormones, toxins, andother products harmful to the body. If the seconddetoxification pathway is dysfunctional, the meta-bolic products of the first pathway build up andcan become even more toxic, decreasing immuneresponse and accumulating as oxygen free radicals.These metabolites can cause tissue injury and for-mation of adhesions.53 Healthy elimination ofthese metabolites assures that the body doesn’t geta chance to reabsorb them.

Nutrition, exercise, and healthy lifestyle prac-tices play a preventive role in providing immunesupport and a healthy body’s response to addedstressors and imbalances of hormones. Womenwho exercise and eat less fat and sugar produce lessestrogen. Vegetarian women excrete two to threetimes more estrogen in their feces and have half asmuch estrogen in their blood as meat-eaters.54

Additional approaches in the area of mind-bodymedicine recognize that belief systems and emo-tional health affect optimal physical health.

Nutrition

The goods news is that there are numerous nutri-tional influences related to endometriosis. Thismeans we can take an active part in preventionand management of the condition.

A recent retrospective study of over 500women with endometriosis concluded that therewas a significant decrease in risk of developingendometriosis with a greater consumption ofgreen vegetables and fresh fruit, and an increasein risk was associated with high intake of beefand other red meat.55

Foods high in fiber are associated with opti-mal transit time in the intestines and an optimalbalance of friendly microorganisms within thelarge intestine.56 These microorganisms, betterknown as gut flora, crowd out the other types offlora that play a role in metabolizing estrogen.Studies suggest that an intake of less protein andhigh fiber or a vegetarian diet lead to a decreaseof biologically active estrogens in blood plasma.54

While higher protein diets are found to provideenzymes for the detoxification pathways of estra-diol,57 vegetarian diets are of greater value due totheir lower fat content. Animal protein diets,especially egg yolks, poultry, and red meat, con-tain large amounts of arachidonic acid, whichpromotes inflammatory prostaglandins and thusinflammation and pain. By enhancing your dietwith vegetable protein, soy, almond and othernut butters, and salmon, you tip the inflamma-tory pathway toward anti-inflammatory pro-staglandins that inhibit tumor growth—andpossibly endometrial growth. Interestingly, arecent study in Japan demonstrated that moder-ate isoflavone intake from soy was significantlyassociated with a decreased risk of premeno-pausal hysterectomy. This data led the authors toconclude that moderate soy intake may decreasethe risk for diseases like endometriosis, whichcommonly precipitate premenopausal hysterec-tomies.58 Another study of 50 women with endo-metriosis examined the effect of dietary changes,specifically the reduction of glycemic carbohy-drates, the addition of omega-3 and omega-9fatty acids, and the elimination of foods with caffeine and tyramine, and found a significantreduction in symptoms after eight weeks.59

By increasing intake of vegetables, specificallythose that enhance liver function, the buildup oftoxins and metabolites that produce cell damageis prevented. Liver-friendly foods to increase arecarrots, kale, and the cabbage family vegetablesdue to their known help in phase II of the liver’sdetoxification pathway. Indole-3-carbinol (I3C),found in broccoli, brussels sprouts, cabbage, and


cauliflower, favors the less active form of estro-gen.60 Other liver-cleansing foods include beets,carrots, artichokes, lemons, dandelion greens,watercress, and burdock root. Onions, garlic, andleeks contain organosulfur compounds thatenhance the immune system and induce enzymesthat detoxify the liver. In addition, they containthe bioflavonoid quercitin, which is known tostimulate the immune response, protect againstoxidation, block the inflammatory response, andinhibit tumor growth.61 By eating as many of yourvegetables as possible in an organic form, you cutdown on your intake of pesticides that may alsomimic estrogen.

Use seasonings such as turmeric (curcumin)that protect against environmental carcinogens,decrease inflammation, and increase bile secretion.Ginger is helpful with many types of inflamma-tion—and helps with liver detoxification. Adding atablespoon of soaked and ground milk thistle seedseach day can also help with liver function. Grind atablespoon of fresh flaxseeds and place on cereals orsalads. The increase in lignans from these seeds aidsin providing fiber as well as an oil that helps in theanti-inflammatory pathway. Seasoning with fucus(a seaweed) helps stimulate T cell production andabsorb toxins.62

Foods to omit or decrease include sugar, caffeine, egg yolks, poultry, red meat, and alco-hol. Sugar is known to increase estrogen levels in men; presumably the effect is similar inwomen.63 Endometriosis is found to be corre-lated with caffeine consumption. Women con-suming 5,000 to 7,000 mg of caffeine per monthhad a 1.2 times greater incidence of endometri-osis, while those consuming over 7,000 mg permonth had a 1.6 times increase.64 One cup ofcoffee contains 120 mg of caffeine; one cup of black tea contains 60 mg; one cup of decaf-feinated contains about 2 mg of caffeine.

The Environmental Protection Agency esti-mates that 90 percent of human dioxin exposure isthrough food, primarily meat and dairy prod-ucts.65 Egg yolks, meat, and poultry cause the lipid

pathway to be tipped toward prostaglandins andleukotrienes that cause inflammation, smoothmuscle contraction, and vascular constriction.Alcohol use depletes stores of B vitamins in theliver and also has estrogenic effects on the body.


Before beginning the discussion on nutritionalsupplements, it is important to explain the con-cepts of free radicals, antioxidants, and free radi-cal scavengers. There are several ways to define afree radical, but a definition I like is, “an atom orgroup of atoms that has at least one unpairedelectron and is therefore unstable and highlyreactive.” Antioxidants such as vitamins C and E,selenium, carotenes, and others are moleculesthat defend the body from cellular damage byending the free radical chain reaction before vitalmolecules are harmed. These are often referred toas “free radical scavengers.”

Vitamin C. Studies using vitamin C showincrease in cellular immunity and decreases in

Dietary Recommendations

• Eat a high-fiber diet.• Eat a high-protein vegetarian diet.• Increase intake of vegetables, nuts, and seeds.• Use turmeric, ginger, milk thistle, and

flaxseeds.• Omit or decrease alcohol, dairy, red meat,

sugar, and caffeine.• Eat cold water fish (salmon, tuna, sardines,

mackerel, herring) 2 or 3 times per week.• Eat organic foods.

Vitamin C

Take 6–10 g in divided doses daily, starting with1,000 mg a day, then add 1,000 mg every 4 or 5 daysuntil the stools become loose. At this point, backdown to the previous dose of vitamin C so that thestools are normal in consistency.


autoimmune progression and fatigue.66 In addi-tion, vitamin C enhances immunity and decreasescapillary fragility and tumor growth, all of whichare involved at various levels in endometriosis.Studies on autoimmune progression indicate theeffectiveness of high levels of vitamin C.67

Beta-Carotene. Beta-carotene helps enhanceimmunity. Recent research shows that retinoidscan help decrease IL-6, an inflammatory media-tor, which has been implicated in endometri-osis.68 In addition, studies show that use ofbeta-carotene increased T cell levels after sevendays.69 Beta-carotene was also shown to be pro-tective against early stages of tumor growth.70

Impairment of phagocytosis (the engulfing ofmicroorganisms, other cells, and foreign particlesby white blood cells) is seen in vitamin A–deficient states.71 Although vitamin A was used inthis study, one-third of beta-carotene is convertedto the active form of vitamin A, retinol. Additionalstudies suggest that immune function is due tocarotenoids rather than vitamin A.72

Beta-Carotene

50,000–150,000 IU daily

Vitamin E. Recent research demonstratesthat free radicals may contribute to the inflam-mation and excessive growth of endometrialtissue seen in endometriosis, and in these circum-stances, antioxidants such as vitamin E and N-acetyl cysteine can act to inhibit this abnormalproliferation.73, 74

Vitamin E also helps to correct abnormalprogesterone/estradiol ratios in patients withmammary dysplasia (increased growth of cells).75

Since parallels have been found between abnor-mal tumor growth in cancer and abnormalgrowth of lesions in endometriosis, vitamin Esupplementation may be advantageous. Whilesecondary dysmenorrhea is usually involved withendometriosis, studies on the use of vitamin Ewith primary dysmenorrhea76 show benefit per-

haps through the inhibition of the arachidoniclipid pathway. Inhibiting the arachidonic path-way helps prevent the release of chemicals thatwould normally cause edema, inflammation, andsmooth muscle contraction.

Vitamin E

400–800 IU daily

Essential Fatty Acids. Gamma-linolenic acid(borage, black currant, and evening primrose oils)and alpha-linolenic acid (flaxseed, canola, pump-kin seed, soy, and walnut oils) help decrease theinflammatory response on the tissue level throughpathways that produce prostaglandins in the body.Depending on one of three main pathways ofprostaglandin production, the effects can be help-ful or harmful to the body. Animal fats produce apathway of prostaglandin products that increaseinflammation, muscle constriction, and edema.However, gamma-linolenic acid and alpha-linolenic acid produce the opposite effects. Thesefatty acids taken in supplemental form can pro-duce the prostaglandins that are involved ininhibiting tumor growth, dilating smooth muscle,and decreasing inflammation.77 Since endometri-osis tissue, called implants, are thought to secretechemicals that cause leakage from nearby capillarybeds, decreasing the permeability of these vesselscould help control the tissue destruction andadhesions, decreasing irritation in the pelvis.Recent research demonstrates that having a higheromega-3 to omega-6 fatty acid ratio may have asuppressive effect on the in vitro survival ofendometrial cells, leading the authors to concludethat omega-3 fatty acids may be useful in the man-agement of endometriosis by decreasing inflam-

Essential Fatty Acids

Eicosapentaenoic acid: 1,080 mg dailyDocahexaenoic acid: 720 mg dailyAlpha-linolenic or gamma-linolenic acid: 300 mg

daily


mation.78 In an animal model, fish oils were foundto decrease prostaglandin production and inhibitthe growth of endometrial implants.79

B Vitamins. B vitamins help the liver to inac-tivate estrogen. Studies suggest that supplemen-tation of B vitamins may cause the liver tobecome more efficient in processing estrogen.80

B Vitamins

50–100 mg B-vitamin complex; B6 should not exceed200 mg daily

Selenium. Selenium aids in the synthesis ofantioxidant enzymes responsible for detoxifica-tion reactions within the liver. In addition, sele-nium stimulates white blood cells and thymusfunction.81 Individuals with decreased seleniumlevels have suboptimal cell-mediated immunity,decreased numbers of T cells, and associatedinflammation.82

Selenium

200–400 mcg daily

Lipotropics. Lipotropics aid in promotingliver function and detoxification reactions. Sup-plements that contain choline (a B vitamin),betaine, and methionine promote the flow of fatand bile (containing estrogen metabolites) fromthe liver out through the large intestine.83

Lipotropics

1,000 mg choline and 1,000 mg methionine or cys-teine 3 times a day

Botanicals

Herbal Medicines for Pain Relief. Theherbs appropriate for acute pain relief in endo-metriosis are the same herbs used for menstrualcramps. Valerian, crampbark, black cohosh, andother helpful herbs are discussed in Chapter 13.A recent study of a cyclic administration of two

Japanese herbal formulas of peony and licorice(Shakuyaku-kanzo-to) and peony and dong quai(Toki-shakuyaku-san) was found to decreaseendometrial pain in all patients studied and waseven reported to promote ovulation.84 Anotherstudy reported both hormonal and inflammatorymodulation that led to decreased volume ofendometrial implants in an animal model ofendometriosis through the use of Tripterygiumwilfordii, another Chinese herb.85

Traditional Herbal Therapies

Chaste Tree (Vitex Agnus Castus). Chastetree has traditionally been used as a treatment forhormone imbalances in women. Through actionon the pituitary gland, chaste tree has a proges-terone effect by increasing luteinizing hormone(LH). Useful for fibroids, premenstrual syn-drome, perimenopause, and various menstrualcycle disorders, it also has an indication in endo-metriosis, perhaps because less estrogen is avail-able to stimulate endometrial tissue.86

Dandelion Root (Taraxacum Officinale).Dandelion root is one of nature’s most detoxify-ing herbs. It works principally on the liver andgallbladder to help remove waste products. Bysupporting the liver, excessive estrogens andtoxins can be deactivated. Researchers in Japanhave found a link between dandelion and antitu-mor activity.87 In addition, dandelion leaf con-tains vitamins A, C, and K and calcium, as wellas choline, a lipotropic substance.

Prickly Ash ( Xanthoxylum Americanum).Prickly ash is known for its specific action oncapillary engorgement and sluggish circulation.Through its stimulation of blood flow through-out the body, prickly ash helps enhance the trans-port of oxygen and nutrients and the removal ofcellular waste products. For women with pelviccongestion, this herb enhances circulationthroughout the pelvis.

Motherwort ( Leonurus Cardiaca). Mother-wort is antispasmodic and gently soothes the


nerves. As women with endometriosis generallyexperience uterine cramps and pain, motherwortis useful in promoting relaxation during times ofextreme “bearing-down” pain in the uterus andother regions.88 As a mild sedative, motherworthelps with the needed rest during menstrualcramps.

Herbal Tincture for Chronic Treatment

Chaste tree, dandelion, prickly ash, motherwort combi-nation: 1⁄2 tsp 3 times daily for 3 months

Turska’s Formula. Turska’s formula is afavorite old naturopathic treatment for decreasingaberrant cancer cell growth. A tincture of this for-mula is useful in treating endometriosis due to the

similarities of cancer to cell growth found in thepelvis. This formula contains monkshood (Aconitenapellus), yellow jessamine (Gelsemium semper-virens), bryony (Bryonia alba), and poke root (Phy-tolacca americana). Monkshood and yellowjessamine contain alkaloids that have been knownto disrupt the assembly of microtubules that even-tually help in the formation of cells that differen-tiate and give rise to connective tissues, blood,lymphatics, bone, and cartilage. Quite possibly,these herbal alkaloids interfere with the inductionof abnormal ectopic lesions within the pelvis (con-sistent with the theory of cells left behind inembryonic development). Bryonia is also knownto provide antitumor effects. Poke root containsglycoproteins known to stimulate lymphocyte

Sample Treatment Plan for Endometriosis

Nutrition

• Increase the following in your diet:

Vegetables (especially cauliflower, brusselssprouts, and carrots)

Protein (tofu, beans, salmon, soy nuts, and smallamounts of turkey and chicken)

Fiber (whole-grain breads, rice, raw vegetables,and flaxseed)

Omega-3 oils (especially cold water fish: salmon,tuna, sardines, mackerel, and herring)

• Decrease or eliminate the following:

All saturated animal fatsAll foods containing sugar, caffeine, chocolate, or

alcohol

• Avoid pesticides and heating food in plasticcontainers.

• Drink purified water.

Daily Supplements

• Vitamin C: 6–10 g• Vitamin E: 400–800 IU• Fish oils: 1,080 mg EPA and 720 mg DHA• Beta-carotene: 50,000–150,000 IU• Selenium: 200–400 mcg

• Lipotropics: 2–4 capsules• Flax oil, evening primrose oil, or borage oil:

2 to 4 capsules per day

Botanicals

• Acute tincture:

Black cohosh: 1 ozWild yam: 1 ozCramp bark: 1 ozValerian: 1 oz1⁄2–1 tsp every 2–4 hours for acute pelvic pain

• Chronic tincture:

Chaste tree: 1 ozDandelion: 1 ozPrickly ash: 1 ozMotherwort: 1 oz1⁄2 tsp 3 times a day

• Turska’s formula: 5 drops 3 times daily• Progesterone cream:

Option 1: days 1–6, no cream; days 7–26,1⁄4–1⁄2 tsp twice a day




transformation for immune enhancement. Pokeroot also has anti-inflammatory properties. Due toits potential toxicity, however, this tincture can beprovided only by a licensed health professional.

Turska’s Formula

5 drops 3 times daily

See Resources section for sources.

Natural Progesterone

Progesterone has been known to modify theaction of estradiol by decreasing the retention ofreceptors, causing a fall in serum estradiol levels.Women without enough progesterone are unableto balance out estrogen, leading to problems that result from a relative excess of estrogen. Inaddition, progesterone has the effect of sedatingpainful uterine contractions. Chapter 13 dis-cusses in more detail how progesterone inhibitsuterine contractions and reduces pain. It is possi-ble that this uterine sedative effect extends topain relief in the pelvic region in general. I havenot used natural progesterone alone as a treat-ment for endometriosis, but it has been myobservation that progesterone is an importantpart of a comprehensive treatment plan.

Natural progesterone creams can be appliedin various regimens. For some women I recom-mend 1⁄4 teaspoon two times a day for threeweeks on and the week of menses off, or applytwice daily from day 15 of the cycle to day 26.Other women just need to use it the week beforetheir menses is due. Still other cases requirehigher doses of natural oral micronized proges-terone in a cyclic dosing pattern.


Conventional medical treatment for endometri-osis usually involves diagnosis plus medical orsurgical treatment. Because one cannot feelendometriosis most of the time or detect it by

ultrasound or CAT scan, laparoscopy (a surgicalprocedure to view the interior of the abdomenand pelvis) remains the standard for diagnosis.Studies have repeatedly shown that 78 to 82 per-cent of women with chronic pelvic pain of morethan six months’ duration that does not respondto nonsteroidal anti-inflammatories or oral con-traceptives have endometriosis. A recent develop-ment in the treatment of endometriosis istreatment of presumptive disease without laparo-scopic proof. Some physicians now offer thisoption, and if no response is seen in six months,they then proceed with laparoscopy.

Often, women with chronic painful periodsor pelvic pain are initially treated with non-steroidal anti-inflammatory medication such asibuprofen, naproxen, or meclofenamate. Assymptoms progress, patients usually resort toprescription analgesics and/or hormones. Sinceestrogen is known to stimulate the growth ofendometriosis, treatment is aimed at suppressionof estrogen synthesis. By achieving states ofpseudopregnancy (through birth control pills) orpseudomenopause (through cessation of thebody’s own production of estrogen and proges-terone), women have found significant symptomrelief. Benefit from birth control pills is thoughtto be due to reduced menstrual bleeding, anovu-lation, and lesion regression. However, stimula-tion of a lesion does occur, possibly due to adecrease in concentration of progesterone recep-tor sites and lesions.

In the past, danazol was regarded as a highlyeffective drug because of its suppression of thepituitary and inhibition of estrogen and adrenalhormone production. Relief quite possibly is dueto reduction of endometriosis associated withautoimmune abnormalities. However, male pat-tern hair growth, irreversible low voice, hotflashes, depression, weight gain, acne, reducedbreast size, muscle cramps, fatigue, and othersymptoms related to the medication have causeddanazol to become a less popular alternative, andit has mostly fallen out of use.


Prescription drugs called gonadotropin-releasing hormone agonists (GnRH agonists),such as Lupron, Synarel, and goserelin, are used toproduce a menopausal state. Upon stimulation ofthe receptors of the brain by these hormones, adecrease in production of LH (luteinizing hor-mone) and FSH (follicle-stimulating hormone)is achieved and causes the individual to have alow estrogen state. This causes dramatic relief of symptoms within two to three months. Sideeffects due to low estrogen, similar to thoseaccompanying natural menopause (insomnia,hot flashes, vaginal dryness, and osteoporosis) dooccur. Current add-back therapy with low-doseestrogen or a progestin reduces symptomswithout reducing effectiveness. Higher doses ofhormone therapy such as oral contraceptives may make the lesions grow, so very low doses ofhormones are recommended. After the GnRHagonist is discontinued, recurrence of endometri-osis frequently occurs, so ovarian suppressionregimens like oral contraceptives or Depo-Provera injections are commonly used followingGnRH therapy.

Treatment with progestins helps endometrialtissue to atrophy. However, side effects includenausea, weight gain, fluid retention, breakthroughbleeding, and sometimes depression.

Combinations of estrogen and progestin suchas those found in low-dose birth control pills sup-press FSH and LH. Mild-to-moderate pain relief isachieved because the body’s own estrogen produc-tion is decreased. In addition, since the volume ofmenstrual flow is also decreased, less blood is theo-retically available for reflux into the pelvic cavity.

Current research shows promising results inthe use of the antiprogesterone Ru-486 due tothe regression of endometriosis and possible min-imal side effects. Clinical trials are underway. Useof medications that enhance the immune systemare also being studied.

Laparoscopic surgery has the advantage ofextensive use of microscopic imaging so that sur-geons can view lesions in greater detail. In addi-

tion, laparoscopy allows for a shorter recuperationtime when compared to a laparotomy. During alaparotomy, the surgeon makes a larger incision inthe abdomen, allowing for larger endometriomasor adhesions to be excised.

Surgery has produced cure for some individ-uals, while it has proved to be disappointing to others. Whether laparotomy or laparoscopy,surgical treatment varies as to type of surgery,technique, and surgeon experience. Conservativesurgery removes superficial endometriosis lesionsand/or endometriomas while leaving the uterusand ovaries intact. Recurrence rates vary from 5to 20 percent per year, with a rate of 40 percentafter five years. Differences in recurrence rateswith surgery may be due to the method of endo-metriosis implant removal and the skill of thesurgeon. Laser surgery is able to penetrate deeply,but without the possibility of biopsy (provingendometriosis), while excision by electrocautery,which allows for meticulous biopsy, takes timeand additional effort. The knowledge and experi-ence of the surgeon are important in the identifi-cation of the implants, since color, consistency,appearance, and location of the implants can bevariable. In addition, some surgeons remove theclear peritoneal covering, as they believe thatendometrial implants reside in this tissue.

The disease frequently recurs unless a womanhas had a hysterectomy with bilateral salpingo-oophorectomy (removal of uterus and bothovaries and fallopian tubes). Aggressive surgeryconsists of removing implants, ovaries, anduterus, and sometimes, even more aggressive sur-gery involves removing the peritoneum as well.While surgery removes implants that adhere tothe ovaries, uterus, and other pelvic organs, theeffects of ovary removal and the resulting abruptcessation of hormone production have to betaken into consideration. While beneficial forsome individuals, medical or surgical manage-ment is not effective in all circumstances.

Physicians have seen an increase in endo-metrioid cancer in endometriosis implants. And


endometriosis can grow into bowels or causebowel obstruction or fistulas. Therefore, findinga health-care provider who is very experiencedwith endometriosis treatment is very important.


As with any pain of unknown origin, a licensedprimary health-care practitioner should be con-sulted to rule out other causes of pain beforeextensive use of analgesic medications, botanicalformulas, or supplements. The cultural bias thatmenstrual periods are supposed to be painful—aswell as a reluctance to seek help due to past abuse,trauma, or fear—can be a detriment to healing.Although the norm is changing, in the past manywomen with endometriosis were told that the pain was “in their head” or psychosomatic. Anincreased understanding of the pain, pattern ofsymptoms, and loss of quality of life for those whoexperience endometriosis has drawn attention andresearch to this disruptive problem.

Abnormal bleeding, pain that increases inintensity, continued pain with or without menses;

lower back pain; or pain with urination, bowelmovements, and vaginal intercourse should bebrought to the attention of your health-carepractitioner, who will listen to your symptoms,take a medical history, and do a pelvic exam. Thisphysical exam is valuable in determining whetherthere are masses, areas of sensitivity, or abnormalfindings suggestive of endometriosis. Dependingon the exam, an ultrasound, MRI, and/or bloodwork may be recommended. In addition,depending on these results, further recommenda-tions may be made (such as a laparoscopy thatcan diagnose and potentially treat the endometri-osis at the same time).

If you are reluctant to seek out help due topast trauma or just a feeling of discomfort, it isessential that you find a health-care practitioneryou can trust. Have a friend (or even therapist)come with you to the office and even to theexam room to hold your hand, ask questions,and be there for you. Since the key to preventionof further pain is early diagnosis, prompt med-ical intervention can lead to more effective assis-tance in supporting your body’s own ability toheal itself.


89

OVERVIEW

Virtually all knowledgeable health-care providersagree that the terms fibrocystic breast disease or fibro-cystic breast condition should be abandoned in favorof a more accurate, physiologically based descrip-tion. First of all, the benign breast conditions thatare present in almost all of us to some degree shouldnever have been given the “disease” label in the firstplace.1 Moreover, the widespread misconceptionthat women with painful or lumpy breasts are atincreased risk of breast cancer borders on the tragic.Unfortunately, our health-care system requires adiagnostic code to reimburse services, and “fibro-cystic breast disease” has one, even though the med-ical literature is replete with reasons why itshouldn’t. This reinforces misinformation and fearand obscures the safe and simple means that existfor obtaining relief and reassurance.

Tender or lumpy breasts are one of the mostcommon reasons why women consult their gyne-cologists for assessment and treatment. Sincepainful breasts are not always lumpy, and lumpybreasts are not always painful (and neither situa-tion is usually abnormal), it is useful to createdescriptive categories of symptoms and condi-tions to replace the generic term fibrocystic.

Physiological, Cyclical Pain and Swelling

Many women notice painful or sensitive breastsjust prior to menstruation. This has been attributedto a more prominent estrogen than progesteroneeffect on breast tissue at this time. Sometimes lessprogesterone is made late in the cycle, as in irregu-lar ovulation (inadequate luteal phase). Otherwomen may have average amounts of progesteronebut increased tissue sensitivity to estrogen with

related fluid retention. Most of us tolerate this wellenough once reassured it is normal, and the symp-toms always resolve with menses. Women who takeexogenous estrogen, such as oral contraceptives orestrogen replacement therapy during menopause,may be similarly affected.

Mastalgia

Mastalgia refers to any breast pain severe enoughto interfere with the quality of a woman’s life,causing her to seek treatment. Physiological,cyclical mastalgia is this severe about 15 percentof the time and comprises the bulk of this group.Women who suffer from noncyclical pain aremore rare, and the pain is less likely to be hor-monal in cause. Pain may be due to old trauma,acute infection, or sometimes something relatedto the chest wall. In contrast, breast cancer occursas a unilateral painful firm lump only about 5percent of the time. Painful swellings that fluxwith the cycle and do not change over time arenot worrisome as cancer signals.

Breast Nodularity or Diffuse Lumpiness

Breast lumpiness—the most worrisome categoryin most women’s minds—may be either cyclic ornoncyclic, and might or might not include pain.The distinction between these and normalbreasts is often simply a matter of degree.Normal breasts are irregularly textured becausethe tissue they are made of is not homogeneous.It is a mix of glands, fat, and connective tissue.Glands can be more or less prominent and moreor less obscured by fat or fluid, so all breasts feeldifferent. Symmetry is important; finding amirror-image thickening in the opposite breastindicates a normal condition.

7F I B R O C Y S T I C B R E A S T S C H A P T E R



Nondominant Masses

Even densities that are not symmetrical arelargely due to benign nonprogressive causes, butthey do require careful distinction from domi-nant masses. When careful palpation around theedges of a nonsymmetrical lump reveals that thedensity merges in one or more places with thesurrounding breast tissue, it is considered non-dominant and may be comfortably observed forchange over time. When these lesions are biop-sied or, preferably, a sample of cells is taken in theoffice using a needle to be looked at microscopi-cally (fine-needle aspiration), some 70 percentwill show nonproliferative changes (adenosis,fibrosis, microcysts, mild hyperplasia, and more);some 20 percent will show proliferative changeswithout atypia—mostly epithelial hyperplasia.None of these conditions places one at increasedrisk for cancer, and all are self-limited. Only afraction, roughly the 5 percent that show atypi-cal hyperplasia, carry a significantly increased riskof breast cancer (relative risk at 4 percent), espe-cially when coupled with a positive family his-tory (relative risk at 9 percent).2 It was this tinysubgroup that led to the original cancer scareattached to fibrocystic breasts.

The most useful tool a woman can bring toher own breast health is her knowledge of andfamiliarity with the architecture of her ownbreasts, particularly as it varies over time. Noth-ing is more helpful in avoiding an unnecessarybiopsy than a self-knowledgeable woman whohas observed the monthly variation in her ownbreasts and knows which tissue thickens cycli-cally. Think of the self-exam as a familiarizationprocess, not a diagnostic one. The majority ofbreast cancer occurs in women over age 60, andmost women don’t get breast cancer at all. We allhave plenty of time to learn our textures so thatour own hands are the most sensitive to anychanges that may occur. This will occur effort-lessly over time with regular self-exams.

Dominant Masses

These outright noncyclical unilateral lesions areclearly distinct on all sides from the surroundingbreast tissue. They persist over time, and exceptin the very young demand some kind of assess-ment. Most commonly they are either fibroade-nomas or gross (obvious) cysts. A fibroadenomais a rubbery, smooth, benign fibrous tumorcommon in younger women. In women underage 25, it can be observed over time. Fibroadeno-mas generally do not grow bigger. Large cysts aremore common in women aged 25 to 50—an agegroup when cancer just begins to appear. Theyare softer, usually squishier, and can be made todisappear by draining them through a needle inthe office; unless they recur frequently, no furthertreatment is necessary. Recurrent large cysts havebeen shown to slightly increase cancer risk insome studies but not in others;3, 4 fibroadenomasdo not. Unfortunately, noncyclical unilateraldominant masses can sometimes be cancerous.


Women with fibrocystic tissue causing breast pain,discomfort, and lumpiness will find comfort in analternative perspective on their situation. Giventhat this condition is not really a disease, a womancan direct her energies toward relieving symptomsand optimizing breast health, as well as increasingher motivation toward general health practicesand self-care.

KEY CONCEPTS

• Practice monthly breast self-exams; know yourbreasts; be able to detect new and unusualchanges, thickenings, and lumps.

• Have a yearly breast exam by a licensed physician.

• Relieve symptoms of pain and tenderness.• Have changes, if any, evaluated by a physician.

91F I B R O C Y S T I C B R E A S T S

The liver is the primary site for estrogen clear-ance or estrogen metabolism. Compromised liverfunction can lead to a state of estrogen domi-nance, contributing to texture and density changesin the breast. To assure that estrogens are beingmetabolized properly, it may be necessary to pro-vide nutritional and herbal support for the liver.

Digestion and elimination are fundamental fac-tors involved in hormone-related health problems.Women having fewer than three bowel movementsper week have a risk of fibrocystic breasts four tofive times greater than women having at least onemovement per day.5 The longer it takes food tomove through the colon, the more waste productspass into the bloodstream, creating a potentiallytoxic physiological environment. Bacterial flora inthe large intestine, such as Lactobacillus acidophilus,improve the transit time of bowel toxins, as well asimproving the excretion and detoxification of estro-gens. Women on a vegetarian diet excrete two tothree times more detoxified estrogens than womenon an omnivorous diet.

Nutrition

Epidemiological evidence supports a diet rich inwhole fruits and vegetables in the prevention offibrocystic breast conditions. A recent studydemonstrated that a reduced risk of proliferativeand atypical breast lesions was associated withconsumption of fresh fruits and vegetables,whereas a small but significant reduction of riskwas associated with soy consumption, possibly bydecreasing cellular proliferation in the breasttissue.6 Another study examined the effect soyconsumption has on breast tissue via direct imag-ing using breast enhanced scintigraphy (a nuclearmedicine diagnostic imaging test). After one yearof daily soy consumption, the researchers reporteda number of promising subjective and objectiveresults: patients and their physicians reported areduction in both breast tenderness and fibrocys-tic changes; a small but statistically nonsignificantdecrease in both the average and maximal count

breast activity on scintigraphy; and a significantreduction in the variability of tissue activity.7

Maybe somewhat surprisingly, another studyshowed a decrease in benign breast changes withalcohol consumption.8 Since alcohol slows downthe metabolism of estrogen, it is not clear why thisstudy demonstrated these results.

Avoid Methylxanthines (Caffeine). Removalof caffeine from the diet, an idea that originatedwith Ohio surgeon Dr. John Minton, is probablythe most well-known alternative treatment forfibrocystic breasts. Of the 20 uncomfortablewomen who followed his advice to stop all caffeineintake, 13 said their breasts felt better as a result.9

Dr. Virginia Ernster conducted the first ran-domized study of a larger number of women, inwhich for four months 158 women eliminatedcaffeine (coffee, tea, cola, and chocolate) fromtheir diets as well as caffeinated medications(theophylline and theobromine). She found asignificant reduction in clinically palpable breastfindings in the abstaining group compared withthe control group, although the absolute changein the breast lumps was quite minor and consid-ered to be of little clinical significance.10

Several other studies have been done, leavingus with mixed reports: three studies show noassociation between caffeine or other methylxan-thines and benign breast disease,11–13 and twostudies show a correlation with caffeine con-sumption.14, 15 Such is the way of science.

PREVENTION

• Avoid caffeine (black tea, coffee, decaffeinatedcoffee, cola, chocolate, and medications with caffeine). Even decaffeinated coffee has othermethylxanthines, caffeine-like chemical compounds.

• Assure regular, daily bowel movements.• Eat a diet high in fruits, vegetables, soy foods,

and whole grains.• Decrease dietary fats, especially saturated fats.


In clinical practice, I always recommendavoiding caffeine for women with painful/lumpybreasts. Many women gain mild to dramaticresults with this simple approach, and somewomen receive no benefit. A fair experimentwould be to completely abstain for three monthsand observe any changes in the pain, swelling,and discomfort. A decrease in the nodularity willgenerally take longer, as long as eight months ofcomplete abstention.

Dietary Fat. How dietary fat affects thehuman breast is still controversial, although someresearch has looked at low-fat diets in womenwith fibrocystic breasts and at how low-fat dietsaffect the hormone levels in these women.Reducing the fat content of the diet to 16 per-cent of total calories (in contrast to the averageAmerican diet of 40 percent fat), while increasingcomplex carbohydrate consumption, has beenshown to reduce the severity of premenstrualbreast tenderness and swelling, as well as reduc-

ing the actual breast swelling and nodularity insome women.16 Reducing the dietary fat intaketo 20 percent of total calories results in signifi-cant decreases in circulating estrogens in womenwith benign breast disease.17

Since fibrocystic breasts are a result of estro-gen dominance, it is logical that decreasing estro-gen in the body or its influence on breast tissuewould improve the symptoms of breast pain andswelling. However, a slight reduction in fatintake has repeatedly showed very little, if any,effect on breast problems, including breastcancer. A more rigorous approach to lowering theamount of fat in the diet is clearly needed.

The simplest way to accomplish the necessarylevels of fat reduction is to avoid animal fats in allforms; a vegan diet (vegetarian, without anyanimal products at all, including dairy or eggs) isnaturally a very low-fat diet. Of course, vegetari-ans, and even strict vegans, can succumb to fat inother forms like french fries, potato chips, andother greasy fried foods. A vegan diet rich in wholegrains, legumes, fruits, vegetables, seeds, nuts,olives, and seaweed that is enriched with oils forstir-frying and in salad dressings results in a dietthat derives about 15 to 20 percent of its caloriesfrom fat.


Vitamin E. For more than 35 years, clinicianshave used vitamin E in the medical managementof benign breast disease. This practice was initiallybased on positive reports from small numbers ofpatients as far back as 1965 and from subsequentstudies in 1971, 1978, and 1982.18–21 When larger

Caffeine Content of Common Items

Beverage Caffeine (mg)Coffee, drip (8 oz) 150Coffee, perk (8 oz) 60–120Coffee, instant (8 oz) 70Coffee, decaffeinated (8 oz) 2–5Tea, black, 5-minute steep (8 oz) 60–100Tea, green (8 oz) 20Hot cocoa (5 oz) 2–10Coca-Cola (12 oz) 34

Food Caffeine (mg)Milk chocolate (1 oz) 1–15Bittersweet chocolate (1 oz) 5–35Chocolate cake (1 slice) 20–30

Over-the-Counter Drugs Caffeine (mg)Anacin, Empirin, or Midol (2) 64Excedrin (2) 130NoDoz (2) 200Aqua-Ban (2) 200Dexatrim (1) 200


• Avoid caffeine.• Decrease dietary fat to 20 percent of calories.• Increase dietary fiber (whole grains, legumes,

fruits, and vegetables).• Increase seafood and seaweed.• Increase soy foods.


numbers of women were studied, vitamin E didnot fare so well, showing no significant effectseither subjectively or objectively,22, 23 and the ear-lier results have never been duplicated.

However, this is not to say that some womendon’t find symptom relief from taking vitamin E.Two studies demonstrated that vitamin E is clin-ically useful in relieving pain and tenderness,whether cyclical or noncyclical.21, 24 The studieshave been done with varying dosages: 150, 300,or 600 IU daily. In clinical practice, practitionersgenerally recommend from 400 to 800 IU of D-alpha tocopherol with a minimum trial period oftwo months. Since vitamin E in these dosages iscompletely safe to use, this is a simple and appro-priate self-treatment method for a benign breastcondition.

Vitamin E (Natural)

400–800 IU daily

Omega-6 Fatty Acids. The pain and tender-ness of benign breast disease associated with cyclicmastalgia have been alleviated with evening prim-rose (Oenothera biennis) oil, the only one of themany essential fatty acids to be scientifically stud-ied in relation to fibrocystic breasts.

The evening primrose plant has been com-monly known as tree primrose and sun drop.Evening primrose can be found in many parts of North American and is native in the NorthTemperate Zone, especially at high altitudes. Thenative peoples of North America, as well as theEnglish and Pilgrims, were well aware of the heal-ing properties of the leaves and bark as an astrin-gent, nervine (an herb that affects the nerves andincludes relaxants, tonics, and even stimulants),and sedative. It was often used for stomach andliver complaints, coughs, and female reproductiveproblems. Even the roots were eaten as a veg-etable. The seeds were recommended as a coffeesubstitute in wartime and have a strong flavorsimilar to poppy seed oil. The therapeutic value ofthe seed oil is a more recent discovery. It is this

seed oil and its essential fatty acid content thatholds the most interest today in maintaininghealth and preventing disease.

Evening primrose oil is rich in essential fattyacids—polyunsaturated fats that are as essentialas vitamins and minerals for the maintenance ofgood health. The oil contains 74 percent linoleicacid (LA) and 9 percent gamma linolenic acid(GLA). Although other oils such as borage oiland black currant oil contain higher amounts ofGLA, evening primrose oil is by far the mostpopular and familiar source of this fatty acid.Evening primrose oil also contains 11 percentoleic acid, 6 percent palmitic acid, and 2 percentstearic acid.

Under ideal conditions, the body uses LA toproduce GLA. In turn, GLA is used to producebeneficial hormone-like compounds called pro-staglandins. Specifically, GLA is used to produceseries one prostaglandins such as prostaglandinE1 (PGE1).

Prostaglandins affect the function of virtuallyevery system in the body. These molecules areused in the regulation of inflammation, pain,blood pressure, fluid balance, and blood clotting.Prostaglandins also affect hormone productionand function.

The key to understanding the importantneed for supplementing with oils rich in GLA,such as evening primrose oil, is that many of uscannot convert LA to GLA efficiently. Dietarydeficiencies, disease conditions, processed oils,trans-fatty acids, heated oils, alcohol, aging, viralinfections, and sugar consumption block, slowdown, or interfere with the enzyme that catalyzesthe conversion of LA to GLA. The result is thatvirtually all North Americans are deficient inGLA. Supplementing with evening primrose oilcan enrich the body’s GLA supply and restore theproduction of beneficial prostaglandins derivedfrom GLA. Research completed over the last 20years has confirmed that supplementation withevening primrose oil has beneficial effects innumerous diseases and conditions. Benefits for


health problems supported and/or suggested byscientific trials using evening primrose oil includepremenstrual syndrome, fibrocystic breast pain,eczema, rheumatoid arthritis, diabetes, heart dis-ease, osteoporosis, and ulcerative colitis. Otherconditions for which it may provide benefitinclude menopause and pregnancy.

The pain and tenderness of benign breast dis-ease associated with premenstrual breast pain andfibrocystic breasts has been alleviated withevening primrose oil in more than one scientificstudy. In 1985, when 291 women took threegrams per day of evening primrose oil for three tosix months, almost half of the 92 women withcyclic breast pain experienced improvement com-pared with one-fifth of the patients who receivedthe placebo. For those women who experiencedbreast pain throughout the month, 27 percent(just over one-fourth of the 33 women) respondedpositively to the evening primrose oil, comparedto 9 percent on the placebo.25 Another 73 womenwith breast pain with or without lumpiness ran-domly received three grams per day of eveningprimrose oil or placebo. After three months, pain and tenderness were significantly reduced inboth cyclical and noncyclical groups, while thewomen who took the placebo did not significantlyimprove.26 In the course of treatment, it has been detected that women with breast pain have unusu-ally low concentrations of GLA and metabolitesfrom GLA. When patients receive supplements ofevening primrose oil, the concentration of GLAmetabolites increases and the concentration of sat-urated fats in the breast decreases. This may alsohave long-term implications for prevention ofbreast diseases such as breast cancer.

Although symptom relief can be achievedthrough the use of evening primrose oil, it shouldnot be relied on to actually reduce the number ofdeveloping cysts.

Other omega-6 fatty acids that may have ben-eficial effects but have not been studied in relationto fibrocystic breasts are flaxseed oil, black currantoil, and borage oil. Borage oil and black currant

oil contain higher amounts of GLA, so poten-tially, one could take fewer capsules to achieve thesame benefit. For example, borage oil contains 23percent GLA versus only 9 percent in the eveningprimrose oil. That would mean instead of the 6capules of evening primrose oil it would take toachieve the 3,000 mg of evening primrose oil thatwas used in the study, you could conceivably useat half as many capsules of borage oil.

Evening Primrose Oil (Omega-6 Fatty Acids)

1,500 mg twice daily

Vitamin A. Basic science research supportsthe use of vitamin A by demonstrating the pres-ence of specific retinoid receptors in breast tissuethat can modulate our genetic predisposition,thereby decreasing the risk for both benign andmalignant breast changes.27

In a study of patients with fibrocystic breastdisease, 12 women were treated with 150,000 IUof vitamin A daily for three months, and 5 of the9 women who completed the study showed com-plete or partial response.28 Some of the patientsexperienced mild side effects of vitamin A toxic-ity, including dryness of the skin and mouth.

Although the potential toxicity of vitamin A indoses this high makes it an impractical approach tofibrocystic breast disease, it is possible that beta-carotene could be substituted, since it has a similaractivity without the side effects of vitamin A, or adiet high in yellow and orange fruits and vegetables.

Beta-Carotene

50,000–150,000 IU daily

Iodine/Thyroid Hormone. It has beenknown for a long time that for the thyroid glandto secrete thyroxine (its hormone), it requiresiodine. Prescription thyroid hormone replacementwith low or even normal thyroid function mayresult in improvement of fibrocystic breasts.29, 30

These results suggest that iodine deficiency may bea causative factor in fibrocystic breasts.


Although the exact mechanisms of action onbreast tissue are not known, the breast has anaffinity for both thyroid hormone and iodine.The only areas of the breast in which iodine canbe found are in the terminal and interlobularduct cells, which are also the areas primarilyinvolved in cystic changes. Without iodine, thebreast tissue becomes more sensitive to estrogenicstimulation, which in turn produces microcystshigh in potassium. The potassium is believed tobe an irritant that produces fibrosis and eventu-ally cyst isolation.

Four types of iodine have been studied in thetreatment of fibrocystic breasts, only one ofwhich has been truly effective and free of sideeffects on the thyroid gland. According toresearch by Dr. William Ghent, although allforms of iodine relieve subjective clinical symp-toms, the fibrocystic breast reacts differently tothese different forms of iodine: sodium iodide(Lugol’s solution), potassium iodide, caseinatediodine (protein-bound), and aqueous (diatomic)iodine. Symptom relief varied a great deal withthe different iodines, but only the aqueous ordiatomic iodine achieved both symptom relief in74 percent of the women and also objectivereduction in nodules and resolution of fibrosis in65 percent of the patients, without adverseeffects on the thyroid gland.31

Women get different amounts of iodine intheir diet, depending on the iodine content ofthe soil and water, as well as the types of foodthey prefer to eat. Plant foods grown in the so-called goiter belt areas of the country (the GreatLakes region, the Midwest, and the Intermoun-tain states) lack iodine because the soil and waterare iodine deficient. Today, iodine deficiency isconsidered rare in the United States due to thewidespread distribution of foods from areas ofthe country sufficient in iodine and due to theavailability of iodized salt. Certain foods, such asseafood and seaweeds, are naturally high iniodine and might be used to supplement a dietlow in iodine.

Aqueous Iodine

3–6 mg daily (prescription item)

Additional Supplements

• B-complex: 10 times the recommendeddaily dietary allowance

• Methionine: 1 g per day• Choline: 1 g per day• Lactobacillus acidophilus: 1 tsp 3 times

per day• Flaxseed oil: 1 tbs per day

Botanicals

Herbal therapies for addressing the symptoms ofbreast pain, swelling, and cystic nodules in thebreast are largely arrived at from traditional usesof herbal medicines and from observational expe-rience in clinical practice. Herbal diuretics areuseful in decreasing breast swelling and the dis-comfort associated with it. The most effective ofthese is dandelion leaf (Taraxacum officinale).Unlike synthetic diuretics, dandelion leaf doesnot deplete potassium; instead, it actually con-tains a high percentage of potassium. However,since potassium is possibly implicated in fibrosisand potential cyst isolation, dandelion may notbe the ideal diuretic to use. Diuretics consideredto be effective for fibrocystic breasts includecleavers (Galium aparine), yarrow (Achillea mille-folium), and uva ursi (Arctostaphylos uva-ursi).

Additionally, poke root (Phytolacca ameri-cana), an herb used in traditional naturopathicmedical practices, can be applied as an oil to thebreasts and rubbed in like a lotion, reducingpainful lumpiness and nodularity.

Herbal support for the liver improves howthe liver metabolizes hormones. In this case, ourgoal is to encourage the normal pathways for themetabolism, excretion, and recirculation of estro-gens. Traditional herbs that support the liverinclude burdock root, dandelion root (not leaf ),milk thistle, celandine, fringe tree, and beet root.


Additional Natural Therapies

Natural Progesterone. Once we agree thatfibrocystic breasts are, at least in part, due to ahigh-estrogen/low-progesterone problem, then it is logical to use progesterone therapy as a treatment. Specifically, many practitioners andwomen patients have experienced that the appli-cation of natural progesterone in a cream or gelform routinely resolves the problem. Dr. JohnLee, the leader in the use of natural progesterone,states that he cannot recall a single case in hisown practice in which the results were not posi-tive.32 Lee suggests using the natural proges-terone cream or gel as prescribed by a health-carepractitioner until the cysts are gone and thenreducing the dose to the smallest amount that isstill effective, to be continued monthly as neededthrough menopause.

I cannot confirm the effectiveness or safety ofthis practice, and the research is not yet clear onthe safety of long-term natural progesterone andbreast health. There is more information aboutthis in Chapter 12.

Natural Progesterone Cream

1⁄4–1⁄2 tsp applied to breasts and palms twice a dayfrom ovulation to menses


Conventional medical literature has tended tofocus more on pathologic descriptions of diseaseand on verifying or disproving related cancer riskrather than on exploring therapeutic options forsymptom relief. In spite of conflicting data in the1980s, many women added vitamin E and elim-inated coffee from their diets with noticeablesubjective improvement and no side effects otherthan those imparted by caffeine withdrawal.Low-fat, high complex carbohydrate diets canreduce cyclical pain, and the results of studieswith evening primrose oil have been mixed.

Cyclic breast pain and swelling are felt to behormonal, so treatment is aimed at hormonalmanipulation, usually by suppression. More oftenthan not, oral contraceptives help to relieve mildor severe premenstrual pain, although for smallernumbers of women the pain is worsened by thistreatment. This paradox is explained by the factthat oral contraceptives suppress ovarian produc-tion of hormones and replace this with an averagesynthetic dose of both estrogens and progesterone.If the replacement level is higher than the naturalone, sore breasts may result; usually, the replacedlevel is lower, and then the pain is relieved. Con-tinuous oral contraceptives (no placebo break)seem to help better than cyclic regimens.

Many so-called effective conventional treat-ments cause such serious side effects that it is hardto imagine any cases that would warrant their use.Danazol, which interrupts LH and FSH secretion

Herbal Recommendation

• Yarrow leaf capsules: 2–6 per day; or yarrowleaf liquid tincture or extract: 1⁄4–1 tsp per day

• Phytolacca oil: apply to breasts nightly for 2weeks, then reduce to 3 times per week

Sample Treatment Plan for Fibrocystic Breasts

Three-Month Period

• Avoid caffeine and other sources of methylxanthines.

• Lower dietary fat to 20 percent and increasedietary fiber (whole grains, legumes, fruits,vegetables, and soy foods); increase seafoodand seaweed (for the natural iodine).

• Vitamin E: 400 IU twice per day• Evening primrose oil: 1,500 mg twice per day

If there is no change after three menstrual cycles,then incorporate a more assertive approach utilizingsome of the other therapies listed, or see a naturo-pathic physician for individualized recommendationsand, especially, prescription aqueous iodine.


from the pituitary gland, was once touted as themost effective breast pain reliever. However, it is amale hormone and can cause facial hair, voicedeepening, and other androgenic changes, quiteunacceptable side effects for most women, and itcan cost more than $200 per month. It is nolonger used to treat fibrocystic breasts.

Similarly, GnRH agonists work at the hypo-thalamic level to eradicate estrogen via a tem-porarily induced menopausal condition. Thisclass of drugs may make danazol obsolete, butthey again do not present a good long-term solu-tion due to the side effects, including reversiblebone loss, and they cost even more money.

Tamoxifen, an antiestrogen, has been used totreat breast cancer and can help cyclic breastpain, up to a 90 percent reduction in pain. How-ever, it causes menopausal side effects, its long-term effects are unknown, and it increases theincidence of endometrial cancer. On the otherhand, it has been shown to reduce breast cancerrisk in women who are at higher risk, includingthose women who have atypical hyperplasia ofthe breast, which is determined only by a biopsy.For benign breast disease, it is difficult to imag-ine a situation where the benefits of tamoxifenwould outweigh the risks and side effects.

Bromocriptine is a nonhormonal drug ther-apy that lessens the levels of prolactin, the hor-mone that manages lactation changes, and seemsto work well, although it is often not toleratedbecause of nausea or dizziness.

The side effects of most of the expensivedrugs used to eliminate breast pain and lumpi-ness are probably too extreme to warrant theiruse for most women until the simpler remedieshave proven inadequate. If elimination of caf-feine, adding vitamin E, and switching to a low-fat, high complex carbohydrate diet do not bringresults, the next logical step for a conventionalpractitioner would most likely be a trial of oralcontraceptives.


A woman might decide to see a licensed health-care practitioner because she needs a breast examor wants to determine the exact nature of herbreast pain/tenderness or lumps. The practi-tioner will ask about her symptoms as well asother pertinent factors in her medical history andwill perform a physical examination.

If the practitioner considers it necessary, sheor he might recommend a mammogram and/orultrasound to determine the nature of a specificlump and may encourage aspiration of a mass todetermine whether it is cystic or solid. The prac-titioner will no doubt recommend that highlysuspicious lumps be surgically biopsied.

A lump that is new or one that is increasing insize, or a lump that does not change over the courseof the menstrual cycle, are all causes for concernand might lead to a professional evaluation.


99

OVERVIEW

Genital herpes is the most prevalent sexually trans-mitted infection (STI) in the United States.1–3

Data about the prevalence of genital herpes in theUnited States has been collected from theNational Health and Nutrition Examination Sur-veys between 1976 and 1980 (NHANES II) andfrom 1988 to 1994 (NHANES III). According toNHANES III, 45 million Americans over the ageof 12 are infected with Herpes simplex 2 (HSV-2 orgenital herpes). The prevalence increased 30 per-cent between 1988 and 1994, with the greatestincrease among teenagers, and quintupled amongwhite teenagers and doubled among whites intheir twenties. Some 25.6 percent of women and17.8 percent of men test positive for the virus intheir blood, and blacks have a higher prevalence(45.9 percent) than do whites (17.6 percent).4

Testing positive in the blood is different thanhaving a genital herpes eruption history. In fact,only 10 to 20 percent of seropositive individualshave had a genital herpes lesion, showing us thatthe majority of cases are subclinical or undetected.

There are six members of the herpesvirusfamily that are known to infect humans: HSVtype 1 (HSV-1) and HSV type 2 (HSV-2), vari-cella zoster virus, human cytomegalovirus,Epstein-Barr virus, and herpesvirus type 6.Today, HSV-2 is the leading cause of genitalulcer disease in the United States. As many as onein five Americans is believed to be infected withHSV-2—the virus type more closely associatedwith genital herpes. Another virus type, HSV-1—the type more closely associated with infectionsof the mouth, lips, pharynx, and eyes earlier inlife through oral/genital contact—is believed tobe responsible for 10 to 50 percent of new casesof genital herpes.5 About 80 percent of people

with their first episodes of genital herpes are 18to 36 years of age. The highest annual incidenceof genital herpes among women occurs at 20 to24 years of age and is estimated to be 210 per100,000 women.

The diagnosis of typical genital herpes isfairly straightforward most of the time butinvolves local and systemic signs. There are threedistinct syndromes: primary herpes, first-episodenonprimary herpes, and recurrent herpes. Thereare, however, atypical manifestations, and theseare the ones that are not so straightforward.

The severity of symptoms varies in extent andduration according to whether the episode is the patient’s first infection with either HSV-2 orHSV-1, called primary herpes; initial genital infec-tion in a woman who has already had an infectionwith the other HSV type (initial, or first-episodenonprimary herpes); or a recurrence of a genitalinfection with either type. A woman’s first episodeof genital herpes (primary herpes) is usually themost severe form of the disease. Symptoms usuallystart appearing within a week after infection, ifthey are going to appear at all. However, symp-toms can start one day and up to 26 days afterexposure to the virus. Typically, infection is char-acterized by extensive, multiple clusters of painfullesions involving the genitals, anus, perineum, orsurrounding areas. Symptoms and lesions of pri-mary genital herpes vary in severity, extent, andduration. Initial symptomatic episodes of HSVnot only tend to be more severe but are followedwithin the first year of a greater likelihood of clin-ical recurrences as well as shedding of the viruswithout any symptoms (also known as subclinicalshedding, when the outer layer of the skin or tissueharbors the virus without symptoms and thensheds, transmitting the virus). These subsequent

8G E N I TA L H E R P E S C H A P T E R



episodes of HSV-2 are usually associated withmore symptoms and more frequent outbreaksthan HSV-1 of the genital area and occur aboutfour to five times a year in about one-third ofwomen who have symptomatic outbreaks.

Both HSV-1 and HSV-2 infect the skinand/or mucosal tissue of the genital area and themouth, and once this occurs, the virus infects thesensory and autonomic nerves and then ascendsto the nerve ganglia in the spinal cord where itestablishes a lifelong home where it can be peri-odically reactivated. With this episodic reactiva-tion, the virus migrates from the ganglia alongthe sensory nerves to the target site, which resultsin either an actual outbreak or a shedding with-out an outbreak or with atypical symptoms,called subclinical shedding.1, 3 In fact, the major-ity of primary infections with HSV-1 and HSV-2are subclinical. This presents a great difficulty insexual transmission, because the virus can betransmitted to another, even when you do notknow you are infected or have ever been infected.Men are more likely to have asymptomatic HSV-2infections than women.6

The classic herpes lesion begins as a redpapule, evolving within two to three days to avesicle containing clear fluid, and then progress-ing to a pustule. When the surface breaks open,a tender ulceration occurs that may explain thesymptomatic burning pain. Lesions ulceratemore rapidly in moist areas than on dry skin, sothat painful genital ulcerations are more apt tooccur on the external vulva area. Several succes-sive lesions may appear in the first three to fourweeks of primary herpes. The lesions of primaryherpes may heal in one to six weeks.

In more than two-thirds of women, primaryherpes is accompanied by systemic symptomsthat may include fever, malaise, body aches,headaches, and nausea. Meningitis-like symp-toms, such as stiffness of the neck and sensitivityto light, are also common. Nearly three-quartersof women will also suffer from herpetic cervicitis,with vaginal discharge and intermenstrual spot-

ting. Swollen lymph nodes in the groin area arealso common. Discomfort with urination is alsocommon, sometimes as a result of herpes in theurethra and in other cases because the urinecomes into contact with lesions on the labia.

Diagnosis

A practitioner can best make a diagnosis ofherpes based on the medical history, inspectionof the area, and a laboratory test to provide con-firmation. The focus of the history is the onsetand clinical course of the genital lesions. Eventhough very personal, it is important that thepractitioner know the following details of thewoman’s sexual history:

1. Pregnancy history2. Currently sexually active or not3. Sexually active with men, women, or both4. If birth control is used, what kind5. Knowledge about partner or partners’ sexual

history6. Condom use for protection from sexually

transmitted infections7. Types of sexual activity: oral sex with part-

ner, mutual oral sex, penile/vaginal sex,penile/anal sex

The practitioner also needs to know whether thelesions started as blisters or pimples and whetheror not they were painful. Knowledge about anysystemic symptoms of both partners is importantas well.

The physical examination involves inspectingthe lesions, examining the genital area thor-oughly, including the anal area and the inguinallymph nodes (those in the groin). Inspecting thevaginal area with a speculum requires carefulexam of the vaginal wall and the cervix. If sys-temic symptoms such as fever, headache, or neu-rologia symptoms are present, a more thoroughneurological examination needs to be performed.

The information gleaned from a good historyand physical help to distinguish a genital HSVinfection from other possible problems, includ-

101G E N I T A L H E R P E S

ing vaginal candida, herpes zoster, syphilis, chan-croid, allergic contact dermatitis, trauma, Behçet’ssyndrome, a heat rash, a rash from shaving thepubic area, a drug reaction, or a secondary infec-tion from something like scabies.

Laboratory testing to confirm the diagnosis isindicated for most people who are having theirinitial genital eruption, even in women with atypical clinical symptom picture. Some lesionsare classic in appearance, and perhaps a clinicianwill make a judgment that a laboratory test is notnecessary. However, viral cultures are the mostsensitive test for confirming the diagnosis of gen-ital herpes. Determining the virus type has valuefor future considerations. For example, individu-als with genital HSV-1 (as many as 30 percent ofwomen with primary herpes) have a much lowerrisk of symptomatic recurring outbreaks. In addi-tion, women with primary genital herpes are atincreased risk for other STIs and should possiblybe tested for chlamydia, gonorrhea, syphilis, andHIV infection.

The 2002 STD guidelines from the Centersfor Disease Control (CDC) state that isolation of HSV in a cell culture and then immuno-fluorescent staining can differentiate HSV-1from HSV-2 and is the preferred viral test inwomen who have an active genital lesion. Thereare a few problems with these tests: transportinga cell culture can be difficult, the sensitivity ofthe tests declines as lesions heal, and the test is farmore accurate for initial episodes than for recur-ring lesions. If the cell culture is used, then test-ing the blood is used to confirm the results.1–3

Other testing methods include direct immuno-fluorescent antibody (DFA) test, direct enzyme-linked immunosorbent assay (ELISA), andantigen detection tests. Only the DFA antigen testcan distinguish HSV-1 infection from HSV-2.The most useful tests for HSV genital infectiondetection are type-specific serologic assays for theHSV antibodies.

The most serious and feared complication ofgenital herpes is the transmission from an infected

pregnant mother to her newborn child. Consulta-tion with a health-care practitioner during thepregnancy is advisable both in women with recur-rent genital herpes and in women who mayuncommonly acquire their primary infectionduring pregnancy. Viral cultures late in the preg-nancy may be advised, and consultations about adelivery by cesarean section may be justified.Other complications for the infant include menin-

KEY CONCEPTS

• Genital herpes is most commonly associatedwith HSV-2.

• Risk factors for HSV-2: female, African-American,Mexican-American, older, low education level,poverty, cocaine use, a history of two to four ormore lifetime sexual partners, unprotected sex,having a sexual partner with genital herpes,living in the southeastern United States (higherrate of seropositive individuals).

• The majority of primary genital herpes infectionsare asymptomatic or unnoticed.

• All HSV infections establish latency and are con-sidered incurable. The present infection mayactually be a recurrence of an asymptomaticinfection acquired some time in the past.

• Systemic symptoms are more common with pri-mary infections, and symptoms are generallymore severe in women than in men.

• Seek the advice of a health-care practitioner indiagnosing an initial genital lesion; differentiateherpes from other causes of genital ulceration.

• Recurring eruptions are common and are gener-ally less severe than initial episodes.

• Treating acute episodes can reduce symptomsand shorten the duration of the eruption.

• Immune supportive therapy and antiviral therapycan reduce the frequency of recurrences and canreduce symptoms in acute episodes.

• The individual with herpes, the sexual partner,and the health-care practitioner all need to real-ize that genital herpes is a sensitive issue. Opencommunication, trust, and respect are essentialfor an informative dialogue and effective man-agement of genital herpes.


gitis, urinary or rectal dysfunction, infection in theeye, and erythema multiforme (a skin disease).

The impact of genital herpes on a person’spsychological and sexual health can be quite intru-sive and profound. Many people withdraw frominterpersonal relationships because of stress relatedto their infection or because of fear of spreading

the disease to others. Disruption of one’s sexual lifecan also manifest as significantly reduced sexualpleasure and a strong sense of sexual inhibition.Many people also worry that they will be rejectedby future partners and are pessimistic about thepossibility of establishing normal sexual relation-ships. Since many people become emotionallyupset upon learning of the diagnosis, a health-careprovider can be extremely valuable in helping todeal with anger, guilt, or anxiety. Education andcounseling include information about the natureof HSV infection, most importantly prevention of its transmission. It is important that patientsalso understand that the primary infection mayhave been asymptomatic and that even an initialoutbreak may be a reactivation of an infectionacquired months or even years previously.


A susceptible host plus exposure to the herpessimplex virus add up to acquiring the disease.Improving the health of the host and enhance-ment of the immune system is essential in pre-venting and controlling herpes. There is someevidence that a defect in the immune system ispresent even in otherwise healthy individualswho have recurrent HSV infection. Support ofthe immune system, dietary factors, stressors,skin health, and preventing and treating othernon-herpes infections are all avenues for usingnatural therapies in reducing the likelihood ofcontracting herpes and in reducing the frequencyand intensity of recurrent herpes infections.

Nutrition

A health-supportive diet is fundamental to goodhealth and an optimal immune system. Althoughbiochemical differences may require that some ofus eat more of some foods and less of others,health-supportive diets are based on the guide-lines listed below.

A dietary approach for preventing recurringherpes outbreaks that reduces high-arginine foods

PREVENTION

• Genital herpes is a sexually transmitted disease.Education about recognizing the disease and itsprodromal symptoms of itching, numbness, andtingling and protection during sexual contact orabstaining during outbreaks are important inpreventing transmission.

• The virus can shed; thus, transmission of thedisease to another individual is possible evenwithout symptoms. The use of barrier methods isrecommended for any person who has evidenceof prior infection with HSV-2.

• The safest method of protecting yourself and asexual partner is to use some sort of barriermethod to prevent contact. The use of male con-doms, female condoms, dental dams, or house-hold plastic wrap are all recommended options.

• Informing one’s sexual partner of a history ofherpes is the responsible thing to do. Beforehaving sexual contact with a new partner, askquestions about his or her past sexual history,history of sexually transmitted infections, andpast habits and lifestyle that may have exposedthe partner to the virus and other sexuallytransmitted infections.

• A willingness to practice “safer sex” techniquesis an important health issue to discuss with asexual partner. One should understand that HSVinfection can be spread by oral-genital contactas well as genital-genital sexual contact.

• Transmission from one body site to another ispossible, and infected areas should be patted,rather than wiped, dry. Be especially carefulabout transmitting the infection from anotherpart of the body to the eye.

• Enhance the immune system.• Some individuals may need to consider prophy-

lactic suppressive antiviral medication.


and increases high-lysine foods has become quitepopular. This concept arose out of two findings.First, we know that the replication of the herpessimplex virus requires the manufacture of proteinsrich in arginine, and arginine itself may be a stim-ulator of HSV replication. Second, laboratoryresearch has shown that lysine has antiviral activitythat blocks arginine7 and that an arginine-deficientenvironment suppresses HSV replication.8

Thus, theoretically, reducing one’s intake ofarginine and increasing one’s intake of lysineshould be effective in reducing HSV replication.In fact, many people do observe an increased susceptibility to outbreaks if they eat chocolate or peanuts, foods that are high in arginine. Otherhigh-arginine foods include almonds, cashews,and sunflower seeds. Foods high in lysine includemost vegetables, beans, fish, turkey, and chicken.


L-Lysine. Scientific studies on the effective-ness of lysine supplementation have not shownconsistent results, and a least one study citesdietary variability of lysine and arginine intake asa possible confounding factor that is often diffi-cult to control and is not often assessed in stud-ies.9 One study that did show positive results was done in 52 patients with recurrent infections(oral, genital, or both). Test subjects received L-lysine (one gram three times daily) or a placebo.They also avoided nuts, chocolate, and gelatin.

After six months, the treatment was rated as effec-tive or very effective by 74 percent of those receiv-ing the lysine, compared to 28 percent of thosereceiving placebo. The mean number of herpesoutbreaks was 3.1 in the lysine group comparedto 4.2 in the placebo group, and lysine-treatedpatients reported milder symptoms. No signifi-cant side effects were reported in either group.10

Another experimental study was done with 41patients who took a daily dose of 1,248 mg oflysine. This demonstrated a decreased recurrencerate and a decreased severity of symptoms duringrecurrences, but not a reduced healing time.11

For people who want to rely on lysine supple-mentation alone, my recommendation is to takeone gram daily for maintenance and one gramthree times daily during acute outbreaks. Lysinecan also be found in topical ointments to beapplied directly to herpes eruptions. These may behelpful in reducing symptoms but have not beenadequately studied to prove their effectiveness.

Lysine

Acute: 1 g 3 times dailyMaintenance: 1 g daily

Vitamin C and Bioflavonoids. Supplementa-tion with vitamin C may have therapeutic value inthe treatment of recurrent external genital herpeseruptions. Using 600 mg of vitamin C and 600mg of bioflavonoids three times daily for threedays after the initial onset of symptoms (in theprodromal phase) was found to be the optimaldosage for the most rapid disappearance of symp-toms.12 In addition, in vitro evidence supports theuse of ascorbate in combination with copper toinactivate HSV-2.13 In women with active lesions,a randomized double-bind, placebo-controlledclinical trial was done on the topical use of awater-based solution of Ascoxal, an ascorbicacid–containing formulation, in the treatment ofrecurrent mucocutaneous herpes. A solution-soaked cotton pad was applied to the lesion threetimes for two minutes with 30-minute intervals


• Maximize your intake of vegetables, wholegrains, legumes, and fruit.

• Drink 4 to 8 glasses of water daily.• Reduce fat intake.• Eliminate refined sugar and chocolate.• Avoid food additives, coloring agents, pesti-

cides, and herbicides.• Reduce salt and alcohol intake.• Reduce or avoid almonds, cashews, sunflower

seeds, and peanuts.


on the first day only. Both subjective and objectiveaccounts demonstrated decreased symptoms andhealing time. In addition, viral culture after thefirst day yielded HSV significantly less frequentlywhen compared to placebo.14

Vitamin C and Bioflavonoids

Prodromal period: 600 mg vitamin C with 600 mgbioflavonoids 3 times daily for 3 days

Vitamin E. Applying topical vitamin E to alesion may provide pain relief.15 Although clinicalobservations have been made of only four pub-lished cases (in oral primary herpes, not genital), itwould seem logical that vitamin E applied to gen-ital eruptions may provide a similar benefit. Drythe area around the lesion with warm air andapply vitamin E oil with a cotton swab. Leave inplace for 15 minutes. After the 15 minutes, painrelief should be evident. Repeat as needed.

Further evidence for the use of vitamin E wasfound in an animal study that employed a patentedcombination antioxidant cream including vitaminE, sodium pyruvate, and membrane-stabilizingfatty acids. It demonstrated that the ingredientsworked synergistically to reduce genital HSVlesion development, duration, and severity signifi-cantly when compared to placebo or acyclovir.16

Vitamin E

Apply vitamin E oil to dry area around lesion; leave inplace for 15 minutes. Repeat as needed.

Zinc. A number of zinc salts have beenshown to have antiviral activity against HSV. Invitro17 and animal studies have supported use ofzinc topically with genital infection.18–20 Supple-mentation with zinc has been observed to reducethe frequency, duration, and severity of genitalherpes eruptions. A compound of zinc (25 mg)and vitamin C (250 mg) was given twice daily forsix weeks. In some cases, the eruption was com-pletely suppressed, and in others the eruptionsdisappeared within 24 hours of their onset.21

Zinc and Vitamin C

25 mg zinc with 250 mg vitamin C twice daily for 6weeks

Botanicals

Lemon Balm (Melissa Officinalis). Lemonbalm ointments have been used topically in Ger-many for oral cold sores, and products are nowavailable in the United States. Laboratory evi-dence demonstrates the anti-HSV-2 activity ofMelissa at nontoxic concentrations in vitro.22, 23

The German cream Lomaherpan is a concentrateof 70:1 lemon balm extract. Several clinical stud-ies have shown impressive results. One studydemonstrated that when the lemon balm creamwas used on patients with an initial oral herpesinfection, or cold sore, not a single recurrenceoccurred. Not one patient using the cream devel-oped another cold sore. The cream was alsoshown to be effective in reducing the healingtime in cases of genital herpes.24

Another study, a double-blind, placebo-controlled, randomized trial, used a standardizedtopical cream (active ingredient: 1 percent Lo-701—dried extract from Melissa officinalis L.leaves) in 66 patients with a history of recurrentherpes labialis of at least four episodes per year.With applications four or five times a day, subjectsnoted shortening of the healing period, preventionof infection spreading, and rapid relief of the typ-ical symptoms of herpes. The authors also con-cluded that the intervals between the periods withherpes might be prolonged with this treatment.25

The cream should be applied two to fourtimes a day during an active eruption. No sideeffects have been observed.

Lemon Balm

Apply topically 2 to 4 times a day.

Licorice (Glycyrrhiza Glabra). Licorice hastraditionally been used by naturopathic physi-


cians, herbalists, and other health-care practi-tioners to support the body’s immune system andto defend against the effects of disease-causingviral infections. Laboratory studies demonstrate acomponent of Glycyrrhiza glabra root, gly-cyrrhetinic acid, is active against viruses, specifi-cally in HSV where it inhibits the growth,activity, and ability to replicate, irreversibly inac-tivating the herpes simplex virus.26 In clinicalpractice, I have observed that topical prepara-tions of licorice containing glycyrrhetinic acidhave helped to reduce both healing time anduncomfortable symptoms associated with genitalherpes. Apply the ointment or gel several timesdaily. If used daily over several weeks or months,licorice may cause fluid retention and therebyraise blood pressure in certain individuals.

Licorice

Apply ointment or gel several times daily.

Siberian Ginseng (Eleutherococcus Sentico-sus). A randomized double-blind, placebo-controlled trial of a standardized extract of eleuthe-rococcus showed a decrease in severity, duration,and frequency of outbreaks when used for at leastthree consecutive months. Although not com-monly used by alternative practitioners for thetreatment of herpes, this study supports eleuthero’srole in suppression of herpes outbreaks.27

Siberian Ginseng

• Dried root: 500–3,000 mg dried root capsules• Tincture (herb and alcohol or herb, alcohol,

and water): 1 tsp 3 times per day• Fluid extract: 1⁄2–1 tsp 2–3 times per day• Extract (33% alcohol extract): 40–120 drops

1–3 times per day• Solid extracts made from dried, powdered root

(at least 1% eleutheroside F): 100–200 mg 3times per day

Bee Propolis. Propolis is a resinous substancethat bees make by combining substances from

plants with waxes and glandular secretions. Theyuse this resin for the construction and repair oftheir hives. It is also placed at the entrance to thehive where the worker bees brush up against it asthey enter the hive. This sterilizes the bees frominfection. The composition of propolis variesdepending on the plants in the area that the beesvisit. Some propolis may be higher in flavonoids,other propolis may be higher in diterpene com-pounds. Historically, propolis has been used forits antibacterial, antifungal, antiviral, antiproto-zoan, antitumor, anti-inflammatory, immunomo-dulatory, and antioxidant activities. In vitro datasuggests propolis has both antibacterial andantiviral properties against a variety of microor-ganisms, including HSV.28–30

Two of my favorite natural topical therapies forherpes lesions are honey and bee propolis. A smallstudy comparing topical application of honeyversus acyclovir cream found a statistically signifi-cant shorter duration of episodes and faster healingtime when using honey compared to acyclovir.31

Another larger, randomized, single-blind studyshowed that more subjects’ lesions healed after 10days of treatment with a 3 percent propolis oint-ment than with placebo or acyclovir.32

Bee Propolis

Apply 3% bee propolis ointment several times per day.

Aloe Vera. Aloe vera is a cactus, and the gelat-inous substance inside the leaf is known to havemany beneficial properties. It’s not surprising thatsome research shows some effects for the herpesvirus, and mucosal epithelial tissue appears to bea good site for the medicinal effects of aloe. Invitro data suggests that chemical constituents ofaloe vera inactivate HSV-2 both alone and syner-gistically with acyclovir.33, 34 Human clinical trialson men support its use topically as a 0.5 percent

Aloe Vera

0.5% cream, apply 2–4 times daily


hydrophilic cream, but not as a gel, to shortenhealing time and decrease symptoms.35, 36

Myrrh (Commiphora Myrrha) and Gold-enseal (Hydrastis Canadensis). I am not awareof any research studies using myrrh and gold-enseal for genital herpes eruptions, but the tradi-tional use of both of these herbs is longstanding.As an antiseptic and as an anti-inflammatory forinflammations and sores of the mucous mem-branes, these two herbs have been very reliableand may go a long way not only toward improv-ing the health of the epithelial tissue of themouth and genital region but also stimulating animmune response locally in that tissue.

Myrrh

Oral tincture: 10–30 drops 3 times per day

Goldenseal

Oral tincture: 10–30 drops 3 times per day

Additional Botanicals. Many botanicalshave the ability to provide immune supportthrough various mechanisms. Other plants havevery specific antiviral properties as well.

The antiviral activity of Saint-John’s-wort(Hypericum perforatum) has been demonstrated.Laboratory studies have shown that two con-stituents in Saint-John’s-wort, hypericin andpseudohypericin, exhibit strong antiviral activityagainst herpes simplex virus 1 and 2 as well asinfluenza types A and B, in addition to a virus inthe mouth that causes vesicular stomatitis.37

Momordica charantia, or bitter melon, has beenshown to have antiviral activity against bothHSV 1 and 2 such that its effectiveness in vitro isnot only greater than acyclovir, but it is alsoeffective against acyclovir-resistant strains.38

Medicinal mushrooms are known for theirantimicrobial activity against a number ofmicroorganisms. Recent in vitro evidence sug-gests that fungal beta-glucans extracted fromPleurotus tuber-regium exerts its antiviral effect by

binding to the virus, thereby preventing theinfection of the host cells.39

Echinacea has shown in vitro antiviral activ-ity against HSV-1,40 but a human study did notdemonstrate any statistically significant reduc-tion in recurrent genital herpes.41

Viracea, a proprietary blend of benzalkoniumchloride and derivatives from Echinacea pur-purea, was found to have anti-HSV-1 and -2 activity in vitro, even on strains that wereresistant to acyclovir.42

Chapparal (Larrea tridentate), specifically itsleaf resins, have been shown to have significantantiviral activity. The natural ingredients in theleaf resin appear to the inhibit replication of thevirus.43 Preparations are available in either cap-

Sample Treatment Plan for Genital Herpes


During an Acute Episode

• Apply ice, preferably during the prodrome stageduring symptoms of itching, numbness, or tin-gling or even after the eruption has appeared,for 10-minute applications several times duringthe day. This limits the discomfort and swellingand can keep an outbreak from fully erupting.

• Apply lemon balm ointment several times perday.

• Apply licorice gel (glycyrrhetinic acid) twiceper day.

• Lysine: 1,000 mg 3 times per day• Vitamin C: 600–800 mg with 600–800 mg bio-

flavonoids 3 times per day• Zinc: 25 mg per day

Prevention

• Follow a diet that is high in lysine foods (veg-etables, beans, fish, turkey, and chicken) andavoid foods high in arginine (chocolate, allnuts and seeds).

• Lysine: 1,000 mg per day• Safe sex protection


sules or a topical lotion. One or two capsulesdaily of the leaf resin may reduce the frequencyof outbreaks, and the topical lotion, whenapplied at the first sign of a tingling sensation,may prevent the outbreak from occurring.

Botanicals such as thuja (Thuja occidentalis),lomatium (Lomatium disectum), and astragalus(Astragalus spp.) have been traditionally used bynaturopathic physicians, herbalists, and otherhealth-care practitioners to support the body’simmune system and to defend against the effectsof disease-causing viral infections. These herbsare typically administered in liquid extracts, cap-sules or tablets, or teas. Lomatium may cause atemporary skin rash if used in an improper dose.


Many patients prefer to use antiviral therapy tosuppress infections and to reduce recurrentepisodes. The primary goals of antiviral therapyare to limit the severity of the infection and togive the patient a sense of control over the diseaseprocess. Antiviral therapy is offered to normalimmunocompetent patients with either primaryor nonprimary genital herpes. In the vast major-ity of cases, oral antiviral therapy is sufficient,although more severe cases may require hospital-ization and intravenous acyclovir.

Episodic therapy appears to work best forwomen who have a clearly identifiable prodrome.Patients who desire continuous suppressive therapyneed to discuss with their physician the advantagesand disadvantages of this regimen. Medical consid-erations, psychosocial needs, and cost are all factorsinfluencing the wisdom of such a regimen.

The advent of herpes viral testing accuracyand knowledge of the asymptomatic carrier hasled to an increase in the use of antiviral herpestreatments. The meds used to treat the virus areessentially the same as they have been for the past10 to 20 years, but recommendations for usageand dosing have changed. The three meds most

commonly prescribed are acyclovir, valacyclovir,and famciclovir. Acyclovir (Zovirax) was the firstFDA-approved drug for treatment of herpes andis available as capsules, tablets, oral suspension,topical ointment and cream, and sterile powderfor IV infusion. Valacyclovir (Valtrex) comes in500 and 1000 mg caplets, famciclovir (Famvir)in 125 mg, 250 mg, or 500 mg tablets. The sideeffect profile of all of these meds is the same. Theside effects are uncommon, but those reportedare nausea, vomiting, and headache. They seemto be dose-dependent. There does not appear tobe any long-term harm with the use of thesemeds, and there are few, if any, drug interactions.Essentially, this is a very safe medication class.

These meds are used for episodic treatment andfor prevention. We now know that 5 to 10 percentof people are asymptomatic herpes shedders, sosuppressive daily therapy is recommended for:

1. A person with an initial herpes outbreak2. A person who is known to be an asympto-

matic shedder3. Patients with oral or genital herpes who have

more than four episodes a year

The recommendation is for a year or more,depending on the patient’s interest. The usualrecommendation is for a year following the firstepisode of herpes, and longer if there are othercofactors.

The dosing has also changed from the origi-nal recommendations. Acyclovir, which is avail-able generically, is recommended as follows:Ointment for genital topical therapy used severaltimes a day until the lesions have resolved andcream for oral lesions with the same dosing.Orally, it is now 400 mg twice daily for 10 daysfor an initial episode, then 400 mg twice daily for5 days for recurrences. 400 mg once daily is thesuppression dose.

Valacyclovir has a variety of dosing recom-mendations: For an initial outbreak of genitalherpes, use 1,000 mg three times a day for 10days. For recurrent outbreaks, use 500 mg twice


daily for 5 days. For suppression, use 500 mg perday. For oral herpes, the recommendation is 2 gin the morning and 2 g in the evening on one dayonly. For recurrent outbreaks, many practitionersprescribe the 1,000 mg caplet and suggest thatpatients cut it in half for economic reasons andtake one half caplet twice daily.

Famvir is dosed at 125 to 250 mg twice dailyfor 10 days for the initial episode and 125 to 250 mg twice daily for 5 days for the recurrentepisodes. The suppression dose is 250 mg oncedaily. It is interesting that with this product, thesuppression dosing is greater than the activetreatment dosing, because the drug is more rap-idly taken up by the virus when it is in its activereplication phase. Hence, more drug is neededfor suppression than for active treatment.

The drugs are eliminated through the kidneys,so one may need to reconsider dosing in patientswith renal impairment. The drugs are approvedthroughout all ages of pediatric use, and theywould need to be specifically dosed by a pediatri-cian. So far, no resistant strains are reported.

The most important treatment remains pre-vention. Condoms do not prevent the spread ofHSV genitally. Health practitioners continue tosuggest that patients refrain from sexual activity,including oral sex and kissing, when an activelesion is present. We now recognize that 5 to 10percent of people with a history of herpes doshed virus without an active lesion. Talking toyour partner about his or her sexual history andsafe sex practices are probably the most importantsteps in dealing with herpes.


The most appropriate method for accurate diagno-sis of a genital lesion is to see a licensed health-carepractitioner qualified to perform a gynecologicalexam. Accurate diagnosis of genital lesions is notonly an important key to effective and appropriate

treatment but also a key to determining sexualbehavior and habits with sexual partners. Labora-tory testing using viral cultures and blood tests forantibodies are the most common methods thatmay be recommended by your practitioner.

A qualified health-care practitioner can beextremely helpful in providing education andcounseling to the person who has newly acquiredherpes. Education includes information about thenature of HSV infection, various treatmentoptions, effect on pregnancy, and prevention oftransmission. Counseling includes helping patientsto deal with fears, shame, guilt, and feelings ofsocial isolation as well as developing strategies forcommunicating with present and future sexualpartners.

Women who are pregnant need to informtheir practitioner of their history of herpes. Anyoutbreaks during the pregnancy should berecorded and reported so that appropriate testing,treatment, and management can be done duringthe pregnancy and delivery. Whether your practi-tioner is a midwife, alternative practitioner quali-fied to perform home births, obstetrician, orfamily physician, she or he needs to know yourinfection status to make appropriate recommen-dations for your health and your baby’s.

Women with recurrent genital herpes infec-tions may need to seek more aggressive or indi-vidualized care from an alternative practitionerthan the therapies discussed in this chapter.Homeopathy, additional herbal/nutritional com-bination products, or Chinese herbal medicinemay be more effective in an individual case.

Some women may choose to use conven-tional pharmaceutical antiviral therapy, althoughthis is not usually medically necessary. There arecases of primary or nonprimary genital herpes,however, when antiviral therapy is indicated forimmunocompromised individuals. Cases wheresymptoms and complications are severe enoughto warrant hospitalization may require intravenousantiviral therapy.

109

OVERVIEW

Most of us are aware that heart disease is a pri-mary affliction for men, but cardiovascular disease (CVD) is also the leading cause of deathin women. More than 500,000 women die ofcardiovascular-related causes annually in theUnited States.1 Taking into account other athero-sclerotic disorders resulting from damaged andnarrowed arteries, such as strokes, almost 4 ofevery 10 women will die of these diseases,approximately 100,000 prematurely (before theage of 65).2 Starting at age 50, more women dieof cardiovascular diseases than of any other con-dition,3 and women younger than 55 years oldwho have a heart attack have a worse prognosisand higher incidence of heart attack–relateddeath than do men of the same age who have aheart attack, as well as a greater chance of havinganother heart attack.4, 5 Cardiovascular disease isalso a major cause of disability in older women.For black women, the risk of heart-related death istwice as high as for white women.6

Even though heart disease is the leading causeof death in both men and women, the rates ofcoronary disease (but not necessarily death) at virtually every age are higher in men than inwomen.7 When women are in their thirties andforties, the difference between men and women isfour- to fivefold. After that, the difference shrinkswith increasing age. Coronary artery disease(CAD) is less common in premenopausal women,and the incidence of CAD tends to be about 10 to15 years later than men, until the age of 70.8

Overweight women and those with the applefat distribution (with abdominal fat) are atgreater risk for developing coronary artery dis-ease than are slim women and those with thepear fat pattern (fat stored around the hips).9

Abdominal obesity also increases the risk of high blood pressure and diabetes and may lowerthe HDL (good) cholesterol level and raise thetriglyceride level. A desirable waist-to-hip ratiofor middle-aged women is less than 0.8. To getyour waist-to-hip ratio, measure your abdomenat the largest point and divide it by your hipmeasurement.

Overall weight, usually calculated in terms ofbody mass index (BMI), is also an important toolfor assessing one’s risk for coronary artery disease.To calculate your body mass index, divide yourweight in kilograms by the square of your heightin meters. You can also refer to the height andweight chart in Appendix B to help you to deter-mine your body mass index. A desirable bodymass index is less than 25. The Nurses’ HealthStudy found that women with a BMI of 29 ormore had triple the risk of coronary artery diseasecompared with women who were lean and witha BMI of less than 21.10 Women with a BMI of25 to 28.9 had almost double the risk. As manyas one-third of white women and one-half ofblack women are 20 percent or more over theirdesirable body weight.

Between the ages of 30 and 60, and in each ofthe decades in this age group, women who havehad either surgical or natural menopause havetwice the rate of CAD compared to women intheir age group who still have premenopausalovarian function.11 Women who have had bothovaries removed have a higher rate of CAD at anearlier age than women who undergo naturalmenopause.12 The explanations for this are multi-ple, but the estrogen produced by the ovaries helps to maintain higher HDL levels, which pro-tect the cardiovascular system, keep the LDL levelslow, and slow the aging of the arteries. Whether

9H E A R T D I S E A S E C H A P T E R



women still have their ovaries or not, the rate ofcardiovascular disease increases with age13 andincreases significantly after the age of 70.14

One of the largest and most controversialdebates in modern medicine revolves around hor-mone replacement therapy (HRT or HT). Formore than thirty years, observational researchstudies on HRT consistently reported signifi-cantly reduced rates of cardiovascular disease inwomen who used either estrogen alone or estro-gen plus progestins,15 and HRT was routinelyprescribed for primary prevention of cardiovascu-lar disease. Then, in 1998, the Heart and Estro-gen/Progestin Replacement Study (HERS)16

found that the hormones did not protect womenwho already had evidence of cardiovascular dis-ease from heart attacks, and moreover, that morewomen treated with HRT died of heart disease inthe first year of the study than those given aplacebo. This study was followed soon after, in2002, with one called the Women’s Health Initia-tive,17 which found that conventional HRT (Pre-marin and Provera) was not associated with adecrease in heart disease, but actually with a slightincrease. It was also associated with a slightincrease in strokes and clots. As researchers con-tinued to study the women in the estrogen-onlygroup (Premarin), they did not find an increase inthe risk of heart disease, but still did find a slightincrease in strokes and clots.18 In addition to theestrogen plus progestin HERS study and theestrogen-only WHI study, numerous other ran-domized controlled trials have been done sincethe HERS trial. No beneficial effects of estrogenon heart disease risk were observed in either theestrogen in the prevention of reinfarction trail(ESPRIT)19 or in the women in the PapworthHRT atherosclerosis study (PHASE).20

Most recently, studies show that HRT mightin fact be beneficial if taken during peri-menopause or very early menopause,21, 22 offer-ing a window of cardioprotection if started in theearly menopausal years. Estrogen has favorableeffects on several heart disease risk factors: HRT

increases high-density lipoprotein (HDL) choles-terol, decreases low-density lipoprotein (LDL)cholesterol, reduces oxidation of LDL choles-terol, lowers uptake of LDL in blood vessels,binds to vascular estrogen receptors, reduces vascular tone, preserves endothelial function,increases prostacyclin release, decreases throm-boxane A2 formation, decreases fibrinogen,reduces plasminogen activator inhibitor, anddecreases fasting blood glucose and insulin.23

As you can see, the last 9 or 10 years in par-ticular have seen a flurry of trials on the subjectof HRT and heart disease, and with all of thesestudies, commentaries, confusions, contradic-tions, controversies, questions, and opinionsabound. Despite the more recent reassuring newsabout the effects of HRT when given early,women and their physicians are still left with noconsistent clear message or guide as to what tothink regarding HRT and cardiovascular disease.Because of this inconsistency, it is important toassess each woman individually to determinewhether HRT is right for her. In addition, physi-cian advisory organizations no longer recom-mend that HRT be used to reduce the risk ofheart disease.

The question really is, does hormone replace-ment therapy benefit women, and, if so, whichhormones, in what form, in what dose, and inwhom is it beneficial?

In determining the best plan of action, it isimportant that each woman is individuallyassessed for her heart disease risk. Utilizing acomprehensive medical history, physical exami-nation, and selected laboratory and heart func-tion testing, it is possible to assess a woman’s riskfor coronary artery disease and the risk of heartattacks. Based on this assessment, a strategy canbe put in place utilizing lifestyle changes, nutri-tional and botanical supplements, and in somecases prescription medications to prevent andtreat cardiovascular disease. To assess eachwoman individually and comprehensively anduse a holistic integrative therapeutic plan is a

111H E A R T D I S E A S E

long overdue approach in the management ofheart disease in women.

What Is Heart Disease?

Before we go too far, let’s clarify what we meanby cardiovascular disease. Generally, when werefer to the risk of heart disease in menopausalwomen we mean coronary artery disease, includ-ing coronary artery atherosclerosis, myocardialinfarction (MI), acute coronary syndromes, andangina. These conditions are intimately relatedto hypertension and hyperlipidemia. The termheart disease is most often used to describe coro-nary atherosclerosis, hardening of and depositionof plaque in the arteries of the blood vessels thatsupply the heart. Other forms of heart diseaseinclude congestive heart failure, arrhythmias,mitral valve prolapse, and cardiomyopathy, butthese are unrelated to issues of menopause andhormones. The focus of this chapter is the pre-vention and treatment of coronary artery disease(CAD) and atherosclerosis, hypertension, hyper-lipidemia, and myocardial infarction.

Risk Factors for Heart Disease

Major risk factors for coronary artery disease(CAD) include high blood pressure, abnormalcholesterol profile (dyslipidemia), and diabetes.Optimal levels of lipids and lipoproteins forwomen are LDL cholesterol (LDL-C) less than100 mg/dL, triglycerides less than 150 mg/dL,non-high-density lipoprotein cholesterol lessthan 130 mg/dL, and HDL cholesterol (HDL-C)over 50 mg/dL. Updated guidelines from the2001 National Cholesterol Education Program(NCEP III) expert panel on detection, evalua-tion, and treatment of high blood cholesterol inadults (called the adult treatment panel, or ATPIII) are more complex than just this and empha-size more aggressive lowering of elevated LDLlevels, especially in women with higher risk fac-tors for heart disease. If you have peripheral vas-cular disease, coronary artery disease, abdominalaortic aneurysm, diabetes, or metabolic syndrome,

discuss testing and management with your prac-titioner as well as all available options, includingexercise, weight management, dietary changes,aspirin, drug treatment, and nutritional supple-ment interventions.

Triglycerides are an important risk factor forcardiovascular disease in women, but especiallywhen increased triglycerides are present in associ-ation with low HDL levels. If the triglyceridelevel is greater than 400 mg/dL and HDL choles-terol is less than 50 mg/dL, the risk of heart dis-ease is significantly increased.24 Patients withelevated triglycerides and a family history forheart disease most likely have familial hyperlipi-demia. Triglyceride levels from 200 to 400mg/dL are considered elevated but borderline.Weight loss alone can return elevated triglyceridelevels to normal. Smoking, dietary simple carbo-hydrates, obesity, and lack of exercise are allrelated to elevated triglycerides.

When determining one’s risk for heart disease,there are some critical things to look for. Womenwhose father had a heart attack or stroke beforeage 50, or mother before age 65 (unrelated to cig-arette smoking), are at a genetic disadvantage. It’simportant for these women to work harder in theareas of prevention because they are at increasedrisk just by virtue of their family history.

Hypertension is the most common chronicdisease in older women and a significant riskfactor for stroke, congestive heart disease, andkidney disease. Beginning at age 50, hyperten-sion is more common in women than in menand even more so in black women. See Table 9.1for new blood pressure guidelines set in 2003.Isolated systolic hypertension (systolic BP of 160mm Hg or greater) or combined hypertension(systolic BP of 160 or greater and diastolic BP of90 or greater) is directly related to increaseddeath rates from cardiovascular disease.

Impaired tolerance to glucose is another riskfactor for heart disease. Women with higher thannormal blood sugar or who are clinically diabeticare at increased risk. The diabetic woman has three


to seven times the risk of cardiovascular diseaseand of dying prematurely from atherosclerosisthan a nondiabetic woman.25 Diabetes is astronger predictor of cardiovascular disease inwomen than in men.26 Women are more prone tosuffer unrecognized or “silent” events related toischemia.

In addition to these risk factors, there are twosyndromes, both called syndrome X, associatedwith heart disease risk. The first one was named byDr. Harvey Kemp of Harvard in 1967 to describewomen with normal coronary angiograms whohad angina-like chest pain with or without posi-tive treadmill tests.27 Some of these women turnedout to have abnormal circulation in the smallcoronary arteries, and their coronary flow didn’tadjust itself appropriately.

The second syndrome X, also called Reaven’ssyndrome or metabolic syndrome,28 was coined in1988 by Dr. Gerald Reaven of Stanford Univer-sity. It is a syndrome of increased truncal (midsec-tion) obesity—a waist-to-hip ratio greater than1:1—and is defined as a cluster of symptoms thatappear to occur secondarily to cellular resistance toinsulin. Individuals who secrete larger amounts ofinsulin because the normal insulin action isimpaired are predisposed to glucose intolerance,hyperinsulinemia, dyslipidemia, and hyperten-sion. The relationship between resistance toinsulin, non-insulin-dependent diabetes mellitus,hypertension, and cardiovascular disease has beenextensively documented.29 Evidence suggests thathyperinsulinemia may be seen in as many as 25

percent of the nondiabetic population. As many as50 percent of individuals with high blood pressuremay have syndrome X.30 Overweight individualsare more susceptible to this condition, but asmany as 50 percent of hyperinsulinemic patientsmay be of normal weight.31 Individuals who haveglucose intolerance and hyperinsulinemia shouldeat a diet lower in carbohydrates, whether simpleor complex. A diet that is 40 percent carbohy-drates, 30 percent fat, and 30 percent protein mayhelp to correct the hyperinsulinemia.

The diagnosis of coronary artery disease andevaluation of the potential for risk of cardiovas-cular disease (CVD) are fundamental steps toimprove women’s health and decrease their risk ofacquiring and dying from cardiovascular disease.Screening tests, noninvasive diagnostic testing,and testing to help determine risk and prognosisoffer the opportunity to identify women atincreased risk, begin proactive prevention strate-gies, and provide the basis for treatment options.

For women who do not have symptoms ofCAD, the goal is to identify risk factors for devel-oping CAD. Risk prediction charts are available,and one risk chart, the Framingham risk score(FRS), includes traditional risk factors for CAD,including age, smoking history, blood pressure,obesity, sedentary lifestyle, and cholesterolvalues.32 From this score, it is determined if therisk is low, intermediate, or high. This is then cor-related with expected rates of death or heartattack. Prevention strategies are then determinedfor each woman. In general, the risk of heart dis-

Table 9.1 Blood Pressure Guidelines

Blood Pressure Systolic Pressure Diastolic PressureCategory (mm Hg) (mm Hg)

Normal less than 120 less than 80

Prehypertension 120–139 80–89

Stage 1 hypertension 140–159 90–99

Stage 2 hypertension 160 or higher 100 or higher


ease and heart events are low in premenopausalwomen and therefore screening is less importantuntil menopause. Important exceptions to this arewomen who have diabetes, women with periph-eral arterial disease, and overweight women withpolycystic ovarian syndrome.

The U.S. Preventive Services Task Force(USPSTF) recommends against routine screen-ing in adults who are low risk for CAD.33 Forthose at higher risk (a history of a nonfatal heartattack, older age, high blood pressure, smoker,abnormal cholesterol levels, diabetes, obesity, andbeing sedentary), appropriate testing is veryimportant to prevent future cardiac events. It isimportant to make a distinction between routinescreening and tests done for individuals who aresymptomatic or who are suspected to have CAD.For women who have a normal resting electro-cardiogram (ECG) and who have good exercisetolerance, a routine exercise treadmill test withECG is recommended as the initial test to evalu-ate suspected CAD. For women who have anundetermined or intermediate risk exercise ECGtest, cardiac imaging is recommended. Again, dia-betic women merit special attention and will needto be evaluated more assertively due to their eight-fold higher risk of cardiovascular death comparedto women who are not diabetic.

For women who are symptomatic—forexample with angina pains—and are intermedi-ate or high risk, noninvasive cardiovascular riskscreening, including exercise ECG testing, stressechocardiography (an ultrasound imaging of the heart called echocardiogram, done whileexercising), and cardiac imaging looking for ath-erosclorosis are recommended. Stress echocardio-graphy can provide important information aboutthe function of the left ventricle of the heart,valvular disease, and any stress-induced ischemiaor previous infarction. This particular test hasbecome an important tool in testing women,because it is more specific and accurate than stan-dard exercise ECG in women. An abnormal exer-cise stress echocardiography test is associated

with an increased risk of future cardiac events inwomen, and a normal test is associated with alow risk of cardiac events. Even in symptom-freewomen who are suspect for CAD, stress echo-cardiography is a cost-efficient and better testthan an exercise ECG, particularly in womenwho are at intermediate risk for coronary arterydisease.

Cardiac imaging tests include what is calledgated myocardial perfusion single-photon emis-sion computed tomography (SPECT), a nuclear-based technique. SPECT imaging is currentlythe most commonly performed stress imagingtest in the United States. However, it may havelimitations in women, possibly due to theirsmaller heart and the interference of the breasttissue. Different nuclear isotopes and pharma-ceuticals can be used to enhance the diagnosticvalue of the SPECT test. Whichever SPECTtechnique is used, these tests are able to furtherevaluate and/or predict cardiac disease, and thisinformation can be used to determine the extentof the treatment intervention that is needed toimprove their symptoms and future health.

Several new imaging technologies haveemerged in the detection of subclinical CAD:computed tomography (CT), magnetic reso-nance imaging (MRI), and carotid intima-mediathickness (IMT). Consultation with a cardiolo-gist is important in determining the value orneed for such tests.

Increasingly, blood tests for cardiovascularbiomarkers, which may serve as markers forCVD, are being done in healthy women. Testsfor lipoprotein (a), C-reactive protein, fibrino-gen, homocysteine, and subfractions of HDL-Cand LDL-C are a few of the more frequentlyused. It is difficult to say with certainty, at thistime, in whom and how often these should bedone. Currently, the scientific community hasnot agreed on guidelines for their use or whethersuch testing ultimately does a better job than thetraditional physical exam with cholesterol panelsand blood glucose testing. In my practice, for


women who have had one regular lipid panelwith abnormalities, I am inclined to order theseadditional, more sophisticated blood tests. Themore risk factors they have, such as obesity, diabetes, and others, the more eager I am to eval-uate them in as comprehensive a manner as pos-sible. These additional blood tests can be easilydone to serve that purpose.

There are heart disease risk factors unique towomen. These include oral contraceptive use, pregnancy, having had both ovaries removed, and premature menopause. Additional risk factors notrelated to gender include increased body fat, espe-cially if it is in the abdominal area; history of smok-ing; being sedentary; diabetes mellitus; high bloodpressure; poor lipid ratios; and family history.


Conventional and alternative medicine practition-ers agree that, in most cases, atherosclerosis andcardiovascular disease are directly related to dietand lifestyle. While family history and genetic predisposition play an important role in cardiovas-

cular disease, risk factors such as cigarette smok-ing, exercise, dietary habits, and stress can be mod-ified to reduce a person’s risk. In fact, a recentstudy found that the following factors are to becorrelated to increased hypertension: excessivesodium intake, low potassium intake, physicalinactivity, low intake of fish oil, low calciumintake, low magnesium intake, excessive coffeeconsumption, and excessive alcohol intake.34

Dietary and lifestyle changes are the founda-tions of heart disease prevention and treatment.Dr. Dean Ornish and his team of researchersconducted the first significant clinical trial todetermine whether comprehensive lifestylechanges affect coronary atherosclerosis. Dr. DeanOrnish’s landmark study, called the LifestyleHeart Trial, published in 1990, found thatlifestyle changes (a low-fat vegetarian diet, mod-erate aerobic exercise, stress management, smok-ing cessation, and group support)35 changedserum lipids as much as cholesterol-loweringdrugs. After one year in the program, patientsalso showed significant overall regression of theircoronary atherosclerosis. These results have beenreplicated in several recent studies.36–38 It is inter-esting to note that patients who made less com-prehensive changes in lifestyle showed significantprogression of their atherosclerosis, suggestingthat the conventional 30 percent–fat diet recom-mendation made to patients with cardiovasculardisease is not low enough. See the nutrition anddietary factors section for more about the DeanOrnish low-fat diet.

Smoking is the most important risk factor forcardiovascular disease and heart attacks, even inpremenopausal women. Smokers have three tofive times the risk of coronary artery disease asnonsmokers, and smoking accounts for one-fifthof CVD deaths.39, 40 Even smoking only one tofour cigarettes a day doubles a woman’s risk ofCVD. Smoking a pack or more per day maydouble to quadruple that.41 Tobacco smoke con-tains chemicals that damage the lining of thearteries, raise the cholesterol level, promote the

Risk Factors for Coronary Artery Disease

Medical Conditions

HypertensionDiabetes mellitusHyperlipidemia/lipid abnormalitiesSyndrome X (insulin resistance)Obesity and/or excess abdominal and upper body fat

(apple shape)

Lifestyle

Sedentary lifestyleHigh-fat dietCigarette smokingAlcohol—more than two drinks per dayStress

Family History

Coronary artery disease


ability of platelets to clump together, elevatelevels of fibrinogen (a clot-forming protein), andelevate the blood pressure. Smoking is especiallyproblematic in women who use oral contracep-tives. This combination increases the risk ofCVD by up to 39 times due to blood clots.42 Thegood news is that women who stop smoking canreduce their risk of CVD to that of a nonsmokerwithin two years of quitting.

Exercise is a vital part of a lifestyle routinethat can have lifelong benefits in preventing heartdisease and strokes. Regular exercise lowers cho-lesterol levels, improves the blood supply andtherefore the oxygen delivered to the heart,increases the strength of the heart muscle andthus improves the volume of blood it can move,

reduces blood pressure, helps to inhibit bloodclots, reduces overall body fat, and minimizesdamage from stress.

In many women, stress is the major cause oftheir high blood pressure. Relaxation techniquessuch as deep breathing, biofeedback, meditation,yoga, progressive muscle relaxation, and hypnosishave all been shown to have some value in lower-ing blood pressure.43 Many recent studies on var-ious stress reduction techniques have also shownimprovement in blood pressure and other meas-

KEY CONCEPTS

• Determine your individual risk for cardiovasculardisease; make an appointment with a knowl-edgeable health-care practitioner for medicalhistory, physical exams, and tests.

• Monitor blood pressure regularly.• Monitor fasting levels of total cholesterol, HDL

cholesterol, LDL cholesterol, cholesterol/HDLratio, triglycerides, and blood glucose. Consultwith your health-care provider regarding at whatage to start and how frequently ECGs, stressECGs, stress echocardiograms, and cardiac orcarotid artery imaging may be needed on anindividual basis depending on symptoms andsuspicion of CVD.

• More sophisticated testing as needed or desired:homocysteine, alpha-lipoprotein (a), fibrinogen,C-reactive protein, HDL subfractions, LDL subfractions.

• Heart disease, and especially heart disease ear-lier in life, is a preventable disease; appropriatediet and exercise, emotional balance and stressmanagement, and herbal and nutritional supple-mentation may substantially reduce CVD risk.

• Benefits and risks of hormone replacement ther-apy need to be discussed with a health-careprovider familiar with up-to-date research onthis topic.

PREVENTION

Prevention of Heart Disease

• Get regular aerobic exercise for 30 minutes, 5–7days per week.

• Increase fish, whole grains, fruits, vegetables,legumes, olive oil, and nuts and seeds intake.

• Eat lean meats and poultry without the skin.• Eat low-fat or fat-free dairy (preferably organic).• Decrease consumption of foods high in saturated

fats, cholesterol, sugar, and simple carbohydrates.

• Work toward or maintain a healthy body weight.• Do not drink more than one alcoholic beverage

per day.• Stop smoking and avoid secondhand cigarette

smoke.

Prevention of Hypertension

• Limit sodium intake to less than 2,400 mg perday.

• Practice stress management techniques.• Work toward or maintain a healthy body weight.• Exercise daily for 30 minutes or more.

Prevention of Hyperlipidemia

• Decrease consumption of saturated fats andhigh-cholesterol foods.

• Increase consumption of fruits, vegetables, andwhole grains.

• Exercise daily for 30 minutes or more.• Increase consumption of olive oil, nuts, and

seeds.


ures of CVD, including decreased mortality andoxidative stress.44–49

A fundamental tenant of alternative medicineis that lifestyle changes that include smoking cessation, appropriate exercise, diet, and the useof dietary ingredients, nutritional supplements,and herbal extracts can prevent or reduce risksand treat cardiovascular disease. Considerablescientific research exists that demonstrates theeffect of these natural therapies and interventionsin lowering cholesterol, improving blood lipidratios, lowering blood pressure, preventing clotsand strokes, inhibiting fibrinogen, loweringhomocysteine levels, strengthening the cardiacmuscle, and preventing the oxidative damage tovessel walls, all of which are implicated in cardio-vascular disease risk. Ingredients such as fiber,soy, antioxidants, folic acid, vitamins B6 and B12,magnesium, fish oils and flax oil, garlic, haw-thorn berry, and others are just some of the manynatural therapies that give alternative practition-ers a great deal of confidence in their ability tohelp women to prevent and treat heart disease.Most alternative practitioners employ a diverse,holistic health plan in their approach to prevent-ing and treating CVD. Recent research supportsthe use of supplements like fish oil, oat bran, andplant sterols in combination with diet and exer-cise interventions as a way to favorably effect alllipid parameters,50 and diets focused on decreas-ing cholesterol have long-term success on parwith statin therapy.51

Nutrition and Dietary Factors

Dietary habits are a fundamental area where wecan exert a great deal of influence on our hearthealth.

Fats. Lowering the level of dietary fat hasbeen in the news for a long time now. The Amer-ican Heart Association says that 30 percent orless of our total calories should be from fat. Manyalternative practitioners advise even lower intakesbecause of some of the additional benefits, such

as reduction of breast, ovarian, and uterinecancer risk.

In addition to amount of fat, the type of fatis also important. Understanding the harmfuleffects of some fats and the beneficial effects ofothers can be confusing. A little explanation ofterms and concepts may go a long way in clarify-ing the issue. Fats are the most concentratedsource of food energy. Each gram of fat provides9 calories, compared with only 4 calories pergram for carbohydrates or protein. All fats aremade from carbon, oxygen, and hydrogen. Theseelements are arranged in molecules called fattyacids. The three major classes of dietary lipids aretriglycerides, phospholipids, and sterols (such ascholesterol). Ninety-five percent of the dietaryfats are triglycerides. A triglyceride is a glycerolmolecule with three fat molecules attached.These fat molecules are called fatty acids. Lipaseenzymes, found in our bile, break apart thetriglyceride molecules. The triglyceride is con-verted into a monoglyceride, which the body canthen absorb, along with the individual fatty acidsand the glycerol.

Fatty acids and monoglycerides are absorbedand transported by lipoproteins. These lipopro-teins are the very low-density lipoproteins(VLDL), low-density lipoproteins (LDL), andhigh-density lipoproteins (HDL) that we havediscussed earlier in the chapter. VLDL and LDLtransport the fats from the liver to the cells in thebody, and HDL returns the fats to the liver. Ele-vations of LDL or VLDL are associated with anincreased risk for atherosclerosis (narrowing ofthe arteries), which compromises blood flow tothe heart, which can cause a heart attack, andcreates an artery prone to releasing a blood clot,which can lead to a stroke. Elevation of the HDLis protective and is associated with a lower risk ofheart attacks.

Types of Fatty Acids. A distinction should bemade between different types of fatty acids. Sat-urated fatty acids are solid at room temperature


and are typically animal fats (found in beef,lamb, butter, cheese, and lard). Saturated fats ingeneral are not good for the heart; they con-tribute to LDL cholesterol and should be eatenin sparse amounts for a heart-healthy diet. Atriglyceride is a saturated fat when the carbonmolecules in the fatty acids are saturated withhydrogen molecules and can’t carry any more.When some of the hydrogen molecules areremoved, what remains is an unsaturated fattyacid, or unsaturated fat. Unsaturated fats areliquid at room temperature and, therefore, arecalled oils. Most vegetable oils contain mainlyunsaturated fats. These are not as bad for you assaturated fats, and they contain healthy essentialfatty acids (discussed later), but they aren’thealthy in large quantities. Polyunsaturated fattyacids contain more than one double bond alongthe fatty acid chain. Replacing saturated fattyacids in the diet with polyunsaturated fatty acids(PUFAs) from vegetable oils will lower both totalcholesterol and LDL levels and decrease bloodpressure.52 However, it may also lower HDL.

The third general type of fat is monounsatu-rated fat. These fats contain one double bond.Monounsaturated fatty acids, as found in oliveoil, show either no effect on HDL or an increasein HDL, thereby promoting a better effect than

either PUFAs or saturated fats. Of all the types of fat, monounsaturated is the healthiest for your heart.

An omega-9 oil, such as oleic acid (found inolive oil), is a monounsaturated fat that has theunsaturated bond at the ninth carbon moleculeon the chain. Monounsaturated oils like canolaand olive are ideal for cooking as they are madechiefly of oleic acid that is more resistant todamage from the heat from cooking and lightfrom storage. The high content of oleic acidmake these two oils far superior to the highlypolyunsaturated oils like corn, safflower, and soythat are easily damaged by heat and light andaren’t as heart-healthy. The fatty acids in theseless desirable oils are changed to lipid peroxideswith cooking, which have a toxic effect on theinside of the arteries. In a healthy cardiovascularprevention regime, one would, therefore, prefer-entially eat the seeds and fruits that containmonounsaturated oils; use canola, sesame, andolive oil for cooking; and leave the rest of the oilson the supermarket shelves. (See Table 9.2 for thefatty acid composition of different dietary oils).53

We don’t hear a lot about sesame oil, but anumber of studies have proven its cardiovascularbenefits. One study showed a significant decreasein blood pressure measures in patients after 45

Table 9.2 Fatty Acid Composition of Various Dietary Oils

% GLA % LA % ALA % Oleic % SaturatedOil (Omega-6) (Omega-6) (Omega-3) (Omega-9) Fat

Flax 0 14 55 20 9

Safflower 0 75 0 13 12

Soy 0 50 9 26 15

Olive* 0 8 0 76 16

Coconut 0 3 0 6 91

Corn 0 59 0 24 17

Canola 0 30 7 49 7

*Is especially high in the preferential monounsaturated fat, oleic acid.


days of using sesame oil and an increase in meas-ures when patients reverted back to other oils. Inaddition, sesame oil decreased weight, body massindex, waist and hip measurements, blood sugar,hemoglobin A1c, total cholesterol, LDL, and tri-glycerides.54 Another study found that sesame oilwas superior to sunflower and nut oils in its abil-ity to decrease oxidation of lipids, improve lipidparameters, and decrease blood pressure.55

Olive oil, with a monounsaturated fatty acidrich in oleic acid, is especially heart-healthy. Mostof the beneficial effects of olive oil, especially thericher virgin olive oil, are attributed to its highmonounsaturated fatty acid content. However, italso has other components that may help explainits cardiovascular benefits. Virgin olive oils havemore phenols, which appear to provide the great-est benefits by increasing HDL cholesterol levelsand reducing the oxidative damage on lipids. Phe-nols are a class of naturally occurring compoundsfound in fruits, vegetables, tea, red wine, andgrape juice that are in essence antioxidants. Thesecardioprotective phenols included flavonoids,resveratrol, and curcumin. A daily 25 ml dose ofany type of olive oil has been shown to reducelipid cardiovascular risk factors56 by decreasingoxidative damage on lipids, increasing HDL cho-lesterol levels, and improving the glutathione bal-ance that protects against oxidative stress.

Hydrogenated oils (an unsaturated oil thathas been made into a saturated fat) should beavoided for cardiovascular health. Hydrogenatedoil raises LDL, lowers the protective effects ofHDL, and can in fact increase the incidence ofheart disease. Foods such as margarine, cakes,cookies, candies, and doughnuts often containpartially or totally hydrogenated oils. This is alsotrue of many oils sold in supermarkets; in orderto prolong their shelf life, hydrogenated fats areused in many so-called cooking oils.

Another important fat classification, and onethat’s come under a good bit of scrutiny lately forbeing especially unhealthy, is trans fats. Trans fats

are made during the process of hydrogenating oilsby chemically modifying a natural oil in a processthat converts some of the cis unsaturated fattyacids to the trans form. When we metabolize transfat, it behaves similar to saturated fat, leading to ahigher risk of heart disease and other chronic dis-eases. Trans fats have adverse effects on HDL-Cand LDL-C. Trans fatty acids also have an adverseeffect on cell membranes, making them stiffer, andin general are associated with increased inflamma-tory and oxidative damage.

Trans fatty acid levels are determined by theamount of hydrogenated oils in a food. Foodssuch as doughnuts, french fries, margarine, mostcookies, and any food that contains “partiallyhydrogenated oils” contain trans fats. Soybeanoils, corn oils, and safflower oils contain rela-tively high amounts of oleic and linoleic acids,which can convert to elaidic acid during thehydrogenation process. Elaidic acid is the mostcommon form of trans fatty acids because of itsproduction by hydrogenation of our mostcommon dietary oils. Elaidic acid is found inamounts as high as 60 percent in hard margarine.Being armed with a bit of knowledge about transfats and the foods that contain them and know-ing what to look for on labels will help you tosteer clear of the damaging effects of trans fats.

Many women are fearful of eating more nutsdue to their fat and calorie content, but nuts actu-ally contain healthy fats, as does olive oil. Higheramounts of nuts are associated with cardioprotec-tive effects. Increased intake of walnuts in particu-lar, with their alpha-linolenic acid content,appears to have a triglyceride-lowering effect.57 Inaddition, beneficial oils in nuts help to decreaseinflammatory markers associated with CVD risk,such as C-reactive protein (CRP).58 Nuts andseeds to increase in the diet in addition to walnutsinclude almonds, filberts, sesame seeds, pumpkinseeds, and flaxseed.

Cholesterol. Cholesterol is a waxy substancefound in animal tissue. It is produced by the liver


(about 1,000 mg per day) and is a component of allcell walls. Blood-circulating cholesterol is suppliedby the liver and the intake of animal foods. Dietsthat are high in cholesterol and saturated fats (beef,pork, lamb, butter, cheese, palm oil, coconut oil)contribute to poor lipid ratios and elevated choles-terol. Lowering the cholesterol in the diet will lowerthe blood cholesterol in most individuals.59

Essential Fatty Acids. The body can make mostof the fatty acids it needs from the carbon, hydro-gen, and oxygen provided by food. These havebeen arbitrarily classified as nonessential fatty acids.(This is a most unfortunate classification. It tendsto mask the fact that the so-called “nonessential”fatty acids are as critical to cellular life and metab-olism as are the so-called “essential.” The nonessen-tial fatty acids are manufactured by the cells fromraw materials. The others must be supplied byfood. We cannot survive without both.) Essentialfatty acids (EFAs) are polyunsaturated fats thatmust be obtained from foods. The two essentialfatty acids are linoleic acid and alpha-linolenic acid.Linoleic acid is the main omega-6 fatty acid.Alpha-linolenic acid is the main omega-3 fattyacid, which the body can convert to eicosapen-taenoic acid (EPA) and docahexaenoic acid(DHA). Linolenic acid has been found to decreaseatherosclerotic plaques, systolic blood pressure, andrelated mortality in that high dietary consumptionis related to low incidence of atherosclerosis.60–63

The body uses the omega fatty acids to createeicosanoids. One of the most important classes ofeicosanoids is the prostaglandins. Prostaglandinsexert a local hormone-like effect on target cellsand tissues. For example, in the cardiovascularsystem, they affect dilation or constriction ofblood vessels and clot formation.

The omega-6 and omega-3 fatty acid groupseach produce separate, distinct prostaglandins.Both types of fatty acids are needed, but in theright ratio. There is some disagreement as to theright ratio between omega-6 and omega-3 fattyacids. Our early ancestors probably ate roughly

equal amounts of omega-6 and omega-3 essentialfatty acids. In the modern industrialized coun-tries, most people eat from 10:1 to as high as30:1 omega-6 to omega-3. Based on the researchof Yeluda and Carasso,64 many modern alterna-tive practitioners recommend a ratio of 4:1. Thisratio of fatty acids will produce a favorable production of the friendly prostaglandins, series1 and series 3, and a limited amount of theunfriendly series 2 prostaglandins. Overall, wewant to reduce omega-6 fats and increase omega-3 fats in our diet. Increasing dietary fish, flaxseed,and walnuts and decreasing saturated fats willhelp to improve this ratio.

The eicosanoids from eicosapentaenoic acidare also associated with cardioprotective effects.EPA has been shown, in particular, to decreasesystolic blood pressure, in part due to its effectson intracellular sodium transport,65 while doca-hexaenoic acid has been shown to increaseHDL.66 In animal studies, dietary fish oil hasbeen shown to improve vascular function anddecrease oxidative stress.67

Fish oils contain EPA and DHA. Cold-waterfish such as salmon, tuna, mackerel, herring, andhalibut in particular are excellent sources ofomega-3 fatty acids. Fish oils prevent clots,inhibit inflammation in the vessel walls, causevasodilation, and promote a regular cardiacrhythm. Similar to aspirin, fish oils block theproduction of thromboxane A2, which is apotent vasoconstrictor and promoter of the stick-iness of blood.68 Fish oils may also lower bloodpressure and triglycerides, but they may raiseLDL.69–71 Other studies show that fish oils lowertotal cholesterol, LDL and triglycerides, whileincreasing HDL.72 In a large study of male physi-cians, those who ate fish at least once per weekhad a 52 percent lower risk of sudden cardiacdeath.73 Fish oils with a seed oil of alpha-linolenic acid and vitamin E have also beenshown to reduce the inflammatory marker C-reactive protein (CRP), associated with cardio-


vascular disease.74–79 Norwegian researchers con-cluded that eating fish like mackerel, herring, andsalmon will significantly reduce the risk of heartdisease. As little as one serving of 300 grams of fishper week will provide the benefit. They suggestedthat the minimal dietary requirement for EPA andDHA should be about 200 mg per day.80

Keep in mind that fish oil has anticoagulationeffects that may act synergistically with medica-tions like warfarin, and therefore caution shouldbe exercised in supplementing with fish oil inpeople who are taking these medications.81

Lipid-lowering medication was found to decreasebeneficial omega-3 fatty acids and increase path-ogenic arachidonic acid after only three monthsof use, leading the authors to conclude that thesemedications should be combined with diets low

in arachidonic acid and high in omega-3 fattyacid.82 Fish consumption not only improves lab-oratory values but also decreases evidence of car-diovascular disease at the blood vessel level interms of stenosis and other markers of atheroscle-rosis in postmenopausal women who consumedtwo or more servings of fish per week.83

Fiber. Increasing the fiber in the diet isanother vitally important nutritional habit toacquire. Fiber sources that form a gel such as psyl-lium seed or oat bran bind bile and cholesterol inthe intestines and promote their excretion. Thisaction improves the cholesterol by decreasing LDLlevels while increasing HDL levels.84 A diet highin whole grains, fruits, vegetables, and legumes isthe optimal high-fiber diet. Soluble fibers such aspectin or oat bran have the most consistent bene-ficial effects on cholesterol levels.85 Most studieson fiber have shown rather impressive lipid reduc-tions, with the higher the initial cholesterol, thegreater the benefit. One of the ways fiber helps tolower cholesterol is to increase the rate at whichfood passes through the digestive tract, therebyincreasing the loss of cholesterol in the stool. Areview of 20 scientific trials on the effect of oatproducts on cholesterol demonstrates that amodest reduction in blood cholesterol can beachieved by eating oat products daily.86 Eating onebowl of oat bran cereal or oatmeal daily (3 gramsof oat fiber) lowers the total cholesterol by 8 to 23percent. These results have been achieved in aslittle as three weeks.

A more recent study showed that dietary fiberintake is inversely correlated with several cardio-vascular disease risk factors. The highest totaldietary fiber and nonsoluble dietary fiber (morethan soluble) intakes from fruit, vegetables, andcereals were significantly associated with adecrease in a number of cardiovascular risk factors including overweight, hypertension, lipidmarkers, and homocysteine.87 Part of fiber’seffect on lipids is because these higher fiber diets are in fact diets low in cholesterol intake.88

Five Omega-6 and Omega-3 Fatty Acids to Remember

LA: Linoleic acid. An omega-6 fatty acid found invegetable oils, nuts, and seeds. Given the properconditions, the body converts LA to GLA and eventually into prostaglandin 1.

GLA: Gamma-linolenic acid. LA gets converted toGLA by enzymes in the body. Certain foods, habits,and events (saturated fat, partially hydrogenatedoils, stress, aging, drinking alcohol) disrupt thisconversion so that only 5 to 10 percent of LA getsconverted to GLA. It may be better to get GLAdirectly from evening primrose oil, black currantoil, or borage oil supplements.

ALA: Alpha-linolenic acid. This is an omega-3 fattyacid not commonly found in foods. Seven seed oilscontain some ALA, with flaxseed oil being therichest natural source. Through several biochemicalsteps, the body converts ALA to EPA and then toprostaglandin 3.

EPA and DHA: Eicosapentaenoic acid and doca-hexaenoic acid. These two omega-3 fatty acids arefound in cold-water fish oils. EPA is a buildingblock for the body to make prostaglandin 3; DHA is important for the brain, nervous system, andvision.


Another study found that soluble fiber addedsimply as a breakfast bread source was found tosignificantly decrease blood pressure and triglyc-eride and cholesterol levels in diabetic patients.89

Increased fiber intake (more than 3 grams ofcereal fiber daily or more than six servings ofwhole grains per week) is also associated withdecreased progression of coronary atherosclerosisin postmenopausal women.90

A number of large, recent epidemiologicalstudies published in medicine’s most respectedjournals found that overall, increased intake ofdietary fiber is associated with decreased cardiovas-cular disease in adults91, 92 and menopausalwomen.93, 94 Another study looked at the combi-nation of 10 mg of simvastatin and 15 grams ofpsyllium (Metamucil) and found that the combi-nation decreased LDL cholesterol better than thesame dose of medication alone and found reduc-tions comparable to 20 mg of simvastatin afterfour to eight weeks of treatment without signifi-cant changes in HDL or triglycerides.95 One studyof a very low saturated fat diet plus a cholesterol-lowering drug, compared to a diet high in plantsterols, including soy foods and high-fiber wholegrains, concluded that dietary intervention may beas effective as the medication.96 Continuing to eata diet higher in fiber as we age also provides car-dioprotection. A large study found that increasingfiber later in life can decrease risk of cardiovasculardisease in the elderly.97

Research has also shown that the sugars infruit (fructose) significantly raise blood triglyc-eride and cholesterol levels. If your triglyceridesare above 150 mg/dL, or if you have additionalsignificant risk factors for heart disease such aselevated blood pressure or diabetes, avoid toomuch fruit, fruit juice, and other simple sugars.Limit them to one serving per day. Sugar can beeaten in small amounts only if your triglyceridelevel is below 150 mg/dl. All sugars can increasetriglycerides, but a high amount of fructose, esp-cially fructose added as a sweetener, is actuallymore damaging than sucrose and glucose. It gets

even worse if you eat high-fructose corn syrup, avery common sweetener used in packaged foods.Fructose increases LDL and does not improveHDL. A recent study showed that foods with ahigh glycemic index have a negative effect onHDL levels.98

If you have elevated triglycerides, you can eatall the whole grains that you want, althoughsome diets, such as the popular Zone diet, pres-ent some provocative, controversial ideas thatmay be contrary to this.

One of the best ways to achieve a high-fiberand low-fat diet is the vegan diet. This is a vege-tarian diet in which absolutely no animal prod-ucts are consumed. Strict vegan diets, which aretypically very low in saturated fat and dietarycholesterol and high in fiber, can help maintainor achieve desirable blood levels by especiallylowering the total cholesterol and the LDL cholesterol.99

Specific fruits or vegetables may also have a par-ticular positive effect on serum lipids. Raw carrotsmay have a more potent effect on lowering choles-terol than do oat products. Eating a raw carrot atbreakfast every day for three weeks has been shownto reduce serum cholesterol by 11 percent andincrease fat excretion by 50 percent.100

Evidence also exists demonstrating thatpeople with a low intake of fruits and vegetableshave an increased risk for heart disease.101

Numerous studies have continued to show that adiet high in carotenes and flavonoids found infruits and vegetables reduces the risk of heart dis-ease and strokes.102 It is thought that the antiox-idants (C, E, carotenes, and flavonoids) found infruits and vegetables reduce the risk of cardiovas-cular disease by scavenging free radical species.The antioxidants protect the unsaturated fattyacids from peroxidation, thus preventing athero-sclerosis. Lipid peroxide concentrations are infact higher in individuals with atherosclerosis.103

Good dietary sources of carotenes as well as vita-mins C and E are green leafy vegetables, yellow-orange fruits and vegetables, red and purple


fruits and vegetables, legumes, grains, and seeds.Good dietary sources of flavonoids are citrusfruits, berries, onions, parsley, legumes, green tea,and red wine.

Soy. Soy foods contain a group of non-steroidal plant chemicals called phytoestrogens.These compounds are similar in their chemicalstructure to estradiol, and to equol, a phytoestro-gen metabolite, but they are not actually estro-gens. Phytoestrogens are categorized into threemain classes: isoflavones, lignans, and coumes-tans. Isoflavones contribute significantly to ourdietary phytoestrogen intake. Isoflavones arefound in legumes and are highest in soybeans.These isoflavones are associated with the proteinpart of the soybeans and are not found in soy oilsor soy lecithin.

One potential dietary influence for a choles-terol-lowering strategy is to consume more soyprotein. This is perhaps my favorite recommenda-tion to women because soy also offers many otherpotential benefits, including mild reduction ofmenopausal symptoms and potentially reductionin the risk of breast cancer and uterine cancer.Observations in large Asian populations, whosediet includes soybeans as a basic food group, showa lower incidence of CVD than in populationswho consume a traditional Western diet.104

Much research has been done on soy and itsrelationship to blood pressure, cholesterol, andeven some inflammatory biomarkers of cardio-vascular disease. In general, the studies are varied,with some showing clear benefit and some notshowing any. Perhaps the best evidence comesfrom a review of 38 scientific studies. This meta-analysis concluded that consumption of soy pro-tein rather than animal protein significantlydecreased serum concentrations of total choles-terol, LDL cholesterol, and triglycerides.105

The use of soy for menopausal symptoms andheart disease protection continues to receivegreat interest from women, practitioners, and sci-entists. Most recently, a large meta-analysis of

studies published from 1966 to 2005 found thatsoy protein intake was significantly related todecreased total and LDL cholesterol and trigly-cerides and increased HDL.106 Other studies ofpre- and postmenopausal women found that soyis beneficial for improving lipid parameters,107, 108

with even more favorable effects in type 2 diabetic women with hyperlipidemia,109 decreas-ing lipid peroxidation better than estrogen,110

improving platelet function,111 decreasing homo-cysteine,112 and working synergistically withstatins to achieve favorable cholesterol levels.113

New research states consuming 25 grams of soyprotein (containing 50 mg of isoflavonoids) dailyfor five weeks may decrease systolic blood pres-sure by nearly 6 percent.114

There are many other positive soy studies, too numerous to list here, but to be fair, let’s talkabout those soy studies that have not showed lipid-lowering effects. A recent study looked at daily soyconsumption in the form of a 50-mg isoflavone barand found no significant change in lipids, exceptan increase in HDL, when consumed for eightweeks. The isoflavone-enriched bar did improve C-reactive protein (CRP), a marker of inflamma-tion that mediates the initiation and progression of atherosclerotic plaque lesions, but had no sig-nificant effect on other plasma inflammatorymarkers.115 A controlled trial of 202 healthy post-menopausal women aged 60 to 75 concluded thatthe use of a soy protein supplement containingisoflavones did not improve plasma lipids whenstarted at age 60 or older.116 A 2006 review articleconcluded that the evidence for soy lowering cholesterol was not overwhelmingly impressive.117

Interestingly, when soy intake (30 grams ofsoy, including 4 grams of phytosterols) was stud-ied in the setting of a low glycemic index diet (a diet that does not raise blood sugar levelsquickly), it demonstrated more improvement inlipid parameters than the standard AmericanHeart Association Diet.118 It may in fact be thatsoy is most effective as part of an overall healthydiet and lifestyle plan. Substituting soy protein


for animal protein increases the variety of nutri-ent intake and adds fiber, monounsaturated fats,minerals, and antioxidants while avoiding thesaturated fats found in animal protein. Otherstudies have found that supplementing the dietwith a soy protein and soy fiber lowers LDL andtotal cholesterol119 and that eating any legumes,including soy, at least four times per week canlower the risk of cardiovascular disease.120

Despite the lack of effect in some studies on soy and lipids, when we look at the role of soyin other aspects important to women’s health—reducing the incidence and severity of hotflashes, loss of bone mass, vaginal dryness, andfemale-related cancers—the most convincingeffects of soy are in fact in the area of its actionon lipids. The North American Menopause Soci-ety seems to agree with this perspective in a 2000consensus opinion.121

With many good reasons for women to eatsoy, blood pressure may be another area of bene-fit. New research states that consuming about 25grams per day of soy protein can decrease bloodpressure.114, 122–124

Good Carbs, Bad Carbs. It seems we all lovecarbohydrates. Complex carbohydrates, such asfound in brown rice, whole wheat, rye, oats,barley, millet, whole fruits, and vegetables arehigh in both fiber and vitamin content and there-fore the preferred form of carbohydrates. Refinedcarbohydrates, on the other hand, must be placedin the group of unhealthy foods. Sugar, a refinedcarbohydrate, is a significant factor in the devel-opment of atherosclerosis.125

High-sugar diets lead to elevations in trigly-cerides and cholesterol and also to an increase ininsulin production. Elevations in insulin levelsare associated with risk of cardiovascular diseaseby increasing cholesterol, triglycerides, and bloodpressure. The prudent woman would decrease allsources of refined sugar in the diet by avoidingcandies, pastries, and desserts; she would alsoavoid sweetened cereals, white breads, or any

food containing refined carbohydrates. Decreas-ing the total carbohydrate intake in favor ofincreased protein may be advisable as well. Arecent study of women found that weight loss ofas little as 5 percent with a plan that includeddecreased carbohydrates and increased exerciselead to a decrease in the ability of LDL choles-terol to cause atherosclerosis.126 Of course, thiswould presume the carbohydrates left in the dietto be complex and not refined.

If your triglycerides are above 150 mg/dL, or ifyou have additional significant risk factors for heartdisease such as elevated blood pressure or diabetes,limit fruit, fruit juice, and other simple sugars toone serving per day. Sugar can be eaten in smallamounts only if your triglyceride level is below 150mg/dl. All sugars can increase triglycerides, butfructose is actually more damaging than sucroseand glucose. It gets even worse if you eat high-fruc-tose corn syrup, a very common sweetener used inpackaged foods. Fructose increases LDL and doesnot improve HDL. A recent study showed thatfoods with a high glycemic index have a negativeeffect on HDL levels.98

Foods with a high glycemic index are thosefoods that raise blood sugar levels quickly. Thesefoods include items such as white bread, refinedcereals, white rice, and white flour pasta. Thesefoods greatly stress blood sugar control and cause arapid rise in blood sugar. In response, the bodysecretes insulin from the pancreas. Over time, toomuch insulin is secreted, called hyperinsulinemia,and the body tissues become resistant to theinsulin. These two consequences of a high glycemicindex diet can promote the growth of cancer andincrease the risk of heart disease and diabetes.

Reading labels on packaged foods is a goodstrategy for reducing intake of refined sugars. Anylabel that says sucrose, glucose, maltose, lactose,fructose, sugar, corn syrup, or white grape juiceconcentrate is a source of added dietary sugar.

Salt. With all this talk of lowering cholesteroland improving the cholesterol ratios, it is easy to


forget how important it is to balance the bloodpressure and how foods may have a positive or anegative effect on this. For example, a diet low inpotassium and high in sodium is associated withhigh blood pressure. By contrast, a diet high inpotassium and low in sodium can protect againstelevation of blood pressure.127, 128 It has becomecommon knowledge that too much salt in ourdiet may contribute to high blood pressure. Notso commonly known is that high blood pressureis also related to too little potassium in our diet.In fact, restricting salt alone may not be enoughto lower the blood pressure. Potassium must beincreased. Most Americans ingest twice as muchsodium as potassium. Nutrition researchers rec-ommend a 5:1 potassium-to-sodium ratio that iseasily accomplished by a diet high in fresh fruitsand vegetables, which are rich in potassium.

Dietary recommendations in the treatment of hypertension were evaluated by the federalgovernment in the Dietary Approaches to StopHypertension (DASH) studies. The DASH dietis high in fruits, vegetables, and low-fat dairyfoods and low in saturated and total fats. It isalso low in cholesterol but high in fiber, potas-sium, calcium, and magnesium. The DASHdiet, along with a sodium intake of less than2,400 mg per day, results in significantly lowerblood pressures—systolic pressure that is 7points lower in patients without hypertensionand 11.5 points lower in those with hyperten-sion.129 The characteristics of the DASH diet aredescribed in Table 9.3.

Caffeine. The peer pressure to become acoffee drinker is no greater than the conflictingevidence around the health impact of coffee.Some studies say it raises cholesterol; some donot. Some say caffeinated coffee is the problembut decaffeinated is not; others show no differ-ence between the two. There is no one consistentanswer on the effect of coffee on heart disease.What does seem to be true is that caffeinatedcoffee drinkers also drink more alcohol, consume

more dietary saturated fats and cholesterol, aremore likely to be smokers, and are less likely tobe current exercisers.130

I encourage all my patients to decrease theircoffee intake to not more than one regular coffeedrink per day. Using any stimulant to falsely raiseenergy and obscure the fact that we are tired orstressed or just plain doing too much in our livesdoes not seem consistent with respecting ourbodies’ normal rhythms. For women who haveelevated cholesterol, elevated blood pressure, orgenerally higher risks for heart disease, thenumber of studies that do show a connectionbetween coffee and hyperlipidemia, hyperten-sion, and coronary heart disease seem to deliveran obvious message: just say no.

In hypertensive individuals, the use of caf-feinated beverages is questionable. Two studiesshowed slight elevations in blood pressure or apotentiation of the stress-related rise in bloodpressure in hypertension-prone males. In a thirdstudy, caffeine (75 mg per day) had no effect onthe blood pressure of young, healthy subjects.131

In a recent study, caffeine consumption was notfound to be related to the incidence of hyperten-sion but consumption of cola was.132

Caffeine also appears to have adverse effectson serum lipid profiles. In men, coffee intakeinduced higher levels of cholesterol.133, 134 More-over, when men with elevated cholesterol levelsrefrained from coffee for five weeks, their serumcholesterol dropped by 10 percent. Those whocontinued to abstain from coffee showed a 13percent average drop at ten weeks, and those whoreturned to coffee gradually reached prestudylevels of total cholesterol.135 In women, choles-terol levels increased with increasing amounts ofcoffee with a low of 214 mg/dL at one-half toone cup per day and a high of 234 mg/dL at fourcups per day.136 Almost all of the difference wasdue to an increase in low-density lipoproteincholesterol. Cholesterol was not affected bydecaffeinated coffee in this study.


Table 9.3 The DASH Diet—Basic Components (2,000 calories per day)

Food Daily Serving SignificanceGroup Servings Sizes Examples of Food

Grains and 7–8 1 slice bread Whole wheat bread, Sources of energygrain products 1⁄2 cup dry cereal whole-grain cereal, and fiber

1⁄2 cup cooked rice, oats, gritspasta, or cereal

Vegetables 4–5 1 cup raw leafy Tomatoes, potatoes, Sources ofvegetables carrots, peas, squash, potassium,

1⁄2 cup cooked broccoli, turnip greens, magnesium,vegetables collards, kale, spinach, fiber, flavonoids,

6 oz veggie juice artichokes, beans, antioxidantssweet potatoes

Fruits 4–5 6 oz fruit juice Apricots, bananas, Sources1 medium fruit dates, oranges or juice, of potassium,1⁄2 cup dried fruit grapefruit or juice, magnesium, fiber,1⁄2 cup fresh, frozen, mangoes, melons, flavonoids,

or canned fruit peaches, pineapples, antioxidantsprunes, rasisins,strawberries,tangerines

Low-fat or 2–3 8 oz milk Skim or 1% milk; Sources ofnonfat 1 cup yogurt nonfat or low-fat calcium, proteindairy foods 1.5 oz cheese yogurt, buttermilk,

and cheese; part-skimmozzarella cheese

Meat, including 2 or 3 oz cooked meat, Select lean; trim away Sources ofpoultry and fish fewer poultry, or fish visible fats; broil, roast, protein and

or boil instead of frying; magnesiumremove skin frompoultry

Nuts, seeds, 4–5 1.5 oz or 1⁄3 cup nuts Almonds, filberts, Sources of energy,legumes per 1⁄2 oz or 2 tbs seeds mixed nuts, peanuts, protein, fiber,

week 1⁄2 cup cooked walnuts, sunflower magnesium, proteinlegumes seeds, kidney beans,

lentils

There are multiple reasons that coffee has thiseffect on serum cholesterol. Unfiltered coffee inparticular137, 138 increases coronary artery diseaserisk and mortality in men and women.138, 139

This effect is possibly explained by the presenceof the diterpines (removed by filtering), cafestol,

and possibly kahweol in unfiltered coffee.Another explanation came to light in a recentlypublished Norwegian study140 that indicated adose-response between coffee consumption andblood homocysteine levels: the larger the coffeeintake, the greater the homocysteine levels.


Homocysteine is formed during the breakdownof certain amino acids and is known to increasethe risk of heart disease when it accumulates inthe blood.

Alcohol. Many sweeping statements have beenmade about the benefits of alcohol in preventingheart disease. If we look at the connections be-tween heart disease and alcohol more closely, wefind that these general statements are in fact para-doxical and can be misleading. Heavy use of alco-hol causes damage to the heart muscle and is alsorelated to high blood pressure, strokes, and ar-rhythmias (irregular heartbeats). On the otherhand, people who abstain from alcohol, whencompared to those who drink, are at greater risk ofmajor heart disease events such as heart attacks. Tounderstand the alcohol-heart connection, it is im-portant to distinguish between light, moderate, orheavy alcohol use. A working definition is helpful:Heavy use is three or more drinks per day. One totwo drinks per day is low to moderate, and lightwould be something less than one daily drink.

There is now strong evidence that light tomoderate alcohol consumption protects againstheart disease. Low to moderate alcohol intake,one drink per day, may reduce the risk of cardio-vascular disease.141 In the Nurse’s Health Study,one drink per day reduced the risk of heart dis-ease by 40 percent.141, 142 Another study reportedthat women who had one drink per day had a 30to 40 percent lower risk of all cardiovascular diseases as well as a lower death rate than heavydrinkers and very light drinkers.143 And morerecently, consumption of 15 grams (one drink) to30 grams (two drinks) of alcohol per day by post-menopausal women was shown to improve lipidprofiles and therefore decreased their cardiovas-cular disease risk.144 Alcohol tends to raise HDLcholesterol, which likely contributes to its cardio-protectiveness. Alcohol also has a beneficial effecton decreasing blood clotting.

It is not clear whether there are any signifi-cant differences between red wine, white wine,

liquor, and beer. However, researchers haveobserved the “French paradox”: in France, satu-rated fat intake and mean cholesterol levels arehigh, but heart disease mortality is low. Widepublicity about this paradox has asserted that red wine consumption in France is high and isresponsible for the unexpected results. As a con-sequence, a general perception exists that redwine is especially beneficial. Nonalcoholic ingre-dients in the red wine may in fact be responsiblefor this benefit, including antioxidants and flavo-noids, namely the antioxidants in red grapes thatprevent the oxidation of LDL cholesterol.

Alcohol ingestion, however, harbors potentialdangers that may outweigh its alleged benefits. In my opinion, daily ingestion of alcohol cannot be responsibly recommended to women. Well-documented evidence indicates that alcohol mayincrease serum estradiol by 300 percent in post-menopausal women who take hormone replace-ment.145 Alcohol also increases the incidence of breast cancer,146–148 osteoporosis,149 depres-sion,150 pancreatitis, liver cirrhosis, gastritis, degen-erative nervous system conditions, fetus damage,substance abuse, and cancers of the mouth, phar-ynx, larynx, esophagus, and liver.151 These, and theharmful cardiovascular consequences of heavydrinking, add up to considerable increase in diseaseand death.

From a medical perspective, all heavydrinkers should reduce their intake. It is myopinion that moderate drinkers should alsoreduce to light intake, and in individual cases,abstinence (those with breast cancer, those with ahistory of substance abuse, possibly those takinghormone replacement therapy, and maybeothers). Daily alcohol probably does not belongin a healthful life. Stick to the occasional celebra-tions, and utilize other methods of reducing yourrisk of cardiovascular disease.

Chocolate. It has been hypothesized forsome time that chocolate can reduce the risk ofcardiovascular disease. High levels of antioxi-


dants, including stearic acid and flavonoidscalled procyanidins, catechins, and epicatechins,are found not only in chocolate but also in tea,red wine, and various fruits and vegetables.Cocoa is particularly rich in these flavonoids. It isthought that the flavonoids reduce leukotrienes,potent vasoconstrictors, and contain prostacy-clins that vasodilate and inhibit blood stickiness.

This benefit is only found in dark chocolate,however. Milk chocolate binds to the antioxi-dants in chocolate and makes them unavailable.It is also higher in fat content. Dark chocolate,with 70 percent cocoa or more, also known asbittersweet or semisweet chocolate, contains littleor no added sugar and is made from cocoa butter,which has a neutral or even beneficial effect oncholesterol. Dark chocolate is also made withoutthe use of hydrogenated or partially hydro-genated oils, which have a negative impact oncholesterol.

Dark chocolate decreases LDL cholesterol oxi-dation, reduces the risk of blood clots, increasesblood flow in arteries, and may even lower bloodpressure. It may or may not have a beneficial effecton cholesterol levels. According to laboratoryexperiments and randomized trials, the suggestionis that the flavonoids in chocolate are likely protec-tive against death from cardiovascular disease.152 Itis thought that eating 50 grams (about one two-ounce bar) of dark chocolate per day may reduceone’s risk of CVD by 10.5 percent.153

Heart-Healthy Diets. There are a number ofdiet recommendations that utilize nutritionalbenefits to improve and maintain cardiovascularhealth. The following are some of the mostrespected, well-known, and effective cardiovascu-lar diets.

The Step 1 and Step 2 Cholesterol-LoweringDiets. The Step 1 and Step 2 diets were created bythe National Heart, Lung, and Blood Association’sNational Cholesterol Education Program (NCEP)and have been endorsed by the American HeartAssociation (AHA). These diets were designed to

reduce the risk of cardiovascular disease by focusingon reducing elevated cholesterol levels.

The Step 1 diet advises to reduce total fatintake to less than 30 percent of daily calories,with 8 to 10 percent of calories coming from sat-urated fats. Polyunsaturated fats should compriseless than 10 percent of daily calories. Monoun-saturated fats (olive oil, avocados, soy) should belimited to less than 15 percent of total calories.The intake of cholesterol should be less than 300mg per day. Protein should be about 15 percentof total calories, and total calorie intake shouldbe determined based on what amount wouldhelp to maintain normal body weight.

The stricter Step 2 diet requires greater disci-pline and perhaps the guidance of a dietician/nutritionist. Step 2 differs from Step 1 in that lessthan 7 percent of daily calories comes from satu-rated fats and cholesterol intake is limited to lessthan 200 mg.

If you have a diet that differs from the Step 1diet, and you have hyperlipidemia, then startwith this diet. If you are already following theStep 1 diet, or a similar diet, and your cholesterolis still abnormal, especially an elevated LDL,then you should start the Step 2 diet. In eithercase, a lipid panel test should be done after threemonths of the diet.

In general, a Step 1 diet typically reduces thetotal cholesterol by 5 to 7 percent. The Step 2 diettypically drops the level of LDL another 3 to 7 per-cent. The dietary changes, along with an exerciseprogram designed to reduce weight, should be donein women who are overweight. Even a small weightloss of 5 to 10 pounds has been associated with agreater reduction in LDL cholesterol than just theStep 1 diet and no weight loss. Weight loss alsoresults in raising HDL-cholesterol levels, loweringtriglycerides levels, and lowering blood pressure.154

The TLC Diet. In 2001, the National Choles-terol Education Program released new guidelinesfor the management of cholesterol in the “ThirdReport of the Expert Panel on Detection, Evalu-


ation, and Treatment of High Blood Cholesterolin Adults, Adult Treatment Panel III (ATP).” TheAmerican Heart Association has adopted theNCEP III guidelines, calling for more intensivelife-habit interventions to lower cholesterol andreduce the risk for heart disease and of heartattacks. They call this the Therapeutic LifestyleChanges (TLC) diet. Its target is to lower LDLcholesterol. See the following sidebar for the rec-ommendations of the TLC diet.

AHA Recommendations. The American HeartAssociation dietary recommendations are designedto reduce high cholesterol, high blood pressure,and excess weight. These are the dietary guidelines:

• Eat a variety of fruits and vegetables. Choosefive or more servings per day.

• Eat a variety of grain products, includingwhole grains. Choose six or more servingsper day.

• Include fat-free and low-fat milk products,fish, legumes (beans), skinless poultry, andlean meats.

• Choose fats with 2 grams or less of saturatedfat per serving, such as liquid and tub mar-garines, canola oil, and olive oil.

• Balance the number of calories you eat withthe number you use each day. (To find thatnumber, multiply the number of poundsyou weigh now by 15 calories. This repre-sents the average number of calories used inone day if you’re moderately active. If youget very little exercise, multiply your weightby 13 instead of 15. Less-active people burnfewer calories.)

• Maintain a level of physical activity thatkeeps you fit and matches the number ofcalories you eat. Walk or do other activitiesfor at least 30 minutes on most days. To loseweight, do enough activity to use up morecalories than you eat every day.

• Limit your intake of foods high in caloriesor low in nutrition, including foods like softdrinks and candy that have a lot of sugars.

• Limit foods high in saturated fat, trans fat,and/or cholesterol, such as full-fat milkproducts, fatty meats, tropical oils, partiallyhydrogenated vegetable oils, and egg yolks.Instead choose foods low in saturated fat,trans fat, and cholesterol.

• Eat less than 6 grams of salt per day (2,400mg of sodium).

Therapeutic Lifestyle Changes (TLC) Diet

Limits for LDL-Raising Nutrients

Saturated fats Less than 7% of totalcalories

Trans fats Minimal or noneDietary cholesterol Less than 200 mg per day

Therapeutic Options for Lowering LDL

Plant stanols/sterols 2 g per daySoluble fiber 10–25 g per dayTotal calories Adjust total calorie intake

to maintain desirablebody weight

Physical activity Include enough moderateexercise to expend at least200 calories per day

Recommendations for Nutrient Intake

Percentage of Nutrient Total Calories

Total fat 25–35%*Saturated fat Less than 7%Polyunsaturated fat Up to 10%Monounsaturated fat Up to 20%Carbohydrates** 50–60%Protein Approximately 15%

(including soy protein)

*Range of percentages for total fat allows for increasedintake of unsaturated fat in place of carbohydrates in peoplewith metabolic syndrome or diabetes.**Carbohydrates should be mainly from foods rich in complexcarbohydrates and fiber, including whole grains, legumes,fruits, and vegetables.


• Have no more than one alcoholic drink perday.

Not all low-fat diets have provided cardiovas-cular prevention. In the Women’s Health Initiativedietary modification trial, 48,835 postmenopausalwomen aged 50 to 79 years were randomlyassigned to an intervention of intensive behaviormodification to reduce total fat intake to 20 per-cent of calories and increase intakes of vegetablesand fruits to five servings per day and grains to atleast six servings per day.155 After an average of 8.1years, this diet did not significantly reduce the riskof CAD, stroke, or CVD in postmenopausalwomen and achieved very modest effects on CVDrisk factors. What this tells me is that an evenmore rigorous diet and lifestyle changes need to beachieved in order to improve risk factors andreduce CVD risk.

The Mediterranean Diet. The Mediterraneandiet, perhaps one of the healthiest diets in theworld, emphasizes increased fiber, olive oil, fruits,vegetables, grains, and legumes and decreasedrefined cereals, meat products, eggs, and saturatedfats. This diet has been shown to have a beneficialeffect on cardiovascular health in a number oflarge studies.156 The Mediterranean diet has alsobeen shown to have beneficial effects on risk fac-tors for cardiovascular disease and may evenexceed that of the low-fat diet. Compared with alow-fat diet, three months on a Mediterraneandiet that included olive oil (one liter per week) orpackets of walnuts, hazelnuts, and almondsdecreased cardiovascular risk factors.157 Both ofthese diets were associated with significant reduc-tions in blood pressure, lower fasting glucoselevels, lower insulin levels in those without dia-betes, lower triglycerides, increased HDL-C, andlower C-reactive protein levels.

Ornish Lifestyle Modification Program. Thelow-fat diet has been promoted by Dr. DeanOrnish since the publication of his bestsellingbook Dr. Dean Ornish’s Program for Reversing

Heart Disease. What is now known as the OrnishLifestyle Modification Program is based on thefollowing four components:

1. A very low-fat, high complex carbohydratediet rich in fruits, vegetables, whole grains,beans, and legumes

2. Regular exercise3. Stress management4. Family/community support systems to

maintain healthy behavior

The main focus is a plant food–based dietcontaining whole fruits and vegetables, wholegrains (brown rice, whole wheat breads, whole-grain cereals, whole wheat pasta), dried beansand legumes, soy products, lean poultry, fish, eggwhites, and nonfat dairy. Plant oils are to be usedonly lightly, and red meat, butter, and animal fatsare to be avoided, as are processed foods, high-fatfoods, sweets, and caffeinated drinks. Alcoholand salt are to be consumed in moderation. TheOrnish Lifestyle Modification Program claims topromote weight loss, improve cardiovascularhealth, help to regulate blood sugar and insulin,and lower cholesterol levels.

Whether it is the TLC diet, the Step 1 or Step2 diet, the Mediterranean diet, or the Ornishdiet, they all offer a great step toward reducingthe risk of heart disease. One might be moresuited to you over the other. Consider readingmore about each, experimenting, or speakingwith your health-care practitioner and/or a qual-ified nutritionist to determine which approach isbest for you.


Although dietary changes alone can have a pow-erful effect in reducing the incidence of heart disease, they may not be enough for everyone.Lowering cholesterol, lowering blood pressure,inhibiting blood clots, preventing oxidativedamage to the vessel walls, and several othermechanisms are all effects that can be achievedwith the therapeutic use of nutritional/herbal


supplements. This is an exciting and successfularea for alternative medicine to make an impacton a large segment of the population. Given thatheart disease is the number-one cause of death inmen and women in America, these conceptsdeserve the attention and respect of individualsand practitioners of all disciplines and all schoolsof thought.

Antioxidant Combinations. Combinationnutritional supplements are difficult to evaluatebecause of the multi-ingredient combinations andthe different doses of each single ingredient fromone product to another. Numerous observationalstudies have, however, evaluated the effect ofantioxidant combinations on cardiovascularevents.158–161 In one study, vitamins C and Ereduced coronary death and death due to all causesin elderly patients.158 In another, an antioxidantsupplement significantly lowered risk for myocar-dial infarction (heart attack) in men and womenover 55.159 A Finnish study showed no significanteffect of an antioxidant supplement on death dueto coronary artery events;161 however, only 3 per-cent of the people actually used an antioxidant sup-plement. In the very large U.S. observational studyof more than 1 million men and women,160 therewere modest reductions in CVD deaths amongwomen using antioxidants supplements who hadno previous history of CVD.

Prevention trials with antioxidant combina-tions have unfortunately not produced hoped-forresults. In the Heart Protection Study, a combina-tion of vitamin C, vitamin E, and beta-caroteneappeared to cause no difference in either deathrates due to any cause, heart disease–relateddeaths, heart disease events, or vascular events ofany kind.162 Other quality studies of an antioxi-dant supplement for secondary prevention ofCVD (people who already had evidence of heartdisease or had a previous cardiac event) showed nosignificant effects on the rate of return of narrow-ing of a coronary artery, the rate of restenosis (areturn of narrowing of the coronary artery after

surgery), or the rate of cardiovascular events threeyears later.163–165

Major clinical trials of antioxidant use for theprimary (initial) prevention of CVD are cur-rently underway and include tens of thousands ofparticipants. In the near future, with an adequateamount of high-quality scientific data, we hopeto gain greater clarity as to the impact of antiox-idant combination products and multivitamincombinations on cardiovascular disease.

Vitamin E. In the past, I went so far as to saythat of all the vitamins or minerals, vitamin E mayoffer the greatest protection for women againstheart disease because of its ability to be easilyincorporated into the LDL-cholesterol moleculeand prevent free radical damage and, as a result,prevent atherosclerosis and CAD.166 A number ofclinical trials have shown that vitamin E supple-mentation (alone or in combination with otherantioxidants) leads to increased resistance of LDLto oxidative damage.167, 168 Doses between 500and 1,500 IU have shown significant reduction inLDL oxidation.169 Women who took vitamin Esupplements for more than two years had abouthalf the risk of CVD.170 A recent study evaluatingchildhood and adulthood dietary intake of vita-min E found that people who consumed the mostvitamin E in their diet had a decreased risk ofhypertension.171

The New England Journal of Medicine pub-lished a report showing that women who took atleast 100 IU of vitamin E per day for several yearshad 40 percent decreased likelihood of having a coronary event when compared with non-vitamin E users.172 Continued research has nowdemonstrated that doses between 400 and 800IU per day dramatically reduce the risk of nonfa-tal heart attacks, but do not reduce the numberof deaths from CAD.173 Doses of 400 to 1,000IU per day provide additional cardiovascularbenefit by inhibiting platelet aggregation,increasing HDL-cholesterol, and stimulating thebreakdown of fibrin (a clot-forming protein).


Levels of vitamin E in the blood may be moredirectly related to the development of a heartattack or stroke than are total cholesterol levels.Whereas high blood pressure was predictive of aheart attack 25 percent of the time, and highcholesterol 29 percent of the time, low bloodlevels of vitamin E was predictive almost 70 per-cent of the time.174

There are, though, negative studies on vita-min E’s effect in cardiovascular disease. Althoughvitamin E was shown in animal studies to be beneficial for hypertension,175, 176 a human trialfound that relatively modest doses, 500 IUmixed tocopherols per day for six weeks, led toan increase in blood pressure and heart rate indiabetic patients.177 A very large study, called theHOPE trial, had a significant influence in dimin-ishing the role of vitamin E for cardioprotectionin the minds of many consumers and practition-ers. In women and men, 55 years of age or older,who were at high risk for cardiovascular disease,treatment with 400 IU vitamin E per day for anaverage of 4.5 years had no apparent effect oncardiovascular outcomes.178 The HOPE-TOOtrial was extended for another four years andstudied men and women at least 55 years oldwho had vascular disease or diabetes.179 Again,there were no differences in the main cardiovas-cular outcome between those who took vitaminE and those who took the placebo. In essence,there was no significant effect of vitamin E onmyocardial infarction (MI), stroke, cardiovascu-lar death, unstable angina, or total death rate. Infact, investigators observed an increase in heartfailure rates in patients assigned to the vitamin E.It is not known whether this was due to chanceor whether the alpha-tocopherol form of vitaminE became a pro-oxidant in these patients withsignificant disease.

One of the most damaging reports on vita-min E was a meta-analysis on high-dosage vita-min E that compiled the results of 19 studiesfrom 1966 through August 2004 to concludethat large doses of vitamin E (400 IU per day or

more) may increase death rates, at least in thosepeople with chronic illnesses.180 It is importantto point out that this type of analysis has seriousflaws. To summarize an insightful commentarywritten by a well-known clinician, Allan Gaby,M.D., for the Emerson Ecologics website (emersonecologics.com), in these different studies,patients were randomly assigned to take vitaminE, in doses ranging from 16.5 to 2,000 IU perday, or a placebo for at least one year. Most of thepatients had one or more chronic diseases includ-ing heart disease, diabetes, Parkinson’s disease,Alzheimer’s disease, or kidney failure. Otherswere at high risk of developing heart disease.When all 19 studies were combined, the risk ofwhat is called all-cause mortality, or death due toany cause, did not differ significantly betweenpeople assigned to vitamin E supplementationand those who were in the placebo group. Instudies using doses of vitamin E less than 400 IUper day, the vitamin E supplementation was associated with a small although not statisticallysignificant reduction in the death rate. In the 11studies using more than 400 IU per day, vitaminE supplementation increased the risk of death by4 percent.

A number of other influences may haveaffected this small but statistically significantincrease, including additional nutrient supple-mentation, serum cholesterol levels, and the highpercentage of participants with significant healthproblems such as high blood pressure, diabetes,cigarette smoking, and severe coronary artery dis-ease. There may have also been a problem in thetype of vitamin E used. (There are four differenttypes of vitamin E: alpha-, beta-, gamma-, anddelta-tocopherol, and gamma-tocopherol is themost effective as an antioxidant.)

With these flaws, and in contrast to the largebody of scientific evidence that shows the bene-fits of vitamin E in slowing the progression ofAlzheimer’s disease, treating intermittent claudi-cation, fibrocystic breast disease, premenstrualsyndrome, osteoarthritis, and more, I continue


to advise the use of vitamin E supplementation.While controversial, I am not willing to give up on the potential benefits of vitamin E and cardioprotection.

Vitamin E

400–1,000 IU per day

Vitamin C. Vitamin C is probably not amajor player in blood pressure, hyperlipidemia,or other influences on cardiovascular disease.However, vitamin C has a positive effect on thecardiovascular system and, along with folic acid and zinc, has been found to be low in theblood of hypertensive patients.181 Vitamin Cprotects LDL cholesterol from oxidation,182

raises HDL cholesterol, and lowers total choles-terol triglycerides.183 In one recent study, 500 mgof vitamin C for 10 weeks led to significantdecreases in total cholesterol and apoB, a bio-marker for cardiovascular risk.184 But a combina-tion product that included 500 mg vitamin C,160 mg bioflavonoids, 600 mg magnesium, and900 mg vitamin B complex led to decreased clotformation in adults with hyperlipidemia.185 In arecent study, 36 IU vitamin E and 250 mg vita-min C two times per day dramatically decreasedatherosclerosis in hypercholesterolemic patientsat both three and six years.186 Despite theseencouraging results, a long-term study of 500 mgvitamin C daily did not significantly affect anylipid measures except triglycerides in womenwho had high triglycerides.187

Smokers may gain a particular advantagewith vitamin C. Nicotine has been known toreduce blood vitamin C levels. An increasedintake of dietary vitamin C has been associatedwith decreased risk of cardiovascular disease insmokers,188 who are typically deficient, andintake of vitamin C supplementation was associ-

ated with decreased cardiovascular disease in aretrospective study of over 85,000 women.189

Recent long-term studies of vitamin C do notsupport its use in hypertension, however. A studyof 500 mg daily for over five years was shown tohave no effect in a group of over 400 subjects.190

Coenzyme Q10. CoQ10 can be used forhigh blood pressure control, atherosclerosis,angina, mitral valve prolapse, congestive heartfailure, and cardiomyopathy. As an antioxidant,CoQ10 protects against atherosclerosis by pre-venting the oxidation of LDL. In a recent study,150 mg CoQ10 in combination with the lipid-lowering medication fenofibrate worked betterthan drug therapy alone in improving total cho-lesterol, triglycerides, and blood pressure.191 Alarge review study showed that CoQ10 adminis-tration led to decreases in systolic and diastolicblood pressure of 16 and 10 mmHg respec-tively.192 A study using 60 mg CoQ10 twice dailyfor 12 weeks led to an average decrease in systolicblood pressure readings of nearly 18 percent.193

These findings were similar to a previous studylooking at 60 mg CoQ10 twice daily for eightweeks in patients already receiving conventionalcardiovascular treatments.194 This study alsofound decreases in blood sugar, insulin, and tri-glycerides and increases in HDL. CoQ10 may becoadministered with conventional medication toincrease duration of antihypertensive effect up totwice as long.195 Other studies of up to 600 mgper day allowed patients to decrease the dose ordiscontinue the conventional medication whiledramatically improving cardiovascular function-ing196, 197 and decreasing subsequent cardiovascu-lar events and mortality by nearly half in patientswith a prior history of MI.198 CoQ10 also workstogether with vitamin E in preventing damage tolipids and to the vessels.199

It may be that CoQ10 can benefit thosewomen who choose to take HRT and are con-cerned about the potential for increased risk ofheart disease. A recent study showed that the

Vitamin C

1,000 mg or more per day


common dose of Prempro led to a decrease inCoQ10 and vitamin E levels in the blood,thereby increasing menopausal cardiovascularrisk factors in women who use HRT.200 Use ofstatins to treat high cholesterol has been associ-ated with muscle pain and decreased exercise tol-erance that has been correlated with a reductionin CoQ10.201–204

CoQ10

50–150 mg per day

Calcium. Calcium is most well known for its effects on bone health, but it can also be usedto treat elevated cholesterol and hypertension.Calcium supplementation may produce modestreductions in blood pressure, usually only 1 or 2points. But in those whose blood pressure is verysensitive to salt intake or whose dietary intake ofcalcium is low, supplementation may be moreeffective. Calcium has been related to decreasesin systolic blood pressure,205, 206 and an analysisof 40 well-controlled studies found that calciumlowers blood pressure measurements.207 Anotherlarge review of studies of calcium for hyperten-sion in pregnancy found that higher calciumintakes were correlated to decreased blood pres-sure, as well as resultant preeclampsia anddeath208 and that the combination of calciumand linoleic acid decreases pregnancy-inducedhypertension as well.209, 210

Not all studies have shown benefit, and a largereview of three randomized controlled trials inves-tigating the combinations of magnesium, potas-sium, and calcium found no evidence that thesesupplements improved blood pressure or mortal-ity.211 Calcium probably has only a small role inlowering cholesterol, but a recent randomized con-trolled trial suggests that calcium may have a rolein decreasing cholesterol via its ability to improvethe function of bile in the liver, thereby increasingcholesterol excretion,212 and another study on 223menopausal women showed that calcium supple-mentation did decrease cholesterol slightly and

with more significant increases in HDL.213 Cal-cium carbonate 400 mg three times daily canreduce cholesterol and LDL cholesterol by about 4percent and increase HDL by 4 percent.214

While reducing cholesterol and blood pres-sure may not be calcium’s strong suits, the bene-fits to bone health, tooth retention, weight loss,PMS, and reduction in the risk of colorectalcancer make it one of our most important dietarynutrients and nutritional supplements.

Calcium

400–1,200 mg per day calcium carbonate or otherform

Magnesium. Many scientists and healthpractitioners believe that magnesium is one ofthe most important nutrients for cardiovascularprotection and treatment. Drs. Burton and BellaAltura of NY Health Science Center have donesome of the most consistent research in magne-sium over the last 30 years. They, and others,assert that magnesium contributes to thestrength of contraction of heart muscle,215

increases HDL levels,216 inhibits platelet aggrega-tion and prolongs the clotting time,217–219

decreasing the risk of heart disease, strokes, for-mation of atherosclerotic plaque, and blood clotsthat can result in heart attack or stroke.

At least 10 independent clinical studies showthat patients with hypertension exhibit serumand/or tissue hypomagnesemia. On the average,patients with long-term hypertension have atleast a 15 percent deficit in total magnesium.220

A recent review of studies showed that supple-mentation with magnesium appears to modestlydecrease blood pressure,221 yet another largereview showed no effect at all.222 Magnesium maybe more effective in decreasing blood pressure andimproving arterial function when combined withpotassium.223 Evidence from both animals andhumans suggests that magnesium levels in dietand blood may affect blood lipids; the lower themagnesium intake, the higher the serum lipid


levels. In addition, a recent study showed thatsupplementation of 600 mg daily for 12 weeksproduced improvements in all lipid parameters inboth type 1 and 2 diabetics.224, 225 There is strongevidence suggesting a relationship betweenuncontrolled type 1 and type 2 diabetes and mag-nesium deficiency,220 thus magnesium deficiencymay predispose diabetic patients to an increasedincidence of cardiovascular disease and death.

Magnesium also improves cardiac perform-ance by enhancing blood flow in the coronaryarteries. It also prevents oxidation of lipoproteinsand subsequent atherosclerosis.

Magnesium

400–1,200 mg per day in divided doses

Niacin. Niacin (nicotinic acid) has been shownto favorably affect all lipids and lipoproteins, and itcan be used either alone or in combination withother lipid-lowering agents.226 We’re not sureexactly how it works, although it likely inhibitsmobilization of free fatty acids from peripheral fattissue to the liver. As a result, niacin reduces hepaticsynthesis of very low-density lipoprotein (VLDL)and triglyceride levels. Because there is less VLDLavailable, LDL levels decrease.227

The Coronary Drug Project was the first trialto study the effect of niacin on cardiovascularendpoints.228 Niacin therapy in men with priorMI reduced the five-year incidence of nonfatalreinfarction by 27 percent. In addition, after amean follow-up of 15 years all-cause mortalitywas 11 percent lower in niacin-treated men com-pared with placebo-treated patients.229

Niacin—specifically nicotinic acid—may beused to reduce total cholesterol, TG, and LDLlevels and to raise HDL values. It is currently thebest treatment to raise HDL levels,227 and it canreduce the risk of nonfatal MI.230 Niacin lowersLDL levels by about 5 to 25 percent, TG by 20 to50 percent, lipoprotein(a) by 34 percent,231 and thetotal cholesterol/HDL ratio by 27 percent226 whileincreasing HDL levels by 15 to 35 percent.232

Niacin has been compared to several conven-tional pharmaceutical drugs used to reduce choles-terol levels. A study published in 1994 comparedniacin and lovastatin over a period of 26 weeks in136 patients who were at high risk for coronaryheart disease.233 Lovastatin produced a greatereffect on reducing LDL cholesterol, but niacin pro-vided better overall results. Niacin far exceededlovastatin in increasing HDL cholesterol, which isa more significant indicator in reducing the risk forheart disease, and some estimates suggest that itcan raise HDL by as much as 35 percent.234 Niacinhas also been found to decrease inflammatorymarkers like C-reactive protein235 and increaseadiponectin, a hormone that not only decreasesatherosclerosis but improves glucose tolerance,body mass index, and fatty liver disease.236, 237 In astudy of patients with previous history of heartattack, niacin was found to decrease the risk ofrepeat MI and death in patients with and withoutmetabolic syndrome.238

Conventional practitioners and alternativepractitioners alike acknowledge that severalgrams of niacin per day will lower total choles-terol and LDL cholesterol, raise HDL,239 anddecrease atherosclerosis both alone and whenused with conventional treatments like statins.The niacin and statins seem to act synergisticallyto improve lipid parameters at lower doses, in ashorter amount of time, and more effectivelythan when either is used alone.240–242

The major problem with the therapeuticdosage (1.5 to 3 grams per day) has to do withside effects. Flushing responses are common.Anecdotally, some clinicians decrease the effectsof niacin’s flushing by having the patient startwith a low dose, like 500 mg per day, increasingthe dose weekly to achieve the desired dose, andtaking the dose before bed or coadministeringwith 81 mg baby aspirin. More seriously, liverfunction findings can become abnormal, andindividuals with liver disease should not takeniacin. Immediate-release niacin is recom-mended, as sustained-release niacin has been


associated with severe liver toxicity in doses ofmore than 2 grams per day. Niacin can also exac-erbate elevated serum glucose levels in diabeticsand can worsen gout. Niacin in doses of morethan 1 gram per day are best taken under theguidance of a physician, with monitoring ofliver-function tests.

Niacin (Nicotinic Acid)

500 mg 1–3 times per day

Pantethine. Pantethine is the activated formof vitamin B5 (pantothenic acid) and a key com-ponent of coenzyme A (CoA). CoA plays a sig-nificant role in lipid metabolism and is involvedin the transport of fats. The cells of our bodyneed CoA to utilize fats in the form of energy.Pantethine, at the typical dose of 300 mg threetimes per day, has been shown to significantlyreduce serum triglycerides, total cholesterol, andLDL cholesterol, while also increasing HDL cho-lesterol.243, 244 This same dose was found to beeffective at decreasing adverse lipid parameters inpostmenopausal women.

Pantethine

300 mg 3 times per day

Potassium. The role of potassium in thebody crosses over into many physiological eventsthat include nerve transmission, muscle contrac-tion, enzymatic reactions, carbohydrate synthe-sis, basic cell functions, and acid-base balance.Inadequate potassium intake in the diet mightplay a role in the development of high bloodpressure, stroke, and cardiovascular disease. Inaddition to increasing the potassium foods in ourdiet, several studies now show that potassiumsupplementation can reduce blood pressure. Ithas been shown that potassium supplementationof 2.5 grams per day can lower the systolic bloodpressure an average of 12 points and diastolicblood pressure an average of 16 points.222 Potas-sium supplementation may be even more benefi-

cial in people over age 65 who often do notrespond well to antihypertensive drugs.

Potassium supplements are available by pre-scription and over the counter. The FDA restrictsthe potassium over-the-counter dose per tablet to99 mg due to potential problems with nausea,vomiting, diarrhea, and ulcers that may result fromhigher doses of the mineral. The frequency andseverity of side effects associated with potassiumsupplementation are negligible when comparedwith the frequency and severity of side effects asso-ciated with conventional antihypertensives.

Potassium dosing should be based on individ-ualized need and potassium level in the blood.The common dose for treating hypertension is48 to 90 mEquivalents daily. Drug/potassiuminteractions are possible, and a consultation withyour health-care provider should occur if you aretaking ACE inhibitors, angiotensin receptorblockers, or potassium-sparing diuretics. In addi-tion, certain drugs influence the nutrient levelsand depletion of potassium.

Decreasing sodium and increasing potassiumintake helps prevent heart disease, high bloodpressure, and strokes. The standard American diethas a poor potassium/sodium ratio; the idealpotassium-to-sodium ratio is greater than 5:1. Adiet rich in fruits and vegetables can produce amore beneficial ratio because most of these foodshave significantly greater potassium than sodium.Amongst the highest are bananas, apples, carrots,oranges, lima beans, and potatoes.

Potassium

99 mg–2.5 g per day

L-Arginine. L-arginine is an amino acidinvolved in many areas of our physiology, includ-ing the production of nitric oxide, an importantmessenger in the regulation of our blood vessels.We synthesize arginine from other substances,but dietary intake is the primary source of ourarginine levels. Arginine is the precursor of nitricoxide, a gaseous molecule involved in relaxation


of the smooth muscles of our vessels, whichresults in vessel dilation (vasodilation) and inhi-bition of blood platelets clumping together.

The key to arginine’s cardiovascular benefits isits ability to induce endothelial nitrous oxide pro-duction whereby an enzyme in the endothelium(lining) of the blood vessel, nitric oxide xynthase,catalyzes a reaction that produces nitrous oxideand ornithine. The nitric oxide diffuses into theunderlying muscle of the vessel and causes relax-ation and dilation. Nitric oxide also helps to pre-vent atherosclerosis in the vessels, along with itsdilation and clot prevention effects.

Supplementation with arginine has beenshown to increase artery dilation in normal people,people with hyperlipidemia, and in those withhypertension;245, 246 significantly improve bloodflow and function in patients with congestive heartfailure;247, 248 and in some, but not all trials,improve blood flow, vasodilation, exercise toler-ance, and quality of life in those with angina.249, 250

Therapeutic doses for cardiovascular effects seem torange from 6 to 12 grams per day. L-arginine is avery safe supplement and has been associated withonly minor problems lasting a few days, includingdiarrhea, bloating, abdominal pain, or allergic reac-tions. The exceptions are those patients with kidneyfailure or liver disease. For these patients, supple-mental arginine may not be able to be metabolizedor excreted as well and should be monitored.

L-Arginine

6–12 g per day in divided doses, 3 g at a time

L-Carnitine. L-carnitine is an amino acidfound naturally in the body. We obtain some L-carnitine from the diet in foods such as red meatsand dairy products, but our bodies also synthesizecarnitines from two other amino acids, methionineand lysine. L-carnitine has a key role in the energyproduction within our cells and is required totransport long-chain fatty acids into our cells.

Two to three grams per day of L-carnitine hasresulted in reductions in total and LDL choles-

terol in individuals with hyperlipidemia251 andalso decreased triglycerides in those with highblood pressure.252 Lipoprotein(a) levels, an inde-pendent biomarker of cardiovascular disease risk,have also been reduced with 2 grams per day ofL-carnitine, even in those with type 2 diabetes.253

In addition, some preliminary evidence suggestscarnitine may be able to attenuate the muscularside effects of statin therapy.254

Numerous other cardiovascular effects of L-carnitine are beyond the scope of this chapter,but improvement in exercise tolerance, func-tional improvement in angina, peripheral vascu-lar disease, treatment of heart failure, andreduced death rates from heart attacks are allareas of clinical effectiveness of L-carnitine.

L-Carnitine

2–3 g per day

Folic Acid, Vitamin B6, Vitamin B12. Muchresearch over the years has shown that elevatedplasma levels of homocysteine are associated with significant increases in coronary artery disease,255–257 myocardial infarction,258, 259 periph-eral occlusive disease, cerebral occlusive dis-ease,260, 261 dementia, and Alzheimer’s disease.262

Two recent meta-analyses of observational studiesconcluded that a 25 percent reduction in plasmahomocysteine concentration was associated with decreases of 11 to 16 percent in the risk ofischemic heart disease and 19 to 22 percentreduction in the risk of stroke.263, 264 Folate, vita-min B12, and vitamin B6 are inversely related tohomocysteine levels, and anyone with a nutri-tional deficiency that leads to low concentrationsof either one or more of these nutrients is atincreased risk for elevated homocysteine levels.Testing for homocysteine levels is availablethrough commonly available simple blood tests.

The first meta-analysis of the HomocysteineLowering Trialists’ Collaboration concluded thatfolic acid supplementation lowered homocysteinelevels by about 25 percent.265 The second meta-


analysis found a 23 percent reduction in homo-cysteine concentration was the maximum observedwith 800 mcg per day of folic acid.266 A 20 percentreduction was seen with 400 mcg and 13 percentwith 200 mcg per day. Due to folic acid fortifica-tion of foods in the United States, our plasmafolate concentration has increased, and subse-quently our homocysteine levels have decreased.For those of us who eat a diet fortified with folicacid in some of the foods, folic acid supplementa-tion is likely to lower homocysteine concentrationsby only about 15 percent.

Women are more responsive to the homocysteine-lowering effects of folic acid thanare men, and the Women’s Health Initiativedemonstrated that the risk of vascular disease wasstronger than the association observed in males inthe Physician’s Health Study.267 High consump-tion of foods containing folate and vitamin B6

may reduce the risk of heart attack268 in women bynearly 50 percent.269 A study of 80,000 femalenurses showed a direct link between the ingestionof these two B vitamins and reduced coronary dis-ease. The results suggested that eating more fruits,vegetables, and whole grains or obtaining thesevitamins through supplementation may be asimportant as quitting smoking, lowering choles-terol, or controlling high blood pressure in lower-ing heart disease risk. Folic acid and the loweringof homocysteine has recently been less impressiveas a heart disease prevention strategy.

Folic Acid

400 mcg–2.5 mg per day

Vitamin B6

10–25 mg per day

Vitamin B12

400–1,000 mcg per day

Essential Fatty Acids. As I discussed in thenutrition section, a diet rich in omega-3 oilsresults in a much lower risk of heart disease.

Besides changes in diet, supplementation of var-ious oils is also warranted for many individuals.The daily consumption of fish oils can signifi-cantly lower blood pressure in people with hyper-tension, and low consumption may increase theincidence of hypertension, especially in dietswith a low fish intake.270

A group of researchers at the Johns HopkinsMedical School evaluated the results of 17 clinicaltrials using fish oil supplementation and foundthat consuming 3 grams or more per day of fish oilled to reductions in blood pressure of individualswith hypertension,271 lowered systolic pressure byan average of 5.5 mm Hg, and lowered diastolicpressure by 3.5 mm Hg. The effect was found to be greater at higher blood pressures. A meta-analysis of 36 trials of fish oil supplementation andblood pressure, with an average dose of 3.6 gramsper day, showed that fish oil had a small effect inlowering blood pressure, especially in older peoplewith hypertension.272 Another meta-analysis of 31trials also showed a small but statistically signifi-cant drop in blood pressures of about 3 points /1.6points at 3.3 to 7 grams per day.273 Granted, theseare small decreases, but fish oils in conjunctionwith other nutrients, botanicals, and lifestylechanges can be used as part of a comprehensivetreatment plan to achieve a reduction in bloodpressure, stroke, and risk of coronary events.

There are numerous studies on the effect ofomega-3 fish oils and triglycerides. In a review ofhuman trials, about 4 grams per day of omega-3fatty acids from fish oil decreased serum triglyc-eride levels by 25 to 30 percent.274 Both the EPAcontent and the DHA content of fish oils havethe triglyceride-lowering effects. Among post-menopausal women, fish oil supplementation of2.4 g EPA and 1.6 g DHA per day not only lowered triglycerides by 26 percent but alsoimproved the triglyceride/HDL ratio.275

Another issue pertinent to women is that forthose who are on hormone replacement therapy,C-reactive protein (CRP) and triglycerides levelscan be higher. A recent clinical trial of 30 women


on HRT showed that 7 grams per day of fish oilsupplementation significantly decreased CRPand triglyceride levels.78

It may be most effective to supplement fish oilswith statin medications for lowering cholesterol.In one clinical controlled trial, 59 patients whoalready had coronary heart disease and hyper-triglyceridemia who were taking statins were ableto significantly lower their levels of triglyceridesand very low density lipoprotein (VLDL) whentaking the fish oil and the statin.276

Another drug/fish oil study showed that 3.36grams per day of fish oils were able to furtherdecrease the triglycerides, total cholesterol, andapolipoprotein E than just the statin alone.277

The most compelling reason to give fish oils is ifit in fact lowers heart disease. We have evidencefor this from 15 large studies of more than60,000 individuals where a decrease in deathsfrom ischemic heart disease was observed inthose who consumed fatty fish or omega-3 fattyacids.278 In one of these studies, 1 gram per day of omega-3 EFAs was associated with a 20percent decrease in total deaths, a 30 percentdecrease in cardiovascular deaths, and a 45 per-cent decrease in sudden deaths.279

Flaxseed oil, nature’s richest source of omega-3fatty acids, is the vegetable alternative to fish oil. Itcontains twice as many omega-3s and is usually lessexpensive. Flaxseed oil provides the body withalpha-linolenic acid (ALA), which it uses to makeEPA, whereas fish oil provides EPA directly. Thereis some concern that humans do not readily con-vert ALA to the EPA and DHA, and thereforeflaxseed oil would be a less efficient method ofgaining EPA and DHA. However, there are studieson supplementation with flaxseed oil that suggestprotective effects against cardiovascular disease byinhibiting the excessive clotting of blood.280 Arecent study of flaxseed’s effect on cholesterol inpostmenopausal women found decreases in LDL,triglycerides, and other lipid parameters.281

Other seed oils may also provide some posi-tive effects on lipids. For example, a black cur-

rant seed oil dose of 3 grams per day was shownto decrease LDL more than fish oil.282 A morerecent commercially available product, hempseed and hemp seed oil, may also prove to bebeneficial in the lowering of lipids, homo-cysteine, CRP, and others. Evening primrose oilrich in gamma-linolenic acid (GLA) may alsohave a role in prevention of heart disease283 bydecreasing LDL cholesterol.

Fish Oil

1 g per day of EPA and DHA2–4 g per day of EPA plus DHA may be useful in

patients with elevated triglycerides

Wild salmon ranges from 1.0–1.5 g EPA plus DHA per3 oz serving, with a little more DHA than EPA. Differ-ent species range in their EPA and DHA content. Wildsockeye salmon has approximately 600 mg DHA and430 mg EPA per 3 oz serving.

Flaxseed Oil

1 tbs per day

Evening Primrose Oil

3–4 g per day

All supplemental oils should be taken with meals.

Botanicals

Flavonoids. Flavonoids are a group of com-pounds found in many fruits, vegetables, nutsand seeds, and numerous medicinal plants. Over4,000 different flavonoids have been identified infoods and plants. Quercetin, rutin, catechin, andhesperidin are the most frequently used in medi-cine. Flavonoids inhibit the peroxidation oflipids by acting as free radical scavengers.284

Quercetin specifically has been shown to inhibitLDL oxidation.285 In addition to these directantioxidant effects, flavonoids inhibit plateletaggregation, protect vitamin E from oxidation,and chelate iron. In numerous dietary studies,flavonoids have been shown to reduce cardiovas-cular disease.286, 287


Green, oolong, and black tea are made fromthe leaves of the Camellia sinensis plant and arerich in cardioprotective flavonoids. Green tea isespecially rich in the flavonoids called catechins.These include catechin, epicatechin, epicatechingallate, epigallocatechin gallate, and proantho-cyanidins. Epigallocatechin gallate is consideredthe most significant active component of greentea. Theaflavins are the pigments found in blacktea, formed from the catechins during the fermen-tation of green tea to form black tea. Green teacatechins have been studied fairly extensively aspreventive agents for cardiovascular disease.288–290

Two recent significant studies prove the car-diovascular benefits of green tea. Taking aflavonoid-rich green tea extract (375mg) for threemonths along with a low-fat diet decreased totalcholesterol by 11.3 percent and LDL by 16.4 per-cent in men and women with mild to moderatehypercholesterolemia.291 Another study, theOhsaki study,292 found that green tea consump-tion was inversely associated with mortality due toall causes and inversely associated with cardiovas-cular disease. Compared with individuals whoconsumed less than one cup per day of green tea,those who consumed five or more cups per day

had a 16 percent lower risk of all-cause and CVDmortality during 11 years of follow-up.

Several studies have examined the potentialeffects of tea on blood pressure. While there maybe transient increases in blood pressure due tothe caffeine, regular use appears to be associatedwith lower blood pressures.293 Both green tea andoolong tea intake of 120 mL /day or more cansignificantly reduce hypertension.294 In the largepopulation-based Rotterdam Study of Dutchmen and women, the risk of heart attacks waslower in those who drank more than 375 ml (oneand a half cups) per day.295

Garlic (Allium Sativum). Garlic is popularas a lipid-lowering agent, but it has a modesteffect. While analyses have demonstrated thatgarlic can reduce total cholesterol levels by 5 to12 percent, recent reports suggest these studiesmay have been too brief to draw conclu-sions.296–298 There is great variability in researchresults, which may in part be due to the greatvariation in the potency of and the extracts ofgarlic used. Even the studies showing a positiveeffect lack long-term follow-up, standardized lab-oratory measurements, and adequate dietarycontrols. While evidence supports at least ashort-term benefit, the effect is typically a smallbut statistically significant decrease in lipid levels.Since 1975, over 32 human studies have beenpublished demonstrating the lipid-loweringeffects of garlic.299 Two meta-analyses of thesestudies indicate that one to three months oftreatment using 600 to 900 mg of garlic powdertablets reduced total serum cholesterol an averageof 9 to 12 percent and triglycerides from 8 to 27percent.300, 301 A recent study of 30 patients whoconsumed 5 grams of raw garlic for 42 days foundsignificant decreases in total and LDL cholesteroland increased HDL cholesterol. These benefitswere reversed after 42 days of no garlic.302

Garlic has also been shown to lower blood pressure slightly,303 inhibit clotting,304 and regulateheart rhythms.305, 306 Garlic is not as aggressive at

Flavonoids

Quercetin

200–400 mg 3 times per day

Citrus Bioflavonoids

1,000–6,000 mg per day

Green Tea

More than 1 cup per day, and especially more than 5cups per day or

1 capsule or more per day of green tea catechinextract

Black Tea

More than 11⁄2 cups per day


lowering serum cholesterol and triglycerides assome of the newer pharmaceuticals, but it alsodoes not have any of their side effects. For womenwith a modest elevation of cholesterol, it will pro-vide a safer and effective alternative. For womenwith severe hypercholesterolemia, appropriatedrugs may be used and later replaced by garlicwhen the desired drug effect is complete.

Garlic is not contraindicated during preg-nancy and lactation, and 800 mg per day wasfound to be a safe and effective way to decreasegestational hypertension.307

Problems with ingestion of garlic are usuallyminor. In sensitive individuals they may includeheartburn and flatulence. Some people do notappreciate the odor or taste of garlic. Odor-freeor enteric-coated products may avert these unde-sirable effects. Individuals are rarely allergic togarlic. However, people taking anticoagulantdrugs should take garlic with caution and bemonitored by a health-care practitioner.

Garlic

1 fresh raw clove of garlic per day orGarlic pill providing a minimum of 4,000 mcg allicin

daily

Ginger (Zingiber Officinale). The sameginger that is used in cooking and ginger ale has been shown to inhibit platelet aggregation(blood platelets sticking together),308 lower cholesterol,309–312 inhibit atherosclerosis,313 anddecrease blood pressure.314 Ginger stimulates the conversion of cholesterol to bile acids andincreases bile secretion, thereby lowering choles-terol by promoting its excretion and impairing itsabsorption. Most research studies have used onegram of dry powdered ginger root.

Ginger

1 g per day powdered ginger root

Globe Artichoke (Cynara Scolymus). Theleaf extract of the artichoke has been found to have

some lipid-lowering activity. One clinical trialused 1,800 mg of artichoke extract versusplacebo for six weeks for the treatment of highcholesterol levels.315 The decrease in total choles-terol values was 18.5 percent in the artichokegroup versus 8.6 percent in the placebo group.Also, LDL values fell by 22.9 percent. Forpatients with gallstones or other bile-ductobstructions, globe artichoke supplementationshould be avoided due to the choleretic activityof the extract. This product is currently availableas a nutritional supplement in the United States.

Globe Artichoke


Procyanidolic Oligomers (PCO). Extractsfrom grape seeds and the bark of the maritimepine tree are high in a group of flavonoids calledproanthocyanidins, also called procyanidins.Mixtures of proanthocyanidin molecules arereferred to as procyanidolic oligomers (PCO).These commercially prepared extracts of grapeseeds and pine bark, or PCO extracts, possesspotent antioxidant activity that is far strongerthan even vitamin E or vitamin C. In animalstudies, PCO extracts have been shown to pre-vent damage to the arterial lining, lower bloodcholesterol levels, and shrink cholesterol depositsin the arteries.316, 317 Human studies have con-firmed these findings in smokers,318 and a combi-nation of 100 mg grape seed extract and 200 mcgchromium two times daily was found to signifi-cantly decrease total and LDL cholesterol up to20 percent.319

PCO

50–300 mg per day

Gugulipid (Commiphora Mukul ). Themukul myrrh tree, native to India, Pakistan, andAfghanistan, is the source of standardizedgugulipid extract. The extract is further concen-trated to isolate compounds known as guggul-


sterones. The two guggulsterones important in the management of hyperlipidemia are Z-guggulsterone and E-guggulsterone. Gugulipidappears to prevent the oxidation of LDL and mayregulate the level of bile acids, helping the body toexcrete cholesterol. Guggulsterones are thought tobe the main active constituents responsible forthese effects. Studies have shown that gugulipidcan decrease total cholesterol levels by 11.7 per-cent, LDL by 12.5 percent, and TG by 12.0 per-cent, with no change in HDL values.320 Mostcommercial extracts are standardized to 5 percentguggulsterone content, and the typical treatmentdose is 500 mg (providing 25 mg of guggul-sterones) three times per day.321

A comprehensive review of available researchon gugulipid suggests conflicting evidence at thistime.322 When using the standardized extractpreparations, only mild abdominal discomfort isreported in a small number of people.

Gugulipid

500 mg with 25 mg guggulsterones, 3 times per day

Hawthorn (Crataegus Oxyacantha). Haw-thorn leaves, berries, and blossoms contain flavo-noids. One of these, proanthocyanidin, hasespecially good cardiovascular effect. Hawthornpreparations are modestly effective in reducingblood pressure,323 in the prevention and treat-ment of atherosclerosis, lowering cholesterol, andpreventing the oxidation of LDL.324 Hawthornpreparations improve the blood supply to theheart by dilating the coronary arteries, increasethe force of contraction of the heart muscle, andregulate cardiac rhythm.323 A very recent study of79 diabetic hypertensive patients who received1,200 mg hawthorn versus placebo for 16 weeksfound significant reductions in diastolic meas-ures, no drug-herb interactions, and only fewmild side effects.325 Two randomized control trialfound decreases in both systolic and diastolicmeasures when treatment was administered forabout three months.326, 327

Hawthorn

Choose one of the following:

Tincture (1 part herb to 5 parts alcohol): 405 mlper day

Freeze-dried berries: 1.0–1.5 g per dayFlower extract (1.8 percent vitexin or 20 percent

procyanidins): 100–250 mg per dayBerries or flowers (dried as a tea): 3–5 g of dried

herb per day

Plant Sterols/Stanols. Plant sterols are natu-rally occurring cholesterol derivatives from veg-etable oils, nuts, soy, corn, woods, and beans.The hydrogenation of plant sterols producesstanols. Sterols and stanols are often referred togenerically by the term phytosterols. Phytosterolshave a chemical structure similar to cholesterol,and the consumption of these plant sterolsreduces the absorption of cholesterol and thusreduces circulating cholesterol levels. Evenmodest additions have been found to lower totalblood cholesterol and LDL cholesterol by about10 percent.328 Sterols and stanols from a dietaryintake of plant sterols in the range of 1.5 to 2.5grams per day reduce LDL cholesterol by 8.5 to10 percent.329 A recent study found that dietaryintervention with plant sterols could reduce cho-lesterol levels by about 30 percent, or approxi-mately the same extent as one of the statin drugs,levostatin.330 Most studies have found no effectof these sterols on triglyceride levels, but someindividuals have shown effects in recent stud-ies.331–333 Sterols do not seem to lower HDLlevels.

Sterols and stanols are often added to selectedbrands of margarines, semisolid food spreads,and salad dressings. As of 2000, the FDA author-ized sterol-containing products to state that theyreduce the risk of heart disease. The lowest effec-tive dose for such a claim is 1.3 grams per day.Sterols and stanols are also available in dietarysupplements. The supplement forms of phyto-sterols are advantageous in that they do not


require refrigeration, are convenient to take, andare largely calorie free.

Dietary sterols include sitosterol, campe-sterol, and stigmasterol. Soybean oil is the prin-cipal source of sterol esters, followed by canola,sunflower, and corn oils. Sterols reduce total cho-lesterol levels and LDL cholesterol because theyare natural competitors of cholesterol absorptionand resorption.

Plant Sterols and Stanols

Average dose of 3.4 g per dayNCEP III recommends 2 g per day

Policosanol. Policosanol is a mixture of alco-hols extracted from sugar cane, wheat germ, ricebran, or beeswax. Policosanol has been used toreduce total cholesterol, LDL cholesterol, andtriglycerides and to increase HDL cholesterolbased on over 10 years of critical trials and 30 or so positive clinical trials. One recent meta-analysis of natural interventions for abnormaland elevated lipids concluded that policosanol ismore effective than plant sterols.334

However, evidence to the benefits of poli-cosanol is conflicting. In May of 2006, a random-ized controlled trial studied four different doses ofpolicosanol compared to each other and a placebogroup.335 None of the treatment groups had adecrease of LDL cholesterol of more than 10 per-cent, and no statistically significant differenceoccurred between policosanol and placebo. It maybe that combining policosanol with other lipid-lowering natural agents, and especially fish oils,will offer the most effect. Animal and humanstudies that combined 5 or 10 mg policosanolwith 1 gram omega-3 fatty acids showed adecrease in total cholesterol, triglycerides, andLDL and an increase in HDL greater than whenfish oils alone were used.336, 337 Despite this con-

flicting evidence, I still recommend policosanol inmy clinical practice due to the results I witness.

Red Yeast Rice. Red yeast rice is made fromcooked white rice fermented by the yeastMonascus purpureus, which is then sterilized anddried. Red yeast rice has been used as a dietarystaple, to make rice wine, and as a food preserva-tive and is a cholesterol-lowering agent. Themain active ingredient in red yeast rice is mona-colin K (lovastatin),338 which inhibits theenzyme that initiates the synthesis of cholesterol.Omega-3 fatty acids, isoflavones, and plantsterols in red yeast rice are likely also responsiblefor its beneficial effects on lipids. In one of theearly studies on red yeast rice (using 2.4 g/dCholestin), after 8 weeks cholesterol levels werelowered in men and women by 17 percent, LDLby 22 percent, and triglycerides by 12 percent,with HDL values unchanged.339

However, there is significant variability in qual-ity and potency of commercial red yeast rice prod-ucts. In addition, the lovastatin content in dietarysupplements of red yeast rice was lowered due tochallenges by the FDA and others. Due to legalissues, Cholestin is no longer available. There are,however, other effective red yeast rice products.

Red Yeast Rice

2.4 g per day

Additional Botanical Therapies. A vastrange of herbs have been used for decades, oreven centuries, to treat heart and vascular systemconditions. Some of these herbs are categorizedhere according to their dominant action:

Diuretics: dandelion leaf, lily of the valley, parsley

Heart tonics: broom, bugleweed, figwort, haw-thorn, lily of the valley, motherwort, night-blooming cereus

Aids to circulation: broom, cayenne, ginger,hawthorn, horse chestnut, lime flowers,mistletoe, yarrow

Policosanol

10–80 mg per day


Nervines (reduce anxiety and stress): lemonbalm, hops, lime flowers, motherwort, pas-sionflower, skullcap, valerian

Antihypertensives: rauwolfia, hawthorn, mistle-toe, garlic, yarrow, crampbark

Anti-atherosclerosis: lime flowers, hawthorn,mistletoe, yarrow

Exercise

Numerous studies show the great heart-healthbenefits of exercise.340–371 Physical exercise isassociated with a reduction in obesity, improvedbody fat distribution, a reduced risk of type 2diabetes, reduced blood pressure, and reducedcholesterol levels. In women of all ages, exercisehas been shown to reduce the risk for cardiovas-cular disease by altering CVD risk factors. Inaddition, it diminishes the stiffness of arteriesand decreases damaging plaque in blood vessels.Finally, exercise reduces the risk of arrhythmias,normalizes blood lipids, and increases insulinsensitivity. A recent study suggests that exerciseand modest diet changes can decrease cholesteroland resultant atherosclerosis comparable to cer-tain statins. Most important, by staying activewith moderate levels of physical activity, we canprevent cardiovascular disease independent ofother risk factors and improve our life expectancy.

Aerobic exercise in particular is known to raiseHDL cholesterol levels, and in women, HDLmay be the most important cholesterol issue inpredicting coronary artery disease. Williamsfound an average 0.13 mg/dL plasma HDLincrease for each additional kilometer run byfemale runners per week. Similarly, other studieshave reported modest to significant increases inHDL cholesterol following aerobic training. Inone of these studies, the increase in HDL wasmeasured at 7.6 mg/dL when exercise was com-bined with smoking cessation in women.

In addition to aerobic exercise, strength train-ing has been found to reduce CVD risk factors aswell. In one study, previously sedentary women

performed 12 resistance exercises for one hour,three times per week. After five months of exercise,they showed decreases of 13 and 14 points in totalcholesterol and low-density lipoprotein cholesterol(LDL), respectively, from baseline values. Anotherstudy noted that previously hypertensive adoles-cents who reduced their blood pressure by aerobicexercise were able to maintain blood pressure con-trol by taking weight-lifting exercise after discon-tinuing aerobic exercise. These results are evenmore surprising when one considers the lack ofeffect noted for aerobic exercise in plasma total andLDL and triglycerides in women.

The type of exercise chosen appears less signif-icant than its intensity or duration on its effects onCVD risk factors. Exercise recommendations havechanged over the years and will likely continue tochange with time. Public health recommendationsvary by organization. I recommend engaging in 40 to 60 minutes of moderate-intensity physicalactivity such as brisk walking on most days of theweek or at a vigorous intensity for 20 minutes perday. It should be noted here that the effects ofexercise on CVD risk factors are not permanent.Code and colleagues found that, in both men andwomen, the effects of exercise on blood pressuredisappeared within weeks after the return to asedentary lifestyle.

Benefits of Exercise

Exercise:

1. Normalizes blood lipids2. Elevates protective HDL levels in dose-response

fashion3. Significantly reduces LDL4. Reduces and stabilizes blood pressure5. Increases insulin sensitivity6. Stabilizes weight and decreases fat mass and BMI7. Is beneficial in congestive heart failure8. Reduces CVD mortality9. Is an essential in rehabilitation after heart

attack, stroke, or bypass surgery10. Alleviates stress


For several decades, exercise has been advo-cated for the treatment of men who have had aheart attack or stroke. Recent encouraging resultssuggest that it should also be prescribed forwomen in similar situations. Ades and colleagues

studied 60 older patients (41 men and 19 women)who had had previous MI or bypass surgery andparticipated in a rehab program that includedtreadmill running for 25 minutes, stationarybiking for 15 minutes, and machine rowing for 10 minutes for three and twelve months.371 Theresults showed improved fitness and increasednumber and size of capillaries in the thighs.

Women should be encouraged to graduallyincrease their exercise and engage in an exerciseprogram that is safe, convenient, and hopefullysatisfying and even fun, at least at times. There isno single best exercise but rather what’s best foryou. Regular, lifelong exercise offers womenmore CVD benefits than any one drug, nutrient,or herbal intervention.

Stress Management

Women’s hearts appear more vulnerable to stressthan men’s. Arnold suggests that negative stres-sors such as lack of social support and perceivedlack of control contribute to CAD risk.375 A sim-ilar inference can be made from the dataobtained by Blumenthal and colleagues.376 Inpatients with CAD or ischemia, these authorsfound that a stress management program wasapproximately three times more effective atreducing cardiac events than exercise.

Many simple techniques can be effective inmanaging stress and reducing its baleful influ-ence. Techniques such as deep-breathing exer-cises, biofeedback, transcendental meditation,yoga, progressive muscle relaxation, and hypnosishave all been shown to reduce stress and lowerblood pressure.377 The antihypertensive effect ofthese techniques is not dramatic. However, theyconstitute an important factor in a holistic pro-gram to lower blood pressure and treat and pre-vent heart disease.

Natural (Bio-Identical) HormoneReplacement Therapy

Whether a woman should go through the meno-pausal years without hormone therapy or

Exercise Recommendations

Prevention of Cardiovascular Disease

Follow the exercise guidelines outlined in Appendix A.

Treatment of Existing Cardiovascular Disease

1. Consult a health-care provider before beginninga new exercise program.

2. Use caution and moderation. Note that in menwho seldom exercise, cardiac arrest is 56 timesmore likely during vigorous exercise than at rest.In men who exercise frequently, the risk is 5times greater.372

3. Walking program for heart patients:373

Distance Time Weeks (miles) (min/mile)1–2 1 203–4 1 17–205–6 1 157–8 1.5 159–10 1.5 14

To maintain the conditioning effect, exercise 20to 30 minutes three to five times a week. If you stopexercise for more than two weeks, start again at alower level and gradually build back up to your origi-nal program.

Examples of Moderate Exercise for Mild CAD374

• 30 minutes of brisk walking each day• 10 minutes of brisk walking 3 times a day• Swimming, biking, or working out on an exercise

machine such as a treadmill, stair-climbingmachine, rowing machine, or stationary cycle atmoderate intensity for 30 minutes daily

Begin slowly and increase speed gradually over time.If you have never exercised before, start with a fewminutes each day and increase time gradually everyweek until you reach 30 minutes per day.


whether she should use bio-identical or conven-tional hormone therapy is a complex decision.The decision is especially difficult when one con-siders the many unanswered questions aboutmenopause, cardiovascular disease, and naturaland conventional hormones. The method Ifollow is to systematically evaluate each womanwith a thorough medical history, physical exam,and laboratory testing. Based on these tests andthe patient’s preferences and concerns, the prac-titioner and patient can together develop a per-sonalized plan that is right for the patient.

A woman’s risk for cardiovascular diseasechanges over time. The plan needs to changeaccordingly to carefully balance the benefits versusthe risks of therapy. Both practitioner and patientneed to be open-minded so that informed andappropriate decisions are reached.

Conventional HRT may be appropriate for some women. When it is appropriate, itbehooves physicians to advise the use of the leastobjectionable options. Phytoestrogens and bio-identical hormone therapy are perhaps the mostappropriate for some women, and I would assert,most women. No single protocol or approach isequally appropriate for all women. Determiningif my patient is at low, medium, or high risk forCAD has been a critical tool in the path to therecommendations I finally make. (See theoverview section at the beginning of this chapterfor more about issues pertinent to HRT and car-diovascular disease.)

Natural (Bio-Identical) Progesterone

The use of natural or bio-identical progesteronecreams and oral micronized natural progesteronehas grown in popularity over the last severalyears. However, only recently have natural prog-esterone creams been shown to have biologicalactivity. Progesterone is synthesized from dios-genin or stigmasterol found in Mexican wildyams and soybeans. This hormone end producthas come to be known as natural or bio-identicalprogesterone both because it is plant derived and,

more important, because it is biochemicallyidentical to the progesterone produced by thehuman ovary. Natural progesterone is biochemi-cally different than progestin, which is com-monly misstated as progesterone. The mostcommon progestin used for menopausal womenis medroxyprogesterone acetate (MPA), betterknown as Provera.

There are few studies on natural proges-terone. However, the development of oralmicronized progesterone (OMP) in the last 10 to15 years, together with the few side effects andpopularity of natural progesterone, have encour-aged scientific research and medical interest inthis natural hormone. For more information onthe indications and effects of natural proges-terone, please refer to Chapter 12.

To date, unfortunately, very few studies haveaddressed the possible cardiovascular effects ofthese preparations in postmenopausal women.The study with the biggest impact on the percep-tion of natural progesterone was the Postmeno-pausal Estrogen/Progestin Interventions (PEPI)trial.378 Although the postmenopausal women inthis study were also given estrogen, the PEPI trialdemonstrated similar lipid changes for estrogenand progesterone that are known to occur withadministration of estrogen alone, except for HDL,which was significantly reduced. Perhaps whatmerits reflection here is that, despite its otherundesirable effects, estrogen alone has the mostfavorable effect on lipids. When estrogen is com-bined with natural progesterone, HDL cholesteroldoes not improve quite as much, and when givenwith progestin, HDL improves even less.

A recent study compared the effects of natu-ral progesterone and synthetic progestin (in theform of conjugated equine estrogen) and foundthe following: the conjugated equine estrogen(CEE) group had an increase in HDL levels of14.4 percent after six months; the estrogen plusprogestin had an increase in HDL of 4.58 per-cent; and the estrogen plus natural progesteronehad an increase in HDL of 5.44 percent.379 Total


cholesterol levels were significantly decreasedonly in the estrogen plus progestin group; triglyc-eride levels were increased only in the estrogenplus natural progesterone group; and themicronized progesterone was not superior tomedroxyprogesterone acetate.

There is evidence showing that oralmicronized progesterone (OMP) may lowerblood pressure. In fact, OMP administered indoses of 200, 400, and 600 mg per day to hyper-tensive postmenopausal women and older mensignificantly reduced systolic blood pressure ascompared to placebo in a two-week treatmenttrial.380 With the maximum dose, systolic bloodpressure was decreased approximately 19.7 mmHg and diastolic blood pressure about 9.6 mmHg. At the lower doses, the decreases in systolicblood pressure were less significant. Both OMPand progestins can cause fluid retention, althoughnatural progesterone to a lesser extent.

Studies demonstrate that synthetic progestinsand natural progesterone have markedly differenteffects on the coronary vessels381 and on theirsmooth wall muscle cells.382 The results of thesetwo studies indicate that synthetic progestinsmay induce spasm of the coronary arteries,whereas estrogen and/or natural progesteronepromoted dilation.

Although many women are presently usingnatural progesterone creams as an alternative toconventional HRT, relatively little research hasbeen done on these products—with little infor-mation about their impact on cardiovascular riskfactors. For more information on the use of nat-ural progesterone alone or in combination withdifferent estrogens in menopause, please refer toChapter 12.

Perhaps most interesting is that in theWomen’s Health Initiative, women who were onestrogen only did not have an increased inci-dence of cardiovascular disease but did have anincreased risk of stroke,383 differing from the firstWHI study estrogen and progestin group.17 Fora discussion on other research and how the

timing of when a woman starts HRT may affectthe risks and the benefits, see the overview sec-tion of this chapter.

Natural (Bio-Identical) Estrogens

Natural estrogens are what we have come to callplant-derived bio-identical hormones. Theyinclude estradiol, estrone, and estriol. Mexicanwild yam contains diosgenin and soy contains stig-masterol that can be converted into an estrogenbiochemically identical to that produced by ourovaries. Bio-identical estradiol and estrone in apatented delivery system and in premanufactureddosages are available by prescription from a regular pharmacy. Bio-identical estradiol, estrone,and estriol can also be compounded in customized,individualized dosages of any strength, any combi-nation, and in many different delivery systemsincluding lozenges, sublingual tablets, creams, gels,capsules, and even injections. The distinctionsbetween bio-identical estrogens and other forms ofHRT are presented in Chapter 12. This sectionwill focus on their effect on the cardiovascularsystem.

Theoretically, if we have a dose of a bio-identical estrogen that is equivalent in strength tothe dose of the conventional estrogen, the cardio-vascular benefit or risk should be the same.Nonetheless, any hormone therapy that is consid-ered to be an alternative to the leading form of ther-apy (conjugated equine estrogens, i.e., Premarin)must at some point be compared in order to proveits worthiness and acceptability among patients andhealth-care practitioners. A few studies have lookedat oral micronized estradiol alone or in combina-tion with bio-identical progesterone and comparedit to conjugated equine estrogens (CEE) plusmedroxyprogesterone acetate (MPA) to evaluatepossible effects on CAD. Ten menopausal women,administered the natural estrogen/progesteronecombination, experienced a decrease in total cho-lesterol. In contrast, this parameter did not changesignificantly at 12 months over the initial choles-terol readings in the five women who were given


CEE and MPA. Both groups experienced anincrease in HDL cholesterol.384 Another studyreported the results of a combination pill contain-ing 2 mg of oral micronized estradiol, 1 mg ofestriol, and 1 mg of a synthetic progestin in 265women, who were followed for over four years;serum cholesterol and triglyceride levels decreasedsignificantly, but HDL levels were not measured.385

Estriol is the other natural estrogen that canbe used either alone or in combination withestradiol (called bi-est) or with estradiol andestrone (called tri-est). Estriol is used for a varietyof treatments and is discussed in more detail inChapter 12. Little is known about what estriolmay or may not do with regard to CVD. How-ever, two studies indicate positive effects ofestriol administration on lipid profiles and car-diac function. Japanese researchers found that 2mg per day of estriol was effective in decreasingtotal cholesterol and triglycerides and increasingHDL levels in elderly women (age 70 to 84), but

not in middle-aged postmenopausal women (age50 to 65).386 The other study followed post-menopausal women using estriol and found anincrease in their cardiac function and improvedblood flow in the extremities.387 Even so, I wouldnot currently consider estriol a viable approachfor treating or preventing heart disease.

When it comes to cardiovascular disease, I con-tend that ethically, practitioners using bio-identicalhormone therapy must have the same benefit-riskconversation with patients as a conventional prac-titioner who prescribes the typical Premarin/Provera would have. That said, in my opinion,there is enough evidence at this point that oralmicronized progesterone is more cardiac friendlyon lipids and coronary arteries than are the syn-thetic progestogens or progestin (such as Provera).Other than this point, I would advocate for fol-lowing the current guidelines from the NorthAmerican Menopause Society and their PositionStatement on HRT in Menopausal Women:388

Sample Treatment Plan for Cardiovascular Disease or Hyperlipidemia


• The National Cholesterol Education Program(NCEP) recommends that dietary therapy beginwith reducing dietary saturated fat by minimizingor eliminating beef, pork, lamb, cheese, butter,milk, chocolate, and fried foods.

• Consider the Mediterranean diet: increaseintake of fruits; vegetables; whole grains;legumes, especially soybean products; nuts;seeds; olive oil; and fish.

• Reduce sodium to less than 2,500 mg per day.• Quit smoking.• Do not exceed one alcoholic beverage (5 oz)

per day.• Practice regular aerobic exercise (30 minutes or

more, 5–7 times per week)—e.g., a brisk walk.• Reduce or eliminate coffee (both caffeinated

and decaffeinated).• Strive for healthy body weight.• Practice stress management such as meditation

or relaxation exercise 15 minutes each day.

Daily Supplements for CardiovascularDisease

Plant sterols/stanols: 2.0–3.4 g per dayVitamin E: 400–800 IU per dayGarlic: 1 capsule per day containing 4,000–5,000

mcg allicinGreen tea: 1 capsule extract or 3–5 cups tea per

dayCoQ10: 100 mg per dayEPA/DHA fish oil: 1 g per dayFolic acid: 800 mcg per day

Daily Supplements for Hyperlipidemia

Policosanol: 20–40 mg per dayNiacin (nicotinic acid): 500–1,500 mg per dayPlant sterols/stanols: 2.0–3.4 g per dayEPA/DHA fish oil: 2–4 g per day if triglycerides are

elevatedPantethine: 300 mg 3 times per dayOther supplements based on specific situation


Sample Treatment Plan for Hypertension


• Consider the DASH diet or Mediterranean diet:increase intake of fruits; vegetables; wholegrains; legumes, especially soybean products;nuts; seeds; olive oil; and fish.

• Consider avoiding all sodium; at the least,reduce sodium to less than 2,500 mg per day.

• Quit smoking.• Do not exceed one alcoholic beverage (5 oz)

per day.• Practice regular aerobic exercise (30 minutes or

more, 5–7 times per week)—e.g., a brisk walk.• Reduce or eliminate coffee (both caffeinated

and decaffeinated).• Strive for ideal body weight.• Practice stress management such as meditation

or relaxation exercise 15 minutes each day.

Daily Supplementation

Dandelion leaf capsules: 2 capsules dailyGarlic: 1 capsule containing 4,000–5,000 mcg

allicin, twice per dayCoenzyme Q10: 100 mg per dayPotassium: 99 mg–2.5 g per dayHerbal tincture:

Motherwort: 2 ozPassionflower: 2 ozRauwolfia (available through health-care

practitioner—not to exceed .3 mg of reserpine per day)

Hawthorne: 2 ozDose: 1 tsp twice daily

• “Data from studies such as the WHI and theHeart and Estrogen/progestin ReplacementStudy (HERS) should be extrapolated onlywith caution to women younger than 50years of age who initiate HT. The data shouldnot be extrapolated to women experiencingpremature menopause (under 40 years of age)and initiating HT at that time.”

• “Premature menopause and premature ovar-ian failure are conditions associated withearlier onset of CHD [coronary heart dis-ease], but there are no clear data as towhether ET [estrogen therapy] or EPT[estrogen/progestogen therapy] will reducemorbidity or mortality from these condi-tions. The benefit-risk ratio may be morefavorable for younger women.”

• “Nonoral routes of administration ofET/EPT may offer advantages and disadvan-tages, but the long-term benefit-risk ratiohas not been demonstrated. Differenceswould be related to the role of the first-passhepatic effect, the hormone concentrationsin the blood achieved by a given route, and

the biologic activity of component ingredi-ents. There is some evidence that transder-mal 17 beta-estradiol does not increase thelevel of C-reactive protein, and also that itmay be associated with lower risk of deepvenous thrombosis than oral estrogen.”

• “The effect of ET on CHD and stroke is notyet clear. ET does not have a significant effecton stroke risk in postmenopausal womenwith known ischemic cerebrovascular disease,but for healthy older women, effects of ETon stroke risk are not clear. However, unlessconfirming data become available, ET shouldnot be used for primary or secondary preven-tion of these conditions.”


There is still much that is unknown about car-diovascular disease, hormone replacement, andthe aging process in women. The results of theWomen’s Health Initiative (WHI) have dramati-cally changed how HRT has been prescribed inthis country. It is no longer routinely prescribed


to reduce the risk of cardiovascular disease, as itwas for over 30 years. The approach now is muchmore individualized, and there is still lack of agree-ment if the timing of when HRT is startedimpacts its influence on cardiovascular disease. Aswith all therapies, HRT must be examined againstthe backdrop of benefit versus risk. The naggingquestions for women continue to be, “Should I orshouldn’t I?” and “Are the risks greater than thebenefits?” Further discussion of these concerns ispresented in Chapter 12.

Conventional practitioners are as eager toeducate their patients on the importance of pre-venting heart disease as holistic care providersare. For several years now, patients have beenencouraged by their conventional physicians tostop smoking, increase exercise, lower theirdietary fat, increase fruits and vegetables, loseweight, and reduce their stress. It has becomemuch more common to recommend diet andlifestyle changes as a first line of treatment formild hyperlipidemia and mild hypertension.

Those individuals who are at increased riskfor heart disease should discuss the potentialbenefits and harms of aspirin therapy with theirpractitioner. Low-dose aspirin is a foundation ofheart disease secondary prevention, due to itsability to inhibit platelet aggregation. Recur-rence rates for heart attacks are also consistentlylower in women (and men) who already havecoronary disease when they are treated with alow dose of aspirin.389 In a meta-analysis of fourlarge primary prevention trials using low-doseaspirin, a 15 percent reduction was seen in car-diovascular events and a 30 percent reductionwas observed in MI rates.390 More recently, alarge randomized placebo-controlled trial oflow-dose aspirin was done in the Women’sHealth Study (WHS).391 In 39,876 women whodid not have coronary disease, a 24 percentreduction was observed in the risk of ischemicstrokes, compared with those women who didnot take aspirin. Unfortunately, there was nooverall reduction in MI or total cardiovascular

events except in women who were 65 years orolder. In that age group, aspirin therapy didreduce overall cardiovascular disease by 26 per-cent and the risk of MI by 34 percent.

The U.S. Preventive Services Task Force(USPSTF) has found good evidence that aspirindecreases the incidence of heart disease in adultswho are at increased risk. However, they alsoacknowledge that aspirin increases gastrointesti-nal bleeding episodes and that it may alsoincrease the incidence of hemorrhagic (bleeding)strokes. Their conclusion is that for those indi-viduals who are at high risk for heart disease, thebenefits outweigh the risks. The American Dia-betes Association has also concluded that clini-cians should consider aspirin for primaryprevention of heart disease in diabetic patientswho are older than 30 or have risk factors for car-diovascular disease and no contraindications toaspirin. The American Heart Association recom-mends aspirin for “patients who’ve had a myocar-dial infarction (heart attack), unstable angina,ischemic stroke (caused by blood clot) or tran-sient ischemic attacks (TIAs or ‘little strokes’), ifnot contraindicated.” You should not startaspirin therapy without first consulting yourpractitioner. Also inform your practitioner if youare taking aspirin and must have a simple surgi-cal procedure, even a dental extraction, as itincreases the risk of excessive bleeding.

When treating hyperlipidemia, most conven-tional practitioners will follow the NCEP, ATPIII guidelines. Step 1 involves identifying thelipid levels with blood testing; step 2 is to iden-tify the presence of any atherosclerotic diseasethat confers a high risk for heart disease events.Step 3 is to determine the presence of major riskfactors other than an LDL level above 160. Thesemajor risk factors include:

• Cigarette smoking• Blood pressure of 140/90 or higher or some-

one on high blood pressure medication• Low HDL, less than 40 mg/dL


• A family history of premature heart disease(before age 55 in father, brother, or son;before age 65 in mother, sister, or daughter)

• Age (men 45 and older and women 55 andolder)

Step 4 is to determine a woman’s 10-yearheart disease risk according to Framinghamtables of greater than 20 percent risk, 10 to 20percent risk, or less than 10 percent risk; Step 5is to determine the risk category. At this point,your practitioner will initiate advice. Initiatingthe Therapeutic Lifestyle Changes (TLC) is thefirst attempt at lowering your lipids, if your LDLis already at its goal. The specifics of the TLC aredescribed in the nutrition section. Per the ATPIII guidelines, drug therapy is advised, accordingto the scheme shown in Table 9.4.

Ideally, drugs will be advised simultaneouslywith TLC for women whose 10-year risk is greaterthan 20 percent. For those in lower risk categories,drugs may be added after a three-month trial ofjust the therapeutic lifestyle changes.

There are many drug or quasi-drug treatmentsthat your conventional practitioner may consider.The major classes of lipid-lowering agents used inconventional medicine include HMG-CoA reduc-tase inhibitors (statins), bile acid sequestrants,fibric acid derivatives, and nicotinic acid.

The group of drugs called the statins lowerLDL and triglycerides, and some may raise HDL.Currently, these include lovastatin, pravastatin,simvastatin, fluvastatin, atorvastatin, and cerivas-

tatin. They each come in several strengths. Bileacid sequestrants decrease LDL and increase HDLbut do not lower triglycerides. These includecholestyramine, colestipol, and colesevelam. Nico-tinic acid is used in three different forms: theimmediate-release nicotinic acid (1.5–3 grams perday), the extended-release form (Niaspan, 1–2grams), or the sustained-release form (nicotinicacid, 1–2 grams). Nicotinic acid lowers LDL,although not as much as some of the newerstatins; raises HDL better than all the statins; andlowers triglycerides as much or better than thestatins. Finally, fibric acids are drugs that are usedprimarily to lower triglycerides. These includegemfibrozil, fenofibrate, and clofibrate.

The treatment of high blood pressure isresponsible for more primary care visits than anyother chronic medical condition. However,approximately 75 percent of treated hyperten-sion patients are receiving inadequate care, asdefined by their inability to achieve and maintaintheir target blood pressure.

The American Heart Association (AHA) offers10 ways to control your high blood pressure:

1. Know your blood pressure and have itchecked regularly.

2. Maintain a healthy weight.3. Avoid using salt in cooking or the salting of

your foods. Avoid packaged salty foods.4. Eat a diet low in saturated fat according to

the AHA recommendations (see nutritionsection).

Table 9.4 ATP Guidelines for Drug Therapy

Risk Category LDL Goal LDL Level for TLC LDL for Drug Therapy

CHD or 10-year < 100 mg/dL >_ 100 mg/dL >_ 130 mg/dLrisk > 20% (100–129 mg/dL: optional)

2� risk factors < 130 mg/dL >_ 130 mg/dL 10-year risk 10–20%:(10-year risk <– 20%) >_ 130 mg/dL; >_ 160 mg/dL

0–1 risk factors < 160 mg/dL >_ 160 mg/dL >_ 190 mg/dL

(160–189 mg/dL: optional)


5. Limit your alcohol intake to one drink perday.

6. If you are taking any medication, take it asprescribed. Do not make any changes with-out consulting your prescribing practitioner.

7. Make regular follow-up appointments withyour practitioner.

8. Follow exercise advice.9. Advise your immediate relatives to have

their blood pressure checked.10. Manage stress optimally.

There are many different medications tolower high blood pressure, called antihyperten-sives. Diuretics rid the body of excess fluids, andeven sodium, and are often used as the initialtherapy. Beta-blockers reduce the heart rate andthe amount of blood the heart pumps. Sympa-thetic nerve inhibitors reduce the blood pressureby inhibiting the nerves that cause blood vesselconstriction. Vasodilators cause the muscle wallsin the blood vessels to relax, and therefore allowthem to dilate and widen. Angiotensin-convert-ing enzyme (ACE) inhibitors work to lower bloodpressure by interfering with the body’s productionof angiotensin, a chemical that causes the arteriesto constrict. The angiotensin II receptor blockersblock the effects of angiotensin, and the calciumchannel blockers are calcium antagonists that canreduce the heart rate and relax the blood vessels.Some individuals will need only short-term treat-ment or may be able to reduce their dose after ayear or more of normal blood pressure. Othersmay need to be on blood pressure medicationsindefinitely. Keep in mind that reducing weight,eating healthier, exercising regularly, reducingsodium, and reducing or managing stressors maykeep you from having to take blood pressuremedications or enable you to decrease or discon-tinue them. When drug treatments are needed, as you can see, there are many to choose from,and it takes knowledge, skill, and experience foryour practitioner to offer the best medication foryou. You may need to go through trial periods on

different medications to see not only which worksbest, but which works best with the fewest sideeffects. An additional reminder, though: Don’tjust stop your medication on your own if you get discouraged or are experiencing side effects.Call your medical office. The following sidebarcontains a list of some of the drugs used to treathigh blood pressure. This is not a complete list, asthere are many and new ones all the time.

The use of pharmacologic agents to lowerlipids and/or blood pressure is an appropriateregimen for patients who have not responded toa rigorous lifestyle modification program andnutritional and/or herbal supplementation. It isimportant to recognize, however, that despite the effectiveness of alternative therapies, not allpatients are able to make the necessary changesor comply with the supplementation regimen. Aminority of patients have conditions that willresist their own and their physician’s best efforts.

SEEING A LICENSED PRIMARYHEALTH-CARE PRACTITIONER(N.D. , M.D. , N.P. , P.A. , D.O.)

The signs and symptoms of coronary artery disease in women can be different from thosefound in men. Women more often have cases of silent myocardial infarction, have chest painwhile having normal coronary vessels, and have a higher incidence of mortality with their firstincidence of chest pain due to coronary arteryspasm. Diagnostic testing in women may not beas reliable either. Exercise stress testing is less predictive, and angiograms reveal less extensivedisease in women than in men.

One’s risk of heart disease changes with time,and risk must be assessed periodically. For meno-pausal women, it starts with the annual physicalexam, which should include a thorough medicalhistory, physical exam, blood pressure and pulsecheck, weight, listening to heart and lungs, andother physical findings. Lipid panels checking for total cholesterol, HDL, LDL, triglycerides,and the cholesterol/HDL ratio and thyroid and


glucose testing are done at different frequenciesdepending on health status and risk factors. Whileannual routine screening may be more often thanmost practitioners will recommend for womenaged 50 and older, I do in fact prefer that approachto optimize the preventive medicine approach. Ifdeemed necessary, biomarkers of cardiovascularrisk, EKG, stress EKG test, and stress echocardio-grams may also be recommended. The results ofthese tests will help determine the most appropri-ate next step, whether it is a more aggressive diag-nostic test and/or treatment intervention.

For women with abnormal findings, it isimportant to seek the advice of someone who canhelp determine if therapeutic doses of some ofthe natural therapies discussed in this chapter aresuitable and sufficient for success. A treatmentplan can be agreed on; then, with follow-up eval-uation and testing after an appropriate interval,the next step in the process can be determined.Some women may need to take cholesterol- orblood-pressure-lowering pharmaceutical agents ifan aggressive natural treatment plan has notbrought adequate results, at least on an interim

Drugs Used to Treat High Blood Pressure

Diuretics

HlorthalidoneFurosemideHydrochlorothiazideNdapamideMetolazone

Potassium-Sparing Diurectics

Amiloride hydrochlorideSpironolactoneTriamterene

Combination Diuretics

Amiloride hydrochloride plushydrochlorothiazide

Spironolactone plushydrochlorothiazide

Beta-Blockers

AcebutololAtenololBetaxololBisoprolol fumarateCarteolol hydrochlorideMetoprolol tartrateMetoprolol succinateNadololPenbutolol sulfatePindolol

Propranolol hydrochlorideTimolol maleate

ACE Inhibitors

Benazepril hydrochlorideCaptoprilEnalapril maleateFosinopril sodiumLisinoprilMoexiprilQuinapril hydrochlorideRamiprilTrandolapril

Angiotensin II ReceptorBlockers

CandesartanIrbesartanLosartan potassiumValsartan

Calcium Channel Blockers

Amlodipine besylate Diltiazem hydrochlorideFelodipineIsradipineNicardipineNifedipineNisoldipineVerapamil hydrochloride

Alpha Blockers

Doxazosin mesylatePrazosin hydrochlorideTerazosin hydrochloride

Combined Alpha and Beta-Blockers

CarvedilolLabetalol hydrochloride

Central Agonists

Alpha-methyldopaClonidine hydrochlorideGuanabenz acetateGuanfacine hydrochloride

Peripheral AdrenergicInhibitors

GuanadrelGuanethidine monosulfateReserpine

Blood Vessel Dilators

Hydralazine hydrochlorideMinoxidil (use in severe cases or

in conjuction with treatment ofkidney failure)


basis, and with appropriate monitoring andfollow-up. The determination of whether to usenatural or conventional HRT and its dosage canbest be made by a practitioner who appreciatesthe role and value of each and the benefits andrisks of HRT.

Another reason to see a licensed health-carepractitioner (naturopathic doctor, medicaldoctor, osteopathic doctor, nurse-practitioner, orphysician’s assistant) is if you are on prescription

medications, for whatever reason, and want touse the natural supplements for your blood pres-sure or cholesterol. There are some significantdrug/herb/nutrient interactions that are impor-tant to be aware of, and in a few circumstancesthere are herbs and nutritional supplements thatare contraindicated with select medications. Analternative practitioner in particular can assurethe safest method of taking natural supplementswith pharmaceutical medications.


155

OVERVIEW

Impaired fertility affects over 6 million women in the United States alone, and recent estimatessuggest that approximately 10 million coupleshave sought infertility services. Infertility is con-sidered a common condition and affects 10 to 15 percent of reproductive age couples. Femaleinfertility accounts for about 50 percent of thecases, 19 percent are due to male factor infertil-ity, 17.6 percent are due to a combination, andabout 10.5 percent of the cases are caused byunknown factors.1 Female infertility most oftenis due to tubal and pelvic disease (40 percent) orfrom a previous pelvic inflammatory infection,asymptomatic chlamydia or gonorrhea, or ovula-tory dysfunction (40 percent). Endometriosis, adiminished number of oocytes in the ovary, uterineabnormalities, immunologic factors, chromoso-mal abnormalities, environmental chemicals andtoxins, and cancer chemotherapy or radiationcan also cause infertility.

Infertility is defined as a failure to conceiveafter 12 months of frequent intercourse withoutcontraception in women under 35 years of age orfailure to conceive after six months of intercoursewithout contraception in women 35 years of ageor older. Infertility is further broken down intotwo types: primary infertility is in women withno history of prior pregnancy, and secondaryinfertility is with a history of prior pregnancy.

Eighty-five percent of couples will conceiveafter the first year of trying, with an increase to93 percent after two years. Most spontaneouspregnancies occur within three years, and there isa poor prognosis for success without treatmentafter that. This final point underscores theimportance of timely specialty referrals to repro-ductive endocrinologists for evaluation for assisted

reproductive therapies for infertile couples whowish to have a child. Many ob-gyns, primary carephysicians, and complementary care providersmay do couples a disservice by waiting too long tomake these referrals.

If pregnancy has not been achieved withinone year in a woman less than 35 years old, eval-uation of both partners should be initiated.Women who are 35 years old or older; womenwho have a history of irregular menses, pelvicpain, or dyspareunia (pain with intercourse); andwomen with a previous pelvic surgery, PID, orendometriosis should be evaluated earlier.

A detailed medical history is necessary todetermine many things that are pertinent to fertility:

• Previous pregnancy history and outcome• Menstrual cycle details• Contraception history• Duration of time without contraception• Coital frequency• Surgeries, hospitalizations, illnesses, PID,

STIs, Pap smear history• A review of other systems and history of any

thyroid problems, nipple discharge, acne,facial hair, or hair loss

• Medications, allergies• Family history of serious illnesses, congenital

birth defects, and reproductive health problems

• Lifestyle factors: smoking history, alcoholuse, exercise

A physical evaluation should include heightand weight, observation for signs of excess andro-gens (facial hair, acne, and hair loss), abdominalhip and waist circumference, and breast, thyroid,abdominal, and pelvic exam.

10I N F E R T I L I T Y C H A P T E R



Laboratory testing can be extremely complex,and the order of what is done may vary dependingon the medical history and physical exam. Initialexams often include thyroid testing, prolactinlevels (for those with irregular cycles or symp-toms), mentrual cycle day 3 follicle-stimulatinghormone (FSH) and possibly estradiol levels toassess ovarian reserve, a mid-luteal phase proges-terone test to confirm ovulation, hysterosalpin-gography (HSG) to assess the fallopian tubes andany abnormalities of the uterus, and analysis of

semen. Other tests may be indicated such asandrogen levels, blood sugar, insulin levels, orglucose tolerance testing. Pelvic and transvaginalultrasound (TVUS) looks for uterine fibroids,ovarian cysts, and ovarian follicles, and a salinesonohystogram (SHG) is useful in evaluating the uterus for polyps, intrauterine adhesions, and submucosal fibroids. Some women who havea history of pelvic adhesions, tubal disease, orendometriosis may need to have a laparoscopicsurgical evaluation.

Causes of Infertility in Couples

Pelvic or Structural Factors (35%)

• Infection: pelvic inflammatory disease, sexuallytransmitted disease, septic abortion,endometritis, pelvic tuberculosis

• Surgical history: dilation and curettage, rup-tured appendicitis, adnexal surgery, leiomyoma(fibroids)

• Contraception and pregnancy history: priorintrauterine device use, DES exposure in utero,ectopic pregnancy, frequent abortion

• Endometriosis

Ovulatory or Hormonal Factors (15%)

• Secondary amenorrhea• Abnormal uterine bleeding• Obesity• Luteal phase defect (short luteal phase)• Decreased ovarian reserve• Premature ovarian failure (early menopause)• Polycystic ovary syndrome• Elevated prolactin• Elevated TSH• Prior use of antiestrogens (Lupron, Depo-

Provera, danazol)

Male Causes (35%)

• Varicocele (42% of cases)• Unexplained (22% of cases)• Obstructive azoospermia (14% of cases)• Cryptorchidism (3%)• Testicular surgeries or injury

• Genitourinary infection or sexually transmitteddisease

• Postpubertal mumps• Hypogonadism• Genital radiation or chemotherapy• Hypospadias• Testicular cancer (less than 0.1% of cases)• Retrograde ejaculation or other dysfunction• Development abnormalities: vas deferens

absence (related to cystic fibrosis), impairedtesticular function (chromosome abnormality)

• Exposure to excessive heat (hot tubs, saunas),toxic chemicals, pesticides

• Medication or drug use (gonadotoxins): med-ications including allopurinol, colchicine,chemotherapy, cimetidine, cyclosporine, eryth-romycin, gentamicin, neomycin, nitrofurantoin,tetracycline, spironolactone, and sulfasalazine;drugs including nicotine (first- or secondhand),alcohol, cocaine, steroids, and marijuana

Unexplained (10%)

• Depression

Unusual Problems (5%)

• Immunologic

Rare Causes

• Substance use (alcohol, marijuana, caffeine,tobacco)

157I N F E R T I L I T Y

A day 3 FSH level (or day 3 and day 10 levelsif doing a full clomiphene citrate challenge test) isimportant and helpful information in predictingif a woman is less likely to become pregnantbeyond what would be predicted by age alone. Anelevated FSH level on cycle day 3 (or day 10) ofgreater than 11 to 12 IU/L is associated with poorchance of conception and poor results with invitro fertilization. A FSH test that is 25 IU/L ormore or an age of 43 years or more are each asso-ciated with a chance of pregnancy that is close tozero even with attempts at ovulation induction orwith assisted reproductive technologies.


Complementary medicine has a role in the man-agement of infertility both before and after areferral has been made to a reproductive endocri-

nologist. After a detailed history and physicalincluding pertinent lab work, treatment can betargeted to address any identified underlyingcauses. Unfortunately, in many cases, no causecan be determined. In these causes of unex-plained infertility, the first step is to address basicissues of diet and lifestyle.

Environmental and Lifestyle Factors

Both overweight and underweight women haveincreased rates of infertility. Women who areoverweight are more likely to experience prob-lems with ovulation and miscarriages. An in-crease in abdominal fat decreases insulinsensitivity, which is related to ovulation dysfunc-tion. Women who are underweight have infre-quent or even lack of ovulation. This iscompounded when combined with an eating dis-order or excessive exercise. In a woman with abody mass index (BMI) less than 25, weight lossof as little as 5 percent can be significant in help-ing to normalize menses and ovulation, especiallyin cases of polycystic ovary syndrome.2–4 Weightgain in an underweight woman is important aswell. Overall, the preponderance of evidence sug-gests that a normal body weight increases thesuccess of assisted reproductive therapies such asin vitro fertilization.

KEY CONCEPTS

• Female infertility is most often due to a previouspelvic inflammatory disease, asymptomaticchlamydia or gonorrhea, or ovulatory dysfunction.

• Other causes of infertility include endometriosis,diminished oocytes in the ovary, uterine abnor-malities, immunologic factors, chromosomal abnor-malities, environmental chemicals and toxins,cancer chemotherapy, and cancer radiation.

• Maintain optimal weight.• Manage stress.• Support fertility with a healthy diet.• Natural methods for infertility are most effective

in anovulatory dysfunction.• Acupuncture can increase pregnancy rates in

women undergoing fertility treatment.• The decision to pursue conventional fertility

treatments depends on age, the duration andcause of the infertility, the results of ovarian-reserve testing, finances, other health issues,emotional well-being, and thoughts and emo-tions about adoption or surrogate options.

• Seek a fertility specialist if considering conven-tional fertility treatments.

PREVENTION

• Prevent pelvic inflammatory disease by practic-ing safer sex and avoiding sexually transmittedinfections.

• Avoid environmental toxins.• Reduce stressors.• Avoid smoking and excess alcohol and reduce

caffeine.• Maintain optimal weight.• Minimize exposure to environmental chemicals

and toxins.• Treat any underlying medical conditions related

to infertility (exometriosis/endometriosis, poly-cystic ovarian dysfunction)


Focusing on daily exercise and a whole foodsdiet free of processed foods, alcohol, and caffeineis important to help normalize weight as well asblood sugar. However, a very recent study sug-gests that vigorous exercise of greater than fourhours per week may interfere with the success ofin vitro fertilization (IVF) and that nonexercisersmay have more success with IVF than exercisers.5

Moderate regular exercise is probably indicatedfor most individuals. In addition, in cases of exercise-related reproductive dysfunction, mostof the evidence suggests that it isn’t the intensityof the exercise but the lack of adequate nutrition,specifically total calories and protein, that causesthe fertility issues.6, 7

Smoking, caffeine (even decaf ), and alcoholhave been linked to decreased fertility, so avoid-ance is important in both partners in coupleswith fertility issues. Nicotine is toxic to thereproductive system. Smoking has been shown tocause both primary and secondary infertility inwomen.8, 9 One study demonstrated that 38 per-cent of nonsmokers conceived in their first cycleattempt compared to only 28 percent for smok-ers. Smokers were over three times as likely totake over one year to conceive versus nonsmok-ers. Heavy smokers are affected more than lightsmokers.10 Smoking has also been shown todecrease success of fertility treatments.11 In onereport, female smokers had lower ovarian reservesand required more drug intervention to induceovulation than did the nonsmokers.12

Other considerations are the genetic damageand chromosomal errors caused by smoking.Cadmium, nicotine, and some of the nicotinemetabolites have been identified in the ovaries(and testes) and genital fluids of smokers. Cellswithin the ovaries are affected by one particularnicotine metabolite, cotinine, which causesoxidative damage and developmental problemsof the follicles.13, 14

Psychological stressors deserve to be addressedas well since the process of dealing with infertilitycan be very stressful and emotionally taxing.

Stress can both contribute to infertility and be aconsequence of difficulty in conceiving. Manywomen and couples decide to discontinue theirfertility treatments because of too much stress and upset. In addition, research suggests that past or current stress and mental illness, especiallydepression, may be the cause of many cases ofunexplained infertility. This can be especiallyproblematic because continued inability to getpregnant often fuels depression, leading to avicious cycle of emotional upset and a veritableroller coaster of monthly hopes and letdowns.

Higher levels of premenstrual tension andstress are associated with lower pregnancy rates.15

Stress hormones have inhibitory effects on thereproductive system, and, therefore, stress needsto be addressed in anyone receiving fertility serv-ices. In addition, it appears that stress decreasesantioxidants, which are often low in both part-ners in an infertile couple. Any treatment ofinfertility should probably start with stress assess-ment and reduction techniques for both part-ners. Psychological counseling and a variety ofrelaxation techniques including biofeedback,yoga, tai chi, Qi gong, and meditation can behelpful aspects of the treatment plan for anyonewith past or present stress or depression.

In the last few years, there has been a lot ofpublic health information available on the importance of avoiding alcohol while pregnant,but when it comes to the influence of alcoholconsumption on female fertility, mild to moder-ate alcohol use has not been well studied. It seems,however, that alcohol does reduce conceptionrates with a dose-related connection. Researchdemonstrated that female alcohol intake was associated with two to three times the risk ofspontaneous abortion, and alcohol intake duringthe week of conception increased the risk of earlypregnancy loss.16 In another study, there was agreater than 50 percent reduction in the proba-bility of conception during a menstrual cycle in which women consumed alcohol. In this samestudy, caffeine consumption did not independently


affect conception rates, but it may enhance thenegative effect of alcohol.17

Caffeinated beverages have been associatedwith decreased fertility, increased miscarriages, andlower birth weights.18 More than five cups of coffeeper day, or more than 500 mg of caffeine per day,is associated with a delayed time to conception,although we don’t really understand the mecha-nism. One possibility is that caffeine may impairestrogen production or the metabolism of estro-gens.19 Substances other than caffeine in coffee,tea, and other beverages may also be responsible forreduced fertility. Numerous caffeinated beverages,including coffee, soft drinks, black and green tea,and even decaffeinated coffee, contain tannins, and some contain even more tannins than regularcoffee. In animal experiments, tannins havereduced fertility in mice and hens.20, 21

Increasingly, environmental pollution andexposure to heavy metals, pesticides, estrogen-likesubstances, and other chemicals are implicated incases of infertility in men and women. Dependingon the specific exposure, duration, and load, dif-ferent aspects of fertility can be affected. Thesetoxic exposures may affect sperm count, sperm

formation, sperm viability, ovulation, egg viability,and hormone levels.

Nutrition

In addition to the issues related to weight, caf-feine, and alcohol mentioned previously, there aresome specific nutritional influences on fertility inwomen. In women who have a short menstrualcycle, increasing soy in the diet or taking soyisoflavone supplements may increase the length ofthe follicular phase and delay ovulation.22 Some-thing as simple as flaxseed can lengthen the lutealphase of the cycle (the second half ) and increasethe frequency of ovulatory menstrual cycles inwomen who don’t ovulate regularly.23

As far as weight loss is concerned, one can getseriously confused these days about the value ofcarbohydrate versus protein diets. When it comesto fertility, one study demonstrated that it didnot matter whether the diet was high-carbohydrateor high-protein: both groups who stuck to low-calorie diets lost weight and had improved men-strual cycles and fertility.24, 25

It is, of course, important to limit certain kindsof fish that have a higher mercury content in preg-nancy, but evidence indicates it may be wise to do the same in cases of infertility. Studies showthat infertile couples consumed more fish and hadhigher levels of mercury in their blood than fertilecouples.26 Consumption of biphenyl-contaminatedfish also has an adverse effect on fertility.27 Substi-tuting fish oils from a reliable manufacturer forfish consumption is a good way to keep omega-3fatty acids in the diet. Prior to pregnancy, a mini-mum daily intake of eicosapentaenoic acid (EPA)and docahexaenoic acid (DHA), found in fish andfish oils, is about 650 mg of each.

Wild salmon ranges from 1.0 to 1.5 gramsper three-ounce serving, with a little more DHAthan EPA. The different species of salmon (sock-eye, chinook, coho) range in EPA and DHA, andwild sockeye contains approximately 600 mgDHA and 430 mg EPA per three-ounce serving.Whether you take fish oil supplements daily or

Caffeine Content

Item Caffeine (mg)Coffee, brewed (8 oz) 60–120Coffee, instant (8 oz) 70Coffee, decaffeinated (8 oz) 2–5Double espresso (2 oz) 45–100Tea, black, 5-minute

steep (8 oz) 60–100Tea, green (8 oz) 20Barq’s Root Beer (12 oz) 22Coca-Cola (12 oz) 34Pepsi (12 oz) 38Chocolate milk (8 oz) 4Milk chocolate (1 oz) 1–15Dark chocolate (1 oz) 20Ben & Jerry’s Coffee Fudge

Frozen Yogurt (4 oz) 42


eat fish several times per week, try to averageabout 650 mg of EPA and DHA per day. Specificneeds for DHA increase during pregnancy (seeChapter 16). (During pregnancy, cod liver oilmay be a questionable choice due to the highcontent of vitamin A, a teratogen, in fish liver.28)


Vitamin E. Some simple vitamin and min-eral supplementation may be key to fertility inselected women, and because oxidative stressaffects the female reproductive system and conse-quently fertility, antioxidants are important con-siderations in enhancing fertility. Vitamin E is apowerful antioxidant, combating free radicaldamage, and can play a beneficial role in femalefertility. Most of the research on vitamin E is per-tinent to male fertility, such as making spermmore fertile. In one study, vitamin E was given toboth men and women and resulted in a signifi-cant increase in fertility, and also assisted theachievement and maintenance of pregnancy inwomen with repeated miscarriages.29 Other stud-ies show that adding antioxidants, including vita-mins C and E, to the diet of animals significantlyreduced the decline of regular ovulation relatedto aging.30 This may have importance for womenin their 40s, who begin to experience reducedfertility due to diminished ovarian reserve.

Vitamin E

400–800 IU per day

Selenium. The mineral selenium is anotherantioxidant that protects from free radicaldamage. Free radicals are created when normalbiochemical reactions cause oxygen molecules tobecome unstable. They are also formed by smok-ing, barbecuing, and deep-frying food, andmore. Selenium can protect normal tissue fromoxidative damage caused by the free radicals,including preventing chromosome damage. Sele-nium may also be able to provide protectionfrom exposure to toxic heavy metals including

cadmium and lead that can adversely affectsperm development. Selenium mostly affectsmale fertility by maximizing sperm formation,optimizing testosterone production, and increas-ing sperm count. (For more information on malefertility, see the section titled “Male Fertility”later in this chapter.)

Selenium

100–200 mcg daily

Zinc. The most widely studied nutritionalsupplement for fertility in both men and womenis zinc. Zinc plays a vital role in cell division, anddeficiencies are associated with reduced fertility,increased miscarriages, and chromosome damage.Less than optimal zinc levels not only reduce con-ception rates, but babies have lower birth weights,more birth defects, and can have a less developedbrain and nervous system.31 Zinc deficiency isespecially important for sperm development.

Zinc

30 mg per day

L-Arginine. L-arginine is an amino acid nec-essary for the synthesis of protein and is foundnaturally in numerous animal protein foods.Arginine supplementation of 16 grams per dayhas been shown to improve uterine blood flowand fertilization rates in women who had previ-ously failed in vitro fertilization.32 Additionaleffects for enhancing sperm count and spermquality are discussed in the male fertility section.

L-Arginine

16 g per day

Para-Aminobenzoic Acid (PABA). PABA isa part of the folic acid molecule and is found ineggs, milk, meat, and several grains. The role ofPABA produced by the body is not really known,but as an oral supplement it is FDA-approved for


difficult conditions such as scleroderma, vitiligo,pemphigus, and dermatomyositis. It is approvedfor use as a sunscreen because it acts as a filter toblock out ultraviolet radiation. In fertility, PABAsupplementation of 100 mg four times dailyresulted in pregnancies in 12 of 16 women witha history of infertility.33

PABA


Multiple Vitamin-Mineral. A double-blindtrial found that taking a multivitamin-mineral supplement increased female fertility.34 A multivit-amin and mineral in the form of a prenatal prepa-ration has much of what is needed, but womenwho are deficient in vitamins like folic acid andB12

35–37 and minerals like magnesium and sele-nium38 may need additional supplementation.

Botanicals

Chaste Tree (Vitex Agnus Castus). Chastetree stimulates the release of luteinizing hormone(LH) from the pituitary gland and mildly inhibitsFSH. The result is an indirect ability to raise ormodulate progesterone levels.39 Chaste tree alsomodulates the secretion of prolactin from thepituitary gland, and in one study prolactin was sig-nificantly reduced while shortened luteal phasesand progesterone deficits were normalized.40

Chaste Tree

Liquid extract 1 tsp per day or 0.6–0.75% standard-ized extract, 175–215 mg per day

Black Cohosh (Cimicifuga Racemosa).Similar to chaste tree, black cohosh can also stim-ulate pituitary secretion of LH and therefore leadto ovulation and subsequent production of prog-esterone by the corpus luteum.41, 42 Black cohoshmay be especially valuable for women in their40s whose FSH levels may be starting to increaseas the ovary ages.

Black Cohosh

20–40 mg standardized extract twice daily

Rhodiola (Rhodiola Rosea). Rhodiola mayenhance fertility. It has been shown to enhancethyroid function without causing hyperthy-roidism in animals, and egg maturation wasenhanced as well. These and other preclinicalresearch led to treating 40 women with amenor-rhea and infertility with rhodiola (100 mg) twicedaily for two weeks. Normal menses were restoredin 25 women, 11 of whom became pregnant.43, 44

Additional Botanicals. Numerous plantshave been used in traditional herbal medicine fortheir ability to regulate the tone of the uterus. Incases of infertility of undetermined cause, theseuterine tonics are thought to prepare the uterusfor implantation of a fertilized egg. These herbsinclude dong quai (Angelica sinensis), blue cohosh(Caulophyllum thalictroides), crampbark (Viber-num opulus), false unicorn or helonias (Chamae-lerium luteum), and squaw vine (Mitchella repens).

Dong quai can tonify a weakened uterus byimproving the metabolism within the uterus45 aswell as regulating hormonal control and improv-ing the timing of the menstrual cycle.46 Bluecohosh can improve the muscular tone of a hypo-tonic uterus and thereby was thought by earlytraditional herbalists to improve fertility. Cramp-bark has been used more in cases of miscarriagerather than actual infertility. It has been used tra-ditionally both as a uterine sedative and a uterinetonic. False unicorn or helonias has been used toimprove uterine tone and decrease what has beencalled pelvic congestion. This herb also tends tobe used more for women who have a history ofmiscarriage or abnormal bleeding during thepregnancy rather than true infertility. Squaw vineis a uterine tonic that increases the circulation toand in the uterus, thereby also reducing uterinecongestion. It can both sedate a hypertonic uterusas well as tonify a hypotonic uterus.


Ginseng species are an important considera-tion in infertility due to their ability to enhanceoverall health, vitality, stamina, and endurance.Siberian ginseng may be able to promote regula-tion of reproductive hormones, thereby regulat-ing the timing of ovulation.47

Phytoestrogens can be particularly useful in theIVF fertility treatments by improving implanta-tion, pregnancy, and delivery rates.48 In addition,phytoestrogens may also reverse the antiestrogeneffects of clomiphene citrate, a medication fre-quently used in the treatment of infertility.49

A plant that many are not familiar with,tribulus (Tribulus terrestris), has been studied asan ovarian stimulant. A study of women takingtribulus every day has demonstrated the ability oftribulus to normalize ovulation, whereby some ofthe women also became pregnant.50 When usingthe tribulus simultaneously with an ovulation-induction drug, the results with the combineduse were better than the drug by itself.

Polycystic ovary syndrome (PCOS), alsoknown as chronic anovulatory syndrome, is theassociation of hyperandrogenism with chronicanovulation in women without specific underly-ing diseases of the adrenal or pituitary glands.One of the characteristics is infertility, althoughsome PCOS patients may randomly ovulate andare fertile that month. PCOS is a complicateddisorder that takes a very comprehensive, multi-factorial approach. Several herbs may have a role.Flaxseed, nettles, and green tea stimulate sex-hormone-binding globulin, which can lower theelevated estrogens and androgens. Saw palmettocan inhibit 5-alpha reductase, which then inhibitsthe conversion of testosterone to dihydrotestos-terone, and smilax and sanguinaria may be able toproduce a progesterone effect. All of these mech-anisms—plus modifying insulin resistance and/orlowering a hypersecretion of insulin, treating theunderlying endocrine problem, and inducingovulation—are the keys to treating PCOS.

Additional Therapies

Recent research also supports the use of manualsoft-tissue therapy for pelvic adhesions, whichmay be implicated in some cases of infertilitywhere there has been a history of surgery, infec-tion, inflammation, or trauma. Adhesions formas a result of the natural healing process but causeproblems by attaching to internal structures andaffecting normal anatomy, mobility, and func-tion. The manual therapy can improve tissuemobility and restore function by breaking thecollagen cross-links that have formed during thehealing process. The specific technique studied isthe Mojzisova method, which combines bothsoft-tissue and osseous manipulation and is usu-ally performed by specially trained physicaltherapists.51

Celiac disease, which may cause deficienciesin a number of nutrients, requires special consid-eration for appropriate diagnosis and manage-ment. Gluten avoidance has been shown toimprove fertility rates in sensitive patients.52–54

A Note About Acupuncture

Acupuncture has been shown to improve pregnancyrates in women undergoing fertility treatment. Pelvicultrasound studies have confirmed that acupuncturetreatments can improve pelvic blood flow, and thismay account for its effectiveness. Another possiblemechanism for the ability of acupuncture to improvefemale fertility is a favorable effect on gonadotropin-releasing hormone, and therefore on the secretion ofgonadotropins and improved thickening of the liningof the uterus (the endometrium). In addition,acupuncture can also be helpful in improving spermcount, menstrual cycle regulation, ovulation induc-tion, and decreasing stress and depression. Acupunc-ture, as with many complementary therapies, is bestwhen combined with conventional treatment whenindicated. Research studies thus far have had smallsample sizes and difficulty in providing proper con-trol, so the results should not be overemphasizeduntil further studies can be done. Acupuncture by alicensed professional with experience working withfertility issues appears to be safe and well tolerated.


Celiac disease may lead to decreased absorptionof fat-soluble vitamins, thereby causing deficien-cies that may impair male fertility as well.

Topical or vaginal progesterone may helpnormalize menstrual cycles, improve implanta-tion rates, and maintain pregnancies in womenwith history of repeated miscarriages but shouldonly be used under the care of a physician.55, 56

MALE FERTILITY

Low sperm counts have been attributed to anumber of factors, including exposure to pesti-cides, welding, antibiotic and other medicationuse, a history of mumps, gastrointestinal com-

plaints, decreased intake of fruits and vegetables,family history of female fertility disorders, andnicotine and caffeine intake.57 Therefore, itseems prudent when dealing with a couple whowant to improve their fertility that these factorsbe addressed promptly, especially in patients whohave demonstrated sperm abnormalities.

Supplements

A number of supplements can improve spermquality and quantity, including vitamins C, B12,and E; L-arginine; L-carnitine; selenium; zinc;and folic acid.58

Vitamins C and E. Vitamin C and otherantioxidants can decrease sperm DNA damagethat can interfere with fertility.59 Vitamin C defi-ciency has been linked with significant decreasesin sperm count, motility, and vitality and with anincrease in morphologically abnormal sperm.60

Vitamin E and selenium have been shown toreduce lipid peroxidation and, therefore, improvesperm quality. One study looked at men who hadnormal sperm counts, but low rates of fertilizationduring in vitro fertilization treatments. After onemonth of daily vitamin E supplementation, thefertilization rates increased from 19 percent to 29 percent, suggesting that the antioxidant effectsof vitamin E may make the sperm more fertile.61

The combination of oral vitamin C and vita-min E (one gram of each), administered to malepatients with DNA damage who had previouslyfailed fertility treatments for two months, wasshown to decrease DNA-fragmented sperm, anda second fertility treatment led to improvementof clinical pregnancy and implantation rates.62

Vitamin C

500–3,000 mg 3 times daily

Vitamin E

500–1,000 IU per day

L-Carnitine. The amino acid L-carnitine isessential for normal functioning of sperm. It seems

Sample Treatment Plan for Infertility Due to Lack of Ovulation or Infrequent Ovulation Cycles


Diet

Whole foods diet high in vegetables, whole grains,nuts and seeds, fruits, low-fat organic dairy

Protein: 60 g dailySoy foods: 1 serving dailyFlaxseed: 2 tbs per dayFish: 2–3 times per week

Lifestyle

Avoid caffeine, alcohol, and smoking.Seek optimal body weight.


Vitamin E: 400 IU per dayVitamin C: 2,000 mg per dayZinc: 30 mg per daySelenium: 100 mcg per dayPrenatal vitamins: 2 per day

Botanicals

Chaste tree (0.6% aucubin extract capsule): 215 mgper day

Rhodiola: 200 mg per day


that the higher the levels of L-carnitine in spermcells, the higher the sperm count and the moremotile the sperm. L-carnitine given as a supple-ment helped to increase the sperm count and thenumber of normal sperm after four months.63

L-Carnitine

3,000 mg daily

B12. A deficiency of B12 leads to reducedsperm counts and reduced sperm mobility. Inmen who had sperm counts under 20 million/ml,1,000 mcg of vitamin B12 per day led to anincrease to 100 million/ml.64 In another study ofmen with low sperm counts, 6,000 mcg of vita-min B12 per day showed improvements in thesperm counts of 57 percent of them.66


It is important to be aware of the latest conven-tional treatment options for infertility and togain insight into when is it timely to seek special-ized fertility care. The decision to pursue conven-tional modes of infertility treatment depends onage, the duration and cause of the infertility, theresults of the ovarian-reserve assessment/testing,finances, other health issues, emotional stamina,and thoughts and feelings about adoption or surrogate options. Treatment options includeintrauterine insemination (IUI) in the naturalmenstrual cycle, ovulation induction usingclomiphene citrate or gonadotropins (with orwithout IUI), and in vitro fertilization.

Intrauterine insemination involves introduc-ing a concentrated suspension of washed sperminto the upper uterine cavity. The success of IUIvaries depending on the cause of infertility. IUIalone, without ovulation induction medications,increases the chance of fertility in a natural cycleby only 1 to 2 percent in couples with unexplainedinfertility. When clomiphene citrate (CC) is addedin these couples, the fertility rate increases to 8 to10 percent.

Three main types of medication are used toinduce ovulation. Clomiphene citrate is the mostcommon, but aromatase inhibitors (AI) andinjectable gonadotropins are also used when thereis no response to other treatments. Clomiphenecitrate is not only the most commonly used med-ication, but it is also the most effective, inexpen-sive, and easiest to use and requires less monitoringthan the other medications. Clomiphene citrate is primarily used to induce ovulation in womenwith abnormal ovulation patterns, in women witha luteal phase defect (abnormal length of thesecond half of the cycle), or in women who haveunexplained infertility. It is also used to assess ovar-ian reserve. It is not generally effective in womenwho have amenorrhea due to low estrogenic statessuch as hypothalamic amenorrhea.

Clomiphene citrate is well tolerated most ofthe time and does not often have any serious sideeffects. However, because it depletes estrogenreceptors, side effects include hot flashes, nauseaand vomiting, breast discomfort, and headaches.It can also have detrimental effects on cervicalmucus and the endometrial lining. Severe sideeffects occur in less than 2 percent of womenusing it. CC can lead to an increase in multiplegestations at a rate of about 6 to 10 percent.Most of these tend to be twins; less than 1 per-cent are triplets or higher-order multiples. Pastconcern about increasing the risk of ovariancancer has faded with recent research showing noincreased risk. About 80 percent of women usingCC will ovulate, but only 50 percent of those willconceive. Over the course of using CC for six tonine cycles, the rate of pregnancy goes up toabout 70 to 75 percent in those who begin toovulate while on CC. Obesity, elevated androgenstates, and late reproductive age diminish theresponse to CC.

Inducing ovulation with gonadotropins isindicated in women who fail to ovulate with CC,don’t conceive on CC despite ovulatory cycles,have endometriosis, have unexplained infertility,or are of advanced reproductive age, or if CC is


contraindicated. Gonadotropin therapy involvesinjecting either FSH and LH, or FSH alone.FSH stimulates the development of multiple fol-licles and therefore carries a higher risk of multi-ple birth than does CC use. Overstimulation(hyperstimulation) of the ovaries is also a risk.These cycles require close monitoring with serialestradiol levels and ultrasounds. This therapy isusually combined with IUI.

Aromatase inhibitors (AIs) are best known forthe treatment of breast cancer, but they’ve beenused more recently to induce ovulation. By usingAIs in the follicular phase of the menstrual cycle(the first half, before ovulation), estradiol levelsare reduced and the hypothalamus and pituitarydon’t receive their normal feedback message. This results in increased secretion of the pituitarygonadotropins, which can stimulate ovulation.AIs are usually given at a dose of 2.5 to 5 mg perday on days 3 to 7 of the cycle. AIs are indicatedfor women with infrequent or no ovulation andfor unexplained infertility.

Other drugs that are used on a selective basis and along with other therapies includegonadotropin-releasing hormone agonists, gonadotropin-releasing hormone antagonists,and human chorionic gonadotropin.


It’s important to remember that a significantnumber of pregnancies occur in previously infertilecouples without any treatment at all. The mainreason to see a health-care provider is to pursue athorough investigation of the reasons for yourinfertility. Remember, infertility is defined as a fail-ure to conceive after 12 months of frequent inter-course without contraception in women under 35years of age or failure to conceive after 6 months of

intercourse without contraception in women 35years of age or older. At age 35, and especially afterage 40, time becomes of the essence, so it is a goodidea to seek the advice of a practitioner promptly ifa desired pregnancy is delayed.

A practitioner with expertise in fertility canproceed with a methodical evaluation, treat anyabnormalities that are found, provide educationabout the reproductive system, offer advice aboutyour fertility potential, provide counsel regardingall options, and provide clinical and emotionalsupport.

Infertility in women lends itself to an integra-tive approach using conventional therapies alongwith natural therapies. A health-care team ofdiverse practitioners—including a reproductiveendocrinologist, a naturopathic physician, andperhaps an acupuncturist specializing in women’shealth and/or a psychotherapist—who are com-fortable working collaboratively provides an opti-mal environment for patient care.

RESOURCES FOR PATIENTS

A number of excellent resources are available tocouples that are having difficulty conceiving.

RESOLVE. An informational clearinghouse forinfertile couples: offers educational materi-als, a medical call-in hour, help line, physi-cian referrals, member-to-member supportsystem, local chapters and support groups.Website: resolve.org/main/national/index.jsp?name=hom.

Preserving Fertility pamphlet. Available atresolve.org/main/national/niaw/presfert.pdf.

Conquering Infertility by Alice D. Domar, Ph.D. (Penguin, 2004). A mind/body guide to enhancing fertility and coping withinfertility.


167

OVERVIEW

Interstitial cystitis (IC) is a multifactorial syn-drome whose diagnosis and cause remain elusive.Poorly understood, IC remains a significantwomen’s health problem. About 90 percent of ICpatients are female.1 IC typically begins in youngor middle-aged women.

IC is characterized by pelvic and/or perinealpain, urinary urgency, urination at night, painincreased by holding urine (which leads to fre-quency), and a constant urge to urinate. The painof IC can range from a mild burning or discomfortto severe debilitating pain in the bladder, lowerabdomen, perineum, pelvis, vagina, low back, andthighs. Menstruation and sexual intercourse aggra-vate symptoms in as many as 75 percent ofwomen. There are often flare-ups and remissions.

When a woman has the classic symptoms ofurinary urgency, frequency (more than eight timesper day), bladder pain, and urinating at night(more than twice); has no evidence of a urinarytract infection; and reports continuous pain or painwith menstrual flow, then other pelvic diseases suchas endometriosis should be given some considera-tion. If urinary leakage (incontinence) is present, anevaluation for the cause of the incontinence shouldbe done. Painful or difficult urination (dysuria)may indicate a urinary tract or vaginal infection ora structural problem in the urinary tract.

Diagnostic tests for IC are mostly done to ruleout other causes. Keeping a daily diary of when youfeel the need to urinate may be useful. Your health-care practitioner may use the O’Leary-Sant Index,which measures pain, voiding symptoms, and qual-ity of life. A physical exam can help to rule outother diseases and pelvic pathology. Urinalysis andurine cultures are normal in patients with IC. Ifblood is visible in the urine under a microscope,

then cytology tests should be done. Vaginal and cer-vical cultures are done if the practitioner suspects asexually transmitted disease. Some urology experts,especially urogynecologists, may choose to recom-mend a potassium sensitivity test, which instillspotassium into the bladder, to see if the bladder hasincreased in permeability. If the usual pain getsworse, the test is considered positive for IC.

On cystoscopy, bladder ulcers called Hunner’sulcers and reduced bladder capacity are detected inless than 10 percent of individuals with IC. If theseulcers are seen, this is considered definitive for IC.More commonly, IC is characterized by petechialbladder mucosal hemorrhages, inflammation, andno ulcerations.

IC is more common in patients with irritablebowel syndrome, spastic colon, abdominalcramping, hysterectomy, rheumatoid arthritis,fibromyalgia, hay fever, asthma, and allergies tofoods and medications.

Drug and surgical interventions have beenused to treat this condition with limited successand potential side effects. Despite continuedresearch on IC, safe, noninvasive treatmentoptions are lacking.

Several causes have been proposed for IC,although none have been proven. The contribut-ing factors fall into two main categories: bladderepithelial permeability and inflammation. Theexact causes are difficult to distinguish and arelikely to be interrelated in any one patient.Because of this, a variety of treatment options maybe used. These include vitamin A (as palmitate),bioflavonoids (from citrus), L-arginine, quercetin,N-acetyl glucosamine, corn silk, kava root, andOregon grape root.

Although the cause of IC is unknown, it isimportant to consider the possible causes to

11I N T E R S T I T I A L C Y S T I T I S C H A P T E R



understand the therapeutic basis for naturaltreatments. Because IC is a multifactorial syn-drome, it is likely that several of these factors maybe true in your case. Short descriptions of possi-ble factors in IC follow:

• Bladder epithelial permeability. One ofthe more recent theories for IC is that the bladder epithelium is abnormally permeable,allowing components of urine to penetrate andirritate the bladder. The most common explana-tion of the permeability is that the bladderepithelium is deficient in glycoproteins and glycosaminoglycans (GAG). Several studies haveshown that IC patients had decreased levels ofglycoproteins and GAG in both the bladder andthe urine.

• Mast cell activation. This theory proposesthat bladder mast cells are activated and releasehistamine, prostaglandins, leukotrienes, andother substances that affect bladder smoothmuscle and sensory nerve terminals. Several stud-ies have shown that IC patients have increased

urine levels of these mast cell mediators. Some ICbladder biopsy samples contain mast cells, but itis known that these cells are not specific to ICand can also be found in other bladder disorders.

• Autoimmune causes. Autoimmune theoriesare based on detecting antinuclear antibodies,increased urinary excretion of eosinophiliccationic protein, and the tendency of IC to affectwomen. Other evidence includes IgM in theuroepithelium, immune deposits in vessel walls,and T and B cell nodules in patients with IC.

• Inflammation. Most biopsies of IC bladdersshow mild chronic inflammation to significantinfiltration of T cells, B cells, plasma cells, neu-trophils, eosinophils, and mast cells. Inflammatorymediators such as interleukin-6 are also increased.

• Infection. The possibility of an infectiouscause has been suggested by the presence ofmicroorganisms embedded in the bladder wallof patients with IC and bacterial ribosomalmRNA in tissues of bladder biopsies.

• Reflex sympathetic dystrophy. Bladdersympathetic innervation may be interrupted byinjury to peripheral nerves from prior UTIs,hysterectomy, or childbirth. This may lead to anincreased transmission of pain impulses fromthe bladder and reduced circulation, facilitatinginflammatory cell infiltration and leading tobladder ulceration, fibrosis, and atrophy.

Each of these theories has supportive anddetractive evidence. As stated earlier, the cause ofIC may vary in different people, or multiple fac-tors may be in operation.


Therapeutic options, both conventional andalternative, are as varied as the theories on thecause of IC. Almost no studies have been done tohelp practitioners identify which patients wouldlikely respond best to which treatments. Treat-ment choices are made individually for eachpatient, and in most cases, several treatments

KEY CONCEPTS

• IC is a noninfectious chronic condition charac-terized by pelvic and/or perineal pain, urinaryurgency, urinary frequency, bladder pain, andurination at night.

• IC is difficult to diagnose with any test; testsare mostly done to rule out other causes of thesymptoms.

• There is no proven cause, but bladder permeabil-ity and inflammation direct the variety of treat-ment options available.

PREVENTION

• No specific prevention strategies have beenestablished, but minimizing bladder irritantsseems logical. Classic offenders are coffee,chocolate, alcohol, carbonated drinks, citrusfruits, and tomatoes.

169I N T E R S T I T I A L C Y S T I T I S

should be used concurrently until symptom reliefoccurs. After that, a careful, gradual process ofreducing dosages or simplifying the treatmentinterventions is appropriate.

The most commonly used treatment by bothconventional and alternative practitioners isdietary changes. Patients with IC will oftenreport that certain foods increase their symp-toms. Classic offenders are coffee, chocolate,alcohol, carbonated drinks, citrus fruits, andtomatoes. Acid or potassium content is often sus-pected as the mechanism. Responses to thesefoods is hugely variable, and there is no consis-tent diet that works for all IC patients.

The following natural treatment plan mayseem complex, but consider that the averagepatient with IC has symptoms three to four yearsprior to diagnosis. In my experience with treatingIC patients over a one-year period with this proto-col, significant improvements are usually seenwithin the first three months. Continued improve-ment (75 percent better or greater) is seen after sixmonths while maintaining the same doses. Withinthe second six months and beyond, gradual reduc-tion of dosage can be done on an individual basis.I have found that IC patients are so thrilled withtheir improvement that they hesitate to reduce thesupplements and do so carefully. With this naturalmedicine approach, IC patients can proceed withoptimism and be reassured that there is likely helpfor their very chronic condition.

Nutrition

Some foods and beverages seem to exacerbatesymptoms for many women. Although not fullyinvestigated, about 53 percent of patients withIC associate a flare-up of their symptoms withdietary influences, especially citrus fruits andother acidic foods and beverages.2 Many womenfind it helpful to avoid certain foods. If you avoidthese foods for two weeks and your symptomsimprove, this is good news for the bladder.Making these dietary changes is a good self-helpstrategy in managing this condition.

Glycosaminoglycans and Bladder Epithe-lial Permeability. The bladder epithelial perme-ability hypothesis is a compelling and active areaof research. This theory asserts that the bladderepithelium is abnormally permeable in IC, sourine components penetrate and irritate thebladder. Several lines of indirect evidence sup-port this hypothesis:

1. Some IC patients have increased pain aftereating foods such as citrus fruits and toma-toes that are acidic and high in potassium.

2. Some IC patients have pain when potassiumchloride is instilled into the bladder, whilemost healthy controls do not.3, 4

3. Taking fluorescein orally yields higher bloodfluorescein levels in IC patients than in con-trols, attributed to increased fluoresceinreabsorption across the bladder wall.5

4. In one of the only direct bladder permeabilitystudies, radio-labeled diethylenetriamine pen-taacetic acid (DTPA) was instilled in the blad-der and blood samples showed that ICpatients had higher blood levels of DTPA than

Foods to Avoid

Alcohol Lentils ApplesLima beans Aspartame LimesAvocados Mayonnaise BananasNuts* Cantaloupes OnionsCarbonated drinks Oranges Cheese**Peaches Chicken livers Pickled herringChilies/spicy foods Pineapple ChocolatePlums Citrus fruits PrunesCoffee Raisins Corned beefRye bread Cranberries SaccharineGrapefruit Sour cream GrapesSoy sauce Tomatoes GuavaStrawberries Vinegar LemonsTea Yogurt

*Except almonds, peanuts, and pine nuts**Except American, cottage, ricotta, and cream cheeseSource: K. Whitmore2


healthy controls, although the small study of10 IC patients and 9 controls was not able todemonstrate statistical significance.6

5. Glycosaminoglycans (GAGs) normally linethe epithelium and are thought to con-tribute to the permeability barrier. Severalstudies have shown that IC patients havedecreased levels of GAGs in both the blad-der and urine.7–12

GAG supplementation is used to treat ICbased on the rationale that the GAG may supple-ment or replace the deficient epithelial GAGs.The GAG studies with published trials includePPS (pentosan polysulfate sodium) Elmiron,13–19

heparin,20 and hyaluronic acid (Cystostat).21 Thesestudies showed treatment efficacy over placebofor each of these treatments. No studies havebeen published on over-the-counter preparationsof chondroitin sulfates and glucosamine prepara-tions; however, a link has been established betweenchondroitin and IC.22 A GAG in the form of N-acetyl glucosamine or glucosamine sulfate canbe used as part of a multifactorial approach torepair the bladder epithelium.

Glucosamine Sulfate

750 mg twice daily

N-Acetyl Glucosamine

500 mg twice daily

Vitamin A. Vitamin A has been shown toinhibit mast cell growth and proliferation, anddeficiency may aggravate the clinical manifesta-tions of inflammatory reactions due to mastocy-tosis.23–26 Vitamin A also helps to elevate urinarynitric oxide levels. (See the section on L-arginineand inflammation for more information on therole of nitric oxide in IC.) In addition, vitamin Adeficiency has been linked to a higher level oftissue damage due to inflammation, both as anetiological and aggravating factor, and supple-mentation may decrease inflammation in these

cases.22, 27, 28 Vitamin A also plays an essential rolein maintaining and protecting epithelial integrityand mucosal surfaces and their secretions,including those of the bladder.26, 29

Vitamin A may also be of benefit in the man-agement of IC as it is essential to proper immunefunction30, 31 and stimulates epithelial repair andgrowth.30, 32, 33 Vitamin A increases immuneresponse mainly due to its effect on T-helper cells.34

In addition, evidence supports the theory that Vitamin A may also attend to the GAG repair.35

Vitamin A

5,000 IU per day

L-Arginine and Inflammation. Nitric oxide(NO) may play an important role in the patho-genesis of IC in that it activates the cyclooxyge-nase (COX) enzymes, leading to production ofproinflammatory prostaglandins that exacerbatethe inflammatory response.36 NO also plays arole in IC in the regulation of smooth musclerelaxation, immunological responses, and blad-der neurotransmission and blood flow.37, 38

Luminal nitric oxide is elevated in IC, correspon-ding to symptom severity, and can be used as amarker for mucosal inflammation in suchcases.39–41 Nutrients such as arginine (a precursorto NO synthase) and antioxidants like vitamin A help to elevate urinary nitric oxide levels andmay play an important role in the managementof interstitial cystitis.36, 40, 42, 43 Oral supplemen-tation with arginine changes urine levels ofNO,44 and three studies demonstrated symptomimprovement over placebo.40, 45, 46 Anotherstudy reported that a six-month course of oral L-arginine increased nitric oxide–related enzymesand metabolites in the urine of patients with IC.This result was correlated with a decrease in ICsymptoms.37

L-Arginine

500 mg twice daily


Calcium Glycerophosphate (Prelief ). Cal-cium glycerophosphate has been shown to helpreduce bladder pain and urinary urgency in ICpatients when it is used with acidic foods andbeverages. Calcium glycerophosphate, sold underthe trade name Prelief, is a food-grade mineral,available in granulated form. When added toacidic foods and beverages, it removes the acidand helps to reduce bladder pain and urinaryurgency associated with these foods.

However, from a naturopathic medicinestandpoint, this should be done sparingly. This islike taking a heartburn medicine but still eatingspicy Polish sausages. The food is still aggravatingyou, you are just temporarily protected from theimmediate bodily response. The fact that thesefoods are causing symptoms means that they arecausing irritation and inflammation.

Calcium Glycerophosphate (Prelief)

2 packets 3 times daily with meals

Add 2 packets of powder to a serving of acidic foodor beverage. (It will not dissolve in alcoholic drinks.)Also take 2 packets at bedtime if desired. You can usemore if needed.

Botanicals

Kava (Kava Methysticum). A permeable or“leaky” bladder may allow chronic diffusion ofurinary potassium, leading to sensory symptomsand tissue damage. This appears to be a majorfactor in the pathogenesis of interstitial cystitis.47

Kava is known historically as a urinary antispas-modic, and recent reports support its use as asmooth muscle relaxer, likely through inhibitionof calcium channels.48 In addition, kava blockssodium and calcium ion channels in neural tissueand thereby alters potassium potentials.47 Abnor-mally elevated potassium levels may induceheightened nervous and electrical sensitivity andincrease mucosal sensitivity in patients with IC.Kava may help to reduce this effect by alteringthe potassium channel activity. In addition, IC

has been reported to be aggravated by stress49, 50

and associated with panic disorder,51 two condi-tions that may be ameliorated by kava.52

Kava Extract

Kavalactones: 70 mg 3 times daily

Quercetin. Another proinflammatory culpritin IC is the mast cell, an immune modulatory cellthat secretes its damaging contents in a processcalled degranulation in response to factors such asstress and toxins. Mast cells can directly damagethe bladder mucosa, leading to bladder inflamma-tion. Some researchers speculate that treatment of IC must include mast cell stabilizers.45, 53, 54

Quercetin and other bioflavonoids may be helpfulin mast cell stabilization, inhibiting degranulationand the release of damaging mediators.55–59

Quercetin and other bioflavonoids also con-tribute in other ways to mitigate the inflammatoryprocess. Quercetin may be beneficial to connectivetissue by limiting inflammation and associatedtissue degradation, improving circulation, and promoting a strong collagen matrix.60, 61 Quercetinalso plays a part in modulation of the inflamma-tory response, at least in part by modulating pros-taglandin synthesis and cytokine production.62

Quercetin

500–1,000 mg twice daily

Bioflavonoids

500–1,000 mg twice daily

Oregon Grape Root (Berberis Aquifolium).Oregon grape root, a berberine-containingbotanical, is an immune modulator, specificallyin mucosal membranes, and, like vitamin A, maybe effective in treating allergic and inflammatoryconditions like IC due to its effect on T-helpercells.63, 64 In addition, evidence suggests thatberberine may also decrease inflammation byinhibiting arachidonic acid metabolism inendothelial cells.65


Oregon Grape Root

500 mg per day

Corn Silk (Zea Mays). Another botanical,corn silk, has been found to be a potent inhibitorof proinflammatory cytokines as well.66 Corn silkalso has historical evidence for its application in avariety of urinary conditions and may be helpful inthe treatment of IC due to its demulcent effects.67

Corn Silk

300 mg 3 times daily

Additional Botanicals. Other botanicalsmight be considered for their anti-inflammatoryproperties, such as licorice (Glycerrhiza glabra)and feverfew (Tanacetum parthenium). Botanicalswith demulcent properties allow for mucosalprotection and soothing. These include licorice,

slippery elm (Ulmus fulva), marshmallow (Altheaofficinalis), oat seed (Avena sativa), and comfrey(Symphytum officinale).

It can be crucial to use herbs that providepain relief while the other therapies attempt torepair the lining of the bladder. Common choiceswould be kava (Piper methysticum), crampbark(Viburnum opulus), wild yam (Dioscorea villosa),and valerian (Valeriana officinalis).

CONVENTIONALMEDICINE APPROACH

The most likely conventional IC expert will bethe urogynecologist. Dietary modifications arestandard recommendations. A diet low in acidicfoods and avoidance of beverages such as coffee,tea, and carbonated and/or alcoholic drinks canbe helpful in reducing symptoms. The practitioneralso will often recommend Prelief, a nutritionalsupplement discussed earlier in this chapter.

Sample Treatment Plan


Nutrition

Avoid the following foods:

Alcohol Lentils ApplesLima beans Aspartame LimesAvocados Mayonnaise BananasNuts* Cantaloupes OnionsCarbonated drinks Oranges Cheese**Peaches Chicken livers Pickled herringChilies/spicy foods Pineapple ChocolatePlums Citrus fruits PrunesCoffee Raisins Corned beefRye bread Cranberries SaccharineGrapefruit Sour cream GrapesSoy sauce Tomatoes GuavaStrawberries Vinegar LemonsTea Yogurt

*Except almonds, peanuts, and pine nuts**Except American, cottage, ricotta, and cream cheese

If the preceding list is too strict, avoid the following:

TomatoesCoffeeChocolateAlcohol

Supplements

N-acetyl glucosamine: 500 mg 3 times daily; orglucosamine sulfate: 750 mg 2 times daily

L-arginine: 500 mg 3 times dailyQuercetin: 500–1,000 mg twice dailyVitamin C (buffered, noncitrus source):

1,000–2,000 mg dailyCorn silk: 300 mg 3 times dailyKava extract: 1 capsule 3 times dailyVitamin A: 5,000 IU daily


The only oral medication approved for IC by the FDA is pentosan polysulfate sodium (PPS, Elmiron). Other oral medications includeamitriptyline, imipramine (used for pain), hydrox-yzine, antispasmodics, muscle relaxants, andnumerous pain medications. PPS is the most stud-ied conventional medicine for IC. Unfortunately,it only shows about a 30 percent efficacy rate.

Medicine can also be instilled into the bladder.Until PPS, DMSO was the only approved med-ication for IC. The medication is placed directlyinto the bladder through a catheter weekly orbiweekly. Another intravesicular (within the blad-der) therapy is Bacillus Calmette-Guerin (BCG).The mechanism is unknown, but the solutionmay modulate the immune response in the blad-der. Intravesical heparin, hyaluronic acid, andintravesical PPS are other options.

Experimental therapies are being explored,including electrical nerve stimulation to activatethe inhibitory circuits and decrease the sensationof pain, intravesical injection of botulinium toxin,gene therapy, and nerve growth-factor inhibitors.Surgical interventions are currently considered alast resort. These include surgical removal of visi-ble ulcers, laser denervation, or removing a part ofthe colon and attaching it to the bladder toincrease bladder capacity. These surgical proce-dures are still associated with a high rate of relapse,persistent pain, permanent or intermittent needfor catheterization, and additional surgeries.


The symptoms of IC can range in severity frommild and intermittent to chronic and very severe.The main reason to see a licensed health-carepractitioner is to diagnose the cause of the symp-toms. That is easier said than done, and often IC symptoms are misdiagnosed as a urinary tractinfection, endometriosis, a sexually transmittedinfection, or a vaginal infection. On the otherhand, sometimes these, rather than IC, are thecause of the symptoms. Rarely, bladder cancermay be the cause if blood in the urine is present.

The diagnosis of IC is based upon the pre-senting signs and symptoms. A good medical history, physical exam, and tests are done todetermine the cause of the symptoms. A cys-toscopy or intravesical potassium sensitivity testmay be recommended. Once the diagnosis of IChas been made, either with certainty or as a pos-sibility, treatment can proceed. IC is a conditionthat lends itself well to alternative therapies—notonly because they typically work as well or betterthan the conventional options, but also becausethere is no medical danger if conventional treat-ment options are declined. Whether alternativeor conventional medicine or an integration of thetwo is used, symptom improvement is the ulti-mate measure of success.


175

OVERVIEW

There are currently 43 million American womenwho are postmenopausal, and their numbers areexpected to increase to 60 million by the year2020. By the year 2015, nearly 50 percent of thewomen in the United States will be menopausal.This rapid expansion in the menopausal popula-tion is related both to an increase in longevity (toan average life expectancy of approximately 84years) and to the maturation of the baby boomergeneration into the menopausal age group.

Understanding the terminology and defini-tions can be helpful in understanding the naturalbiological process of aging. The term menopauseis derived from meno (month, menses) plus pausis(pause, cessation); in other words, it is a pause inmenstruation. A spontaneous or natural meno-pause is the permanent cessation of menstruationfollowing the loss of ovarian activity and isstrictly defined as the point after 12 consecutivemonths of no menses following the final men-strual period. The average age of menopause hasbeen estimated to be between 50 and 52. In theMassachusetts Women’s Health Study, the largestand most comprehensive study of middle-agedwomen, the median age for menopause was 51.3years.1 The range is generally from age 40 to 58years of age, although some women reach meno-pause prematurely in their thirties and a few aslate as in their sixties. Despite our aging popula-tion and greater life expectancy, the age of meno-pause has not changed in the last few centuries.Three important factors influence the age ofmenopause: current smoking, familial factors,and genetic factors involving the estrogen recep-tors. Other influences may also affect the timingof menopause: increased body mass index (beingoverweight), more than one pregnancy, history of

no pregnancy, toxic chemical exposures, treat-ment of childhood cancers with chemotherapyand radiation, epilepsy, and cognitive scores inchildhood (the higher the score, the later themenopause). There appears to be no linkbetween age of menopause and history of hor-monal contraception, socioeconomic or maritalstatus, race, or age of first menstrual cycle.

Premenopause refers to the period of life fromthe first menstrual period up to the final men-strual period, but this term is often used incor-rectly. To avoid confusion, it’s probably best tonot even use this term. Perimenopause is theperiod immediately before menopause. Peri-menopause starts with changes in the menstrualcycle and ends 12 months after the final men-strual period. In the early stage of peri-menopause, the menstrual cycle length begins tovary by as much as 7 days from the normal cycle.So, rather than having a 28-day cycle, maybe thecycle begins to be a 20- to 21-day cycle from day1 of the menses to the next day 1. In the laterstage of perimenopause, we start to see two ormore missed menses in a year, and the cyclebeing 60 days or more. Some people call peri-menopause the menopause transition or the climacteric. The average age of onset of the peri-menopause or menopause transition is age 47.5.For most women, this transition lasts about fouryears. Only a very small number of women stophaving their menses abruptly. Most of us experi-ence the irregular pattern of bleeding.

Postmenopause begins after the time of thefinal menstrual period, whether it was a naturalor medically induced menopause, and continuesuntil the end of life. It is defined as stage �1(early postmenopause) and stage �2 (late post-menopause). The early postmenopause stage is

12M E N O PA U S E C H A P T E R



five years, which includes the first year since thefinal menstrual period and the next four years.

Menopause should be regarded as a normal,natural event of aging except when it is broughtabout by surgery, medications, or radiation. As wediscuss problems that can be associated with meno-pause for some women, it can quickly be viewed asa disease process and a sign of pending fragility, dis-ability, and even death. It is important to appreciatethat menopause is or can be the beginning of a new phase of life, with fewer family obligations,new options, new learning opportunities, and newadventures. With a proper understanding of peri-menopause and menopause, and an adequatelyinformed and respectful health-care practitioner,the majority of menopausal women can be healthyand happy and use this time period as an opportu-nity to foster a preventive health-care plan andlifestyle as well as an opportunity to assess their life.

Women can enter menopause by several dif-ferent routes and pass through more than onephase. Premature menopause (also called prema-ture ovarian failure, or POF) is a combination ofsecondary amenorrhea, menopausal symptoms,and a persistent elevation in follicle-stimulatinghormone (FSH) levels greater than 20 IU/Lbefore 40 years of age. One in 100 womenbetween the ages of 15 and 40 will spontaneouslydevelop premature menopause.2 In two-thirds ofcases, no apparent cause for the premature ovar-ian failure will be found.3 These cases are calledidiopathic. In one-third of cases, causes of prema-ture menopause include metabolic and systemicdisease, chromosome abnormalities, immunologicdisorders, infections, lack of blood supply to theovaries, cigarette smoking, ovariectomy or bilateraloophorectomy (both ovaries removed), pelvic irra-diation, and chemotherapy.

Some women may experience a temporarymenopause in which normal ovarian function isinterrupted temporarily and the menses stops (for12 months or more). Some medications that areused to treat conditions such as endometriosis orcertain cancers may cause this.

The term induced menopause is used when the menses ceases after surgical removal of bothovaries. This is referred to as ovariectomy orbilateral oophorectomy and may or may notinclude the removal of the uterus (hysterectomy).A hysterectomy is actually only the surgicalremoval of the uterus. These surgeries can bedone separately or together. The incidence ofhysterectomy and oophorectomy in the UnitedStates is substantial. Women who undergo abilateral oophorectomy have an increased risk ofdeveloping osteoporosis, coronary artery disease,and/or atrophy of the genital area at a youngerage. Probably the most dramatic entry intomenopause is to have both ovaries removed.

From 1994 through 1999, an estimated3,525,237 hysterectomies were performed amongU.S. women aged 15 years or older.4 During this time, the overall hysterectomy rate for U.S.women was 5.5 per 1,000 women. The hysterec-tomy rates for women living in the South (6.5 per1,000) is significantly higher than those in theNortheast (4.3) or West (4.8). For women livingin the Midwest, it was 5.4 per 1,000. About 55percent of women who had a hysterectomy had abilateral oophorectomy (both ovaries removed).Uterine fibroids, endometriosis, and prolapse ofthe uterus are the most frequent reasons for thesesurgeries in women aged 15 years and older. Withnew laparoscopic-assisted hysterectomies, ovariesare removed more easily (and this is unfortunate ifthe ovaries are healthy) and removal of the ovarieshas increased significantly, from 20.4 percent in1994 to 42.5 percent in 1999.

When the ovaries are removed, the onset ofmenopause is immediate. The sudden onset ofhot flashes, mood changes, sleep disturbances,and loss of sexual arousal is accompanied by aslower onset of fatigue, headaches, dry skin, boneand joint pain, loss of vaginal lubrication, andpainful vaginal sex. This overwhelming barrageof symptoms results from the sudden drop inhormone production—estrogen, progesterone,and testosterone.

177M E N O P A U S E

Women who have had a hysterectomy butstill retain one or both ovaries will go throughmenopause more naturally most of the time,although sometimes earlier than they would haveotherwise. Without the uterus and the monthlybleeding, it may be harder to know when meno-pause arrives. All the typical symptoms canoccur, though. If you are fortunate to not haveany of the overt menopausal symptoms, you canestimate that you’ll have gone through meno-pause somewhere between ages 48 and 53. TheFSH blood test may be used to determine meno-pausal status.

Other methods of inducing menopauseinclude chemotherapy, medications, or pelvicradiation therapy, which causes the ablation ofovarian function. Women who have been treatedwith chemotherapy may go into menopause eithertemporarily or permanently. About 30 percent ofthese women will have a return of their mensessometime within the first year. Irradiation of thepelvic or abdominal area can also induce meno-pause. Tamoxifen, another cancer drug usedmostly for women who have breast cancer, caneither induce menopause in premenopausalwomen or increase menopause symptoms in post-menopausal women.

Several drugs can induce menopause that isreversible once the drugs are discontinued. Theseinclude Lupron and Synarel, which are usuallygiven to suppress menses in the case of endome-triosis and to shrink fibroids before surgery.Menopausal symptoms tend to be not as severe asin surgical menopause but worse than naturalphysiologic menopause.

Fortunately, all of the sex hormones are notlost with menopause or even with surgical meno-pause. For example, about 50 percent of ourtestosterone comes from the ovaries and adrenalglands; the other 50 percent comes from manydifferent parts of the body, including the liver, theskin, and the brain. These tissues manufacturetestosterone from precursor hormones that aremade in the ovaries and the adrenals. In other

words, the ovaries and the adrenal glands areresponsible for producing all of a woman’s testos-terone, either directly or indirectly. The adrenalglands also produce androstenedione. Andro-stenedione is converted to estrogen (estrone) inthe body fat and to a lesser degree in some othertissues and organs including the muscle and skin.For some women, this source of estrogen is ade-quate to counter some of the menopausal symp-toms, and they have an easier time.

Although this adrenal source of hormonal sup-port is a blessing, the adrenal glands produce theirmaximal amount of androgens in the presence offully functioning ovaries. The function of thecortex of the adrenal glands is linked to the func-tions of the ovaries due to their shared originalgroup of cells in the developing embryo. If youdon’t have your ovaries, then the adrenal glandswill not produce their potential amount of andro-gens. In natural menopause, the ovaries continueproducing androgens (typically referred to as malehormones) that help maintain the potential forsexual arousal.5 Several studies have shown thatsurgically induced menopausal women have lowersexual desires and subjective arousal compared towomen who have retained their ovaries; treatingthese post-oophorectomy women with estrogenand androgens results in a greater sexual responsethan treatment with estrogen alone.6 Surgicalmenopause may also have a psychological impacton women. Not only is this related to the suddenchange in hormone status, but the severity ofdepression that may develop can often be corre-lated to body image, sexual identity, cultural back-ground, and family issues.7

The natural transition from the reproductiveyears to the postmenopausal years is not necessar-ily a smooth one, even though it is a normalprocess of aging. Though not a disease, there canbe health problems associated with menopause.For many women, symptoms of these hormonalchanges occur intermittently for a number ofyears. Dr. Susan Love calls this period “pubertyin reverse.” Just as the hormonal highs and lows


of puberty brought sleepiness, acne, moodswings, and unpredictable menses, this end of the spectrum with its own hormonal fluctuationsmay bring hot flashes, insomnia, mood swings,acne, poor concentration and memory, andunpredictable menses again.

No two women’s menopause transition is alike.Many women begin to experience an array ofphysical, mental, and emotional symptoms longbefore they meet the definition of menopause.

During perimenopause, several biologicalchanges occur:

• The number of ovarian eggs (oocytes)reaches very low levels

• The menstrual cycle begins to vary, usuallyshortening from one menses to the next.

• The levels of FSH in the body increase. Thisrise is one of the first signs of an aging repro-ductive system. Health-care practitioners oftenmeasure FSH levels to determine if one’ssymptoms are related to menopause. There aretwo problems with this test, however: varyingpatterns of FSH may occur even in the samewoman, and the FSH is often normal even ina perimenopausal woman.

• Ovarian production of estradiol, proges-terone, and testosterone decreases with theonset of true menopause.

• Although hormone levels will eventuallydecrease, lower estrogen levels aren’t experi-enced until six months to one year beforetrue menopause. It’s only in the last year ofperimenopause that estrogen levels begin todecrease. Near menopause, estrogen levelsrise very high and then drop very rapidly.Declining progesterone levels precededeclining estrogen levels. Some of the peri-menopause symptoms may in fact be due tolowered progesterone levels or a relativechange in the relationship of estrogen toprogesterone.

• Eventually, the lower levels of estrogen areno longer adequate to cause a buildup of the

uterine lining, and there is not enough tissueto produce a menses.

• The specific reason why menopause occursis the ultimate loss of follicles in the ovaries.This leads to the loss of progesterone pro-duction and declining estrogen influence.This coincides with an increase in FSH andLH (luteinizing hormone).

The symptoms of decreased hormone levelsand perimenopause are varied, unpredictable,and often go unrecognized as perimenopausalsymptoms. The signs and symptoms of peri-menopause can include menstrual irregularities,hot flashes, vaginal dryness and thinning, skinchanges, fatigue, decreased libido, mood swings,depression, changes in memory and cognition,sleep disturbance, hair loss on the head, hairgrowth and acne on the face, heart palpitations,nausea, headaches, urinary tract infections, jointpains, and the beginning stages of osteoporosisand heart disease.

Menopausal Symptoms

The transition to menopause usually beginssometime in a woman’s 40s. Symptoms tend tobegin and increase over a span of months and canlast about four to seven years. Seventy-five to 90percent of women will have transient symptomsthat resolve within this time period and stopwithout any treatment. Maybe 10 to 25 percentwill have symptoms that persist. Vaginal drynessand thinning and problems related to this tendnot to be transient and in fact tend to get worsewith time.

The changes associated with menopause canbe mild, moderate, or severe. Some women mayhave no significant menopausal symptoms, andothers will have symptoms that are progressiveand problematic for many years. The mostcommon prevalent symptoms are vasomotorsymptoms (hot flashes and night sweats), sleepdisturbances, and vaginal dryness. A comprehen-sive list of symptoms includes the following:


• Decline in fertility (perimenopause)• Irregular bleeding (perimenopause)• Vasomotor symptoms• Sleep disturbances• Urinary problems (urinary leakage, urinary

urgency, urinary frequency, infection, pelvicrelaxation)

• Vulvovaginal changes (dryness, irritation,discomfort during sexual activity, discharge,itching, inflammation, infection)

• Headaches• Mood swings• Depression and anxiety• Memory changes• Sexual function effects• Body aches• Skin, mouth, eye dryness• Fatigue

More rare symptoms might include voice impair-ment, shoulder problems, and sometimes strange,rare, and peculiar symptoms that don’t seem to berelated to anything else but are due to hormonalchanges. These might include numbness and tingling sensations, dizziness, and nerve pain, toname a few.

Hot Flashes, Night Sweats. Hot flashes andnight sweats in perimenopausal and menopausalwomen are often referred to clinically as vasomo-tor symptoms. The traditional vasomotor symp-toms, commonly referred to as hot flashes andreported by about 85 percent of menopausalWestern women, are related to the decline in ovar-ian function.8 Hot flashes are the most commonsymptom associated with the menopausal periodand second to irregular menses during the peri-menopausal period. We still do not understandthe physiology of hot flashes, the mechanism oflowered estrogen levels and hot flashes, the averageage of onset, triggers, duration, frequency, or whythey are prominent in some cultures and absent inothers. A few triggers may affect the frequencyand/or severity of hot flashes in some women.Stress, hot or spicy foods, hot drinks, warm envi-

ronments, alcohol, and caffeine are the mostcommon triggers. Hot flashes are sudden, tran-sient episodes ranging from just feeling warm oroverheated to intense heat and perspiration.Women tend to describe a wavelike sensation overthe body, particularly of the upper torso, face, andhead. If the hot flashes occur at night and are asso-ciated with what can be drenching perspiration,they are called night sweats.

The number of women in the United Stateswho are affected by hot flashes is remarkable.About 75 percent of women will experience hotflashes, and 15 percent are severely affected.9 Theoccurrence of hot flashes is highest in the firsttwo years postmenopause, although informationis scanty on the total time over which hot flashesare experienced. Women with surgically inducedmenopause often report particularly persistent,more intense, and more frequent hot flashes. Ithas been determined by one large study that formost women hot flashes last about 2 years,although some women experience them for 5 to10 years.9 As many as 15 percent of women maystill report hot flashes 16 years after menopause.Hot flash frequency is particularly variable andranges anywhere from several episodes in a yearto every hour throughout each day.

Not all cultures report the same incidence ofhot flashes or other menopausal symptoms. Forexample, Japanese and Indonesian women reportfar fewer hot flashes than do women from Westernsocieties.10 Mayan women in the Yucatan do notreport any symptoms at menopause other thanmenstrual cycle irregularity.11 Many researchershave attributed these differences to biological,psychological, social, and cultural factors.

The clearest explanation for hot flashes is thatthey appear to be the body’s response to a suddenbut transient downward resetting of the body’sthermostat, which is located in the hypothala-mus.12 This temporary alteration of the set pointwould cause the sensation of intense heat andflushing. What we don’t know is what triggersthis event. A logical correlation between low


estrogen levels and hot flashes exists. Estrogenlevels have been found to be lower in premeno-pausal women with hot flashes than in thosewithout hot flashes.13 However, not all studiesare consistent, and some women never have hotflashes, while others have persistent ones, and yet others have them only sporadically. Prior topuberty, girls have low estrogen levels, but nothot flashes. Also, hot flashes are reported duringpregnancy, when the estrogen level is high. Someresearchers believe that hot flashes are due to animbalance in beta-endorphins and other opiatesin the brain that in turn may influence the tem-perature regulation center.14 Estrogen and prog-esterone may alter the activity of these naturallyoccurring opiates, and it is possible that lowerlevels of estrogen and progesterone cause a with-drawal of opioids, triggering a hot flash.

What may seem like a hot flash due to peri-menopause or menopause may in rare cases becaused by another condition such as thyroid disease, epilepsy, infection, insulin-producingtumors, pheochromocytoma, carcinoid syn-dromes, leukemia, pancreatic tumors, autoim-mune disorders, or allergic disorders.

Irregular Uterine Bleeding. In the transitionphase of menopause, changes in the amount offlow and the frequency of the flow are the mainsigns of perimenopause. These changes and irregu-larities in the cycle are due to decreased frequencyof ovulation and unpredictable fluctuating levels ofthe ovarian hormones, estrogen and progesterone.The menses can become lighter or heavier, bleed-ing for fewer days, even less than two, or more daysthan your usual length. The cycles can becomeshorter by at least a week, as well as longer than thepattern you have become accustomed to. At somepoint, most women will just skip one or moremenstrual cycles. Basically, changes can occur anywhich way, and each woman will have to identifywhat is an irregular bleeding pattern for her.

Even though these hormonal changes arenormal, the woman with abnormal uterine

bleeding needs to be evaluated by a licensedhealth-care practitioner. Fortunately, in the vastmajority of cases there is nothing serious, and thesolutions are straightforward and effective. Attimes, the bleeding can become too chaotic, and,of course, there are other causes of abnormalbleeding other than perimenopause such as auterine polyp, hypothyroid, uterine fibroids, andendometriosis, to name a few. Chapter 1, onabnormal bleeding, is an important chapter toread to help understand these distinctions.Normal menstrual blood loss is approximately 40mL. Blood loss greater than 80 mL is consideredheavy, especially if there are blood clots or if youbecome anemic. If the bleeding is prolonged,longer than seven days, and/or the cycle is nowshorter than 21 days, and/or bleeding or spottingoccurs between menses or after sexual activity,then these symptoms require investigation by ahealth-care practitioner and effective treatments.

Although perimenopausal women are at riskfor endometrial hyperplasia (a thickening of thelining of the uterus), the majority with abnormalperimenopausal bleeding do not have hyperplasia.In postmenopausal women who bleed and whoare not taking HRT, the bleeding is generally dueto atrophy (thinning of the lining of the uterus).Any uterine bleeding that occurs after the actualmenopause (12 consecutive months since the lastmenstrual period) should be reported to yourpractitioner. In women on HRT, abnormal bleed-ing can be due to too little estrogen, too muchestrogen, too little progesterone, or too muchprogesterone. It is important to see your licensedhealth-care practitioner in order to determine thecorrect hormonal solution and also to determine iffurther testing with a pelvic ultrasound and/oruterine biopsy is necessary. These issues are dis-cussed further in Chapter 1.

Fertility Changes. The decline in fertilityduring perimenopause is related to several factors,including that word we don’t want to hear, “aging”of the ovaries and the uterus. Other specific


changes are going on as well: rising levels of follicle-stimulating hormone (FSH) and changes in thefeedback mechanism that regulates the menstrualcycle. This increase in FSH is a reflection of thelower number of follicles within the ovaries and theless viable quality of the follicles. Fewer follicles,poor quality, and irregular or lack of ovulation con-tribute to this decline in fertility. The blood level ofFSH on day 3 of the menstrual cycle is a good indi-cator of infertility related to aging ovaries.

On the other hand, some women mistakenlythink that if they are in their mid- to late 40s orearly 50s, having some perimenopause symptoms,and haven’t menstruated for a few months, theycannot become pregnant. On the contrary,unplanned pregnancies are common during thistime period. If pregnancy is not desired, contracep-tion must be used until you have not had a mensesfor 12 consecutive months, or until levels of FSHare consistently above 30 IU/L.

Insomnia/Sleep Disturbances. Sleep prob-lems are especially common in perimenopausalwomen, increasing after age 40 and plateauing byage 50. Sleep problems also contribute to fatigue,poor concentration, low motivation, irritability,depression, and anxiety. Insomnia comes in manysizes and shapes, including difficulty falling asleep,difficulty staying asleep, restless sleep, and wakingearly and not being able to go back to sleep. Theseproblems may last only a few days or a few weeksor become chronic with persistent problems morethan three nights per week. The longer or morefrequent the insomnia, the more it leads to poorcoping skills, fatigue, and depression.

A primary problem for many women withhot flashes and nighttime sweats is sleep disrup-tion. Some women are awakened during sleepdue to a night sweat, but sleep disturbances arenot always a result of hot flashes, and not all hotflashes disrupt sleep. Most nighttime hot flashesare associated with waking up, but almost halfthe time a waking episode is not associated withhot flashes. Sleep disturbances and early morning

awakenings are also signs of depression and anx-iety. These emotional changes are also associatedwith menopause for some women.

In addition to the direct influence of hor-monal changes and hot flashes on insomnia, thistime in a woman’s life, quaintly called midlife,can also be a time of significant life changes and challenges. Job stress, relationship loss, childcare, parent care, or medical problems can alterbrain chemistry and sleep patterns. Insomnia canalso be a result of sleep-related disordered breath-ing due to snoring or apnea, chronic pain such asarthritis or fibromyalgia, thyroid conditions, rest-less leg syndrome, asthma, or medications.

Mood Swings, Depression, and Anxiety.The psychological conditions associated withmenopause have been a source of conflicting scientific data and controversy. Even though therelationship between menopause and depressionhas been extensively studied, the results havebeen inconsistent. Some studies have shownmore frequent depressive moods among peri-and postmenopausal women compared to pre-menopausal women, while other studies havenot. It may be that the psychosocial and culturalfactors that influence variations in moods affectwomen more at the time of menopause.15

The Massachusetts Women’s Health Studyconcluded that women who were depressed pre-menopausally had higher rates of depression inperimenopause; for the women who were notdepressed during the premenopause years, the rate of depression was slightly increased duringperimenopause and was highest for women whoremained perimenopausal for at least 27 months.16

Researchers observed that the rate of depressionbegins to decrease as women move from peri- topostmenopause and is lowest for those womenwho have been postmenopausal for at least 27months. These results show that depression ismoderately associated with perimenopause andthat the depression is transient and will declineabout two years after menopause.


A 1997 study was able to demonstrate thatdepression and anxiety were higher in post- thanin perimenopausal women,17 although not allstudies confirm this. This study also showed thatdepression and anxiety scores were reduced tovalues below those of perimenopausal womenwhen the women took hormone replacementtherapy (HRT). Women who take estrogen aloneseem to do best mood-wise, compared to womenwho take estrogen plus synthetic progestogens,called progestins.18

Mood changes may not be as prominent asdepression or anxiety. Many women are plaguedby irritability, melancholy, weepiness, shorttemper, feeling overwhelmed, and a lower toler-ance of stressors. Up to 10 percent of peri-menopausal women experience mood changes.Some of these mood changes are due to sleepdeprivation with or without night sweats. Inthese circumstances, successful treatment for themoods requires treatment of the night sweatsand/or insomnia.

Decreased Memory and Concentration.Trouble concentrating, planning, and learningnew things and difficulty remembering names,words, or what you went into the kitchen toretrieve are common changes experienced bywomen in the menopause and menopause transi-tion. Many of us experience some degree ofchange in memory and concentration and clarityof thinking as we age, but there are also specificcognitive changes that occur when estrogen,progesterone, and androgens are rapidly with-drawn from the system, most commonly short-term memory loss. The relatively rapid transitionfrom the menstruating/reproductive years tomenopause appears to be a factor in these cogni-tive changes, and related to these hormonaldeclines, especially in estrogen. Estrogen affectsnumerous neurotransmitters in our brain, includ-ing acetylcholine, serotonin, noradrenalin, anddopamine. All of these have influences on concen-tration, learning, and memory. This is most dra-

matic after childbirth or after bilateral oophorec-tomy (both ovaries being removed). Short-termmemory impairment is also a common cognitivechange in women with natural menopause. Diffi-culty concentrating, difficulty with previouslysimple technical tasks, decrease in memory, andlack of mental clarity are typical states that canthen be worsened by difficulty sleeping and sleepinterruptions.

An evaluation of significant cognitive impair-ment may be necessary to assess for a thyroidimbalance, medication problems, overuse of seda-tives or alcohol, and dementia. Alzheimer’s disease(AD) is the most common cause of dementia andaffects 1.5 to 3 times more women than men.19

For women on hormone therapy, adjustments inthe dose may improve mental function.

Vaginal Dryness and Thinning. Vaginaldryness, vaginal thinning, and what is calledatrophy are very common problems for meno-pausal women but usually do not become trou-blesome until several years after menopause.Estrogen is responsible for the thickened, elastic,lubricated tissue of the vagina and vulva (externalgenital area). When estrogen levels decline, thevulva loses its collagen, fat, and water-retainingability. As a result, it becomes flattened, thin, anddry and loses tone. With estrogen loss, the vaginaalso shortens and narrows, and the vaginal wallsbecome thinner, less elastic, and pale in color.Problems of vaginal dryness, vaginal discharge,and pain with vaginal sex are reported by two outof three women at the age of 75.20 The changethat is usually noticed first is a feeling of drynessof the vagina. The cause is atrophy of the mucus-producing glands of the vaginal wall. With a lossin lubrication and a thinning of the tissue, thevagina is more prone to infections and mechani-cal injury from vaginal penetration. Small pin-point bleeding, itching, and burning can result.Other tissue in the same area also becomes thinand atrophied. The urethral tissue (exit route forurine), the labia (the “lips” of the external genital


region), and the vaginal wall can all atrophy.These changes can result in increased bladderinfections, involuntary loss of urine (inconti-nence), and prolapse of the bladder, rectum, oruterus. As the atrophy progresses, women mayexperience an increase in urinary urgency or dif-ficulty holding the urine.

Urinary Problems. Urinary incontinenceand recurring urinary tract infections becomemore common in postmenopausal women. Uri-nary incontinence (recurring involuntary leakageof urine) is common and affects from 10 to 30percent of women between the ages of 50 and64. Urge incontinence occurs when there is asudden strong desire to urinate, and stress incon-tinence is urinary leakage with coughing, laugh-ing, sneezing, or lifting. Stress incontinence ismore common during perimenopause and doesnot tend to increase over time, whereas urgeincontinence tends to increase with time.

Other urinary changes include increased uri-nary frequency, sudden urges to urinate evenwhen the bladder is not full, frequent nighttimeurination (nocturia), and increased frequency ofurinary tract infections. As estrogen levelsdecline, the end of the urethra, where we urinate,becomes shorter, and this reduces our defenseagainst the bacteria that cause urinary tract infec-tions (UTI). Lower estrogen levels also cause ourvagina, urethra, and bladder to become morealkaline, which also leaves these areas prone toinfections. Vaginal estrogen therapy is an impor-tant option in restoring the acidic environmentof the vagina and the bladder.

Changes in Sexual Response and SexDrive. Changes in sexual response and libido arecommon throughout life, can be due to a host of influences, and tend to increase with aging.With an increasing number of menopausalwomen, an aging population, and an increasedopenness about the topic of sexuality, women areincreasingly coming to their health-care practi-tioners wanting help in this area.

According to at least one large study, as manyas 30 percent of women have low sexual desire,and about 50 percent of these feel distressedabout it.21 Not all sexual problems come in theform of low desire. Female sexual disorder (FSD)is defined in four main categories: desire disor-ders, arousal disorder, orgasmic disorders, andpain disorders. Sexual desire disorders includehypoactive sexual desire disorder (HSDD),which is a recurrent consistent deficiency orabsence of sexual thoughts, fantasies and/orinterest in sexual activity, and sexual aversion disorder, a persistent or recurrent aversion toand/or avoidance of sexual contact with a part-ner. HSDD increases with age and is morecommon in women after age 60. In fact, it isthought that HSDD is more related to age thanto menopause.22, 23 Sexual arousal disorder isdefined as the inability to attain or maintainsexual excitement and a lack of response to sexualstimulation such as lubrication. Orgasmic disor-der is difficult, delayed, or absent orgasm afteradequate sexual stimulation and arousal. Sexualpain disorders include dyspareunia, genital painassociated with vaginal penetration; vaginismus,involuntary spasm of the musculature of theentrance to the vagina that interferes with pene-tration; and sexual pain related to sexual stimula-tion other than intercourse.

Numerous variables affect sexual function,including emotional and psychological factors,medical problems causing fatigue and/or pain,certain medications (see the following sidebar),and hormonal influences.

Testosterone is necessary for a normal sexdrive in women and men, helping to determinedesire, arousal, and sexual sensation. During per-imenopause, estrogen levels are fluctuating butultimately are declining, and testosterone pro-duction is also declining. The hormonal issuesinfluencing sexual function in women aren’ttotally understood, but fluctuating testosteronelevels have been associated with a decrease inlibido (desire).24, 25 Most, but not all, sexual


problems in postmenopausal women are relatedto estrogen loss to the genitals. Decreased estro-gen levels are responsible for most of the changesand decrease in lubrication during sexual arousal,vaginal tone, vaginal elasticity, and genitalengorgement. This can manifest as a lack of ade-quate vaginal lubrication with sexual arousal,bleeding after vaginal sex, and pain with vaginalsex. Vaginal dryness is not only associated withpainful vaginal sex, but also with a decrease insexual desire.26 It is not hard to understand whyanticipation of painful sex would dampen one’sdesire for sex. With a loss of estrogen, relaxationof vaginal tissue and decreased muscle tone also occur, which leads to a decrease in sexualresponse.

A woman’s total estrogen production decreasesby 70 to 80 percent in menopause, while andro-gen production decreases by about 50 percent. Ifone has a surgical menopause, the plasma levels of testosterone are decreased significantly morethan in women in natural menopause,27 and thiscan result in an even greater incidence of sexualdysfunction than in women who went through anatural physiologic menopause.

Acne, Facial Hair, and Hair Loss. Manyperi- and postmenopausal women have problemsrelated to the change in the ratio of estrogen totestosterone. Even though both hormones havedeclined, there is a relative increase in testos-terone because there is less estrogen to block itseffects. In addition, women have individual sen-sitivities to androgens. Some women only reactto very high levels, while others are especiallysensitive to what are considered normal androgenlevels. In addition, women have different kindsof receptor site and tissue sensitivity. Some willdevelop acne, some thinning hair, and someexcess body and/or facial hair.

Excessive hair growth occurs in areas wherehair follicles are the most androgen-sensitive.These include the face, chin, skin under the jaw-bone, upper lip, sideburn area, and cheeks. Othersensitive areas include the area below the bellybutton, the lateral pubic area, midline of thechest, around the nipple area, and the low backover the sacrum. Hirsutism (excess body hair) ismost notably correlated with elevated free testos-terone, but testosterone must be converted by anenzyme in the skin to be fully active in the skin.This enzyme is probably higher in women whohave excess body and facial hair. These enzymelevels may change in postmenopausal women, orthe hair follicle may become more sensitive to theactivated testosterone in some postmenopausalwomen.

Hair thinning and hair loss are often trau-matic for women and cause a great deal of anxi-ety. Androgenic alopecia (hair loss) is the most

Selected Medications That Can Affect Sexual Function

Reduction in Sexual Desire

AntipsychoticsBarbituratesSelective serotonin reuptake inhibitors (SSRIs)Tricyclic antidepressantsBeta blockersDigoxinSpironolactoneOral contraceptivesHistamine H2-receptor blockers

Reduction in Arousal

AntihistaminesAntihypertensivesSSRIsTricyclic antidepressants

Reduction in Orgasmic Response

AmphetaminesAntipsychoticsNarcoticsSSRIsTrazodoneTricyclic antidepressants


common alopecia in humans and is geneticallydetermined. Androgens modulate hair growth.The follicle responds to the androgens and isdependent on the amount present and the pres-ence and number of androgen receptors. Thethinning of hair that can be seen in menopausalwomen is more likely to be diffuse but is mostcommon on the top of the head (the vertex) and next most common at the crown. Somewomen have a receding hairline and thinning atthe temples.

Weight Gain. One of the more troublingchanges to women during the menopause transi-tion is weight gain, which is often about fivepounds. We don’t understand very clearly if orhow a drop in hormones, and if or how prescrib-ing hormones, affects weight. What we do knowis that aging itself and lifestyle are associated withweight gain. Lean body mass, muscle mass, andthe metabolic rate decrease with age, whichmeans we burn fewer calories. These changes,combined with being more sedentary as we age,can easily lead to weight gain. Hormonal changesin menopausal women are probably associatedwith an increase in insulin resistance, leading toincreased fat storage, increased abdominal fat,and weight gain.

Headaches. Hormonal changes may play arole in headaches, especially in perimenopauseand especially in women with migraine head-aches. Migraine headaches tend to be worse onone side of the head and worse with light andnoise, can be associated with nausea and vomit-ing, and tend to be moderate to severe. The hor-monal changes associated with the menopausetransition can increase the frequency and inten-sity of headaches, especially for those womenwho have a history of menstrual-related head-aches. During times of more stable estrogenlevels, such as during pregnancy, or once meno-pause has been reached, most women will expe-rience a resolution of their headache patterns,especially migraine headaches.

Skin, Eye, and Dental Changes. We alreadytalked about how hormone changes can berelated to acne. Specifically, acne can be the effectof excess testosterone on the glandular secretionsin the skin. Estrogen also has important func-tions in the skin. It determines the skin collagen,skin thickness, and texture. Collagen, a majorprotein in the skin, is dependent on estrogen,and 30 percent of skin collagen is lost during thefirst few years after menopause. As time goes on,more collagen is lost, resulting in increasinglaxity of the skin, wrinkling, and loss of elasticity.The skin also becomes dry more easily.

A variety of changes occur in the eye relativeto hormonal status. Postmenopausal womenreport dry eyes, burning, pressure, light and tem-perature sensitivity, blurring, tearing, eye fatigue,swollen eyelids, and a feeling of scratchiness. Dryeye syndrome can, oddly enough, cause excesstearing, and it appears to also be affected bydrops in testosterone levels.

Fluctuations in hormones during peri-menopause and lower levels in menopause areinvolved in inflammation of the gums, sensitivityof the teeth, tooth loss, and a burning sensationin the mouth and tongue. These symptoms maybe a sign of more serious problems as well. Toothloss may be associated with low bone density andosteoporosis. Burning sensations in the mouthcan be a symptom of diabetes or anemia, andgum inflammation may be related to anincreased risk of cardiovascular disease.

Heart Palpitations. A palpitation can feellike a rapid heart rate, missed heartbeats, or irreg-ular heartbeats. Not all heart palpitations arerelated to a decrease in estrogen levels but may bea symptom of anxiety, panic disorder, fears, ordepression. Fortunately, women in their 40s andearly 50s, during the most common time of themenopause transition, are not likely to have aserious cardiac problem. Nonetheless, thesesymptoms should be evaluated, especially if theyoccur with exercise, are associated with shortness


of breath or chest pain, or if you have a familyhistory of early heart disease or heart attack (menless than age 50 and women less than age 60).

Joint Pains. Another symptom commonlyreported during menopause is joint pain and/orbody aches. This is not currently well under-stood, but it is likely there is a connectionbetween hormones, immune function, andinflammation in the joints. Osteoarthritis, specif-ically, is a common joint disease that increaseswith age and affects women more than men.

Osteoporosis and Cardiovascular Disease.While the symptoms of hot flashes, mood swings,insomnia, sexual dysfunction, and the rest areannoying at best, and can significantly impactquality of life, the most significant changes associated with menopause are osteoporosis andcardiovascular disease. These conditions can dra-matically alter and even shorten one’s life. For acomprehensive discussion on osteoporosis, refer toChapter 14, and for heart disease, refer to Chapter9. Prevalence, risk factors, evaluation, and alterna-tive and conventional approaches and treatmentsare covered in these chapters.

Menopause Evaluation

The onset of perimenopause is an importanttime for a comprehensive health and lifestyleevaluation. A thorough medical history, com-plete physical exam, and selected tests dependingon your age, your symptoms, and other medicalproblems should be done by a licensed health-care practitioner.

While it may seem surprising, there is no onetest for menopause. Tests to determine ovarianfunction are not routinely done because the diag-nosis of perimenopause or menopause is largelyable to be made based on the medical history.Practitioners can use hormone testing on an indi-vidual basis, mostly to differentiate menopausefrom thyroid problems, abnormal causes of a lackof menses such as elevated prolactin levels, orpremature ovarian failure (premature meno-

pause). The follicle stimulating hormone (FSH)test is not as accurate as we would like, but if it isconsistently elevated above 30 mIU/mL, a diag-nosis of menopause can be established. The diffi-culty with FSH tests is that they can fluctuateimmensely, especially in perimenopause. Theother problem is that FSH tests are frequentlynormal in perimenopausal women. It can also bevery difficult to use the FSH test if women are onhormonal contraceptives or hormone replace-ment therapy (HRT or HT).

There is a recent popular notion that saliva orserum testing can be done to determine estrogen,progesterone, and testosterone levels or individ-ual estrogen levels including estriol, estrone, andestradiol. However, saliva testing has yet to beproven accurate for the testing of these hor-mones, although the FDA has approved salivatests for cortisol and DHEA levels. I will focusmy comments on blood serum testing.

For the perimenopausal woman, it is difficultto gather conclusions on test results when thehormones are in such a fluctuating state. Thereare so many peaks and valleys and so mucherratic hormone activity that testing offers littlevalue in most situations. For the women takingHRT, it is tempting to think that we could testthe blood to determine what dose to take. This isa popular recommendation in some consumermenopause books. However, I would point outthat there is no mathematical grid comparingvalues of estrogen or progesterone or of testos-terone levels in the blood and how that wouldequate with a certain dose of the comparable hor-mone. There are reference ranges for these hor-mones, but practitioners don’t know exactly whatdose to give to keep a woman in the referencerange. Women absorb and metabolize hormonesdifferently. The form of hormones and the deliv-ery method—oral, transdermal, sublingual, orinjection—also behave differently from womanto woman. In selective cases, testing may be ahelpful guide. These are generally cases in whicha woman is on HRT and not doing well, and


despite the practitioner’s best efforts with a goodmedical history and adjusting the dose, she stilldoes not feel well. But clearly, the majority of thetime, it requires the practitioner’s experience andmenopause expertise and time to listen to thepatient to know what dose, what dosing adjust-ments, and what forms and deliveries of hor-mones may work best. Even if testing is done, thedecision basically comes down to good clinicaljudgment and the willingness of the woman andher practitioner to try various approaches.

Testing can be done to facilitate assessing awoman’s risk for diabetes, heart disease, and osteo-porosis. Risk assessment for heart disease is dis-cussed in Chapter 9 and for osteoporosis, Chapter14. Diabetes risk assessment is a combination ofhistory and physical exam, glucose screening, andlipid panel testing. Diabetes mellitus is diagnosed

when a fasting plasma glucose test is 126 mg/dL orgreater on two or more occasions or the blood glu-cose is 200 mg/dL or greater two hours after a doseof glucose is ingested.

Other important situations also warrant test-ing and are discussed in the appropriate chaptersin this book. To name a few, abnormal uterinebleeding may need thyroid blood tests, pelvicultrasound, or endometrial biopsy. Urinary tractinfections can be tested with urinalysis and urinecultures. Cervical cancer can be screened for with Pap smears. Breast cancer can be screenedfor with mammograms.


The fundamental goals of an alternativeapproach to menopause are to provide relief fromcommon menopausal symptoms and to preventand/or treat osteoporosis, heart disease, andother diseases of aging. The goal is to do this withmethods that do not increase the risk of life-threatening diseases such as breast cancer, bloodclots, and strokes.

In order to accomplish these fundamentalgoals, the menopausal woman and her practi-tioner must embrace an individualized approach.An alternative and comprehensive approach isdistinct in that the evaluation of each womanlends a great deal of attention not only to indi-vidual symptoms, but also to her individual risksfor future diseases. This requires a comprehensivehealth history; judicious use of tests to assess risksfor osteoporosis and heart disease; an apprecia-tion of risk factors for breast cancer, diabetes, andAlzheimer’s disease; a willingness to individualizethe treatment very carefully; and an ability to uti-lize the whole spectrum of interventions, includ-ing diet, exercise, stress management, nutritionalsupplements, herbal therapies, all available hor-mone options, and prescription and over-the-counter pharmaceuticals.

Although more and more conventional HRTregimens are becoming available and new non-

KEY CONCEPTS

• Find a good menopause practitioner to workwith. Seek the advice of practitioners who caninform you about the spectrum of options.

• Seek out an initial comprehensive evaluation.• Managing menopause symptoms is distinct from

prevention of significant diseases such as heartdisease and osteoporosis.

• Attempt to determine individual risks for signifi-cant diseases—osteoporosis, heart disease,breast cancer, and diabetes.

• Hormone testing is not routinely recommendedand offers limited help in knowing how tomanage your menopause symptoms.

• Be well informed about the process of menopause.

• Be well informed about the spectrum of alterna-tive and conventional treatment options.

• Realize that menopause and aging are processesthat evolve over time.

• What you decide today is not permanent; youcan change your treatment decisions based onyour changing health, changes in medical under-standing and research, and newly availabletreatment options.


hormonal drugs are being developed, a practi-tioner who has an understanding of the wholespectrum of options from the most natural to themost conventional is in the ideal position toproperly advise and prescribe a customized opti-mal treatment and prevention plan. A licensednaturopathic physician is currently the only pri-mary health-care provider trained in all theseoptions, although he or she may have to refer forsome selected expertise in osteoporosis, heart dis-ease, gynecology, or endocrinology. In the past,conventional medicine largely approached thesituation as “HRT for all and forever.” Since2002 and the first Women’s Health Initiativeresearch results,28 women and many of their doc-tors abandoned HRT almost overnight.

At the other extreme is an absolute fear andbias against using HRT for any reason or for anyamount of time. The use of nonhormonal natu-ral therapies has thrived in this environment,both in the form of women treating themselvesand for those seeking advice from licensed alter-native practitioners. In either case, cautionshould be exercised in presuming that just treat-ing the symptoms of menopause is adequate.Keep in mind our fundamental goals: symptomrelief, disease prevention, and disease treatment.While there are many effective nonprescriptionnatural therapies for symptom relief, this doesnot adequately address greater long-term con-cerns such as bone density, blood pressure, cho-lesterol levels, breast health, or vaginal tissuehealth. The identification of disease risks may notbe very important in the early perimenopausalyears, but it acquires increasing importance as thepostmenopause years accumulate. This is why Irecommend that women seek the advice of alicensed naturopathic physician with a strongexperience in women’s health, and menopause inparticular.

In this section on natural medicine, we willfocus on symptom relief. See the chapters onheart disease and osteoporosis for prevention andtreatment of those diseases.

The Naturopathic Approach

In the naturopathic approach to menopause,therapeutic intervention is determined followinga comprehensive assessment of symptom severityand scope and an evaluation of risk factors forosteoporosis, heart disease, Alzheimer’s, diabetes,and breast cancer. A determination of low,medium, or high risk, especially for osteoporosisand heart disease, is especially directive in provid-ing choices regarding alternative and/or conven-tional therapies. Once the symptoms have beenpinpointed and the risks have been assessed, thentreatments are recommended. Treatment consid-erations include a spectrum of options. The seventreatment categories are:

1. Diet, exercise, lifestyle, and stress management

2. Nutritional supplementation3. Botanical supplementation4. Compounded bio-identical hormones5. “Friendlier” conventional HRT6. “Less friendly” conventional HRT7. Nonhormonal prescription medications

You may be surprised to see the inclusion ofconventional hormone replacement therapy inmy list of options. Choosing to use hormones,whether compounded bio-identical or conven-tional pharmaceutical preparations, is a matter ofweighing the benefits and the risks. Hormonaltherapies should be utilized in the lowest dose,shortest duration, and safest way possible thatmeets the goals that have been identified. Theseissues are addressed in the section on hormones.

Diet/exercise/lifestyle and/or nutritional sup-plements and/or botanical therapies will be effec-tive for the management of menopause symptomsin the majority of women. When these are notadequate, individualized formulations of bio-identical hormone options should be used. Ifthese are not adequate, then “friendlier” hor-mone therapy (also bio-identical) is preferredover “less friendly” (synthetic and semisynthetic


and not bio-identical) HRT. (The distinctionsbetween the different kinds of hormones are dis-cussed in the hormone section.) Determining thetreatment approach is a combination of subjec-tive and objective findings resulting from themedical history, physical exam, any lab or diag-nostic imaging tests, and the personal perspectiveand values of each woman. The specifics of theseoptions and therapies will be expanded on as wediscuss nutrition, exercise, nutritional supple-mentation, botanicals, bio-identical hormones,conventional HRT, and nonhormonal drugs.

Nutrition

An alternative approach to menopause isn’t com-plete without proper nutrition. This includes gen-eral considerations such as a diet rich in wholenatural and unprocessed foods, with an emphasison fruits, vegetables, whole grains, beans, seeds,nuts, and healthy fats, and low in saturated fats,fried foods, white flour, alcohol, sugar, and salt.

The Value of Soy. One of the importantdietary recommendations for all menopausalwomen may be to increase foods that are high inphytoestrogens, although their benefits may bemore for preventing osteoporosis, heart disease,and even breast cancer than for the relief ofmenopause symptoms such as hot flashes.

A large number of plants, especially legumes,contain compounds called phytoestrogens.Phytoestrogens are mainly, but not exclusively,nonsteroidal in structure and are either of plantorigin or derived from the body’s metabolism ofprecursors present in dietary components. Themost important dietary phytoestrogens are thephenolic phytoestrogens, which include theisoflavones and the lignans. Soybeans are therichest food source of isoflavones, containing 1to 2 mg of isoflavones per gram of soy protein.The two main isoflavones of soy are genisteinand daidzein. Isoflavones have a unique ability toweakly bind to estrogen receptors in the bodyand seem to have both a weak estrogen effect as

well as an antiestrogen effect, depending on thetissue involved and the dose consumed.

There are hundreds of studies on soy anddozens on hot flashes, some showing effect andothers not, making it difficult to make conclu-sions. For now, I’d like to pass on the results oftwo systematic reviews of isoflavones and meno-pausal symptoms and one consensus opinionfrom the North American Menopause Societythat offer a good summary of the research. Thefirst systematic study was a review of the literaturefor the randomized controlled clinical trials onsoy and perimenopausal symptoms.29 Ten trialswere evaluated, and only four were positive andshowed benefit for perimenopausal symptoms.There were no serious safety concerns with soyproducts for the treatment periods, which wereup to six months. In the second systematic review,25 trials involving approximately 2,300 womenmet the study criteria.30 Soy and red cloverisoflavones were evaluated in this review, includ-ing soy foods, beverages, or powders; soy extracts;and red clover extracts, for a total of 25 studies.Only one soy food trial and two soy extract trialsshowed the ability to reduce hot flushes.

The final report comes from a consensusopinion of the North American Menopause Soci-ety,31 which acknowledges that some data doessupport the efficacy of isoflavones in reducingthe incidence and severity of hot flashes but thatmany studies have not found any difference. Italso concluded that there was not adequate datato evaluate the effect of isoflavones on breast andother cancers, bone mass, and vaginal drynessbut that there were convincing health benefits ofisoflavones and lipids in reducing low-densitylipoproteins and triglycerides and increasinghigh-density lipoproteins. Perhaps the best evi-dence that soy lowers cholesterol comes from areview of 38 scientific studies. This meta-analysisconcluded that consumption of soy protein ratherthan animal protein significantly decreased serumconcentrations of total cholesterol, LDL choles-terol, and triglycerides.32


In terms of menopause symptoms and hotflashes in particular, I’m sure the three reviews aredisappointing news for advocates of soy. It’simportant to appreciate, though, that statisticalsignificance is not the same as clinical signifi-cance for any one person. For some women, andthis has been borne out in some studies, soy pro-tein and soy isoflavones can be helpful in reduc-ing the frequency and severity of hot flashes. Forthe specifics in regard to bone effects and cardio-vascular effects, please refer to the osteoporosisand heart disease chapters.

If you choose to increase soy foods or take soy beverages, powders, or supplements, a wordabout dosages and addressing some of the highlypublicized controversies about soy is important.A reasonable approach would be to ingest a dailylevel of isoflavones that does not exceed theamount consumed in ethnic diets that containhigh amounts of isoflavones. From a review ofthose diets, it appears that this amount is some-where between 50 to 150 mg of isoflavones perday for adults. The isoflavone content of soyfoods varies with the form. A listing of theisoflavone content of some of these soy foods willoffer some help in calculating your daily intake(see Table 12.1).

There have been some controversies aboutsoy, and based on the actual research, these neg-

ative comments and concerns about soy are insome cases incorrect and in other cases highlyexaggerated. Some have pointed out problemswith thyroid function, inhibition of mineral andprotein absorption, and concerns about hor-monal effects.

Some of the controversy about soy lies notonly in its ability to bind to estrogen receptors but in its content of phytates and trypsininhibitors, interference with thyroid function,and difficult digestibility for some individuals.Soy foods, especially cooked soybeans, are diffi-cult for some people to digest, causing gas andstomach upset. Soy’s content of trypsin inhibitorscan block the enzymes needed for protein diges-tion. When the protein is improperly digested,fermentation and gas production ensues. How-ever, many researchers believe that so few trypsininhibitors are left behind after processing the soyfood that for most people, their digestion is notaffected.

The phytate content in soybeans has beenanother cause for concern with soy foods. Phy-tates are compounds found in grains and legumesthat can compete with the uptake of mineralssuch as calcium, magnesium, iron, and zinc.Although the phytate content of soybeans ishigher than that of other grains or legumes, themineral-blocking effect of phytates is reduced

Table 12.1 Isoflavone Content of Soybeans

Soy Food Amount Isoflavones (mg)

Textured soy protein granules 1⁄4 cup 62

Roasted soy nuts 1⁄4 cup 60

Tofu, low-fat and regular 1⁄2 cup 35

Tempeh 1⁄2 cup 35

Soy beverage powders 1–2 scoops 20–50 (varies with manufacturer)

Regular soy milk 1 cup 30

Low-fat soy milk 1 cup 20

Roasted soy butter 2 tbs 17

Cooked soybeans 1⁄2 cup 35


when eaten with meat or fish. If you eat soyproducts in the context of a healthy, varied diet,you should get adequate minerals. Phytates arealso reduced in fermented products such astempeh and miso.

The genistein and daidzein in soy can alsoinhibit thyroid hormone synthesis. High-soybean diets have been implicated in diet-induced goiter. This problem is not likely tooccur with an average amount of soy in the dietand again in the context of a healthy, varied diet,especially a diet that is adequate in iodine, whichis now mostly the case in this country. In somesusceptible individuals, or in some who take veryhigh doses of nutritional supplementation of soyisoflavones (above 200 mg per day) or have anextreme diet low in other nutrients and high insoy, it is prudent to be aware of potential butextremely rare problems with soy ingestion.

One of the greatest fears for women contem-plating menopause treatment options is the con-cern about estrogen replacement therapy andbreast cancer. Although we will be addressing this in the hormone and conventional medicinesections of this chapter, there are several lines ofevidence and logic that support the conclusionthat not only is soy safe, but there is actually arelationship between increased soy intake andbreast cancer prevention. Several studies con-cluded that Asian women who consume a tradi-tional low-fat, high-soy diet have a four- tosixfold lower risk of developing breast cancer.33

The constituents in soy are remarkable in theiractivities against a variety of cancers via severaldifferent mechanisms. Dietary phytoestrogensalso inhibit cancer cell growth by competing withestradiol for the type II estrogen binding sites.34

Even more convincing evidence for the breastcancer protection benefit of soy comes fromanimal studies.35 Soy supplementation hasreduced the number and size of tumors inducedwith a carcinogenic substance.

The most comprehensive review of the litera-ture on soy and its effects on the breast comes

from a paper citing over 280 references.36 Inreviewing animal, laboratory, and human studies,the study’s authors conclude that while there issome conflicting data as to whether soy is protec-tive against breast cancer or is safe or harmful forbreast cancer patients, it is clear from reading thisresearch that the data significantly favors safetyand even protection if consumed from a youngage. The authors concluded that moderation inintake is probably wise and should mimic theAsian soy intake of one to two servings per day.Doubts as to the significance of the breast cancerprotective effects of soy and the safety of soy willremain until there has been a prospective studyon soy comparing women on a high-soy dietwith women on a low-soy diet over the span ofmany years with identical risk factors in otherareas. One specific word of caution to breastcancer patients undergoing treatment withtamoxifen: until it has been determined if soy isbeneficial in addition to tamoxifen or if it inter-feres with tamoxifen, I would recommendagainst daily soy ingestion while on tamoxifen.

For the most part and in most individuals,soy foods will not interfere with thyroid func-tion, protein digestion, or the uptake of minerals,and they are more associated with reducing therisk of hormone-dependent cancers than withincreasing it. Any potential negatives with soy arenot likely to occur with one to two servings ofsoy foods daily, with adequate iodine in the diet,using soy in the context of a healthy, varied dietand focusing on organic sources. Organicallygrown soybeans are grown without pesticides andare not from genetically modified seeds. This isan important issue for soy foods in particular, asgenetically modified soy crops have increasinglydominated in the agriculture business. Fortu-nately, there are farmers and manufacturers whoare committed to raising and producing organicsoy products.

The optimal use of soy would be to start earlyin life and eat a diverse array of soy foods with atotal dietary intake of 50 to 150 mg of soy


isoflavones per day. If you don’t like soy foods, takea high-quality soy protein powder or capsule.

Flaxseed. Another significant dietary sourceof phytoestrogens to consider is flaxseed.Flaxseed contains lignans, two of which,matairesinol and secoisolariciresinol, are knownto have estrogenic activity. Other lignans aremodified by intestinal bacteria to form estrogeniccompounds. Lignans from plants such as flaxseedare absorbed in the circulation and have bothestrogenic and antiestrogenic activity37 much likesoy, although to a lesser degree.

Flaxseed flour and its defatted meal (flaxseedmeal) are the highest plant producers of lignans.The lignan content of flaxseed meal is 75 timeshigher than that of seaweeds (the second highestlignan-containing group) and 804 times higherthan that of fruits (the lowest lignan-containinggroup).37

The evidence that lignans can reduce the riskfor cancer is still unclear, although the biologicproperties of lignans and data from various cul-tures suggest that they do. Many lignans haveantitumor, antioxidant, weak estrogenic, andantiestrogenic characteristics.38–42 Adding to theevidence, urinary excretion of lignans has beenfound to be lower in nonvegetarians and in post-menopausal women with breast cancer as com-pared with healthy women.43–45

Foods for Bone Health. Several dietary factorsaffect bone health and are involved in the develop-ment of osteoporosis: insufficient calcium intake,vitamin D deficiency, low calcium and high phos-phorus intake, low fatty acid intake, insufficientdark leafy greens, a high-protein diet, excess saltintake, and excess alcohol. See Chapter 14 fordietary and lifestyle factors, supplements, herbs,hormones, and other conventional medications forprevention and treatment of bone loss.

Foods for Heart Health. Heart disease is theother major concern in the postmenopausal years.The prevention of heart disease is largely deter-mined by diet and lifestyle. Women who make the

necessary dietary changes have a significant advan-tage in being able to age healthfully and reduce therisk of heart disease. Lowering the level of trans fatsand saturated fats while increasing omega-3 fatsand monounsaturated fats from olive oil are keys toa nutritional preventive approach to heart disease.Diets that are high in cholesterol and saturated fats(beef, pork, lamb, butter, cheese, palm oil, andcoconut oil) contribute to poor fat ratios and ele-vated cholesterol. Even though total fat intakeshould be reduced, switching from saturated fats tovegetable oils will lower total cholesterol levels.Olive oil is your best choice for salads and cooking.

Increasing fiber in the diet with whole grains,fruits, vegetables, and legumes is the optimalhigh-fiber diet. Soluble fiber such as the pectin inapples or oat bran has the most consistent bene-ficial effect on cholesterol levels.46 Specific fruitsor vegetables can also have a positive effect onblood levels of fat. Raw carrots, for example, mayhave a more potent effect in lowering cholesterolthan oat products.47 People with a low intake offruits and vegetables have an increased risk forheart disease.48 See Chapter 9 for dietary andlifestyle factors, supplements, herbs, hormones,and other conventional medications for preven-tion and treatment of heart disease.


Following are the nutritional supplements that areused to treat some of the symptoms of menopause.For an in-depth look at some of the nutritional


Reduce saturated fats (cheese, butter, beef, pork).Avoid trans fats (deep fried foods, margarine, par-

tially hydrogenated oils).Reduce refined grains and flours, sugar, and salt.Use only a modest amount of low-fat dairy products.Increase fruits, vegetables, legumes (especially soy),

whole grains, nuts and seeds, olive oil, and cold-water fish (salmon, tuna, mackerel, herring, hal-ibut, and sardines).


supplements used to treat and prevent heart dis-ease and osteoporosis, consult Chapters 9 and 14.

Bioflavonoids. Bioflavonoids, such as rutin,hesperidin, and quercetin, are usually known fortheir antioxidant and anti-inflammatory proper-ties and their ability to strengthen capillaries.Some evidence exists to show that giving bio-flavonoids in combination with vitamin C willhelp to relieve menopausal hot flashes.49

Bioflavonoids

1,000 mg per day plus 1,000–1,500 mg vitamin C

Vitamin B6. Vitamin B6, or pyridoxine, playsa critical role in the manufacture of serotonin aswell as other amino acid neurotransmitters. Vita-min B6 levels are typically quite low in depressedpatients, especially women taking birth controlpills or conjugated equine estrogens (Pre-marin).50–52 An insufficiency of vitamin B6 mayalso cause insomnia and irritability. Since depres-sion, insomnia, and irritability are typical meno-pausal symptoms, this vitamin may be a helpfuladdition to a supplement program.

Vitamin B6

50–200 mg per day

Warning: chronic intake of dosages greater than 200 mg per day can be toxic over a period of manymonths or years.

Evening Primrose Oil. Currently, naturalproducts for menopause often include eveningprimrose oil (EPO) because it has a reputationfor alleviating vasomotor symptoms such as hotflashes. However, a study on the effects of gammalinolenic acid (GLA) from evening primrose oilfound it to offer no benefit over placebo in treat-ing menopausal flushing.53

Cyclic breast pain is a common symptom inmenstruating women before their period. In peri-menopausal women, this symptom can be exacer-bated or can occur in women who have not had

the problem in the past. Results of research andclinical trials have consistently shown that EPO iseffective in relieving breast pain and premenstrualcyclic breast pain.54–56 (See Chapter 7 for moreinformation about this and other treatments forpainful and lumpy breasts.)


1,500–3,000 mg per day

Gamma-Oryzanol. Gamma-oryzanol is asubstance found in grains and is isolated fromrice bran oil. This ferulic acid compound is pres-ent in rice, wheat, barley, oats, tomatoes, aspara-gus, olives, berries, peas, citrus fruits, and otherfoods. The concentrations are higher in wholegrains than in refined grains and flours.

Gamma-oryzanol was initially shown to beeffective in relieving menopausal hot flashes in theearly 1960s,57 and at least one additional study hasconfirmed that finding.58 The typical dosage ofgamma-oryzanol is 100 mg three times daily.

Gamma-Oryzanol


Vitamin E. The considerable reputation ofvitamin E as a remedy for hot flashes comes fromstudies done as far back as 1945.59–62 The problemis that vitamin E has received very little scientificattention for this use since those early studies. Onlyrecently has there been renewed research interest,largely born of the need to provide menopausalbreast cancer patients with safe and effective medi-cines for symptom relief.63 Patients received fourweeks of vitamin E (800 IU per day), then fourweeks of an identical placebo, or vice versa. Hotflash frequency decreased by 25 percent in the vita-min E group and 22 percent in the placebo group.Although this is considered a statistically significantdifference, the clinical impact of this reduction wasmarginal, and the patients did not particularlyshow a preference for vitamin E over placebo.


Vitamin E


Botanical Medicines

Phytoestrogens. As discussed in the nutri-tion section, phytoestrogens are plant-derivedsubstances that are able to activate the estrogenreceptors in mammals. They are mainly, but notexclusively, nonsteroidal in structure and areeither of plant origin or derived by the body’smetabolism of precursors present in dietary com-ponents. Phytoestrogens are present in virtuallyevery plant in varying amounts.

Phytoestrogens are capable of exerting weakestrogenic effects in some parts of the body, andthey also have antiestrogenic effects due to theirability to occupy estrogen receptor sites andblock the estrogen produced by our own bodiesfrom binding. Since the phytoestrogens are somuch weaker than the body’s estrogen, the neteffect is significantly less estrogenic stimulationin the target organ.

Phytoestrogens are found in many medicinalherbs with a historical use in conditions that arenow treated by estrogens. The weak estrogeniceffects of phytoestrogen-containing herbs canprovide some benefit in relieving menopausesymptoms. One advantage of phytoestrogens isthat they have not been associated with increas-ing the risk of breast cancer. In fact, epidemio-logic data and experimental studies in animalshave demonstrated that phytoestrogens areextremely effective in inhibiting mammarytumors, not only because they occupy estrogenreceptors but also through other unrelated anti-cancer mechanisms.64, 65

The common phytoestrogen compounds, theisoflavones, have a similar structure to the body’ssex hormones. They have the ability to bind toestrogen receptors on human cells, and inwomen they have a preference for binding to thebeta form of the estrogen receptor. As a result,

they preferentially express estrogenic effects inthe central nervous system, blood vessels, bone,and skin without causing stimulation of thebreast or uterus, at least in typical doses.66

Dong Quai (Angelica Sinensis). Dong quai,also known as tang-kuei, dang-gui, and Chineseangelica, is an aromatic herb widely used through-out Asia. In Asia, dong quai is to women’s healthwhat ginseng is to men’s. It has predominantlybeen used as a female remedy to treat menopausalhot flashes, menstrual cramps, lack of menstrua-tion, or frequent menstruation and to promote a healthy pregnancy and easy delivery. Thecoumarins in dong quai are found largely in theroot. The potential estrogen-like activity of dongquai has been assumed because of its observed tra-ditional uses and clinical effects, and evidenceincludes its ability to cause an initial increase inuterine contraction, followed by relaxation67 andits effect in increasing uterine weight when givento mice.68 These observations may be a partialexplanation as to why dong quai may be useful inmenopause, although clearly there is some benefitat least for issues related to missed menses or fre-quent menstruation.

In a 12-week study conducted by Kaiser Per-manente, using dong quai as a solo agent for therelief of menopausal symptoms such as hotflashes and sweats did not prove to be effective.69

More research is needed on use of dong quai incombination with other herbal preparations.

Dong quai may increase the flow of a periodor bring on a menses. In a perimenopausal womanwho is either already having heavy flow problemsor may have missed a menses for several months,this may be alarming. In this case, dong quai isprobably not the best herbal choice for yourmenopausal symptoms.

Dong Quai

Dry herb used in combination with other herbs in cap-sule form or

Tincture: 1⁄2–1 tsp 1–3 times per day


Ginkgo (Ginkgo Biloba). Ginkgo is theworld’s oldest living species of tree with fossilrecords as old as 200 million years. The leaves ofyoung, cultivated trees are used in modern herbalpreparations. Two groups of active constituents—the terpene lactones and the ginkgo flavone glyco-sides—are the most critical compounds ofstandardized herbal products. Many forms andmethods of preparation of ginkgo are available,although a high quality of Ginkgo biloba extract istypically standardized to 24 percent ginkgoflavone glycosides and 6 percent terpene lactones.The actions of these constituents include improv-ing blood flow to the brain70 and to the hands andfeet.71, 72 Although ginkgo extract has not beenspecifically studied in menopausal women withmemory or cognition problems, it has been usedto improve memory.

Clinical studies have demonstrated the efficacyof Ginkgo biloba extract (GBE) for the treatment ofmemory loss, depression, and disorientation associ-ated with cerebrovascular insufficiency in geriatricpatients.73–75 Two studies have shown gingko to beeffective for patients with mild to moderate pri-mary dementia of the Alzheimer’s type or multi-infarct dementia.76, 77 Patients who received ginkgoshowed memory and attention improvements andsignificant improvement in cognitive function testsand depression. Relative differences for dementiawere not observed. I think it is important toinclude ginkgo for menopausal women becausechanges in mental clarity, memory, and concentra-tion are common, and it may be that ginkgo willhave an increasing role in improving these symp-toms for this group of women.

Another commonly reported change in peri-and postmenopausal women is a drop in their sexdrive. Extract of ginkgo appears to be remarkablyeffective in reversing antidepressant-inducedsexual dysfunction in women as well as men.78

Although the sexual dysfunction in this studywas drug-induced rather than the result ofchanging hormones, I recommend trying thissafe and simple approach.

Ginkgo Biloba

40–80 mg standardized extract capsules or 1⁄2–1 tsptincture 3 times per day

Ginseng (Panax Ginseng). There are manytypes and grades of ginseng and ginseng extractsthat include related species. Panax ginseng, alsoknown as Korean or Chinese ginseng, is the mostwidely used. A standardized extract of ginsenghas been shown to improve depression and well-being in 384 postmenopausal women.79 Anotherrandomized controlled trial found that onemonth of Korean red ginseng increased energyand decreased insomnia and depression.80

Historically, ginseng has been used as a “tonicfor invigoration and fortification in times offatigue and debility and for declining capacity forwork and concentration.”81 Ginseng can help inreducing mental or physical fatigue,82–85 enhanc-ing the ability to cope with physical and mentalstressors by supporting the adrenal glands,86 ortreating the atrophic vaginal changes due to lackof estrogen.87

Panax Ginseng

Standardized extract capsules: 200 mg 5% ginseno-sides or 100 mg 10% saponin ginsenoside per day

High-quality root: 4–6 g per day

Licorice (Glycyrrhiza Glabra). The majoractive constituent in licorice root is glycyrrhizin.Much of the attention on licorice root has cen-tered on its anti-inflammatory, antibacterial,antiviral, and expectorant (promotion of theelimination of mucus from the lungs or bronchi)properties, but for menopausal symptom reliefwe are more interested in the estrogenic activityof some of its phytoestrogen components, includ-ing beta-sitosterol, formononetin, coumarin, andothers, in particular beta-sitosterol, which is1⁄400th as active as estradiol.88 However, the gly-coside of glycyrrehetinic acid has been shown tohave an antiestrogen activity, inhibiting the effect


of estradiol on uterine growth in ovariectomizedanimals.89 It may be that licorice has both hor-mone and antihormone effects, or it may in factlower estrogen levels while simultaneously raisingprogesterone levels. This creates some confusionin thinking about why and when to take it, andat this time we cannot really clear up the confu-sion because there is insufficient research toaccount for the use of licorice as a single meno-pausal herb. Licorice may, however, be used incombination with other herbs as part of an effec-tive formulation for symptom relief.

Licorice

Dry form used in combination with other herbs in cap-sules or

Tincture: 1⁄2–1 tsp 1–3 times per day

Red Clover (Trifolium Praetense). Redclover, a member of the legume family, has beenused worldwide as a source of hay for cattle,horses, and sheep, and the leaves and youngsprouts have been used by humans as a source ofprotein. Historically, it has also been recognizedas a medicinal plant for humans and, morerecently, as a menopausal herb.

At least six clinical trials have been conductedon the effect of red clover isoflavones on vasomo-tor symptoms. Three show benefit, and three donot. The first two published studies on red cloverand vasomotor symptoms showed no statisticallysignificant difference between the red clover stan-dardized extract and the placebo.90, 91 Two otherstudies showed positive results in reducing hotflashes.92, 93 The two most recent studies con-tinue the contradictions. In a 2002 study, 80 mgof isoflavones per day resulted in a significantreduction in hot flashes as compared to base-line.94 Another recent study, called the ICEstudy, compared two different doses of red cloverisoflavones with placebo. The reductions in themean daily hot flash count at 12 weeks were sim-ilar for groups receiving 82 mg of isoflavones, 57mg, and the placebo. However, in comparison

with the placebo group, the hot flashes werereduced more rapidly in the group receiving 82mg of isoflavones.95

Other effects of red clover also have implica-tion in menopausal women. One publishedstudy showed that red clover isoflavones mayreduce the risk of coronary vascular disease byincreasing arterial elasticity, although it did notimprove cholesterol levels.96 Red clover isoflavonesmay also slow bone loss of the spine.97

There have been no significant adverse orintolerant reactions with red clover, no signifi-cant change in blood parameters used to measuretoxicity, and no evidence of uterine bleeding orincreased endometrial thickness. In fact, an 80mg red clover extract did not increase the thick-ness of the lining of the uterus in postmeno-pausal women, despite its high content ofphytoestrogens.98

I cannot offer women who have a history ofbreast cancer the same degree of reassurance aboutusing red clover as I can with black cohosh. I donot consider it definitely contraindicated, becausein fact red clover has a rich history in herbal med-icine as a treatment for cancers of all kinds. Onecan see the logic of its use in cancer because of itsgenistein and daidzein constituents, both knowninhibitors of tumor growth and cancer cell divi-sion. However, the results of an experiment thatcompared the relative effects of several differentherbs on estrogen-receptor positive breast cancercells in vitro raised concern.99 Surprisingly, thebreast cancer cells in the laboratory responded thesame to red clover as they did to estradiol. Thequestion of safety or concern with using red cloverextracts in postmenopausal women with a historyof estrogen receptor positive breast cancer remainsunanswered.

Red Clover

Standardized extract of 40 mg total isoflavones, 1 tablet 1–2 times per day or

Dry herb capsule (500 mg): 1 per day


Nonphytoestrogen Herbs

Black Cohosh (Cimicifuga Racemosa). Blackcohosh, Actaea racemosa or Cimicifuga racemosa, isa member of the buttercup family and is used for avariety of women’s health conditions. In the last 25years, it has emerged as the most studied of theherbal alternatives to hormone replacement ther-apy for menopause symptoms. Since the 1980sand up through 2005, numerous studies, includingseveral randomized controlled trials, have been car-ried out using a standardized extract of blackcohosh, with encouraging but mixed results.100–106

In one of the largest studies, 629 women withmenopausal complaints received a liquid standard-ized extract of black cohosh at 40 drops twice perday for six to eight weeks. As early as four weeksafter beginning the therapy, a clear improvement inthe menopausal ailments was seen in approxi-mately 80 percent of the women. After six to eightweeks, complete disappearance of symptomsoccurred in approximately 50 percent.107

In 2006, one study using a standardizedextract of black cohosh seemed to indicate bene-ficial effects on bone metabolism by stimulatingbone-building cells and a weak effect on matura-tion of vaginal cells,108 and another showed noeffect on menopausal symptoms.109

In a third study, the Herbal Alternatives forMenopause (HALT) Study, five groups werestudied: black cohosh (160 mg/daily), a multi-botanical herbal formula including black cohosh,a multibotanical formula plus dietary soy, conju-gated equine estrogen (0.625 mg/daily), andplacebo.110 Hot flash frequency and intensity didnot differ between the herbal interventions andplacebo at 3, 6, or 12 months with one excep-tion. At 12 months, symptom intensity was sig-nificantly worse in the group that received themultibotanical formula plus dietary soy versusthe placebo group. The unfortunate news here isthat black cohosh extract, in a higher dose thanis generally used in clinical practice, did not showbenefit in the relief of hot flashes.

In a double-blind, randomized, placebo-controlled study, a combination of black cohoshand Saint John’s wort was studied.111 The SaintJohn’s wort plus black cohosh group was signifi-cantly superior to the placebo group on scalesmeasuring menopause symptoms and depression.

The average recommended dose of the stan-dardized extract of black cohosh is 40 to 80 mgper day. The clinical studies performed prior to1996 used doses of 40 to 140 mg of standardizedextract. Although there is still some confusionabout which dose of black cohosh may be mosteffective, the dosage used in most clinical trials todate is 20 to 40 mg of the standardized extracttwice daily.

Despite the two negative studies in 2006, thecollective study findings and clinical anecdotalevidence on black cohosh teach us that it is effec-tive for menopause symptoms of hot flashes,mood swings, sleep disorders, and body aches.

Left unanswered is, how does black cohoshwork? Early studies found it to have estrogenicactivity,112 whereas other studies in the last fewyears have demonstrated no phytoestrogens inblack cohosh and no estrogen-like effects on LHor FSH. In addition, prolactin levels, estradiol,and endometrial thickness were not affected byblack cohosh.113, 114 Most recently, scientistsfrom the University of Illinois have reported thatconstituents in black cohosh bind to opiatereceptors and activate responses, including coretemperature regulation.115 At the moment, themechanism of action is not clear, although somehave postulated an effect on serotonin levels.

Over these same 25 years, safety and toxicitystudies have also been conducted on blackcohosh, and it has been subjected to increasedscrutiny, as has hormone replacement therapy.Two areas that receive the most attention arewhether black cohosh is safe in breast cancerpatients and if there are any adverse effects onliver function.

We don’t know with certainty that blackcohosh is safe to use in breast cancer patients, but


we have compelling safety data that offers muchreassurance. There are two recent excellent reviewsof the literature on the safety of black cohosh.116,

117 The more comprehensive Low Dog paperaddresses safety in special populations, such asbreast cancer survivors. Recent studies find thatthere is no estrogenic action of black cohosh, thatit does not effect serum levels of estradiol, LH,FSH, and prolactin.113, 114 In addition, in vitrostudies have shown that black cohosh did notcause increase in proliferation of estrogen receptorpositive breast cancer cells, and it had an additiveeffect of inhibiting proliferation when given withthe antiestrogen drug tamoxifen.118–120 A veryrecent study demonstrates that black cohoshinhibits the growth of human breast cancer cells.99

The other area that has received a lot of atten-tion in the last two years is whether black cohoshhas adverse effects on liver function. Reports andhuman clinical trials including more than 2,800patients demonstrate the low incidence of adverseevents associated with black cohosh. The WorldHealth Organization (WHO) CollaboratingCenter for International Drug Monitoring data-base of adverse reactions to pharmaceutical andherbal products revealed a total of 35 adversereactions to black cohosh as of July 31, 2000. Thereactions were primarily general and temporarysymptoms and were not concentrated on a partic-ular organ system. This list did include one caseof liver failure, one case of hepatitis, and one caseof elevated liver enzymes. These cases were relatedto unspecified amounts of black cohosh andunspecified products. Some studies on animalsreported increased liver weights associated withvery large doses over an extended period of time.

Australia, Canada, and selected Europeancountries have elected to require a warning labelon black cohosh about liver effects. In the UnitedStates, the National Institutes of Health (NIH)concluded in 2004 that there was no competentevidence to support concerns about safety in theuse of black cohosh in breast cancer patients andthat there is inadequate evidence that black

cohosh preparations are causally associated withhepatotoxicity. No warning labels are required onblack cohosh products in the United States. Inthe recent Osmers study, liver enzyme testing was done, and there was no adverse effect on liverfunction tests.103 Another recent long-termobservational study published in the journalMenopause in 2006 found no endometrial prolif-eration, no negative effect on breast health, and nohepatotoxicity after 52 weeks of 20 mg of blackcohosh extract in postmenopausal women.121

These facts, and a review of the scientific literature, do not present a compelling case for concern.116, 117 The only true contraindication toblack cohosh that I can point out is for the cancerpatient taking cisplatin. This is based on an in vitrostudy in which black cohosh slightly protectedmouse mammary tumor cells from cisplatin.122

Black cohosh did not alter the response of the cellsto radiation or 4-HC and had an enhancing sensi-tizing effect for doxorubicin and docetaxel. Veryoccasional side effects have been reported thatinclude gastrointestinal discomfort, headache,nausea, vomiting, weight gain, and vertigo.

Standardized extracts of black cohosh continueto be one of the most reliable herbal approaches to treating a wide array of perimenopausal andmenopausal symptoms. The most commondosage is 40 mg daily, but many achieve betterresults with 40 mg twice daily. One should expectresults within four weeks. In my experience, about85 percent of women will receive benefit, andmaybe 50 percent will achieve complete ameliora-tion of their hot flashes and night sweats. Blackcohosh can also be safely and effectively used withhormone therapy. Lower doses of hormone ther-apy are often achieved by also using black cohoshextract at the same time.

Black Cohosh

Standardized extract capsules (40 mg per capsule):1–2 capsules twice per day

Standardized liquid extract: 1⁄2–1 tsp twice per day


Chaste Tree (Vitex Agnus Castus). As an herbfor the management of menopausal symptoms, Ibelieve chaste tree has been overpromoted. Thefruits of chaste tree contain essential oils, irridoids,pseudoindicans, and flavonoids, and the effect ofchaste tree is on the hypothalamus-hypophysisaxis. It increases secretion of LH and also has aneffect that favors progesterone.123–125 The result isa shift in the ratio of estrogen to progesterone andconsequently a “progesterone-like” effect. One ofthe most common changes that occurs in themenopause transition is irregular bleeding.Whether it be frequent or infrequent, heavy orlight, ultimately a change and cessation will occur.In the process, some will experience significantbleeding problems because of menses that areeither too frequent or too heavy. These problemsare some of the most convincing indications forchaste tree.

The first major study on chaste tree was pub-lished in 1954.126 Although this study was pre-dominantly treating women with amenorrhea(lack of menses), a dramatic improvement wasseen in 40 patients with cystic hyperplasia of theendometrium (excessive thickening of the uterinelining). The impressive effect lends credence to itsprogesterone effect. Chaste tree was also studied inwomen with frequent menses and heavy menses,although they were not perimenopausal.127 Inwomen who had frequent menses, the durationbetween periods was lengthened, and in womenwith excessive bleeding, a shortening of thenumber of heavy bleeding days occurred.

Chaste tree is the most important herb tonormalize and regulate the menstrual cycle. It isnot a fast-acting herb, so do not hesitate to use itover a long period of time. Results may not beachieved until after three to six months.

Saint John’s Wort (Hypericum Perfora-tum). Saint John’s wort is the most thoroughlyresearched natural antidepressant. The majorityof these studies have not been conducted onmenopausal women, but in 37 of 39 clinicaltrials, Saint John’s wort was shown to be superiorto the placebo or equal to the conventional pre-scription antidepressant medications. In general,studies have shown improvement in individualswith mild to moderate depression.128 In a recentreview of studies, a total of 37 trials, including 26comparisons with placebo and 14 comparisonswith synthetic standard antidepressants, wereevaluated. The authors concluded that “current evidence regarding hypericum extracts is incon-sistent and confusing. In patients who meet criteria for major depression, several recentplacebo-controlled trials suggest that the testedhypericum extracts have minimal beneficialeffects while other trials suggest that hypericumand standard antidepressants have similar benefi-cial effects.”129

One non-placebo-controlled clinical trialconducted in women with menopause symptomsfound that 900 mg of Saint John’s wort for 12weeks significantly improved psychological and

Chaste Tree

Standardized extract capsules (175 mg of 75% agnu-side): 1 capsule per day

Standardized liquid extract: 30–60 drops per day

Sample Treatment Plan for Mild Depression, Irritability, and Mood Swings


Diet:Reduce alcohol, avoid sugar and simple

carbohydrates.Eat whole grains, vegetables, nuts, seeds, adequate

fish or low-fat dairy, proteins, and legumes.Eat regularly three meals per day.

Lifestyle: Get 30–60 minutes of exercise daily. (SeeAppendix A.)

Botanicals:Black cohosh: 40 mg standardized extract twice

dailySaint John’s wort standardized extract: 300 mg 3

times per day


psychosomatic symptoms as well as a feeling ofsexual well-being.130

As mentioned earlier, in a double-blind, ran-domized, placebo-controlled study using a com-bination of black cohosh and Saint John’s wort,the study group was significantly superior to theplacebo group on both a general menopauserating scale and a depression scale.111

Saint John’s Wort

Standardized extract of 3 percent hypericin: 300 mg 3times per day

Kava (Piper Methysticum). Kava is a plantindigenous to Melanesia, Micronesia, and Polyne-sia. Its properties have been most often associatedwith analgesic, sedative, anxiolytic, muscle relaxant,and anticonvulsant effects. While kava is typicallynot often thought of as an herb for menopause,anxiety, irritability, tension, nervousness, and sleepdisruption are common perimenopause and meno-pause symptoms in which kava can offer some help.Kava has been used as a social and ceremonial bev-erage for generations by the people of Fiji and otherislands of the South Pacific, at least in part to createa relaxed, stress-free atmosphere. Kava has beenshown to have significant effects in reducing anxi-ety in a number of studies.131

Three randomized, controlled trials haveinvestigated the value of kava for menopausalsymptoms.132–134 The first two showed signifi-cant reduction in anxiety and general menopausesymptoms and the third a reduction in the anxi-ety scale, with kava plus HRT showing the great-est improvement.

In 2003, another valuable study evaluated theeffects of kava on anxiety, depression, and meno-pause symptoms in perimenopausal women forthree months.135 Eighty women were random-ized to one of three groups. The control groupknowingly received 1,000 mg of calcium per day,the second group received the calcium and 100mg of kava, and the third group received the calcium and 200 mg of kava. There was a clear

and similar reduction in depression and anxietyin the two kava dosing groups compared with the calcium alone control group, but not a cleardecline in general menopause symptoms scores.

Kava

Standardized extract (70% kavapyrones): 100–210 mgper day

Additional Botanicals and CombinationHerbal Products for Menopause

The natural food stores and drug stores are brim-ming with herbal menopause products thesedays. You will find the herbs we have discussed inmost of them in one combination or another,and perhaps in combination with nutritionalsupplements, soy, or additional herbs that con-tain phytoestrogens or have some other thera-peutic benefit specific to menopause. Most ofthese combination products have not beenresearched, even though individual ingredientshave been. I am aware of only one herbal combi-nation product that has been researched in adouble-blind, placebo-controlled trial. I was oneof two principal investigators on this study,which set out to research the effects of a botani-cal formulation containing phytoestrogens onmenopausal symptoms, serum lipids, and someof the hormone indicators of menopause.136

The treatment group took two capsules ofburdock root, licorice root, motherwort, dongquai, and wild yam root three times per day.After three months, women receiving the herbalproduct showed a greater response rate thanwomen in the placebo group. One hundred per-cent of women taking the botanical formula hada reduction in their symptom severity, while only67 percent of women receiving the placeboshowed a decrease. Seventy-one percent ofwomen taking the herbal formula reported areduction in the total number of symptoms, whileonly 17 percent of the women taking the placeboreported a decrease in the total number of their


symptoms. The botanical formula was most effec-tive in treating hot flashes, mood changes, andinsomnia.

Numerous other herbs can be helpful forindividual menopause symptoms. The GermanCommission E (the German agency similar toour FDA) has approved hops for mood issuessuch as anxiety and restlessness and for sleep disruptions.137 Hops contain a group of non-steroidal phytoestrogens called prenylflavonoids.In one study, 67 menopausal women were giveneither a placebo or a 100 mcg or 250 mcg stan-dardized hop extract for 12 weeks.138 At 6 weeks,the 100 mcg dose was significantly superior tothe placebo, but not after 12 weeks. Even so,there was a more rapid decrease in menopausesymptoms for both doses of hop extract, espe-cially the hot flash score. The higher dose was notany better than the lower dose.

Valerian has been used for centuries by manydifferent cultures and has been used in moderntimes, mostly for anxiety and insomnia. Threerandomized clinical trials have showed improve-ment in sleep quality, although none of these stud-ies were specific to menopausal women.139–141

Motherwort is another plant that has beenused historically in situations that are relevant toperimenopause and menopause. It can ease heartpalpitations and act as a calming agent, known as a nervine. The German Commission E hasapproved its use for nervous cardiac problems.142

OVERVIEW OF HORMONEREPLACEMENT THERAPY

Hormone replacement therapy (HRT), nowoften called HT as well, has been used since the1950s to treat menopause symptoms and to pre-vent osteoporosis and heart disease. Several keystudies, of the last nine years in particular, havechallenged previously held beliefs about thesafety and efficacy of long-term HRT use. TheWomen’s Health Initiative (WHI) was the mostfamous of these studies and was a large-scale, randomized, controlled clinical trial of 16,608

menopausal women aged 50 to 79.28 This study,of 0.625 mg conjugated equine estrogens (Pre-marin) and 2.5 mg medroxyprogesterone acetate(Provera) was halted prematurely after 5.2 yearsdue to a slight increase in the risk of breast cancerin women receiving the HRT. Women in thehormone group also appeared to have higherrates of strokes, heart attacks, and blood clotsthan the placebo group. The HRT users also hada reduced risk of colorectal cancer and fractures,but overall the risks outweighed the benefits.This study marked a significant moment in his-tory for HRT, and millions of women discontin-ued their HRT as a result of the findings. In thefive years since the WHI, many studies have beencompleted, shedding new light on why decadesof observational studies of postmenopausalwomen using HRT differed from the WHI studyand why there seems to be such disparityamongst some of the key studies in the area ofmemory, heart disease, and breast cancer in par-ticular. While reviewing each of these studieswould be informative, I would like to summarizeand utilize the 2007 position statement of theNorth American Menopause Society (NAMS)and its expert advisory panel of clinicians andexperts in the field of women’s health.143 The pri-mary goal of understanding HRT research inperi- and postmenopausal women is to come tosome determination as to the risks and benefits ofestrogen therapy (ET) and estrogen-progestogentherapy (EPT) for symptom relief and diseaseprevention and treatment. For a more compre-hensive discussion on osteoporosis and heart dis-ease, and on the benefits and risks of ET andEPT, I refer you to Chapters 14 and 9.

The NAMS panel offered two main categoriesof recommendations: those where the panel wasable to reach consensus and those where they werenot. There are several factors involved in the lack ofconsensus recommendations: the timing of whenHRT was started in relation to perimenopause andmenopause accounts for part of the difficulty.Starting HRT in early perimenopause has a differ-


ent risk-benefit profile than starting 5, 10, or evenmore years beyond the last menstrual period. Inaddition, the panel acknowledged that there isinsufficient scientific data on the risks of long-termuse of HRT for symptom control versus the long-term use for reduction of risk of certain diseasessuch as osteoporosis, heart disease, or even demen-tia. Another difficulty faced in drawing conclusionsfrom the HRT research is that not all the groups ofwomen studied are comparable. Some groups havemore women on statins (drugs for high cholesterol)and others have more overweight women, smokers,or previous users of HRT. These are just some ofthe significant variables involved in comparing onestudy to the next.

Recommendations for the Use of HRT

The following summarizes the areas of consensusrecommendations for the use of HRT,143 alongwith some additional input for clarification anddiscussion.

Evaluation Prior to Starting HRT. Allwomen should have a complete health evalua-tion, including a medical history and physicalexamination and a mammogram within the pre-vious 12 months before HRT. Decisions on bonedensity testing are made based on each situation.

Hot Flashes. The primary indication forusing HRT is for the treatment of hot flashes andnight sweats.

Vaginal Symptoms. Most systemic and vagi-nal ET and EPT products are approved for treat-ing symptoms of vulvar and vaginal atrophy.These symptoms include vaginal dryness, painfulvaginal sexual activity, and atrophic vaginitis. Ifone or more of these symptoms are the onlymenopause symptom, then a local vaginal estro-gen is recommended rather than products thatdeliver a systemic effect.

Progestogens. Progestogens include bio-identical progesterone and progestins (which are synthetic). The primary purpose for the use

of these products is to provide protection to the lining of the uterus when estrogen is given.Postmenopausal women who have a uterus andwho are given estrogen need an adequate dose ofa progestogen in order to prevent endometrialcancer. For women who have no uterus, a proges-togen is generally not prescribed with the systemic estrogen. (Some practitioners, and espe-cially alternative-minded practitioners, believethat giving a bio-identical progesterone can haveadditional health benefits other than protectingthe uterus from the estrogen. A discussion on this is included in the section on bio-identicalprogesterone later in this chapter.) A progestogenis generally not indicated when a low-dose vagi-nal estrogen is used for local vaginal effects.

Coronary Heart Disease. “The majority ofobservational and preclinical studies support thepotential benefits of systemic ET/EPT in reduc-ing coronary heart disease (CHD) risk. Mostrandomized clinical trials do not. Emerging datasuggest that these disparities in findings may berelated to the timing of initiation of ET/EPT inrelation to the proximity of menopause. It is cur-rently not clear if ET/EPT can prevent CHD inwomen who do not have evidence of CHD(called primary prevention). There is current evi-dence that initiating ET/EPT in perimenopausalor early postmenopausal women may indeedoffer protection, but this needs further evalua-tion. For women who already have evidence ofCHD, EPT does not provide prevention offuture cardiovascular problems (called secondaryprevention). For the moment, the NAMS panelstates that the use of ET/EPT is not recom-mended for the purpose of coronary heart diseaseprevention in women, no matter their age. It isalso important to note that in the WHI study ofestrogen only, there was no increased risk ofCHD.144

Venous Thromboembolism (Blood Clots).Postmenopausal women who use ET or EPT havean increase in the risk of venous thromboem-


bolism (VTE). This tends to appear during thefirst one to two years after starting the hormones,and it tends to decrease over time. In the WHI,there were 11 additional cases per 10,000 womenper year of using EPT and 2 additional cases per10,000 per year in the ET-only women aged 50 to59. It is thought that lower doses of estrogen maybe safer, and possibly estrogen delivered transder-mally as well (creams, gels, and patches).

Stroke. Both ET and EPT appear to increasethe risk of ischemic strokes (deficiency of bloodsupply caused by a clot) in postmenopausalwomen, although clinical trials have not beenconsistent. There were 8 additional strokes per10,000 women per year in the WHI EPT groupand 12 additional strokes per 10,000 women peryear in the WHI ET only group. This is consid-ered rare for the EPT group and slightly aboverare for the ET group. The risk is even lower inwomen who are 50 to 59 years old or within thefirst five years of menopause. Women whoalready have cardiovascular disease have a higherrisk of stroke even without the use of hormonetherapy. The panel concluded that no HRT regi-men should be used for the primary or secondaryprevention of stroke, and HRT should be partic-ularly avoided for women who have an elevatedbaseline risk of stroke.

Diabetes Mellitus. Large good studies sug-gest that HRT reduces the onset of diabetes mel-litus (DM). Women in the EPT group of theWHI had a 21 percent reduction in DM or whatresulted in 15 fewer cases per 10,000 women peryear of hormone use. Even so, the panel does notrecommend the use of EPT for the sole purposeof DM prevention.

Breast Cancer. According to the WHI, breastcancer risk slightly increases in women on EPTafter five years of use. This risk was rare, slightlyless than having a first-degree relative with breastcancer, but resulted in four to six additional breastcancers per 10,000 women per year in EPT usersfor five or more years. It is not clear if there is a dif-

ference between women who use HRT daily andthose who cycle their hormones by going off for afew days per month. In the ET arm of the WHI,there was no increase in the risk of breast cancereven after seven years of use, and in fact there wereeight fewer cases of breast cancer per 10,000women per year of use of estrogen only.144

EPT increases the proliferation of breast cells,breast pain, and density of mammograms. ETonly does this to a lesser degree. In fact, it is pos-sible that EPT may interfere with the radiologi-cal interpretation of mammograms. (Otherresearch has shown that women who take EPTand acquire breast cancer get diagnosed earlier onmammograms and have less invasive disease,smaller tumors, and better outcomes.)

Osteoporosis. Both ET and EPT reduce therisk of osteoporotic fractures. For women whohave osteoporosis or are at high risk for fractures,ET/EPT is a treatment option. One shouldweigh the benefits and the risks of this and othertreatment options.

Depression. Short-term ET may have anti-depressant activity in perimenopausal womenbut not in older postmenopausal women. Thepanel did not support the use of ET or EPT forthe treatment of depression.

Dementia and Cognitive Decline. StartingEPT after age 65 is not recommended for the prevention of dementia or cognitive decline.The Women’s Health Initiative memory studyshowed an increase in the risk of dementiaduring the five years in women 65 and older.145

It is not yet clear as to whether ET or EPT canprevent dementia when hormones are startedduring perimenopause or early postmenopause.

Premature Menopause and PrematureOvarian Failure. Women who have the onset ofmenopause early, and especially prior to age 40,have lower risks of breast cancer, but earlier onsetof bone loss and CHD. It is not known if ET orEPT affects these conditions in this populationof women. It is logical to think that younger


women who start ET or EPT may experiencemore benefits, but this is not known.

Risks and Benefits. An overriding perspec-tive of ET and EPT use offered by the NAMSpanel is that HRT should be used based on cer-tain goals and evaluating the benefits and risksfor each individual woman. This should also takeinto account the cause of menopause (surgical,medications, normal physiology), time sincemenopause, and scope and severity of symptomsand their impact on quality of life, as well as theunderlying risk of cardiovascular disease, stroke,clots, DM, dementia, and depression.

Dosing. Lower doses should be consideredand can provide adequate symptom relief inmany women, while also being able to stabilizebone loss. Some women will not achieve ade-quate results with lower doses or may need anadditional vaginal estrogen for local vaginalsymptoms. These lower ET and EPT doses arebetter tolerated in terms of less breast tenderness,for example, and may have a better risk-benefitprofile, although this is not known for certain.

Non-Oral Hormones. There is some evi-dence that transdermal estradiol suppliedthrough patches, gels, or creams is less likely tocause blood clots because it initially bypassesmetabolism by the liver, which has clotting fac-tors. There is no evidence that transdermal estro-gens are any safer for the breast.

Additional Issues. Some additional guide-lines are offered by the advisory panel. Theresults of the WHI are relevant especially forwomen in their mid-60s but should be extrapo-lated with caution for perimenopausal women,women younger than 50 who use HRT, and forwomen early in their menopause. Short-term use (less than five years) in symptomatic peri-menopausal and early menopausal women isgenerally considered beneficial with very smallrisks.

Long-term use of the lowest effective dose ofET or EPT is a decision that many women may

want to make based on the benefits they receivein relieving their menopause symptoms. Thesebenefits may outweigh the risks. Other womenwho may want to use HRT long term are womenwith osteoporosis who also have moderate tosevere menopause symptoms. Another group iswomen who have low bone density for whomother nonhormonal therapies cause too manyside effects or do not work to slow bone loss. Forwomen who have been on HRT and decide tostop, symptoms have about a 50 percent chanceof recurring.

The panel’s position on bio-identical hor-mones that are compounded for an individual bya special pharmacy is that any risk-benefit datapertaining to other kinds of hormones alsoapplies to these compounded hormones. Theyalso expressed a concern as to quality controlissues with some bio-identical compounded hor-mone prescriptions. (In my opinion and experi-ence, quality control is not an issue withcompounding pharmacies that are operated bylicensed pharmacists with oversight by state andfederal agencies.)

There were only two areas where the panel didnot reach consensus. How to discontinue HRTwas one area. Some clinicians recommend abruptdiscontinuation of HRT, while others taper thedose. In general, it doesn’t seem to affect thereturn of menopause symptoms. In women whohave a history of severe symptoms, tapering thedose is a compelling approach, and I find it to bepreferable. However, there is not current data tosuggest whether stopping abruptly or reducinggradually over time is better. The other area withlack of agreement is whether taking estrogen andprogestin every day has a different effect thancycling the estrogen and progestin or just cyclingthe progestin. There is some concern that dailyprogestin may be related to the adverse breastcancer and cardiovascular effects, but the data isconflicting on this topic.

The panel concluded that each woman willhave to decide for herself based on her own goals


and her own concerns relevant to benefits andrisks of long-term HRT. An age of less than 60 andwithin the first four years of menopause are themore optimal times to use HRT. The potentialrisks are small, and even rare, except for stroke,especially for women who use estrogen only. Forwomen younger than 50 and at low risk for CHD,stroke, osteoporosis, breast cancer, and coloncancer, the risks or benefits for HRT are evensmaller than those described in the WHI. Again,it is important to emphasize that each womanshould have an evaluation prior to hormone useand should be informed of potential risks.

Bio-Identical or Natural Hormones

One of the greatest areas of confusion in meno-pause medicine today is the subject of bio-identical or natural hormones. The bio-identicalhormones include estradiol, estrone, estriol,progesterone, testosterone, and dehydroepian-drosterone (DHEA). These hormones are dis-tinct from many of the commercially availableprescription hormones—some of which are syn-thetic, while others may be derived from a natu-ral substance but are still not bio-identical.Bio-identical hormones are made from eitherbeta-sitosterol extracted from the soybean orfrom diosgenin extracted from Mexican wildyam root. Those compounds are made into thedesired hormone that is biochemically identicalto the hormone the body produces. By defini-tion, a “natural” hormone is plant derived andbio-identical. The bio-identical estrogens includeestriol, estrone, and estradiol. By contrast, non-bio-identical hormones are intentionally differ-ent in chemical makeup from the body’s naturalhormones and include conjugated plant estro-gens, conjugated equine estrogens, syntheticestrogens, synthetic progestogens, called prog-estins, and synthetic testosterone. It is the chem-ical structure of a hormone, not its source, thatdetermines if a hormone is bio-identical or not.

For the past 50 years, conjugated equineestrogen, under the brand name Premarin, has

been the most commonly prescribed estrogen inthe United States. Conjugated estrogens arederived from pregnant mares’ urine. In the 1970sit was believed that Premarin consisted of only10 estrogens—17 beta-estradiol, 17 beta dihy-droequilin, 17 beta dihydroequilenin, 17 alphadihydroequilin, 17 alpha estradiol, estrone, equi-lin, 17 alpha dihydroequilenin, delta 8-9 dehy-droestrone sulfate, and equilenin. Since then,advancements in technology have revealed thatthe original 10 estrogens make up less than 40percent of the hormonal content of Premarin.Using modern analytical techniques, today over200 individual components have been identified,including androgens and progestins.146 The com-position of Premarin is complex, and differentestrogens produce various effects in different tissues. Herein may lie a theoretical basis for apotentially different effect of conjugated equineestrogens versus bio-identical estradiol. Dr. JoelHargrove has shed some light on these distinc-tions for years.147 His hypothesis is that a non-bio-identical hormone may act like an environ-mental toxin to the genetic material within the cellbecause even though it can bind to the receptorhormone complex, it is a foreign substance.

Besides the effect on the genes themselves,bio-identical hormones and non-bio-identicalhormones may very well leave what Dr. Hargrovecalls a “different metabolic footprint” on the restof the body with different metabolic conse-quences. They may be directly cytotoxic to estrogen-sensitive tissues, bind differently to dif-ferent kinds of estrogen receptors, alter bindingof other hormones to those receptors, or alter theliver’s metabolism of carcinogens. It is this dis-tinction and potential difference in metabolicconsequences, as well as the shorter half-life ofbio-identical hormones, that motivates me to usealmost exclusively bio-identical hormones.

Bio-identical estrogens are available as eithera patented conventional hormone prescriptionmade by a pharmaceutical company and dis-pensed from a regular pharmacy with a prescrip-


tion, or in a nonpatented form from a specialtypharmacy called a compounding pharmacy, alsoavailable only by prescription. There are a fewkey advantages to the compounded forms. First,health-care providers can create customizeddosing regimens and potencies to fit each indi-vidual woman, which can be adjusted in smallunits to taper a woman onto or off of treatment.Second, the pharmaceutical company versionshave additives, binders, adhesives, or preserva-tives included in their formulations because theypatent one or more of those or the delivery tech-nology rather than the estrogen itself. As moreand more practitioners recognize, these chemicalsubstances can cause reactions and side effects inmany individuals. These can include skin reac-tions, headaches, digestive problems, or others,only because of the chemical additive, notbecause of the estrogen itself.

Third, bio-identical hormone formulationshave a vast array of delivery options to attend tothe specific individual needs of each patient.Capsules, sublingual lozenges or pellets, creams,gels, vaginal creams or gels or tablets, nasalsprays, and even pellets that are implanted underthe skin are available in an infinite array ofdosing combinations. These exceed the limitednumber of doses and deliveries that are availablein either the pharmaceutical company bio-identical hormone preparations or the syntheticand semisynthetic prescription items.

Finally, bio-identical estrogens include estra-diol, estriol, and estrone, as I mentioned earlier.Bio-identical progesterone, testosterone, andDHEA are also available. Any combination ofthese hormones can be formulated in a com-pounded hormone prescription: any dose, anycombination, and the numerous delivery options.

I am not suggesting that bio-identical hor-mones are innately good and other hormones areinnately bad. I want to stress that there currentlyis no scientific evidence that bio-identical estra-diol has a better safety profile than the non-bio-identical estrogens of synthetic estrogens,

conjugated equine estrogens, or conjugated plantestrogens. (There are, however, some clear andpotential advantages to bio-identical proges-terone over progestogens.) Much of the decisionas to which kind of hormone to take depends onthe woman.

Some would argue that the advantage of con-ventional pharmaceutical company HRT is thatit has undergone years of scientific study. Whilethis is true, there has been little effort to makedistinctions between different kinds of estrogens.Also, as you will see, combining estriol withestradiol, and the use of bio-identical proges-terone and testosterone with the estrogens, pro-vide the potential maximum benefit and a moreindividualized approach for each patient.

Bio-Identical Estrogens

Estrogen is the major hormone that has beenused to treat menopausal symptoms. There arethree dominant estrogens in the body: estradiol,estrone, and estriol. Estradiol is the primaryestrogen produced by the ovaries. Estrone isformed from estradiol. Estriol is produced inlarge amounts during pregnancy and is a break-down product of estradiol. Before menopause,estradiol is the body’s predominant estrogen;after menopause estradiol levels drop so thatestrone becomes the predominant estrogen. Bio-identical estrogen preparations mirror these threenaturally occurring estrogens in your body.

Estriol. Naturally occurring estriol is pro-duced by the body almost exclusively duringpregnancy. Practitioners of alternative medicineprimarily use estriol to treat menopausal symp-toms because it is considered to be the safestform of estrogen—it is thought to be less car-cinogenic than estradiol and estrone and is aboutone-fourth the potency.

Several researchers have studied the use ofestriol on postmenopausal women. Symptomsthat were alleviated with estriol treatmentincluded hot flashes, insomnia, and vaginal dry-


ness and itching during intercourse. A commonproblem associated with menopause is atrophicvaginitis, a condition that occurs when estrogen islacking in the body. Symptoms may include vagi-nal dryness, pain with penetration, increased fre-quency of vaginal and urinary tract infections,urinary incontinence, and urinary frequency andurgency.

Estriol can be taken orally, in capsules ortablets, and intravaginally in a cream, gel, or sup-pository to treat urinary incontinence, urgency,persistent urinary tract infections, and recurringvaginal infections. I often prescribe estriol vagi-nal cream or suppositories for dry or itchy tissuerelated to low estrogen, vulvar/vaginal discom-fort with sexual activity, urinary incontinence,and recurrent urinary tract and vaginal infectionsin women who are peri- or postmenopausal.These creams most likely work by restoring thevaginal flora, which improves vaginal and blad-der health, and increasing lubrication, elasticity,and thickness of the vaginal skin cells.

Estriol cream is equal to the estradiol ring indecreasing vaginal dryness, decreasing atrophicsigns (signs of thinning), and decreasing the vagi-nal pH to a more preferred acidic environment.However, the estriol cream may not be quite asgood at decreasing the itching.148 Estriol has alsodecreased the incidence of bladder infections.149

A common prescription is 1 mg of estriol pergram of cream. One gram of cream is inserted inthe vagina daily for two weeks as a loading dose,then twice a week as a maintenance program.

Estriol

Oral estriol: 1–4 mg per dayVaginal cream (1 mg/g): insert 1 g every night for 2

weeks, then twice weekly as a maintenance dose

Estriol and Endometrial Cancer. Althoughthere has been a good deal of study as to theeffects of estriol therapy on the endometrial oruterine lining (conventional estrogen therapiescause a thickening or overgrowth of the lining,

called endometrial hyperplasia, that can lead tocancer), there have been mixed results. In typicaldoses from 1 to 4 mg, there appears to be nothickening of the lining of the uterus. If I wereprescribing higher doses, I would advise usingestriol along with a proven progestational agentto protect the lining from this thickening effect.

Estriol and Heart Disease Risk. Estriol hasnot been studied as extensively as conventionalHRT in terms of its affect on the risk for heartdisease; however, a few studies indicate positiveeffects of estriol, while others have found estriolto have no effect on blood cholesterol levels, aprecursor of heart disease.150 There is no clearrisk or benefit related to estriol and heart disease.

Estriol and Bone Density. Estriol also hasbeen minimally studied regarding its effects onbone density and loss; therefore, I do not useestriol to slow or prevent bone loss or to treat lowbone density. The research is just not convincingenough at this point. However, estriol taken withcalcium lactate supplements may help preventbone loss that occurs during menopause.

Estriol and Breast Cancer. Women oftenopt against conventional HRT because they areafraid that it might put them at risk for breastcancer. Many practitioners and researchers agreethat there is a slight increased risk, and deliveringthe safest possible hormone options continues tobe a goal. This has led some to study and useestriol for reducing the risk of and treating breastcancer.

Henry Lemon, M.D., a leading researcher onestriol, has concluded that small doses of estriolgiven in a noncontinuous dosing or cyclic sched-ule provides protection from breast cancer.Although his hypothesis and work is interestingand provides an appealing basis in which to useestriol, his findings have not been followed upwith rigorous clinical trials. The results of otherresearch has not been promising.151 Estriol,estrone, and estradiol all stimulated humanbreast cancer cells in tissue cultures. However,


estriol may reduce the negative effects of thecancer drug tamoxifen for women already diag-nosed with breast cancer.152

Prescribing Estriol. Estriol seems to be help-ful in treating many of the symptoms of meno-pause such as hot flashes. However, the jury is stillout as to whether estriol will protect you fromconditions such as osteoporosis and if it providesany heart disease protection or adverse cardiovas-cular effects. Women who currently have breastcancer or who are survivors must weigh the bene-fits and risks after being provided with well-balanced information. The prudent thing to do,given current research, is for breast cancer sur-vivors to avoid the use of oral estriol. Vaginalestriol for vaginal dryness, however, is a preferredform of vaginal estrogen for breast cancer sur-vivors. In a study of 11 postmenopausal womenwith vaginal atrophy who were treated for eightweeks with 0.5 mg/day of estriol vaginal creamdaily for three weeks then twice weekly for fiveweeks, there was no change in blood levels ofestradiol or estrone.153 In another study of 74postmenopausal women with vaginal atrophytreated with vaginal estriol cream, while bloodestriol levels rose initially followed by a gradualdecline, the levels of the stronger estrogens,estrone and estradiol, were unchanged.154 This isconsidered reassuring for breast cancer survivors.

A popular practice for prescribing com-pounded natural estrogens is to combine thepotentially safer estriol with small doses of estra-

diol and estrone. Currently, practitioners whoprescribe a triple-estrogen compound typicallyuse a formula of 80 percent estriol, 10 percentestradiol, and 10 percent estrone. Progesterone isadded to the formula at a minimum of 100 mgper day to protect the uterus from the potentialeffects of the estrogen in thickening the lining ofthe endometrium. Using estrogen only, withoutthe proper dose of progesterone, in women witha uterus might put them at risk for endometrialhyperplasia or even endometrial (uterine) cancer.

I use a bi-estrogen formulation containingestriol and estradiol, which is increasingly popularbecause of concerns that estrone may be associatedwith more carcinogenic estrogen metabolites andthus an increase in the risk of breast cancer.

Bio-Identical or Natural Progesterone

Many people make the mistake of using the termprogesterone when they really mean its syntheticcounterpart, progestin. Progesterone is the othernatural hormone your ovaries make, other thanestrogen, and its main function before meno-pause is to support pregnancy. Progestin is theterm applied to the synthetic derivatives, whichdiffer in biochemical structure from proges-terone. Progestins are the synthetic hormonesused in conventional hormone replacement ther-apy and birth control pills and are what oftenaccount for the side effects that some women feelwhen taking these medications such as irritabil-ity, depression, bloating, and mood swings.These side effects are due to the progestins’ ten-dency to cause water retention, affect brainchemistry, and alter other steroid pathways. Pro-gestogen is a term applied to any substance pos-sessing progesterone qualities. It can refer toprogesterone or a progestin.

During the perimenopausal phase, when awoman may have months or years of irregularovulation, her production of progesterone beginsto decline. Progesterone falls to almost zero inthe beginning of menopause, while estrogenlevels decline to about 40 to 60 percent of pre-

Tri-Estrogen and Bi-Estrogen Formulation Dosages

Tri-estrogen formulation (estriol 1 mg/estradiol .125mg/estrone .125 mg/progesterone 50 mg): 1 cap-sule twice daily (equivalent to 0.625 mg Premarin� 2.5 mg Provera)

Bi-estrogen formulation (estriol 1 mg/estradiol .250mg/progesterone 50 mg): 1 capsule twice daily(equivalent to 0.625 mg Premarin or 2.5 mg Provera)


menopausal levels. The progesterone deficiencyexplains many of the perimenopausal symptomssuch as mood swings, hot flashes, vaginal dry-ness, and irregular menses.

In treating perimenopause and menopausesymptoms, progesterone can be used for the reliefof symptoms and to balance the effects of estro-gen on the uterus. It has a critical role in prevent-ing endometrial hyperplasia (an overgrowth orthickening of the uterine lining) and uterinecancer. Progesterone is often touted in the natu-ral products marketplace as effective for the pre-vention and treatment of osteoporosis, butclinical trials show that neither oral natural prog-esterone nor progesterone patches or creams canslow, prevent, or reverse bone loss.

I can’t stress enough that if you are peri- orpostmenopausal and are taking any form of estro-gen, you must also take a proven form and dosageof progesterone (or progestin) to protect youruterus from hyperplasia and cancer. The excep-tion is women who have had a hysterectomy; theydo not need to take progesterone or progestins.However, there are times when adding naturalprogesterone rather than increasing the dose ofthe estrogen, even in women without a uterus,may alleviate some menopausal symptoms. Somewomen’s insomnia, fatigue, mood swings, andother menopause symptoms may be more respon-sive to progesterone than to estrogen.

It is important to note that all progestins (the synthetic progestogen) can have undesiredside effects.155 Premenstrual symptoms such asincreased breast tenderness, edema, irritability,and abdominal cramps are fairly frequent, caus-ing as much as 40 percent of women to not taketheir prescriptions properly. More serious sideeffects are rare and include high blood pressure,blood clotting, and altered carbohydrate lipidmetabolism.156 If you try the synthetic progestinsand find you cannot tolerate them, bio-identicalprogesterone is an excellent option. In fact, bio-identical progesterone is a preferred option notonly to minimize these symptoms, but it also

may have a positive affect on cholesterol profilesand help to keep the coronary arteries in theheart dilated.

If you are taking estrogen and are one of thefew women who cannot tolerate either the syn-thetic or natural progesterone, you must be mon-itored by a primary care practitioner to watch forcertain cancers such as uterine cancer.

Progesterone is available with a prescription inthe form of an oral capsule, sublingual drops, sub-lingual pellets, lozenges, or transvaginal or rectalsuppositories; it also may be injected. Progesteroneis also available over the counter as a cream.

Progesterone Creams. The most popularform of progesterone is the topical cream. Thegoal of natural progesterone cream is to supportthe waning daily production of progesterone inthe body and keep progesterone at normal levels.The goal is not to supply pharmacological levels(higher doses), as is the case with oral progesterone.Unfortunately there is currently considerable con-fusion and misinformation about progesteronecreams. There are two basic categories of creams:

• Those that contain wild yam and no progesterone

• Those that contain diosgenin extract (a phy-toestrogen compound) from wild yam thatis converted into natural progesterone in alaboratory

The problem is that the creams that contain onlywild yam are not effective as a progesterone agentbecause the body cannot convert the diosgeninto progesterone.

The confusion is further exacerbated by thevaried strengths of the creams. The wild yamcreams with bio-identical progesterone addedcome in a wide range of dosages. Some of theseproducts have less than 2 mg of progesterone perounce of cream, some have between 2 and 15 mgper ounce, and some have as much as 400 mg perounce or more. It is important to know exactlywhat you are getting because the strength of the


cream will dictate how it is used and what symp-toms it should be used for.

As a practitioner, when using the proges-terone creams, I largely use the creams that haveat least 400 mg per ounce because they yield thebest results for most women suffering from PMS,menopause symptoms, and irregular bleeding. Ingeneral, these doses of bio-identical progesteronein cream form tend to be effective for mildersymptoms of menopause.

In general, women tolerate bio-identical prog-esterone cream extremely well, and most find iteffective for alleviating some menopausal symp-toms. Very few women experience side effects(reported as less than 4 percent by the manufac-turing companies), but these may include breasttenderness, drowsiness, depressive moods, head-aches, and irritability. In my experience as a clini-cian, I have found very few side effects.

Bio-identical progesterone cream is typicallyused for menopausal symptoms such as hotflashes, mood swings, sleep disruption, and irreg-ular and/or heavy bleeding. Absorption of prog-esterone from the creams through the skin isvariable from person to person. A study evaluat-ing different concentrations of progesteronecreams has demonstrated that the progesteronecan be measured in the blood if the cream is

applied on a regular basis.157 This same study alsodemonstrated significant improvement in hotflashes and night sweats. However, another studyon transdermal progesterone cream delivering 32mg daily did not show evidence that it suppliedsufficient hormone to enter the body to achieve abiologic or therapeutic effect on lipid levels orbone mineral markers or to improve vasomotorsymptoms or moods.158 Bio-identical proges-terone cream has yet to be adequately studied toshow sufficient protection of the uterus whengiven with an oral estrogen or estrogen patch.

I do not recommend that progesteronecreams be used to prevent heart disease, osteo-porosis, breast cancer, endometrial hyperplasia,or uterine cancer. There is continuing researchon the benefits of progesterone creams, but todate there is insufficient evidence that they pro-tect women from any of these conditions.

Oral Micronized Progesterone (OMP).While bio-identical progesterone creams are pop-ular with women in menopause, only the oral,injectable, and vaginal gel forms, available byprescription only, are available in high enoughconcentrations to protect against endometrialhyperplasia, a thickening of the uterus that canlead to cancer.

Studies demonstrate that oral micronizedprogesterone (OMP) is effective in preventingendometrial hyperplasia associated with estrogenuse.159 It does not undermine estrogen’s bone lossbenefits, nor does it improve bone density whenit is added to estrogen replacement,160 and it doesnot appear to increase the risk of heart disease.161

However, I can’t stress enough that if you areperi- or postmenopausal with an intact uterusand taking any kind of estrogen, you must alsotake a proven form and dosage of progesterone(or progestin) to protect your uterus from hyper-plasia and uterine cancer. If you do not toleratesynthetic progestins, bio-identical progesteroneis an excellent option. If you are one of the smallnumber of women who do not even tolerate bio-


Apply natural progesterone cream (400 mg proges-terone per ounce) to the palms, inner upper arms, orinner thighs.

Perimenopausal Women

Days 1–7: do not use progesterone cream duringmenses

Days 8–21: 1⁄4 tsp twice a dayDays 22–28: 1⁄4–1⁄2 tsp twice a day

Menopausal or Postmenopausal Women

1⁄4 tsp twice daily continuously


identical progesterone and you are taking anestrogen, then you and your uterus must be reg-ularly monitored by a primary care practitioner.

OMP is available by prescription from a com-pounding natural pharmacy in any dose yourprovider prescribes. It is also available from aconventional pharmacy under the trade namePrometrium. For perimenopausal women whoare taking estrogen every day, oral progesteronecan be given at a dose of 100 mg per day everyday, or it can be given at 200 mg per day on days15 to 26 of the cycle.

These doses are based on an average dose ofestrogen replacement or less. For higher doses ofestrogen, the dose of progesterone will need to beincreased as well, typically doubled. Progesteroneis prescribed on a cyclical basis (as opposed toevery day) for women who are still bleeding. Thiscycling of the progesterone allows them to stillhave a monthly period, the onset of which occurswithin a few days of stopping the progesterone.

Sublingual Progesterone. Sublingual (underthe tongue) progesterone has basically the sameuses for menopause and premenstrual symptomsas the creams and the oral progesterone. How-ever, it is generally stronger than the creams andweaker than the usual oral doses. Typically, thetablets must remain under the tongue for 20minutes while they dissolve before the proges-terone is fully absorbed.

One advantage of sublingual tablets—as wellas creams and vaginal and rectal suppositories—is that they are not significantly metabolized bythe liver, as is the case with oral progesterone.This is thought to minimize side effects. However,there is very little information available as tohow sublingual progesterone works and its possi-ble longer-term side effects, so I take care whenrecommending this form of progesterone. Themain issue is that sublingual progesterone andprogesterone creams have not yet been proven toprotect the uterus from the effects of estrogen replacement.

Rectal administration of progesterone has notbeen well studied. Nasal sprays of progesterone(in oil) produce relatively low serum levels,which are sustained for only a few hours.163 Eventhough these levels are low, they can producesome secretory changes in the endometrium andmay prove with further study to be sufficient toreverse endometrial hyperplastic effects of estro-gen replacement therapy.

More About HRT and Breast Cancer. Theissue of progestogens and breast cancer is com-plex and not very well understood. It is difficultto come to a comfortable conclusion on thismatter. One of the largest studies to date, theNurses’ Health Study, showed that adding a syn-thetic progestin to estrogen failed to reduce theincidence of breast cancer and actually increasedit.164 Women taking estrogen alone had a 36 per-cent increase in their risk of breast cancer; thoseon estrogen plus progestin had a 50 percentincrease; those on progestins alone had a 240

Oral Micronized Progesterone (OMP)

Perimenopausal woman taking continuous estrogenand/or a monthly menstrual cycle is desired: 100 mgtwice daily (or 200 mg once daily) 12 days per month

Perimenopausal woman taking estrogen and/or amonthly menstrual cycle is desired: 1 mg estradiol(or equivalent) plus 50 mg OMP twice daily (or 100mg once daily) 3 weeks on and 1 week off (duringmenses)

Postmenopausal woman taking continuous estrogenand a monthly cycle is not desired: 1 mg estradiol(or equivalent) plus 50 mg OMP twice daily (or100mg once daily) continuously

In my experience, women have few side effects withOMP in doses of 200 mg or less. Higher doses, 400mg per day, are sometimes prescribed for amenorrhea,or lack of menstruation, in women who are not yettruly menopausal, or to manage heavy acute uterinebleeding. However, in high doses OMP can cause sideeffects, including dizziness, abdominal cramping,headaches, breast pain, nausea, diarrhea, fatigue, irri-tability, and abdominal bloating.162


percent increase—although this number may bemisleading because the number of women ononly progestins was very small. The Nurses’Health Study also was able to report on durationof use. For women who had been taking estrogenand progestin for five to ten years, there was a 46percent increase in their risk of breast cancer. Atthe end of 2000, the Nurses’ Health Study pub-lished its estimates of breast cancer risk associatedwith HRT in postmenopausal women.165 Theresults were expressed as percentage increases inthe cumulative risk of breast cancer and werefrightening to many: the use of estrogen alone for 10 years leads to a 23 percent increase by age70, and the use of estrogen plus progestin for 10years leads to a 67 percent increase by age 70. Itis important to realize that the result is not anactual mathematical conclusion but the conclu-sion of the model, the consequences of a smalldifference in risk that gets magnified as the mathis carried out into the future. Also, it is importantto realize that risk estimates represent a projec-tion, not an actual measurement.

Another study done in Seattle had contradic-tory findings to the Nurses’ Health Study.166 Thisstudy found no effect on the risk of breast cancerfrom either estrogen alone or estrogen and prog-estins together. In the WHI group of estrogenplus progestin users, there was a slight increase in breast cancer after five years of use.28 In the estrogen-only arm of the WHI, estrogen did notincrease the risk of breast cancer, even after sevenyears of use.144

At the other end of the pendulum, investiga-tions that have found no increased risk of breastcancer with HRT or ERT use receive much lessattention. The Iowa Women’s Health Study isprospectively following a cohort of women who were selected in 1985.167 After six years offollowing these women, a statistically significantincrease in the risk of breast cancer could not bedetected in women who had either ever usedHRT or who were currently using it. Anotherreport through eight years of follow-up looked at

whether postmenopausal HRT increased therisks for breast cancer and death from breastcancer in women with a family history of breastcancer.168 There was no significant increase in therate of breast cancer even in women with a familyhistory of breast cancer who were using HRTlonger than five years. These results are consistentwith other reports that there is no additional riskin using HRT/ERT in women who have a first-degree relative with breast cancer.

The latest analysis from the Iowa Women’sHealth Study, an 11-year follow-up, showed anassociation between women who had ever usedpostmenopausal HRT and the risk of breast can-cers that were more localized and had a betterprognosis.169 The study did not find an increasedrisk of invasive ductal or lobular carcinoma inwomen who had used HRT either less than ormore than five years. A slight increased risk ofbreast cancer was observed in current users andthose with less than five years of use; currentusers with more than five years of use had noincrease in risk. These results are the opposite ofthose seen in the Nurses’ Health Study—womenwho are using HRT for more than five years have the increase in risk.164 Two other recentstudies, the Carolina Breast Cancer Study170 andanalyses from the National Health and NutritionExamination Survey (NHANES),171 found noincreased risk with postmenopausal hormones.These recent studies perpetuate the inconsistencyin research on this issue that has been true in thelast 25 years. This provides some logic to thepoint of view that if there is an increased risk ofbreast cancer associated with ERT/HRT, the riskmust be small because otherwise by now, afterthis many years, we would have seen more con-sistency in the data and the size of the risk esti-mates would be large rather than slight.

A reminder about duration of use offers somereassurance amidst the confusion. No studiesfind an increased risk of breast cancer with short-term use of HRT, and the conflicting results ofmore than 60 studies demonstrate that if there is


an increased risk with long-term use, it is a slightincrease.

The effect of bio-identical progesterone onthe risk of breast cancer in menopausal womenwho are taking bio-identical EPT is basicallyunresolved. Some evidence does exist that bio-identical progesterone might help to preventbreast cancer. In a 1995 study, women who werescheduled for breast reduction surgery appliedprogesterone cream to their breasts for two weeksbefore the surgery.172 The cells in the removedbreast tissue showed less cell division in thewomen who used the progesterone cream, andthe researchers concluded that progesteroneapplied directly to the breast might even helpprevent breast cancer. In perhaps the most com-pelling study to date, done in France, transder-mal bio-identical estradiol plus oral micronizedbio-identical progesterone was not associatedwith an increased risk of breast cancer whereastransdermal estradiol with progestins did increasethe risk, similar to the WHI results.173

For women already at risk for breast cancer orwho have had breast cancer, no good studies existon the effects of progestins or progesterone.

Friendlier and Less-FriendlyConventional HRT

Friendlier conventional HRT includes all estro-gens manufactured by a pharmaceutical com-pany that are made with bio-identical estradiolor estrone. As stated previously, the differencesare the binders, fillers, preservatives, adhesives,and additives used in these products. Oral capsules of 1 mg bio-identical hormones areequivalent to 0.625 mg of conjugated equineestrogens (CEE). Estrogen patches that contain0.05 mg of bio-identical estradiol are equivalentto 0.625 mg CEE (Premarin) or to 1 mg of oralbio-identical estradiol. Estradiol cream and gelare also now manufactured by pharmaceuticalcompanies.

Less-friendly conventional HRT uses hor-mones that are composed of estrogens and prog-

estins that are not identical to a woman’s own estro-gen or progesterone. Conjugated equine estrogensare derived from the urine of pregnant mares.Esterified estrogens are in part estrone sulfate andin part equilin sulfates. (See Appendix C for a charton current conventional hormone options.)

Androgens. The normal postmenopausalovary produces testosterone as well as andro-stenedione and small amounts of estrogen. Fol-lowing menopause, a woman’s androgen (malehormone) production decreases by as much as 50percent. Ovarian androgen production stopsabruptly with surgical menopause and moregradually with natural menopause. A substantialnumber of menopausal women who are givenestrogen replacement at standard dosages con-tinue to have menopause symptoms such as hot flashes, night sweats, and insomnia. Thesewomen may have enhanced symptom relief whenthey are switched to estrogen plus androgen, usually testosterone. Studies have shown thattestosterone increases the bioavailable estrogen,both that produced by the body and that given in a pill.174

Estrogen and testosterone therapy has beenexplored not only for its ability to improve vaso-motor symptoms but also to improve sexualdesire and sexual satisfaction. For example, adouble-blind study of women who were dissatis-fied with their HRT regimen showed that sexualdesire, satisfaction, and frequency of sexual activ-ity were increased when they used the estrogen/testosterone combination.175 Another study ofearly postmenopausal women, both natural andsurgical, were switched from estrogen alone toestrogen/testosterone therapy.176 Overall symp-tom relief was greater with estrogen/testosteronetherapy than with estrogen-only therapy. Sexualdrive and satisfaction increased. Results of otherstudies have shown that the combination of 1.25mg of esterified estrogen and 2.5 mg of methyl-testosterone given daily for two years signifi-cantly reduced the intensity of hot flashes and


vaginal dryness in women with surgical meno-pause.177 A study comparing the effects of estro-gen and an estrogen/testosterone combinationon sex drive showed improvement in 50 percentof women on estrogen alone, but 90 percent ofwomen when testosterone was added.178

There have been some concerns about estro-gen/testosterone therapy reversing the increasedHDL cholesterol achieved with estrogen alone.The combination of esterified estrogens andmethyltestosterone has been shown to decreasetriglycerides, LDL, HDL, and total cholesterol in postmenopausal women. However, a two-yearstudy of estrogen/testosterone therapy producedno change in LDL levels but did show significantreductions in triglycerides and very low-densitylipoprotein, and also reduced HDL levels. So thestory is mixed, and further studies are needed todetermine the actual impact of these changes oncardiovascular disease. If testosterone is used, itwould be prudent to monitor blood lipid levelsfor any adverse effects.

For treatment of osteoporosis, adding testos-terone to estrogen therapy appears to produce agreater increase in bone density compared withestrogen therapy alone. In a double-blind study,66 surgically menopausal women without osteo-porosis received either 1.25 mg of esterifiedestrogen alone or 1.25 mg of esterified estrogenand 2.5 mg of methyltestosterone daily for twoyears. Both groups already had bone loss at thespine, hip, and wrist. Only the combination ofestrogen with testosterone significantly increasedspinal bone density after one year and two years.

Standard formulations of CEE and methyl-testosterone combine either 0.625 or 1.25 mg of CEE with 5 mg of methyltestosterone. Otherformulations contain either 1.25 or 0.625 mgesterified estrogens, combined with 2.5 or 1.25mg of methyltestosterone, respectively.

Through a compounding pharmacist, onecan obtain bio-identical testosterone. I generallyuse 1 to 3 mg of bio-identical testosterone for-mulated into the bi-estrogen or tri-estrogen for-

mulation, and the pills are taken one capsuletwice daily. Testosterone cream applied to thegenital region has received mass media attentionon “The Oprah Winfrey Show.” It is used as analternate method of delivering the testosterone.Common prescriptions are anywhere from 1 to 4mg per gram of cream. These are applied to theexternal genital region right before sexual activityto enhance sensation to touch and orgasm. Useshould not exceed twice per week to avert localtestosterone side effects such as enlargement ofthe clitoris that can occur if testosterone cream isused daily and in the stronger dosages. A goodresource for both menopausal women and theirhealth-care practitioners is a book called TheHormone of Desire.179

The North American Menopause Society(NAMS) invited a panel of clinicians andresearchers who were experts in the field oftestosterone therapy to review the scientific evi-dence regarding the role of exogenous testos-terone in postmenopausal women.180 Theirconclusions were as follows: Postmenopausalwomen with decreased sexual desire with noother cause other than being postmenopausalmay be candidates for testosterone treatment.Because of lack of adequate evidence for testos-terone increasing sexual function, testosteronetreatment without also giving estrogen therapycannot be recommended. Other causes of lowlibido are to be ruled out and laboratory testingof testosterone levels should be used only tomonitor for supraphysiologic levels before andduring therapy, not for the purpose of diagnosingtestosterone insufficiency. Monitoring would beincluded in an office visit follow-up to assesschanges in sexual function. Transdermal and top-ical gels or creams are preferred over oral formsdue to their minimal effect on the liver. Testos-terone therapy is contraindicated in women withbreast or uterine cancer and in women with car-diovascular or liver disease. Testosterone shouldbe given at the lowest dose for the shortest timethat meets treatment objectives.


Bio-Identical Testosterone

Oral: 2–6 mg per dayCream (1–4 mg/g): apply twice weekly to external

genitalia before sexual activity

Dehydroepiandrosterone (DHEA). Dehy-droepiandrosterone (DHEA) is another of theandrogens. It is the most abundant circulatingsteroid in humans. DHEA is called a precursorhormone because it is produced in large amountsin the body and other steroid hormones are madefrom it, including estrogen and testosterone. In awoman, 90 percent of DHEA comes from theadrenal glands; the remaining 10 percent is manu-factured by the ovaries. Our DHEA level peaks atage 25 and then declines gradually to only 15 to 20percent of our maximum by the time we turn 70.

Many claims have been made about DHEA’seffect on the immune system, and its anti-agingproperties are said to include better memory, lessfatigue, more energy, relaxation, and increasedability to handle stress. It is also touted as havingpositive effects on bone density and helping toprevent cancer and cardiovascular disease. How-ever, the exact effect DHEA has on the body’scells is unclear. I have seen DHEA increaseenergy, improve stress response, improve musclemass, and occasionally increase libido.

A daily oral intake of 50 mg of DHEA for apostmenopausal woman may restore DHEAlevels to those of a young adult. At this dosage,DHEA is converted to other more potent andro-gens, including testosterone. In pharmacologicaldoses of 1,600 mg, DHEA is converted toestrone and estradiol. Unfortunately, there areonly a handful of randomized placebo-controlledstudies examining the effects of giving DHEA tohumans. Although animal studies are promising,we need more research on its particular effects onpostmenopausal women.

One of the most significant effects of DHEAmay be its ability to enhance a sense of generalwell-being. This effect was found at doses of 50

mg and 100 mg daily.181 Few adverse effects havebeen reported with DHEA, although in women,androgenic side effects such as facial hair growthand acne can occur with doses as low as 50 mg.A dose of 25 mg daily may be more appropri-ate.182 I typically give 5 to 20 mg per day towomen who are either low in DHEA accordingto test results or to women with fatigue, loss ofvitality, and/or low sex drive.

DHEA

5–50 mg per day

Exercise

The benefits of exercise for perimenopausal andpostmenopausal women are wide and deep.Women can receive substantial reductions in car-diovascular disease,183 a reduced risk of breastcancer,184 an increase in bone density,185 a lower-

Sample Treatment Plan for Hot Flash Symptom Relief

Diet:Follow a whole foods diet high in fruits, vegeta-

bles, whole grains, and legumes.Emphasize soybean products and flaxseed.Reduce total fat, animal fats, and simple

carbohydrates.Eat modest amounts of organic low-fat dairy.

Exercise: Regular weight-bearing, strengthening, andaerobic exercise with light weight training

Herbal: Choose one of the following:Black cohosh standardized extract capsules (40

mg): 1–2 capsules 1–2 times per dayConsider herbal combination formulations: dong

quai, licorice root, motherwort, burdock root,hops, Saint John’s wort, red clover, maca

Bio-identical progesterone cream (400 mg/oz ormore): apply 1⁄4 tsp twice daily 3 weeks on and1 week off if perimenopausal

Bio-identical estrogens/progesterone (estriol 1mg/estradiol 0.25 mg/progesterone): 1 capsule (50mg) twice daily (1 week off if perimenopausal)


ing of body fat and body mass index, and animproved sense of well-being.186 The ability ofexercise to reduce the incidence or severity of hotflashes during menopause is not clear. It appearsthat for women who are not overweight, moder-ate exercise may be beneficial for hot flashes andmore vigorous exercise may exacerbate them.

Exercise Recommendations. Physical exer-cise that includes strength, cardiac, and flexibilitymodalities (see Appendix A) ensures a meno-pause without exaggerated symptoms and pro-tects against heart disease and osteoporosis whenit is initiated early in life, is appropriate andmoderate, and lasts throughout life.

However, if you have reached menopause andhave been sedentary, start slowly and progressgradually. Consult an exercise consultant to learnthe safest program both for aerobic and strength/weight training.

Solutions to Selected Problems

Insomnia. In determining individualizedtreatments for insomnia, it is imperative to iden-tify and address the underlying cause as well asprovide options for short-term relief. The basicsstart with good sleep hygiene. This includesgoing to bed at the same time each night andavoiding or reducing naps. A comfortable bedand room temperature along with low levels oflight and noise contribute to better sleephygiene. It is often advised that the bedroomshould not be used for eating or television watch-ing but rather only for sleep and intimacy. If youare not able to fall asleep after 20 to 30 minutesin bed, get out of bed and engage in a quiet activ-ity and then return to bed when sleepy.

Nutritional practices may influence sleep.Caffeinated drinks may have to be avoided alto-gether or at least within 12 hours of sleep. Someindividuals have nighttime hypoglycemia. Adrop in blood glucose level causes the release ofchemicals that can stimulate the brain. Consum-ing complex carbohydrates with protein can help

maintain sleep through the night by regulatingnighttime blood glucose levels.

Relaxation techniques such as biofeedback,progressive muscular relaxation, meditation, andwarm baths can help sedate some people. Sooth-ing music may also reduce anxiety and stress.One study showed that after listening to musicwhile trying to go to sleep, the level of sleepinesswas significantly increased and the time to sleeponset was much lower. The music became moreeffective each night of continued use.187

Some studies of insomnia in postmenopausalwomen demonstrate that HRT significantlyimproves sleep quality, shortens sleep onset, andreduces nighttime restlessness and awakenings.188

Sleep efficiency and time spent awake after sleeponset appear to be significantly better when usingoral micronized progesterone with estrogenreplacement therapy but not when using syn-thetic medroxyprogesterone acetate (MPA).189

Insomnia is not only a frequent medicalproblem, but it’s also a difficult problem. Insom-

Sample Treatment Plan for Insomnia


Diet:Avoid stimulants, especially during the second half

of the day (coffee, caffeinated tea, chocolate, caffeinated sodas).

Have a protein snack before bed.Lifestyle: Get regular exercise, practice good sleep

hygiene.Herbal:

Black cohosh extract: 40 mg twice dailyValerian: 1–2 capsules or 1–2 tsp liquid extract

before bedNutritional supplement: 2 mg melatonin before bedFor difficult cases:

Add hormone prescription, with oral micronizedprogesterone taken right before bed.

Consider adding 5-HTP, higher doses of melatonin,or other herbal combinations of hops, valerian,and passionflower.


nia is usually a symptom of an underlying hormonal, nutritional, pharmacological, orpsychological problem. Some women may needevaluation for sleep apnea, treatment of psycho-logical issues, or pharmacological treatment.

Melatonin. One of the better-known naturaltreatments for insomnia is melatonin. Oneplacebo-controlled trial on melatonin found that0.5 mg of melatonin daily for two weeks short-ened the amount of time it took to fall asleep buthad no effect on sustaining sleep or improvingthe quality of the sleep.190 In another study, 2 mgof melatonin per day was effective in improvingsleep efficiency.191 Melatonin has also been effec-tive in patients with long-term insomnia whowere using benzodiazepines.192 Most patientswere able to decrease their benzodiazepines by 50percent during the second week of using 2 mg ofmelatonin nightly and discontinue it by the fifthor sixth week. It is thought that individuals whoactually have a melatonin deficiency are mostresponsive to melatonin for insomnia.

5-Hydroxytryptophan (5-HTP). 5-HTP is aform of tryptophan that has been reported innumerous double-blind studies to decrease thetime required to get to sleep and to decrease thenumber of night awakenings.193–196 The typicaldosage range of 5-HTP is 100 to 300 mg about45 minutes before bed.

Valerian. This herb has been used for decades,if not centuries, as a sedative, including as an aidfor insomnia. Studies have confirmed the effec-tiveness of valerian. In a double-blind study fromSwitzerland, valerian improved sleep latency,reduced night awakenings, and improved sleepquality, especially in women.197 Several trials havelooked at valerian in combination with otherherbal sedatives such as passionflower and lemonbalm. In one clinical trial, 33 percent of men andwomen without insomnia who took valerian andlemon balm 30 minutes before bed reported animprovement in sleep quality. Only 9 percent inthe placebo group reported improvement.198

Other Botanicals. Numerous plants have seda-tive actions and have been used historically to promote sleep and improve sleep quality. Theseinclude hops, skullcap, chamomile, lemon balm,oat straw, lavender, bitter orange, Californiapoppy, and kava. Preparations can include pow-dered capsules, tinctures, and teas. Most of theseherbs are mild sedatives and are unlikely to sufficealone, but are typically used in combinations.

Sexual Function

Ginseng. The most well-known herb to im-prove energy and stamina, as well as for sexual rejuvenation, is ginseng. American ginseng hastraditionally been used for weakness, loss ofmuscle tone, low endurance, loss of work efficiency,and decreased sexual function. The ginsenosides inAmerican ginseng exert an estrogen-like action onthe vaginal epithelium that improves the lubrica-tion and elasticity of the vaginal tissue, contributingto sexual response and comfort. In animal stud-ies, ginseng increased testosterone levels inmales.199 Given the potential influence of testos-terone on sexual function in women, this maypartly account for its effect in women as well.Therapeutic effects of ginseng on the reproduc-tive system of female animals also include accel-erating ovarian function, enhancing ovulation,and stimulating egg production.200

(Enhancing pelvic and specifically genital cir-culation is also a consideration for which onemight consider ginkgo. Ginkgo was also dis-cussed earlier in the botanicals section as an aidto improve sexual function in women takingantidepressants.78)

Several studies show the ability of ginseng to battle fatigue and stress. One study of nurseswho took ginseng showed improved scores in jobcompetence, mood, and mental and physicalperformance.84

Ginseng has also been shown to enhance theability to cope with various mental and physicalstressors, largely due to its effect on the adrenalglands, which are involved in maintaining our


hormonal balance. Finally, in a double-blind,placebo-controlled trial of 232 patients withfatigue, it was found that ginseng improved fatigue,anxiety, nervousness, and poor concentration.201

Damiana. All students of herbal medicine areprobably familiar with damiana’s time-honoredreputation as an aphrodisiac. It is unclear how theconstituents of damiana bring about this effect,and indeed no studies have proven this effect onwomen, but it has been shown to enhance sexualbehavior in animals. A combination product thatincluded ginseng, damiana, and gingko was shownin a small placebo-controlled study to improvesexual desire and satisfaction.202 Mexican Indiansand generations of herbalists have looked to dami-ana to improve sexual interest and response.

Ashwagandha. In cases of general debility,nervous exhaustion, loss of muscle strength, andthat all-familiar “brain fog,” the ashwagandhaplant that grows and is cultivated in India andeven the Himalayas is well-known in folk medi-cine of that region as a traditional treatment ofthese problems. This plant is regarded in India asa tonic and adaptogen, with properties similar toginseng. In one study, physical endurance wasdoubled in participants given extracts of ashwa-gandha (Withania somnifera).203

Rhodiola. Rhodiola, also known as goldenroot or arctic root, has been used for centuries toincrease physical endurance and exercise per-formance204 and as a folk custom to ensure fertil-ity. Effects on regulation of the menstrual cycleand the successful treatment of 25 of 40 womenwho had stopped having menses altogether sup-port its use in matters related to hormones andsexual function.205

Maca. Maca has been used in Peru for fivethousand years. Alkaloids from the root of theplant act upon the two key glands in the brain,the hypothalamus and the pituitary, supportingand boosting energy levels and encouraging theproduction of ovarian hormones such as estrogenand testosterone.206

Look for these herbs in popular combinationproducts to enhance sexual desire as well as toaddress other menopause issues.

The Importance of Lubrication. The amountof estrogen in the vagina is the main determinantof vaginal health, including the pH, the balanceof organisms, the integrity of the tissues, and theamount of lubrication. As estrogen levels declinewith menopause, many changes can occur,including thinning of the vaginal wall tissue,vaginal dryness, loss of vaginal tone, and suscep-tibility to infections. Symptoms such as painwith vaginal sexual activity, itching and burning,and even urinary leakage may result. For sexualfunction and comfort with vaginal sexual activ-ity, lubrication during sex not only is helpful forcomfort, but for some is a necessity. There aremany over-the-counter lubricants, and in thecontext of natural medicine, we can look forlubricants that are less irritating due to a lack ofchemicals and hypoallergenic bases. Somethingas simple as vitamin E oil can be used as a lubri-cant. Products are available that contain vitaminE oil and allantoin and are water based so theyare nondrying and nonirritating. Other naturalvaginal moisturizers are oil based rather thanwater based. Common ingredients are mineraloil, glycerin, yerba santa, castor oil, and more. Itis important to check to see which ones areappropriate to use with condoms and to remem-ber that lubricants do not contain spermicideand so do not provide contraception.

The most effective way to improve lubricationover the long term is prescription vaginal estrogens.Please refer to the section on hormones earlier inthis chapter for how to use vaginal estrogens forthinning, dryness, and pain of the vagina andproblems related to these atrophic changes.

Topical Ingredients to Enhance Arousal.Numerous botanical and nutrient topical productsnow exist to enhance female arousal and orgasmwhen applied to the vulva (external female genitalarea). One such product is a feminine massage oil


that contains borage seed oil, evening primrose oil, extracts of angelica and coleus, and severalantioxidants. A randomized, double-blinded,cross-over study was conducted to evaluate the effi-cacy of this product in women who had been diag-nosed with female sexual arousal disorder. Thetreatment resulted in increases in sexual pleasure inmore than 90 percent of women.207

Another over-the-counter topical cream thatsupports female sexual arousal contains nitricoxide, which is the chemical produced by thebody to promote the dilation of blood vessels inthe female genital tissues. L-phenylalanine and L-tyrosine are amino acids that the body uses toproduce neurotransmitters important in the initi-ation of blood vessel dilation. Niacin, also knownas vitamin B3, is known for its ability to dilateblood vessels as well. In addition, oils such as L-menthol from mint oil, rosemary oil, and cinna-mon oil can increase local blood flow and havewarming and stimulating effects when formulatedin a cream and applied to the genital tissues.

As discussed earlier in the hormone section,topical testosterone cream is also a valuable toolto enhance genital arousal and orgasm.


Conventional medicine treatment of menopausehas changed fairly dramatically in the years follow-ing the initial publication of the Women’s HealthInitiative (WHI) report in 2002. Many womenwho were taking hormone therapy for preventionof heart disease and osteoporosis were instructedto stop their hormones, because the WHI sug-gested that there might be a slight increase inbreast cancer and strokes in asymptomatic womentaking hormones. We have known that there is aslight increase in deep venous thrombosis, whichwas confirmed by this study. The study alsoshowed an improvement in prevention of osteo-porosis and colon cancer, but these beneficial ef-fects were considered not to be worth the risk. Therecommendation that all menopausal women be

placed on hormone therapy, which was a mainstayof conventional medicine for the preceding 40 to60 years, has changed. After the WHI report, theAmerican College of OB/GYN (ACOG) and theNorth American Menopause Society (NAMS)convened panels of specialists to look at the infor-mation and make recommendations. These rec-ommendations are for the general patient, withprovisos that each individual woman should becounseled and her risk and goals assessed, andsome deviation from these guidelines may be pos-sible at the discretion of the practitioner and pa-tient. There are three commonly agreed-upon usesfor hormone therapy:

1. Decrease of menopausal symptoms2. Prevention of osteoporosis in women who

are intolerant of other medications used totreat osteoporosis

3. Topical use of hormones for urogenital atrophy

They also recommend that hormones be usedat the lowest effective doses for the shortest effec-tive period of time. What this means is that theprovider should try different doses and find onethat is most effective in the reduction of awoman’s symptoms. That does not mean it has tobe the lowest dose possible. The shortest periodof time means that women should periodicallygo off their hormones to see if their menopausalsymptoms have reduced or gone away. These recommendations are not applicable to womenwho are using hormones for treatment of osteo-porosis, which should be a lifetime treatment.Women with atrophic urogenital symptoms willneed to use their hormones lifelong, but the top-ical vulvovaginal estrogens pose no meaningfulrisks. The lowest effective dose, in the shortestperiod of time, pertains primarily to a womanusing hormones for menopausal symptoms.

They recommend that all women with anintact uterus have a progestogen administeredalong with the estrogen to prevent endometrialhyperplasia and uterine cancer. The regimens of


treatment with progestogens varies greatly butare divided into two basic approaches:

1. Continuous daily therapy2. Cyclic treatment, adding a progestogen 12

to 14 days per month, and recently there is a“long sequential cyclic” regimen of 14 daysevery 3 months

Woman who do not have a uterus are notrequired to use a progestogen. Women who have auterus and are progestogen intolerant can have theoption of annual uterine lining evaluation withtransvaginal ultrasound or an endometrial biopsy.When using transvaginal ultrasound, women withan endometrial thickness of 4 mm or less are con-sidered not to have disease and do not need anendometrial biopsy unless there is persistentabnormal bleeding or other medical reasons.Women with more than 4 mm thickness may havea normal lining but need an endometrial biopsyand/or a saline sonohystogram. Or, instead of thetwo-step approach of ultrasound and then biopsy,women may instead have an endometrial biopsyyearly to assess the lining tissue.

Another alternative is the use of the proges-togen intrauterine system known as a MirenaIUD. This is not an FDA-approved use of thisdevice as of this writing. The Mirena IUD pro-vides a large local progestogen environment forprevention of hyperplasia and cancer withoutany significant systemic absorption. There is nojustification for the use of unopposed estrogensin a woman with a uterus unless she is doing reg-ular assessments of her uterine lining. There areonly a few reasons why women without a uterusare given progestogens along with estrogen:

1. To increase menopause symptom relief2. To reduce the risk of endometriosis in

women who had active disease during theirsurgery to remove the uterus and ovaries

The use of hormone therapy for other reasonsis widespread, but is not approved by the FDA,ACOG, or NAMS. There have been empiric

reports over the years that the use of estrogenreduces the onset or severity of dementia, macu-lar degeneration, cataracts, tooth loss, and skinwrinkling, and many women choose to use hor-mones for these quality-of-life issues. This goesback to the decision to individualize eachwoman’s therapy based on her goals and risk factors. Properly counseled about the risks ofhormone therapy, many women are continuingto use hormones for these issues. That choice isbetween the woman and her provider.

A pharmaceutical company’s FDA applicationinformation shows that 0.014 mg of transdermalestradiol in the form of a weekly patch has beenshown to be effective for prevention of osteoporo-sis, but it does not develop blood levels highenough to increase or build an endometrial lining.Therefore, the FDA is allowing this medication tobe used as an unopposed estrogen in women witha uterus. The information in the package insert forthis medication suggests a progestogen challengetest at 6- to 12-month intervals. Another contro-versial unopposed estrogen use is topical vaginalproducts. Several studies suggest that there is min-imal to no increase in blood estrogen levels withthe use of the vaginal ring, creams, and tablets.Over the years, there have been suggestions that awoman with a uterus using these products begiven a progestogen withdrawal challenge test onan annual basis. These recommendations are vari-ably applied. Again, discussion with the womanabout her choices is probably the most importantmanagement suggestion.

So, what hormones are currently being used?The delivery systems and types of hormones havechanged dramatically over the past 10 to 20years. This discussion will provide some informa-tion on the most commonly prescribed products.There are, however, two first important guidingprinciples for hormone therapy managementthat should be discussed.

First is the bioequivalence of oral and trans-dermal estrogen products. The following doses of the different types of estrogen supposedly


provide the same blood levels after administra-tion, and so they are considered biologically equivalent:

Oral conjugated estrogen: 0.625 mgOral estradiol: 1.0 mgPatch estradiol: 0.05 mgBiest/Triest: 2.5 mg orallyEstradiol gel (Estrogel): 2 squirtsEstradiol cream (Estrasorb): 2 packets

A dosage higher than these amounts would givehigher-than-average blood levels, and dosageslower than these amounts would give lower-than-average blood levels. It is acceptable to varythe estrogen dosage to meet the woman’s symp-tom requirements.

The second guiding principle is that there isa minimal acceptable dosage of progestogen thatwill prevent hyperplasia or uterine cancer. Onecannot go below the recommended amounts ofprogestogen or frequency intervals without therisk of hyperplasia and uterine cancer, so the rec-ommended progestogen dosages should not bevaried. For information on the various types ofconventional estrogen products and the recom-mended progestogen dosages, see the NorthAmerican Menopause Society website, meno-pause.org. This site offers a menopause guide-book that outlines all of the currently availableconventional estrogen and progestogen productsas well as a 47-page committee consensus opin-ion on progestogen usage. (See Appendix C for alist of conventional hormone preparations andsome details about dosing.)

For purposes of the summary discussion inthis chapter, these are the conventional hormoneguidelines:

1. Estrogens. The most commonly used estro-gens are the oral forms, and they come as estra-diol (by product name and generic), conjugatedanimal-source estrogens (Premarin), a mixtureof esterified vegetable estrogens (Enjuvia, Cen-estin, Menest), esterified estrogens with methyltestosterone (Estratest and Syntest), and various

generic forms. Estrogens also come in combina-tion products containing an estrogen plus a pro-gestogen and in transdermal patches, gels, andcreams, as well as in a vaginal ring that providestransdermal systemic estrogen levels (Femring).Even some conventional practitioners areincreasingly using compounded hormone ther-apy, which has the benefit of a variety of dosingforms and can be compounded as an oral cap-sule, a transdermal cream or gel, a vaginal tablet,or a sublingual-dissolving medication.2. Combination products. The combinations

of estrogen plus progestogen products are verypopular because the woman can take one med-ication and get both hormones. These come inoral forms and in two patch brands. There isalso a combination estrogen plus progestogenvaginal product called NuvaRing, which is alow-dose birth control product that has beenused for perimenopausal symptom relief andcycle control. And again, there are compoundedhormone products from the compoundingpharmacies.3. Progestogens. There are several commer-

cially available non-bio-identical progestins incommon usage today: Provera or Cycrin(medroxyprogesterone), Aygestin (norethin-drone acetate), the minipill Micronor (norethin-drone), and Megace (megestrol). Bio-identicalprogesterone is available in a product calledPrometrium, in two dose forms. Compoundingpharmacies can compound bio-identical proges-terone in oral, sublingual, transdermal, or vagi-nal form. There is also a vaginal bio-identicalprogesterone, FDA approved for use in infertil-ity, that comes in a 4 percent and 8 percent geland can be used for vaginal application of sys-temic progesterone.4. Vaginal estrogens. Vaginal estrogen prod-

ucts that are used only for urogenital atrophicproblems are very weak estrogens and are notlikely to increase blood levels. For many years,vaginal creams have been available in eitherestradiol or conjugated estrogens, but in the


past 10 years or more, we have also had thethree-month indwelling vaginal ring estrogencalled Estring and vaginal tablets of estradiolcalled Vagifem. Compounded vaginal estrogenproducts in variable doses are also available.Conventional practitioners by and large do notuse these and are particularly unaware of how touse vaginal estriol, as discussed in the alternativemedicine section on hormone therapy.

Nonhormonal medical options have in-creased in popularity and understanding. For low bone density, a bisphosphonate such as Fosamax, Actonel, or Boniva or a selective estro-gen receptor modulator (SERM) such as Evista(raloxiphene) may be prescribed. Or for severeosteoporosis, parathyroid hormone (Forteo)—which works on the bone in an entirely differentway than hormones, SERMs, or bisphospho-nates—may be recommended.

For insomnia, there are many different optionsdepending on age, type of use (daily versus inter-mittent), and abuse potential of the patient. Most sleep aids are benzodiazepines, some are antihistamines, and a new one (Rozerem) works on melatonin receptors. Consult a physician wellacquainted with the use of these medications.

For anxiety and depression, there are thecommon SSRIs (Prozac, Paxil, Celexa, Zoloft),newer SNRIs (Effexor, Cymbalta) and tricyclicantidepressants, and sedatives.

For vasomotor symptoms, a blood pressuremed, a seizure drug, SSRIs, SNRIs, and ergotscan be prescribed. None of these medications’actions on relieving sweats and flushes are under-stood—practitioners have just observed thatsome women on some medications had signifi-cant improvement in their symptoms. Most ofthe drugs are safe and easy to use, but some are expensive. The blood pressure med used isClonidine, usually 0.1 to 0.2 mg daily at bed-time. The anti-epileptic drug gabapentin (Neu-rontin) is administered as 300 mg three times aday. Effexor and Paxil have shown a reduction in

sweats and flushes in studies at 37.5 to 75 mgand 10 to 20 mg daily, respectively. However,SSRIs and SNRIs have been occasionally shownto cause vasomotor symptoms in men andwomen. Bellergal Spacetabs, an ergot and bel-ladonna combination, were used for many yearsfor vasomotor symptoms but are no longer madeby its pharmaceutical company. Some com-pounding pharmacies supply it. There are nostudies on it, but empirical reports have shownmixed results. It is used one to two times daily.

Sexual problems are commonly reported bywomen in midlife, and the treatment is verycomplex. Libido can be decreased because ofestrogen deficiency, sudden surgical loss of testos-terone from an oophorectomy (not from naturalovarian aging), or the administration of an oralestrogen, which can lower serum testosterone.Libido can decrease because of pain with inter-course, decreased skin sensation from loss ofestrogen, chronic medical problems, medica-tions, or most often from the woman’s psychoso-cial environment. Sexual performance problemscan have similar roots but are often the result ofother diseases (hypertension, diabetes, athero-sclerosis) that affect clitoral and pelvic blood flowor from medications used to treat other diseases(notably antidepressants). A few studies havebeen done on the use of testosterone to improvesexual function and have shown conflictingresults. The work done by Dr. David Archerusing testosterone patches (pending FDAapproval) shows improvement in women whohad bilateral oophorectomy but not those whohave undergone natural menopause. Testosteroneis not well absorbed orally, and it has potentialhealth risks such as permanent voice change, hairgrowth on the face or body, loss of head hair,lipid elevations, acne/oily skin, and emotionalside effects. More research is needed on the roleof hormones in sexual dysfunction in women.

In summary, the conventional practitioner’s useof hormone therapy and the standard of practicethese days is limited to three areas of use: meno-


pausal symptoms, osteoporosis prevention or treat-ment, and vaginal or urogenital atrophic symp-toms. The formulations of type, dose, and deliveryhave significantly increased, and it is important towork with a provider who is capable and knowl-edgeable about the various products. Most womenwill do well on most hormone products, but forthose women whose symptoms do not respondeasily to these products, a knowledgeable meno-pause clinician can provide better guidance. It isimportant for a woman with a uterus to use a pro-gestogen along with estrogen replacement. Womenwho have had a hysterectomy do not typically needprogestogens. Hormone therapy is used for nonap-proved, nonstandard reasons, and the patient needsto be counseled about risks and needs to define hergoals. This is an acceptable practice as long asproper counseling is provided.


Most women who are perimenopausal can feelcomfortable starting on their own with the diet,exercise, herbs, nutritional supplements, and nat-ural progesterone creams described in this chapterfor the relief of menopause symptoms. Womenwho do not find adequate relief from these thera-pies will need to see a licensed primary careprovider (naturopathic doctor, medical doctor,osteopathic doctor, nurse-practitioner, or physi-cian’s assistant) who preferably is educated in therange of options, not just conventional HRT.

My advice to all women is to at some time have a full evaluation by a practitioner whois educated in all the natural, hormonal, andpharmaceutical nonhormonal options. The only primary care practitioners that are trained inthe medical school setting about all of theseoptions are licensed naturopathic physicians. The purpose of this evaluation, as discussed inthe overview section and the overview of alterna-tive medicine, is to conduct a medical history,physical exam, and necessary laboratory andimaging studies to determine the risk for osteo-porosis and heart disease. After a determinationof whether you are at low risk, medium risk, orhigh risk for these conditions, a treatment planwill be recommended.

Using natural therapies versus using conven-tional or bio-identical HRT or some combina-tion of the these is a very personal decision. A well-informed patient who also has the goodfortune of having a well-informed, respectful,open-minded practitioner is in the best positionto make appropriate decisions. Remember thatany decision you make is reversible. Decisionscan and do change over time. Menopause, aging,and our concerns about long-term health prob-lems evolve over time, and balance is necessary.Naïveté is inappropriate, and over-medicalizationof menopause is also inappropriate. Menopauseis a normal and natural event of aging. It can bea time of strength, empowerment, personalgrowth, and positive, life-changing insights anddecisions.


225

OVERVIEW

Menstrual cramps are one of the most commonproblems that women face, affecting over 50 per-cent of menstruating women. The term dysmen-orrhea, derived from the Greek and meaning“difficult monthly flow,” is commonly used torefer to painful menstruation. Dysmenorrhea isbest classified as primary or secondary. In pri-mary dysmenorrhea, painful menstrual crampsoccur that have nothing to do with any physicalabnormalities or identifiable pelvic disease. Sec-ondary dysmenorrhea is painful menstrualcramps due to some specific pelvic or systemiccondition such as endometriosis, pelvic inflam-matory disease, adhesions, ovarian cysts, celiacdisease, thyroid conditions, congenital malfor-mations, narrowing of the cervical opening,polyps, or uterine fibroids. We will be focusingon primary dysmenorrhea in this chapter,although the treatments in this chapter for acutepain relief can be used in both primary and sec-ondary dysmenorrhea.

Treatment for secondary dysmenorrhea isdirected to treating the underlying cause of thecondition, whether it is endometriosis, fibroids,or another condition. Menstrual cramps are asignificant personal and public health problemfor women. Of the 50 percent of menstruatingwomen who are affected by menstrual cramps,about 10 percent have severe pain that rendersthem incapacitated for one to three days eachmonth.1 It is estimated that 600 million workhours are lost in a year in the United Statesbecause of untreated and incapacitating dysmen-orrhea. Social and family life is also disrupted bythe painful episodes.

Primary dysmenorrhea occurs most com-monly between the ages of 20 and 24. Women in

13M E N S T R U A L C R A M P S C H A P T E R

this age group experience the most severe pain.Women older than 24 have less painful cramp-ing, and the overall incidence of primary dys-menorrhea tends to decrease with age—morerapidly in married women than in unmarriedones, possibly due to pregnancy and childbear-ing. Women who begin to menstruate at ayounger age and have longer menstrual periodshave increased severity of pain and more days ofpain. In smokers, cramps tend to last longer. Infact, a recent study showed that there is a definiterelationship between the amount of cigarettesmoke exposure and menstrual cramps.2 Beingoverweight is also an important risk factor formenstrual cramps, and it doubles the odds ofhaving a long painful episode.3 Conversely, beingunderweight has also been shown to be an inde-pendent risk factor for dysmenorrhea.4

Primary dysmenorrhea usually appears within6 to 12 months after the first menstrual period.The pain usually begins several hours before orjust after the onset of menstruation and is oftenthe most severe the first or second day of men-struation. It tends to be spasmodic and isstrongest in the lower part of the abdomen abovethe pubic hairline, although it can often radiateto the back and along the inner aspects of thethighs. More than 50 percent of women withmenstrual cramps also have additional symptomsincluding nausea and vomiting, fatigue, diarrhea,lower backache, and headache. Women withsevere cases may also become dizzy and evenfaint. The symptoms may last from a few hoursto one day but seldom last longer than two tothree days. Some women have more congestivesymptoms that are characterized by a dull achingin the low back and pelvis, bloating, and weightgain, along with some systemic symptoms



including breast tenderness, headaches, and irri-tability.

Primary dysmenorrhea is diagnosed whenother causes of pelvic pain have been excluded.Certain characteristic clinical features distinguishthe diagnosis.

The cause of primary dysmenorrhea may beone of several factors, including behavioral andpsychological factors; lack of blood flow, andtherefore oxygen, to the uterus (ischemia); andincreased production and release of uterine pro-staglandins. Increased prostaglandins, specificallyPgF2-alpha and PgE2, cause uterine contractionsthat lead to ischemia and pain. The levels of bothPgF2-alpha and PgE2 are low during the firsthalf of the menstrual cycle and the early part ofthe second half, then rise sharply and reach theirhighest levels shortly before and during the onsetof menses. Studies have found that women withdysmenorrhea produce 8 to 13 times more PgFthan do women without dysmenorrhea.1 Thisincrease in prostaglandin production may berelated to the decline in progesterone levelstoward the end of the cycle just before the onset

of menses. Dysmenorrhea occurs only in cycleswhere ovulation has occurred. In cycles withoutovulation, there is no increase in progesteroneproduction in the second half of the cycle andthen decline right before the onset of menses, asin a normal cycle, and there is subsequently noincrease in the prostaglandin concentration inthe lining of the uterus. These mechanisms formthe basis for many of the therapies used, bothnatural and conventional.


An alternative approach to menstrual cramps dueto primary dysmenorrhea needs to provide effec-tive pain relief while at the same time correctingthe underlying dysfunction that is creating thepain. Because it is a functional problem and nota disease state that is causing the pain, we cantruly focus on a holistic approach by looking foraggravating factors in the diet, lifestyle, environ-ment, and emotional realm. Dietary principlesemphasizing good nutritional habits—eliminat-ing junk foods, saturated fats, and trans fats;increasing omega-3 oils from fish, hemp oil, andflax oil; and increasing whole grains, fruits, andvegetables—provide a range of nutrients neededto prevent and treat menstrual cramps. Stressreduction can help relieve tension in the lowerback and pelvic area that can worsen cramps.Improvements in posture improve the position-ing of the spine and promote proper circulationand nerve stimulation to the pelvic organs.

Providing acute pain relief is one of the great-est challenges for natural medicine, whether it ispelvic pain, headaches, or musculoskeletal pain.Mild and moderate levels of pelvic pain are moretreatable with natural therapies than is severepain, although some women with severe pain will experience relief from the therapies thatfollow. Even when acute pain relief is not accom-plished with alternative therapies, a treatment planfor the interim days of the month is important in order to reduce the severity of the recurring

Clinical Features of Dysmenorrhea

• The initial onset is at or shortly after the firstmenstrual period (menarche). If dysmenorrheastarts two years or more after menarche, thenother causes and secondary dysmenorrheashould be considered. Endometriosis is difficultto distinguish from primary dysmenorrheabecause they produce similar symptoms. Onedistinction is that endometriosis tends to getworse with time.

• Duration of the pain is usually 48 to 72 hours,starting a few hours before or just after theonset of the flow. Pain that starts several daysbefore the menses is less likely to be primarydysmenorrhea.

• The pain is cramping, or labor-like, althoughsome women have more congestion and bloating.

• Findings on pelvic exam are normal.

227M E N S T R U A L C R A M P S

menstrual cramp episodes over time. Having anatural therapeutic treatment plan for thechronic problem and using over-the-counter orprescription conventional medicines for acutepain relief can turn out to be the most effectiveplan. Over time, hopefully, the need for painmedications will decrease.

Many alternative practitioners have experi-ence with natural therapies not included in thisbook such as acupuncture, homeopathy, andhands-on techniques that may offer effective helpfor many women with menstrual cramps. I oftenencourage women to try an herbal or nutritionalproduct for a couple of hours during acute pain.If no relief is accomplished within that amountof time, then switch to a pharmaceutical methodof pain control. As each successive month oftreating the chronic problem goes by, a measureof the success of that treatment will be a de-creased need to use the pain relief medication.

It is important not to overlook the role of stres-sors in our personal lives that can be at least partof the cause of our pain and can also affect ourability to deal with pain. A recent study of over380 otherwise healthy women demonstrated thatwomen who experienced high stress were twice aslikely to experience dysmenorrhea in the following

cycle, especially among those women with a priorhistory of painful menses.5 Psychotherapy canhelp a woman gain insight into these influencesand learn how to reduce and manage stressors.Research has shown that behavior therapy hasbeen highly effective in reducing the symptoms ofspasmodic dysmenorrhea.6

Biofeedback treatment with a relaxation prac-tice has also proven to be significant in reducingdysmenorrhea.7 After two months of biofeedbacktreatments, sufferers of menstrual cramps haddramatic declines in the severity and duration of

KEY CONCEPTS

• Primary dysmenorrhea should be distinguishedfrom secondary dysmenorrhea.

• Typical menstrual cramps are due to primary dysmenorrhea.

• Causes of secondary dysmenorrhea include endo-metriosis, pelvic inflammatory disease, adhesions,ovarian cysts, celiac disease, thyroid conditions,congenital malformations, narrowing of the cervi-cal opening, polyps, and uterine fibroids.

• Seek adequate pain relief in addition to tryingto correct the underlying mechanism that iscausing the problem.

• About half of all women experience menstrualcramps.

PREVENTION

• Good posture and spinal alignment may decreasethe tendency toward menstrual cramps.

• Stress reduction may help to relax the pelvic andlow back muscles.

• Some women may find that their menstrualcramping is worsened when they use tampons;these women should switch to sanitary napkins.

• A copper IUD (Paraguard) for contraception may worsen spasmodic menstrual cramping. Aprogestin-containing IUD (Mirena) and hormonalcontraception can improve chronic dysmenor-rhea. Barrier methods of contraception have nobearing on dysmenorrhea.

• Maintain a healthy weight.• Avoid smoking.• Food allergies may contribute to water reten-

tion, gas, and bloating, which may contribute tocongestive menstrual pain.

• An increase in exercise may improve blood flowto the uterus and create an optimal pelvic mus-culature that will tend to reduce the incidenceof menstrual discomfort.

• Maintain optimal digestive function. Irregularbowel habits may be correlated to primary dysmenorrhea.

• Reduce foods that may contribute to an excessof the prostaglandins that cause uterine con-tractions: dairy products, beef, pork, lamb, poul-try, eggs, deep-fried foods, and trans fats foundin potato chips, french fries, and partiallyhydrogenated packaged foods.


their symptoms as well as a decline in theamount of medication they were taking. Medita-tion, visualization, and relaxation techniques areused by many women both as a primary form ofpain management and also in combination withother therapies. My advice would be to seek theadvice of a trained person to help you learnwhich method may be most appropriate andeffective for you.

Nutrition

A healthy diet is fundamental to an effectivemenstrual cramps treatment program. In fact,something as simple as eating breakfast regularlywas found to be inversely related to the incidenceand severity of dysmenorrhea.8 Many womenexperience relief from cramps just by switchingto good nutritional habits. There are two basicaspects to making changes in the diet. One is todecrease the intake of foods that may be con-tributing to the condition, and the other is toincrease the intake of foods that provide a widerange of important nutrients necessary to bringabout a functional change in the pelvic area. Onestudy supports this theory by demonstrating thatdietary intake of fish, eggs, and fruit was associ-ated with less dysmenorrhea while wine intakewas associated with more dysmenorrhea.9 Inaddition, another study advocates a vegetariandiet as a way to increase sex-hormone-bindingglobulin and decrease body weight and the sever-ity and duration of menstrual cramps.10

The most important foods to avoid are thosethat are high in arachidonic acid. This is thepolyunsaturated fatty acid that the body uses toproduce the series-2 prostaglandins (PgE2)—theones that cause muscle and uterine contractions.Egg yolks, red meat, and poultry are the mainsources of arachidonic acid.

In addition, many people are allergic to dairyproducts or lack the enzymes to digest them.Digestive problems such as bloating and gas canintensify with menstrual cramps, adding to theoverall discomfort. Reducing or even eliminating

the intake of milk, cheese, cottage cheese, butter,ice cream, and yogurt may be enough to have asignificant impact for as many as one-third ofwomen with menstrual cramps.

Saturated fats from nondairy sources can alsointensify menstrual cramps by stimulating thePgE2 series. Most of our saturated fats comefrom animal products, although a few are fromvegetable sources such as palm oil or coconut oil.Animal foods to reduce or avoid that contain sat-urated fat include beef, pork, lamb, and evenchicken and turkey. Even though chicken andturkey are lower in saturated fat, they are actuallyhigher in arachidonic acid than red meats.

Salt can be another aggravating factor forwomen with menstrual cramps. Too much dietarysalt can increase fluid retention and worsen bloat-ing that contributes to the congestive symptoms ofmenstrual cramps. Canned and frozen foods, fastfoods, and processed/packaged foods are all sus-pect for high amounts of salt. Read the labels care-fully. You may be surprised to find that some ofthe things you thought were healthy, such as cer-tain salad dressings, are actually loaded with salt.Even a bean burrito at a fast-food restaurant willbe high in salt. Look for “no salt” labels on yourpackaged foods, and go light on the saltshaker inthe kitchen and at the table.

Although sugar in the diet may not be directlyrelated to menstrual cramps, sugar does interferewith the absorption and metabolism of some Bvitamins and minerals. Deficiencies or less thanoptimal amounts of some of these nutrients mayworsen muscle tension and increase the contractilenature of the uterus. High-sugar foods are oftenthe same foods that are high in saturated fats.

Women with monthly menstrual cramps runthe risk of overusing alcohol because of its seda-tive and pain-relieving effects. This overuse maylead to other problems, including alcoholism andsubstance abuse. Nonaddictive pain relief med-ications would be far preferable. Alcohol alsodepletes the nutrient status of many B vitaminsand minerals such as magnesium. These deficien-


cies and nutritional imbalances can lead to diffi-culty in regulating muscle function and worsenmuscle spasms during menstruation. Alcohol mayalso interfere with the liver’s ability to metabolizehormones effectively and efficiently. This may leadto heavier flows. A heavier amount of blood createsmore clots, and the passage of clots will trigger anincrease in the uterine muscle spasms.

The best medicinal foods for menstrualcramps are those foods that increase the antispas-modic prostaglandins, the PgE1 and PgE3 series.Certain fish, including salmon, tuna, halibut, andsardines, contain omega-3 oils, specifically eicos-apentaenoic acid (EPA), a fatty acid that helps torelax muscles by the production of PgE3.11 Manyseeds and nuts are sources of linoleic acid andlinolenic acid, also precursors to these muscle-relaxing prostaglandins. The best sources of bothof these fatty acids are flaxseed, hemp seeds, andpumpkin seeds. Sesame seeds and sunflower seedsare excellent sources of linoleic acid. The oils fromthe seeds of flax, hemp, pumpkin, sesame, andsunflower are the best oils to use in salad dressings.Flax, hemp, and pumpkin oils should not beheated, but sesame and sunflower are acceptablecooking oils. In many cases the seeds, nuts, andfruits from which these oils are extracted arehealthy choices as well.

To round out the healthy changes in the diet,emphasize whole grains, legumes, vegetables, andfruits. Whole grains such as brown rice, oats,millet, barley, rye, amaranth, and buckwheat pro-vide sources of magnesium, calcium, potassium,fiber, vitamin E, B-complex vitamins, and protein.Specifically, intake of dietary fiber has been shownto be inversely proportional to menstrual pain.12

Both calcium and magnesium reduce musculartension, fiber helps to regulate the bowel function,and potassium has a diuretic effect that can aid inreducing bloating. Beans are also good sources ofcalcium, magnesium, potassium, and protein.Many vegetables are high in the calcium, magne-sium, and potassium that help to relieve and pre-vent muscle spasms. Fruits are an excellent form of

natural anti-inflammatory substances like bio-flavonoids and vitamin C. These nutrients notonly strengthen the blood vessels that can aid cir-culation to areas of muscle tension in the pelvisbut also reduce the pain from menstrual crampsthrough their anti-inflammatory effect.


Vitamin B1 (Thiamine). A large, well-designed study found that 100 mg of thiaminedaily helped to alleviate dysmenorrhea com-pletely in 87 percent of study subjects, while only5 percent had no relief.13

Vitamin B1

100 mg daily

Vitamin B3 (Niacin). Niacin or vitamin B3

has been shown in clinical research to be effectivein 87.5 percent of women with menstrualcramps.14 Niacin was given in 100 mg dosestwice daily throughout the month, and thenevery two to three hours during the periods ofmenstrual cramps. Although a sometimesuncomfortable niacin flush could easily occur atthe escalated dosing, none of the women in thestudy stopped the medication due to the flush-ing. Interestingly, the women who received norelief of their menstrual cramps were frequentlythe women who reported no flushing. Thevasodilating effect of niacin (which causes flush-ing) may indeed be the main treatment effect.Vasospasm of the uterine arteries may be respon-sible for the menstrual pain.

Vitamin B3 (Niacin)

100 mg twice daily throughout the month100 mg every 2–3 hours during episodes of menstrual

cramps

Vitamin C and Rutin. In a follow-up study,the author of the niacin study also found thatrutin with ascorbic acid increased the effective-ness of niacin in the treatment of menstrual


cramps.15 In twice as many women as the niacin-only study, the same dose of niacin (100 mgtwice daily regularly and every two or three hoursduring menstrual cramps) was given while alsoadding 300 mg of vitamin C and 60 mg of rutindaily. These additions slightly improved theresponse in up to 90 percent of the women. Thisincreased effectiveness was thought to be due toimproving the permeability of the capillaries,thus potentiating the vasodilating effect of theniacin. In most cases, niacin was not effectiveunless it had been taken 7 to 10 days before theonset of the menstrual flow.

Vitamin C

300–3,000 mg per day

Rutin

60–1,000 mg per day

Vitamin E. Vitamin E was studied back in the1950s for the treatment of spasmodic dysmenor-rhea. It was used in doses of 150 IU ten days pre-menstrual and during the first four days of themenstrual period. In approximately 70 percent ofthe women tested, it helped to relieve menstrualdiscomfort within two menstrual cycles.16 A morerecent, large, well-designed study evaluated vita-min E at a dose of 200 IU two times per daybeginning two days before the start of menses andcontinuing through the third day of the cycle andfound a significant decrease in dysmenorrhea andoverall blood loss after two months.17 I generallyrecommend higher amounts of vitamin E becausethere are so many other benefits for women,including relieving cyclic breast pain, raising ben-eficial HDL cholesterol, and providing antioxi-dant protection.

Vitamin E


Calcium. Calcium supplementation formenstrual cramps has been used by women as a

self-care treatment for many years. Muscles needcalcium to maintain their normal muscle tone; if they are deficient in calcium, they can moreeasily cramp. This is true of the uterine muscle aswell. Low calcium intake is associated with men-strual water retention and greater pain during themenses.18 The typical American diet suppliesabout 450 to 550 mg of calcium per day, fallingshort of the recommended daily allowance of1,000 mg per day in menstruating women.

Calcium

Supplement the diet so that total calcium is 1,000 mgper day

Omega-3 Fatty Acids. Essential fatty acidsare the raw materials from which prostaglandins,beneficial hormone-like substances, are made.There are two essential fatty acids: linoleic acid(omega-6 family) and linolenic acid (omega-3family). Linoleic and linolenic acids cannot bemade by the body and must be supplied daily inthe diet from either food or supplements. Thetypical American diet is often much higher inomega-6 oils than it is in omega-3 oils. As a result,many of us end up with the PgE2 prostaglandinsthat cause muscle contractions and pain.

Another problem is that our bodies need acertain amount of linoleic acid to convert togamma linolenic acid (GLA), which leads to theproduction of the PgE1 prostaglandins (the anti-spasmodic and anti-inflammatory prostaglan-dins). The conversion of linoleic acid to GLAand the beneficial prostaglandins requires thepresence of magnesium, vitamin B6, zinc, vita-min C, and niacin. Women who are deficient inthese nutrients won’t be able to make this conver-sion adequately. Supplementation with flax oil(high in omega-3 fatty acids), hemp oil, borageoil, black current oil, and evening primrose oil(all high in linoleic acid and GLA) is one way offavorably altering the synthesis of the beneficialprostaglandins; the end result likely will be feweruterine contractions and less menstrual pain.


As mentioned earlier, after the rise of proges-terone in the second half of the menstrual cyclefollowed by its decline right before menstruation,omega-6 fatty acids, particularly arachidonic acid,are released. Subsequently, an increase in PgF2-alpha and PgE2 occurs, causing uterine contrac-tions leading to ischemia and pain. Instead ofinhibiting ovulation and therefore the proges-terone effect, or inhibiting the synthesis of pro-staglandins with nonsteroidal anti-inflammatoryagents, the omega-3 fatty acids, eicosapentaenoicacid (EPA), and docahexaenoic acid (DHA) com-pete with omega-6 fatty acids and result in theproduction of the friendlier antispasmodic andanti-inflammatory prostaglandins, series 1 and 3.

Based on these observations and mechanisms,using fish oil containing omega-3 fatty acids as asupplement seems beneficial. Dietary supple-mentation with fish oils was tested in 42 adoles-cent girls with dysmenorrhea.11 The first groupof 21 girls received fish oil (1,080 mg EPA and 720 mg DHA) and 1.5 mg vitamin E dailyfor two months, followed by a placebo for anadditional two months. In the second group, 21girls received a placebo for the first two months,followed by fish oil for two more months. At the conclusion of the study, on a 7-point scale, a score of 4 being moderately effective anda 7 meaning totally effective, 73 percent of thegirls rated the supplementation greater than orequal to 4. Another, more recent study looked atsupplementation with krill oil in decreasingmenstrual symptoms, including cramps com-pared to standard fish oil, and found the krill oil to be superior in decreasing the severity ofdysmenorrhea as evidenced by a decreased use ofanalgesics.19

Fish Oils

1,080 mg EPA and 720 mg DHA per day

Evening Primrose Oil (EPO)

500–1,000 mg up to 3 times per day

Melatonin. I have no personal experienceprescribing melatonin for menstrual cramps, butI think it has potential based on some of itsknown biochemical effects. It has been proposedthat insufficient melatonin secretion during thesecond half of the menstrual cycle (the lutealphase) is a factor in primary dysmenorrhea.20

This hypothesis is based on several factors: (1)melatonin levels are low at ovulation and increasepremenstrually three- to sixfold and reach theirpeak at menstruation;21 (2) melatonin decreasesuterine contractility;22 (3) melatonin exerts anal-gesic effects;23 (4) melatonin stimulates proges-terone secretion;24 and (5) melatonin inhibitsuterine prostaglandin synthesis and release.25

Since melatonin has been shown to have allthese effects, supplementation in order to achievehigh concentrations during menstruation mayserve to oppose the effects of prostaglandins andtherefore prevent the occurrence of dysmenorrhea.

Melatonin

2.5 mg per day, taken 3–4 days prior to onset of menses

Botanicals

Rose. A recent study suggests that rose teaconsumption helped to decrease both pain andpsychological distress of women during menses.26

In addition, another study showed that abdominalmassage of rose, lavender, or clary sage essential oil in a base of almond oil was more effective than almond oil alone in decreasing the severity ofdysmenorrhea.27

Valerian (Valeriana Officinalis). Valeriantraditionally has been used primarily as a sedativeand antispasmodic for the treatment of anxietydisorders, sleep disorders, and a diverse array ofconditions associated with pain. Valerian con-tains an important class of compounds calledvalepotriates and valeric acid, which are foundexclusively in this perennial plant native to NorthAmerica and Europe. It is not difficult to see how


valerian would help to relieve pain, anxiety, andinsomnia because both valepotriates and valericacid are capable of binding to the same receptorsin the brain as the pharmaceutical drug Valium.28

Although valerian has not been scientificallystudied for menstrual cramps, it has been shown to relax the spasmodic contractions of intestinalmuscles.29 Both the uterus and intestines containsmooth muscles. In clinical practice, valerian isusually a significant feature of an alternative medi-cine approach to painful menstruation. It is mostpractical to take valerian in tincture form or cap-sules. Many people prefer valerian capsules becausethe tincture has a very bitter taste. Attempts to dis-guise the taste can be made by placing the tincturein a small amount of fruit juice and then followingthat with several swallows of plain juice. Valerianmay make you tired and sleepy, so it is advisable tostay home and rest or take a nap.

Valerian

1 tsp tincture or 1–2 capsules every 3–4 hours or asneeded for pain

Crampbark (Viburnum Opulus) and BlackHaw (Viburnum Prunifolium). Both of thesespecies of viburnum are mentioned repeatedly inthe traditional botanical reference books as uter-ine relaxants and general antispasmodics.30 Theyhave been used mainly for menstrual cramps,bearing-down uterine pains, and chronic uterineand ovarian pains. Animal studies have con-firmed that both species have an antispasmodiceffect on the uterus.31 Laboratory studies onhuman uterine tissue also have confirmed thatViburnum prunifolium exhibits a relaxant effecton the uterine tissue.32

When the menstrual pains are of either a congestive or spasmodic nature and include lowback pains, especially if the pains radiate downthe thighs, there is no better herbal choice thancrampbark.

The root bark of black haw is reported tocontain several active constituents that are uter-

ine relaxants, one of which is scopoletin, whichhas been historically used as a specific medicinefor menstrual cramps with severe low back andbearing-down pelvic pains. For menstrual painsassociated with a profuse menstrual flow andintermittent severe pains, black haw would prob-ably be a more specific choice than crampbark.American Indians used the root and/or stem forthe treatment of painful menses, to prevent mis-carriage, and as a postpartum antispasmodic.

Crampbark

1⁄2 tsp tincture or 1 capsule every 2–3 hours

Black Haw

1⁄4 tsp tincture or 1 capsule every 2–4 hours

Caution: Both viburnum species should be avoidedduring pregnancy except in the hands of an experi-enced herbal practitioner.

Ginger (Zingiber Officinale). Ginger is typ-ically known for its stimulatory effects on diges-tion and easing the nausea of an upset stomach.The pungent constituents in ginger, shagaol andgingerol, also have an inhibitory effect on inflam-matory and spasmodic prostaglandins. Althoughginger has not been studied specifically in rela-tion to menstrual cramps, it does have antispas-modic effects on the smooth muscle of theintestines. Given that the uterus is also made up ofsmooth muscle, and ginger has a long history oftraditional use for treating spasmodic dysmenor-rhea, I use it in clinical practice with great confi-dence in combination with other herbs.

Ginger

1–2 g of dried ginger powder 1–2 times daily

Black Cohosh (Cimicifuga Racemosa).Black cohosh has gained increased attention inthe last few years largely as an herb for the reliefof menopause symptoms. However, when I wasfirst studying botanical medicine, this herb wasknown more for its relaxant effect on the uterus


in dysmenorrhea, false labor pains, and threat-ened miscarriage. It can be helpful in both con-gestive and spasmodic menstrual cramps of evena severe nature. If the menses is also associatedwith PMS irritability and anxiety, delayed orirregular menstrual cycles, or scanty flow, thenblack cohosh would be an even more indicatedherbal choice for menstrual cramps.

Black Cohosh

1⁄4–1⁄2 tsp tincture or 1–2 capsules every 2–4 hours

Other Traditional Herbs to Consider.Herbs such as false unicorn root (Chamaeliriumluteum), wild yam (Dioscorea villosa), passion-flower (Passiflora incarnata), German chamomile(Matricaria chamomilla), blue cohosh (Caulo-phyllum thalictroides), and hops (Humulus lupu-lus) have an independent antispasmodic orsedative effect on the uterus in their own right.They are often used in combination with eachother or in formulations with some of the moredominant choices such as crampbark, black haw,valerian, and black cohosh.

Additional herbs may also be considered fortheir different actions. For example, herbs thathave an anti-inflammatory effect, such as whitewillow and ginger; diuretic herbs that decreasethe pelvic congestion, such as parsley, dandelionleaf, or horsetail; and herbs that promote circula-tion, such as ginkgo, may also have a role in reduc-ing the pain experienced from dysmenorrhea.

Natural Progesterone. As stated earlier, it isbelieved that the drop in progesterone premen-strually results in an increased production ofarachidonic acid by the endometrium. This stim-ulates PgE2 release and uterine contractions. Ifwe can temper or delay this drop in progesteronepremenstrually, then, in effect, natural proges-terone can be used to inhibit the uterine contrac-tions, ischemia, and pain during menstruation.

Remember, though, that some decline inprogesterone is necessary in order to trigger the

onset of blood flow. Natural progesterone mayallow a slower decline or a delayed decline. Thus,some women do indeed find that a natural prog-esterone cream, applied topically for 3 to 12 daysprior to onset of menses, will reduce menstrualcramps.


Apply 1⁄4 tsp of cream (>400 mg/oz) 2 times per dayfor 3–12 days before the expected onset of menses.

Exercise

The effects of both special exercises33–35 and gen-eral regular physical exercise on primary dysmen-orrhea have been studied. No discrepancies existin the results from the first group of studies—special exercises are reported consistently toreduce or eliminate menstrual pain. For example,one researcher found symptom reduction in 89.3percent of 129 dysmenorrheic women whoadhered to his program of special exercises. Sim-ilarly, another researcher, investigating 141 dys-menorrheic girls 14 to 18 years of age from twodifferent high schools, found that 92 percent ofparticipants in one of the schools were “cured” orimproved after being given a set of specific exer-cises to reduce menstrual pain.36 (A girl was con-sidered cured “if she was free of pain for at leastthree menstrual periods” following the perform-ance of the prescribed exercises.) The experimentwas conducted from mid-September 1956 tomid-June 1957. The results for the second schoolwere 76 percent “cured.”

The three studies on the effects of general reg-ular physical exercise on dysmenorrhea offer conflicting results. One group of investigators37

conducted a 12-week experiment that comparedtwo groups of dysmenorrheic women who volun-teered to either walk/jog or to act as sedentary controls. The experimental group reported signifi-cantly less severe menstrual symptoms than thecontrols. In contrast, another group of investiga-tors reported a 30 percent increase in menstrual


Sample Treatment Plan for Dysmenorrhea


• Increase salmon, tuna, halibut, sardines, her-ring, fruits, vegetables, and whole grains.

• Decrease dairy, salt, sugar, red meat, poultry,and eggs.

For Acute Pain Management

• Calcium carbonate: 1,000–1,500 mg duringpain

• Valerian: 1 tsp tincture or 1–2 capsules every3–4 hours

• Crampbark and/or black haw: 2 capsules every3–4 hours

• Relaxation techniques• Consider combination products containing

niacin, borage, vitamin E, calcium, crampbark,

valerian, and black cohosh: 3 capsules every3 hours during acute pain (see theResources section for formulation sources)

Use Throughout the Month

• Niacin: 100 mg twice daily• Fish oils: 1,080 mg EPA and 720 mg DHA

daily• Vitamin E: 200–400 IU daily• Crampbark and/or black haw and/or black

cohosh: 1–2 capsules daily• Consider combination products containing

niacin, borage, vitamin E, calcium, cramp-bark, valerian, and black cohosh: 2 capsulesfor daily pain (see the Resources section for formulation sources)

symptoms in regularly exercising over sedentarystudent nurses.38 However, a more recent, con-trolled study again validated the hypothesis thatregular exercise decreases menstrual symptoms infinding that “high exercisers experienced the great-est positive effect and sedentary women the least.”39


Two groups of drugs are highly effective againstdysmenorrhea: oral contraceptives and prostag-landin synthetase inhibitors, also known as non-steroidal anti-inflammatory drugs (NSAIDs). Thechoice of medication depends on whether awoman needs oral contraceptives for birth control,whether she has any allergies to aspirin or con-traindications to oral contraceptives such as priordeep venous thrombosis, whether she has a historyof gastric ulcers, and her age.

Women desiring birth control should proba-bly use oral contraceptives as the first agent ofchoice. Combination oral contraceptives reduceprostaglandin levels and menstrual flow, andapproximately 80 percent of patients achievenear-complete relief of dysmenorrhea. A newer

regimen of oral contraceptive use may be evenmore effective. Reducing the pill-free interval toapproximately four days reduces the volume ofmenstrual bleeding beyond the usual reductionseen in the seven-day pill-free interval and sup-presses ovulation more effectively, further reduc-ing the production of prostaglandins. Paincontrol with oral contraceptives is probably theresult of reduced volume of menstrual fluid andsuppression of ovulation, which reduces uterineprostaglandin levels.

You may need to try several oral contracep-tives before you find one you are comfortablewith. The majority of oral contraceptive sideeffects come from the progestin. Use the medica-tions for several months before you decidewhether they are effective, rather than giving upafter the first cycle, and be willing to try differentbrands if necessary. Oral contraceptives, if suc-cessful, can be used throughout a woman’s entirereproductive cycle and into her early 50s. If dys-menorrhea is reduced but not significantly elim-inated, an NSAID can also be added.

For women who do not need contraceptionor do not tolerate or choose to take oral contra-


ceptives, prostaglandin synthetase inhibitors canbe used. These nonsteroidal anti-inflammatorydrugs reduce menstrual fluid prostaglandins andtheir metabolites, resulting in decreased uterinecontractility and menstrual pain. They alsosomewhat decrease the amount of menstrualflow. They are most effective if given beforecramping begins and are usually only taken fortwo to three days per cycle.

There are several groups of prostaglandin syn-thetase inhibitors, including medications such asaspirin, ibuprofen, naproxen, and mefenamicacid. The aryl-propionic acid derivatives such asibuprofen and naproxen are easily available overthe counter and have been highly successful.Patients achieve a significant reduction in dys-menorrhea 60 to 90 percent of the time. Aspirin

has not been shown to be any more effective thana placebo and is not generally used by women formenstrual cramps. However, aspirin in associa-tion with other proprietary agents in a combina-tion medication such as Midol is reported bypatients to be effective.

Another category of NSAIDs includes meclofe-namate (Meclomen) and mefenamic acid (Ponstel).They have been available for more than 20 yearsand have been highly effective. They are used whencramps begin. COX-II inhibitors such as Celebrexhave been very effective in the treatment of dys-menorrhea. However, some head-to-head trialswith the other NSAIDs have not shown them to bemore effective, and they are significantly moreexpensive and possibly have an increase in sideeffects. Side effects of all prostaglandin synthetase

Exercise Recommendations for Menstrual Cramps

If not exercising regularly, incorporate exercise intoyour daily routine. (See Appendix A.)

Try the following special exercises for moderateto severe dysmenorrhea (adopted from Haman33 andGolub36). For mild menstrual pain, do only one or twoof the exercises. Do these exercises twice a day for 10consecutive days before menses.

Exercise 1

• Stand at a right angle to the wall with leftelbow on the wall on a level with the leftshoulder.

• Tilt pelvis forward.• Keeping knees slightly flexed, to avoid hyper-

extending them, move left hip until it toucheswall.

• Return to original position.• Repeat 5 times.• Repeat sequence with right elbow on the wall.

Exercise 2

• Stand facing the wall with both elbows on wallon a level with shoulders.

• Without moving elbows or feet and keepingknees slightly flexed, to avoid hyperextending

them, move pelvis away from wall and thentoward it until pelvis touches the wall.

• Return to original position.• Repeat 5 times.

Exercise 3

• Stand with feet 12 inches apart and armsraised to the side at shoulder level.

• Keeping knees slightly flexed, to avoidhyperextending them, twist trunk to theright and bend forward, attempting to touchthe right ankle with the left hand.

• Return to original position.• Repeat sequence in the opposite direction.• Repeat 5 times.

Exercise 4

• Stand with feet a few inches apart and armsat the sides.

• Swing arms forward and upward, simultane-ously raising the right leg backward.

• Return to the original position.• Repeat with the left leg.• Repeat 5 times.


inhibitors can include headaches, stomach or intes-tinal upset (specifically gastritis or ulcers), and atendency to feel fatigued. Serious complicationsinvolve kidney damage and gastrointestinal bleed-ing. Recommended doses for acute menstrual painare as follows:

Ibuprofen: 600 mg every 6 to 8 hoursNaproxen (Naprosyn): 500 mg every 12 hoursNaproxen sodium (Aleve): two 220-mg tablets

every 6 hoursNaproxen sodium (Anaprox DS): 550 mg every

6 to 8 hoursMefenamic acid (Ponstel): two 250-mg tablets

at the onset of pain, followed by one tabletevery 8 hours

Meclofenamate (Meclomen): 100 mg every 8hours

Celebrex: 200 to 400 mg once daily

For those who do not respond to oral contra-ceptives or other medications, it is best to considerlaparoscopy to rule out endometriosis or anotherpelvic disease. Usually, when the oral contracep-tives or the NSAIDs work, the practitioner willconsider that the patient has primary dysmenor-rhea, which is not associated with another pelvicdisease. If the patient has a negative laparoscopyand oral contraceptives or NSAIDs do not helpthe dysmenorrhea, she may be carefully watchedand administered intermittent narcotic medica-tions under the ongoing supervision of a physi-cian. Narcotic medications should be avoidedwhen possible because of the potential for toler-ance and abuse. They should be used only whenother options and diseases have been excluded.

The levonorgestrel intrauterine system in theMirena IUD substantially reduces menstrual flowapproximately 80 percent as a bonus to the excel-lent contraception it provides. It has also beenfound to significantly reduce menstrual cramps andmight be a good option for women seeking bothcontraception and treatment of menstrual cramps.


We need to remember that primary dysmenorrheais pain during menses that exists without any iden-tifiable pelvic disease. You must be certain thatyour menstrual pain is indeed primary dysmenor-rhea and not pain due to pelvic disease such asendometriosis, adenomyosis, uterine fibroids,pelvic infection, or an ovarian tumor. These condi-tions need to be diagnosed by a licensed health-carepractitioner capable of ordering the tests necessaryto exclude these pelvic diseases if you are notresponding to simple treatments.

If your pain is being well managed by con-ventional treatments, but you are experiencingsome unwanted side effects, an alternative practi-tioner can work collaboratively to reduce theseside effects. Alternative practitioners may also beconsulted for their expertise in using effectivealternative therapies and higher doses of naturalanti-inflammatories, herbs that may not be easilyaccessible for self-treatment, or for a comprehen-sive treatment plant looking at the relationship ofthe menstrual cramps to the whole system andwhole person.

237

OVERVIEW

As the U.S. population ages, certain diseases andmedical conditions more common among agingAmericans are gaining greater public attention.Osteoporosis, a serious and disabling disease andthe most prevalent metabolic bone disease inWestern societies, is one such condition. Fortu-nately, osteoporosis can and should be preventedand, when present, treated. Osteoporosis affects75 million people in Europe, the United States,and Japan. In the United States alone, it affects25 million people and causes 1.5 million frac-tures annually.1

In the United States the rates of osteoporosisand fractures vary with ethnicity, with African-Americans having the highest bone mineral density (BMD) and Asian-Americans having thelowest. After adjusting for body weight, one largestudy of postmenopausal women revealed thatwhite American women and Hispanic Americanwomen had the highest risk of osteoporotic frac-ture. This was followed by Native Americans,African-Americans, and Asian-Americans.2 Sowhile Asian-Americans have the lowest BMD,they also have a lower fracture rate, which wethink may be related to body size.

Most cases of osteoporosis occur in post-menopausal women, and the rates increase withdeclining BMD and with age. Of white Ameri-can women, 13 to 18 percent who are 50 years orolder have osteoporosis of the hip.3 An additional37 to 50 percent have low bone mass (osteope-nia) of the hip, again increasing with age andworse in women age 80 and older.

Osteoporosis is defined as a skeletal diseasecharacterized by low bone mass and a deteriora-tion in bone microarchitecture leading to bonefragility and susceptibility to fracture4 and is

responsible for about 90 percent of all hip andspine fractures in white American women aged65 to 84.5 The World Health Organization(WHO) has defined osteoporosis as a bone min-eral density that is 2.5 standard deviations (SD)below the mean peak value in young adults.6

This is called the T-score. A T-score that isbetween 1 and 2.5 SD below the mean is calledosteopenia.

These definitions are useful because they pro-vide objective criteria, but they have limitationsbecause they ignore the importance of otherdeterminants of bone strength. The definitionsalso ignore other risk factors for fractures in elderly women such as a maternal history of hip fracture, age, and poor balance. For example,most postmenopausal women with fractures donot have a bone density score that meets theWHO osteoporosis criteria.7 The World HealthOrganization, the National Osteoporosis Foun-dation, and other expert panels are in the processof releasing new guidelines to estimate a woman’srisk of an osteoporotic fracture, using a bonedensity test along with these other risks. Thesenew guidelines will provide better direction fortreatment interventions.

Although low bone mass, as measured by bonedensity, is important in determining a person’s riskof fracture, other risk factors are equally important.These include maternal history of a hip fracture,previous vertebral fracture, previous hip fracture,high fall risk, and others.8 Assessing a person’s like-lihood of a fall (use of sedative medications, inabil-ity to stand unaided from a sitting position, poorvision, muscle weakness) is very important as well.Low bone mass may be due to osteoporosis and/orpoor bone quality. Vitamin D deficiency and othercauses of hyperparathyroidism can lead to poor

14O S T E O P O R O S I S C H A P T E R



bone quality as well. Clinically, the term osteoporo-sis is used in reference to loss of bone associatedwith relatively atraumatic fractures of the ribs,spine, wrist, and hips.

Fractures associated with osteoporosis are dis-tinguished by three characteristics:9

• Greatly increased incidence with aging, withfractures occurring 2 to 100 times moreamong adults over age 75 than amongyounger people

• Greater incidence among women than men• Associated with modest trauma

The three most common fracture sites are thespine, hip, and forearm. For a 50-year-old Amer-ican woman, the risk of having an osteoporoticfracture in her remaining years is estimated to be 40 percent,10 and two-thirds of the fracturesoccur after age 75. Osteoporosis-related fractureswill develop in half of all women and one-fifth ofall men older than 65 years.11 Hip fractures, witha median age of 82, are particularly life altering.Within the first year following a hip fracture, themortality rate is increased by up to 20 percent, asmany as 25 percent of the survivors will be con-fined to long-term care facilities one year afterthe fracture, and 50 percent will have at leastsome long-term loss of mobility.12

Vertebral fractures (fractures of spinal verte-brae) occur a little younger, on average in awoman’s mid-70s. Multiple vertebral fractures,or one severe one, can cause severe pain, loss ofheight, and an exaggerated curvature of the mid-spine called thoracic kyphosis. These pains anddeformities can restrict bending and reachingand can greatly increase the risk of additional ver-tebral fractures.13, 14 Fractures of the thoracicspine can also restrict lung function, cause diges-tive problems, 15 lower self-esteem and bodyimage, and result in depression.16

Vertebral fractures are twice as common aseither hip fractures or distal radius (wrist) frac-tures. The incidence of wrist fractures starts to riseimmediately after menopause, with an incidence

of about 15 percent by age 80, but a peak inci-dence about 20 to 25 years sooner. Each year,172,000 wrist fractures occur that are the result ofmoderate trauma and rapid postmenopausal boneloss. The female to male ratio is 5:1. Wrist frac-tures are rarely fatal and cause much less disabil-ity than do hip and spinal fractures.17, 18

How Osteoporosis Affects the Bone

There are two types of bone: trabecular and cor-tical. The skeleton is living tissue composed ofabout 75 percent cortical bone and 25 percenttrabecular bone. The trabecular bone is the insidepart of the bone where the bone marrow is. It iscomprised of a network of structural tissue thatprevents it from compressing with pressure (forexample, from a fall). The cortical bone is thehard exterior of the bone that protects the bonefrom external trauma. Vertebrae are made up of90 percent trabecular bone and only 10 percentcortical bone; the hip is 50:50, and the extremi-ties are 90 percent cortical bone. Trabecular boneis concentrated in the vertebrae, pelvis, other flatbones, and at the ends of long bones like theupper and lower leg.

Trabecular bone is metabolically much moreactive and has a higher turnover rate than corti-cal bone. To provide support for the body, boneis continuously rebuilt to maintain an optimalstructure. Any damage or fatigue effect is con-stantly repaired through a process of bone break-down (resorption) and rebuilding (formation)called bone remodeling. Bone formation andresorption are interdependent processes; if one isaltered, it directly affects the other. The cells thatcause bone resorption are called osteoclasts andstimulate the production of acid and enzymesthat dissolve bone mineral and proteins. Bonebuilding cells, or osteoblasts, promote bone for-mation by creating a protein matrix, which con-sists primarily of collagen. This becomes calcifiedand results in mineralized bone.

Normal bone remodeling is a process that isbalanced by bone resorption and bone formation.

239O S T E O P O R O S I S

In childhood, bone formation far exceeds boneremodeling, leading to longer, denser bones.During the adult years, bone resorption andbone formation are in balance, and total bonemass remains relatively stable. As we age, theosteoblasts and osteoclasts may no longer func-tion in a balanced fashion. When there is animbalance between bone resorption and bone for-mation, bone loss occurs, bone mass decreases,and fracture risk increases.

Bone loss can be osteoclast-mediated, as seenin osteoporosis, or osteoblast-mediated, as seenin bone cancers. In osteoporosis, osteoclast-mediated bone loss outpaces the ability ofosteoblasts to fill in the empty spaces. Certainproblems cause different types of bone loss. Trabecular bone loss occurs with low estrogenlevels, steroid use, and immobilization. So, whenwomen choose not to take estrogen after meno-pause, they are more likely to lose trabecularbone and therefore may be at higher risk for ver-tebral and hip fractures. Cortical bone loss occurswith calcium and vitamin D abnormalities suchas vitamin D deficiency and leads to an increasedrisk of extremity fractures. An extreme form ofthis is rickets, which presents with bowing of thefemurs that results from small microfractures ofthose bones. Because of the differences in corticaland trabecular bone, many practitioners prefer tomeasure both the hip and the spine when doingbone density testing.

The Role of Menopause in Osteoporosis

As we age, bone resorption increases. This in-crease is worsened by a decrease in bone forma-tion in women after menopause. Within the firstfew years of menopause, there is rapid bone lossdue to lower levels of ovarian estrogen produc-tion. With less estrogen in the body, bone resorp-tion is no longer inhibited. This decline inestrogen is the most significant factor in the in-creased bone loss associated with menopause.19

In the spine, bone loss of 2 percent per yearbegins about two to three years before the last

menstrual period, and this accelerated rate of loss ends three to four years after menopause. Atthe hip, bone loss has an age-related rate ofdecline of about 0.5 percent per year. Over thesefive to seven years, it totals approximately 10.5percent loss for the spine and 5.3 percent for thehip.20 A slow and small amount of bone lossoccurs from then on. Women older than 70 faceother challenges that may accelerate their boneloss again such as increasing age and secondaryhyperparathyroidism due to a drop in calciumabsorption.

In women who have premature menopause(at or before age 40), whether spontaneous or bymedical causes such as having both ovariesremoved, chemotherapy, or pelvic radiation,there is a greater risk of low BMD compared toother women their age who are not meno-pausal.21 By the age of 70, when risk of fractureis greater in general, this issue of early prematuremenopause becomes moot because no matterhow menopause was attained, women will havethe same risk of low BMD or fractures.

The Role of Heredity, Nutrition, andLifestyle in Osteoporosis

Genetic predisposition contributes significantlyto bone mass and to the development of osteo-porosis later in life. Heredity has the greatestinfluence on a woman’s peak bone mass, andstudies have suggested that 80 percent of thedeterminant of peak bone density is due togenetic factors.22, 23 Female children of womenwho experienced an osteoporotic fracture werefound to have 3 to 7 percent lower bone massthan would be expected for their age.24, 25 Addi-tional studies have shown that relatives of womenwith osteoporosis tend to have lower bonemass.26 The racial differences observed in bonemass also suggest the role of a genetic factor.

Dietary factors and nutrient deficiencies alterbone growth and remodeling and may result inlower bone mass. Girls or women with a dietaryabnormality such as anorexia nervosa have signifi-


cantly lower bone mass than their healthy counter-parts.27 A balanced diet of plenty of vegetables,especially dark green leafy vegetables, nuts, seeds,whole grains, low-fat dairy, fish, and small amountsof animal meats play an important role in thedevelopment and maintenance of healthy bone.Adequate calcium and vitamin D intake is neededto achieve the genetically determined peak bonemass, to maintain bone mass once this peak hasbeen achieved, and to maintain the strength andintegrity of the skeleton throughout our lives.28

The intake of calcium is most importantduring the bone-building years of childhoodthrough adolescence and in old age. Duringpuberty, calcium is required for bone growth andfor the achievement of maximal calcification.Postmenopausal women and men over 65 requirea greater intake of calcium because absorption ofcalcium is less efficient, but the dietary intake ofcalcium is usually lower because of intolerance todairy products or elimination of dairy productsas part of a low-fat diet.

Lifestyle factors, such as the level of physicalactivity, cigarette smoking, alcohol consumption,and additional nutritional influences can pro-foundly impact bones. We will expand on thesein the overview of alternative treatments.

Assessing Osteoporosis Risk andDiagnosing Osteoporosis

The evaluation of risk and diagnosis of osteo-porosis is made by a careful medical history, athorough physical examination, laboratoryanalysis, and measuring bone density.

No one test or risk factor, alone or in combi-nation, will accurately predict which patients willor will not experience osteoporotic fractures. Ingeneral, the more risk factors present, the greaterthe potential for lower bone mass and the higherthe risk of fracture. However, predictions fromrisk factors cannot pinpoint all persons who willbe affected. Risk factors for osteoporosis accountfor only 20 to 40 percent of bone mass variance.29

Therefore, risk factors alone do not provide

adequate assessment of low bone mass, but ratherare important guides in the clinical assessment ofosteoporosis risks that contribute to optimal pre-ventive management. Ultimately, an individualwoman’s risk of fracture is the most relevantparameter for her future health care.

It is important to distinguish between riskfactors for osteoporosis as defined by BMD andrisk factors for osteoporotic fractures. For osteo-porosis defined by BMD, major risk factors are:

• Postmenopausal• Advanced age• Genetics• Lifestyle factors (low calcium, low vitamin

D intake, smoking)• Thinness

The most common risk factors for osteo-porotic fracture are female, advanced age, lowBMD, previous fracture as an adult (other thanthe skull, facial bone, ankle, finger, and toe). Amore comprehensive list of risk factors for osteo-porotic fractures includes:

• Female• Postmenopausal and advanced age• Previous fracture as an adult (other than

skull, facial bone, ankle, finger, and toe)• History of hip fracture in a mother or father• Body weight less than 127 pounds or body

mass index (BMI) less than 21• Characteristics: short, slender, fair-skinned,

blonde, blue-eyed• Current smoking, of any amount• Low calcium or vitamin D intake• More than two alcoholic drinks per day• Early menopause (physiologic, surgical, or

drug-induced)• Increased risk of falling (impaired vision,

dementia, poor health or fragility, sedentary,history of recent falls)

When trying to determine a woman’s risk oflow bone mass and risk of fracture, questionsshould be asked to determine risk factors as


stated in the two preceding lists. There are alsovarious medications, disease states, and geneticdisorders that are secondary causes of bone loss.This information should also be explored with amedical history. Most of these risks can be deter-mined on a questionnaire. They don’t diagnoseosteoporosis, but identifying these risk factorscan help to determine causes of osteoporosis andhelp to guide the best treatment strategy.

After menopause, the risk of falling should alsobe determined. Factors related to an increased riskof falling include

• A history of falls, fainting, or loss of consciousness

• Muscle weakness• Balance problems• Dizziness• Difficulty standing or walking• Arthritis

• Poor vision• Medications that affect balance and

coordination

Physical exam should assess height, weight, siteof back pain and localized spinal muscle spasms,spinal contours and deformities, and dental health.A loss of height can be a sign of a fracture in thevertebrae. Normal age-related height loss is up to1.0 to 1.5 inches. Height should be measuredyearly, and a loss of height that is greater than 1.5inches increases the possibility that a vertebral frac-ture has occurred.30 Vertebral fractures also causeacute or chronic back pain, especially in themiddle part of the back, called the thoracic spine.If there are multiple vertebral fractures, calledcompression fractures, the most obvious sign is anabnormal curvature called kyphosis. If back pain,height loss, and kyphosis are all present, this war-rants an x-ray of the spine to determine if there is

Medications, Diseases, and Disorders That Increase the Risk of Osteoporosis

Medications

• Oral or intramuscular use of glucocorticoids formore than three months

• Excessive thyroid hormone• Long-term use of the anticonvulsant phenytoin• Heparin• Cytotoxic drugs• Gonadotropin-releasing hormone• Intramuscular medroxyprogesterone contracep-

tive agent• Immunosuppressive drugs (cyclosporine)

Genetic Disorders

• Osteogenesis imperfecta• Thalassemia• Hemochromatosis• Hypophosphatasia

Calcium Balance Disorders

• Elevated urinary calcium• Vitamin D deficiency

Endocrine Disorders

• Cortisol excess• Cushing’s syndrome• Gonadal insufficiency• Hyperthyroidism• Type 1 diabetes

Gastrointestinal Diseases

• Cirrhosis• Malabsorption syndromes (celiac disease,

Crohn’s disease)• Total gastrectomy (removal of the stomach)

Other Disorders and Conditions

• Multiple myeloma• Lymphoma and leukemia• Systemic mastocytosis• Anorexia nervosa• Rheumatoid arthritis• Chronic renal disease


osteoporosis and/or vertebral fractures. Even exces-sive height loss without back pain warrants an x-ray to confirm a spine fracture. Women who haveone vertebral fracture are at high risk for a subse-quent fracture,31 which makes diagnosing a singlevertebral fracture that much more important.

Body weight should also be recorded. A bodyweight less than 127 pounds or a body massindex less than 21 kg/m2 is a risk factor for lowBMD. Thinness is associated with low bone den-sity and a twofold increased risk of fracture, espe-cially in older women.32

Laboratory Tests. Laboratory tests areimportant in determining the cause of the lowbone density or osteoporosis. Secondary causesof bone loss should be identified because thecause needs to be treated, not just the resultingeffects, the bone loss. Laboratory studies and biochemical markers are done on an individualbasis. Some women may need some or all ofthese tests initially because their risk is deter-mined to be high from the history and physicalexam. Other women will want or need these testsbecause their bone density is significantly low,and possible metabolic causes will be importantto determine. Tests may need to be repeated overtime in order to monitor the effectiveness of thetreatments that have been employed. It’s impor-tant to fully understand, however, that these testscannot diagnose osteoporosis, predict bone den-sity, or determine fracture risk.

Tests that should be routinely performedinclude a complete blood cell count, serum cal-cium, alkaline phosphatase, thyroid-stimulatinghormone, albumin, and urinary calcium excre-tion to detect malabsorption of calcium or arenal calcium leak. Selected cases warrant addi-tional testing of 25-hydroxyvitamin D levels inthe serum, parathyroid hormone, and serumelectrophoresis to determine the cause of theexcessive bone loss or fractures.

There are some newer tests that are biochem-ical markers of bone turnover. Again, they do not

diagnose osteoporosis or determine future boneloss or fracture rates. However, they can be usedto determine a response to treatment. These testsof bone turnover can be done prior to beginninga treatment for osteoporosis and then again in afew months to determine if the treatment isworking to slow bone turnover. Tests for bio-chemical markers of bone turnover can be donemore frequently than a bone density test and canbe done early, even within weeks after beginningthe treatment. The role of these tests in routineclinical practice has not been established, how-ever, and therefore it is difficult to determine thescope of their usefulness.

It might be tempting to think that all meno-pausal women should have a bone density test. Iwould discourage that way of thinking because atest is really only helpful if it influences the treat-ment. If a woman really wants the test, I have noobjection to ordering it for her. However, I tendto follow the recommendations for BMD testing(described later) of the North American Meno-pause Society:

• Postmenopausal women with medical causesof bone loss

• All postmenopausal women who are 65years or older

• Postmenopausal women younger than age65 who have one or more of the followingrisk factors for fracture:

Fracture after menopause (other than skull,facial bone, ankle, finger, and toe)

Weight less than 127 pounds or BMI lessthan 21

Hip fracture in mother or fatherCurrent smoker

Bone density testing can clarify an already diffi-cult decision and can optimize the use of bothconventional and natural medicine therapies.

Imaging Techniques. Bone imaging tech-niques include radiographic techniques and


ultrasound of the heel. Radiographic techniquesinclude dual energy x-ray absorptiometry (DXA),CT scan, x-rays, dual photon absorptiometry(DPA), single-photon absorptiometry (SPA), andx-ray absorptiometry (SXA). DXA is the preferredtest of the commonly used densitometry tech-niques and is more accurate in measuring bonedensity of the lumbar spine and proximal femur.DXA offers a lower dose of radiation and ashorter examination time than other imagingmethods. Because of its enhanced precision andaccuracy, DXA has become the gold standard forbone densitometry. The total hip, femoral neck,and lumbar spine are the three most importantmeasurements. The lowest score of the three is themost important. Repeat tests in women who arenot receiving treatment generally do not need tooccur until three to five years later. For womenreceiving treatment for osteoporosis, BMD test-ing is typically done after two years, althoughselected cases may warrant testing at one year.

Ultrasound of the heel is less expensive, iseasily administered, and uses no radiation. Theheel bone is 100 percent trabecular bone, the sametype of bone that makes up 90 percent of the ver-tebrae and 50 percent of the hip. Ultrasoundmeasurement of the heel bone may provide a lessexpensive screening test for osteoporosis. Reviewshave concluded that ultrasound of the heel was agood predictor of fractures of the spine.33 Its lim-iting factor is that the scans are not useful indetecting small changes in density over time andtherefore cannot be used to monitor the effective-ness of treatment of osteoporosis. Women withabnormal results would be referred for DXA test-ing to more precisely assess bone mineral density.

In women who are receiving treatment forosteoporosis, DXA scans are usually done aftertwo years of treatment. It is important to realizethat even if there is no increase in BMD on theDXA scan in the first two years, there may be significant increases in the third year, even on thesame therapy. In addition, if proven fracture-reducing drugs are being used (bisphosphonates

and estrogen therapy), a reduction in fracture riskoccurs even if the bone density is not increased.On the other hand, if there is a decrease in theDXA scan, while on proven osteoporosis treat-ment medications, further testing should be doneto determine if there are any secondary causes ofbone loss.


Osteoporosis is far easier to prevent than to treat.An osteoporosis prevention perspective needs tostart in the teenage years. Education shouldinclude several key areas:

Medical problems, early in life and current, thatcan lead to osteoporosis

Medications that can interfere with calciummetabolism

The role of nutrition and exercise early in lifeand their necessity in achieving peak bonedensity

Awareness of the long-term consequences forbone health of anorexia

Awareness of the negative effect of smoking andexcess alcohol

For women in their 40s, 50s, and older whohave just begun to think about osteoporosis, thetime for reaching peak bone density at age 30 to35 is already past. We all lose bone density as weage, and if you achieved 100 percent of maxi-mum by 30 or 35 and you do not have a condi-

World Health Organization Definitions

1. Normal bone mineral density (BMD): Within1 standard deviation (SD) of young adult gender-matched means

2. Osteopenia: BMD between 1 and 2.5 SD belowyoung adult means

3. Osteoporosis: BMD more than 2.5 SD belowyoung adult means

4. Severe osteoporosis: BMD more than 2.5 SDbelow young adult means and the presence ofone or more fragility fractures


tion or genetics that cause rapid bone loss, thenall is well usually. If your peak bone density wasonly 85 percent of maximum, then you can’tafford as much normal age-related bone lossbefore your bone density becomes osteopenicand then osteoporotic.

Several approaches are available to preventosteoporosis and to treat both those who are athigh risk and those who have developed the condi-tion. Natural medicines are especially key in pre-vention and in helping women with mild low bonedensity. Once osteoporosis has been diagnosed,many of the natural interventions such as diet,exercise, nutritional supplementation, and herbalmedicines could be used aggressively in mildercases to slow bone loss and possibly improve bonedensity, bone strength, bone architecture, and bonehealth in general. In general, it is my position thatin cases of diagnosed osteoporosis, natural inter-vention should be used to supplement an antire-sorptive therapy intended to stop or slow the rateof bone loss and reduce the rate of fractures. Themost common proven antiresorptive therapiesinclude estrogens, bisphosphonates, and selectiveestrogen receptor modulators (SERMS).

All postmenopausal women, no matter theirrisk for osteoporosis or bone density status, shouldbe encouraged to practice prevention strategies. A

balanced diet, adequate calcium and vitamin D,regular exercise, not smoking, low alcohol intake,and fall prevention are important steps for bonehealth as well as other health benefits.

Natural interventions for mildly low bonedensity and osteoporosis include dietary andlifestyle factors, exercise, nutritional supplemen-tation, the use of phytoestrogens, and natural(bio-identical) hormone replacement therapy.Each of these areas deserves special attention.

Nutrition

Several dietary factors affect bone health and areinvolved in the development of osteoporosis:insufficient calcium and vitamin D intake, highphosphorus intake, a high animal protein diet,excess salt intake, and other mineral deficiencies.A diet that maximizes consumption of fruits andvegetables and minimizes dietary fats is beneficialfor bone development.

Women older than age 65 who do not eatenough and women who practice frequent dieting

KEY CONCEPTS

• Osteoporosis-related fractures will develop inalmost half of all women older than 65.

• Osteoporosis is a serious and disabling diseaseand is far easier to prevent than to treat.

• Women with a family history of osteoporosis,and especially hip fractures, are at the highestrisk of developing the condition. Eighty toninety percent of the determination of thedevelopment of osteoporosis is a family historyof osteoporosis.

• Fracture risk can be determined from a medicalhistory, physical exam, laboratory testing, and aDXA bone density test.

PREVENTION

• Do not smoke.• Reduce or avoid alcohol consumption and do not

exceed one drink per day.• Do regular weight-bearing exercise, especially

comprehensive weight lifting throughout life.• Ensure proper nutrition: organic low-fat dairy,

soy foods, adequate calcium and vitamin D,whole grains, dark leafy green vegetables, nuts,seeds, healthy oils, and fish.

• Avoid being underweight.• Minimize caffeine intake.• Reduce animal protein.• Avoid falls and injuries.• Get regular annual health checks; laboratory

testing and bone-density testing may be appropriate.

• Consider hormone replacement therapy (bio-identical hormones or conventional hormones) ifyou have several risk factors.

• Take nutritional supplements for bone health.


or have eating disorders are susceptible to insuf-ficient intake of vitamins and minerals and there-fore may have insufficient bone mass. Elderlywomen are particularly vulnerable to the negativeeffects of weight loss impacting their bonehealth. Weight loss in this group may lead toaccelerated bone loss and a higher risk of frac-tures, particularly of the hip.34

Studies have shown that excessive animal pro-tein in the diet may promote bone loss. It particu-larly causes an increase in urinary excretion ofcalcium. Raising daily animal protein intake from47 to 142 grams doubles the excretion of calciumin the urine.35 Calcium is mobilized from thebone to buffer the acidic breakdown products ofprotein. In addition, the amino acid methionine,highest in meat, dairy products, and eggs, is con-verted to homocysteine, which in high amountsmay also cause bone loss. All of these mechanismsof a high animal protein diet contributing to cal-cium and bone loss should raise serious concernabout popular high animal protein diets.

On the other hand, insufficient protein mayalso be a problem, especially in women olderthan 75, and adequate protein intake may helpto minimize bone loss.36, 37 Protein supplementa-tion of 20 grams per day in older patients whohave had a hip fracture have been shown todecrease recovery time and result in lower rates ofcomplications and a lower death rate the firstseven months after the fracture.38

A vegetarian diet is associated with a lowerrisk of osteoporosis,39 even though vegetarians donot have greater bone mass in their 20s, 30s, and40s. Several studies have shown that vegetariansdo have significantly higher bone mass later inlife, which would indicate that vegetarians losebone more slowly than nonvegetarians.40, 41

Many high-protein animal foods also containhigh amounts of phosphorus, which mobilizescalcium from the bones in order to maintainhomeostasis in the bloodstream.

High-phosphorus beverages are also implicatedin osteoporosis. A study in children demonstrated

a severe impact of soft drinks on calcium levels.Fifty-seven children with low blood calcium levelswere compared to 171 children with normal cal-cium levels.42 Of the 57 children who had lowblood calcium levels, 66.7 percent drank morethan four 12- to 16-ounce bottles of soft drinks perweek. Only 28 percent of the 171 children withnormal serum calcium levels consumed that manysoft drinks per week. For all 228 children, a strongcorrelation was seen in the serum calcium level andthe number of bottles of soft drinks consumedeach week. The more soft drinks consumed, thelower the calcium level in the blood. Due to thehigh intake of soft drinks in the United States, wecan probably expect to see increased osteoporosisin the “Pepsi generation” for many years to come.The American per-capita consumption of softdrinks is about three quarts per week.

Other nutritional factors also accelerate cal-cium loss and may be implicated in osteoporosis.Refined sugar may raise the risk for osteoporosisby increasing the loss of calcium from the bodyand by causing a significant increase in fastingserum cortisol levels. A serving of refined sugarincreases the urinary excretion of calcium,43 andan excess of corticosteroids can cause osteoporosis.High sodium intake can also cause an increase inurinary excretion of calcium in some individu-als.44 Refined grains and flours may also play apart in the development of osteoporosis. Due totheir lack of nutrient-rich germ and bran, there isa significant loss of vitamins and minerals inthese foods. The refining process produces whiteflour stripped of B6, folic acid, calcium, magne-sium, manganese, copper, and zinc.

One of the best general dietary preventivehabits to acquire is to eat a lot of dark green leafyvegetables. Kale, collard greens, romaine, spinach,Swiss chard, and other dark greens are a rich sourceof vitamins and minerals, including calcium, vita-min K, and boron. As you will learn in the nutri-tional supplements section, vitamin K is involvedin the mineralization of bone, and boron decreasesthe urinary excretion of calcium and magnesium.


Soy foods appear to also have some role inpreventing or slowing bone loss. Soy contains aclass of compounds called phytoestrogens. Thephytoestrogen especially high in soy foods isisoflavone. Phytoestrogens and isoflavones arediscussed in more detail in Chapter 12; here we’llfocus on their effect on bone health. Soybeanscontain phytoestrogens called isoflavones and aparticular isoflavone called daidzein. Daidzein issimilar to a semisynthetic product called Ipri-Flavone, which is used to treat osteoporosis. Soyis the only dietary source of daidzein, which is anonsteroidal estrogen-like molecule. Soy alsoincreases the menstrual cycle length by one tofive days, especially the follicular phase. This mayhave a positive effect on bone density due tolonger exposure to elevated estrogen levels.

Soy appears to have a proestrogen effect onbone in some experimental evaluations. Thebone density of ovariectomized rats for which soy replaced casein in the diet was compared toanother group that received estrogen. The addi-tion of soy inhibited bone loss, although not tothe same extent as was achieved with estrogentreatment.45 Another study of ovariectomizedrats also reported a positive effect of the soy phy-toestrogen genistein in maintaining bone.46

These authors also reported that genistein sup-presses the bone resorption cells (osteoclasts)both in the test tube and in vivo.

Several human studies have provided furtherinsight into the possible role of soy in bonehealth. A study conducted at the University of

Illinois found that menopausal women had anincrease in mineral levels and density in theirlumbar spines after taking 55 to 90 mg ofisoflavones for six months.47 The placebo groupshowed the lowest bone density and the greatestbone loss, while the estrogen group showed thehighest bone density and the slowest bone loss.What was surprising was that the soybean pro-tein diet was effective in preventing bone loss inthe fourth lumbar vertebra and, although less so,in the right hip as well. Soybean protein seems tohave more of an effect on trabecular bone (morepredominant in the spine) than on cortical bone(more predominant in the hip). The soybeanprotein did not show as great an ability to pre-vent bone loss as the estrogen group, but the pos-itive effect it showed is encouraging.

The study of the relationship between soyisoflavone intake and bone mineral density wasconducted from the Study of Women’s HealthAcross the Nation, a U.S. cohort study of womenaged 42 to 52 years.48 For African-American andCaucasian women, median intakes of genisteinwere too low to pursue analyses. For Chinesewomen, no association between genistein andbone mineral density was found. Premenopausal,but not perimenopausal, Japanese women whoseintakes were greater had a higher bone density ofthe spine and femoral neck. Mean spinal bonedensity of those women in the highest genisteinintake group was 7.7 percent greater than that of women in the lowest group. Bone density of the femoral neck was 12 percent greater in thehighest intake group versus the lowest.

Other positive studies on soy and bone den-sity also give some credence to the role of soy for bone health. In a study estimating the dailyintakes of soy isoflavones in the diets of 478 post-menopausal Japanese women who reported soyconsumption, high consumption of soy productswas associated with increased bone mass.49

Soy is also a good source of calcium. A dietthat includes greater amounts of soy productscan account for a meaningful amount of calcium,

Calcium Content of Selected Soy Foods

Soy Product Calcium (mg)Tofu, firm (1⁄4 block) 553Tofu, regular (1⁄4 block) 406Soy milk, calcium-fortified (1 cup) 80–300Soy milk (1 cup) 7Soybeans, roasted (1⁄4 cup) 119Soybeans, boiled (1⁄4 cup) 88Tempeh (1⁄4 cup) 77


and some soy foods can offer as much or morecalcium than a serving of dairy products.

An adequate intake of calcium and vitamin Dis fundamental for bone health and is an impor-tant adjunct to drug treatments for osteoporosis.In fact, a review of almost three dozen clinicaltrials found that bone mineral density of the hipincreased more in the estrogen plus calciumgroup, compared with the estrogen groupalone.50

Most menopausal women look to calcium supplementation to meet their calcium needs.However, dietary sources of calcium should beemphasized as part of a well-balanced diet toensure intake of other nutrients found in high-calcium foods. Dairy products are good sources of calcium. In addition, dairy products have ahigh elemental calcium content and absorptionrate and are affordable. There are now many dairyproduct alternatives as well, such as calcium-fortified soy foods, calcium-fortified rice milk,and others.

Some foods can actually inhibit calciumabsorption. I don’t advocate avoiding thesefoods, but it is important to be aware that theoxalate contained in foods such as spinach andthe phytates found in whole grains can inhibitcalcium absorption.

Foods high in calcium include kelp, Swissand cheddar cheese, carob flour, dulse, collardgreens, turnip greens, molasses, almonds,brewer’s yeast, parsley, corn tortillas, dandeliongreens, Brazil nuts, watercress, goat’s milk, tofu,dried figs, buttermilk, sunflower seeds, yogurt,beet greens, wheat bran, whole milk, buckwheat,sesame seeds, olives, broccoli, walnuts, cottagecheese, and spinach. Calcium and vitamin D arediscussed in detail in the nutritional supplementsection.

The influence of dietary fats on mineralabsorption is complex and only understood inpart. Several key observations have been made,although many of the factors that influenceabsorption are still unknown. For example,

increasing linoleic acid in the diet significantlyreduce calcium in the stool, indicating thatomega-6 essential fatty acids (EFAs) stimulatecalcium absorption.51 Calcium absorption willalso be significantly increased when the diet issupplemented daily with fish oil, evening prim-rose oil, a mixture of both, or sunflower oil.52

Deficiencies of EFAs modify bone fatty acidlevels and have profound effects on the degree ofmineralization of the bone. This is observed inanimals fed EFA-deficient diets, who developosteoporosis. The role of EFAs is discussed inmuch more detail in the nutritional supplementsection of this chapter.

Alcohol and Smoking. Consumption ofalcohol also appears to promote bone loss. Scien-tific evidence links consumption of alcohol (sevenounces or more per week) with lower bone mass,increased bone loss, an increase risk of falls, and ahigher incidence of hip fracture.53 A meta-analysisshowed that consuming two alcoholic drinks perday significantly increases the risk of fracture,54

and even heavier consumption has additional neg-ative effects on bone density. The good news isthat a small amount of alcohol, one to two ouncesper week, is associated with a higher bone mineraldensity in women age 65 years and older55 and adecreased risk of hip fracture.56

The results of most studies show that smok-ers lose bone more rapidly and have a lower bonemass than nonsmokers.57 Some research showsthat postmenopausal women who smoke have asignificantly higher fracture rate than womenwho don’t smoke.58 In female smokers, the risk of hip fracture is increased by 1.5 to 2.5-fold.14

It’s not clear what mechanisms are involved inthe adverse effects of smoking on bone densityand fracture. Some evidence suggests that smok-ing may alter calcium absorption59, 60 and lowerestrogen levels.61 All in all, it appears that womenwho smoke tend to lose bone more rapidly, havelower bone mass, and reach menopause abouttwo years earlier than nonsmokers.62–64



Calcium. When women think about whatthey can do to prevent osteoporosis, most womenthink of calcium supplementation. Calciumimproves bone health, increases bone mineraldensity, and improves the effectiveness of osteo-porosis medications. Although most studies donot show a positive effect of calcium in reducingfracture risk, in the Women’s Health Initiative(WHI) trial, hip fractures were significantlyreduced in older women on the calcium supple-ment program.65 Calcium supplementation hasalso been shown to decrease bone loss in post-menopausal women.66 The effects of calcium sup-plementation have been greatest in women whosebaseline calcium intake was low, in older women,and in women with osteoporosis.67

As women age, especially after menopause,calcium requirements increase due to bothreduced intestinal calcium absorption and lessefficient kidney conservation of calcium. Eventhough these two mechanisms are in play, how-ever, the primary influence on calcium absorp-tion is the amount of calcium that is ingested, via either diet or supplementation. Selected populations of postmenopausal women may nothave adequate calcium intake, including olderwomen, women who are lactose intolerant (andso must avoid dairy foods), vegans (who con-sume no animal or dairy products), and womenon poor diets in general. Even in the UnitedStates, postmenopausal women have dietaryintakes of calcium of about 600 mg per day,which is below the recommended amount. TheNational Academy of Sciences (NAS) recom-mendations68 (last revised in 1997) and theNational Institutes of Health (NIH) recommen-dations69 (last revised in 1994) are the two mostwell-accepted guidelines for calcium intake inwomen (see the following sidebar).

To determine how much calcium you shouldtake in a supplement, you must first estimatewhat your dietary intake is. Start by assuming

that you get 250 mg per day, not counting anydairy foods or calcium-fortified foods, if you eattwo or three meals per day. Most women take inan additional 300 mg per day in the form of oneserving of dairy. If you take in more than oneserving per day of dairy, add another 300 mg foreach additional serving, as well as for each serv-ing of a calcium-fortified soy food. If you drinkone glass of milk per day and eat no soy foods orother calcium-fortified foods, for example, youraverage daily intake is 250 mg � 300 mg � 550mg per day. So, if you are 55 and postmeno-pausal, you need an additional 650 to 950 mgper day to reach a total that falls within the rec-ommendations of 1,200 to 1,500 mg per day forpostmenopausal women under 65.

There is a great deal of confusion and contro-versy about which form of calcium is best. I dis-courage women from using either oyster shell orbone meal calcium. These calcium supplementsmay contain substantial amounts of lead. In1981, the FDA cautioned the public to limitintake of calcium supplements made from eitherdolomite or bone meal because of the potentiallyhigh lead levels. Unfortunately, even othersources of calcium from various chelates may also

Recommendations for Calcium Intake

National Academy of SciencesRecommendations

Age 31–50 1,000 mg/dayAge 51 and older 1,200 mg/day

National Institutes of HealthRecommendations

Premenopausal women aged 25–50 1,000 mg/day

Postmenopausal women under 65 using estrogen therapy 1,000 mg/day

Postmenopausal women not using estrogen therapy 1,500 mg/day

All women aged 65 and older 1,500 mg/day


contain minute amounts of lead. In a 1993 studyof lead content in calcium supplements, lead wasthe highest in bone meal, unrefined calcium carbonate, and dolomite and lowest in calciumchelate supplements and refined calcium carbon-ate.70 Calcium chelates are bound to citrate,fumarate, malate, succinate, and aspartate.

When the calcium is taken on an emptystomach, calcium citrate is absorbed better thancalcium carbonate. In addition, it may be that aswomen age and have lower stomach acid produc-tion, lower fat absorption, and take in less vita-min D due to less exposure to sunshine anddecreased fat absorption, calcium citrate may bea better choice to combat these compromisingeffects on calcium absorption. In most women,though, especially in perimenopausal womenand postmenopausal women up to age 65, thereis no known best form. Calcium carbonate isabsorbed well when taken with food. Calciumcitrate can be taken with food or on an emptystomach, making it more flexible as to timing ofyour supplement regime.

Calcium supplementation is extremely safe,and even in amounts of total calcium intake upto 1,500 mg per day there is no increase in therisk of a kidney stone.71 However, in womenwith a history of kidney stones, calcium supple-ments are contraindicated except with medicaltesting/assessment and supervision. Calciumintake greater than 2,500 mg per day, taking intoaccount diet and supplement, should be avoided.Some women become constipated or have nauseaand indigestion with calcium supplementation,especially calcium carbonate. In these cases, cal-cium citrate will less likely cause these problems.

Another issue that makes it difficult to deter-mine the optimal dose of calcium is that higherdoses of calcium may interfere with the absorp-tion of other nutrients. In two separate studies,researchers have shown that a high dietary cal-cium intake adversely affects zinc absorption andbalance in humans.72, 73 This may be especiallyimportant in elderly women due to their com-

promised zinc absorption, their possible mar-ginal zinc status to begin with, and their high riskof osteoporosis. A zinc deficiency can result inskin changes, growth retardation, loss of appetite,changes in vision, decreased insulin function,dysfunction in prostaglandin synthesis, andimmunologic abnormalities. Zinc is also essentialfor normal bone formation; it enhances the bio-chemical actions of vitamin D, is required for theformation of osteoblasts and osteoclasts, and isrequired for the synthesis of various proteinsfound in bone tissue. Zinc levels have been foundto be low in the serum and bone of elderly peoplewith osteoporosis,74 and also in people with boneloss at the alveolar ridge of the mandible.75 Thisnegative interaction between calcium and zincabsorption raises concerns about how higher cal-cium intakes may affect the absorption of otherminerals needed for bone health.

Another area of great disagreement is whatratio of calcium to magnesium is best. Someresearchers and clinicians recommend twice asmuch calcium as magnesium; others recommendequal parts calcium and magnesium; others rec-ommend 1.5 parts calcium and 1 part magne-sium; and still others recommend twice as muchmagnesium as calcium. The most scientificresearch support exists for two parts calcium toone part magnesium. (See the section on magne-sium later in this chapter.)

The optimal time to take calcium supple-mentation is the last question to consider. Theabsorption of calcium is dependent on itsbecoming ionized in the intestines. Calcium carbonate has to be solubilized and ionized bystomach acid in order to be absorbed. Manypeople have insufficient stomach acid, and stom-ach acid secretion decreases with age. In studiesof postmenopausal women, about 40 percent arefound to be severely deficient in stomach acid.76

For this reason, I recommend taking a form of calcium that is already in a soluble and ionizedstate, such as calcium citrate, calcium lactate, orcalcium gluconate. In these ionized products,


about 45 percent of the calcium is absorbed fromcalcium citrate in patients with reduced stomachacid, as compared to 4 percent absorption for calcium carbonate.77

All of these issues make it difficult to choosefrom the myriad options of form and dosing incalcium supplementation. In general, I wouldfollow the dosages of either the NIH or NAS. Ifyou don’t mind taking more pills, then I wouldalso recommend taking calcium citrate over cal-cium carbonate, or at least a combination. (Cal-cium citrate is much bulkier, and you have totake more pills to get adequate amounts of theelemental calcium.) Even though I can no longerargue for advantages in absorption in general ofcitrate over carbonate, fewer digestive sideeffects, the flexibility of taking the calcium withor without meals, and the possibility of enhancedabsorption as you age make a good case for cal-cium citrate. In the end, though, the amount ofyour total calcium intake is far more importantthan the kind of calcium.

Recommended Daily Calcium Intake

Women aged 25–50: 1,000 mg/dayWomen aged 51 and older: 1,200–1,500 mg/day

Vitamin D. Vitamin D is the only vitaminthat’s also a hormone, and it is the only vitaminwe don’t have to consume from our diet. VitaminD is normally produced in the skin throughultraviolet exposure of a derivative of cholesterol(7-dehydrochlesterol) to produce previtamin D,which is then metabolized to 25-hydroxyvitaminD in the liver and then to 1-alpha dihydroxyvit-amin D3 in the kidney, at which time it becomesfunctional. This hormone is now able to carryout its function, including calcium absorption,phosphate absorption in the intestine, calciummobilization in the bone, and calcium reabsorp-tion in the kidneys. Vitamin D also maintainsnormal parathyroid status, is an important regu-lator of the immune system, and is important formuscular strength.

Vitamin D enhances intestinal calcium absorp-tion, thereby contributing to a favorable calciumbalance in the system. Increased calcium absorp-tion also reduces parathyroid hormone–mediatedbone resorption. In the United States, most infantsand young children have adequate vitamin D con-sumption from fortified milk. During adolescence,however, the consumption of dairy products dropsoff and inadequate vitamin D intake is more likelyto adversely affect calcium absorption.

In general, calcium intake alone may have onlya slight protective effect for bone mass and fracturerisk, and it is more beneficial to supplement witha combination of calcium and vitamin D. Severallarge studies of vitamin D (400 and 800 IU perday) plus calcium (1,000 mg per day) have notshown a significant effect on fracture risk.78, 79

However, there are studies that do show a signifi-cant effect. One such study in people aged 65years or older showed that both calcium and vita-min D consumption can significantly reduce theincidence of nonvertebral fractures.80 Anotherstudy of postmenopausal women undergoing hipreplacement surgery showed that women with hipfractures were more likely to have a vitamin Ddeficiency than those undergoing elective jointreplacement.81 More recently, the NoNOF studyof survivors of hip fractures demonstrated thatvitamin D supplementation, either orally or byinjection, suppresses parathyroid hormone,increases bone mineral density, and reduces falls.82

The effects were more marked with cosupple-menting with 1,000 mg of calcium per day.

Perhaps the most compelling study is a meta-analysis of randomized clinical trials in post-menopausal women with a mean age of 71 to 85,which found that 700 to 800 IU per day of vita-min D was associated with significant reductionin hip and wrist fractures83; 400 IU per day hadno effect. Finally, more recent results from theWomen’s Health Initiative found that 1,000 mgper day of calcium plus 400 IU of vitamin D wasassociated with a small but significant 1 percentincrease in bone mineral density of the hip.65


Experts have typically thought that the mod-erate protective effect of vitamin D on fracturerisk is due primarily to bone mineral densitychanges. However, there is a good body of evi-dence that vitamin D may also directly improvemuscle strength and, as a result, reduce fracturerisk by preventing falls. While randomized con-trolled trials have found that vitamin D reducedfractures within two to three months84 and hasbenefits in improving muscle strength,85–87 theeffect of vitamin D on falls has not been wellestablished and results of randomized trials havebeen mixed. A meta-analysis in 2004 attemptedto determine the overall efficacy of vitamin D inpreventing falls in the elderly, especially women.88

Based on five randomized clinical trials involving1,237 individuals, vitamin D reduced the risk offalling by 22 percent, compared with individuals,but especially women, who received calcium or a placebo. A recent study on vitamin D sup-plementation and fall prevention was done inAustralia89 in which 625 older residents of nurs-ing homes and assisted-living facilities (95 per-cent women) were randomized to receive eithervitamin D (ergocalciferol; 10,000 IU weekly or1,000 IU daily) or a placebo. None of the partic-ipants had a vitamin D deficiency. All partici-pants also received 600 mg of elemental calciumdaily. During two years of follow-up, the inci-dence of falls was significantly lower in the vita-min D group compared to the placebo group(1.37 versus 1.86 falls per person/year). Thosewho received vitamin D were also less likely tosustain a fracture (8 percent versus 11 percent),although this was not statistically significant.

How much vitamin D is enough? Therequirements for vitamin D were last set in 1997by the Food and Nutrition Board of the Instituteof Medicine and may be inadequate (see sidebar).

A popular approach of using cod liver oil tosupplement vitamin D deserves awareness and abit of caution. One tablespoon of vitamin D–fortified cod liver oil supplies 1,400 IU of vita-min D but also contains high levels of vitamin A,

which can exacerbate calcium loss and be associ-ated with low bone density.

Magnesium. The conventional scientific viewis that magnesium is essential for parathyroid hor-mone (PTH) production and release. PTH isessential for the activation of vitamin D and there-fore absorption of calcium across the gut wall.However, magnesium is an intracellular ion anddifficult to measure. A magnesium level is a reflec-tion of extracellular magnesium. There are severalconditions that can lead to magnesium deficiencyand therefore hypoparathyroidism and vitamin Ddeficiency. These include diuretic use (urinaryloss), alcohol abuse (nutritional deficiency), dia-betes (urinary loss), and chronic diarrhea (malab-sorption). Otherwise, magnesium deficiency israre. From the conventional scientific viewpoint,the main reason why magnesium is part of calciumsupplements is that carbonates are constipatingand magnesium has a laxative effect, and thereforethe combination is usually better tolerated.

Even though calcium has received the mostattention, alternative medicine views the impor-tance of magnesium in skeletal metabolism andcalcium regulation in a little bit different andperhaps broader context. Magnesium influencesboth matrix and mineral metabolism in bone.Magnesium depletion causes cessation of bonegrowth, decreased osteoblastic and osteoclastic

Current Dietary Recommendations for Vitamin D

Adequate Tolerable Age Intake Upper Limits0–50 200 IU/day 2,000 IU/day51–70 400–800 IU/day 2,000 IU/dayOver 70 800 or more IU/day 2,000 IU/day

Higher doses than those listed as adequate or evenupper limits will be needed by women who have hadtheir vitamin D levels tested and found to be low orlow normal. Dosage for these women should be moni-tored with follow-up tests.


activity, osteopenia, and bone fragility.90 Ade-quate serum magnesium levels are necessary forproper calcium metabolism; adequate calciumintake may not ensure proper bone health ifmagnesium status is abnormal.

Magnesium deficiency has been shown morethan once to be related to osteoporosis. Magnesiumstatus appears to have a major influence on the typeof calcium crystals present in the bones, and there-fore its deficiency is associated with abnormal calci-fication of the bone.91 This may in part explainwhy some women who have reduced bone mineraldensity do not have an increase in fracture rates.These women may have a lowered bone mass, butthey have excellent structural calcification, due inpart to adequate levels of magnesium.

In order to assess the effects of magnesium onbone density, a group of osteoporotic postmeno-pausal women were given magnesium over aperiod of two years. At the end of the study, mag-nesium therapy appeared to have prevented frac-tures and resulted in a significant increase inbone mass density after the first year of treat-ment. There was, however, no change in densityfrom then on to the end of the study.92 The find-ing that magnesium supplementation actuallycaused an increase in bone density rather thanjust a stabilization of current bone density is significant. Other factors may have influencedthe increase in bone density, but the results ofthis study warrant further investigation into thepotential effect of magnesium on bone density.

Dr. Guy Abraham published a study support-ing the importance of magnesium above that ofcalcium. His study demonstrated an 11 percentincrease in bone density in the group that wasgiven dietary advice, hormones, and nutritionalsupplements (500 mg calcium citrate, 600 mgmagnesium oxide, vitamin C, vitamin B-complex,vitamin D, zinc, copper, manganese, and boron).The group that received the dietary advice plus thehormones but no supplementation had an averageincrease of only 0.7 percent.93 An 11 percentincrease in bone density is greater than that found

in studies of calcium or hormone replacementtherapy taken either separately or together. However, in most studies on bone density orosteoporosis-related fractures, the benefits of calcium have been observed without magnesiumsupplementation. A study looking at calciumabsorption found no benefit on calcium absorptionin postmenopausal women taking magnesium.94

Continued research to elucidate magnesium’s rolein bone metabolism and calcium-magnesium inter-actions is needed as well as clinical treatment trialsthat vigorously evaluate magnesium as a potentialtreatment for postmenopausal osteoporosis.

Foods high in magnesium include kelp, wheatbran, wheat germ, almonds, cashews, molasses,brewer’s yeast, buckwheat, Brazil nuts, dulse, fil-berts, peanuts, millet, whole wheat, pecans, wal-nuts, rye, tofu, beet greens, and coconut.

Magnesium

500–750 mg per day

Manganese. Manganese may be one of themost important trace nutrients related to osteo-porosis. Manganese deficiency causes a reductionin the amount of calcium laid down in the boneand thereby an increased susceptibility to frac-ture. Manganese stimulates the production ofmucopolysaccharides that provide a structure onwhich calcification takes place.95

Manganese

15–30 mg per day

Boron. Dr. Forrest Nielsen studied the effectof boron on bone loss in postmenopausalwomen. Published in 1988, his results indicatedthat boron supplementation reduced the urinaryexcretion of calcium by 44 percent, reduced urinary magnesium excretion, and markedlyincreased the serum concentrations of 17 beta-estradiol and testosterone.96 These findingsdefinitively implicate boron in calcium and mag-


nesium metabolism, hormonal stabilization, andthe subsequent prevention of bone loss.

Boron

3 mg per day

Zinc. Zinc is essential for normal bone for-mation,97 enhances the biochemical actions ofvitamin D,98 and is required for the formation ofosteoblasts and osteoclasts and for the synthesisof various proteins found in bone tissue. Zinclevels have been found to be low in the serumand bone of elderly people with osteoporosis.74

Zinc

15–20 mg per day

Copper. Copper deficiency may be a relatedcause of osteoporosis. Copper deficiency is knownto produce abnormal bone growth in growing chil-dren. Copper supplementation has been shown inlaboratory studies to inhibit bone resorption.99 Itssupplementation is deemed necessary in womenat risk for or with diagnosed osteoporosis.

Copper

1.5–3 mg per day

Folic Acid. Accelerated bone loss in meno-pausal women may in part be due to the increasedlevels of homocysteine, a breakdown product ofmethionine. Homocysteine has the potential topromote osteoporosis if it is not eliminated adequately. Since folic acid is involved in thebreakdown of homocysteine, supplementing post-menopausal women with this nutrient results insignificant reductions in homocysteine levels.100

This association of homocysteine levels and osteo-porosis was recently seen in a study showing thathigh homocysteine levels were associated withalmost twice the risk of nonvertebral osteoporoticfractures in women.101 However, in the samestudy, there was no association between homo-

cysteine levels and BMD at either the femoral neckor the lumbar spine. Despite these associations, itis not yet clear that giving folic acid is a therapeu-tic tool in preventing bone loss or fractures. Fornow, it remains an interesting association, and folicacid is easy enough to include in a holistic bonehealth approach and prevention program.

Folic Acid

400–800 mcg per day

Vitamin B6. Vitamin B6 also plays a role inhomocysteine metabolism. In genetic homo-cystinuria, B6 supplementation has been shownto reverse the elevated levels of homocysteine.102

Vitamin B6 has been studied and prescribed forits role in osteoporosis prevention in other capac-ities as well. Animal studies have shown B6 defi-ciencies to cause increased fracture healingtime,103 impaired growth of cartilage and defec-tive bone formation,104 and more rapid develop-ment of osteoporosis.105 Vitamin B6 may alsostimulate the production of progesterone and,through this hormone’s activation of osteoblasts,have a distinct role in preventing osteoporosis.

Vitamin B6

50–100 mg per day

Vitamin C. One of the actions of vitamin Cis to promote the formation and cross-linking ofsome of the structural proteins in bone. Animalstudies have shown that vitamin C deficiency cancause osteoporosis.106 Moreover, it has beenknown for decades that scurvy, a disease causedby vitamin C deficiency, is associated with abnor-malities of bone.

Vitamin C

500 mg or more per day

Vitamin K. Vitamin K has been thought forsome time to be a contributing factor in the


prevention of bone loss. It is required for the pro-duction of osteocalcin, the protein matrix onwhich mineralization occurs. Octeocalcin attractscalcium to bone tissue, enabling calcium crystal formation to occur. Vitamin K also plays a key rolein the formation, remodeling, and repair of boneby helping the calcium adhere to the site of thisprotein matrix. Individuals with osteoporosis havebeen found to have lower serum vitamin K levelswhen compared to age-matched controls.107 Theamount of vitamin K that is required for optimalbone health appears to be greater than that neededfor normal clotting of blood.108

Recently, a review and meta-analysis of 13published clinical trials made an even strongercase for the role of vitamin K in osteoporosis.109

In 12 of the 13 clinical trials, this meta-analysisconcluded that supplementation with large dosesof vitamin K can prevent bone loss of the hip andvertebrae. (The one trial that showed no effectwas a study of premenopausal athletic womenwho were given 10 mg per day of vitamin K1.)Even more impressively, fracture data was avail-able in seven of the studies. The rates of hip fractures were reduced by 77 percent, other non-vertebral fractures by 81 percent, and vertebralfractures by 60 percent.110

Most of the studies in this meta-analysis wereof postmenopausal women, but some of thestudies included patients who had diseases thatare associated with higher risk of osteoporosis,including patients with primary biliary cirrhosisand some on glucocorticoids. These results infracture reduction exceed those typically seenwith alendronate (about 50 percent), and fewerside effects are associated with vitamin K com-pared to the approximately 17 percent side effectrate of reflux and esophagitis with bisphospho-nates. However, the longest study in this meta-analysis was only three years, which is a shortamount of time in the world of bone density andfracture data, and further research is neededbefore drawing conclusions on the comparativevalue of vitamin K supplementation.

Vitamin K2

45 mg per day

Essential Fatty Acids

Essential fatty acids (EFAs) have not been talkedabout much in relationship to osteoporosis, butthere is a growing body of evidence and research towarrant attention. Most of the research and focuson osteoporosis has been around the loss of calciumfrom bone before and during osteoporosis, reducedbone strength, and increased risk of fractures. Whathas received less attention is that osteoporosis maybe a marker for other serious potential health prob-lems apart from fractures. Not only must we con-sider demineralization of bone, but ectopiccalcification and the possible connection betweenectopic calcium deposits, particularly in the arteriesand kidneys, and bone decalcification.

Specifically, low bone density may be related tovascular problems, and essential fatty acids andtheir regulation of calcium metabolism may be akey player in influencing the sites at which calcifi-cation occurs. The role of essential fatty acids haslargely been ignored in relation to osteoporosisdespite animal and human studies indicating thatEFAs enhance calcium absorption, enhance theeffects of vitamin D, reduce urinary calcium excretion, increase bone calcium, reduce ectopiccalcification elsewhere, and increase bone proteinsynthesis and bone strength.

The first published paper that clearlydescribed the relevance of EFAs on calciumshowed that in EFA-deficient animals, the kid-neys became highly calcified, apparently becauseof a shift of calcium from the bones.111 Otherearly studies demonstrated that EFA deficiencyin animals was associated with loss of normal col-lagen synthesis and of normal connective tissuein bone, loss of normal cartilage, demineraliza-tion of bone, and bone weakness.112–114

This early body of research established thatEFA deficiency led to severe osteoporosis in ani-


mals and that the osteoporosis was associatedwith significant ectopic calcification. Not untilthe 1990s, however, did new observations lead torenewed interest in EFAs and calcium. Theseobservations indicated that prostaglandin (PG)formation could stimulate bone growth, thatrenal calcium stones were rare among the Inuit(Eskimos) of the Arctic, seemingly due to theirhigh intake of EFAs from fish oils, and that EFAmetabolism might form a basis for the associa-tions between osteoporosis and coronary arterydisease, peripheral vascular disease, and stroke.

Before we get too far along, it’s important tohave some familiarity with the basics of EFA bio-chemistry. There are two families of EFAs ofimport in this conversation, the omega-6 seriesand the omega-3 series. Linoleic acid (LA) is theparent compound of the omega-6 series, andalpha-linolenic acid (ALA) is the parent com-pound of the omega-3 series. Each of these ismetabolized by a series of enzymatic reactions in which their metabolites play key roles within the body. The most important metabolites areprobably dihomo-gamma-linoleic acid (DGLA)and arachidonic acid (AA) of the omega-6 seriesand eicosapentaenoic acid (EPA) and doca-hexaenoic acid (DHA) of the omega-3 series.

Essential fatty acids are required constituentsof every membrane within the body. They arerequired for the normal functioning of everymembrane and for the normal functioning ofcalcium release from storage. EFAs are also partof most of the signaling systems within every cell.

How calcium is excreted and how much isexcreted are major factors in the metabolism ofbone and the development of kidney stones, aswell as the overall calcium balance in the body.Probably the major factor controlling calciumexcretion is calcium intake, but we also knowthat prostaglandins are involved in calcium reab-sorption and excretion. Significantly elevatedlevels of urinary prostaglandin E2 (PgE2) arepositively correlated with urinary calcium excre-tion.115–117 Calcium stones forming in the urine

are also correlated with increased PgE2 andincreased calcium excretion. Although the pre-cise role of EFAs and prostaglandins in hypercal-ciuria is not understood, the balance of researchdemonstrates that excessive production of PGEfrom arachidonic acid is a factor.

If we could reduce urinary calcium excretion,this could not only have a bone-preserving effectbut also reduce the formation of stones. Researchin the early 1990s explored enhancing dietaryEPA with fish oils to protect against stone dis-ease. What was found was that the fish oils wereable to reduce urinary calcium excretion. Thiswork was preliminary and fundamental tounderstanding how EFAs and prostaglandinmetabolism could affect calcium excretion andreabsorption. Although the work was undertakenin an effort to prevent kidney disease and kidneyfailure, it supports the idea that EFAs affect cal-cium metabolism and could be used to improvebone health and bone density.

The influence of dietary fats on mineralabsorption is complex and only understood inpart. Several key observations have been made,although many of the factors that influenceabsorption are still unknown. For example,increasing linoleic acid in the diet significantlyreduces calcium in the stool, indicating thatomega-6 EFAs stimulate calcium absorption.51

Calcium absorption will also significantlyincrease when the diet is supplemented with fishoil, evening primrose oil, a mixture of both, orsunflower oil daily.52

Animal studies have revealed many mecha-nisms related to EFAs and calcium absorption.Probably the largest body of work establishedthat there is a significant relationship amongEFAs, the actions of vitamin D, the transport ofcalcium across the membrane, and an increase inmembrane fluidity followed by an increase in calcium absorption.

As mentioned earlier in the nutrition section,deficiencies of EFAs modify bone fatty acid levelsand have profound effects on the degree of miner-


alization of the bone. Animals fed EFA-deficientdiets also develop osteoporosis. Evidence is alsobuilding that prostaglandins have an influence onbone metabolism. Prudent use of EFAs may reducethe degradation of bone matrix collagen, while alsoincreasing bone mineral content. Animal studiesusing different ratios of evening primrose oil (highin gamma-linolenic acid or GLA), fish oil (rich inEPA and DHA), sunflower oil, and flaxseed oilsuggest that supplementation with high doses ofevening primrose oil and fish oil is more effectivein inhibiting bone loss than is supplementationwith linoleic and alpha-linolenic acids.118

The relationship between osteoporosis andcardiovascular disease has several correlations.One is that those individuals with osteoporosisand a subsequent hip fracture have an increasedrisk of mortality due to strokes. Calcium is notsimply lost from the bone in osteoporosis, butsome of that calcium is deposited in the arteriesand kidneys. The calcification process in athero-sclerosis is very similar to what occurs in bone. Itmay be that metabolic issues that regulate calcifi-cation are common to both diseases. Individualswith osteoporosis frequently have ectopic calcifi-cation in other tissues as well, especially the discsbetween the vertebrae.

Loss of bone calcium with concomitant calci-fication in the kidneys was observed as far back as 1931 in a study by Borland and Jackson wherean induced EFA deficiency elicited both prob-lems.111 More recently, supplementation withEPA and GLA was shown to prevent ectopic cal-cification. This is better understood by looking atthe role of EFAs in membrane health, calciumabsorption, calcium excretion, and bone mineral-ization. It is also worth speculating that sincedeficits of long chain EFAs are important in cardiovascular disease, the associations betweenosteoporosis and heart disease may be dependenton a commonality of impaired EFA metabolismand poor sources of dietary fat.

While preventive measures of a well-balanceddiet, avoiding smoking and excess alcohol, regu-

lar weight-bearing exercise, and proper vitaminand mineral intake should be the hallmarks inthe prevention of osteoporosis, the informationand data on essential fatty acids should not onlymotivate us to improve sources of dietary fat, italso suggests that EFA supplements are a viablemethod of decreasing the risk of osteoporosis.

Essential Fatty Acids: Omega-3 and Omega-6

Approximately 1 g per day of EPA and DHA

Botanical Medicine

Red Clover (Trifolium Pratense). Red clover isa member of the legume family rich in flavonoids,glycosides, phytoestrogens, and other vitamins andminerals. This native American herb was histori-cally used to treat whooping cough, gout, andcancer. Some researchers speculate that red clovermay have an estrogenic effect on the bone. Theystudied the effects of a special red clover extract,Rimostil, containing Clovone, a specific blend ofisoflavones (biochanin A, formononetin, genistein,and daidzein), on serum lipids, bone density, and endometrial thickness in postmenopausalwomen.119 Fifty postmenopausal women were ran-domly assigned to receive either 28.5 mg, 57.0 mg,or 85.5 mg of Rimostil for six months, followed bytwo months of a placebo. Bone density was meas-ured at baseline, three months, and six monthsusing a DXA scan. (Lipid levels and uterine liningthickness were also measured in this study.) Allthree doses of Rimostil were associated with a 2.9to 4 percent increase in bone density from zero tosix months in the proximal radius and ulna (clos-est to the elbow). No significant change in bonedensity occurred at the distal radius and ulna.

Another placebo-controlled clinical trialattempted to determine the effect of red cloverisoflavones on bone density in women aged 49 to65.120 One group received one tablet of a stan-dardized extract of red clover (26 mg biochaninA, 16 mg formononetin, 1 mg genistein, and 0.5mg daidzein), and the other received a placebo.


This trial lasted one year, and 86 women in thered clover group and 91 in the placebo groupcompleted the study. Dietary calcium and vita-min D were similar in both groups. At the end of12 months, women in the red clover group hadless bone loss of the lumbar spine than women inthe placebo group. Bone density decreased by1.08 percent in the red clover group and by 1.86percent in the placebo group. The differences inthe hip bone between the red clover and placebogroups were not significant. Two markers of boneformation were also tested in this study. For post-menopausal women in the study, there was anincrease in these markers in the red clover group,and a decrease in one marker and a lower increasein another marker in the placebo group. Theseresults suggest that red clover isoflavones may beable to slow bone loss in the lumbar spine.

Red Clover Standardized Extract

28–85 mg per day of red clover isoflavones

Ipriflavone. A synthetic derivative ofisoflavones, Ipriflavone was only available in Italyand a handful of other countries until recently. It is now available over the counter in naturalfood stores or from alternative practitioners. Two multicenter, two-year clinical trials evaluated the efficacy and bioavailability of Ipriflavone inpostmenopausal women with low bone mass.121

Women were randomly selected to receive eitheroral Ipriflavone (200 mg three times daily) or aplacebo, plus 1 gram oral calcium daily. Bothstudies were reported in the same paper. Study A showed a bone-sparing effect of 1.6 percent inthe spine, and study B, 3.5 percent in the wristafter two years. A significant difference wasfound between the treatment groups and theplacebo groups in both studies.

It seems as though Ipriflavone has a directability to inhibit the osteoclastic (bone-losing)cell activity, but how it does this is unknown.Although the effects on bone density using Ipri-flavone tend to be small, between 1.15 and 3.7

percent, these results provide yet another optionfor many women who cannot, will not, or do notneed to take stronger, more effective conven-tional treatments. It remains to be seen whetherIpriflavone can have a positive effect on the hip, a far greater concern. Although the effect onthe spine and wrist is encouraging, these smallincreases in bone density do not necessarily meanthere is a reduced fracture rate, the true test of aneffective treatment for the prevention and treat-ment of osteoporosis.

One well-publicized study in 2001 was notable to document any benefit for Ipriflavone inwomen with significant bone loss and withosteoporosis.122 It was also noted through bloodtests that some of the women taking Ipriflavonedeveloped lower lymphocyte counts. For thisreason, I recommend Ipriflavone only for womenwith mild bone loss or for those who are athigher risk for bone loss, but not for women withsignificant bone loss. I also recommend getting ablood test, a complete blood count (CBC), everysix months to check the lymphocyte counts.

In the studies that do show benefit, Ipri-flavone was given with a calcium supplement.

Ipriflavone


Herbs in High Mineral Content. Through-out the centuries of traditional herbal medicine,many herbs have been known for their high min-eral content. It is difficult to use herbs as a substi-tute for mineral supplementation because weknow so little about the precise mineral content ofa given herb. However, using these high-mineralherbs to augment mineral supplementation maynot only improve one’s mineral status but alsooffers other health benefits. High-mineral herbsinclude nettles, oatstraw, red raspberry leaves,chamomile, horsetail, and dandelion greens.

Natural or Bio-Identical Progesterone. Theterm natural progesterone, now more popularly


called bio-identical progesterone, refers to proges-terone made from derivatives found in the Mex-ican wild yam or in soybeans. It is important torealize that commercial bio-identical proges-terone is made in a manufacturing laboratory by extracting either diosgenin from Mexican wildyam or beta-sitosterol from soybeans, then con-verting the natural substance into progesteronethrough various enzymatic and biochemical reac-tions. This progesterone is biochemically identi-cal to the progesterone produced by a woman’sovaries. Because of this, it is called bio-identicalor natural progesterone. This is distinctly differ-ent from synthetic progestational agents, properlycalled progestins, the most common of which ismedroxyprogesterone acetate (MPA).

Accelerated bone loss has been shown tooccur after menopause, but evidence also existsindicating that normal menstruating womenbegin to lose spinal bone prior to meno-pause.123–127 Evidence also exists that this boneloss prior to menopause is related to progesteronedeficiency and that progesterone, like estrogen,plays an important role in bone metabo-lism.128–130 Dr. Jerilyn Prior postulated a hypo-thetical relationship between phases of the boneremodeling cycle and the normal menstrualcycle. Ovarian steroid levels are low at menstrua-tion, so increased bone resorption occurs at thistime. As estrogen production increases beforeovulation, resorption begins to reverse. Finally,bone remodeling begins as progesterone levelspeak in the mid part of the second half of themenstrual cycle.131

Dr. Prior and colleagues went on to study 66premenopausal women over one year.128 In thesewomen, 29 percent of all menstrual cycles weredisturbed by a lack of ovulation or short lutealphase (number of days between ovulation andonset of menses), even though nearly all of thesewomen continued to have regular 30-day cycles.These subtle ovulatory disturbances did notresult in any symptoms, but they did correlatewith decreases in spinal bone density. The

women with the shortest luteal phases, and there-fore with decreased progesterone production,had the greatest decline in spinal bone density,losing 2 to 4 percent of bone per year. Theseresults have been cited as a strong suggestion thatthe maintenance of peak bone density through-out a woman’s adult life requires normal ovarianproduction of progesterone as well as estrogen.

Dr. Prior and colleagues also studied theeffects of synthetic progestin, medroxy-progesterone acetate (MPA, also called Provera),10 mg for 10 days each month, in athleticwomen who had stopped having a menstrualcycle. The regimen led to significant increases inspinal bone density.132 These studies indicate that progesterone and MPA appear to have osteo-tropic (bone-building) effects. This is some of theresearch that alternative practitioners cite whenmaking a case for administering natural proges-terone for the treatment and prevention of osteoporosis. An error is often made when practi-tioners assume that administering bio-identicalprogesterone is the same as administering the synthetic analogue MPA, and this often occurswhen advocates of bio-identical progesteroneattempt to make a case for its use in osteoporosismanagement.

There is good theoretical evidence from thesestudies and additional laboratory and animalstudies that the body’s progesterone and MPAhave a stimulatory effect on bone formation and reduce bone turnover. What is not clear iswhether giving bio-identical progesterone in apill or cream has similar effects. When it comesto preventing or reversing osteoporosis, no otherproduct has been the subject of as much contro-versy as the use of topically applied bio-identicalprogesterone. A large segment of women seekingalternatives to conventional hormone replace-ment therapy and many alternative practitionershave accepted the premise, most often promotedby the late Dr. John Lee, that topically appliednatural progesterone cream will not only preventosteoporosis but will actually increase bone min-


eral density and prevent fractures. In his publica-tions, Dr. Lee had become the strongest advocateof the role of progesterone in preventing andreversing osteoporosis. He asserts that almost allwomen can successfully prevent and reverseosteoporosis and improve their bone density byas much as 15 percent with this cream and thatestrogen replacement therapy is very seldom anecessary component.

Although I respect much of the groundbreak-ing work done by Dr. Lee, this particular prem-ise is based almost exclusively on a hypothesisthat lacks adequate scientific evidence. Otherresearchers have investigated the therapeuticeffects of natural progesterone cream, includingits effects on bone in menopausal women. Onerandomized clinical trial compared the effect of atransdermal natural progesterone cream (32 mgdaily) with a placebo cream. Eighty postmeno-pausal women in Australia were randomlyassigned to each group. Women were evaluatedusing the familiar Greene Climacteric Scale andthe Menopause Quality of Life Questionnaire, aswell as blood lipids and bone markers, over 12weeks.133 No detectable change was seen in vaso-motor symptoms, moods, libido, lipids, or meta-bolic markers of bone turnover. There was aslight elevation of blood levels of progesterone.The authors concluded that the use of 32 mg oftransdermal progesterone was not sufficientlyabsorbed into the bloodstream to achieve biolog-ical effects.

At least two studies, though, have shown thattransdermal natural progesterone of 30 mg perday134 and 40 mg per day135 did modestly elevatelevels of progesterone in the blood after 15 daysand 42 days respectively. A transdermal cream of 20 mg daily in a randomized clinical trialresulted in statistically significant improvementin vasomotor symptoms, but no improvement inmood or bone mineral content.136

Transdermal progesterone cream for vasomo-tor symptoms does have efficacy, which is dis-cussed in the chapter on menopause (Chapter

12). That said, too many women are inappropri-ately selecting natural progesterone cream astheir main and possibly only treatment interven-tion for osteoporosis. A careful process of siftingthrough the benefits of alternative and conven-tional medicine and the weaknesses or downsideof any natural or conventional therapy is espe-cially warranted when it comes to osteoporosis.

Another way to take bio-identical proges-terone is as oral micronized progesterone (OMP).It is also often used in menopause management,although it has not received the attention andcommercial interests for general consumer usebecause it is available only by prescription.Results from the Postmenopausal Estrogen/Progestin Interventions Trial (PEPI) have alsoprovided us with some insight on natural proges-terone and bone density.137 Participants in theplacebo group lost an average of 1.8 percent ofspinal bone density and 1.7 percent of hip bonedensity by the 36-month visit, while thoseassigned to one of the four treatment groupsgained bone density at both sites ranging from3.5 to 5.0 percent and a total increase of 1.7 per-cent bone density in the hip. Although thechanges in bone density were significantly greaterin the treatment groups when compared toplacebo, the results among the treatment groupswere not significantly different from each other.

Treatment groups were either (1) 0.625 mgconjugated equine estrogens (CEE) daily alone;(2) 0.625 mg CEE and 10 mg MPA per day for12 days per month; (3) 0.625 mg CEE and 2.5mg MPA daily; or (4) 0.625 mg CEE and 200mg OMP per day for 12 days per month. I ampresenting this in some detail because, in thisstudy, it appears that it was the estrogen therapycomponent that increased bone density and notthe various progestogen regimens, either syn-thetic or natural.

So does natural progesterone alone, withoutestrogen, either topically or orally, have an abilityto increase bone density? From the data we haveso far, I would have to say no, it does not seem


to. Estrogen, not progesterone, is the main hor-mone that provides benefits for the bone.

Natural or Bio-Identical Estrogens. Naturalor bio-identical estrogens are made in the sameway as natural or bio-identical progesterone,except that the end product is either estrone,estradiol, or estriol. Compounded estrone usedby alternative practitioners is the same hormonethat is used in at least two prescription conven-tional estrogens (Ogen and Ortho-est), with the caveat that the prescription drug has fillers,binders, preservatives, and/or excipients. Theseare added in order for the particular product to receive a patent; a particular individual mayabsorb and tolerate one form better than another.

Bio-identical estrone is also available, by pre-scription, from a compounding pharmacy. Thesepharmacies are able to formulate the dose re-quested by the practitioner and adjust the dosingand the delivery method based on very individualneeds. Bio-identical estrogens are free of unneces-sary fillers and available in individualized dosesand delivery forms (capsules, tablets, sublingualtablets, lozenges, creams, gels), an important advantage in using natural estrogens. In addition,estrone can be used either alone or in combina-tion with estradiol and estriol as is appropriate toeach woman and each set of circumstances.

Bio-identical estradiol is also available from a compounding pharmacist and also individual-ized by dose and delivery for each woman. Bio-identical estradiol is the same hormone as theestradiol that is used in many conventional pre-scription estrogens (Estrace, Gynediol, and allthe current estrogen patches on the market suchas Estraderm, Climara, Vivelle, Alora, andMenostar). Again, the difference in the com-pounded bio-identical estradiol is that it isdevoid of the binders, fillers, preservatives, andadhesives found in the patented product. As withcompounded bio-identical estrone, compoundedbio-identical estradiol also carries with it theextra advantage of very individualized dosing,

combined options with estriol or estrone, andnumerous delivery methods depending onpatient preference or tolerance.

Whether it is compounded estrone/estradiolor the commercial pharmaceutical companyform, these forms of estrogen have bone mineraldensity effects similar to those of conventionalconjugated equine estrogens (CEE). A study of32 postmenopausal women compared 0.625 mgCEE and 5.0 mg MPA with micronized 1.0 mgestradiol (considered to be an equivalent dose to0.625 CEE) and 200 mg OMP, administereddaily and continuously for 13 cycles.138 Lumbarbone density improved by 5 percent in theCEE/MPA group and 3.8 percent in themicronized estradiol/OMP group. Hipbone den-sity improved by 2.6 percent in the CEE/MPAgroup, and 3.1 percent in the micronized estra-diol/OMP group. Statistically, the numbers forthe two groups are considered similar. Low-doseestradiol (0.5 mg), equivalent to 0.3 mg of CEE,has also been shown to be effective in maintain-ing vertebral mass.139 Although the authors ofthis study were able to show that 0.5 mg of estra-diol effectively preserved spinal bone density,more traditional (1.0 mg) and higher-dose (2.0mg) estradiol actually increased spinal bone massby 1.8 percent and 2.5 percent, respectively.

Based on this information, it seems that 0.5mg estradiol can be used to maintain bone mass,whereas 1.0 mg of micronized 17 beta-estradiolis considered the optimal dosing for enhance-ment of bone mass in postmenopausal women.No significant differences were seen with usingthe synthetic progestin (MPA) compared withthe natural progesterone (OMP). Even the newlowest dose transdermal patch, Menostar 14 mcgpatch (.014 mg), which delivers one-quarter ofan average dose of estradiol, shows some abilityto slow bone loss, although not to as great adegree as the average-dose patches of .05 mg.

Most people have not heard much aboutestriol, and I discuss it in more detail in Chapter12. The question in this chapter is whether


estriol will effectively prevent bone loss. A fewstudies done in the last couple of years in othercountries have been able to shed some light onthe effects of estriol on bone. Although not allestriol studies have shown positive results withbone mass, several Japanese studies have. Seventy-five postmenopausal women with bone densitiesat least 10 percent or more below peak bone den-sity were given estriol, 2 mg/day, with 800 mgdaily of calcium lactate. After 50 weeks, an averageincrease in bone mineral density of 1.79 percentwas seen on the routine DXA scan.140

In another Japanese study, 17 women whowere 10 years postmenopause were given estriol,2 mg/day, and 2 g/day of calcium lactate for one year. Another group was given only the calcium lactate. Bone density was significantlyreduced after one year in the calcium-only group,while the estriol-plus-calcium group had a 1.66percent increase in bone density, using the DXAscan again.141 A third Japanese study compared50- to 65-year-old women and elderly womenwho received either estriol, 2 mg/day, plus 1g/day calcium lactate or 2 mg/day of estriol alonefor 10 months.142 Increases of about 5 percent inthe lumbar spine were seen in both age groups ofwomen who took the estriol and the calcium.Women of both age groups in the calcium-alonegroup had a decrease in bone mineral density ofthe lumbar spine. High doses of estriol, one at 4to 6 mg/day and one as high as 12 mg/day, werestudied in Scotland, but they were not provedprotective against bone loss.143

As with bio-identical progesterone, studies onestriol also leave us with a lack of sufficient con-firmation about its bone-protective benefits.

Exercise

When bones are stressed by weight, the bonecells (osteocytes) sense it. Osteocytes, in cooper-ation with other bone cells, initiate a cascade ofevents leading to increased bone mass that limitsthe deformation to a predetermined set point(0.1 to 0.5 percent) in any given dimension.

When the load on bone exceeds the set point,more bone is deposited than removed. When theload is below the set point, the opposite effecttakes place, and bone is lost.144, 145

This statement explains why swimming andmoderate walking generally do not lead toincreased bone mineral density (BMD),146 butweight lifting,147–149 jogging/running,150 gym-nastics,151, 152 and certain sports like basketballdo. The set point theory of bone mass increase inresponse to strain also explains why a few studiesshowed no effect153 or a negative effect154 of exer-cise on BMD—a load below the set point fails totrigger a response.

Regular physical exercise of appropriateintensity and duration that overloads the skeletalsystem above its set point increases BMD inwomen of all ages within the limits set by hered-itary factors, nutrition, and the hormonal statusof the individual. In children and adolescents;155

in college-age women;156, 157 in women in their40s; and in young,158, 159 older,160, 161 and veryold162 postmenopausal women, exercise has beenshown to be essential to the development andmaintenance of bone health.

In sedentary women, trabecular bone lossbegins to occur in the third decade of life andcortical bone loss in the sixth.163, 164 The 35 to 45percent reduction in muscle strength observed inwomen at 80 years of age parallels the observedbone loss at that same age.165 Conversely, theage-related loss of bone parallels decreased phys-ical activity.166 Moreover, women who exerciseretain bone mass throughout life,167 achievegreater peak bone mass that contributes to theconsolidation and strength of bone following theend of linear growth,168 and have significantlylower risk of fractures in later life.154, 169

Furthermore, Recker and associates demon-strated that, independent of calcium intake ororal contraceptive use, the more college-agewomen exercised, the greater BMD theyachieved. These increases were highly significantdespite relatively small increments in exercise. A


1996 review of the literature on peak bone massand exercise confirms these results and adds thatexercise can maintain normal bones sufficientlystrong until very old age and can strengthenweak bones when used in concert with adequatenutrition.170 The author of this review con-cludes—as is the case in many studies—that evensmall increases in initial bone mass grow to a sub-stantial difference if the increased bone mass ismaintained by a lifetime of regular exercise.

Exercises that involve weight training canincrease the mass of bones if the exercise alsoincreases muscle mass and muscle strength.

Women who are in the early postmenopausalyears can achieve small but statistically significantbenefits on bone mass from strength training.171

A meta-analysis found that women who exer-cised could increase their spinal BMD byapproximately 2 percent.172 Menopausal womenwho use estrogen along with weight training havebetter BMD increases than do women who useestrogen alone.173

Strength or weight training can be done as littleas twice a week to achieve these benefits and can bedone on very inexpensive home equipment thatincludes as little as a chair, a bench, and some handweights. One word of caution is for women whoalready have osteoporosis. Heavy weight-bearingexercises and vigorous stretching and lifting can beenough to trigger a fracture of the spine.

One of the more important aspects of physi-cal activity, especially in women who are 75 andolder, is its role in reducing the risk of falls.Muscle strengthening and exercises to improvebalance have been shown to reduce the risk offalls and related injuries by 75 percent.174


If you are not already exercising regularly, consultwith your licensed health-care professional in cooper-ation with a qualified exercise expert. Together withthem establish:

• A schedule of exercise• The types, intensity, and duration of exercise

Consider the following guidelines:

• Begin slowly.• Increase intensity very gradually.• Train with weights for six weeks before intro-

ducing intensive aerobic exercise (such as run-ning or speed walking) into your program.

• Begin each exercise session with joint warmingexercises (see Appendix A) for 5 minutes.

• End each exercise session with 5 to 10 minutesof stretching exercises.

• Use caution and moderation throughout yourlifetime of exercise.

Therapeutic Scheme for Management of Osteoporosis

• Determine risk for osteoporosis: mild, moderate, or severe.

• Be aware of seven levels of intervention thatcover the majority of clinical situations:

Level 1: Diet, exercise, lifestyle, and stressmanagement

Level 2: Nutritional supplementationLevel 3: BotanicalsLevel 4: Compounded bio-identical hormonesLevel 5: Pharmaceutical company bio-

identical hormones (Use with oralmicronized progesterone if uterus is still intact.)

Level 6: Synthetic and semisynthetic non-bio-identical hormones in cases thatdo not respond to other medicines(Use with oral micronized proges-terone if uterus is still intact.)

Level 7: Prescription bone-specific medications

• Recommendations according to risk:

Level Mild Moderate Severe1. X X X2. X X X3. X4. X X5. X X6. X X7. X X


Exercise throughout life is as critical as a life-time of adequate nutrition. The important ques-tion for doctors is not to help their femalepatients of any age decide whether or not to exer-cise. It is rather to study ways to personalize theexercise prescription and motivate the patient tobegin and continue exercising for life.

Numerous books are now available that pro-vide an excellent introduction to your lifetime of exercise. Use simple low-impact exercises andstretching for two or three months before you

branch out into the more comprehensive exerciseprogram described in Appendix A.

If you are already exercising regularly, con-sider introducing into your program:

• Variations of speed in your aerobic exercises• Different exercise positions, particularly in

weight training, that challenge your bonesfrom different angles

• Alternating practicing sports such as basket-ball, volleyball, tennis, and so on with a reg-ular exercise routine

Sample Treatment Plan for Osteoporosis Prevention

See the conventional medicine section if you have adiagnosis of borderline osteoporosis or osteoporosisor have already had a fracture postmenopause. Thedietary and nutritional supplement recommendationsshould then be used in combination with conven-tional therapy. If you do not want to take or are not able to take hormone therapy or conventional osteoporosis-specific medications despite a diagnosisof osteoporosis, this sample treatment plan may notbe adequate to prevent bone loss or reduce the riskof fracture. Continue to see a licensed health-carepractitioner and monitor bone density.


• Soy foods: 1 to 2 servings per day• Dark leafy greens: 1 to 3 servings per day• Low-fat dairy, especially low-fat cultured

yogurt: 1 serving per day• Decrease animal meats (except for fish) and

substitute vegetarian choices, but with ade-quate vegetarian and/or fish protein

• Avoid alcohol, caffeine, and sugar

Regular Exercise

• Weight-bearing and aerobic exercise 150 min-utes per week

• Weight training twice per week• Most important, keep finding ways to motivate

yourself:

Be moderate—avoid burnout.Form a circle of friends who also love to exercise.

Nutritional Supplementation

• Calcium: 1,200–1,500 mg per day• Magnesium: 400–750 mg per day• Vitamin D: 400–800 IU per day minimum for

women 51 to 70 and 800 IU per day forwomen over 70; consider even higher amountsof 1,000–2,000 IU if you have been tested andhave a vitamin D deficiency

• Trace minerals: boron (3 mg), zinc (15 mg),chromium (100 mcg), manganese (15 mg), andcopper (1.5 mg)

• Other nutritional cofactors such as vitamin K2,45 mg per day

• Essential fatty acid supplement: 2–4 g fish oilor 4 g fish oil/evening primrose oil per day

• Women at low risk: recommended diet, regularweight-bearing exercise, nutritional supple-mentation, no hormone therapy necessary

• Women at medium risk: recommended diet,daily weight-bearing exercise, nutritional sup-plementation, natural hormones (estriol, estra-diol, and progesterone or estriol, estrone,estradiol, and progesterone; dose equivalent to0.3 mg or 0.625 mg Premarin, depending onindividual—see Appendix C), or conventionalHRT or bone-specific medications

• Women at high risk: recommended diet, dailyweight-bearing exercise, nutritional supplemen-tation, conventional estradiol (1 mg per day)and oral micronized progesterone (200 mg perday for 12 days per month or 100 mg daily), orconventional HRT or bone-specific medications



Once the diagnosis of osteoporosis has beenmade, the most frequently instituted medicationsare the bisphosphonates, nonhormonal in-hibitors of bone resorption that act by decreasingosteoclast activity (the cells that destroy bone).These drugs have very poor gastrointestinal ab-sorption and can cause esophageal ulcers, gastriculcers, and possibly gastrointestinal bleeding.The instructions for the use of these medicationsare very specific: the patient should take the med-ication immediately upon awakening and withan empty stomach, following the ingestion of themedication with a full glass of water. It is impor-tant that she remain upright for 30 to 45 minutesto prevent reflux and medication problems in theesophagus. Initially, these medications were useddaily, and patient compliance was quite poor;being able to take these medications weekly ormonthly has been one of the biggest advances inbisphosphonate therapy.

The medications that are most commonlyused these days are alendronate (Fosamax), a 70-mg tablet once weekly for treatment or a 35-mgtablet once weekly for prevention in patients whoare at very high risk for osteoporosis and haverapid bone loss but have not actually been diag-nosed as having osteoporosis yet. The next inorder of frequency of use is risedronate (Actonel),a 35-mg tablet once weekly. The newest is iban-dronate (Boniva), which is a 150-mg pill oncemonthly. There are intravenous forms of bispho-sphonates that can be used on a quarterly basis,but because of their cost and the need for IVadministration, they are not frequently used.

Concerns have been raised about bisphospho-nates causing osteonecrosis of the jaw. While aserious problem, it is incredibly rare. Approxi-mately 150 cases of osteonecrosis of the jaw asso-ciated with bisphosphonate therapy have nowbeen reported. Most of these patients, but not all,have received intravenous therapy, have malignan-

cies, and have had dental intervention. Dentalimplant failures have also been seen in patientsreceiving oral bisphosphonates for osteoporosis. Itcould be, especially in those patients who have suf-fered necrosis after dental procedures, that there iscompromised postoperative healing of the bonedue to the inhibition of bone turnover caused bythe bisphosphonate. A nonhealing wound couldthen lead to osteomyelitis, and then necrosis.Another mechanism may be that the bisphospho-nates are decreasing the levels of vascular endothe-lial growth factor. Assuring dental health anddental status may be smart preventive advice priorto even oral bisphosphonate therapy, especially inthose patients who have metastatic cancer, forwhom oral or IV bisphosphonate therapy mayslow their disease progression in the bones.

Estrogen and/or progestin therapy works inthe same manner by decreasing the activity of thecells (osteoclasts) that remove bone. Hormonetherapy was a mainstay for more than 40 yearsfor prevention of bone loss, treatment of osteo-porosis, and reduction of fracture risk. In theaftermath of the Women’s Health Initiative studyin 2002, more women have changed to bisphos-phonate use due to fears about hormone therapy.Currently, however, hormone therapy is FDA-approved for treatment of osteoporosis in womenwho do not tolerate the bisphosphonates, such aswomen who have had esophagitis, gastric ulcers,or GI bleeds and women whose bone densitydoesn’t improve on bisphosphonates. Somewomen are changed to a selective estrogen recep-tor modulator (SERM) also.

None of these agents will work optimallywithout the presence of an adequate amount ofcalcium, and in order to absorb the calcium, oneneeds an adequate amount of vitamin D. Newstudies suggest that 400 units of vitamin D dailyare not adequate for calcium absorption and that800 to 1,000 units per day may be more effec-tive. Vitamin D deficiency is a leading cause ofosteoporosis. When women present with post-menopausal osteoporosis, it is assumed that it is


related to being female and postmenopausal withlow estrogen, but it is also important, as discussedearlier, to rule out other causes of osteoporosissuch as parathyroid hormone problems, concomi-tant steroid use, and vitamin D deficiency.

Calcium is also very important, and manywomen do not tolerate the most common andleast expensive form of calcium, calcium carbon-ate. All calciums appear to be absorbed equallywell when taken with food and in the presence ofvitamin D, but calcium carbonate seems to createmore gastrointestinal symptoms. When bloating,constipation, diarrhea, or gas is present, the cit-rate variety is frequently substituted. The recom-mended daily dosage of calcium between diet andsupplements remains 1,000 mg in women under50 and 1,200 to 1,500 mg in women over 50.

Androgens have had renewed interest as atherapy for osteoporosis. Tibolone, an anabolicsteroid, has been used in many years in Europefor treatment of osteoporosis and is being studiedin the United States. There is concern abouteffects on lipids and the endometrium, as well asbasic side-effect profiles that present with andro-gens, such as acne, facial hair growth, and bodyhair loss. Typically, androgens are not recom-mended for osteoporosis treatment.

Calcitonin is a less well-known medicationthat is primarily used for vertebral compressionfracture pain. It is a peptide that inhibits bone resorption and causes a modest increase in verte-bral bone. Calcitonin does not seem to have anysignificant effect on trabecular bone. Initially, itwas very difficult to obtain, but recombinantDNA production of the medication has increasedits availability. It is an intranasal medication usedonce daily, but its ability to treat general skeletalosteoporosis is limited. It has a very significanteffect, however, on pain improvement in vertebralcompression fractures.

SERMs are selective estrogen receptor modu-lators. They have estrogen-like effects in selecttissues while not actually being estrogen. Theyare called selective receptor modulators because

they have a proestrogen effect on certain tissuessuch as bone and endometrium and an anti-estrogen effect on other tissues such as breasttissue. Clomiphene citrate used for infertility isessentially a SERM. Tamoxifen is probably themost widely recommended SERM. It has beenused for many years in breast cancer treatment. Itimproves skeletal bone density in the same waythat estrogen works, by decreasing osteoclastactivity, but it does have a significant stimulatoryeffect on endometrium and has increasedendometrial cancer in patients.

The third and currently recommended osteo-porosis treatment SERM is raloxifene (Evista). Itdiffers from tamoxifen in that it has no activity onthe endometrium. It stimulates bone growth byreducing the activity of the osteoclasts and reducesserum lipids just like estrogen, but it does notstimulate the endometrium or the breast and hasactually been shown in several studies to reducelifetime risk of breast cancer by 50 to 74 percent.The side effects of raloxifene are vasomotor symp-toms, unexplained leg cramps, and a risk of deepvein thrombosis (DVT) approximately equal tothat of estrogen.

The newest, but very limited, drug for osteo-porosis treatment is parathyroid hormone. It iscalled teriparatide (Forteo), and it actually stim-ulates osteoblast activity, the cells that buildbone. Its effect on the bone is uniquely differentfrom any of the other medications. It is a dailysubcutaneous injectable medication that is mod-erately expensive and used for severe osteoporosisin patients who are not responding to the othermedications or are having a lot of fractures. Themain side effects are dizziness, nausea, jointaches, and leg cramps.

For perimenopausal and young postmeno-pausal women with osteopenia and a T-score notworse than �2.0, I would consider the use of anyof these conventional approaches overtreatment.Other prevention strategies include dietaryadvice, exercise including strength training, vita-min D, calcium, trace minerals and nutrients,


and low alcohol intake. The practitioner shouldmonitor the bone density over time. For womenof this age who actually have osteoporosis, bis-phosphonates may be a good choice. Calciumand vitamin D have important but modest ben-efits in women who already have osteoporosis.

Older postmenopausal women (over 65) whohave either significant osteopenia or osteoporosisare more certain candidates for bisphosphonatesand other conventional treatments, which areproven to reduce the risk of fracture by 50 percent.Hopefully, research will determine the shortestamount of time that is necessary to be treated andthe lowest dose that is required to achieve this sig-nificant benefit, which is not currently known forsome of these medications. Fortunately, there is norapid bone loss after discontinuing bisphosphonatetreatment, compared to the rapid loss that doesoccur after discontinuation of estrogen.

Also in time, research on natural medicinescan be expanded to include the role of nutrientsnot only in bone density, but in bone strength andbone architecture. Some of these areas could bethe use of significantly higher doses of vitamin D,as well as red clover isoflavones, soy isoflavones,manganese, boron, fish oils, and more. In this way,natural therapies could play an increasinglyimportant role in slowing bone loss and reducingfracture rates.


Osteoporosis is one of the most important age-associated disorders and should be considered apotentially disabling disease that warrants sub-stantial preventive efforts and management inter-ventions. Early identification of risk factors forosteoporosis, prevention strategies, vitamin D

status, and assessment of calcium metabolismand bone density provide the basis for determin-ing what is appropriate for each woman. Alicensed health-care practitioner who is educatedabout when to rule out secondary causes of boneloss and the importance of early identification,prevention, and treatment, and who is also awareof the spectrum of alternative and conventionaloptions, is especially crucial for women who areat higher risk or who already have osteoporosis.Your family physician, internist, or endocrinolo-gist is probably the cornerstone for medical ther-apy. Some gynecologists can provide advice andtreatment as well. Some licensed alternative prac-titioners may have expertise in osteoporosis man-agement as well.

Many physicians do not even discuss osteo-porosis, and you may have to insist on a DXA scanto measure bone density. An ultrasound test of theheel, which is much less expensive, may be a help-ful screening test for some women. There is someevidence that a heel test is 85 to 90 percent accu-rate compared with the bone density of the hip ona DXA scan. Many insurance companies do notcover routine osteoporosis screening for womenunder 65 unless they have significant risk factors,but if you have a heel test that shows your bonedensity is below normal, this can be the stimulusfor obtaining a DXA scan. Some practitioners rec-ommend screening women with heel ultrasounds,but by and large the heel test is not yet consideredan accurate test to replace DXA scans for eitherearly detection or monitoring.

The more risk factors you have for osteoporo-sis, the greater the need to have laboratory andbone density testing. Women are especiallyencouraged to seek a licensed health-care practi-tioner who is well educated in the diagnosis andmanagement of osteoporosis.

267

OVERVIEW

Pelvic inflammatory disease (PID) includes aspectrum of infections of the upper genital tract.These include endometritis (infection of thelining of the uterus), salpingitis (infection of thefallopian tubes), tubo-ovarian abscess, and pelvicperitonitis (infection of the serous membranelining the abdominal and pelvic walls). Morethan one million women in the United Statesdevelop PID each year, and one-fourth of themrequire hospitalization.

The infection typically results from the spreadof microorganisms that ascend from the endo-cervix (the canal leading from the cervix into theuterus) to the upper genital organs. The mostcommon organisms are Neisseria gonorrhoeaeand Chlamydia trachomatis. Chlamydia causes 50 percent of PID in Europe and 20 to 30 per-cent of cases in the United States, though the realincidence may be even higher. Gonorrhea remainsthe single most frequent cause in the UnitedStates. Additional organisms implicated in PIDinclude bacterial vaginosis organisms (Mycoplasmaspp., Peptostreptococcus spp., Prevotella spp.),Haemophilus influenzae, Streptococcus pyogenes,and Streptococcus pneumoniae. PID is considered apolymicrobial infection due to the many organ-isms involved. Bacterial vaginosis (BV) producesenzymes that dissolve cervical mucous, and there-fore if you have BV, there is an increased risk ofendometritis (PID in the uterus), and womenwith the highest bacterial loads have increasedrisk of PID of at least twofold.

The problems associated with PID involve itsability to ascend from the lower to the uppergenital tract. How it ascends is not exactly clear.Uterine contractions may be responsible, andeven sperm may play a role in enhancing the

spread of the organisms. Another possibility isthat the bacteria may be transferred into the fallopian tube due to the common occurrence ofretrograde menstruation. The pathogenic organ-isms may spread along with the blood, contribut-ing to PID.

Once the pathogen ascends to the uterus orfallopian tubes, it adheres to mucus-secretingcells and then invades just below the epithelialsurface (the surface of the tissue lining the fallop-ian tubes). An acute inflammatory responseoccurs, causing cell death and tissue damage, andcan result in scarring and tubal adhesions.

One in four women diagnosed with PID maydevelop complications, including ectopic preg-nancy, infertility, recurrent pelvic pain, andrecurrent PID. It is important to recognize thepossibility of PID because of its potential fordeveloping into a lethal condition, a more com-plicated condition, or a condition with long-term consequences. It is also important to bealert to possible surgical emergencies. SometimesPID can be elusive, and there is little clinical evi-dence to support a suspicion of PID, especiallywhen the symptoms are mild and insidious. Theclassic symptoms of lower abdominal pain andtenderness with examination or motion of thecervix occurs in only 20 to 25 percent of patients.A much more common presentation is often amild or subtle pelvic pain. Some women withPID will have discomfort with urination and urinary frequency as well as other urinary tractsymptoms. An increased number of risk factorsfor PID increases the suspicion. These mayinclude the following:

• Age 14 to 24• Heterosexual and sexually active

15P E LV I C I N F L A M M AT O R Y D I S E A S E

C H A P T E R



• Multiple heterosexual sex partners• New heterosexual sex partner• Low socioeconomic status• History of sexually transmitted disease• History of PID• Oral contraceptive users have increased risk

of acquiring gonorrhea or chlamydia ifexposed but a decreased risk of upper tractinfection

• Use of IUD for contraception• Never having been pregnant• Cigarette, alcohol, or illicit drug use• Any instrumentation of the uterus—such as

a uterine biopsy, diagnostic scope, or surgi-cal abortion

• Pelvic or bowel surgery

Adolescents and young single heterosexualadults have the highest incidence of gonorrhea.This organism is believed to be the cause in 33 to80 percent of the PID cases, although mixed gon-orrhea and chlamydial infections occur frequently.About 15 percent of endocervical gonorrhea infec-tions result in PID. A diagnosis of PID in childrenwarrants an evaluation for child abuse.

PID symptoms more often occur during orwithin one week of menses because the openingof the cervix is wider due to menstruation.Microorganisms can then more easily ascend intothe upper genital region and use the flow ofblood as nutrition for their growth.

Women with new heterosexual partners withinthe last 30 to 60 days or multiple sex partners aremore likely to develop PID. If a woman’s partneris not monogamous, then she is also at increasedrisk. A history of a sexually transmitted infection(STI) increases the likelihood of contracting sub-sequent STIs, as does a history of PID.

Barrier contraceptive methods such as con-doms, diaphragms, and cervical caps (FemCap)reduce the risk of STIs, PID, and infertility.1

Their protective benefit comes from decreasingthe risk of acquiring a STI. In addition, thecondom may decrease the risk for developing

PID by eliminating the sperm as the method inwhich the STI can ascend.

Intrauterine devices (IUDs) are associatedwith an increased risk of PID, particularly in thefirst four months after insertion, but then riskreturns to normal at five months.2 The thinkingis that microorganisms in the vagina and cervixare introduced into the uterus during the IUDinsertion. The incidence of PID in IUD users istwo to nine times that of nonusers in most pop-ulations of women studied.1 If a woman withsuspected PID has an IUD, it must be removed.Oral contraceptives (OCs) have both a positiveand a negative effect on the risk of PID. They canincrease the risk of chlamydia infecting the cervix(mucopurulent cervicitis), but they are also asso-ciated with a decreased risk of symptomatic PID.It is thought that the progestin component in theOCs causes the cervical mucus to become thickerand the STI cannot penetrate this. OCs alsodecrease the heaviness of the menstrual flow, andthis decreased blood may result in less retrogrademenstrual flow, making it harder for the bacteriato ascend and cause PID. If a woman using oral contraceptives does acquire PID, it is oftenmilder or possibly even asymptomatic.3

Use of illicit drugs (especially crack cocaine),alcohol, or cigarettes has been associated with anincreased risk of STDs and PID. Substance abusealso increases the potential for HIV infection.Women with HIV are far more likely to have PID.

Vaginal douching may be associated with PIDand even ectopic pregnancy. In several studies,women with PID are more likely to use douchingthan women without PID. One study found thatdouching within the previous two months wasassociated with a 70 percent increase in PID.4

Diagnosis of PID starts with a combinationof a good medical history and physical exam. Themedical history should include a thorough sexualhistory. Symptoms include but are not limited tovaginal discharge, fever, chills, urinary symp-toms, heavy menstrual bleeding, intermenstrualbleeding, and lower abdominal/pelvic pain. A

269P E L V I C I N F L A M M A T O R Y D I S E A S E

physical exam includes taking the temperature; apelvic and abdominal exam with any tendernessof the uterus, fallopian tubes, or cervix serving asa red flag; observing the cervix and looking forredness, swelling, and friability (easy bleeding) ofthe cervix; and evaluating genital tract secretions,particularly for mucopurulent (green or yellow)discharge.

The vaginal secretions should be evaluated forthe presence of white blood cells during micro-scopy. Laboratory testing includes cervical samplesfor Neisseria gonorrhoeae (GC) or Chlamydia tra-chomatis (CT); a pelvic ultrasound showing thick-ened, fluid-filled tubes or tubo-ovarian mass; andacute and/or chronic endometritis on endometrialbiopsy. The gold standard in diagnosing PID is alaparoscopy. During this surgical procedure, thesurgeon looks for swelling of the fallopian tubes,tubal adhesions, tubal erythema (redness), tubalpurulent or serous discharge, and/or a tubo-ovarianmass.

OVERVIEW OF ALTERNATIVE MEDICINE

Gonorrhea is a reportable disease. This meansthat a practitioner must call the public health

department and report the disease if this organ-ism has been cultured. Due to the potential com-plications and seriousness of PID, in concertwith a lack of proven therapeutic results in usingnatural treatments for this disorder, alternativetherapies should be seen as secondary to conven-tional treatment. Women who suffer from PIDand have strong opinions about not being treatedwith antibiotics should be fully educated andinformed so that their decision to decline antibi-otic therapy can be fully considered. A shortcourse of antibiotic therapy is rarely detrimentalto one’s health. In this case, the benefit of thetherapy far outweighs the risk of its use. Like-wise, alternative practitioners should understandthat the integration of antibiotic therapy for thebenefit of the patient is not a failure of naturalmedicine. There are old texts that make referenceto treating PID with natural therapies, but theylack modern methods of evaluation and follow-up. It could be that botanicals used in India,China, or elsewhere have a tradition substanti-ated by modern confirmation testing, but I amnot aware of any confirmed treatments.

Using alternative therapies to support theimmune system, assist in managing pain and

PREVENTION

• Use barrier methods of contraception.• Avoid illicit drugs and cigarettes, and limit

alcohol.• Treat previous STIs with appropriate therapy and

be certain of resolution.• Avoid douching. (It is possible that douching

will cause a vaginal infection of GC, CT, or BV toascend into the uterus and/or the fallopiantubes.)

• Know the sexual history of your partner.• Heterosexual women who have multiple partners

and do not use condoms, cervical caps, ordiaphragms are at higher risk for PID.

• Women with HIV are at even higher risk andneed to practice even greater caution.

KEY CONCEPTS

• Acute or chronic pelvic pain warrants a visit toa qualified licensed health-care practitioner fordiagnosis.

• PID must be differentiated from other causes ofpelvic and abdominal pain.

• PID should be treated primarily with antibiotictherapy, while alternative medicine can offersupportive and adjunct therapies to conven-tional treatment.

• Seek prompt medical attention if you have thesymptoms described in this chapter or suspectyou have PID.

• The sex partner must also be evaluated andtreated. Reinfection will almost certainly occurif the sex partner is not treated.


discomfort, reduce inflammation, and counter-act some of the side effects of the antibiotics arethe main priorities. Drinking plenty of water,getting rest, eating simple light foods, and avoid-ing stimulants are basic guidelines during anyacute infection, including pelvic infections.

General immune support to complementconventional antibiotic treatment is just goodplain common sense. Nutritional and botanicalsupport can stimulate white blood cells thatengulf and destroy bacteria. Herbs and nutrientscan enhance the function of T cells, B cells, andnatural killer cells that support the immunesystem’s response to infection. Vitamin A, vita-min C, the carotenes, vitamin E, zinc, and the Bvitamins all play an important role in immuneenhancement. Increasing antibody response,stimulating helper T cells, enhancing whiteblood cell response and function, and directlykilling the virus or bacteria are just some of theways in which these supplements can be helpfulduring an infection of any kind.

Many herbs have also been shown to have antimicrobial and immunostimulating effects. Allicin extracts from garlic may hold the mostpromise for inhibiting bacterial infections. Gold-enseal and Oregon grape root also have the abilityto inhibit the overgrowth of numerous organisms,although this does not include BV and CT. Themost commonly used herb for immune support is echinacea. Echinacea can increase the produc-tion of T cells, stimulate the white blood cells thatengulf and destroy bacteria, stimulate naturalkiller cell activity, and increase the number of circulating white blood cells in order to deal withthe infection.5 The end result is a strengthenedimmune system. Curcumin is one of the bestherbs to reduce inflammation.

The best complement to counteract the sideeffects of antibiotic use is to add or increase theintake of Lactobacillus acidophilus to help preventa vaginal yeast infection. This can be accom-plished by eating yogurt daily or by taking oralcapsules of Lactobacillus acidophilus. Four to

eight ounces of unsweetened acidophilus yogurtor at least three capsules of Lactobacillus aci-dophilus daily for two weeks may be able to pre-vent the overgrowth of vaginal yeast that oftenoccurs when taking antibiotics. Additionaldietary advice, plus botanical and nutritionaltherapies for the prevention and treatment ofyeast vaginitis, is discussed in Chapter 20.

Ice packs over the pelvic region can reduceinflammation and pain in cases of acute PID.Cold or ice packs placed over the region of theuterus while putting the feet in a tub of hot watercan further assist in reducing the inflammation,congestion, and pain in the pelvic area. Alternat-ing hot and cold sitz baths can also be used toimprove circulation in the pelvic area andimprove the healing time from the infection.This is done by sitting in a bath of hot water,with the water level just above the waist, for threeminutes, followed by sitting in a small secondportable metal or plastic tub of ice cold water for

Sample Adjunct Treatment Planfor Pelvic Inflammatory Disease

This plan should be used as a complement to antibi-otic therapy.

• Eat a light diet during acute infection: veg-etable broths, steamed vegetables, salads, andfruits

• Acidophilus yogurt: 4–8 oz per day as a pre-ventive of yeast vaginitis

• Vitamin E: 400 units twice daily• Vitamin C: 1,000–2,000 mg 3 times daily• Vitamin A: 25,000 units per day and up to

50,000 units for a maximum of 2 weeks• Zinc: 45–60 mg per day• Ice pack over the uterus with a hot footbath• Echinacea: 1⁄2 tsp liquid extract or 2 cap-

sules/tablets every 3 hours during course ofinfection

• High-dose allicin extract: 2 capsules 4 timesdaily for the first 3–6 days, then 2 capsulestwice daily for 1 week, and then 2 capsulesdaily until infection is gone


one minute. This procedure is repeated threetimes in succession, once or twice daily through-out the course of the pain and infection.


Conventional practitioners rely on their judg-ment in assessing the severity of the disease andthe ability of the patient to carry out the treat-ment successfully. It is essential for the practi-tioner to educate the patient about the exacttreatment regimen. If she is able to comply withthe recommendations, she may be a candidatefor outpatient treatment. Infertility may be moresuccessfully prevented by prompt administrationof IV (intravenous) antibiotics, even if thewoman is not acutely ill. In the case of outpatienttreatment, once antibiotics are administered, the patient must have a follow-up visit within 72hours. With the advent of home IV therapy,sometimes IV antibiotic treatment can bereceived at home.

PID therapy must provide broad-spectrumcoverage of the most likely offending organisms.Although several antimicrobial regimens havebeen effective in achieving cure in randomizedclinical trials, few studies have been done toassess and compare elimination of infection ofthe lining of the uterus and the fallopian tubes orthe incidence of long-term complications such asinfertility and ectopic pregnancy. No singleantibiotic regimen has been established. Health-care providers select treatment regimens based on drug availability, cost, the patient’s toleranceof the drug, and other individuating factors.Most practitioners follow the Centers for DiseaseControl treatment guidelines, which wereupdated in 2006:

Regimen A• Levofloxacin (500 mg orally once daily for

14 days) or• Ofloxacin (400 mg orally once daily for 14

days)

Regimen B• Ceftriaxone (250 mg intramuscularly in a

single dose) plus doxycycline (100 mg orallytwice a day for 14 days) or

• Cefoxitin (2 g intramuscularly in a singledose) plus probenecid (1 g orally adminis-tered concurrently in a single dose) plusdoxycycline (100 mg orally twice a day for14 days) or

• Another parenteral third-generation cepha-losporin (for example, ceftizoxime or cefo-taxime) plus doxycycline (100 mg orallytwice a day for 14 days)

These regimens can be used with or withoutmetronidazole (500 mg orally twice a day for 14days). The addition of metronidazole should beconsidered, as anaerobic organisms are suspectedin the majority of PID cases. Metronidazole willalso treat bacterial vaginosis, which is frequentlyassociated with PID and/or follows antibiotictherapy.

It is important to realize how critical it is tofollow the practitioner’s directions and to com-plete the drug regimen as prescribed on the bottle.There may be side effects about which the patientshould be informed to improve compliance.

There are certain criteria for hospitalizationof a woman with PID that include but are notlimited to:

• Concern about the ability of the patient tocomply with treatment and to follow up

• A fever greater than 101 degrees• Signs of an acute abdomen (acute onset of

abdominal pain/tenderness/bloating, nausea,vomiting)

• Lack of improvement within 72 hours

If hospitalization occurs, a more complex regi-men is administered with several combinationsof IV antibiotics. After the patient leaves the hos-pital, two weeks of doxycycline is given.

Intravenous treatment recommendations ofPID are as follows:


• Levofloxacin (500 mg IV once daily) with orwithout metronidazole (500 mg IV every 8hours) or

• Ofloxacin (400 mg IV every 12 hours) withor without metronidazole (500 mg IV every8 hours) or

• Ampicillin/sulbactam (3 g IV every 6 hours)plus doxycycline (100 mg orally or IV every12 hours)

These medications are used in the hospital untilthe patient’s fever has been absent for one or twodays, her pelvic pain has dramatically reduced,she is taking oral food and able to get up and outof bed and take care of herself, and any of theother criteria that a physician chooses to releasethe patient from the hospital.

Treatment of a tubal ovarian abscess, which isa common complication of PID, is more com-plex. If the patient has a fever, with an acuteabdomen, the first line of treatment is surgicaldrainage of the tubal ovarian abscess followed bymultiple IV antibiotics. Sometimes, if a patienthas minimal tenderness, does not have a fever,and is a good candidate for outpatient therapy,she can be given oral medications for two tothree weeks and followed in the office.

Treatment of PID should eliminate signs andsymptoms of the infection and eradicate themicroorganisms while minimizing the damage tothe fallopian tubes as well as long-term complica-tions. Follow-up for outpatient treatment is crit-ical within 72 hours to assure that the patient istaking the medicine accurately and to evaluatethe effectiveness of the treatment.

Pregnant women with suspected PID shouldbe seen immediately and have an ectopic preg-nancy ruled out. PID in pregnancy is uncom-mon and is more likely to occur when HIV ispresent. Hospitalization and IV antimicrobialtherapy are recommended.

Conventional practitioners take great care ineducating the patient about the disease; the im-portance of treatment; the possible consequences;

the importance of treating her male partners, if applicable; and the importance of barrier contra-ceptives and other methods to reduce the risk ofSTIs. To a patient not accustomed to dealing withsevere infections and the need for antibiotics,some practitioners may seem overly aggressive intheir recommendations and insistence. Althoughthis may offend some women, it is important thatthey do not let a less-than-optimal bedside styledistract their attention from the value of whatphysicians know and have to offer.


Women with pelvic pain need to consider notonly PID but also other conditions that canoccur with similar discomfort. Ectopic preg-nancy, tubo-ovarian abscess, ruptured ovariancysts, appendicitis, inflammatory colitis, pancre-atitis, cholecystitis (inflammation of the gallblad-der), cystitis (inflammation of the bladder),diverticulitis (inflammation of a small pouchalong the border of the colon), hepatitis, and atwisted fallopian tube are among the otherpotentially serious disorders that require differen-tiation from PID.

Women with PID typically describe pain thatis sharp, localized, and on both sides of the body.They may also have an oral temperature above101 degrees. Ectopic pregnancy typically pres-ents with one-sided pain but no fever.

If you have these symptoms, call your doctorimmediately. A licensed health-care practitioner(naturopathic doctor, medical doctor, osteopathicdoctor, nurse-practitioner, or physician’s assistant)will proceed with a history, physical examination,and diagnostic testing, including blood work, cul-tures, and possible pelvic ultrasound. An abdomi-nal exam will be done to check for pain in variouslocations. A pelvic exam will check the externalgenital region; a speculum exam will check forinflammation and discharge. A thick, transparent,yellow, gray, or brown discharge coming through


the cervix suggests a chlamydial or gonococcalinfection. An internal exam will check for anenlarged uterus or pain and tenderness. Culturesfor the infectious agents require two to three daysto process and are important in confirming a diag-nosis, but severe symptoms and the potentiallyserious consequences of acute PID require imme-diate treatment even if confirmation has not yetbeen obtained.

Since more than one organism can cause PID,a negative culture result can be misleading. Newerand more accurate tests using antigen detectionmethods or fluorescence antibody marker tech-niques are available for the rapid detection ofchlamydial infection. They can be especially usefulin detecting mild cases or cases that have no symp-toms. Pelvic ultrasound examinations are per-formed when a pelvic mass or abscess is suspected.

They may be able to reveal a cyst, an ectopic preg-nancy, an abscess, or an enlarged tube.

Laparoscopy is considered to be the goldstandard for diagnosing PID. Because diagnosticlaparoscopy is expensive and invasive, requiresspecial training, and may not affect the decisionto treat the patient for pelvic infection, it is notroutinely used in the emergency management ofpatients with PID. A procedure called culdocen-tesis aspirates fluid that has collected behind theuterus. It is rarely used unless the diagnosis isuncertain or a complication is suspected. Thepresence of blood in the fluid sample suggests anectopic pregnancy or a ruptured ovarian cyst.Cloudy or purulent fluid suggests an infection,and the fluid is then tested with cultures for PID.

About 25 percent of women with PID willrequire hospitalization. Criteria for hospitaliza-tion have been established by the CDC. If yourpractitioner recommends that you be admittedto the hospital, I would urge you to entrust your-self to his or her care. You can always use naturaltherapies to augment the treatment. The CDCcriteria for hospitalization include:

• Adolescent patient• A surgical abdomen, a serious condition

characterized by sudden onset of abdominal/pelvic pain, tenderness, and muscular rigid-ity (possibility of appendicitis)

• HIV infection• The diagnosis of PID is uncertain• The patient has not responded to outpatient

treatment• The patient has not been able to tolerate or

follow the outpatient regimen• A surgical emergency is possible• Pregnancy• The patient has a septic appearance (fever,

chills, shaking, or other flu-like symptoms)• Severe illness or nausea and vomiting• Suspected pelvic abscess

Diagnostic Criteria for Pelvic Inflammatory Disease

All three criteria must be present for a clinical diag-nosis (without the use of tests) of PID:

• Lower abdominal tenderness• Bilateral adnexal tenderness• Cervical motion tenderness

Additional criteria useful in diagnosis:

• Oral temperature greater than 101°F• Mucopurulent cervical or vaginal discharge• Palpable pelvic mass• Elevated sedimentation rate or C-reactive

protein—both markers of inflammation• White blood cell count greater than 10,000• Evidence of cervical infection with Neisseria

gonorrhoeae or Chlamydia trachomatis• Tubo-ovarian abscess or fluid-filled tubes on

pelvic ultrasound• Acute and/or chronic endometritis on endome-

trial biopsy• Laparoscopic abnormalities consistent with

PID


275

OVERVIEW

All women want to do everything they possiblycan to optimize the health and well-being ofthemselves and their children. There is no othercondition that inspires women to care for them-selves as well as pregnancy. That said, MotherNature’s talent in producing healthy babies isawesome indeed, and no matter the range ofone’s individual decisions regarding optimalhealth care, most babies arrive intact and healthy.Women who receive prenatal care enjoy thelowest risk of maternal and infant mortality inhistory.

It is important to recognize those things wehave control over and those we don’t. Whilewomen should do their best to take excellent careof themselves during pregnancy, they must notassume personal responsibility for vagaries ofbiology like miscarriages and rare abnormalities.Ninety-eight percent or more of babies are bornhealthy. Keep that number in mind as you readthrough this information. Remember that fetusesare strong little creatures. They pull what theyneed from our bodies pretty effectively. It is thewoman carrying the child, in all but extremecases, who suffers from any deficiencies in nutri-tion or health—the fetus gets preferential treat-ment. Welcome to motherhood!

Pregnancy and birthing are normal physio-logical processes that can be positively supportedthrough adequate rest, preventive nutrition, andthe avoidance of harmful substances. Minimizingstress, getting plenty of low-impact exercise andfresh air, and sleeping well are important factorsleading to a positive overall experience of preg-nancy and birth. The important thing to remem-ber is that each pregnancy is unique, andalthough there are certain universal factors to

consider, the most important preventive medi-cine is the mother’s relationship to her own bodyand her emotional and physical connection tothe child she is carrying.

During pregnancy, hormone secretion changesradically, causing the physical and emotionalchanges experienced by most women fairly earlyin the first trimester. Estrogen and progesteronelevels are about 100 times higher than usualduring pregnancy, dropping immediately afterbirth to prepregnancy levels as prolactin (thepituitary hormone) is produced to stimulate theproduction of breast milk. Throughout preg-nancy, the placenta produces a hormone calledrelaxin, which softens the connective tissues and ligaments that support the uterus, allowing it to expand. The production of endorphins(morphine-like hormones that are the body’s natu-ral painkillers and tranquilizers) is increased duringpregnancy and continues to rise during labor, whenthey reach peak levels.1 These hormonal changescan lead to the experience of morning sickness ornausea in the first trimester, especially when thereare nutritional deficiencies as well.

OVERVIEW OF ALTERNATIVEMEDICINE CONSIDERATIONS

Nearly all pregnant women can benefit from nutri-tional and multivitamin supplementation one yearbefore and all during pregnancy, as well asthroughout labor, delivery, and breast-feeding. Theeffects of poor nutrition during pregnancy can beseen in the increase of birth defects during times offamine.2 But a standard Western diet (high in fats,salt, and sugar and low in complex carbohydrates)also lacks essential vitamins and minerals neededduring pregnancy and breast-feeding, which cancompromise your baby’s health.3 The appropriate

16P R E G N A N C Y C H A P T E R



diet is well balanced and varied and includes freshfruits, vegetables, whole grains, legumes, beans,and fish, with a limit on refined sugars, processedfoods, and saturated fats. Organically grown pro-duce, meats, and poultry are preferable, or inor-ganic produce that has been carefully washed toremove agricultural chemicals.4

In an observational study involving 76 healthypregnant women, 78 percent had “one or moreglaring nutritional deficiencies.”5 Another studyshowed an “overall apparent protective effect ofperi-conceptual multivitamin use” for preventionof certain pregnancy-related illnesses and birthdefects.6 Of special importance are folate (folicacid) and calcium intake, since the requirementfor both of these doubles during pregnancy.

One study found that “The fetus, theneonate, and the pregnant woman have anincreased requirement for folic acid and vitaminB12, and are more likely to suffer from a defi-ciency of these vitamins.”7 Nutrients such as folicacid and vitamins B6 and B12 have been corre-lated with prevention of the more common preg-nancy complications, such as spontaneousabortion, placental abruption, preterm delivery,low infant birth weight, and neural tube defects(such as spina bifida and anencephaly).8 Supple-mentation with calcium—the only mineralwhose requirement doubles during pregnancy9—has been positively correlated with prevention ofpregnancy hypertension,10 preeclampsia,11, 12

preterm delivery,13 and low birth weight,14 aswell as puerperal psychosis (postpartum depres-sion).15 Magnesium supplementation has alsobeen shown to reduce the complications of preg-nancy and improve the health of the infant.16

In addition to taking nutritional supple-ments, certain substances should be avoided inpreparation for and during pregnancy. Smokingduring pregnancy increases the incidence of pre-mature labor,17 low birth weight,18 and infantcomplications.19 These complications may notbe alleviated by increased maternal caloric intake.In addition, women who abuse alcohol and use

illicit drugs are more likely to have inadequatenutrition as well as birth abnormalities anddevelopmental problems in the infant.

Nutrition

During pregnancy, a woman’s physiology changesdramatically to allow for the development of ahealthy fetus. To support the rapidly growingfetus, changes in metabolism, biochemistry, andhormone status are needed to provide the environ-ment and energy required. Appropriate nutritionis important for both the mother and child duringpregnancy and plays a pivotal role in a healthypregnancy. Members of the health-care team assessmaternal nutritional risk, assign goals for weightgain, and recommend dietary changes to achieve

KEY CONCEPTS

• Eat a healthy, whole foods diet, high in healthyoils (low-mercury fish high in omega-3 oils),complex carbohydrates, fruits, vegetables,organic meats and dairy, legumes, and nuts andseeds.

• Avoid situations that would increase risk ofacute illness.

• Manage medical problems safely and effectively,as necessary.

• Have regular prenatal health checks.• Seek assistance from a qualified health-care

practitioner.

TO PREVENT COMPLICATIONS

• Avoid alcohol.• Avoid nicotine.• Reduce exposure to mercury-containing foods.• Avoid recreational drugs.• Avoid over-the-counter drugs, prescription

drugs, and herbs that may adversely affect thefetus. Consult with knowledgeable medical per-sonnel about these choices.

• Exercise regularly; avoid injuries, falls, and high-risk athletics.

277P R E G N A N C Y

those goals. Prenatal evaluation and continuedhealth care are important to monitor the progressof the pregnancy and intervene with correctivechanges when needed.

The nutritional assessment includes informa-tion about diet, eating habits, daily activities, medical and medication history, and the use oftobacco, alcohol, and recreational drugs. An initialphysical examination followed by ongoing examsis essential in assessing the mother’s body massindex (BMI) and appropriate weight gain and fetalgrowth. BMI relates weight to height and thusprovides a better estimate of body fat distributionthan weight alone. The practitioner uses the BMIto determine whether the mother is underweight,normal weight, overweight, or obese. Weight is avery important indicator of fetal health andrequires precise and regular measurement. At eachvisit with your prenatal health-care worker, youshould be weighed to assess your weight gain com-pared to the target goals.

Low prepregnant weight and inadequateweight gain during pregnancy are dominant con-tributors to intrauterine growth retardation20 andlow birth weight.21 Maternal prepregnant weightand weight gain in pregnancy also have an impacton early infant death rates. For women who areunderweight prior to pregnancy, the perinatalmortality risk at birth is lowest when their weightgain during pregnancy is greater than 37 pounds.For women who had normal weight prior to preg-nancy, the lowest risk is with a weight gain of 30to 37 pounds.22 Women who are obese prior topregnancy need to gain less weight for an optimalfetal outcome. Significant risk occurs in obesewomen if there is a greater than 25-pound weightgain during the pregnancy.23 Weight loss in obesewomen is not recommended during pregnancy.Teenagers, especially, often need careful educationabout the importance of nutrition, nutritionalchoices, the importance of healthy weight gain,and guidance throughout the pregnancy.

All pregnant women will benefit from prena-tal nutritional education that focuses on healthy

nutritional practices. Women with limited orpotentially imbalanced dietary habits (vegetari-ans, vegans, anorexics, and women consumingmacrobiotic, high-protein, weight-loss, high-fat,or high–junk food diets) should receive specialattention and be educated on the potential com-plications and risks of these habits to both themother and the fetus. Women with a history ofanorexia, bulimia, obesity, diabetes, chronickidney disease, chronic gastrointestinal disease, orextreme diets may need more individualized edu-cation and nutritional therapy. Vegetarian, vegan,and macrobiotic diets are not necessarily inappro-priate as long as certain parameters are monitored.These include regular physical exams and prenatalchecks, appropriate weight gain, and laboratorytesting. Even women that have done well or seem-ingly well on these diets prior to pregnancy maynot do well when pregnant or nursing.

Other women may suffer from an inadequatecaloric intake because of their fear of weight gain,inadequate education about pregnancy, or insuf-ficient money to purchase enough nutritiousfood. For low-income pregnant and postpartumlactating women, for infants, and for children upto the age of five years at nutritional risk, assis-tance is available through the federal Supplemen-tal Food Program for Women, Infants andChildren (WIC). Food stamp programs and Aidto Families with Dependent Children may alsobe available for women. Other local, private,church, county, and state organizations may alsobe a source of assistance.

Some women are potentially at nutritional risk.These include women who have had several full-term pregnancies, previous low birth weight deliv-eries, and short intervals between births. Womenwith medical conditions such as diabetes, chronicrenal disease, anemia, and phenylketonuria allrequire special attention to dietary counseling. Useof prescribed medications, over-the-counter drugs,vitamin and mineral supplements, laxatives, anddiet aids should all be reviewed by a qualifiedhealth-care practitioner.


The average amount of weight gain is 28pounds. The maternal component of weightaccumulation starts in the first trimester and ismost prominent in the first half of the pregnancy.The growth of the fetus is most rapid in thesecond half of the pregnancy. In the last 12weeks, the weight of the fetus more than triples.

Optimal health during pregnancy not onlyhelps to ensure a healthy baby but also helps toensure good health for the mother after the birth.A strong nutritional foundation during pregnancycan provide mothers necessary support in thepostpartum period, throughout breast-feeding,and during the years to come when the demandsof raising young children are high. When contem-plating pregnancy, the first step a woman needs totake is to commit to eat healthfully. Support offamily and friends during days of not feeling wellalong with assistance with shopping and cookingcan help in keeping that commitment. Almostevery pregnant woman will experience cravings.The main problem with cravings arises when crav-ings for chocolate, sodas, sweets, and ice creambecome substitutes for nutritious foods. Cravingsoften can also be clues about specific nutritionalneeds. A craving for ice cream may indicate anincreased need for protein, fat, or calcium. A crav-ing for acidic foods like pickles may be a clue toincreased need for calcium or salt. A craving forsweets may indicate a need for more protein in thediet. Cravings for chips can indicate a need formore salt and fats. A continued effort should bemade to replace these junk foods with healthiernutritious choices.

The best way to ensure that you are eating wellis to establish a balanced, wide variety of foods,including whole-grain cereals and breads, vegeta-bles and fruits, nuts, seeds, legumes, and comple-mentary amounts of dairy products and meats,especially fish and poultry. If you are unfamiliarwith natural foods, try to find a nutritional practi-tioner who can advise you and begin to makeappropriate changes in your diet. Books on nutri-tion and cooking also can be of help as you incor-

porate healthy foods into your diet. If you alreadyeat a very healthy diet, then it is important toensure that you are eating adequate amounts offood. If you are on a restricted diet or follow a spe-cific dietary system, I advise you to seek the adviceof a health-care practitioner knowledgeable in thearea of nutrition. Generally this would be a licensednaturopathic physician or a nutritionist/dietitian.The following general guidelines for daily foodservings have been proposed as the “daily dozen” inthe book What to Eat When You’re Expecting.24

• Calories: plenty of healthy foods to ensureadequate calories (2,300 daily)

• Protein: four servings (either vegetable oranimal sources—74 g total)

• Calcium foods: four servings daily (dairyand nondairy sources)

• Vitamin C–rich fruits and vegetables: twoservings

• Green leafy vegetables and yellow fruits andvegetables: three servings

• Other veggies and fruits: one or two servings• Whole grains and other complex carbohy-

drates: four to six servings• Iron-rich foods: one or more servings daily• High-fat foods: two servings• Salt: in moderation, to taste• Fluids: at least six to eight glasses• Supplements: nutritious herbs, highly con-

centrated food supplements (soy or greendrinks), and a prenatal vitamin-mineral supplement

The Food and Nutrition Board of the Insti-tute of Medicine has published recommendeddietary allowances (RDAs) periodically since1943. The RDAs are listed by nutrient in thenutritional supplement section that follows.

The question of how many calories per day toconsume is dependent upon many variables. Theinput portion of the energy equation includes the consumed food plus the amount of stored fuelin the body. The output variable in the equationincludes the metabolic rate, thermogenesis (heat


production), and physical activity. The caloric con-tent of the diet required to supply daily energyneeds and achieve optimal weight gain can be esti-mated by multiplying your optimal body weight inpounds by 15.9 and adding 300 to the total. (Al-ternatively, you can multiply your optimal weightin kilograms by 35 and add 300 to the total.)

The postnatal period is another time whenthe physiological demands of lactation andbreast-feeding put additional nutritional strain onthe mother. Optimal milk production requires atotal daily caloric intake of at least 1,800 calories.The energy sources are fat stores and diet, whichneed to supply an additional 500 calories per day.Intake of water, juice, and milk (this can be cow,goat, almond, soy, oat, or rice milk) to satisfy thirstis sufficient for breast milk production needs.

The well-balanced, varied whole foods dietthat was consumed prenatally should be main-tained postnatally. The monthly loss of iron withbreast-feeding is about half that of regular men-struation, and because women do not menstruateduring breast-feeding, their iron stores are usu-ally replenished. Some vitamins and other miner-als, however, may be depleted during lactation.Continued nutritional supplementation with aprenatal vitamin or, even better, a postnatal vita-min, can prevent deficiencies and is importanteven if the diet is sufficient.

After rapid weight loss in the first month, thelactating mother of normal weight may loseweight at a rate of about two pounds a monthwithout affecting milk volume. For the obesewoman, losing four pounds a month is also safe.Intentional weight reduction diets or rapidweight loss during lactation are not advisable. Atone year after delivery, a two-pound residualadditional weight is considered average.


Folic Acid. Folate is the only vitamin whoserequirement doubles in pregnancy.9 Deficienciesof folic acid have been linked in studies to lowbirth weight infants and neural tube defects.

According to one controlled study, women athigh risk (having previously given birth to babieswith neural tube defects) who were given folatesupplementation showed a 72 percent protectiveeffect compared to the placebo group.25 In onestudy, a group of pregnant women given folatesupplementation gave birth to infants withincreased birth weight and Apgar scores and hada decreased incidence of fetal growth retardationand maternal infections.26

Other studies also showed significant preven-tion with supplementation.27–30 Because offirmly established connections between deficien-cies of folic acid and low–birth weight infants and neural tube defects, the U.S. Public Health Service recommends that all women of child-bearing age take daily folic acid supplementationto reduce the risk of congenital birth defects.

Dietary folic acid is a mixture of folates in theform of polyglutamates, which are readilydestroyed by cooking. Higher levels of dietaryfolate intake has been shown in some cases todecrease the incidence of neural tube defects, butwomen hereditarily predisposed to such defectsmay need to take in more folic acid through supplements in order to reach optimal levels.31

Folic acid can be found in green leafy vegetables,nuts, whole grains, liver, watercress (avoid in firsttrimester), parsley, and dandelion. With artificialsupplementation, care must be taken, becauselarge doses of folic acid have been associated witha decrease in zinc absorption, a mineral requiredfor proper fetal growth and immunity,32 as wellas with maternal infection and abnormally slowfetal heart rate.33

Folic Acid

Recommended dietary allowance (RDA):Pregnant: 600 mcg per dayNursing: 500 mcg per dayFood sources: green leafy vegetables, nuts, whole

grains, liver, watercress (avoid in first trimester),parsley, dandelion


Vitamin B3 (Niacin, Nicotinic Acid). VitaminB3 (niacin) supplementation in the first trimesterhas been positively correlated in studies with higherbirth weight, longer length, and greater newbornhead circumference, all signs of healthier infants.34

Good food sources of niacin are wheat germ, fish,and garlic. Herbal sources are alfalfa, burdock rootand seed, dandelion, and parsley.

Vitamin B3 (Niacin)

Recommended dietary allowance (RDA):Age 18 and younger, pregnant or nursing: 30 mg per

dayAge 19 and older, pregnant or nursing: 35 mg per

dayFood sources: wheat germ, fish, garlicHerbal sources: alfalfa, burdock root and seed, dande-

lion, parsley

Vitamin B2 (Riboflavin). Studies show thatvitamin B2 (riboflavin) depletion is commonduring pregnancy (up to 40 percent less at termthan nonpregnant women and men), so ribo-flavin supplementation is recommended to pre-vent metabolic disturbances.35 Good sources ofriboflavin are watercress (avoid in first trimester)and brown rice. Herbal sources include rose hips,parsley, saffron, dandelion, dulse (seaweed), kelp,and fenugreek.

Vitamin B2 (Riboflavin)

Recommended dietary allowance (RDA):Pregnant: 1.4 mg per dayNursing: 1.6 mg per dayFood sources: watercress (avoid in first trimester),

brown riceHerbal sources: rose hips, parsley, saffron, dandelion,

dulse (seaweed), kelp, fenugreek

Vitamin B1 (Thiamine). Direct correlationhas been shown between supplementation ofvitamin B1 (thiamine) early in pregnancy andhigher infant birth weight and size.34 Thiaminedepletion is common during pregnancy, and sup-plementation is recommended.36 Food sources

are green peas, bell peppers, and sunflower seeds.Herbal sources include alfalfa, dandelion, fenu-greek, raspberry leaf, red clover, and seaweed.

Vitamin B1 (Thiamine)

Recommended dietary allowance (RDA):Pregnant or nursing: 1.4 mg per dayFood sources: bell peppers, green peas, sunflower

seedsHerbal sources: alfalfa, dandelion, fenugreek, raspber-

ry leaf, red clover, seaweed

Vitamin B6 (Pyridoxine). Vitamin B6 is“marginally deficient” in about 50 percent ofpregnant women.37 Supplementation has beenlinked to relief of nausea and morning sickness,especially in extreme cases that include vomit-ing.38, 39 In one experimental study, 75 percent ofwomen taking vitamin B6 experienced completerelief from symptoms of morning sickness.40

Higher doses were used for treatment of firsttrimester morning sickness (25 to 200 mg threetimes daily), but are not recommended beforedelivery, as higher doses may shut off breast milkin nursing mothers or cause the baby to havewithdrawal seizures if commercial formula isgiven that does not include enough pyridoxine(B6).41, 42 However, when given during labor,vitamin B6 may prevent many postnatal adapta-tion problems by increasing the oxygen-carryingcapacity of the blood that supplies the fetus.43

Vitamin B6 (Pyridoxine)

Recommended dietary allowance (RDA):Pregnant: 1.9 mg per dayNursing: 2.0 mg per dayTolerable upper intake level (UL):Age 18 and younger, pregnant or nursing: 80 mg per


dayFood sources: whole grains, wheat germ, egg yolk,

peas, carrots


Local application of B6 as a lozenge providedwomen with protection from dental cavities,which are more common during pregnancy.44

Supplementation may also prevent toxemia ofpregnancy (preeclampsia).45 Food sources arewhole grains, wheat germ, egg yolks, peas, andcarrots.

Vitamin B12 (Cobalamin). The coenzymeform of vitamin B12 is a very complex moleculecontaining cobalt, designated in humans ascobalamin, which is required for proper homo-cysteine metabolism. At least 12 different inher-ited inborn errors of metabolism related tocobalamin are known; low plasma vitamin B12

levels have been shown to be an independent riskfactor for neural tube defect in one study.46 Sup-plementation is recommended and may also helpprevent anemia. Food sources are cauliflower andbroccoli. Herbal sources are alfalfa, comfrey,miso, seaweed, and catnip.

Vitamin B12 (Cobalamin)

Recommended dietary intake (RDA):Pregnant: 2.6 mcg per dayNursing: 2.8 mcg per dayFood sources: cauliflower, broccoliHerbal sources: alfalfa, catnip, comfrey, miso, seaweed

Vitamin A. It is important to avoid oversup-plementation of vitamin A during pregnancy.Daily doses of 40,000 units or more of vitamin A during pregnancy may be toxic,47 while doseslower than 10,000 units appear to be safe.48 In astudy of 22,000 pregnant women, those whoconsumed more than 15,000 units of vitamin A per day from food and supplements, or 10,000units as a supplement, showed a significant in-crease in birth defects associated with cranial-neural-crest tissue (several-fold higher incidenceof birth defects).49 Most of these women con-sumed the vitamin A before the seventh week ofpregnancy. Rat studies show a possible link tofolic acid metabolism.50 Elevated levels of vita-

min A in the blood have also been correlatedwith low birth weight.51

Preterm infants have been shown to be defi-cient in vitamin A, which may predispose themto development of chronic lung disease.52

Healthy pregnant women who developed pre-eclampsia were shown to be deficient in vitaminA (but not beta-carotene).53 Preeclampsia is apotentially dangerous condition characterized byhigh blood pressure, swelling, and/or proteinspilling into the urine.

To avoid complications, supplementationwith no more than 6,000 units of vitamin A isoptimal and recommended.54 Beta-carotene,which has the same positive effects as vitamin A,has not been associated with toxicity or terato-genicity in humans or animals.55 Plant sources ofthe nontoxic “provitamin A” beta-carotene areorganic fruits and vegetables, especially yellowand orange ones; for example, one sweet potatoor one cup of carrot juice contains 25,000 IU of beta-carotene.56 Herbal sources are alfalfa,cayenne, comfrey, dandelion, elderberries, lamb’squarters, and seaweed.

Vitamin A

Recommended dietary allowance (RDA):Age 18 and younger, pregnant: 2,500 IU per dayAge 18 and younger, nursing: 4,000 IU per dayAge 19 and older, pregnant: 2,600 IU per dayAge 19 and older, nursing: 4,300 IU per dayTolerable upper intake level (UL):Age 18 and younger, pregnant or nursing: 9,000 IU

per dayAge 19 and older, pregnant or nursing: 10,000 IU

per dayBeta-carotene:No recommended doses or insufficient reliable infor-

mation. Consider UL to be 10,000 IU per day.Anywhere between 10 IU and 10,000 IU per day isan option.

Food sources: yellow and orange fruits and vegetablesHerbal sources: alfalfa, cayenne, comfrey, dandelion,

elderberries, lamb’s quarters, seaweed


Vitamin C. Vitamin C plays a vital role inthe formation of collagen—a major proteinfound in connective tissue, cartilage, and bone. Itis essential to the nerves, healthy gums, and teethand prevents infection. Although one studyshowed that women who took 5,000 mg of vita-min C daily during pregnancy delivered healthyinfants who developed scurvy,57 this “reboundscurvy” is very rare, and the infant recoversquickly without treatment. Supplementationwith vitamin C may be as effective as calcium forleg cramps during pregnancy.58

Food sources of vitamin C are fruits (particu-larly citrus), green chilies, tomatoes, honey, cab-bage, cucumbers, and prunes. Herbal sourcesinclude elderberries, rose hips, parsley, dandeliongreens, nettles, alfalfa, and cayenne.

Vitamin D3

Adequate intake (AI):Pregnant or nursing: 200 IU per dayTolerable upper intake level (UL):Pregnant or nursing: 2,000 IU per dayEnvironmental source: sunshineFood sources: fishHerbal sources: alfalfa, nettles

Vitamin E. Vitamin E declines during preg-nancy, creating deficiencies, and fetal vitamin Elevels are usually low.59 Lower plasma levels inthe mother may be associated with increased riskof preeclampsia, as well as premature andlow–birth weight infants.60 Supplementation hasbeen shown to be effective in preventing chronicmiscarriages.61 Good food sources are parsley,brown rice, and wheat germ. Herbal sourcesinclude alfalfa, rosehips, raspberry leaf, dande-lion, and seaweed.

Vitamin E

Recommended dietary allowance (RDA):Pregnant: 15 mg or 22 IU per dayNursing: 19 mg or 28 IU per dayTolerable upper intake level (UL):Pregnant or nursing: 400 IU per day and up to 900

IU per day during the last two months of pregnancyFood sources: brown rice, parsley, wheat germHerbal sources: alfalfa, rosehips, raspberry leaf, dan-

delion, seaweed, watercress (avoid in first trimester)

Vitamin K. Vitamin K is necessary for bonemetabolism. In most states it is required by lawthat vitamin K be given to newborns in the hos-pital by injection in the foot immediately afterbirth or a shot during labor to prevent hemolyticdisease, which is characterized by anemia, jaun-dice, enlargement of the liver and spleen, andgeneralized edema. Naturopathic doctors recom-mend checking the pregnant mother’s diet forvitamin K deficiency and adding oral supple-mentation of vitamin K in the last month of

Vitamin C

Recommended dietary allowance (RDA):Age 18 or younger, pregnant or nursing: 115 mg per


dayTolerable upper intake level (UL):Age 18 or younger, pregnant or nursing: 1,800 mg

per dayAge 19 and older, pregnant or nursing: 2,000 mg per

dayFood sources: fruits (especially citrus), green chilies,

tomatoes, cabbage, cucumbers, and prunesHerbal sources: elderberries, rose hips, parsley, dan-

delion greens, nettles, alfalfa, and cayenne

Vitamin D. The absorption of vitamin D (aswell as calcium, which vitamin D helps metabo-lize) is enhanced during pregnancy, and sincevitamin D tends toward toxicity, supplementa-tion should be judicious to prevent excessiveamounts of it from spilling into the urine. Fishoil and sunshine are good sources of natural vita-min D, which benefits the development of goodteeth and bones. Herbal sources of vitamin D arealfalfa and nettles.


pregnancy, if needed, rather than automaticallygiving the shots, which have been shown in somestudies to link with childhood cancer.62

Vitamin K (along with vitamin C) is effectivein preventing the nausea and vomiting of earlypregnancy, and it may reduce the risk of intraven-tricular hemorrhage in premature infants.63 Somefood sources are parsley and brown rice. Nettle oralfalfa leaf infusion or tea taken throughout thepregnancy will increase available vitamin K andhemoglobin in the blood; kelp is also helpful.

Vitamin K

Recommended dietary allowance (RDA):Pregnant or nursing: 65 mg per dayFood sources: parsley, brown riceHerbal sources: alfalfa, nettles, kelp

Calcium. Calcium is the only mineral whoserequirement doubles during pregnancy. Lowdietary intake is associated with preeclampsia,64, 65

a potentially dangerous (but preventable) condi-tion characterized by high blood pressure (hyper-tension), swelling, and/or protein spilling intothe urine. Supplementation with calcium mayreduce the risk of preterm delivery, often associ-ated with preeclampsia, and may also prevent thehypertensive disorders of pregnancy.66 Calciumsupplementation can also help to ease leg crampsduring pregnancy.67

Excessive levels of calcium in the body, how-ever, can result in spillage into the urine and anincreased possibility of kidney stones. Supplementwith the form of calcium that does not cause youindigestion or constipation. And attention mustbe paid to the relationship between calcium andother minerals, such as magnesium and zinc.

Raspberry leaf infusion contains calcium in itsmost absorbable form, as do nettle infusions, freshparsley, and watercress. Other food sources of cal-cium include milk products (although consump-tion of these can lead to allergies in the baby), darkgreen leafy vegetables, asparagus, and pumpkinseeds. Avoid bone meal or oyster shell calcium

tablets, which have been found to be high in lead,mercury, cadmium, and other toxic metals.

Calcium

Adequate intake (AI):Age 18 or younger, pregnant or nursing: 1,300 mg

per dayAge 19 and older, pregnant or nursing: 1,000 mg per dayFood sources: parsley, watercress (avoid in first tri-

mester), dairy products, dark green leafy vegetables,asparagus, pumpkin seeds

Herbal sources: raspberry leaf, nettles, horsetail

Chromium, Cobalt, and Copper. Thesethree trace minerals were positively associated instudies with higher infant birth weights, and sup-plementation is therefore recommended.68

Chromium

Adequate intake (AI):Age 18 and younger, pregnant: 29 mcg per dayAge 18 and younger, nursing: 44 mcg per dayAge 19 and older, pregnant: 30 mcg per dayAge 19 and older, nursing: 45 mcg per day

Cobalt

Adequate intake (AI):Pregnant or nursing: presumably as part of B12, 2

mcg per day, and sufficient if you are taking vita-min B12

Copper

Adequate intake (AI):Pregnant or nursing: 2 mg per day

Iron. Some researchers have concluded thatiron supplementation is essential during preg-nancy in order to maintain adequate maternaliron stores. However, because iron supplementa-tion can exacerbate zinc depletion, supplementa-tion is only warranted if iron deficiency isdetected and routine iron supplementationduring pregnancy is clearly indicated.69

If a woman gets sufficient iron in the firsttrimester of pregnancy, studies show a definitepositive association with infant birth weight and


size, although the same is not true for the secondand third trimesters.34 Good food sources arealmonds, honey, beets (including greens), andhigh-quality protein foods like egg yolks andorgan meats (liver, kidney, heart), preferablyorganic. Herbs high in iron are nettles, dande-lion, and alfalfa, as well as kelp.

Iron

Recommended dietary allowance (RDA):Pregnant: 27 mg per dayAge 18 and younger, nursing: 10 mg per dayAge 19 and older, nursing: 9 mg per dayTolerable upper intake level (UL):Pregnant or nursing: 45 mg, if not iron deficientFood sources: almonds, beets (including greens), egg

yolks, honey, organ meats (liver, kidney, heart)Herbal sources: alfalfa, dandelion, nettles, kelp

Magnesium. Magnesium deficiencies are asso-ciated with preeclampsia70, 71 and preterm labor.72

Supplementation must be in the first trimester topositively affect birth weight and size. Researchersthink that magnesium may act by opposing calcium-dependent arterial vasoconstriction andmay also prevent cell damage and death, makingmagnesium sulfate the “drug of choice” in thetreatment of preeclampsia.73 In general, supple-mentation may reduce the complications of preg-

nancy and improve infant health.74 In studies,magnesium-treated women had a 29.5 percentreduction in the risk of hospitalization, as well as a37 percent reduction in days spent in the hospital.Food sources are honey, almonds, barley, driedfruits, and potatoes. Herbs are dandelion, alfalfa,and watercress (avoid in first trimester), as well asseaweed (also called dulse).

Potassium. Potassium levels may be deficientin pregnancy, with the lowest concentrations inwomen with preeclampsia.75 Supplementation isrecommended. Food sources are bananas, pota-toes (especially peels), olives, bran, and greenleafy vegetables. Herbs are nettles, dandelion,alfalfa, and chamomile.

Potassium

Recommended dietary allowance (RDA):Pregnant or nursing: 99 mg per day; should not be

taken unless prescribed by your practitionerTolerable upper intake level (UL):Pregnant or nursing: 99 mg per day; should not be

taken unless prescribed by your practitionerFood sources: bananas, potatoes (especially peels),

olives, bran, green leafy vegetablesHerbal sources: nettles, dandelion, alfalfa,

chamomile

Zinc. Zinc is required for proper fetal growthand immunity. Plasma zinc levels decline about30 percent during pregnancy,76 and low zincintake is associated with spontaneous abortionand premature delivery,77 as well as complica-tions and labor abnormalities.78 Low zinc wasalso associated with the specific complication offetal distress79 and may be associated with centralnervous system abnormalities in infants, includ-ing neural tube defects,80 81 as well as low birthweight infants82–84 and toxemia of pregnancy.85

Supplementation, especially if zinc levels are low,is recommended to reduce the risk of fetal andmaternal complications.86 In one study, laborcomplications (vaginal bleeding, fetal acidosis,uterine inertia) were improved.87 Another study

Magnesium

Recommended dietary allowance (RDA):Age 18 and younger, pregnant: 400 mg per dayAge 18 and younger, nursing: 360 mg per dayAge 19–30, pregnant: 350 mg per dayAge 19–30, nursing: 310 mg per dayAge 31–50, pregnant: 380 mg per dayAge 31–50, nursing: 320 mg per day

Tolerable upper intake level (UL):Do not exceed 400 mg per day during pregnancyFood sources: honey, almonds, barley, dried fruits,

potatoesHerbal sources: alfalfa, dandelion, seaweed (dulse),

watercress (avoid in first trimester)


showed a lower incidence of pregnancy-inducedhypertension (which is associated with pre-eclampsia and preterm labor).88 Some foodsources of zinc are oysters, beets, broccoli, wheatgerm, wheat bran, fish, lentils, and watercress(avoid in the first trimester). Herbs are garlic,ginger root, and parsley.

Zinc

Recommended dietary allowance (RDA):Pregnant: 15 mg per dayNursing: 15 mg per dayTolerable upper intake level (UL):Age 18 and younger, pregnant or nursing: 34 mg per


dayFood sources: beets, broccoli, fish, lentils, oysters,

wheat bran, and wheat germHerbal sources: garlic, ginger root, and parsley

immune system have all been associated with ade-quate intake of docahexaenoic acid (DHA) duringthe development of the fetus.

Essential fatty acids have a unique role duringpregnancy because of the rapid cell growth anddevelopment of new tissues and new organ sys-tems in a developing fetus. Fetal development isassociated with a high EFA requirement, and thissupply is dependent on the amount and avail-ability of EFAs from the mother. Infants born ofmothers with low DHA levels have shorter atten-tion spans,91 and this may have long-term effectson future learning, development, and perform-ance. Children born to mothers who had taken10 ml per day of cod liver oil during their preg-nancy and lactation had higher IQs at age fourcompared to those born to mothers who hadtaken corn oil or placebo.92

Maternal levels of omega-3 fatty acids, espe-cially DHA, decrease during pregnancy.93 EFAsare components of breast milk, and maternallevels may be reduced further in nursing women.For the fetus, a deficiency of EFAs, particularlyeicosapentaenoic acid (EPA) and DHA, may leadto a poorly developed central nervous system.EFA deficiency may also lead to intrauterinegrowth retardation leading to a lower bodyweight and slower growth of the brain. Supple-mentation with a daily complex of essential fattyacids and fish oils during pregnancy providesvital nutrients that supply the necessary EFAs forthe increased nutritional and metabolic demandthroughout the nine months of gestation. Fishoil supplementation has been shown to improvethe DHA status of not only infants at birth butmothers too.94 Other research has shown thatsupplementation with fish oils is a good means ofimproving omega-3s in pregnant women95 andof improving the DHA status in breast milk.96

Trials on omega-3 fatty acids conducted inpregnant women have shown a significant reduc-tion in the incidence of premature delivery.97 Inone such study, fish oil was investigated for itseffects on pregnancy duration, birth weight,

Bioflavonoids. Bioflavonoids are beneficial for women who have recurring miscarriages.When placed on citrus bioflavonoids daily as soonas a period was missed, many stopped aborting.89

One study demonstrated that previously Rh-immunized mothers treated with bioflavonoidsduring their pregnancy delivered babies who wereless erythroblastotic than expected.90

Omega-3 and Other Fatty Acids (EFAs).There is a growing body of evidence about theimportance of omega-3 fats for human health anddevelopment, not the least of which starts withinfant exposure during fetal development. Doca-hexaenoic acid (DHA) is an important componentof phospholipids in the central nervous system andis found in high amounts in the retina, about 25percent. DHA makes up 12 to 20 percent of thefatty acids in the gray matter of the cortex of thebrain and in the brain stem. Inadequate intake ofomega-3s has significant implications for bothmother and infant. The development of the centralnervous system, the brain, the eyes, and the


intrauterine growth restriction, and pregnancy-induced hypertension.98 Omega-3 fatty acid sup-plementation of 2.7 grams per day was comparedto olive oil and/or no supplement. The fishoil–supplemented pregnancies lasted four dayslonger and birth weight was 107 g greater. Inanother study, infants born of mothers who hadbeen given cod liver oil had higher levels of DHAin their umbilical cord, longer gestational length(longer to develop in the uterus), and moremature brain functioning measurements on thesecond day of life.99 Fish oil also appeared to berelated to a reduction in the risk of preterm deliv-ery in those women who had had a previouspreterm delivery. There was no effect of fish oilon intrauterine growth restriction or pregnancy-induced hypertension.100 In addition, this studyreported that preterm delivery and low birthweight of the infants occurs when little to noomega-3 fats from fish or fish oil are consumed.

A more recent study of pregnant women inIceland showed that consuming liquid cod liveroil in the first 15 weeks of pregnancy resulted inbabies with higher birth weight.101 Higher infantbirth weight is related to a lower prevalence ofcardiac disease, high hypertension, and glucoseintolerance in the future.102, 103 Additional goodnews was that the women did not gain moreweight, despite their consumption of increasedcalories and fat from the oil.

Hormone-like substances called prostaglandinsare also involved in the development and clinicalexpression of preeclampsia. These prostaglandinsare modulators of vascular smooth muscle toneand platelet aggregation (blood platelets stickingtogether). Preeclampsia is characterized by increased vasoconstriction, frequently associatedwith increased platelet aggregation, reduced utero-placental blood flow, and premature delivery. In aplacebo-controlled clinical trial, a group of preg-nant women receiving a combination of eveningprimrose oil and fish oil had a significantly lowerincidence of edema.104 Evening primrose oil hasalso been shown effective in preventing pregnancy-

induced hypertension105 (associated with pre-eclampsia and preterm labor).

There is some evidence that evening primroseoil (EPO), taken both orally and vaginally, can be used to promote the preparation of the cervixfor the birth (cervical ripening). Clinically, EPOsupplementation during pregnancy has beenfound by practitioners of natural childbirth to bean efficacious method to stimulate cervical ripen-ing during labor, and the prostaglandin PgE1 isknown to stimulate cervical ripening and hastenthe progression of labor.106 Although practitionersusing this supplement report no adverse effects, a retrospective trial comparing the oil to no sup-plement did not note a difference between groups,and there was a suggestion that there was anincreased incidence of premature rupture of mem-branes, labor augmentation, and assisted vaginaldelivery in the evening primrose oil group.107

The main food sources of essential fatty acidsare raw seeds and nuts or fish. Whole and groundflaxseed and purified flaxseed oil are excellentsources of the two essential oils, linoleic acid andlinolenic acid. Borage oil and black current oilcan be taken in capsule form as nutritional sup-plements. It should be stated, though, that allseed oils are not the same in their makeup ofessential fatty acids, and substituting a seed oildoes not necessarily give the same benefits as thefish oils and vice versa.

Although research clearly shows that moder-ate EFA supplementation is beneficial and safefor pregnant women, caution should be exercisedwhen consuming large doses. Also, there may besome caution about increased fish intake andenvironmental contamination. The U.S. Foodand Drug Administration and the Environmen-tal Protection Agency advise that pregnant andnursing mothers and young children avoid certaintypes of fish and shellfish and limit others. Inpart, this may be due to the methylmercury con-tent in fish such as albacore tuna, shark, sword-fish, king mackerel, and tilefish. Methylmercuryis a known neurotoxin.


Supplementing with fish oils should be donewith purified fish oil supplements, which canreduce or practically eliminate exposure to mer-cury, PCBs, dioxins, and pesticides. Due to howwe have contaminated our ocean waters and thewildlife that inhabits these waters, high-qualityfish oils supplements may in fact be a safer alter-native to fish in food form and enable us to gainthe benefits of omega-3s while reducing the riskof toxicity.108, 109

Omega-3 Fatty Acids

No recommendations have been established by theFDA but the International Society for the Study ofFatty Acids and Lipids recommends 2.87 mg per dayof omega-3 fatty acids with a minimal intake of 300mg per day of DHA for pregnancy or lactation.

Food sources: fish high in omega-3 fatty acids includetuna, salmon, sardines, mackerel, and herring (seeprecautions in text); other sources include flaxseed,hemp seeds, sunflower seeds, walnuts, almonds, andfilberts

Phosphatidylcholine (PC). PC is a primarycomponent of lecithin, sometimes referred to aspure lecithin, from which dietary choline isderived. Dietary choline, after absorption by theintestinal mucosa, is metabolized in the liver tocholine, a critical nutrient for brain and nervedevelopment and function. In mammals, amni-otic fluid has a tenfold greater concentration ofcholine than that in maternal blood,113 and atbirth, all mammals studied have plasma cholineconcentrations much higher than those found inadults.114 When rats were supplemented withcholine, the spatial memory of their offspringwas permanently enhanced, and they showedmore accurate performance on both working andreference memory components of tasks. Fromthese studies,115 researchers believe that choline iscritical for optimal brain development, andtherefore supplementation is suggested.

No recommended dose available.

Lecithin. Lecithin, a derivative of the soy-bean, is needed by the brain to function properlyand helps to break down fatty cholesteroldeposits in the body. Lecithin contains phospho-rus and stimulates the metabolism. Lecithin isalso found in fertile eggs, soy products, and, insmall amounts, in all vegetables that have beenvine ripened.


Taurine. Taurine is an amino acid foundwidely distributed in foods of animal origin (but not milk or milk products). Taurine isbiosynthesized from methionine or from cysteineduring the metabolic process, and disturbancesin enzymatic reactions that take place in thisprocess can lead to mental retardation. Vegetar-ian mothers who consume no meat productsduring their pregnancy, and therefore have a low-taurine diet, as well as others on a protein-,methionine-, or vitamin B6–deficient diet mightbe at particular risk.116

Although dietary deficiency of taurine hasnot been demonstrated to impact fetal develop-

Coenzyme Q10. Coenzyme Q10 is a fat-soluble quinone occurring in the mitochondriaof every cell that is a cofactor in the electrontransport chain on which most cellular functionsrely, making it essential for the health of virtuallyall human tissues. Plasma levels of this enzymerise during normal pregnancy, reaching highs of50 percent above normal by the 36th week.Decreased levels have been linked in studies tospontaneous abortion and threatened abortion,particularly before 12 weeks.110


Methionine (SAM). Methionine is a compo-nent of many proteins, serving as a source ofavailable sulfur for synthesizing both cysteineand taurine, crucial to cellular metabolism. Sup-plementation with methionine in mice reducedneural tube defects by 47 percent111 and also pos-itively affected birth weight and size.112



ment in humans, researchers recommend thatvegetarian women who intend to have childrenoptimize dietary levels of protein and vitamin B6,since there is no taurine present in plants andvegetables. Meat eaters are advised to eat onlyorganic or “free-range” animals in order to avoidthe high concentrations of hormones and pesti-cides found in animal products in industrializedcountries.


Botanicals

There are many herbs that can be used safelyduring pregnancy. Some herbs are characterizedas tonics, others are spices that improve taste anddigestion, other herbs contain specific vitaminsand minerals that aid different organ systems,and still others can be used as medicines to inter-vene and treat conditions or illnesses related tothe pregnancy. However, there are some herbsthat are commonly contraindicated for useduring pregnancy. Although some of these herbsmay be used in very small amounts for specificconditions, it is prudent to avoid them unlessunder the supervision of an expert in herbalmedicine. Some of these contraindicated herbscan be used safely late in the pregnancy or duringlabor with the guidance of an experienced practi-tioner (see the following sidebar).

The following herbs are some of the mostcommon medicinal plants used in traditionalherbal practice for promoting and maintaininghealth during pregnancy.

Dandelion Leaf and Root (TaraxacumOfficinale). Dandelion is a potent source of vita-mins and minerals, especially vitamin A, cal-cium, potassium, and iron. Mildly diuretic andstimulating to bile flow, dandelion leaf helps withthe inevitable digestive complaints of pregnancy,and its root cleanses and tones the liver.117 Inearly pregnancy, dandelion can help to alleviatenausea, upset stomach, and indigestion. As adiuretic, the most active part of the plant is the

leaf. The root or the leaf can be taken as a tea, incapsule form, or as a liquid tincture (a mixture ofplant, alcohol, and water). It can be safely takenthroughout pregnancy as a tonic or to addressone of the indicated specific problems associatedwith pregnancy.

False Unicorn (Chamaelirium Luteum).False unicorn has traditionally been used as auterine tonic before, during, and after pregnancy,especially for women who have a history of mis-carriage. Similar to dandelion, it is used to sup-port liver and digestive function. Due to its bittertaste, this herb is probably best tolerated in cap-sule or tincture form rather than as a tea.

Ginger (Zingiber Officinale). Ginger isprobably best known for its treatment of nauseaand vomiting, whether pregnant or not. Therehave been several good scientific studies on theuse of ginger in nausea of pregnancy and themore severe state called hyperemesis gravidarum(severe nausea and vomiting during pregnancy).In these studies, ginger brought about a signifi-cant reduction in both the severity of the nauseaand the number of attacks of vomiting in themajority of the patients. In all of these studies,there were no adverse effects on pregnancy andpregnancy outcome. In fact, in the most recentstudy of 70 women, there were three sponta-neous abortions in the placebo group and onlyone in the ginger group. More full-term pregnan-cies occurred in the ginger group than in theplacebo group as well. No infants had any con-genital anomalies.118

In a double-blind, randomized, crossover trialthat studied the effectiveness of ginger in hyper-emesis gravidarum, the most severe form of pregnancy-related nausea and vomiting, early inpregnancy, 250 mg of ginger root powder takenfour times a day significantly reduced the severityof the nausea and the number of attacks of vom-iting in 19 of 27 women.119 Ginger is safe to useat any time during pregnancy and is a welcomealternative to some of the antinausea pharmaceu-


ticals, which may be associated with teratogenic-ity (physical defects in the fetus in utero).

Information that has appeared in the writingsof traditional herbalists and the lay press orherbal resources about the danger of gingerduring pregnancy appears to be out of date andnot based on scientific facts. Select sensitive indi-viduals may get some stomach-burning sensa-tions when using ginger. Taking it with food willmost likely relieve that discomfort.

Nettle (Urtica Dioica). Nettle is one of thebest herbs to use in pregnancy due to its appre-ciable amounts of vitamins and minerals, includ-ing calcium and iron. Used throughout the

pregnancy, nettle can help to improve energy,strengthen the blood vessels, reduce varicose veins,alleviate leg cramps, prevent anemia, and decreasethe likelihood of hemorrhage during childbirth.This is an herb that can be taken in all forms,including freshly picked young leaves and as a leafygreen addition to steamed vegetables or salads.

Partridgeberry (Mitchella Repens). Par-tridgeberry or squaw vine is considered one ofthe best uterine tonics. It should be taken for several weeks before the due date. Squaw vine isoften used in combination with raspberry leaf. Itcan be taken as a tea, in capsule form, or as atincture.

Herbs Contraindicated During Pregnancy

The following herbs should not betaken during pregnancy:

Alder buckthorn (Rhamnusfrangula)

Aloe (Aloe vera)Angelica (Angelica archangelica)Arnica (Arnica montana)Autumn crocus (Colchicum

autumnale)Barberry (Berberis vulgaris)Bethroot (Trillium spp.)Black cohosh (Cimicifuga

racemosa)Blessed thistle (Carbenia

benedicta)Bloodroot (Sanguinaria

canadensis)Blue cohosh (Caulophyllum

thalictroides)Broom (Sarpthamnus scoparius)Butternut (Juglans canadensis)Calamus (Acorus calamus)Calendula (Calendula officinalis)

Cascara sagrada (Rhamnuspurshiana)

Coltsfoot (Tussilago farfara)Cowslip (Primula veris)Damiana (Turnera aphrodisiaca)Dong quai (Angelica sinensis)Ephedra (Ma huang) (Ephedra vul-

garis)Feverfew (Tanacetum

parthenium)Ginseng (Panax quinquefolium)Goat’s rue (Galega officinalis)Goldenseal (Hydrastis

canadensis)Gotu kola (Hydrocotyle asiatica)Ipecac (Ipecac ipecacuanha)Juniper berry (Juniperis

communis)Licorice (Glycyrrhiza glabra)Lily of the valley (Convallaria

majalis)Lobelia (Lobelia inflata)Male fern (Dryopteris filix-mas)

Mandrake (Podophyllum peltatum)

Mistletoe (Viscum album)Mugwort (Artemesia vulgare)Nutmeg* (Carum petroselinum)Pennyroyal (Mentha pulegium)Periwinkle (Vinca spp.)Peruvian bark (Cinchona spp.)Pleurisy root (Aesclepius tuberosa)Poke root (Phytolacca americana)Rhubarb (Rheum palmatum)Rue (Ruta graveolens)Sage* (Salvia officinalis)Sarsaparilla (Smilax officinale)Senna (Cassia senna)Shepherd’s purse (Capsella

bursa-pastoris)Stillingia (Stillingia sylvatica)Tansy (Tanacetum vulgare)Thuja (Thuja occidentalis)Wormwood (Artemesia

absinthinum)Yarrow (Achillea millefolium)

*Small amounts of nutmeg and sage used in cooking are OK.

Note: Some of the herbs listed may be recommended by a licensed practitioner with expertise in the use of botani-cals during pregnancy and labor.


Red Raspberry (Rubus Idaeus). Red rasp-berry leaf is the most often mentioned traditionalherbal tonic for general support of pregnancyand breast-feeding. Rich in vitamins C and Eand minerals, especially high in naturallychelated iron (which is well assimilated), it tonesthe uterus, increases the flow of milk, andrestores the reproductive system after childbirth.Raspberry leaf contains fragrine, an alkaloid thatgives tone to the muscles of the pelvic region,including the uterus itself. In addition to tonify-ing the uterus, raspberry is used to prevent hem-orrhage. It deserves its reputation as a pregnancyherb par excellence.

Wild Yam (Dioscorea Villosa and Bar-basco). Wild yam can be used to help preventmiscarriage due to its calming and antispasmodicaction on the uterus. Even though wild yam hasacquired a considerable reputation as a “femaleherb,” perhaps its most traditional uses are as adigestive aid in treating nausea, as an antispas-modic for intestinal and gallbladder colic, and asa liver herb. This herb is best used in capsule ortincture form. To help prevent miscarriage,higher doses of the tincture can be used (1⁄4 to 1⁄2teaspoon every three to four hours).

SUBSTANCES TO AVOID DURING PREGNANCY

Besides supplementing with multivitamins, min-erals, and other appropriate nutrients, a pregnantwoman improves her chances for a complication-free pregnancy and birth by avoiding harmfulsubstances such as alcohol, caffeine, nicotine,and recreational and prescription drugs. Terato-gens are substances that cause birth defects, mis-carriage, or pregnancy complication when apregnant woman is exposed to them, especiallyin the early stages of pregnancy. Environmentalchemicals such as mercury and lead, many pre-scription drugs such as Dilantin and Accutane,recreational drugs including cocaine and alcohol,and even some illnesses including rubella, dia-

betes, and herpes are all potentially teratogenicagents and able to cause loss of a pregnancy, birthdefects, or pregnancy complications. Pesticidesand other contaminants found in the environ-ment (including our food and water) can disruptthe hormonal and chromosomal cycles, leadingto breaks in the DNA and a wide range of defor-mities and abnormalities in all animal species,including humans.

Alcohol

Alcohol consumption during pregnancy is anestablished cause of serious birth defects anddevelopmental delay, described as fetal alcoholsyndrome (FAS). FAS is caused by in utero alcohol-induced damages and results in mentalretardation. Infants born with FAS have facialabnormalities and slow growth. They showimpairment in their intellectual developmentand have difficulties in learning, memory, prob-lem solving, and attention span. They can alsoexperience mental health problems and difficul-ties with social behaviors.120 It is estimated thatthe prevalence of FAS in the United Statesranges between 0.3 to 2.2 per 1,000 live births.Much higher rates can occur in some communi-ties. The focus should be on prevention andaggressively promoting no alcohol use duringpregnancy.

Even mild alcohol ingestion during pregnancyis said to result in hyperactivity, short attentionspan, and emotional problems in children.121

Alcohol consumption during pregnancy con-tributes to birth abnormalities whether the motherdrinks a little or a lot.122 There are two periods ofpregnancy when the maternal consumption ofalcohol is particularly threatening to the develop-ment of the fetus: from the 12th to the 18th weekand from the 24th to the 35th week. Three or fourbeers or glasses of wine a day can cause any one ormore of the following defects: mental retardation,hyperactivity, a heart murmur, facial deformitysuch as a small head, or low-set ears.123


Cigarettes

The sad news is that more than 20 percent ofwomen in the United States smoke. The num-bers are similar in other developed countries andonly slightly lower in developing countries.Unfortunately, many of these women also smokeduring pregnancy—about 11 percent. Not onlydoes smoking harm a woman’s long-term health,it can increase numerous complications andcause serious problems for newborn infants.According to statistics, we could reduce the rateof stillbirths by 11 percent, and newborn deathsby 5 percent, if all pregnant women stoppedsmoking.124

Cigarette smoke contains more than 2,500chemicals, and both nicotine and carbon monox-ide are thought to be related to adverse outcomesin pregnancy. Smoking nicotine has been associ-ated with several complications of pregnancy. Itappears to double a woman’s risk of developingplacental problems,124 including placenta previa (alow-lying placenta that covers part or all of theopening of the uterus), placental abruption (theplacenta peels partially or completely away fromthe uterine wall prior to delivery), and prematurerupture of the membranes. Cigarette smoking isknown to cause lower birth weight and size; moth-ers who smoke 13 or more high-tar cigarettes aday have smaller babies in poorer condition thanthose of nonsmoking mothers.125 Smokers have amiscarriage rate twice as high as that of nonsmok-ers,126 and babies born to mothers who smokehave more than double the risk of dying of suddeninfant death syndrome.127

Women who smoke may experience moreectopic pregnancies (a potentially dangerous sit-uation in which the fertilized egg attaches to, andgrows on, the fallopian tube outside the uterus).Children of smokers may have far more respira-tory illnesses (like asthma) than those of non-smokers. Even secondhand smoke is seriouslyharmful to mother and baby and should beavoided when possible.

The more a woman smokes, the greater therisk to her baby. However, if she stops smokingbefore the end of her first trimester, she is no morelikely to have a lower birth weight baby than anonsmoking woman. Even stopping by the thirdtrimester can improve the baby’s growth.

The good news is that it is possible to stopsmoking and there are numerous resources tohelp you. The National Partnership to HelpPregnant Smokers Quit provides information forwomen and resources for health-care profession-als. The American Legacy Foundation is anotherorganization that helps smokers quit. Smokefree.gov is an online resource for individuals whowant to stop smoking that is sponsored by thefederal government. The American College ofObstetricians and Gynecologists provides goodinformation for health-care providers to offerassistance to their patients. There are many otheradditional resources as well, and some may belocal to your community.

Caffeinated Beverages

A small amount of caffeine will probably not beharmful for most women and their infants. How-ever, there are some studies of concern. Caffeinehas been shown to contribute to growth-retardedor low–birth weight infants.128 Researchers havesuggested that women limit their intake of caf-feine to approximately 300 mg per day duringpregnancy, and since caffeine is known to enterbreast milk, that level might be appropriate fornursing mothers as well.129 One cup of regularcoffee contains about 120 mg of caffeine. Evenwith this limited amount, the coffee or teashould be organic in order to avoid the pesticidesused in agricultural processes.

Pesticides and Environmental Hazards

Environmental factors are becoming more andmore problematic to each generation of pregnantwomen, as many artificial compounds (such asPCBs from plastics) build up in the environment


over time without degrading, become part of the food chain, and are incorporated into ourbodies. Theo Colburn’s groundbreaking study of the links between pesticides, PCBs, and otherorganochlorides in the food chain and hormonaldisruption and birth defects makes clear thatwhatever an individual woman can do to avoidthese compounds in her food and water is wellworth doing.130 Because humans are high on thefood chain, the effects of these compounds onhuman reproduction are potentially exponentialand devastating.

Hazardous substances such as pesticides, lead,and other chemicals brought home from the workenvironment on a parent’s clothing can harm anunborn child.131 Also potentially harmful to thefetus are the mother’s exposure to x-rays duringpregnancy or the father’s preconception exposureto x-rays.132 One study showed that high amountsof lead and barium in drinking water caused anincreased risk of miscarriages.133 Elevated lead inthe body has also been linked to preeclampsia134

and lower birth weight.Mercury has received perhaps the most atten-

tion of any of the pesticides and heavy metals.Methylmercury crosses the placenta and canimpair the development of the central nervoussystem in the fetus. As a result, the federal government has issued guidelines regarding fishintake for pregnant women and for all agegroups. The intake of fish appears to be stronglycorrelated with the concentration of mercury inhair, and it has been observed that women instates with fish advisories who ate 20 or moreservings of fish in a three-month time span hadmercury concentrations in their hair that wassevenfold higher than those of women who ateno fish. The majority of these women exceededthe recommended limit for lead.135 Canned alba-core tuna (or white tuna) and tuna steaks aregenerally considered to be higher in mercurythan light canned tuna. The USFDA currentlyrecommends that pregnant women eat no morethan six ounces of fish per week.

Over-the-Counter and Prescription Drugs

Seemingly harmless over-the-counter drugs likeaspirin, taken by mothers in the first half of the pregnancy, have been linked to lower-than-average IQs in their offspring.136 Valium oiladministered to egg-laying chickens inducedimpaired muscle cell development, suggestingpotential harm from the use of Valium in preg-nancy.137 Medications such as lithium (used totreat bipolar disorder, formerly called manicdepression) and tetracycline (an antibiotic) canharm the fetus; if at all possible, avoidance ofthese substances is recommended. Some anti-seizure medications are folate antagonists and, assuch, can increase the risk for fetal neural tubedefects unless folic acid supplementation isimplemented along with the medication.138, 139

In addition to the products already men-tioned, herbalist Susun Weed provides the fol-lowing list of products to avoid: DES(diethylstilbestrol), laxatives, pHisoHex (or any-thing else containing hexachlorophene), hairdyes, phenobarbital, barbiturates, tranquilizers,epinephrine (adrenaline) shots, sulfa drugs,antibiotics, vaccines, anesthetics, mercury vaporsin dentists’ offices, steroids, hormones, andAccutane (an acne medication).140

Your health-care practitioner can make avail-able a full list of over-the-counter and prescrip-tion medications rated in terms of safety and sideeffects for the fetus during pregnancy and for theinfant during lactation. Please ask your health-care provider(s) before taking any over-the-counter medication, prescription medication, orherbal and nutritional supplements.

Recreational Drugs

Before conception and during pregnancy, espe-cially the first trimester, it is important to avoidusing recreational drugs, even those that mayseem harmless at other times, as consequences toa developing fetus may be serious. Genetic mate-


rial can be damaged by marijuana, for example;in animals, it has been linked to an increase infetal deaths and malformations.141 Cocaine maydecrease sperm concentration in semen, inducedeformities in the shape of the sperm, and reducethe motility after ejaculation.142 Men’s precon-ceptual use of cocaine has been linked to cases ofneurological damage in children.

EXERCISE

The appropriate take-home message on exerciseduring pregnancy is not that women should exer-cise during pregnancy but that they may. Toooften, women have heard that maybe they shouldlimit their exercise. It is not necessary to be sorestrictive in exercise during pregnancy, althoughcertain precautions should be observed. Despiteconflicting opinions, information on exercise and pregnancy is plentiful, and its message isclear: low-impact, moderate exercise is safeduring pregnancy.

In certain instances, exercise can prove bene-ficial to the pregnant woman and her child. Exer-cise can reduce the length of hospitalization,reduce the incidence of cesarean section, andresult in a healthier baby with a higher birthweight. The advantages also extend to the preg-nant mom to be. Women who exercise duringpregnancy seem to do a better job at maintainingtheir ideal body weight after pregnancy and haveless discomfort during their pregnancy.

See the sidebars for some helpful guidelinesfor exercising during pregnancy.

Contraindications to Exercise During Pregnancy

There are instances when exercise should beavoided during pregnancy. These include: pre-eclampsia, pregnancy-induced hypertension, toxemia, preterm rupture of membranes, historyof preterm labor, persistent second or thirdtrimester bleeding, incompetent cervix, or signs ofintrauterine growth retardation.

COMMON COMPLAINTS ANDDISORDERS OF PREGNANCY

Most problems experienced during pregnancy are aresult of the immense hormonal changes, nutri-tional deficiencies, and shift in weight distributionthat happens as a result of sudden weight gain.Backache, digestive discomfort, fatigue, swelling,and mood changes are almost inevitable.

With the judicious use of rest, exercise, andnutrition, most women can successfully weatherthe hormonal roller coaster ride of pregnancy.Walking a mile a day is unanimously recom-

Safety Tips for Exercising While Pregnant

1. Drink enough water or other fluids during andafter exercise to prevent dehydration and hypovolemia.

2. Wear clothing that allows for adequate ventila-tion and prevention of hyperthermia while exercising.

3. Your exercise regimen should emphasize low-impact activities, such as stationary bicycling,swimming, walking, and low-impact aerobics.

4. Do not exercise if you have a fever.5. Supine exercise (exercises in which you lie on

your back) should be avoided, especially in thethird trimester, as they may reduce blood supplyto the fetus.

6. Exercises that require repetitive bouncing andjerky movements and exercises requiring balanceshould be avoided, especially in the thirdtrimester.

7. Activities that involve potential low-oxygenstates, such as scuba diving and mountainclimbing, are contraindicated.

8. Be sure to follow a diet that emphasizes com-plex carbohydrates to replace muscle glycogenlost during exercise, thereby minimizing the riskof fetal ketosis (elevated ketones in the bodytissues).

9. Participation in competitive team sports isacceptable in the first 15 weeks of pregnancy,although there are potential but unproved risksfor fetal loss from pelvic trauma, abdominaltrauma, or both.

10. Avoid exercises such as weight lifting, especiallyin the third trimester.


although it may be linked to an increase in thy-roid hormone (T4) effects on smooth musclerelaxation in the stomach. Physical exercise, espe-cially walking, is recommended for morningsickness. Low blood sugar is implicated in thenausea of early pregnancy and can be regulatedby eating smaller meals more often, eating high-protein snacks before sleeping, and eatingunsalted crackers or matzo before getting out ofbed in the morning.

Insufficient B vitamins may be associatedwith morning sickness; pregnant women areoften deficient in B6 as well as folic acid (the needfor which increases during pregnancy). Foodsrich in B vitamins—such as nutritional yeast,yogurt, bee pollen, spirulina, wheat germ, wholegrains, egg yolk, cabbage, and organic organmeats—might be sufficient to alleviate morningsickness; if not, a B-50 vitamin supplement maybe needed during the first trimester.

Anise, fennel, peppermint, chamomile, orspearmint teas are all helpful; raspberry leaf tea,sipped before getting out of bed in the morning,may help. Wild yam root, according to herbalistSusun Weed, is “specific and powerful for nauseaof pregnancy.”140 As we discussed earlier in thischapter, studies have shown ginger root to beextremely effective in the treatment of the nausea

Summary of Exercise Guidelines

1. Regular frequency of exercise is preferable tosporadic physical activity.

2. Guidelines for exercising safely during pregnancyshould be followed. (See other sidebars in thissection.)

3. Intensity of exercise should be monitoredaccording to symptoms, and exhaustive exerciseshould be avoided.

4. Adequate caloric and nutrient intake should bemaintained.

5. Adequate hydration, proper clothing, and avoid-ance of hot, humid environments should aug-ment heat dissipation, especially in the firsttrimester.

mended by researchers and birth supporters, as iseating healthy (preferably organic) foods everyday (including protein, whole grains, fruits, andvegetables). I recommend that if a pregnantwoman eats meat and/or dairy products, theseshould be “free range” and organic, or at least freefrom the artificial hormones and pesticides usedin the agricultural processes. Dairy products havesome of the highest concentration of estrogen-mimicking artificial compounds and growth hor-mones. Xenoestrogens from pesticides are alsosuspected of causing genetic damage.

Morning Sickness

One of the first and perhaps most annoying com-plaints of pregnancy is the nausea (and vomiting)of “morning sickness,” which generally stopsbeing a problem after the first trimester. No onereally knows what causes morning sickness,

Tips for Safe Weight Training During Pregnancy

1. Do not compete, not even with yourself.2. Begin with very light weights.3. Avoid holding your breath while lifting. Breathe

in during relaxing part of exercise and breatheout during effort part of exercise.

4. Rest between exercises.5. Take a mouthful of pure water between

exercises.6. Do not lift while lying on your back. Pregnant

women should not lie on their backs while exer-cising, especially after the sixth month, becauseblood supply may be reduced to the fetus.

7. Stay cool. Exercise increases body temperature,which may threaten the health of the fetus.Keep your temperature below 100 degrees. Dresslightly in warm weather.

8. Warm up for three to five minutes before per-forming weight-lifting exercises. (See “JointWarming Exercises” in Appendix A.)

9. Perform a few basic stretches of muscles usedduring the exercise session at the end of theworkout. (See Appendix A.)

10. See Appendix A for the “Speak PregnancyExercises.”


and vomiting of severe morning sickness. Startwith 250 mg of ginger root powder four timesdaily; increase if necessary. Fresh ginger root teacan be made by simmering slices of ginger root inboiling water for 15 minutes. Add honey to taste.

Chronic Miscarriage/Abortion

Ten percent of first trimester pregnancies end inspontaneous abortion or miscarriage. Womenwho miscarry always feel guilty; they often feelresponsible for the miscarriage. The fact is, how-ever, that nature is not perfect; all conceptions are not destined to become a child. Having twomiscarriages—even in a row—is not necessarilyabnormal. The causes of miscarriage includeunknown factors, stressors, environmental factors(toxic substances in food, water, and air and pollu-tants in the workplace), smoking, drinking alco-hol, dietary deficiencies, and fetal abnormalities.As discussed earlier in the nutrition section, lowzinc intake has been associated with spontaneousabortion and premature delivery, and vitamin Esupplementation and bioflavonoids may help toprevent miscarriage. In addition, Susun Weed liststhe following herbs as being used in traditionalherbal medicine for preventing miscarriage:140

• Black haw root. This is especially effective.Drink one or two cups of tea or one-halfcup of infusion daily as soon as pregnancy isknown; use throughout entire pregnancy ifdesired.

• False unicorn root. This is recommendedespecially for women who have experiencedrepeated miscarriages. Take three drops oftincture four to five times daily from pre-conception through the first trimester.

• Wild yam root. For threatened miscarriage,make a strong tea by steeping one teaspoonof wild yam root in two cups hot water for15 minutes; take two to four ounces every30 minutes. The tincture is less effective andmay induce nausea or vomiting.

Preeclampsia or Eclampsia (Toxemia)

Preeclampsia is a dangerous condition that maydevelop in the third trimester of pregnancy. Itincludes hypertension (high blood pressure),edema, and protein in the urine. About 6 percentof all pregnant women will develop preeclampsiasometime after completing 20 weeks of gesta-tion; eclampsia occurs in 0.1 percent of cases.143

Western medicine believes that there is noway to prevent preeclampsia but that it can bekept from progressing to eclampsia with goodprenatal care. Herbalist Susun Weed disagrees,calling preeclampsia “the result of malnutritionduring pregnancy,” and says it is easily preventedby eating 60 to 80 grams of protein daily, gettingenough salt, foods high in calcium, adequatecalories, and nourishing herbal supports likeraspberry, nettle, and dandelion leaves through-out pregnancy.140 The Harvard Guide to Women’sHealth links preeclampsia to very young or mucholder women (over 45), women with underlyingmedical problems (high blood pressure, kidneydisorders, autoimmune disorders, and diabetes),and multiple births.144

Once preeclampsia is diagnosed, a skilledprofessional must be called in to help manage thetreatment, since the condition is serious enoughto threaten the mother’s life and damage thefetus. Potassium levels must be increased (inaddition to prescription potassium, eating potatopeels and bananas helps; also mint, chicory, anddandelion leaves). The sodium-potassium rationeeds balancing (drink raw beet juice, up to fourounces daily); supplement with B6 in conjunc-tion with a high-potency B-complex vitamin; eatspirulina; and add seaweed to your daily diet.

The Harvard Guide expresses the current allo-pathic medical perspective when it states unequiv-ocally: “The only definitive cure for preeclampsiais delivery of the baby.”144 However, women withpreeclampsia are generally sent to bedrest unlessthe diastolic blood pressure is greater than 100with bedrest. If significantly preterm, efforts are


made to confirm fetal maturity or mature fetallungs medically before delivery. Usually the earlierin the pregnancy that pregnancy-induced hyper-tension occurs, the more severe it becomes. Themajority of cases at term are usually benign andeasily managed. Catastrophic outcomes of tox-emia include seizures, strokes, and failure of theheart, liver, lungs, or kidneys.

Since preeclampsia is characterized by highblood pressure, it stands to reason that yoga,meditation, and stress reduction techniqueswould be a useful complement to nutritional,botanical, and conventional medications.

Heartburn, Gas, and Constipation

Hormonal imbalances during pregnancy mayresult in softening of the smooth muscle found inthe walls of the digestive tract. The consequentreduction in peristaltic movement causes food topass more slowly through the esophagus, stom-ach, and small and large intestines to the rectum,inducing gas and constipation. Heartburn can becaused by the softening of the muscular valvebetween the esophagus and the stomach so thatpartially digested, acidic food may leak back upinto the esophagus, causing a burning sensation inthe chest. Heartburn and constipation are gener-ally experienced in the later stages of pregnancy.

Susun Weed140 and Rosemary Gladstar145

emphasize eating small meals frequently, chewingfood carefully, and avoiding acid-causing andgreasy foods. Both recommend papaya (especiallyraw, but also in tablets and papaya leaf ) for theenzymes, as well as fennel and anise seeds; Glad-star also recommends cumin and dill seeds inaddition to the fennel and anise, suggesting anold-fashioned remedy for digestive disturbances:combine these four seeds and chew them beforeand after meals.

Be aware that coffee and cigarettes increaseheartburn by irritating the stomach, and remem-ber that whole grains, fresh fruits, and vegetablescombined with nonstressful exercise are the bestsolutions to constipation.

Varicose Veins

Varicose veins can occur in the legs or in the analor vulvar areas in pregnancy, due to hormonalsoftening of the muscular walls of the veins com-bined with the extra weight of pregnancy. Simpleyoga and other nonstressful exercise can help byimproving circulation from the lower body up tothe trunk; it is also good to get your weight offyour legs and put your feet up whenever possible.

A lack of nutritional elements in the diet,especially vitamin C, rutin, and other bioflavo-noids, combined with the extra stress on the cir-culatory system, can cause the fragile capillariesto break. A tendency toward varicose veins andhemorrhoids may also be inherited. Eat foodshigh in vitamin C and bioflavonoids, such asbuckwheat, nettles, rose hips, oranges, lemons,grapefruit, peppers, whole grains, hibiscus flow-ers, and the white rinds of organically growncitrus fruits; also include garlic, onion, chives,and leeks. These help maintain elasticity in theveins and capillaries. Lecithin, vitamin E, andrutin supplements are also recommended for pre-venting and repairing varicose veins.

Backache

It may not be possible to find an herb that is safeduring pregnancy that is also a good treatment for backache. Gentle yoga stretches; walking andswimming; chiropractic adjustments; physicaltherapy; sleeping with pillows to support the legs,back, and belly; wearing flat heels; and gettingplenty of minerals can all help in easing backache.

Bladder Infections

Blood volume increases 50 percent during preg-nancy, causing the kidneys to work harder andmaking the urinary system more vulnerable tostress and infection. Especially in the lasttrimester, burning or frequent urination orcramping in the abdomen may indicate a bladderinfection. Many herbs and nutrients can be usedto treat urinary tract infections, although not allof them are safe while pregnant.


Uva ursi is safe and is one of the most effec-tive herbs to prevent recurrent bladder infectionswhile also having antimicrobial activity in acuteinfections. Used in leaf form, place the leaf in atea ball and place in water that has already cometo a boil. Let it steep for five minutes, then drinkone cup every three hours for two days, then onecup three times a day for an additional week.

Vitamin C and unsweetened cranberry juicecan be used to acidify the urine and fight theinfection by interfering with the ability of thebacteria to stick to the bladder wall. Take 1,000mg of vitamin C three to four times per day for up to one week. Eight to sixteen ounces ofunsweetened cranberry juice per day is recom-mended. Mannose, the simple sugar contained incranberries, is a very effective and safe treatmentduring pregnancy. D-mannose adheres to thebladder epithelium and interferes with the abilityof infection-causing bacteria such as E. coli toadhere to the bladder wall.146

Lactobacillus supplements are also safe inpregnancy. From the studies that are available,probiotics appear to be beneficial for preventingrecurrent bladder infections in women. SeeChapter 5 for further directions on treating blad-der infections.


Nothing would be better in the realm of child-birth than for peace to be made between thosewho endorse modern obstetrics and hospitalbirths and those who applaud the naturalness of pregnancy and labor and prefer home birthwhen uncomplicated. There is merit in bothapproaches. Like all options in health care, onlythe pregnant woman can decide which is rightfor her—but with better cooperation betweenthe groups, her choice would be easier.

When childbirth goes normally—which ismost of the time—it can be safely managed athome. Unfortunately, we have no way of know-ing if a low-risk birth will go awry, and home

births are not equipped to handle complicationssuch as profound fetal distress, prolapsed umbil-ical cords, and maternal hemorrhage. Moreover,these complications can be significantly wors-ened during emergency transport to the hospital.

Modern obstetrics was born after a timewhen all births occurred at home, no matterwhat, and maternal mortality was substantiallyhigher than now. Forceps—we now groan attheir mention—were a lifesaving invention formothers as well as their babies, because prior totheir use, both mother and baby sometimes diedof the “obstructed” pelvis, often after laboring fordays. Life without cesarean sections was also lifewith many more maternal deaths.

Where is the happy medium? How can weavail ourselves of the truly lifesaving aspects ofobstetrics and eliminate the excess? The bestanswer I have is to be as educated as possibleabout options and be open to the obstetrical real-ity that things do not always go as we hope andplan. Be flexible. If possible, have a relationshipwith a conventional provider that you see at leastonce during your pregnancy.

One good option is to consider hospital-based midwife services. The midwives are verycommitted to natural childbirth and, unlike thetypical hospital birth, are present and supportivethroughout your whole labor. They work with a backup physician, someone presumably of their choosing. Even if the physician is called, themidwife will continue to attend you as her pri-mary patient and advocate for your wishes. TheC-section rates for midwife-assisted births arelow, their respect for the birthing process high. Ifyou choose an out-of-hospital birth, be awarethat the main reasons women eventually come tothe hospital are for prolonged labor and/orpain—not emergencies. Have a plan worked outfor what you will do in that situation.

Conventional obstetrics need not be as off-putting as many assume. There are providers whosupport a woman’s wish to have her birth natu-rally. They also support women who choose to


have their labor pains assuaged. Women areoffered the choice of intravenous medication orepidural medication. When an epidural is givenat no sooner than 4 to 5 cm dilation in a womandelivering her first child, the cesarean section rateis not increased over the rate of those womenwho go without epidural anesthesia.

Cesarean section rates vary among physiciansand institutions; it is reasonable to ask a providerfor numbers. Around 15 percent is acceptable,although some will be as high as 20 percent; itdepends somewhat on how “high-risk” the prac-tice is. Moms or babies at higher risk may need tobe delivered more urgently, and therefore moreoften by C-section. Most doctors do not take thedecision to operate lightly, and your doctorshould always discuss the issues with you clearly.Nothing will ever happen without your informedconsent. You never need to have the drug Pitocinto stimulate labor or any other adjunct to laborunless you are in agreement. I encourage womento make their needs and wishes known in allaspects of their health care. That is the only waythe system can become responsive to the evolvingand varied needs of women.


Healthy women with normal pregnancies havethe lowest risk of complications, so medical man-agement choices are largely personal. Most non-M.D. providers use a list of criteria to determinethe low-risk or high-risk status of a pregnantwoman. The criteria should address the mother’sblood pressure, the risk of bleeding, and the lie orposition of the baby in the uterus, as explained inthe following sections.

Blood Pressure

Hypertensive disorders are the most commondisorder of pregnancy, affecting as many as 5 to10 percent of pregnant women.147 One of themain reasons practitioners see pregnant women

so often is to check their blood pressure. Mostwomen’s blood pressures goes way down in preg-nancy. Women with chronic hypertension thatdoes not stabilize at a safe level during pregnancyhave a higher risk of smaller, more at-risk babies.The women themselves are at risk of developingthe complications of hypertension, such as renaldisease. Labor is sometimes induced at term—38 weeks or so—to lighten the load on motherand baby.

Preeclampsia is a different hypertensive disor-der of pregnancy. It is most often a mild disease,characterized by the development of hyperten-sion toward the end of pregnancy. At its worst, itcan cause seizures or eclampsia and significanthematological abnormalities, including loss ofthe ability to clot blood. Kidney failure canoccur. Usually none of these things happen, butbecause the severity of disease does not predictwhich women will have seizures, women withpreeclampsia require protection against this riskwith magnesium sulfate that is given duringlabor and for 24 hours afterward.

Mild forms of preeclampsia are treated withbedrest. Severe forms are treated with bedrest inthe hospital. All efforts are made to avoid deliv-ering babies very prematurely. However, whenmaternal health is significantly compromised,this measure may need to be taken. When severe,there is no cure for this disorder but delivery. It isthought to be caused when the mother’s immunesystem is intolerant of the fetus’s foreign geneticmakeup, and thus it is extremely rare to have asecond severe case in subsequent pregnancieswith the same partner.

Bleeding

Bleeding is never normal in pregnancy. Althoughit doesn’t necessarily indicate a serious problem,it must be assumed to do so until proven other-wise. Placental abruption is a disorder in whichthe placenta pulls away from the uterus prema-turely, causing bleeding and contractions thatcan be life threatening to both the woman and


the fetus. Because the placenta is so large, a lotcan pull away before things are hugely compro-mised, but an evaluation is in order.

Placenta previa—in which the placentacovers the opening to the cervical canal—canalso cause significant hemorrhage and is classi-cally heralded by a small, otherwise insignificant“sentinel bleed.” Ultrasound can diagnose thiseasily. No pregnant woman should have a vaginalexam in the third trimester without first usingultrasound to locate the placenta. Digital explo-ration can cause significant blood loss in the caseof placenta previa.

Abnormal Lie

Many hospitals will support the vaginal birth ofa healthy frank breech infant (butt first).Footling breech—with the feet first—is unsafevaginally, because the feet can come downthrough the partially dilated cervix—as can thecord—before the entire infant will fit. An alter-native to delivering an infant in the frank breechposition is to rotate the fetus, or rather coax thefetus to rotate, from outside, which is successful

about half the time. Neither of these proceduresshould be undertaken at home.

If the fetus measures significantly large orsmall at any point, this should prompt at least anultrasound. Fetal abnormalities associated withpoor growth or too much or too little fluid canpresent this way, and these are best prepared forin advance of delivery. Size discrepancy is often assimple as an error in dating, but figuring out theright due date is still very helpful.

The pregnancies of women with any majorunderlying health problem—such as diabetes orheart or respiratory disorders significant enoughto require ongoing surveillance in the nonpreg-nant state—should be managed with input froma licensed provider. So should those of womenwith kidney disease or autoimmune disorderslike lupus or rheumatoid arthritis. All of theseconditions can make a pregnancy much riskierfor both mother and child. Ultrasound can beinvaluable in assessing fetal growth and well-being. Ongoing surveillance of the pregnancycan alert the woman to any medical problems asearly as possible.


301

OVERVIEW

When finally we understand premenstrual syn-drome (PMS), we will have gone a long waytoward understanding the interplay between thecultural, physiologic, and emotional factors thatregularly affect women’s lives during the premen-struum. A huge piece of work will have beendone toward improving women’s health.

Dr. Maria Gurevich has written, “The persist-ence of PMS as a medical category despite theinconclusiveness of the research, suggests thatPMS is not simply a biomedical entity . . . it is alsoa complex, ideologically and culturally constructedcategory . . . predicated on a number of unarticu-lated, well-entrenched beliefs about the nature ofscience, biology, health and femaleness.”1

Maintaining good health and attitude throughall phases of the menstrual cycle is just not assimple as correcting female physiology gone awrybut also involves on some level transforming ourcultural image of women’s reproductive health,specifically menstruation, from negative (the“curse”) to positive.

However far-reaching these ideals, what we areafter is practical help for the woman who sufferspremenstrually. While precisely defining PMSremains scientifically challenging, any woman cantell you what it is, and a great many will tell youthat they have it. Defining terms carefully helps toextract “pure” PMS from an assortment of over-lapping conditions.

Eighty percent of women experience premen-strual emotional or physical changes, whereasonly about 20 to 40 percent of these women havedifficulties as a result. A much smaller number,about 2.5 to 5 percent,2 feel these changes have asignificantly negative impact on their lives to thepoint where work, relationships, or home life are

jeopardized. Most women who have symptomsdo not seek medical care but instead self-treat,making this an ideal arena for natural self-care.

Some 150 symptoms have been ascribed toPMS—most commonly feelings of anxiousness(premenstrual tension was the first name given to this syndrome), irritability, and anger ormoods vacillating unpredictably among thethree. Some women feel predominantly sad orself-deprecating, others simply fatigued andlethargic. Physical changes include bloating,breast tenderness, food cravings, headache, andgastric upset. No particular assortment of symp-toms is diagnostic; it is the regular recurrence of symptoms on a monthly basis, just before the menstrual period, that matters. Symptomsusually last a few days to a week before menses,sometimes two weeks, beginning at midcyclewith ovulation and lasting until the menses startsor into the first few days of the flow.

As important as the regular timing of thearrival of these symptoms is the predictable reliefand complete resolution experienced with theonset of menses or within one to two days of themenstrual flow beginning. PMS symptoms,whatever they may be for a particular woman, goaway completely just as regularly as they arrive.Most who study this entity require that a womanbe able to predict in advance for at least a coupleof cycles when symptoms will come and whenthey will leave to warrant a diagnosis of PMS.3

It is important to check for other possiblesources of the symptoms that might indicate med-ical conditions a woman may suffer from evenmore dramatically in the premenstruum. Womenwho are afflicted with asthma, migraines, epilepsy,herpes, or disordered eating,4 for example, oftennote a cyclic worsening, a premenstrual magnifica-

17P R E M E N S T R U A LS Y N D R O M E

C H A P T E R



tion, if you will, but this is not considered to bePMS. In addition, obesity has been found to be anindependent risk factor for PMS, and those with abody mass index of greater than 30 had a threefoldincrease in risk for PMS.5 Treatment for the under-lying condition in these cases is more likely to eliminate the premenstrual aggravation than istreatment aimed solely at PMS.

Among women self-presenting to PMS clin-ics for medical care, fully 75 percent had anotherdiagnosis that contributed significantly to theirsymptoms—major depressive or other mood dis-orders being most prominent.6 About 10 percenthad early menopausal symptoms, 10 percentwere affected by hormonal contraceptives, andabout 5 percent each were found to have eatingdisorders or substance abuse issues predominat-ing. Anyone who considers her PMS to be signif-icantly bothersome might be wise to check withher practitioner should her efforts with self-carefail. There may be other, more effective treat-ments, either for the PMS itself or for an under-lying condition.

Most women feel different emotionally andphysically during the premenstruum. The termmolimina refers to those changes women noticethat let them know their menses is approaching:appetite changes, swelling, or menstrual-likecramps. A recurrent pattern of mild but noticeablechanges provides evidence that cycles are ovulatory.Some women enjoy positive changes: enhancedcreativity, heightened sexual desire, intellectualclarity, and feelings of happiness and well-being.7

It is difficult to identify cause in a conditionthat overlaps so broadly with normal physiology,affects so many, and has such a wide array ofsymptoms. Many theories have been exploredand none found completely satisfying. Mostlikely this is because there is such a complexinteraction of factors both physiologic and social.While absolute levels of estrogen and proges-terone are no different in PMS sufferers, weknow that in women in whom both hormonesare pharmaceutically blocked, PMS diminishes

by 75 percent.3 Blocking progesterone only usingRu-486 did not have this effect, nor did itworsen symptoms.8 It is likely that ovarian hor-mones affect the neurotransmitter, neuroen-docrine, and circadian systems that influencemood and behavior differently in each of us. Asresearch continues, we are learning more aboutthe role of neurotransmitters, neurophysiology,and electrical conduction in the brain in thedevelopment, severity, and treatment of PMS.

It is interesting to look at the work done onserotonin to appreciate the role our social envi-ronment may have on PMS. Anita Rapkin, M.D.,studied serotonin levels in women with and with-out PMS and found that serotonin levels fell afterovulation in women with PMS.9 Those withoutPMS had much higher levels of serotonin duringthe last half of the menstrual cycle. Abnormalserotonin metabolism has long been linked todepression. Elevating serotonin levels is how thepopular antidepressant Prozac works.

There is evidence that estrogen levels affectthe serotonin system. More interesting, studies inanimals and humans have demonstrated howsocial interactions in groups can affect our sero-tonin levels. Dominant animals in groups havehigher levels of serotonin, which then fall if theyare removed from their prominent position.Serotonin levels rise in the animals that replacethem in dominance.9 Rapkin postulates thatwomen without PMS may offset ovulation-induced susceptibility to low serotonin and isola-tion behavior through interacting more with“desirable others.” In other words, women ableto manipulate their social environment success-fully are less susceptible to the mood conse-quences of low serotonin.

One begins to see how our culture’s historicalattitude of embarrassment or distaste around men-struation might contribute to susceptible women’sneurotransmitters being adversely affected at aphysiologically critical time, resulting in moodswings, anger, and irritability. This is congruentwith the views of feminist writers who criticize the

303P R E M E N S T R U A L S Y N D R O M E

medicalization of PMS symptoms as disease, argu-ing that medicine has tended to pathologizebehaviors that do not conform to the unnaturalyet pervasive female stereotype. Certainly, noother named condition in women is so commonand so little understood and yet contains so manysignificant pieces to our lives.

In the last few years, premenstrual dysphoricdisorder (PMDD) has been proposed by some tobe a distinct entity clinically different from PMS.Many consider it a new psychiatric disorder.Other experts believe that PMDD is simplysevere PMS with more impairment of normal lifefunctions. However it is classified, PMDD ismore severe than PMS, and the diagnostic crite-ria for this severity are met by only 3 to 8 percent

of women. PMDD includes a minimum of fivespecific symptoms that occur during the latterpart of the luteal phase of the menstrual cycle,right before the onset of menses.10

According to the Diagnostic and StatisticalManual of Mental Disorders (DSM-IV), a womanwould be diagnosed with PMDD if she experi-enced five or more of the following symptomsduring most of the week before her menses, theyinterfere significantly with daily life and relation-ships, and they have occurred in the last year. Atleast one of the first four symptoms must also bepresent to lead to a diagnosis of PMDD.

1. Significantly depressed mood, hopeless-ness, self-defeating thoughts

2. Significant anxiety, tension, feeling irritable, uptight

3. Sudden mood changes of sadness, weepiness, or easily feeling rejected

4. Anger or irritability or increased conflictwith others

5. Lack of motivation for usual activities6. Difficulty concentrating7. Lethargy, easily fatigued, low energy8. Changes in appetite, overeating, food

cravings9. Hypersomnia or insomnia

10. Overwhelmed, feeling out of control11. Additional physical symptoms: breast

tenderness, swelling, headaches, joint ormuscle pain, bloating, weight gain

KEY CONCEPTS

• PMS is characterized by cyclic symptoms duringthe second half of the menstrual cycle with asymptom-free phase during the first half of thecycle.

• Premenstrual magnification may manifest as anincrease in chronic symptoms during the secondhalf of the cycle.

• Premenstrual dysphoric disorder (PMDD) isthought by some to be distinct from PMS, andby others to be a more severe form of PMS. Thehallmarks are when a woman experiences 5 ormore of 11 key symptoms.

• The best evaluation and determination of PMS isa symptom diary relating symptoms to the men-strual cycle.

• Testing should be limited but should rule outthyroid problems and blood sugar problems inparticular.

• Medical evaluation should be done to revealconcurrent disorders of depression and anxiety.

• Treatment should provide symptom relief whilealso addressing any need for lifestyle changesand treating problems in the neuroendocrineconnections (central nervous system brain chem-istry as it is affected by estrogen and proges-terone in particular).

PREVENTION

• A whole foods diet with minimal intake of sugar,refined carbohydrates, dairy products, caffeine,and saturated fats

• Increase dietary fiber including whole grains• Increase essential fatty acids from nuts, seeds,

and fish• Stress management• Regular aerobic exercise• Weight loss


The specific cause of PMDD has not been deter-mined, but the dysregulation of serotonin ap-pears to be a key feature.11


Historically, conventional mainstream medicinehas not been able to offer women a known causefor PMS, nor has it been able to offer a manage-ment approach short of pharmaceuticals with asmany side effects as relief. Fortunately, newresearch has led to a better understanding ofPMS and to new and more successful conven-tional and natural treatments. Self-care with nat-ural therapies is the dominant method womenuse to manage PMS. Women have clearly takenthis familiar monthly problem into their ownhands and more often than not have determinedwhat works for them. Fortunately, PMS is a con-dition for which inadequate self-treatment yieldsdissatisfaction rather than dangerous side effectsor progression of a serious disease.

In an attempt to offer women rationales forviable natural treatments for the relief of PMS,many theories have been offered. While comfort-ing in their attempts to analyze the syndrome,these theories are poorly confirmed in researchstudies yet are still used as a basis for many natu-ral therapies. Popular models such as hormonal-based therapeutics, including elevated estrogenlevels and reduced progesterone levels; elevatedprolactin; and increased aldosterone are not ade-quately confirmed in research. Even though agiven therapy may work for a number of women,its mechanism may still elude our true under-standing. These models are tidy and convenientfor a logical train of thought, but, due to theirlimited ability to help many women, they distractus from potentially having a more accurate under-standing and more effective treatment options.

Clinically, I have not usually found it usefulto use classification systems commonly used byalternative practitioners like PMS-A (anxiety),PMS-C (carbohydrate craving), PMS-D (depres-

sion), or PMS-H (hyperhydration). Yes, womenmay have one or more of these symptoms char-acterized in the particular classification, buttreating women for the correlating hormonalimbalance has not typically been productive inmy experience. In the more difficult cases, it isoften necessary to expand one’s thinking, how-ever, and it may occasionally be helpful toexplore some of these theories.

Another basic foundation for many alterna-tive practitioners in treating PMS is the conceptof the liver’s role in the detoxification process. Ifthe liver function is compromised, then estrogenmetabolism is inadequate, leading to excess estro-gen levels and what is often described as estrogendominance. A “sluggish liver” is then addressedwith various dietary, nutrient, and herbal inter-ventions. It is important to understand that thisis a theory with much speculation and minimalscientific support in its connection with PMS.One cannot argue, however, about the centralrole of the liver and its varied metabolic processeswith subsequent influence on the biochemistryof hormone and enzymatic pathways. There mayin fact be a role for liver function in PMS, butwhat that is remains unknown. On the otherhand, improving liver function pays off in otherways, like exercise does, with many positivehealth benefits to numerous body systems.

Numerous natural alternative therapies areavailable, including lifestyle changes, vitamin andmineral supplementation, herbal medicines, andnatural hormones. Many of these have demon-strated their effectiveness in standard scientificstudies. But at least an equal number have eithershown no effect or an effect that was not signifi-cantly greater than the placebo effect. Herein liesone of the curiosities of medicine, elegantly por-trayed with PMS: why do conventional scientificstudies fail to demonstrate success with many ofthese natural therapies that women consistentlyrely on for successful monthly treatments?

Perhaps the answer is as simple as that statis-tically significant is not the same as clinically


relevant: what works for one person is differentthan what works for another. We are truly indi-viduals with our own unique physiology, stres-sors, and psychological makeup. Double-blind,placebo-controlled scientific studies attempt tofind what works for as many people as possible,not what works best for an individual.

Even in studies where the placebo response isgiven credit, perhaps the belief that the mind canheal the body is the real explanation. The inter-action between neurotransmitters, neurophysiol-ogy, the body’s steroids, circadian systems, mood,and behavior plus plants and nutrients fromnature may remain scientifically elusive, but, tothe credit of women, we have instinctually comeupon safe and effective natural solutions.

One of the significant benefits of treating PMSnaturally is that it serves as a touchstone to moti-vate women to make lifestyle changes that have apositive cascade effect on their general health.

Nutrition

Women who have PMS typically have dietaryhabits that are worse than the standard Americandiet. In a nutritional analysis published in 1983,Guy Abraham reported that PMS patients con-sumed 62 percent more refined carbohydratesthan women who did not have PMS, 275 percentmore refined sugar, 79 percent more dairy prod-ucts, 78 percent more sodium, 53 percent lessiron, 77 percent less manganese, and 52 percentless zinc.12 A diet higher in dairy products can alsocontribute to PMS symptoms such as anxiety, irri-tability, and nervous tension. A dietary survey of39 patients with PMS and 14 women with noPMS found that the women with PMS consumedfivefold more dairy products and threefold morerefined sugar than those women without PMS.13

Dairy products and calcium interfere with magne-sium absorption, and refined sugar increases theurinary excretion of magnesium.14

Further data confirm these findings by showing that women with PMS have increasedconsumption of dietary fat, carbohydrates, and

simple sugars and decreased consumption of pro-tein. This study also showed that PMS sufferershad a higher number of “eating incidences” thanwomen who did not meet the criteria for PMS.15

These increases in eating incidence and carbohy-drate craving in general during PMS may be due in part to a decrease in serotonin during theluteal phase in PMS sufferers, and it follows thatserotonergic treatments like SSRIs or 5HTP maybe helpful in controlling not only mood changesduring this period but also food cravings.16

It is these same food cravings that often serveto worsen PMS symptoms, leading to a viciouscycle of poor dietary choices and mood distur-bance. It has been suggested, however, thatingesting high amounts of carbohydrates may bea form of “self-medication” in that it leads to atransient increase in tryptophan, a precursor toserotonin, and a resultant improvement in moodand energy.17 Choosing high-quality carbohy-drates (including whole grains such as oatmeal,brown rice, barley, rye, and whole wheat)throughout the luteal phase may help decreasePMS mood symptoms.

Another nutritional factor in PMS is theeffect of refined sugars on the retention ofsodium. After a large intake of sugar, insulinincreases quickly, which causes sodium and waterretention. Symptoms such as swelling in thehands and feet, abdominal bloating, and breastengorgement and tenderness result. Complexcarbohydrates are preferred over simple sugars(white sugar, white flour, white rice, etc.) becausethey stimulate insulin release much more slowlyand in a more sustained manner, thereby pre-venting many of these water-retention symp-toms. In fact, one study found that consumptionof a low-fat, high complex carbohydrate diet alle-viated premenstrual breast tenderness.18 Manyother symptoms of PMS may be exacerbated bythe intake of sugary foods and beverages.19

Excessive and incorrect prostaglandin (PG)synthesis has been implicated in the pathogenesisof PMS, and a deficiency of prostaglandin E1


(PgE1) in the central nervous system has beenproposed to be involved in PMS.20 Many nutri-ents are important for the synthesis of PgE1.These include magnesium, linoleic acid (anessential fatty acid), vitamin B6, zinc, vitamin C,and vitamin B3. On the other hand, arachidonicacid is a precursor to PgE2, which has antagonis-tic effects with regard to PgE1. Think of PgE1 asthe good guy and PgE2 as the bad guy. Vegetableoils are rich sources of linoleic acid, and animalfats are the main dietary sources of arachidonicacid; therefore, patients with PMS would be wiseto decrease their consumption of animal fats andincrease their consumption of polyunsaturatedvegetable oils so that they have more of the goodguy, PgE1. A diet high in the other nutrientsmentioned would also promote the synthesis ofPgE1. We will discuss these more in the nutri-tional supplement section.

A recent study showed that an increase in C-reactive protein, a marker of inflammation, was positively correlated with the severity of both physical and psychological symptoms of PMS,21 providing more support for the use of anti-inflammatory dietary choices for PMS sufferers.Foods that can stimulate inflammatory pathwaysinclude, among others, sugar, poultry, eggs, cheese,milk, white flour, white rice, and partially hydro-genated oils. Foods that can reduce inflammationinclude fresh fruits and vegetables, fish, grass-fedbeef, nuts, seeds, curry powder, garlic, and onions.

Limiting the dietary intake of salt can behelpful to some women. Table salt enhances theresponse to the ingestion of glucose, conse-quently increasing the insulin response. As men-tioned earlier, an increase in insulin causesswelling through water retention.

Many women with breast symptoms in theirpremenstrual phase benefit from avoiding caf-feine. Even though scientific studies are contro-versial on this subject, the practical results speakfor themselves. Restricting the intake of coffee(both caffeinated and decaffeinated), black tea,chocolate, and caffeine-containing soft drinks

will especially benefit those with fluid-retentionsymptoms. (See Chapter 7 on fibrocystic breastsfor more information about the detrimentaleffects of caffeine.)

It is estimated that there are two million alco-holic women in the reproductive age group inthe United States.22 Sixty-seven percent of thesewomen relate their drinking to their menstrualcycles, and drinking bouts occur usually duringthe premenstrual phase.23 Alcohol may also playa role in the reactive hypoglycemia of PMS aswell as worsening a variety of other PMS-relatedsymptoms.24

Soy isoflavones may be beneficial for PMS inaddition to the other women’s health conditionsthey seem to positively affect. A recent study sug-gests that increased consumption of dietary soymay be related to a reduction in PMS symp-toms.25 Another study compared the effect ofisolated soy protein containing 68 mg/day soyisoflavones with a placebo in a double-blind fash-ion and found that the soy protein was effectiveat reducing headache, breast tenderness, cramps,and edema after two cycles of treatment.26


It has been hypothesized that women with PMSare deficient in certain nutrients. Nutritionalprofiles and biochemical and hematological eval-uations in 11 women with PMS showed thatthey did indeed have various nutritional deficien-cies.27 Other biochemical investigations havefound no evidence that premenstrual symptomsare caused by either absolute or relative nutri-tional deficiencies.28, 29


• Reduce the intake of alcohol, caffeine, salt,sugar, refined carbohydrates, and dairy products.

• Increase the intake of fruits, vegetables,legumes, nuts, seeds, fish, soy, and healthyoils such as fish, flaxseed, and olive oils.


Nutritional supplements are widely used inthe treatment of PMS despite the inconsistentevidence to support their use. Again we have adiscrepancy between scientific information andwhat a significant number of women report. Apossible explanation for this discrepancy mightbe that vitamin and mineral levels in the periph-eral blood (which is measured in a laboratory) donot parallel the levels in the central nervoussystem (CNS). Researchers J. C. Chuong and E. B. Dawson state, “It is possible that thebioavailability of vitamins and minerals in theCNS, which is related to the activities of severalneurotransmitters (including serotonin), couldchange during the luteal phase in some patientswith PMS. As a result, premenstrual symptomsoccur. However, these changes in vitamin andmineral levels in the CNS may not show up in theperipheral blood levels.”30

Positive results seen in some studies withnutritional supplementation most likely repre-sent a pharmacological response to therapeuticdoses of vitamins or minerals rather than revers-ing an underlying deficiency.

Multiple vitamin and mineral supplementsmay be helpful for women with PMS. A studywas done in 1985 of Optivite, a rather typicalmultiple vitamin/mineral supplement. The quan-tities and proportions of vitamins and minerals in this supplement either met or exceeded the rec-ommended daily allowances except for calciumand vitamin D. In a double-blind, placebo-controlled crossover study, 16 of 23 subjectsreported feeling better during the cycles in whichthey took the supplement, and 7 reported feelingbetter during the placebo cycles.31 Theseresearchers also classified the patients into fourdifferent subgroups (PMS-A, PMS-C, PMS-D,PMS-H) and found that only two of the four sub-groups responded to this particular supplement.

A second study on the same product wasdone in 199132 to assess the effectiveness of avitamin/mineral supplement in controllingsymptoms of premenstrual syndrome. This

double-blind, randomized study of 44 womendivided women with PMS into four subgroupsdepending on their symptoms. Subjects wererandomly assigned to receive either placebo or 6or 12 tablets of the supplement a day for threemenstrual cycles. All subjects had significant dif-ferences in severity of symptoms between the fol-licular and luteal phase of the control cycle. TwoPMS subgroups especially improved: PMS-A(nervous tension, mood swings, irritability, anxi-ety) and PMS-C (headaches, craving for sweets,increased appetite, heart pounding, fatigue).Supplementation with six tablets of Optivitedaily was associated with significant reduction inall symptom categories, including those withPMS-D (depression, insomnia, forgetfulness,crying, and confusion). Those with PMS-H (premenstrual weight gain, breast tenderness,abdominal bloating, and swelling of the armsand legs) did not receive any benefit. If 12 tabletswere taken, then there were significant reduc-tions of symptoms in all groups.

When selecting a multiple vitamin and min-eral supplement, I recommend one that has beenformulated especially for women, as these takeinto account the special nutritional needs ofwomen.

Vitamin B6. A rational basis for the use ofvitamin B6 (pyridoxine) in the treatment of PMSwas first indicated by the work of Adams and hiscolleagues in 1973,33 although it had been pre-scribed since the 1940s. They reported successfultreatment with vitamin B6 of patients complain-ing of depression associated with oral contracep-tion. Since that time there have been over onedozen studies on vitamin B6 and PMS. Some ofthese have shown no effect from vitamin B6, butmost of the studies have shown that there was asubstantial and broad effect on the whole rangeof PMS symptoms. An overview of these studieshas been published in the British Journal ofObstetrics and Gynaecology.34 The studies haveused anywhere from 50 to 500 mg per day.


Vitamin B6 is thought to be unique in its ability to increase the synthesis of several neuro-transmitters in the brain. These neurotransmittersinclude serotonin, dopamine, norepinephrine,epinephrine, taurine, and histamine.35 Lowerlevels of brain neurotransmitters such as serotoninand dopamine have been implicated in the etiol-ogy of PMS.36 In fact, a double-blind crossovertrial demonstrated that 50 mg of B6 per day waseffective at decreasing premenstrual depression,fatigue, and irritability.37 In addition, anotherstudy showed a synergistic effect of 50 mg of B6

combined with 200 mg of magnesium in reducingpremenstrual anxiety.38

Vitamin B6 supplementation is generally considered safe in dosages of 50 to 100 mg daily.When using dosages greater than 50 mg, it may be important to divide it into 50 mg dosagesthroughout the day to assure appropriate utiliza-tion by the liver. One should not exceed 200 mgtotal in one day in order to assure safety. Chronicintake of dosages greater than 500 mg per day canbe toxic if taken daily for many months or years.There are also a few rare reports of toxicity atchronic long-term dosages of 150 mg per day.39

Vitamin B6


Vitamin D. We don’t normally think of vita-min D as a treatment for PMS. Recent researchhas shown, however, that increased intake of vita-min D in both dietary and supplement forms isinversely related to PMS symptoms.40 A combi-nation of vitamin D and calcium decreased thefrequency and severity of menstrual migrainesand other PMS symptoms.41

Vitamin D

Age 19–50: 200 IU per dayTolerable upper limit: 2,000 IU

Vitamin E. Vitamin E is probably not a bigplayer in PMS relief, although some studies

have demonstrated a reduction in premenstrualnervous tension, headache, fatigue, depression,insomnia, and breast tenderness.12, 42 Aberrantprostaglandin (PG) synthesis has been implicatedin PMS, and a deficiency of prostaglandin E1(PgE1) has been proposed to be involved in PMSas well as an increase in another prostaglandincalled PgF2-alpha. It has been hypothesized thatvitamin E inhibits the negative prostaglandin(PgF2) and increases the PgE1. Women continueto use vitamin E to relieve the symptoms of breasttenderness before the period. Despite science thatdoes not confirm a statistically significant benefit,vitamin E remains an important part of self-care.This is discussed more in Chapter 7.

Vitamin E


Essential Fatty Acids. The main strategy ofsupplementing with essential fatty acids is anattempt to raise the body’s own formation ofPgE1. The most popular method of doing so hasbeen to supplement with evening primrose oil(EPO) products in order to supply increasedlevels of gamma linolenic acid. Although thereare several studies that show positive results,some of the studies did not include a placebogroup, and other studies did not show a statisti-cally significant difference between the treatmentgroup and the placebo group.43–45

Four double-blind, crossover, controlled trialsof EPO have demonstrated a significant effectover the placebo group.46–49 One of these studiesused three grams of EPO per day; the others usedfour grams per day. EPO has been shown to bemost effective for relieving clumsiness and head-aches, although all symptoms, including depres-sion, irritability, bloating, and breast tenderness,showed a marked improvement. Other sources ofoils that contain gamma linolenic acid (GLA)and raise PgE1 levels include borage oil, blackcurrant oil, and canola oil. Hemp oil contains avery small amount of GLA.


Another study looked at krill oil and its effec-tiveness at reducing symptoms of PMS. Krill oil isderived from plankton and is high in omega-3 fattyacids, bioflavonoids, and vitamins E and A. Thisstudy looked at two 1-gram capsules of krill oilversus fish oil in the management of PMS symp-toms and found it to be comparable at decreasingswelling, bloating, and weight gain and superior tofish oil in decreasing analgesic use, breast tender-ness, joint pain, dysmenorrhea, and emotionalsymptoms after 45 to 90 days of treatment.50


3–4 g per day

Krill Oil

2 g per day

Magnesium. Magnesium has shown somebeneficial effect in the treatment of PMS. Mag-nesium is depleted by changes in the female sexhormones in the luteal phase leading to a varietyof PMS symptoms, notably migraines and bloat-ing.51 One study suggests that 200 mg of magne-sium daily may reduce premenstrual fluidretention and resultant symptoms like breast dis-tension, peripheral edema, and abdominal bloat-ing after two months of treatment.52

In another study involving 32 women withPMS, 360 mg of magnesium three times dailywas given from midcycle to the onset of men-strual flow.53 In menstrual distress questionnairescores, relief of premenstrual mood fluctuationsand depression during magnesium treatment wassignificant. Although blood serum levels of mag-nesium are not found to be different betweenwomen who have PMS and women who don’t, itseems there is a significant decrease in red bloodcell magnesium levels in PMS patients.54

The mechanism of magnesium and its possiblerole in PMS are not well understood, but we doknow that magnesium is involved in essential fattyacid metabolism and B6 activity. In fact, as men-tioned in the section on vitamin B6, one study

showed a synergistic effect of 50 mg of B6 com-bined with 200 mg of magnesium in reducing pre-menstrual anxiety.38 In addition, another studysuggests that cyclical hormonal changes may causea relative deficiency state that can exacerbate symp-toms associated with PMS.55

Magnesium


Calcium. Reports have suggested that prob-lems in calcium regulation and frank calcium defi-ciency actually mimic many PMS symptoms56–58

and may underlie some of the symptoms of PMS.Therefore, dietary and supplemental forms of cal-cium may have a therapeutic benefit.40, 59

An important randomized, double-blind,placebo-controlled, multicenter clinical trial wasconducted to test this hypothesis. A group of 479women were given either 1,200 mg of calciumcarbonate or a placebo for three menstrualcycles.60 During the luteal phase of the treatmentcycle (from ovulation to menses), a significantlylower symptom complex score was observed inthe calcium group for both the second and thirdmonths. By the third month, calcium effectivelyresulted in a 48 percent reduction in total symp-tom scores from baseline compared with a 30percent reduction in the placebo group. All foursymptom factors (negative mood affect, waterretention, food cravings, and pain) were signifi-cantly reduced by the third treatment cycle.

In addition, as mentioned earlier in the nutri-tional supplement section, research suggests thata combination of vitamin D and calcium maydecrease the frequency and severity of menstrualmigraines and other PMS symptoms with onlytwo months of treatment.41

Calcium

1,200 mg per day

Tryptophan. As alluded to previously, de-creased serotonin and its precursor tryptophan


may exacerbate PMS mood changes, includingdepression, anxiety, and aggression.61, 62 In addi-tion, trials done in recent years to test the effec-tiveness of supplementation of L-tryptophan inreducing symptoms of PMS have shown promis-ing results. These studies, which used daily dosesof 6 grams for 17 days from ovulation to day 3 ofmenses led to significant reductions in moodswings, insomnia, carbohydrate craving, tension,irritability, and dysphoria.63, 64

Tryptophan

6 g per day for 17 days, from ovulation to day 3 ofmenses

Botanicals

Chaste Tree (Vitex Agnus Castus). Thesingle most important plant for the treatment ofpremenstrual syndrome is Vitex agnus castus, alsoknown as chaste tree. The fruits of chaste treecontain essential oils, irridoids, pseudoindicans,and flavonoids. The effect of chaste tree is on thehypothalamus-hypophysis axis. It increases secre-tion of luteinizing hormone (LH) and also has aneffect that favors progesterone.65–67 Chaste treehas also been substantiated in its ability to inhibitprolactin.68 Elevated prolactin levels may be afactor in PMS. Studies of chaste tree for cyclicbreast tenderness confirm its effectiveness in thisdisorder.69, 70 Chaste tree is also thought to posi-tively influence PMS symptoms by affectingopioid receptors in the brain.71

Three studies found that chaste tree reduceda variety of premenstrual symptoms after threecycles of active treatment in a large number ofwomen.72–74 An additional study looked at theeffectiveness of chaste tree versus fluoxetine(Prozac) in decreasing PMS symptoms andfound the two treatments comparable, exceptthat fluoxetine was more effective with psycho-logical symptoms and chaste tree was more effec-tive with physical symptoms.75

Older research led up to these more recent andrigorous studies. Two surveys were done covering1,542 women with premenstrual syndrome whohad been treated with a German liquid extract ofchaste tree for periods of up to 16 years. The meanduration of treatment was 166 days, and the average dose was 42 drops daily. Effectiveness asrecorded by the patients’ doctors was either verygood, good, or satisfactory in 92 percent of thecases.76 Only 2.1 percent of the women noted sideeffects during treatment, and 1.1 percent of themdiscontinued the medicine because of them.

Chaste tree has also been found to be safe foruse with most patients, but caution should be ex-ercised with those on medications that inhibitdopamine. A recent review of research found thatthe most frequent adverse events reported wereheadache, gastrointestinal disturbances, men-strual disorders, acne, itching, and rash, and noknown drug interactions were reported.77

Chaste Tree (Vitex Agnus Castus)

40 drops liquid or extract per day orCapsules of standardized extract: 175 mg per day

Ginkgo (Ginkgo Biloba). We don’t normallythink of ginkgo for PMS. But when you considerthat some PMS symptoms have to do with conges-tion, it makes sense that it might be useful. Adouble-blind, placebo-controlled study was donein 1993 to determine the effectiveness of ginkgoextract on PMS symptoms. A group of 165 womenbetween the ages of 18 and 45 who had fluid reten-tion, breast tenderness, and vascular congestionwere studied. The patients were assigned to receiveeither a ginkgo extract of 24 percent ginkgoflavonglycoside content at 80 mg twice daily or aplacebo from day 16 of their cycle to day 5 of thenext cycle. Based on symptom evaluation by both

Ginkgo (Ginkgo Biloba)

80 mg standardized extract twice daily


patient and doctor, ginkgo extract was effectiveagainst the congestive symptoms of PMS, particu-larly breast pain or tenderness.78

Saint John’s Wort (Hypericum Perforatum).Saint John’s wort has shown promise in prelimi-nary studies of its effectiveness at alleviating PMS mood dysfunction, but more research is stillneeded.79–81 In one observational pilot study,Saint-John’s-wort standardized extract was given ata dose of 300 mg three times daily.81 Nineteenwomen with PMS underwent a preliminaryscreening interview and completed a daily symp-tom rating for one cycle. After taking the Saint John’swort for two complete menstrual cycles, dailysymptoms were rated again. The degree ofimprovement in overall premenstrual syndromescores between baseline and the end of the trial was51 percent, with more than two-thirds of thesample demonstrating at least a 50 percent decreasein symptom severity. The mood subscale showedthe most improvement (57 percent), and thesymptoms with the greatest reductions in scoreswere crying (92 percent), depression (85 percent),confusion (75 percent), feeling out of control (72percent), nervous tension (71 percent), anxiety (69percent), and insomnia (69 percent).

Saint John’s Wort

300 mg 3 times daily

Additional Herbs. Many other herbs that havenot been subjected to scientific research have alsobeen used successfully by women and practitionersfor decades. These include many species of wildyam, licorice root, dong quai, black cohosh, andmore. One study on black cohosh and PMSdemonstrated that it was effective in improvinganxiety, tension, and depression.82 Currently, thereis some thought that black cohosh may act as amild serotonin reuptake inhibitor, which wouldmake it an appealing option for PMS.83

Other plants are used because of their benefitwith specific symptoms; for example, kava extract

for anxiety, dandelion leaf for water weight gain,valerian for sleep problems, and lemon balm forherpes eruptions. You will often find one or moreof these herbs in combination herbal and nutri-tional products that have been specifically formu-lated for PMS symptom relief.

Exercise

Specific exercises are conspicuously absent fromscientific studies looking at the effects of exerciseon PMS. In contrast, although mechanisms ofaction remain elusive, general regular physicalexercise has been the subject of several controlledtrials. In all of these, the results show that womenwho exercise regularly have less strong or fewerPMS symptoms.

Aerobic training (walking, jogging, swim-ming, cycling) appears more effective at reducingPMS symptoms than strength training (weightlifting).84 Frequency of exercise, but not inten-sity, relates to decreased rating of selected men-strual distress symptom clusters;85 gradualincrease in running distances correlates directlywith greater reductions in PMS symptoms.86

Regular exercisers show improvement in all PMSparameters, including concentration, affect,pain, hostility, fear, guilt, and sadness.87

Regularly exercising women report a signifi-cant decrease in anxiety following baseline relax-ation but show greater increase in anxiety duringa stress task than nonexercisers.88

Two reviews of the literature on exercise andPMS emphasize the obvious fact that controlledtrials of exercise training and PMS cannot be per-formed under double-blind conditions, makingit difficult to formulate probable mechanisms forthe observed effects of regular training on PMSsymptoms. According to L. Gannon, exercisemay reduce PMS symptoms by (1) decreasingestrogen levels, (2) improving glucose tolerance,(3) decreasing catecholamines, and (4) elevatingendorphins.89 Gannon concludes, “If PMSsymptoms are caused or exacerbated by dramatic


variations in endorphin levels, exercise may serveto prevent exaggerated elevations and abruptdeclines and, ultimately, to reduce symptoms.”

Yoga postures are another form of exercisethat appears to have benefit and may suit somewomen more. A study of 40 women was done foralmost one year to investigate the effect of yogain relieving premenstrual and menstrual prob-lems.90 The women assigned to the treatmentgroup did yoga postures and meditation. At theend of the 10 months, there were significantlylower scores on the menstrual distress question-naires for those in the yoga group compared tothose in the control group.

Progressive muscle relaxation and deepbreathing can also significantly reduce the moodsymptoms associated with PMS.91

Natural (or Bio-Identical) Progesterone

Perhaps no other PMS therapy has been thetarget of so much controversy as natural proges-terone. This has as much to do with the lack ofscientific research and agreement to support aunified theory as to the cause of PMS as it has todo with the efficacy of natural progesterone itself.Raymond Green and Katharina Dalton advanceda theory in the 1950s that PMS was caused byunopposed estrogen during the luteal phase(second half ) of the menstrual cycle. Dr. Dalton’s

original work with progesterone therapy is thehistorical root on which the use of natural pro-gesterone is based today. Research scientists, andtherefore the majority of the conventional med-ical community, ultimately did not embrace Dr.Dalton’s conclusions about the efficacy of proges-terone therapy for PMS. This was largely basedon what they thought to be inadequate scientificresearch studies, although it is also fair to specu-late that other matters of medical politics and thebusiness of medicine were at play here as well.

Natural progesterone (also called bio-identicalprogesterone) is a white crystalline powderderived from extracts of the Mexican wild yam orsoybean. It requires laboratory manufacturingprocesses and is something altogether differentthan what we know as botanical medicine. Whatmakes natural progesterone natural is not somuch the original plant material but rather thatthe progesterone molecules that result are chem-ically identical to the progesterone hormone pro-duced by a woman’s own ovaries and adrenalglands.

Confusion exists when people think that bio-identical progesterone is found in wild yam andsoybeans or that the human body can convertwild yam and soybean extracts to natural proges-terone. Neither of these is true. Further confus-ing the issue is that many people mistakenly callsynthetic progestogens or progestins proges-terone. Progestins are chemically different thanprogesterone and also chemically different thanbio-identical progesterone.

Dr. Dalton reports that she has used naturalprogesterone via injections (25 to 100 mg daily),vaginal and rectal suppositories (400 to 1,600 mgdaily), and subcutaneous pellets (500 to 1,600 mgevery 3 to 12 months) with results as good as com-plete relief of PMS symptoms in 83 percent ofwomen.92 There have been several studies thatdemonstrated a lack of efficacy of rectal and vaginal suppositories in the treatment of PMS.Sampson and Freeman found these forms of prog-esterone to be no better than placebo.93, 94


• Follow the “General Exercise Program” andexercise instructions outlined in Appendix A.

• The key words in exercising are regularity anddiversity.

• It is important to schedule exercise along withthe other vital activities of the day—meals,sleep, and rest.

• Equally important is to enjoy the exercise youchoose, remembering that best results areobtained from a combination of types of exer-cise—flexibility, stretching, strength, and car-diovascular.


Although the suppository method of deliver-ing natural progesterone for PMS has not heldup to scientific scrutiny, oral micronized naturalprogesterone has. A study by Dennerstein andcolleagues in 1985 found an overall beneficialeffect of using 300 mg per day (100 mg in themorning and 200 mg in the evening) for 10 daysof each menstrual cycle starting three days afterovulation.95 After only one month of treatment,those receiving progesterone could be clearly distinguished from those receiving placebo onmeasures of stress, anxiety, and concentration.Most other symptoms also continued to improvewith each menstrual cycle. The only premen-strual complaint not consistently improved byprogesterone was arousal. A 1993 study alsoreported successful use of progesterone in dosesof 300 mg oral micronized progesterone daily or3 cc rectal solution twice daily.96

More recently, Dr. John Lee had become themost outspoken proponent of the use of naturalprogesterone by using transdermal creams thatare applied to specified areas of the skin. Hereported significant success in his medical prac-tice and has written about it in his treatise onnatural progesterone.97

The availability of natural progesterone intransdermal creams in the retail over-the-countermarket has created perhaps the greatest confu-sion yet in the use of this valuable medicine. It isimportant for the consumer and practitioner tounderstand the difference between wild yam andsoy extracts versus natural progesterone productsderived from these extracts. Wild yam extracts donot contain natural progesterone unless they saythat natural progesterone has been added. Also,different products contain different amounts ofprogesterone. The range is as little as 2 mg perounce to more than 400 mg per ounce. The ruleis user beware and be educated. These productsall have their value, but not necessarily for thetreatment of PMS.

In my clinical practice, I largely use the trans-dermal creams that contain at least 400 mg

progesterone per ounce of cream. For severePMS symptoms that have not responded tonutritional, botanical, and lifestyle changes, andfor those whose symptoms start from a few days toone week before the menses, I recommend apply-ing one-quarter teaspoon natural progesteronecream twice daily starting at midcycle and stop-ping the day before the menses is due. For womenwhose significant symptoms begin at ovulation, Irecommend one-quarter teaspoon per day fromday 8 to day 14 (do not use during days 1 to 7while bleeding), and then one-quarter teaspoontwice daily until the menses begins, as describedabove. The best sites for rubbing in the creaminclude the palms, inner forearms, chest, andinner thighs. Also, it is best utilized when rotatingsites of application. Individual uses may varydepending on symptoms or menstrual pattern.

Since bio-identical progesterone is a hor-mone, I think it is best to seek the advice of aqualified health-care practitioner who is experi-enced with its use for those who use it long term. This assures proper usage and thereforemaximum results. Oral micronized progesteroneand some of the other delivery methods of prog-esterone are prescription items. These productsare used mainly by licensed naturopathic physi-cians but also by progressive medical doctorsand a growing number of chiropractors andacupuncturists.

Natural (Bio-Identical) Progesterone Cream

• If symptoms start from a few days to 1 weekbefore the menses, apply 1⁄4 tsp twice dailybeginning at midcycle (day 15) and stoppingapproximately day 26 or a day or two beforethe menses is due.

• If symptoms begin at ovulation, apply 1⁄4 tspper day on days 8–14 (do not use during days1–7 while bleeding), and then 1⁄4 tsp twicedaily until the menses begins.

Oral Micronized Progesterone

50–200 mg per day on days 15–26



In perhaps no other diagnostic category has theadvice of conventional physicians so overlappedwith that of their naturopathic colleagues. All aresearching! Basic lifestyle issues such as exercise,diet, nutritional supplements, and stress and moodassessment have all been studied and are always thestarting point of treatment. Probably in partbecause we had no consistently effective therapy,conventional physicians have borrowed eagerlyfrom natural medicine, and enthusiastic interest innatural progesterone occurred in the early 1980s.

The first, and most important, step in treat-ing PMS is recognizing it. The woman shouldundergo accurate assessment for other mentaland physical diseases, and then do at least threemonths of symptom charting, possibly with helpfrom her partner. Once the diagnosis of PMS ismade, then the therapy consists of the following:1. Lifestyle therapies. Nonpharmacological

therapies are more effective in less severePMS/PMDD. The first is making lifestylechanges that support the use of aerobic exerciseto maintain a normal BMI and possibly increaseendorphins that may be lacking in the lutealphase. Next are dietary modifications thatinclude having small, frequent meals; reducingintake of caffeine, sugar, alcohol, artificial sweet-eners, salt, red meat, saturated fat, and simplecarbohydrates; and increasing the intake ofcomplex carbohydrates; and foods that are richin calcium and magnesium. A general multivita-min supplement is also recommended.2. Cognitive-behavioral therapy (CBT).

Cognitive-behavioral therapy is a short-term,structured psychotherapeutic treatment thathelps emphasize the role of the patient’s currentthinking in determining behavior. The patient istaught behavioral techniques to help alter herresponse to the premenstrual symptoms. CBThelps in stress management and in teaching thewoman how to alter or cope with her lifestyle.3. Pharmacological therapies. The most

common medication recommended forPMS/PMDD of moderate to severe intensity isan SSRI. These medications can be used just onthe severe-symptom days each month. They areeffective the day they are taken, which suggeststhat SSRIs in this case are not helping byincreasing neurotransmitters. They seem towork in PMS by altering the neurophysiologyand electrical conduction in the brain. SeveralSSRIs have been used. Suggested doses are flu-oxetine (20 mg a day) or the once-weekly tabletsertraline or paroxetine controlled-release (12.5to 25.0 mg per day). The biggest problem with

Sample Treatment Plan for Premenstrual Syndrome

3-Month Plan• Reduce the intake of alcohol, caffeine, salt,

sugar, refined carbohydrates, and dairy products.

• Increase the intake of fruits, vegetables,legumes, nuts, seeds, soy, fish, and flaxseedoil.

• Exercise regularly, focusing especially on aerobic exercise.

• Take a combination nutritional/botanical PMSproduct (available at natural food stores oralternative health practitioners). It shouldinclude vitamin B6; magnesium; gammalinolenic acid from borage, evening primrose,or black currant oil; chaste tree (vitex); vitamin E; Saint John’s wort; and possiblysome traditional herbs for PMS, including dandelion leaf, dong quai, black cohosh, andwild yam. (See the Resources section for for-mulation sources.)

• Take a multiple vitamin/mineral supplement, 1 to 6 capsules per day.

• Take 1,000–1,200 mg of calcium per day.• If this plan doesn't relieve PMS after three

cycles, then use bio-identical progesteronecreams with greater than 400 mg per ounce orprescription oral micronized progesterone.


the use of these drugs is the high incidence ofside effects that can include nausea, headache,fatigue, hyperexcitability, and sexual dysfunctionas well as weight gain. The new serotonin andnorepinephrine reuptake inhibitor venlafaxine,with doses anywhere from 50 mg to 200 mg perday, was shown to have a better effect than theplacebo in reducing PMDD.

Spironolactone is an aldosterone antagonist,used as a diuretic. It has been successful in treat-ing symptoms of irritability, depressed mood,edema, breast tenderness, and food craving.

Oral contraceptives are commonly prescribedfor PMS/PMDD and have reports of as many fail-ures as successes. Probably the most significantproblem with oral contraceptives is the current reg-imen of taking them 21 days on and 7 days off. The7-day drug-free interval allows for less suppressionof ovulation. During that 7-day pill-free interval,follicle-stimulating hormone (FSH) rises, folliclesbegin to grow, and ovulation frequently occurs.Since PMS is only seen in ovulating women, thislack of ovulation suppression may be the reason for the frequent failure of OCs in PMS. There are several new studies that show that a 4-day pill-freeinterval reduces the FSH volumes by 50 percent,helps suppress the development of new follicles,and appears to significantly suppress ovulation. Ashorter hormone-free interval may thus be moreeffective in treating PMS. There is also a birth control pill that contains drospirenone, which isderived from 17 alpha-spironolactone and has antimineralocorticoid and antiandrogen effects. Ithelps prevent fluid retention, and studies haveshown excellent efficacy in symptom relief of PMS.

Uncommonly prescribed medications forPMS/PMDD are the GnRH agonists that sup-press ovulation and make women in effect tem-porarily menopausal. The use of GnRH agonistsplaces women in a low estrogenic state that func-tions like a reversible medical removal of ovaries.These agents have been shown to decrease symp-toms of severe PMS, but they cannot be used

for extended periods of time and have a highincidence of side effects. Add-back therapy withestradiol or a progestogen to reduce the sideeffects also seems to reduce the effectiveness fortreatment of PMS.

Short-acting, water-soluble sedatives such asalprazolam and lorazepam have also been usefuleither in a scheduled dosing (for example, a smalldose three times daily from cycle day 20 untilmenses) or on an as-needed basis to reduce anxi-ety and agitation.

Correction of PMS through surgical removalof the ovaries has been done and remains a veryhigh-risk, symptomatic (due to the abrupt loss ofestrogen), and expensive treatment for PMS. It isdone only in the most extreme circumstancesafter extensive consultations.


PMS is an excellent condition for self-treatmentmost of the time. Mild to moderate PMS is welladdressed by lifestyle changes and safe and effec-tive nutritional and botanical supplements mostof the time. When these measures are not effec-tive or when the symptoms are severe, a licensednaturopathic physician can readily utilize naturalprogesterone therapy, more aggressive dosing of nutritional and botanical supplements, orselected nutrients that specifically and moreassertively target serotonin and other neurotrans-mitters and neurophysiology.

Few conventional medical doctors are trainedin these therapies, although increasing numbersare integrating them into their practice. Severesymptoms of depression, headaches, breast pain,or others may require the use of pharmaceuticalintervention, although this is rarely necessary. Inthese cases, temporary use of such drugs must berecommended judiciously, while the continueduse of natural medicines is integrated into thelong-term plan. Only rarely will PMS not respondto a comprehensive natural medicine approach.


317

OVERVIEW

Sexually transmitted infections (STIs) and theircomplications continue to infect women at epi-demic rates. Each year, more than 15 millionAmerican men and women contract an STI.1

Worldwide, the estimated incidence of STIs isover 250 million cases per year. All women whoare sexually active are at risk for acquiring infec-tion and related reproductive tract problems,although heterosexual women are at substantiallyincreased risk compared to lesbian women. Gon-orrhea and chlamydial infections may produceurethritis, cervicitis, and pelvic inflammatory disease (PID) and are the two types of bacteriathat most frequently cause PID. Human papillo-mavirus (HPV) is the cause of genital warts andcervical dysplasia. Syphilis is responsible formyriad systemic and tissue abnormalities. Herpessimplex virus (HSV) infection is associated withsmall blisterlike skin eruptions and ulcerations.Scabies and pediculosis are fraught with itchingof the skin. As many as 60 percent of hepatitis Bcases are sexually transmitted. HIV infection andAIDS (the most advanced stage of HIV infection)are sexually transmitted diseases as well. Lesscommon STIs, such as lymphogranuloma vener-eum and chancroid, present as pimple-like orulcerative genital lesions.

The purpose of this chapter is to discuss someof the alternative approaches and conventionaltherapies used in the treatment of chlamydia andgonorrhea. Please refer to Chapter 20 (vaginitis),Chapter 3 (cervical dysplasia), Chapter 8 (genitalherpes), and Chapter 15 (pelvic inflammatorydisease) for further information and treatmentrecommendations regarding other conditionsthat can be transmitted through sexual contact.

Chlamydia Trachomatis

Chlamydia trachomatis infection is the mostcommon STI causing a female pelvic infection inthe United States. The infection rate is consid-ered epidemic in women and is estimated at fourmillion new cases each year. Chlamydia is evi-dent in about 20 to 40 percent of sexually activewomen in the United States.2 It can be deceptivebecause as many as 80 percent of women withthis infection do not exhibit symptoms.3 This isof particular concern, because chlamydia canprogress to an asymptomatic pelvic infectionresulting in infertility. Women between the agesof 15 and 25 are at greatest risk of chlamydia, butall heterosexually active women are at risk.4, 5 Therate of C. trachomatis pelvic infection among sex-ually active women is from 5 to 20 percent.6 Thechlamydia organism invades the columnar cellsof the cervix, invades the immune system, andcan either lie in a latent state in the cervix formonths, create asymptomatic cervical infection,or ascend to the upper genital tract, where it canalso be asymptomatic or cause infections of thefallopian tubes or uterus. When symptoms dooccur, it commonly causes urethritis, cervicitis,and PID in women. Common symptoms thatoccur include uncomfortable urination, fre-quency of urination, vaginal spotting, increaseddischarge that may be yellowish, pelvic pain, andpain or spotting with intercourse.

Due to the high incidence of chlamydia andthe high rate of asymptomatic infections, it is rec-ommended that all heterosexually active womenbetween ages 15 and 25 be screened yearly. Byscreening regularly, the incidence of PID can bereduced significantly. Chlamydia is diagnosed onphysical examination, with a smear of the dis-

18S E X U A L LY T R A N S M I T T E D I N F E C T I O N S

C H A P T E R



charge from the urethra and cervix viewed under amicroscope and with special tests and cultures ofthe same discharge. The rectum should also beexamined for a purulent discharge. The vaginaldischarge should also be tested for the presence ofbacterial vaginosis, trichomoniasis, and gonorrhea.The cervix is also examined for hypertrophy(enlargement) of the endocervical epithelium (thecells in the cervical canal), looking for intense ery-thema (redness) and friability (bleeds easily whenit is touched with a cotton-tipped applicator). Thepresence of a mucopurulent discharge from thecervix is a tip-off to a cervical infection. Thisyellow discharge is then tested for chlamydia andgonorrhea.

Being infected with chlamydia is of specialconcern for the pregnant woman because it cancause spontaneous abortion, premature ruptureof the membranes, premature labor and delivery,and postpartum endometritis (infection of theuterus). Due to the frequent asymptomaticnature of chlamydia infection, examinations ofall women suspected of having an STI duringpregnancy should include testing for chlamydiaand gonorrhea. About 60 to 70 percent ofuntreated cases in pregnant women result inneonatal infection in the eyes or lungs.2

Due to the ability of chlamydia infection tobe asymptomatic, it is a particularly problematicpelvic infection. It can ascend to the upper genital tract without detection and then causesignificant damage to the reproductive tractaffecting fertility. Lower abdominal or pelvicpain in a heterosexually active woman may be asymptom of pelvic inflammatory disease (PID),especially when it occurs with cervical inflamma-tion and vaginal and/or purulent endocervicaldischarge. Pain and tenderness on the physicalexam in addition would be enough to have aclinical diagnosis of PID and should be followedwith appropriate testing. (See Chapter 15 formore information on PID.)

Because of the number of women who havecontracted chlamydia and do not exhibit symp-

toms, many women go untreated. Unfortunately,many of these women find out later that their fal-lopian tubes have been scarred, which leads toinfertility.

Neisseria Gonorrhoeae

Neisseria gonorrhoeae is the second most commonSTI causing a female pelvic infection. In 2003,the rate of reported cases in the United States was116.2 cases per 100,000 individuals. Rates havebeen decreasing each year since 1999, and we arecurrently at our lowest reported rate. Approxi-mately 75 percent of the cases occur in women,and the highest rate is among women aged 20 to24 years.7 The highest group at risk is heterosex-ually active women aged 15 to 19.8

The southern United States has the highestrates of gonorrhea, and the rates are 20 timeshigher for African-Americans than for Cau-casians. Young women (and men) who are non-white, unmarried, less educated, and who live inurban settings are the group most commonlyaffected.9

Gonorrhea is most easily transmitted frommales to females assuming lack of condom use.Oral gonorrhea occurs in about 20 percent ofwomen who practice fellatio with males whohave an infection of their urethra. Transmissionbetween women is not impossible, but extremelyrare. The incubation period of gonococcal infec-tion averages 3 to 5 days, with a range of 1 to 14days. The majority of women with gonorrheahave no symptoms, but one-third of womenobserve a vaginal discharge. Urethritis withuncomfortable urination and frequency, cervici-tis, a puslike discharge, abdominal or pelvic pain,vaginal spotting, and pain with intercourse aresymptoms that warrant a suspicion of gonorrhea.

Mucopurulent cervicitis is the most commonSTI pelvic infection in women. Cervicitis is usu-ally caused by gonorrhea, chlamydia, herpes simplex, or a combination, with chlamydia infec-tions being the most common cause. A vaginalinfection along with cervicitis may be due to

319S E X U A L L Y T R A N S M I T T E D I N F E C T I O N S

candida or trichomonas, or the candida or trichomonas may coexist along with the otherorganisms.

Symptoms often do not show up until PIDdevelops. Abdominal pelvic pain is generally anindication of endometritis, salpingitis, or anabscess, and it generally develops a few days fol-lowing the onset of menses. The physical exam ofa woman with gonorrhea reveals a mucopurulentdischarge from the cervical opening, a swollenand friable cervix, and/or bleeding from the cer-vical canal.

Infected mothers may transmit gonorrhea totheir babies during pregnancy or at the time ofdelivery. It most commonly causes conjunctivitisin the baby and can also cause blindness in newborns. Other complications can includeincreased risks of spontaneous abortion, prema-ture labor, early rupture of the fetal membranes,and perinatal infant mortality.

As many as 30 to 60 percent of women withgonorrhea are also infected with chlamydia,10

and therefore gonorrhea and chlamydia shouldbe tested together.

Testing for Chlamydia and Gonorrhea

The U.S. Preventive Services Task Force (2001)and the Centers for Disease Control (CDC)(2006) provide the following guidelines and recommendations for who should be tested forchlamydia and gonorrhea. Their guidelines areslightly different, so I have combined them for optimal recommendations. The followingwomen should be tested for chlamydia:

• Women with mucopurulent cervicitis orPID

• All sexually active or pregnant women 25years old or younger

• Any woman who is at risk, defined liberallyas inconsistent condom use and having anew partner or multiple partners

• Pregnant women at increased risk forchlamydial infection, including women who

are unmarried, are African-American, have aprior history of STI, have new or multipleheterosexual partners, have cervical ectopy (achange in the cervix exposing more colum-nar cells to potential infection), or showinconsistent use of barrier contraception

Women who are treated for chlamydia should berescreened three to four months after treatment.

The optimum frequency of how often toscreen for chlamydia is uncertain. For womenwho have previously tested negative during ascreening test, rescreening should occur if there isa change in sexual partners. Once older than 25,or for women who are in a mutually monoga-mous relationship and have a history of negativescreening tests for chlamydia infection, screeningcan be much less frequent and based on clinicaljudgment. Women who have a history of beingpreviously infected need to be rescreened every 6to 12 months due to high rates of reinfection. Asstated earlier, women with positive infectionsshould be treated and retested after treatment.

According to the U.S. Preventive ServicesTask Force (2005), the following women shouldbe tested for gonorrhea:

• All sexually active women age 25 or younger• All women, especially pregnant women, who

are at higher risk, including women who areunmarried, are African-American, have aprior history of STI, have new or multipleheterosexual partners, are sex workers, usedrugs, have cervical ectopy (a change in thecervix exposing more columnar cells topotential infection), or show inconsistentuse of barrier contraception

• All pregnant women who are 25 years old oryounger or are at risk (screen at the first pre-natal visit)

• Women who live in communities with ahigher prevalence of gonorrhea

Using cultures to test for C. trachomatis andN. gonorrhoeae has historically been the gold


standard and the reference against which allother tests have been compared. However, theseculture methods are more difficult and expensive,so new testing methods have been sought. Thefirst nonculture screening tests that were devel-oped included enzyme immunoassays (EIAs),which detect specific chlamydial or gonococcalantigens, and direct immunofluorescent anti-body (DFA) tests for C. trachomatis. Nucleic acid hybridization tests followed, which detect C.trachomatis–specific or N. gonorrhoeae–specificdeoxyribonucleic acid (DNA) or ribonucleic acid(RNA) sequences. The main disadvantage ofthese tests, especially for C. trachomatis, is thatthey aren’t able to detect a fair number of theinfections. This has led to a new generation oftests, called nucleic acid amplification tests

(NAATs), that are significantly more sensitivethan previous nonculture tests in detecting DNA or RNA sequences. The Gen-Probe PACE2 and the Digene Hybrid Capture II can detectfor both organisms in a single specimen. Rapidin-office tests may be used by some clinics to testfor chlamydia; liquid-based Pap smears and urinetests can also be used to detect chlamydia.

Hepatitis B

Hepatitis B (HBV) is a virus that infects morethan 300,000 Americans annually. It is estimatedthat 1.5 million people in the United States arecarriers of the disease but experience no symp-toms at all. Sexual contact, especially anal sex, isthe leading method of transmitting HBV. Othermethods of transmission include the sharing ofneedles among drug users, exposure to infectedbody tissues or fluids through an open cut orsore, and infected mothers who pass the virus onto their babies. The most common early symp-toms are flulike. Symptoms that arise laterinclude jaundice (yellowing of the skin andwhites of the eyes), abdominal pain, and darkand foamy urine. With treatment, most people

PREVENTION

• Know the sexual disease history of your poten-tial sexual partner.

• The best protection against acquiring a sexuallytransmitted disease is for the male partner touse latex condoms.

• All heterosexual women who engage in unpro-tected sex with one or more men are at risk forSTIs. Women with frequent partners or multiplepartners have more STIs.

• Oral contraceptive use may predispose women tochlamydial infection.11

• Patients diagnosed with one STI should bescreened for other common STIs.

• IV drug users should avoid sharing needles.• Health-care workers should be focused and care-

ful and practice universal precautions in their workplace.

KEY CONCEPTS

• All heterosexually active women age 25 oryounger should be screened annually for gonor-rhea and chlamydia.

• Any sexual contact with a person with gonor-rhea or chlamydia warrants a visit to the doctorfor a physical exam and tests.

• Antibiotic treatment of chlamydia and gonorrheashould be considered the primary treatment,with alternative treatments used as complements.

• Complications of gonorrhea and chlamydia canbe serious and even life threatening, and apregnant woman can pass the infection to herbaby.

• Symptoms of chlamydia and gonorrhea includecervical discharge, difficult or painful urination,bleeding between periods or after intercourse,pain in the pelvic area during sex, a swollencervix and/or bleeding from the cervix, andacute or chronic pelvic pain. However, manywomen have no symptoms at all.

• Appropriate management of an STI includesseeing a health-care practitioner who can iden-tify the disease and treat the woman and hercurrent sexual partner.


begin to feel better within two to three weeks andrecover within four to eight weeks. A very smallpercentage of people who are chronic carriers ofHBV will develop potentially severe and fatalliver diseases such as active hepatitis, cirrhosis, orcancer. Blood tests are used to diagnose both theactive form of HBV and the carrier state. Preg-nant women can be screened for the virus duringtheir prenatal care.


Due to potential infertility from the scarring ofacute PID as well as some of the other complica-tions of chlamydial infection and gonorrhea, myadvice is to consider alternative medicine as anadjunct to conventional antibiotics rather than aprimary treatment. Using alternative therapies tosupport the immune system, to assist in manag-ing pain and discomfort, and to counteract someof the side effects of the antibiotics are the mainpriorities. Drinking plenty of water, gettingenough rest, eating simple light foods, and avoid-ing stimulants are basic guidelines during anyacute infection, including pelvic infections.

General immune support to complementconventional antibiotic treatment is just goodplain common sense. Nutritional and botanicalsupport can stimulate the white blood cells thatengulf and destroy bacteria and enhance thefunction of T cells, B cells, and natural killer cellsthat modulate the immune system in reaction tobacteria and viruses. Such supplements as vita-min A, vitamin C, the carotenes, vitamin E, zinc,and the B vitamins play an important role inimmune enhancement. Increasing antibodyresponse, stimulating helper T cells, enhancingwhite blood cell response and function, anddirectly killing the virus or bacteria are just someof the ways in which these supplements can behelpful during an acute infection of any kind.

Many herbs have also been shown to haveantibacterial, antiviral, and immunostimulatingeffects. The most commonly used herb for

immune support is echinacea. Echinacea canincrease the production of T cells, stimulatephagocytosis of bacteria, stimulate natural killercell activity, and multiply the number of whiteblood cells that circulate in order to deal with theinfection.12 Many herbs have also been shown to have antimicrobial and immunostimulatingeffects. Allicin extracts from garlic may hold themost promise for inhibiting bacterial infections.Goldenseal and Oregon grape root also have theability to inhibit the overgrowth of numerousorganisms, although this does not include bacte-rial vaginosis or chlamydia. Curcumin is one ofthe best herbs to reduce inflammation. The endresult is a strengthened immune system.

The best complement to counteract the sideeffects of antibiotic use is to add or increase theintake of Lactobacillus acidophilus to supportintestinal health and to help prevent a vaginalyeast infection. This can often be accomplishedby eating yogurt containing Lactobacillus aci-dophilus daily or by taking oral capsules of Lactobacillus acidophilus. Four to eight ounces ofunsweetened acidophilus yogurt or at least threecapsules of Lactobacillus acidophilus daily for twoweeks should prevent the overgrowth of vaginalyeast that often occurs when taking antibiotics.In addition, Lactobacillus has been shown toinhibit both gonorrhea and chlamydia and to beinversely related to PID.13–16

Ice packs over the pelvic region can reduceinflammation and pain in cases of acute PID.Cold or ice packs placed over the region of theuterus while putting the feet in a tub of hot watercan further assist in reducing the inflammation,congestion, and pain in the pelvic area. Alternat-ing hot and cold sitz baths can also be used toimprove circulation in the pelvic area andimprove the healing time from the infection.This is done by sitting in a bath of hot water,with the water level just above the waist, for threeminutes, followed by sitting in a small secondportable metal or plastic tub of ice cold water forone minute. This procedure is repeated three


times in succession, once or twice daily through-out the course of the pain and infection.

Nutrition

The nutritional goals during an active STI are toeat health-promoting and immune supportivefoods. Generally, this refers to a diet that is highin fiber, plant-based foods, essential fatty acids,and antioxidant nutrients and low in saturatedfat and refined sugar.

The best dietary sources of antioxidants, andespecially the carotenes, are green leafy vegetablesand yellow-orange fruits and vegetables such ascarrots, apricots, peaches, mangoes, yams, andsquash. Beans, whole grains, and many seeds arealso good sources of carotenes.

Eliminating refined sugar and simple sugars(corn syrup, honey, fructose, maple syrup, whitegrape juice concentrate, and others) will help toassure optimal immune function. Eliminatingsaturated fats such as red meat, butter, cheese,and ice cream, even in the short run, will enablethe body to utilize essential fatty acids such as thefats from olive oil, canola oil, and ocean fish.These essential fatty acids are important in thepromotion of the anti-inflammatory prostaglan-dins PgE1 and PgE3; reducing inflammation is aprimary goal in healing a sexually transmittedinfection.

Keeping the digestion in order with regularbowel habits and free of constipation can beaccomplished with a high-fiber diet rich in wholegrains, fruits, vegetables, and beans. This will notonly minimize digestive side effects if antibioticsare used in the STI treatment, but will also max-imize the elimination of metabolic toxins that areincreased during the infection.

Some naturopathic physicians advocate a verylight diet or even fasting during an active acuteinfection. The rationale is to minimize theburden on the body so that all of its resources canbe utilized for an immune response to fight theinfection. Fasting is also presumably a more effi-cient way of eliminating the metabolic toxins. If

you’re not used to fasting, I would not suggesttrying this approach for any longer than threedays on your own. Drink plenty of water as well.Better yet, you may want to seek advice from aknowledgeable practitioner about this approach.

If you are taking antibiotics, be sure to eateight ounces of unsweetened lactobacillus yogurtdaily to help maintain intestinal health and tohelp prevent the possibility of a yeast vaginitisinfection caused by the antibiotics.

Botanicals

An Indian study of Azadirachta indica (neemseed oil), Sapindus mukerossi (reetha saponinextract), and quinine included 58 women whopresented to a gynecology clinic in India with an

Sample Treatment Plan forChlamydia and Gonorrhea

This plan should be used as a complement to antibiotics.

• Vitamin A: 50,000 IU per day for up to 1 weekand 25,000 IU for 1 additional week (Do notexceed 6,000 IU if pregnant.)

• Vitamin C: 500 mg every 2 hours for 2 daysfollowed by 1,000 mg 3 times daily for 2 weeks

• Carotenoids: 50,000 IU per day for 2 weeks• Zinc: 30 mg per day for 2 weeks• Echinacea: 2 capsules every 2 hours for 2 days

followed by 2 capsules 3 times daily for 2weeks; or 1⁄4 tsp tincture every 2 hours for 2days followed by 1⁄2 tsp 3 times daily for 2weeks

• Lactobacillus: 4–8 oz Lactobacillus acidophilusyogurt daily for 2 weeks or 24 billion or moreLactobacillus acidophilus organisms daily for 2weeks

• High-dose allicin extract: 2 capsules 4 timesdaily for the first 3 to 6 days, then 2 capsulestwice daily for 1 week, and then 2 capsulesdaily until infection is gone

• Ice packs over the uterus with a hot footbathor hot water bottle to the feet; repeat twicedaily as needed


abnormal discharge. They were tested and werefound to have chlamydia, candidiases, trichomo-niasis, bacterial vaginosis, or mixed infections.The women were randomized to receive either acream containing neem seed oil, reetha saponinextract, and quinine or a placebo cream. Thecreams were applied intravaginally at bedtime for14 days. Ten of the 12 patients with chlamydiawho received the treatment cream recoveredwithin two weeks. Ten of the 17 women with bac-terial vaginosis who received the treatment creamrecovered within two weeks. There was no bene-fit in women with candidiasis or trichomoniasis.There was no improvement in symptoms or labtest results in any of the women in the placebogroup. Although there were not enough womento achieve statistical significance, the creamshowed encouraging results and should clearly beinvestigated further. It would be very appropriateto try this cream in bacterial vaginosis. In chlamy-dia infection, it could be used as an adjunct treat-ment along with antibiotics or following theantibiotics to help prevent recurrence.17


Chlamydia is the most common reportable sexu-ally transmitted infection in the United States,with gonorrhea following second. Both of thesebacterial illnesses can be present without symp-toms, and they are highly transmittable. Both arevery preventable with the use of a condom. Thecurrent CDC guidelines (2006) recommend thatall women under the age of 25 have annualscreenings for both chlamydia and gonorrhea,and then anytime a woman has a new partner,screening is recommended. Return visits for arepeat test for cure were recommended in thepast, but now they are only done in the cases ofpregnant women. Single-dose therapy is highlyeffective, especially when administered in theprovider’s office. It is thus recommended that, ifpossible, providers carry a supply of medicationsfor administration to the patient before she leaves

the office or clinic. The sexual partner should betested if at all possible, but the partner shouldalso be treated with antibiotics, regardless of test-ing. Current CDC recommendations are thatany partner exposure within 60 days should beevaluated and then treated. It is often the casethat partner evaluation does not occur or is noteconomically feasible, so many providers rou-tinely treat the partner as well. The ability to testfor chlamydia and gonorrhea has significantlyimproved and now can be done using vaginal,cervical, or rectal swabs, as well as urine testing.Some labs can now also test for chlamydia andgonorrhea on the liquid left over from a liquidPap test. Pregnant women should always bescreened for chlamydia and gonorrhea.

The CDC now recommends that all womenwith positive chlamydia tests have a reevaluationand testing at three months after their therapy tolook for reinfection. This differs from the test-of-cure evaluations that have been done extensivelyin the past and are currently not recommended.Repeating the test in three months to make surethat the patient is not reinfected is important forpreservation of future fertility and prevention oftubo-ovarian abscesses. Treating infected patientsprevents transmission to sex partners. Also, treat-ing pregnant women often prevents transmissionof chlamydia to infants during birth. Treatmentof sex partners also helps to prevent reinfection ofthe initial patient and the infection of other part-ners. Coinfection with chlamydia and gonorrheaoccurs frequently, and patients should be treatedfor both diseases when one is found unless test-ing for the other is negative when tested for both.

The standard antibiotic regimen for treat-ment of chlamydia would include one of the following:

• Azithromycin (1 g orally in a single dose)• Doxycycline (100 mg orally twice a day for

7 days)

Alternative antibiotic regimens would includeone of the following:


• Erythromycin base (500 mg orally 4 times aday for 7 days)

• Erythromycin ethylsuccinate (800 mg orally4 times a day for 7 days)

• Ofloxacin (300 mg orally twice a day for 7days)

• Levofloxacin (500 mg orally once daily for 7days)

Since doxycycline, ofloxacin, and levofloxacin arecontraindicated in pregnant women, azithromy-cin is probably the drug of choice.

The standard antibiotic treatment of uncom-plicated gonorrhea infections involves one of thefollowing:

• Ceftizoxime (125 mg intramuscularly in asingle dose)

• Cefixime (400 mg orally in a single dose)• Ciprofloxacin (500 mg orally in a single dose)• Ofloxacin (400 mg orally in a single dose)• Levofloxacin (250 mg orally in a single dose)

Quinolone-resistant gonorrhea is on the rise,and quinolones are not recommended for thetreatment of gonorrhea in regions where the rateof resistant gonorrhea is high. The main areas inthe United States where quinolones use is notrecommended are California and Hawaii. Someinner-city areas and other regions also have thesewarnings, so it is important for the practitionerto be aware of regional resistance patterns. TheCDC recommends the following treatment forpatients at high risk for quinolone resistance:

• Ceftriaxone (125 mg intramuscularly in asingle dose)

• Cefixime (400 mg orally in a single dose)

Other antibiotic regimens for gonorrheatreatment include single-dose injectable cepha-losporin regimens such as one of the following:

• Ceftizoxime (500 mg intramuscularly)• Cefoxitin (2 g IV) administered with

probenecid (1 g orally)

• Cefotaxime (500 mg administered onceintramuscularly)

None of the injectable cephalosporins offers any advantage over ceftriaxone, which is morecommonly stocked in offices and clinics.Azithromycin (2 g orally) is effective againstuncomplicated gonorrhea, but it is expensiveand causes significant gastrointestinal distressand therefore is not currently recommended for treatment of gonorrhea. The gonorrhea in the United States is not adequately suscepti-ble to penicillins, tetracyclines, and macrolides(erythromycin) for these to be used in treat-ment.

Again, a person being treated for gonorrheawould also be treated for chlamydia, unless testshave shown that chlamydia is not present.


If you have unprotected sexual contact withsomeone who has chlamydia, gonorrhea, or hep-atitis B, I strongly urge you to see a licensed prac-titioner (naturopathic doctor, medical doctor,osteopathic doctor, nurse-practitioner, or physi-cian’s assistant) who is trained and qualified toperform a physical exam and take samples fortesting and also capable of administering ormaking available prescription antibiotics andvaccine. This does not necessarily require a gyne-cologist or other conventional practitioner.Licensed naturopathic physicians are trained toperform and provide these services. State lawdetermines which antibiotics naturopathic physi-cians may prescribe. If a practitioner cannot pre-scribe a particular antibiotic, he or she can eitherrefer you to a conventional practitioner or workin cooperation with a conventional practitionerwho can make a prescription available to you.Nutritional and herbal supplements can then beused in addition to your conventional treatment.


A naturopathic physician can also provide natu-ral therapies to augment your immune sup-port, prevent side effects from the medications,and help you to recover optimally from theinfection.

If you have severe liver disease due to hepati-tis B, I would strongly consider alternative treat-ments as the primary treatment, with carefulmonitoring of liver enzymes and liver biopsywith the help of a specialist.


327

OVERVIEW

Uterine fibroids (also known as leiomyomas ormyomas) occur in 20 to 25 percent of women byage 40,1 more than 50 percent of women overall.They are the most common solid pelvic tumorsin women and the most common indication formajor surgery in women, and they account forapproximately one-third of hysterectomies eachyear.2 According to some studies, in African-American women the incidence of fibroids isthree to nine times higher and the fibroids’ rateof growth is increased.3, 4

You would think for a condition as commonas this that we would have a good understandingof the cause and cure. Nevertheless, the cause offibroids remains poorly understood. Uterinefibroids are not actually fibrous but consist ofmuscle, probably uterine smooth-muscle cellsbut possibly connective tissue or the smooth-muscle cells of uterine arteries. The growth offibroids may be stimulated by estrogen. The ten-dency of fibroids to arise during the reproductiveyears, grow during pregnancy, and regress post-menopausally does implicate estrogen as onefactor in the cause and growth of fibroid tumors.A growth spurt in fibroids is frequently seen inthe perimenopausal period and is likely due toanovulatory cycles with a relative estrogen excessthat commonly occur during this period. Preg-nancy is a condition of elevated estrogen andprogesterone, and even though progesterone isan antiestrogen, the increased blood supplyduring pregnancy leads to an overall stimulatingeffect on the uterine fibroids.5

There have been reports that concentrationsof estrogen receptors in fibroid tissue are higherthan in the surrounding uterine muscle tissue(myometrium)6 but lower than in the uterine

lining (endometrium). Although these findingsmay help to explain why fibroids are sensitive toestrogen, they have not been consistently sub-stantiated in other studies.7, 8 This higher con-centration of estrogen receptors may be due tochanges in estrogen metabolism within the fibroiditself. Pollow and colleagues8 demonstrated a sig-nificantly lower conversion of estradiol intoestrone in fibroids than in the myometrium, sug-gesting that local, concentrated estradiol increaseswithin the fibroid may play a role in the cause andgrowth of fibroids.

The prevalence and size of fibroids are greaterin women who do not ovulate or who haveendometrial hyperplasia or a granulosa cell tumorof the ovary. Even though fibroids do not lead tocancer and are not a cause of uterine cancer, theyare associated with a fourfold increase in the riskof endometrial carcinoma. This is probablybecause too much estrogen without any or enoughprogesterone (called unopposed estrogen) is a con-tributing factor in both conditions.

Fibroids come in all sizes and shapes and usu-ally occur as multiple tumors, although eachfibroid is discrete. Most discernible fibroids arebetween the size of a walnut and the size of anorange, but unusual tumors have been reported up to 100 pounds. Fibroids are classified accord-ing to their location. They are either submucosal(just under the endometrium), intramural (withinthe uterine muscle wall), or subserosal (from theouter wall of the uterus). They can also beintraligamentous (in the cervix between the twolayers of the broad ligament), pedunculated anddangling from a stalk into the uterine cavity(pedunculated submucous), or pedunculated onthe outside of the uterine wall (pedunculated sub-serous). The pedunculated submucous fibroids

19U T E R I N E F I B R O I D S C H A P T E R



can on occasion protrude through the cervix intothe vagina. Other pedunculated fibroids on a longstalk outside the uterus can be mistaken for anovarian mass or attach to the bowel.

The majority of fibroids (an estimated 50 to80 percent)9 don’t cause any symptoms, but whensymptoms do occur they often begin as a vaguefeeling of discomfort and may include a feeling of pressure, congestion, bloating, heaviness, painwith vaginal sex, urinary frequency, backache,abdominal enlargement, and abnormal bleeding.Abnormal bleeding occurs in only 30 percent ofwomen with fibroids. Heavy bleeding (menor-rhagia) results when intramural tumors enlargethe endometrial cavity and increase the surfacearea of endometrium and blood supply to theuterus. Intermenstrual bleeding (metrorrhagia)results when submucous fibroids ulcerate throughthe endometrial lining or cause congestion of thesurrounding blood vessels.

Fibroids can undergo degenerative changes.One type of degenerative change is when the con-tinued growth of the fibroid outgrows the bloodsupply. A more common type of degenerativechange is when there is a loss of cellular detail(hyaline degeneration) as a result of a decrease inthe vascularity of the tumor. Necrosis (cell death)results in cystic degeneration, which lends itself toa softer than usual consistency and can be con-fused with an ovarian mass on exam or pelvicultrasound. Calcification can occur over time andis usually seen in postmenopausal women.

The historical perspective has been thatfibroids are not usually associated with pain exceptwhen degeneration occurs or when the uterus contracts in its efforts to expel a submucousfibroid. Feelings of pressure pains may develop ifthe uterus becomes excessively enlarged withfibroids, or if a single fibroid is larger than 5 cm atits greatest diameter.10 However, if we look a littleharder at some of the research, clinic-based studiessuggest that gynecologic pain is often related tothe presence of fibroids.11–15 Fibroids are com-monly found in women with chronic pelvic pain,

although they may not be the cause or the onlycause of the pain.16, 17

There may also be racial differences when itcomes to pelvic pain and uterine fibroids. Onestudy reported that 41 percent of white and 59percent of black hysterectomy patients with apresurgical diagnosis of fibroids reported severepelvic pain.18 Another study reported a series ofstudies in which pelvic pain and/or menstrual painwas experienced in 34 percent of patients withfibroids.19 In a recent study, the first population-based study of gynecologic pain symptoms andfibroids, dyspareunia (pain with vaginal sexualactivity) and noncyclic pelvic pain, but not dys-menorrhea (menstrual pain), increased in severitywith the presence of uterine fibroids.20 Pregnantwomen with fibroids also have reported pelvicpain more frequently, and it seems that the pelvicpain is related to the size of the fibroid(s) and theirlocation.21, 22

So you might now be confused: do fibroidscause pelvic pain or not? The majority of thetime, uterine fibroids do not cause pelvic pain;however, if you have chronic pelvic pain, fibroidsmay in fact be a cause of that chronic pelvic pain,especially if they can be palpated on the pelvicexam. Some of the urinary complications thatoccur in 5 percent of fibroids are cause for con-cern because they may be due to compression ofthe ureter (outflow tract from kidney to bladder)that can cause enlargement of the kidneys andcompromise of kidney function.

Fibroids are thought to be the cause of 2 to 10percent of cases of infertility. There are several pos-sible reasons for this. The tumors may interferewith implantation of the fertilized ovum, they maycause compression on the fallopian tubes and inter-fere with motility of sperm or egg, or they maycause early miscarriage. They may also cause peri-odic anovulation or abnormal uterine blood flowand may obstruct sperm. Large fibroids may affectpregnancy by interfering with the fetus growth,leading to potential intrauterine growth retarda-tion, premature rupture of membranes, retained

329U T E R I N E F I B R O I D S

placenta, postpartum hemorrhage, abnormal labor,or an abnormal lie of the fetus. Not all practicingobstetricians would agree with these reports, andtheir main observations with pregnant women andlarge fibroids are an abnormal lie or postpartumhemorrhage. The incidence of miscarriage due tofibroids is unknown but estimated to be two tothree times greater than normal.

If a fibroid uterus is present, it can often befelt during a pelvic examination. It usually feelsfirm but can vary from soft to rock-hard. Theuterus can be irregularly shaped or irregularlyenlarged and often feels like it has protrusions.Most of the time it is not painful during theexam. Many times women don’t realize they havea fibroid until the practitioner finds it. This is notcause for alarm. Fibroids are benign growthsmost of the time. The worrisome fibroid is a rap-idly growing one; the rare malignant uterine sar-coma may have to be considered in these cases.

After the pelvic exam, a pelvic ultrasound isthe most useful tool in diagnosing a fibroid. This

imaging test is able to identify fibroids and delin-eate the size and to some degree the location, aswell as identify that the ovaries are normal in size.The ultrasound detects the contours of theuterus, the fibroids (called hypechoic masses),compression of the ureters, any potential enlarge-ment of the kidneys caused by the compression,and, of course, the presence of an enlarged uterus.It is difficult for the ultrasound to detect fibroidssmaller than 2 cm. A magnetic resonance imaging(MRI) test is more accurate in assessing thenumber, size, and location of fibroids, but it doesnot provide significant enough additional infor-mation to be worth the cost. A hysteroscopy candetect submucous tumors. An x-ray can diagnosecalcified fibroids.

The main diagnostic consideration is differ-entiating a possible fibroid from the followingconditions: ovarian malignant tumor, an abscessin the fallopian tube/ovarian region, a diverticu-lum from the colon, a pelvic kidney (rare), endo-metriosis, adenomyosis (endometriosis withinthe muscle wall of the uterus), congenital anom-alies, adhesions in the pelvis, or a rare retroperi-toneal tumor. Not all of these considerations canbe distinguished from the medical history, phys-ical exam, and pelvic ultrasound. Surgery may berequired to distinguish one condition from the

KEY CONCEPTS

• Uterine fibroids are benign and common.• We do not know what causes fibroids.• Fibroids are estrogen dependent (some may even

be progesterone dependent).• The majority of the time there are no symptoms,

but when there is pelvic pain, abnormal bleed-ing, or infertility, uterine fibroids must be considered.

• Abnormal bleeding may be caused by uterinefibroids.

• Abnormal bleeding warrants a visit to yourhealth-care practitioner.

• There are several kinds of fibroids based on location.

• An enlarged uterus or abnormal finding on apelvic exam may require further testing to determine the diagnosis.

• Less than 1 percent of fibroids are malignant,but rapidly growing fibroids warrant furtherexploration.

PREVENTION

• Ensure regular ovulation.• Avoid situations that promote lack of ovulation,

such as stress.• Avoid estrogen-only medications.• Dietary phytoestrogens (soy, flax, red clover) do

not appear to stimulate the growth of fibroids.• Practice good nutritional habits with a diet that

is higher in complex carbohydrates, higher infruits and vegetables, and low in saturated fats,alcohol, sugar, or other foods that interfere withthe liver’s role in metabolizing hormones.

• Maintain a healthy weight. Obesity can lead tohigher estrogen effects on the uterus.


other. Laparoscopy is the definitive method ofexcluding these other diagnoses from fibroids,even though laparoscopy is not typically done todiagnose fibroids. Only when there is great con-cern or lack of clarity about the diagnosis will theprocedure be warranted.


Over the more than 23 years I have been in clin-ical practice, not many health problems haveeluded successful treatment as consistently asuterine fibroids. Women who are seeking analternative to drug or surgical treatment for uter-ine fibroids will not find an easy, reliable alterna-tive to shrink the tumors with natural medicine.Using the protocols in this book, we are usuallyable to successfully resolve or improve mostsymptoms that relate to the fibroids such asabnormal bleeding, pelvic pain or pressure, andbackache. In addition, there are natural therapiesthat may be able to slow the growth of thefibroids to avoid further problems.

When it comes to shrinking fibroids, espe-cially the large ones, natural therapies can onlysignificantly shrink a small minority of cases.There are individual cases that report reductionin size on pelvic ultrasound, disappearance ofsymptoms, and even total disappearance of anyevidence of fibroids. I myself can report caseswhere fibroid growth and the size of the uterushave been significantly reduced. The problem isthat the results are very inconsistent. Often thecases that have shown the most dramaticimprovements are the women who are nearingmenopause or postmenopausal whose fibroidsshrink because of the natural decrease in theirestrogen levels.

It may be possible to reduce uterine fibroidsthrough alternative means and avoid a surgery ordrug treatment that your gynecologist has rec-ommended, but, more likely than not, largefibroids that are causing symptoms that have notbeen successfully dealt with will indeed require

some kind of conventional intervention. Mymain goals with women who have large fibroidsare to (1) deal with problem symptoms, (2) try tostabilize the situation and hold out until meno-pause, and (3) recognize the clinical situationswhen conventional treatment intervention isappropriate and reasonable.

One aspect of being a naturopathic physicianis to more fully educate patients about theirhealth and health problems so that they canmake informed decisions about their health care.With uterine fibroids, I have often been in theposition of discussing surgical options or proce-dures that not all gynecologists discussed withtheir patients. Educating the woman who isfaced with a possible hysterectomy and finding asurgeon or gynecologist who is skilled in thesealternatives may be the most important servicean alternative provider can offer. There are manynew conventional therapies that can be alterna-tives to a hysterectomy in many cases. These new therapies include hysteroscopic resection,embolization, and laparoscopic surgery. How-ever, not all cases of fibroids may be successfullytreated with these methods.

Nutrition

Even though diet changes alone are unlikely toshrink fibroids, good dietary habits are stillimportant. Clinical observation has taught methat all natural therapies work best in the contextof a healthy lifestyle. Improving one’s diet mayhelp in small ways, to decrease heavy bleeding orthe pain and discomfort caused by the fibroids.Besides these potential benefits, dietary improve-ments will improve your general well-being.

Also, women with uterine fibroids may be athigher risk for endometrial cancer due to thehigher estrogen levels. A diet high in saturatedfats is associated with higher blood levels of estro-gen, potentially exacerbating the problem. Low-fiber diets are associated with elevated estrogenlevels and poor excretion of estrogen. Poor nutri-tional habits can also lead to dysfunctional estrogen


metabolism and inhibit the body’s ability tobreak down and excrete excess estrogen.

The tradition of naturopathic medicine holdsthat the health and vitality of an individualdepends on the health of the liver and the wholedigestive system. The liver’s basic functions arevascular, secretory, and metabolic. As a vascularorgan, the liver is a major reservoir of blood and filters over one quart of blood per minute.The liver removes bacteria, endotoxins, antigen-antibody complexes, and other particles from thecirculatory system. The liver’s secretory functionsare the synthesis and secretion of bile. The livermanufactures about one quart of bile daily. Bileis required for the absorption of fat-soluble sub-stances, including some vitamins. The majorityof the bile secreted from the liver into the intes-tines is reabsorbed. The metabolic functions ofthe liver are involved in carbohydrate, fat, andprotein metabolism; the storage of vitamins andminerals; the formation of numerous biochemi-cal factors; and the detoxification or excretioninto the bile of hormones such as estrogen as wellas histamines, drugs, and pesticides.

The liver not only has to process the foodsthat we eat every day but also detoxifies harmfulsubstances, both those we produce from normalmetabolism and those we are exposed to in ourenvironment. In addition, it metabolizes anddeactivates hormones. The liver metabolizesestrogen so it can be eliminated from the body byconverting it to estrone and finally to estriol, aweaker form of estrogen that has very little abil-ity to stimulate the uterus. If the liver cannoteffectively metabolize estradiol, the uterus maybecome overestrogenized and respond withfibroid growths.

Saturated fats, sugar, caffeine, alcohol, andjunk foods are unhealthy and problematic for tworeasons: (1) they interfere with the body’s abilityto metabolize estradiol to estrone to estriol, and(2) some of these foods are deficient in B vitaminsor interfere with B-vitamin metabolism. If B vita-mins are lacking in the diet, the liver is missing

some of the raw materials it needs to carry out itsmetabolic processes and regulate estrogen levels.A recent animal study suggests that lycopene sup-plementation (high in yellow/orange fruits andvegetables and especially high in tomatoes,tomato sauce, and tomato juice) may decrease theincidence and size of leiomyomas.23 Anotherstudy extolled the benefits of a vegetarian diet byfinding that women who suffered from fibroidswere more likely to have high consumption of redmeat and ham and have low consumption offruits and green vegetables.24

Whole grains such as brown rice, oats, buck-wheat, millet, and rye are excellent sources of Bvitamins. Whole grains also help the body toexcrete estrogens through the bowel. The role ofwhole-grain fiber in lowering estrogen levels wasfirst reported in 1982.25 This study found thatvegetarian women who eat a high-fiber, low-fatdiet have lower blood estrogen levels thanomnivorous women with low-fiber diets. Onceagain, we can see why a high-fiber diet mightprevent and perhaps reduce uterine fibroidsthrough the estrogen connection.

A high-fiber diet may also help relieve someof the bloating and congestion associated withfibroids. By bulking up the stool and regulatingbowel movements, some of these symptoms mayimprove. Some women have a hard time tolerat-ing increased fiber in their diet because of com-promised digestive function. In these cases, itmay be necessary to increase fiber slowly andinclude digestive support such as enzymes or acidophilus.

Because there is an association betweenhaving uterine fibroids and a fourfold increase inthe risk of endometrial cancer,1 three dietary rec-ommendations stand out above all else: increasefiber, decrease dietary fat, and increase soy prod-ucts and other legumes. Researchers at theCancer Research Center at the University ofHawaii published a case-controlled, multiethnic(Japanese, Caucasian, Native Hawaiian, Filipino,and Chinese) population study to examine the


role of dietary soy, fiber, and related foods andnutrients on the risk of endometrial cancer.26

The diets of 300 women with endometrialcancer were compared with women in the gen-eral multiethnic population. The researchersfound that high fat intake was positively associ-ated with endometrial cancer, whereas a diet richin fiber, soy, and other legumes reduced the riskof endometrial cancer. The study concluded thatplant-based diets low in calories from fat, high infiber, and rich in legumes (especially soybeans),whole-grain foods, vegetables, and fruits reducethe risk of endometrial cancer.

While I can’t say that lowering fat andincreasing soy and fiber intake will definitely pre-vent or treat fibroids, these nutritional habits dolower the risk of endometrial cancer. Since uter-ine fibroids are associated with an increase in therisk of endometrial cancer, it logically followsthat these diet recommendations could help withfibroids.

Some people have raised the concern thatwomen with uterine fibroids should avoid soyfoods for their high content of phytoestrogens(specifically isoflavones) because phytoestrogensmay have a weak estrogenic effect. The answerappears to be that this is not necessary. Soyphytoestrogens do not have an estrogenic effecton the uterus, at least in the usual doses. This wasmost recently confirmed in a Chinese study.27

This population-based, case-controlled studyobtained detailed information from a food-frequency questionnaire on soy food intake overfive years. The participants were 832 women,ages 30 to 69, who were diagnosed with endome-trial cancer from 1997 to 2001. This group wascompared with 846 control-matched womenselected from the Shanghai Residential Registry,who had an average intake of 42.5 mg of soy-based isoflavones per day.

This study demonstrated that regular con-sumption of soy foods, as either soy protein orsoy isoflavones, was inversely associated with therisk of endometrial cancer. Moreover, this study

indicated that isoflavones are selectively estro-genic and antiestrogenic; they have an estrogeniceffect on some tissues and organs and an anti-estrogenic effect on others. Soy foods may beanalogous to a class of drugs called selective estro-gen receptor modulators (SERMs). In the uterus,soy isoflavones appear to have an antiestrogeniceffect, with the possible exception of when they areused in high doses daily for a longer term.

Long-term high-dose use of soy may be dif-ferent than the usual average typical daily con-sumption of soy. In one study, one group ofpostmenopausal women were given soy tabletscontaining 150 mg of soy isoflavones per day for five years.28 The second group received anidentical placebo tablet for five years. Results ofendometrial biopsies were obtained at baseline,30 months, and five years after the beginning of the treatment. At the five-year endpoint, 70percent of the women on the 150 mg of soyisoflavones had atrophic tissue versus 81 percentwho received the placebo. After five years, theincidence of endometrial hyperplasia was signifi-cantly higher in the isoflavone-treated group,3.37 percent versus 0 percent. There were fivecases of simple hyperplasia and one of complexhyperplasia. No cases of atypical hyperplasia orendometrial cancer occurred during the fiveyears. This is the first study that raises concernsabout long-term, high-dose isoflavone supple-mentation and its effects on the endometrium. Itwould typically take three to five servings of soyfoods per day to achieve 150 mg. One servingper day of soy foods is only 25 to 60 mg per day,depending on the soy food item.

Isoflavones appear to be able to act as a par-tial agonist, binding to the estrogen receptor.Because the action of isoflavones is weaker thanthat of endogenous estrogens at low doses and forshort durations, these phytoestrogens seem to be antagonistic. They are able to counteract theeffects of endogenous estrogens. When treatmentis prolonged and at a higher dose, the agonisteffects are more evident and the isoflavones have


an estrogenic effect. It is important to note thatat 30 months there was no difference betweenthe isoflavone-treated group and the placebogroup. It was only after five years that the dose of 150 mg per day produced an estrogenic effectin a small number of women.

The subject of phytoestrogens is discussed inmore detail later in this chapter and in Chapter12 in the discussion of menopause.


As mentioned earlier, many of the symptoms ofenlarged fibroids can be effectively treated usingnatural therapies. For abnormal bleeding andpelvic pain, refer to Chapters 1 and 13. In thissection, I will largely be discussing the traditionalnaturopathic methods of trying to reduce the sizeof uterine fibroids or to inhibit their growth.These recommendations are based more on tra-dition, theory, logic, and clinical experience thanon scientific evidence.

Lipotropic Factors. Supplements such asinositol and choline exert a lipotropic effect,meaning they promote the removal of fat fromthe liver. Lipotropic supplements are usually acombination vitamin and herbal formulationand sometimes an animal liver extract designedto support the liver’s function in removing fat,detoxifying the body’s wastes, detoxifying exter-nal harmful substances (pesticides, fossil fuels,etc.), and metabolizing and excreting estrogens.These lipotropic products vary in their formula-tions depending on the manufacturer, but theyare all similar and have the same uses in mind.Because the liver is the most important organ ofmetabolism, naturopathic physicians believe thatwhen the liver function improves, metabolismimproves, making this treatment fundamental tothe treatment of many chronic diseases.

Lipotropic Factors

1–4 tablets per day with meals

Pancreatic Enzymes. There are three cate-gories of pancreatic enzymes:

• Lipases: enzymes that help digest fats alongwith bile. A deficiency of lipase results inmalabsorption of fats and fat-soluble vitamins.

• Amylases: enzymes that break down starchmolecules into smaller sugars.

• Proteases: trypsin, chymotrypsin, and car-boxypeptidase break down protein moleculesinto single amino acids.

Supplementation with pancreatic enzymes isusually done to treat pancreatic insufficiency.Pancreative insufficiency manifests itself insymptoms of abdominal bloating, gas, indiges-tion, undigested food in the stool, malabsorp-tion, and nutrient deficiencies. Other clinicaluses of pancreatic enzymes are for treatment ofcystic fibrosis, rheumatoid arthritis, athleticinjuries, and—one of the most controversialuses—the treatment of cancer.

The logic for the treatment of uterine fibroidsis similar to the logic for the treatment of cancer.Enzyme preparations have been used at the Con-treras Clinic in Mexico and by Drs. WilliamKelley and Nicholas Gonzalez as part of a cancertreatment protocol. There is little evidence in the scientific literature to support their use, butthe logic is that the pancreatic enzymes willdigest the protein cell membrane surroundingthe malignant cells. By doing so, the immunecells will then be able to enter the cancer cells andalter the abnormal cell division of the cancercells. In the case of uterine fibroids, the belief isthat the pancreatic enzymes will help to digestthe fibrous/smooth muscle tissue and dissolve thefibroids. When used for this purpose, the pancre-atic enzyme supplement must be taken betweenmeals rather than with meals.

Pancreatic Enzymes

2–4 capsules 3 times per day between meals


Botanical Medicines

Traditional Herbs. Many plants have beenused in traditional herbal medicines designed totreat women with uterine fibroids. The plantsand herbal formulations talked about here areused to try to shrink uterine fibroids; herbs usedto deal with abnormal bleeding and uterinecramping are discussed in Chapters 1 and 13.

Scutellaria barbata, commonly used in tradi-tional Chinese medicine for its purported antitu-mor properties, was shown to inhibit theproliferation of uterine smooth muscle cells andact as an aromatase inhibitor contributing to

decreased fibroid growth in vitro.29–31 Otherbotanicals used in traditional Chinese medicinethat show some promise in treating fibroids invivo include poria and cinnamon.32

Traditional herbalists have developed variousbotanical uterine fibroid protocols and reportmodest success in reducing the size and numberof uterine fibroids. I have used many herbs andherbal formulations over the years in an attemptto shrink fibroids, and I present the protocolbelow from one of the traditional herbalists, RickScalzo, as an option for your consideration. (Seethe Resources for a listing of herbal companies.)

Scalzo’s Protocol

Scudder’s Alterative

Corydalis tubers (Dicentra canadensis)Black alder bark (Alnus serrulata)Mayapple root (Podophyllum peltatum)Figwort flowering herb (Scrophularia nodosa)Yellow dock root (Rumex crispus)

Add 30–40 drops to a small amount of warm waterand take 3 times daily.

Echinacea/Red Root Compound

Echinacea (Echinacea spp)Red root (Ceanothus americanus)Baptisia root (Baptisia tinctoria)Thuja leaf (Thuja occidentalis)Stillingia root (Stillingia sylvatica)Blue flag root (Iris versicolor)Prickly ash bark (Xanthoxylum clava-herculus)

Add 30 drops to a small amount of warm water andtake 3 times daily.

Fraxinus/Ceonothus Compound

Mountain ash bark (Fraxinus americanus)Red root (Ceanothus americanus)Life root (Senecio aureus)Mayapple root (Podophyllum peltatum)Helonias root (Chamaelirium luteum)

Goldenseal root (Hydrastis canadensis)Lobelia (Lobelia inflata)Ginger root (Zingiber officinale)


Turska Formula

Gelsemium root (Gelsemium sempervirens)Poke root (Phytolacca americana)Aconite (Aconitum napellus)Bryonia root (Bryonia dioica)


Other Herbal Extracts to Consider

Chaste tree (Vitex agnus castus)Nettle (Urtica dioica)Burdock root (Arctium lappa)Dandelion root (Taraxacum officinale)Oregon grape (Berberis aquifolium)

Topical Preparations

Poke root oil: rub onto the belly over the uterusnightly before bed.

Castor oil packs: apply over pelvis 3–5 times perweek. (See Appendix D for instructions.)


Herbal Phytoestrogens. There are three typesof naturally occurring estrogen-like substancescalled phytoestrogens found in plants: resorcylicacid lactones, steroids and sterols, and phenolics.Phytoestrogens are present in virtually every plantin at least modest levels, with some plants havingparticularly high levels. Resorcylic acid lactonesare not true phytoestrogens but are mycotoxinsproduced by soil-dwelling molds. Their presencein plants is the result of contamination withmolds. Steroids are the classic steroidal estrogens(estradiol and estrone) and are found in veryminute amounts in a few plants such as apple seed,date palm, and pomegranate seed in the range ofone to ten parts per billion.26, 33, 34 Diosgenin is asteroid derivative and is found in at least 20 plants,including wild yam species. Beta-sitosterol is themost common phytosterol and is distributedwidely through the plant kingdom. It is found inplant oils such as wheat germ oil, cottonseed oil,and soybean oil. Beta-sitosterol is the dominantphytosterol found in garlic and onions. Herbalsources include licorice root, saw palmetto, andred clover. Stigmasterol is closely related to beta-sitosterol. Soybean oil is an important source ofstigmasterol and is a better source for laboratorysynthesis of progesterone than is beta-sitosterol.Some herbal sources include burdock, fennel,licorice, alfalfa, anise, and sage.

The phenolic phytoestrogens are members ofthe flavonoids, the largest single family of plantsubstances, which has over 4,000 individual mem-bers. The term flavonoid derives from the Latinflavus meaning “yellow” because the flavonoids areresponsible for the yellow, red, white, and bluepigments in plants. Phenolics include isoflavones,which are higher in legumes and especially soy-beans than any other plants; coumestans, with oneknown estrogenic member (coumestrol) that isapproximately six times more estrogenic than theisoflavones;35, 36 and lignans, high in grains andcereals and highest in flaxseed.

There has been some concern and contro-versy about how phytoestrogens affect the uterus;

if they have an estrogenic effect, they should beavoided by women with uterine fibroids orendometrial cancer. We talked earlier about soy-beans and how they are actually associated with areduced incidence of uterine cancer.26 I do notbelieve that eating a high soy diet is something tobe concerned about; in fact I recommendincreasing the soy foods in the diet in order toreduce the estrogen burden in the body.

Most of the research on the effects of phyto-estrogens on the uterus is found in relationshipto the agricultural industry and the health ofgrazing animals. In the 1940s, it was reportedthat the red clover sheep grazed on in Australiawas responsible for their infertility.37 A Finnishstudy of pasture legumes determined that redclover contained the highest concentrations ofphytoestrogens38 and that abundant intake of redclover resulted in fertility problems in cattle.39

In one study on the effects of phytoestrogens insheep, it was noted that both coumestans andisoflavones produce changes in the typical stimula-tion with steroidal hormones such as estradiol inall of the target organs.40 Among these changes wasan increase in uterine weight. Other investigatorshave examined the binding of phytoestrogens tothe uterus and vagina. Coumestrol has temporarilyenhanced the uptake of estradiol by the uterus andvagina only one hour after being injected intomice.41 Researchers also noted that coumestrolactually inhibited the uptake of estradiol by theuterus over the long term, and they postulated thatthere was actually an inhibitory effect at the estra-diol receptor sites. Other researchers have notedthat coumestans and isoflavones compete withestradiol for uterine receptor sites but have lessaffinity for them than estradiol.42

Coumestrol has been found to increase uterineweight at a 100 mcg dose when given to rats at acertain time in the development of glands.43 Itappears that the weak estrogenic effect of phyto-estrogens is variable and can even be weakly anti-estrogenic. Variability is based on dose, target tissue,the woman’s hormonal environment, and more.


Higher does of phytoestrogens have stimu-lated some concern. However, it is reassuring thatin countries with a high intake of phytoestrogens(Japan, Thailand, China), women do not have anincrease in uterine fibroids. However, they dohave a four- to sixfold lower incidence of breastcancer44 (also an estradiol target tissue), althoughhow a substance affects one tissue is not necessar-ily translated to how it affects another.

Again, though, I must come back to theeffects of soy on the endometrium, which may bedifferent than some of the other plants, mostnotably red clover. Like data on breast cancer,data on women of different cultures support theconclusion that soy phytoestrogens are not anestrogen stimulus for the endometrium. Rather,they probably act as an estrogen antagonist andare associated with low rates of endometrialcancer in countries where soy phytoestrogenintake is high.45

Based on these studies, my recommendationto those with uterine fibroids is to eat a diet highin soy products; however, my current cautionaryadvice would be to avoid the use of red clover.

In cases where conventional treatment withGnRH inhibitors is needed, thus causing a phar-maceutically induced menopause, Ipriflavone (asemisynthetic soy derivative) supplementationhas been helpful at preventing side effects such asbone loss and increased LDL.46, 47

Natural (Bio-Identical) Progesterone. His-torically, studies have suggested that proges-terone may inhibit growth of uterine fibroids. A. Lipschutz demonstrated that progesteroneadministered to guinea pigs prevented formationof tumors that had been induced by estrogen.48

In 1946, A. Goodman reported six cases of clin-ically diagnosed uterine fibroids that regressedafter using progesterone therapy.49

Dr. John Lee proposes that because uterinefibroids are a result of estrogen stimulation andwhat he calls estrogen dominance, progesteroneis the solution. He asserts that estrogen domi-

nance is a much greater problem than is recog-nized by conventional medicine. “Since manywomen in their mid-thirties begin to havenonovulating cycles, they are producing muchless progesterone than expected, but still produc-ing normal (or more) estrogen. They retain waterand salt, their breasts swell and become fibrocys-tic, they gain weight (especially around the hipsand torso), they become depressed and lose sexdrive, their bones suffer mineral loss, and theydevelop fibroids. All are signs of estrogen domi-nance relative to a progesterone deficiency. Whensufficient natural progesterone is replaced,fibroid tumors no longer grow in size (they gen-erally decrease in size) and can be kept fromgrowing until menopause, after which they willatrophy. This is the effect of reversing estrogendominance.”50 The preferred form of naturalprogesterone for treating fibroids (unless heavybleeding is involved) is a topical cream with atleast 400 mg of progesterone per ounce.

Be advised, however, that there is a countertheory about the relationship of progesterone touterine fibroids. Dr. Mitchell Rein and his col-leagues at Brigham and Women’s Hospital pub-lished a report in 1995 stating that not only isthere no evidence that estrogen directly stimu-lates myoma growth, but that it is actually prog-esterone and progestins that promote the growthof fibroids.51 The authors cite the biochemical,histologic, and clinical evidence that supports animportant role for progesterone and progestins inthe growth of uterine myomas. Their compre-hensive hypothesis is based on an analysis ofmany different technical studies, which they con-clude suggest that the development and growthof myomas involves a multistep chain of events.

Since both of these schools of thought aretheoretical, I encourage all women and theirhealth-care practitioners to educate themselves soas to make the best individual decision. Fibroidsare generally not urgent or life threatening, sothere is room for experimentation and observa-tion to determine the best course of treatment.


Natural (Bio-Identical) Progesterone Cream

1⁄4 tsp of a cream containing at least 400 mg/oz 1 to 2times daily for 1 week after menses; 1⁄4 to 1⁄2 tsp twicedaily for the next 2 weeks. Discontinue for 1 week dur-ing menses. Apply the cream to the inner arms, chest,inner thighs, and/or palms.


Small fibroids that cause few symptoms require notreatment, only observation of growth, which canbe done with annual pelvic exams. If the patientnotices new symptoms, or the physician thinksthere is a change in the fibroid, ultrasound canfollow and assess the location and size of fibroids.Because there is some concern about estrogen’srole in promoting the growth of fibroids, use oforal contraceptives in premenopausal women andhormone therapy in postmenopausal womenshould be prescribed with care, close follow-up,and the lowest doses possible.

In cases of fibroids where heavy bleeding exists,progestogens or estrogen is used to manage thebleeding, and any anemia is treated with iron supplements. Treatment of fibroids with progesta-tional agents (norethindrone, megestrol, medroxy-progesterone acetate) has been used, but there isno consensus regarding the routine use of thesedrugs to shrink fibroids. The progestational agentsproduce a hypoestrogenic effect by inhibitinggonadotropin secretion and suppressing ovarianfunction. They may also have a direct antiestrogeneffect. Even though estrogen and progestogensmay be necessary to control bleeding fromfibroids, most practitioners do not consider themuseful in shrinking fibroids. When used to controlbleeding, there is always a concern about the pos-sible effect on the increase in growth of the fibroid,so fibroids need to be periodically evaluated byphysical exam and/or pelvic ultrasound.

Agents such as leuprolide acetate (Lupron)have been used to temporarily control bleeding,correct anemia, and shrink tumors. This allows alarge tumor to shrink to a more manageable size.

Sample Treatment Plan for Uterine Fibroids

Diet

• Eat a high-fiber, low-fat diet.• Eat a diet high in whole grains (brown rice,

oats, buckwheat, millet, rye, whole wheat).• Eat a diet high in fruits and vegetables.• Eat a diet high in flaxseed, particularly ground

flaxseed.• Eat a diet high in legumes, especially soy

products, 1 serving per day.• Avoid saturated fats, sugar, caffeine, alcohol,

and junk foods.

Nutritional Supplementation

• Lipotropic factors: 1–2 tablets twice daily withmeals

• Pancreatic enzymes: 2–3 capsules 3 times perday between meals

Botanicals

See the Resources section for sources.

• Scudder’s Alterative: 30 drops 3 times perday

• Echinacea/Red Root Compound: 30 drops 3times per day

• Fraxinus/Ceonothus Compound: 30 drops 3times per day

• Gelsemium/Phytolacca Compound (TurskaFormula): 5 drops 3 times per day

See Chapter 1 for abnormal bleeding problems. SeeChapter 13 for pelvic and menstrual pains.


Lupron can be used to change the need for anabdominal hysterectomy to a vaginal or laparo-scopic type, which shortens patient recovery.Lupron suppresses ovarian estrogen secretion,thereby causing temporary and reversible med-ical menopause. The use of GnRH analogs hassuccessfully reduced uterine and tumor size by 40 to 65 percent. Most reduction occurs within8 weeks, and maximum reduction occurs withinabout 12 weeks. After the treatment is discontin-ued, the uterus and fibroids often return to theiroriginal size within three months. On occasion,the use of Lupron may make surgical treatmentunnecessary, but usually the solution is tempo-rary and surgery is inevitable.

One of the most significant disadvantages ofLupron is that it is expensive, costing approxi-mately $600 per month. The other is that it putsthe patient into an instant menopausal state withhot flashes and other side effects, which can becontrolled with very small add-back doses ofeither estrogen or a progestogen. The GnRHanalogs cannot be used long-term (more than sixmonths) because they can lead to irreversiblebone loss and elevated total cholesterol.

The standard surgical treatments for uterinefibroids are a hysterectomy or a myomectomy.Hysterectomy, the removal of the uterus, is theonly approach that provides a permanent solutionfor fibroids. Myomectomies are surgeries thatremove the fibroids but leave the uterus. There aretwo basic approaches: abdominal myomectomies,which are used primarily for the removal of sub-serous, pedunculated, or intramural fibroids, anda hysteroscopic myomectomy, which is used forremoval of submucous myomas.

Hysterectomies can be done with an abdomi-nal incision, a vaginal incision, or by laparoscopy.Except in vaginal hysterectomies, it is possible to leave the cervix, removing the uterine fundus(body) only, which contains the uterine fibroids.There is really no reason to remove either ovariesor cervix to treat the symptoms of fibroids. Byleaving the cervix, the normal length and sensa-

tions of the vagina are maintained. With a vaginalhysterectomy, the entire uterus, including thecervix, is removed. In either case, the decision toleave the ovaries depends on the patient and herdoctor. Most doctors would recommend leavingovaries in women under 45 and might recom-mend removing them in women over 45 becausethey will soon be menopausal, oftentimes to pre-vent ovarian cancer. However, we cannot removeall of our organs to reduce the risk of cancer. Sincethe lifetime risk of ovarian cancer is 1 in 70,women with healthy ovaries should be encouragedto leave them in place when possible. Special cir-cumstances, such as a strong family history ofovarian cancer, might warrant their removal.

Myomectomies are particularly appropriatefor women who wish to retain their childbearingoption or in women with a small submucousmyoma that causes a bleeding problem. Mostmyomectomies for large intramural fibroids aredone abdominally. Laparoscopic myomectomiesfor intramural or subserosal fibroids are very rare,and there are only a few physicians in the UnitedStates capable of performing them. Abdominalmyomectomies have many of the same risks asso-ciated with a hysterectomy and can often be associated with more blood loss. Many womenfeel much more comfortable with retaining theirreproductive organs and should be encouraged to find a physician who is comfortable with the concept of myomectomy when the patientprefers that approach.

Hysteroscopic myomectomies are done withan instrument inserted through the vagina, upthe cervical canal, and into the uterine cavity,providing a view of the interior of the uterus andan instrument that can slice or cauterize the sub-mucous fibroid. Sometimes, when a woman ispast childbearing age, an associated destructionof the uterine lining tissue is performed at thesame time. This is called an ablation and furtherhelps to reduce menstrual flow.

There are other treatments for fibroids, someof which are gaining more popularity and some


of which are still experimental. Uterine arteryembolization is designed to reduce fibroids byobstructing the blood supply that nourishesthem. The procedure is done by a radiologist inthe x-ray department. It entails making a smallincision in the groin and threading a smallcatheter into the femoral artery. The doctorworks the catheter up to the vessels that supplythe uterus under guidance with dye and x-rays.Microscopic plastic particles are injected to closeoff the uterine vessels, temporarily creating acondition of shock for the uterus. Becausefibroids only have one blood supply, the shock isoften enough to cause them to begin to degener-ate (necrose). The uterus, however, has bloodsupply through the uterotubal ligaments andvaginal arteries as well and recovers from the ini-tial loss of blood flow most of the time.

Embolizations have been done for about 10years, and now there is enough data to indicatethat there is a less than 1 percent chance that awoman will need an emergency hysterectomybecause of uterine necrosis after an embolization.There is a 1 to 5 percent chance that the patientcould become menopausal because of a decreasein the blood supply to the ovaries occurringunintentionally at the time of the embolization.The patient can expect significant pain or cramp-ing for up to six months, treatable with painmedications and anti-inflammatories, and mostfibroids will reduce approximately 50 percent intheir size. This is more successful for treatment ofpain from fibroids than bleeding, but it canimprove bleeding.

The new fibroid treatment that conventionalmedicine is investigating is selective progesteronereceptor modulators (SPRMs). Ru-486, the onlycurrently used SPRM, is in investigative trials fortreatment of fibroid pain and bleeding and helpsby reducing the size of fibroids. Most of thesetrials suggest that the medication is well toleratedwith minimal side effects. A second SPRM calledasoprisnil has been shown to significantly shrinkfibroids with minimal side effects and is currently

in phase III trials. It is not known if this is a tem-porary or permanent treatment.

The other area of medical research involvesantifibrinolytic agents. There are other fibrindeposition diseases such as keloids (excessivegrowth of scar tissue) and pulmonary fibrosisthat serve as fibrin disease models. Researchersare beginning to look at medications that reducethe growth and deposition of fibrin for treatmentof fibroids. There are no significant investiga-tional trials underway at the present time.

The newest nonmedical technique being usedto treat fibroids is high-intensity focused ultra-sound. This is done in the radiology departmentwith MRI-guided high-intensity focused ultra-sound. The uterus is scanned for fibroids anddivided into plains at different depths, and theultrasound is directed in small increments intothe fibroid. It is completely noninvasive and isjust beginning to be used. The setups are veryexpensive and the machines are few and farbetween at this point.

The thermal ablation treatment techniquesthat transfer laser, radio frequency, microwave, orcryotherapy through either a percutaneous or atransvaginal probe (which were evaluatedbetween 2000 and 2003) are largely outdatednow and are not thought to be an effective formof treatment.


Four clinical problems that require special con-sideration in fibroid cases are heavy, prolonged,or frequent bleeding; infertility; enlarged kid-neys; and pregnancy complications.

Menstrual flows that are longer than 7 days induration, more frequent than every 21 days,involve intermenstrual spotting/bleeding orexcessive blood loss (more than 80 ml per cyclecompared to the normal average of 33 ml)deserve a visit to your licensed primary care prac-titioner. It is difficult to quantify the number of


pads or tampons used as a criterion for determin-ing excessive blood loss. Bleeding that meets orexceeds saturation of a super tampon or heavypad every hour for six to eight hours or morerequires immediate intervention. Bleeding thatexceeds this deserves an immediate phone call toyour practitioner and urgent management forhemorrhage. Some women tolerate excessiveblood loss better than others. If you are feelinglightheaded, this is cause for concern. A hemo-globin and hematocrit test can determine if youare anemic from blood loss. Additional tests maybe done to determine if your iron stores are low.

Infertile women who have uterine fibroidsmay need to consider the causal relationship. Eventhough fibroids may be a cause of only a small per-centage of infertility cases, if it is the cause, thesolutions aren’t particularly optimistic. It isreported that only a 16 percent pregnancy rate fol-lows myomectomy for infertility. Postoperativeadhesions and the low return question the value ofmyomectomy for this set of circumstances.

Pregnancy in women with uterine fibroids isgenerally problem-free, but each situation is differ-ent. Even though fibroids can grow during preg-nancy, only a very few actually do have continuedgrowth. Six weeks after delivery, many uterinefibroids will decrease in size to become similar tothe size it was prior to pregnancy.

That said, some complications can occurduring pregnancy. An enlarging fibroid duringpregnancy can degenerate and cause pain, infec-tion, and fever. Though debatable, the presenceof fibroids can also affect implantation of the fer-tilized egg with the potential for an early miscar-riage, bleeding later in the pregnancy, prematurerupture of membranes, and postpartum hemor-rhage. Other potential complications include adecrease in the ability of the uterus to contractduring labor or obstruction of the birth canal. In

women who have previously had a myomectomy,the safety of a vaginal delivery is controversial.One school of thought holds that if there hasbeen an incision into the uterine cavity, the deliv-ery must be by cesarean section. Other practi-tioners believe that if there was no infection afterthe myomectomy, the incision into a nonpreg-nant uterus is of no concern in subsequent vagi-nal deliveries.

Remember, the mere presence of uterinefibroids does not require treatment. If you havesymptoms, they can most often be managed withalternative therapies, although excessive bleedingmay require drug or surgical intervention. Even if you have no symptoms, a licensed primaryhealth-care practitioner should examine youevery six months to rule out rapid enlargement.This is especially true for women who are plan-ning pregnancies or approaching menopause.Rapidly enlarging fibroids warrant special atten-tion because of the potential for malignancy. Ayoung woman whose uterus is larger than a 12-to 14-week pregnancy should carefully monitorthe fibroid growth and consider the need for sur-gical intervention, because there are many moreyears for potential further growth and the biggerthe uterus and fibroids, the more technically dif-ficult the surgery.

Women rarely need to rush to any decisionabout surgical intervention, except in the case ofexcessive bleeding problems, a rapidly enlargingfibroid uterus, or prolonged or severe pain. If sur-gical intervention becomes appropriate, remem-ber that you may have a number of surgicaloptions and explore some of the newer tech-niques. If a hysterectomy is indeed the bestoption, and sometimes it is, then be sure to dis-cuss with your surgeon whether you would liketo keep your ovaries; most of the time, there is nopressing medical need to remove them.

341

20C H A P T E R

OVERVIEW

Vaginal infections are responsible for an estimated10 percent of all women’s visits to health-carepractitioners. There are three general categories ofvaginitis: hormonal, irritant, and infectious. Hor-monal vaginitis, also called atrophic vaginitis, isusually found in postmenopausal or postpartumwomen, but occasionally in young girls beforepuberty. (Atrophic vaginitis in menopausalwomen is addressed in greater detail in Chapter12.) Irritant vaginitis can be due to allergies tosuch substances as latex in condoms, spermicides,deodorants, soaps, perfumes, semen, or douches.1

Irritation may also be due to hot tubs, mechanicalabrasion, sanitary napkins, tampons, toilet tissue,or topical medications.

However, most vaginitis is due to a vaginalinfection. More than 90 percent of vaginitis inreproductive-age women is caused by bacterialvaginosis, candidiasis, or trichomoniasis. There areother less common infectious causes of vaginitislike gonorrhea, chlamydia, mycoplasma, campy-lobacter, and even parasites like pinworms and giardia. Among these, gonorrhea, chlamydia, andtrichomona are sexually transmitted. Women whohave sexually transmitted vaginitis require treat-ment with antibiotics to prevent pelvic inflamma-tory disorder; testing and treatment should beoffered to partners as well. To learn more aboutsexually transmitted infections, see Chapter 18.

General symptoms of infectious vaginitisinclude a vaginal discharge, irritation, itching, andodor. Not all infectious causes of vaginitis have thesame symptoms, but they all are associated with avaginal discharge. Though vaginitis is often easilytreated, some women may experience chronic orrecurrent infections that may be resistant to usualtreatments. In addition, untreated vaginitis may

result in more serious complications such as acuteor chronic pelvic inflammatory disease (PID),chronic pelvic pain, and infertility. Vaginitis mayalso increase the transmission of other sexuallytransmitted infections like human immunodefi-ciency virus (HIV) and genital herpes.

Vaginitis is most often a disorder of imbalanceof the normal vaginal flora. Many of the organ-isms that are responsible for vaginitis, like gard-nerella, mycoplasma, staph, E. coli, and candidaare naturally occurring in the healthy vagina.These organisms only become problematic whenthe delicate balance of the beneficial bacterial, likeaerobic lactobacillus, is disrupted. There are anumber of factors that may adversely affect thisbalance by reducing the lactobacilli population,such as lubricants, nonoxynal-9 (spermicide), oralcontraceptives (OCs), hormonal changes, andantibiotics.

Though self-diagnosis is common, it is notrecommended, because it is difficult to make anaccurate diagnosis based on discharge, itching,and odor and because of the possibility of dualinfection. To properly treat vaginitis and avoidpotential treatment complications, it is essentialto know the exact diagnosis.

Bacterial Vaginosis

Bacterial vaginosis (BV) is the most commoncause of vaginal infections and abnormal vaginaldischarge and odor. Unfortunately, it can also beone of the infections most resistant to treatment.BV consists of a significant polymicrobial over-growth. It is the result of alterations in the vagi-nal ecosystem rather than an infection caused byany single microorganism. In BV, the ordinarilylactobacilli-dominant vaginal environment isovergrown with anaerobes (mainly Prevotella,

VA G I N I T I S



Peptostreptococcus species, Eubacterium species,and Mobiluncus) and facultative bacteria (Myco-plasma species, Staphylococcus epidermidis, Strep-tococcus species, and Gardnerella vaginalis). Thisovergrowth results in the degradation of themucus membrane and shedding of the vaginalepithelium, resulting in a discharge, and maylead to potential complications in the uterus andfallopian tubes. The destruction of these mucinsexposes the epithelium to other organisms, withthe subsequent appearance of clue cells (cells thatline the vagina and now have clusters of bacteriaadhered to their surface).2 These are visualizedwith microscopy and are unique to BV.

BV is characterized by decreased or absentLactobacillus species and increased concentra-tions of potentially pathogenic bacteria. Othercharacteristic changes include elevated pH,greater than 4.5; formation of clue cells; odordue to increased vaginal fluid concentrations of diamines, polyamines, and organic acids;3–5

an upregulation of inflammatory cytokines suchas interleukin (IL)-1beta, a noticeable absence orrare presence of white blood cells in the vaginaldischarge; and a decrease in naturally protectivemolecules like secretory leukocyte proteaseinhibitor. Four diagnostic criteria, of which threemust be present, confirm a diagnosis of bacterialvaginosis.

There are three main factors that are respon-sible for the decline of lactobacilli and conse-quential BV:

1. Intercourse without condoms: sperm alkalinizes the vagina, which depletes lactobacilli.

2. Douching, which also depletes lactobacilli.3. The absence of the kind of lactobacilli that

produce peroxide. Broad-spectrum antibi-otics can also eliminate healthy vaginal lactobacilli.6

Bacterial vaginosis may be merely an acute orepisodic condition, may become persistent, ormay resolve itself spontaneously.

More than 50 percent of women with BV areasymptomatic. BV most often occurs among het-erosexual, sexually active women, but is not con-sidered a sexually transmitted disease.7, 8 Amongthose who are heterosexually active, BV is more fre-quent in women who have had intercourse at anearly age, those with more sexual partners, andamong women with concurrent or prior sexually transmitted diseases.9 BV can also existamong sexually abused children and lesbian partners of women with bacterial vaginosis.10, 11

Several factors have been associated with the devel-opment of BV, such as cigarette smoking and racialbackground. Hispanic women are 50 percent morelikely than Caucasian women to develop BV, andAfrican-American women are twice as likely asCaucasian women to have BV.12 The reasons forthese differences are not clear but may be due toless condom use in Hispanic women and increaseddouching in African-American women.

The alterations in vaginal immune responseand vaginal microflora associated with BV leavewomen more susceptible to other infections,including HIV and gonorrhea.13–16 Women withBV are also more likely to shed HIV, and there-fore BV may increase the transmission of HIV.17

There are some potential consequences ofuntreated or undertreated BV.18 The bacteria canmigrate into the uterus and the upper genitaltract and cause pelvic inflammatory disease in aminority of women who have the infection. Theloss of lactobacilli and the resulting degradationof the mucin layer, as well as loss of the local

Diagnostic Criteria

Three of the following criteria must be present toconfirm a diagnosis of bacterial vaginosis.

1. A thin, frothy, gray, odorous discharge2. Vaginal pH greater than 4.5 with pH paper3. A wet-mount lab sample that reveals clue cells4. A positive whiff test (a fish odor detected when

10 percent potassium hydroxide is added to thedischarge)

343V A G I N I T I S

immune response, may allow pathogens toascend to the uterus and fallopian tubes. In preg-nant women, BV can cause premature rupture of membranes and premature labor, and it isresponsible for 70 to 80 percent of all perinataldeaths.19 BV is also responsible for approximatelyone-third of postpartum endometritis (infectionof the uterus).20 Additionally, women with sub-optimal vaginal flora are at increased risk forinfections following gynecologic surgery.

It has been estimated that about 30 percent ofwomen experience a recurrence of symptomaticBV within 30 to 90 days of treatment, and 70percent will have a recurrence within ninemonths.21 With BV, it may not be clear whetherthe repeat episode is a reinfection or a relapse.Reinfection implies that the original problemwas reversed and the patient was completelyasymptomatic before recurrence; relapse indi-cates that the symptoms and microbiology havenever returned to normal even though there mayhave been improvement or a period of improve-ment. Reinfection is a possibility due to exposureto the same factors that caused the first episode.In heterosexual women not using condoms, rein-fection may be due to the alkalinizing effect ofsemen. This alkaline environment fosters over-growth of BV. The treatment for recurrent BVshould focus on preventing relapse, as this is themost common cause of recurrence. Possible rea-sons for relapse include (1) lack of reestablishingthe lactobacillus-dominant vaginal flora, (2) per-sistent overgrowth of pathogenic bacteria, and (3) some of the pathogens have sequestered them-selves in inaccessible sites such as the endometrialcavity.

A simple and useful method for monitoringpatients during treatment for BV is pH paper. Ifa woman has a vaginal pH of less than 4.5 (somesay of less than or equal to 5.0), she has adequatenumbers of lactobacilli and does not have BV.

The goal of treatment is to restore the vaginalpH to less than 4.5 and reestablish normal vagi-nal ecology. Treatment is considered successful if

it clears up the clue cells and amine fishy odorand restores the vaginal flora to healthy levels of lactobacilli. Reexamination following treat-ment is fundamental to assure that the pH hasdecreased to less than 4.5. If it has not, then youare at risk for developing a recurrence. If pHremains greater than 4.5 following treatment,more aggressive use of lactobacillus and/or vagi-nal boric acid suppositories should be utilized.The first follow-up should occur after the desig-nated treatment time of usually 7 to 14 days,then again in one month.

Treatment of BV in nonpregnant women willreduce vaginal symptoms, lower the risk ofpostabortion and posthysterectomy infectiouscomplications, and may reduce transmission ofand infection with other sexually transmittedinfections. Women should refrain from sexual

Prevention of Bacterial Vaginosis

• Practice safe sex, which is helpful in prevent-ing even infections not clearly considered tobe sexually transmitted, such as bacterial vaginosis.

• Consider regular condom use to prevent vaginitis and maintain a normal pH.

• Use condoms until treatment regimen is com-plete to prevent recurrence.

• Eat a diet rich in whole foods with little to nosugar or refined carbohydrates.

• Determine possible allergies to food, pollen,clothing detergent, and semen for recurrentcases.

• Determine possible infection with other organ-isms for recurrent cases.

• Increase intake of acidophilus yogurt and/ortake supplemental lactobacillus supplements,especially when using antibiotics.

• Vaginal estrogen may be necessary to maintainan acidic vaginal environment in postmeno-pausal women.

• In cases of relapse, take boric acid and lacto-bacillus vaginally for 1 to 2 weeks, plus lacto-bacillus orally for 2 to 6 months.


intercourse during the treatment period and untiltheir vaginal ecology is normal. Women who haverecurrent BV following intercourse may need touse condoms or consider having the sexual partnertreated at the same time. Unfortunately, BV canbe the most difficult vaginal infection to treat sat-isfactorily with alternative treatments. However,even conventional treatments can be insufficientwithout a lot of patience and time.

Candida Vaginitis

Although vulvovaginal candidiasis (VVC), morecommonly known as a candida or yeast infection,is often assumed to be the cause of vaginitis, only33 percent of vaginitis cases are in fact VVC.VVC is frequently misdiagnosed by both patientsand practitioners. It encompasses a broad rangeof issues, ranging from those who have coloniza-tion of yeast but are asymptomatic to those who have frequent, recurrent, and symptomaticepisodes. It is estimated that 75 percent of allwomen will have at least one VVC infection intheir life, 45 percent will have multiple episodes,and 5 to 8 percent will have recurrent episodes(RVVC, defined as four or more episodes withinone year).22

Studies throughout the world have shownthat Candida albicans is the most common causeof VVC. It is the organism identified in 85 to 90percent of positive vaginal yeast cultures. How-ever, there are infections with nonalbicans speciessuch as C. glabrata, C. tropicallis, and C. krusei,which are becoming more prevalent in theUnited States. Of the nonalbicans species, Can-dida glabrata is the most common. The numberof VVC cases that are due to nonalbicans speciesis increasing and rose from 9.9 percent in 1988to 17.2 percent in 1995.23 It is thought that thisincrease is due at least in part to the increased useof over-the-counter treatment medications andthat nonalbicans species are becoming less andless susceptible to these agents.24

A diagnosis of VVC is made by a combina-tion of history, clinical examination, microscopy,

and, if necessary, a culture. The usual symptomsof VVC are acute itching and vaginal discharge.The discharge is typically described as cottagecheese–like in character, but it may actually varyfrom watery to thick. Symptoms may alsoinclude vaginal soreness, irritation, vulvar burn-ing, inflammation and swelling of both the inter-nal and external genital tissue, redness, pain withvaginal sexual activity, and urinary discomfort.The symptoms are often worse the week preced-ing the onset of menses with some relief after themenstrual flow.

Self-diagnosis of VVC is unreliable and oftenresults in misdiagnosis. There is even a concernthat physicians are frequently inaccurate in diag-nosing vaginal infections.25 The most candida-specific symptom is itching without discharge,and even this criterion correctly predicts VVC inonly 38 percent of patients.26

The greatest concern in self-diagnosing andself-treating VVC is in women who have recur-rent VVC, defined as four or more candida-confirmed episodes of symptomatic infectionwithin one year. This occurs in approximately 5 percent of women27 and can be dangerous, asthe underlying condition could go undiagnosedbecause the woman is repeatedly treating whatshe thinks are simple vaginal yeast infections.Recurrent VVC commonly affects women whoare immunocompromised as the result of AIDSor other predisposing conditions such as dia-betes, Cushing’s disease, Addison’s disease, hypo-or hyperthyroidism, or leukemia. There are otherpredisposing factors in recurrent infections thatmay also need to be addressed: high-estrogenmedication, antibiotics, hormones, contraceptivedevices, cytotoxic drugs, immunosuppressivedrugs, radiotherapy or chemotherapy, tightclothing, nylon underwear, pregnancy, and exces-sive sugar in the diet.

Reinfection may also come from extravaginalsources. Although the sexual transmission of can-dida is still controversial, there is evidence thatsexual transmission might be a likely source of


recurrent infection. In one study, the researchersfound identical strains of candida in the malesexual partners of 48 percent of women withrecurrent VVC.28, 29 Reservoirs of infection werefound in the oral cavities of 36 percent of 33 het-erosexual couples, the rectums of 33 percent, andthe ejaculate of 15 percent of the men.30 Thisdata suggests that oral-genital contact constitutesa probable mode of sexual transmission. Manyalternative practitioners treat the overgrowth ofcandida in the digestive track as well to addressthe possibility of migration from rectum to vagina.In fact, a 1977 study found that in 98 womenwith recurrent VVC, candida was always found inthe feces of women with current VVC and was notfound in women without VVC.31 Althoughnumerous studies have failed to yield definitiveresults, it may provide a useful avenue of treat-ment in especially chronic and resistant cases.32

The first step in the physical evaluation is todetermine if there is a vulvitis (inflammation ofthe external genital tissue) and/or vaginitis. Somewomen may have vulvar hyperplasia (prolifera-tive cell growth), vestibulitis (inflammation ofthe tissue surrounding the opening to thevagina), genital ulcerations, lichen sclerosis, orother dermatitis conditions. A thorough exami-nation of the external genitalia involves lookingfor erythema, hypopigmentation, hyperpigmen-tation, fissures, vesicles, ulcerations, thinning,and thickening. A woman with VVC will oftenhave vulvar and vaginal redness, swelling, anditching. A thick white discharge may be present,but many women with VVC do not have a dis-charge or do not have the typical thick and whitedischarge.

The diagnosis can often be made in the prac-titioner’s office by using 10 percent potassiumhydroxide (KOH) and microscopy that demon-strates features of yeast. Another diagnostic toolis pH paper. A vaginal pH of less than 4.5 helpsto exclude bacterial vaginosis, trichomoniasis,atrophic vaginitis, or a mixed bacterial/yeastinfection. A vaginal culture may help to establish

that yeast is in fact present for symptomaticwomen with negative microscopic findings andto identify the genus and species.

It cannot be overemphasized how the healthof the entire body affects the internal ecosystemof the vagina. The vaginal pH and microflora,the hormonal cycles, and the vaginal immunetissue are all influenced by our general health anddietary habits, and this in turn determines oursusceptibility to vaginitis. A healthy diet assuresour body’s defense system. A diet low in sugarsand refined carbohydrates is particularly impor-tant in preventing candida vaginitis. In fact, arecent study confirmed that women withimpaired glucose tolerance were at higher risk forrecurrent vaginal candidiasis.33 In general, a well-balanced whole foods diet that is low in fat,sugars, refined foods, and alcohol is optimal inpreventing all infections.

Some women who have severe, stubborncases of chronic candida vaginitis may benefitfrom stricter diets that avoid fermented foods.However, many “anti-candida” diets can be rigor-ous and unnecessarily stressful. Some of thesediets are so restricted that they actually causeother health problems. Women who have self-diagnosed or who have been diagnosed with “sys-temic candida” by an alternative practitionermight want to make sure of this popular over-used diagnosis. Conventional medicine uses theterm systemic candidiasis to describe the situationwhen candida contaminates the blood streamand spreads throughout the body, causing pro-found illness affecting a wide variety of organ sys-tems. This state, according to this definition,only occurs in seriously immunocompromisedpatients, such as HIV-positive individuals. Inindividuals who have no serious immune defi-ciency, any exposed warm, moist part of the bodyis susceptible to candida infection. Commonexamples of this would include vulvovaginitis,oral thrush, conjunctivitis (infection of the innereyelid), diaper rash, and infections of the nail,rectum, and other skin folds. In immuno-


compromised individuals, systemic illnesses suchas myocarditis (infection of the heart muscle),hepatosplenic abscess, pulmonary infection, cen-tral nervous system (CNS) infection, and chronicdisease states may occur.

Alternative medicine has used the term sys-temic candidiasis to describe less intense situa-tions, in an attempt to explain a multitude ofgeneral symptoms such as headache, fatigue, gasand bloating, depression, and more. Perhaps abetter term for this would be systemic candidasyndrome. Ruling out other causes of these gen-eral symptoms is important, and testing the stooland vaginal secretions for candida overgrowthand the blood for the candida antigen providesthe best hope for accurately diagnosing true sys-temic candida infections.

The main concepts of managing VVC areaccurate diagnosis, management of other influ-ences, and being creative and persistent whentreatment does not provide relief or recurrences

occur. Taking shortcuts in history, physical exam,and testing can result in misdiagnosis, unneces-sary treatments, and delays in effective treatment.Most cases of VVC will be very effectively treatedwith natural methods. When this does not work, there are various oral and vaginal regimensincluding butoconazole cream, clotrimazolecream or vaginal tablet, miconazole cream orsuppository, terconazole cream or suppository,fluconazole oral medication, and nystatin vaginaltablets. Treatment options for nonalbicans can-dida infections include more aggressive flucona-zole and terconazole regimens, flucytosinevaginally, and boric acid vaginal capsules.

While VVC may seem trivial to many, forsome the discomfort, the chronicity, and thehealth-care costs incurred are excessive. Treat-ment strategies for candida vaginitis with naturaltherapies will focus on maintaining a normalvaginal pH, restoring normal ecology of thevagina, reducing inflammation, relieving symp-toms, and using natural antifungal agents.

Trichomonas Vaginalis

Trichomonas vaginalis is a motile, flagellate, anaer-obic protozoan and is a far more prevalent sexuallytransmitted infection than either Chlamydia trachomatis or Neisseria gonorrhoeae. About 6 per-cent of all cases of a vaginal discharge are due totrichomoniasis, and about 5 million new casesappear annually.36, 37 The prevalence of diseasevaries widely by population. Multiple sexual part-ners, African-American race, previous history ofsexually transmitted diseases, coexistent infectionwith Neisseria gonorrhoeae, and nonuse of eitherbarrier or hormonal contraceptives are known risk factors for acquisition of trichomoniasis.38

Trichomoniasis is associated with several signifi-cant health consequences, including the transmis-sion of the human immunodeficiency virus(HIV), infertility, atypical pelvic inflammatorydisease (PID), increased risk of postoperativeinfection, preterm births, and cervical dysplasia aswell as adverse pregnancy outcomes such as

Prevention of Candida Vaginitis

Preventing infections is almost always easier thantreating them. Here are some simple strategies:

• Avoid wearing tight clothing.34

• Avoid wearing pantyhose.35

• Consider using condoms to prevent all types ofvaginitis and maintain a normal pH in thevagina.

• Eat a whole foods diet with very little to nosugar and refined carbohydrates.

• Determine possible allergies to food, pollen,clothing detergent, and semen for recurrentcases.


• Increase intake of acidophilus yogurt and/ortake lactobacillus supplements, especiallywhen using antibiotics.

• Vaginal estrogen may be necessary to maintainan acidic vaginal environment in postmeno-pausal women.


preterm delivery, premature rupture of mem-branes, and low–birth weight infants.

The sexual transmission rates are higher fromman to woman than from woman to man, andtransmission is considered rare from woman towoman. Trichomoniasis is rarely transmitted toinfants born to infected mothers, and althoughthe trichomonas organism can survive for shortperiods on moist objects (toilet seats, benches,towels) or exposed bodily fluids (urine, vaginalexudate, semen), no cases of transmission byindirect or inanimate exposure have been docu-mented. Prevalence of trichomoniasis is highestamong women with multiple sexual partners and in women with other sexually transmittedinfections.39–41

The most common complaints associatedwith trichomoniasis are vaginal discharge andvulvovaginal irritation and itching. Discharge ispresent in 50 to 75 percent of infected womenand is classically described as frothy or bubblyand yellow-green. Other associated symptomsinclude dyspareunia (pain with vaginal sexualactivity), dysuria (painful urination), and, in asmall number of patients, some degree of lowerabdominal pain. Vulvar redness is an uncommonfinding, but vaginal redness is noted in as manyas 75 percent of patients. A “strawberry cervix” iscreated by dilatation of capillaries on the cervixwith small hemorrhages and is seen through amagnification device called a colposcope in asmany as 90 percent of cases.42 With the nakedeye it is seen in only 2 percent of cases, but whenit is seen it is an almost sure sign of trichomoni-asis. As these clinical signs and symptoms are notsensitive enough or specific enough to be usedalone, it’s most important to somehow identifythe organism.

The time-honored method for diagnosing trichomonal infections has been microscopic(wet prep) evaluation. The diagnosis is made by directly observing the motile parasite. Thisprocedure detects 60 to 80 percent of cases. Theadvantage of the microscopic examination of the

vaginal discharge is that it can be done in thepractitioner’s office; it’s fast, easy, and low cost;and an immediate diagnosis can be made.

If the trichomonad was not seen, a culture ismore sensitive for diagnosis. A culture in Dia-mond’s medium is both sensitive and specific.However, there is a diagnostic delay because ofthe time it takes for the culture to detect theorganism. Pap smears are not very sensitive intesting trichomoniasis, only 56 percent effectivein one study,43 and are therefore not a very reli-able method.

Newer tests are available now that increaseaccuracy and ease diagnosis. A DNA-based test

KEY CONCEPTS

• Diagnosis is necessary to determine the cause ofthe vaginal infection.

• Be aware of underlying metabolic or immuneproblems in chronic resistant cases of candidavaginitis.

• In recurrent cases of candida vaginitis and bac-terial vaginosis, consider the possibility ofsexual transmission, even though they are nottypically considered STIs.

• The sexual partner should be treated in all casesof trichomoniasis.

• Consider additional testing methods such as cultures and DNA probes in cases that eludediagnosis.

• Self-diagnosis is usually inaccurate and caninhibit successful treatment.

PREVENTION

• Use condoms to prevent all types of vaginitisand maintain a normal vaginal pH.

• Eat a whole foods diet with very little to nosugar and few refined carbohydrates.


• Increase intake of acidophilus yogurt and/ortake lactobacillus supplements.


called the Affirm VP system uses a probe insertedin the vagina that can detect trichomoniasis, bac-terial vaginosis, and candida species from a singlevaginal swab. Additional diagnostic methodsinclude polymerase chain reaction tests, but mostdoctors’ offices do not yet use these. A new 10-minute antigen test for trichomonas is also avail-able. Women who are found to have an infectionof T. vaginalis should also be tested for Neisseriagonorrhoeae (GC) and Chlamydia trachomatis (CT)and, if positive for one or both, should then bescreened for additional sexually transmitted infec-tions, including syphilis, hepatitis B and C, HIV,herpes type 2 virus, and human papillomavirus.

The treatment strategy is to kill the tri-chomonads, reduce inflammation, support thevaginal ecology and immune system, and preventrecurrence.


An important aspect of treating vaginal infec-tions is looking at the problem holistically andsystemically rather than just finding drug alterna-tives to kill unwanted organisms. To this end, we try to improve the vaginal immune system,support the systemic immune system, restore the proper balance of normal microflora in thevagina, restore the normal pH of the vagina,decrease the inflammation and irritation of thetissue itself, provide symptomatic relief, and,when necessary, curb the overgrowth of theoffending organism.

Although this approach sounds basic and log-ical, it is radically different than the conventionalapproach, which is essentially to kill the over-growth of the causative organism. Although insevere acute cases pharmaceutical antifungalsmay ultimately be necessary, organisms arebecoming resistant to these products due to theiroveruse, and newer, stronger treatments are con-tinually developed to address these resistantstrains. Thus, even when the pharmaceutical

over-the-counter or prescription medicationsneed to be used, the principles and methods ofthe natural treatments can be an important partof ensuring a healthy vaginal ecosystem andimmunity for the future.

The health of the ecosystem of the vagina isthe most important concept in treating vaginitis.While the vaginal flora and ecosystem is in a variable state throughout a woman’s lifetime,largely affected by hormonal influences, nothingis more key to this ecosystem than lactobacillus.The vaginal microflora of healthy asymptomaticwomen consist of a wide variety of anaerobic andaerobic bacteria dominated by lactobacillus. The first extensive study of the human vaginalmicroflora was published in 1892 by Doder-lein.44 Since then we have learned that a widevariety of microorganisms are present in ahealthy vaginal ecosystem. The range of bacterialtypes is immense, including Staphylococcusspecies, Gardnerella vaginalis, Streptococcusspecies, Bacteroides species, Lactobacillus species,Mobiluncus, even Candida species, most com-monly Candida albicans, and more. Yet the predominant organisms are members of theLactobacillus genus.

The body’s ability to control the vaginalmicroflora is no easy feat. The normal vaginalmicroflora defend against abnormal vaginal colo-nization. Factors controlling this defense systeminclude the content of the vaginal tissue itself(called the squamous epithelium), the domi-nance of lactobacilli, the subsequent low oracidic pH balance, hydrogen peroxide produc-tion, and hormonal influences (over one’s lifetime as well as monthly cyclic changes). Highor low estrogen states such as pregnancy ormenopause; hormonal medications such as con-traceptive devices, including OCs; femininehygiene products; and vaginal sexual activity,including friction, lubricants, and semen can allcreate a challenge for the vaginal ecology tomaintain homeostasis.


Nutrition

I cannot overemphasize how the health of theentire body affects the internal ecosystem of thevagina. The pH of the vagina, the microflora thatlive there, the hormonal cycles, and the immunetissue in the vagina are all influenced by our gen-eral health and dietary habits, and this in turndetermines how susceptible we are to vaginitis. A generally healthy diet—well balanced, rich inwhole foods, and low in fat, sugars, refined foods,and alcohol—is optimal in preventing infections.A diet low in sugars and refined carbohydrates isparticularly important in preventing candidavaginitis. Some women who have severe, stub-born cases of chronic candida vaginitis may ben-efit from stricter diets that avoid fermentedfoods; however, most of the time these “anti-candida” diets are not necessary.


Vitamin E. We most often think of usingnutritional supplements orally, but in this case Irecommend the use of vitamin E intravaginallyand topically. This use of vitamin E dates back atleast to 1954.45 As demonstrated then as well asin my practice, vitamin E provides a very sooth-ing effect. The tissue becomes less irritated witha decrease in redness, swelling, and congestion.Vitamin E usually relieves burning and itchingwithin one to three days. It can be administeredas either a suppository or from a gelatin capsulethat is inserted into the vagina once or twicedaily for seven or more days. Vitamin E oil orointment can also be applied externally to the

vulvar tissue to relieve discomfort there. VitaminE is especially useful in cases of allergic and irritant-induced vaginitis because it is so soothing.

Vitamin E

Intravaginal suppository or gelatin capsule once ortwice daily for 7 or more days

Vitamin C. Vitamin C has long been toutedfor its beneficial effects on the immune system.According to a recent study, administering 250 mgof vitamin C vaginally for six days significantlyimproves both subjective and objective parametersof vaginitis, like eradicating bacteria and clue cells,increasing lactobacilli, and lowering pH.46

Vitamin C

Insert 250 mg vitamin C tablet in the vagina for 6days

Vitamin A and Beta-Carotene. Both vita-min A and beta-carotene are necessary for thenormal healthy growth of epithelial tissues thatmake up the vaginal mucosa. Vitamin A andbeta-carotene enhance the immune response inepithelial tissues and thereby help mucous mem-branes resist infection. Vitamin A and beta-carotene can be used orally to enhance theimmune response, and vitamin A can be usedintravaginally to stimulate the local immunetissue of the vaginal mucosa. Vitamin A in a cap-sule can suffice, but vitamin A suppositories areavailable in higher doses than a standard capsule.Vitamin A intravaginally is useful in cases ofinfectious vaginitis as well as allergic and irritant-induced vaginitis. Daily use for up to one week isNutrition

• Avoid sugar, refined carbohydrates, fruit juice,and alcohol.

• Reduce fats.• Eat 8 oz of unsweetened acidophilus yogurt

daily.• Increase garlic in the diet.

Vitamin A

Intravaginal suppository or gelatin capsule once dailyfor 7 days; use vitamin E, lactobacillus, or mixedherbal suppository daily for 1 week before repeatingthis dosage.


typical. It can be repeated after one week withoutsuppositories or one week of some alternate likevitamin E, lactobacillus, or a mixed herbal sup-pository to avoid any possible side effects.

Botanicals

Garlic (Allium Sativum). Garlic extracts havebeen shown to inhibit the growth of Candida albicans by blocking the lipid production.47, 48

The major growth inhibitory component ingarlic extract is allicin, and garlic products thathave the highest amount of allicin are the mostdesirable for treatment. Look specifically forproducts with high allicin and the stabilized formof allicin. Garlic is diverse in its uses for vaginitisbecause it is both antibacterial and antifungal.49, 50

I recommend garlic vaginal suppositories forboth candida (yeast) vaginitis and bacterial vagi-nosis. A clove peeled carefully so as not to nickthe garlic can be inserted into the vagina for 6 to 8 hours. The garlic can be threaded like anecklace so that it can be easily removed like atampon. Garlic or garlic capsules can be insertedintravaginally in the evening, and then lacto-bacillus capsules can be inserted in the morningto inhibit growth of the offending organism andrepopulate the healthy microflora.

Goldenseal (Hydrastis Canadensis) andOregon Grape Root (Berberis Vulgaris). Gold-enseal and Oregon grape root contain a sub-stance called berberine that acts both as anantibacterial and as an immune enhancer. Thisimmune effect is especially specific in epithelialmucus membrane tissue as is found in the vagina,mouth, and even the stomach. Berberine hasbeen shown to possess antimicrobial activityagainst a wide variety of microorganisms, includ-ing those found in the vagina, such as Candidaalbicans, Escherichia coli, Staphylococcus aureus,and others.51 Preparations of goldenseal andOregon grape root have been used both orally inteas, caps, and liquid extracts and intravaginallyin douches and suppositories. Because of their

ability to affect both yeast and bacteria, these twoherbs would seem a logical choice in cases wheremultiple infectious agents are involved.

Goldenseal or Oregon Grape Root

Orally (capsules or liquid extracts) or intravaginally insuppositories

Tea Tree (Melaleuca Alternifolia). Tea tree oilhas been studied for trichomoniasis, candidiasis,and other vaginal infections. Most of the evidencesupports its use against candida species.52–54 Onestudy found tea tree effectively inhibited both fluconazole-susceptible and fluconazole-resistantcases of candidiasis in vitro and in animals.55, 56

Perhaps the most impressive study used an emulsi-fied 40 percent solution of Australian tea tree oilwith 13 percent isopropyl alcohol. In the 96 casesof trichomonal vaginitis, clinical cures were seenwith the application of six treatments applied onceweekly with a solution-saturated tampon left inplace for 24 hours (see “Sample Treatment Plan forTrichomonas Vaginalis” sidebar later in this chapterfor specifics).57 Various tea tree oil preparationshave demonstrated antimicrobial activity againstStaphylococcus aureus and Candida albicans, therebyshowing its usefulness in diverse situations.58

Tea Tree Oil

Emulsified 40 percent solution of Melaleuca alternifoliaoil with 13 percent isopropyl alcohol: wash vaginalcanal for 30 seconds once a week for 4 weeks, thenuse vaginal tampon saturated with solution for 24hours following each washing.

Other Therapeutic Agents

Lactobacillus. Several species of lactobacilluspopulate the vagina. Although we often think of Lactobacillus acidophilus as being the mostdominant, other species, such as L. crispatus,L. jensenii, L. fermentum, and L. gasseri are atleast as or more dominant than Lactobacillusacidophilus.


Several factors explain how and why lacto-bacillus does its remarkable job. Through its production of lactic acid, lactobacilli contributeto the low vaginal pH that is instrumental inmaintaining a healthy vaginal microflora.Because vaginal infections are associated with aloss of lactobacilli, it seems logical and hopefulthat lactobacilli would make for a good treat-ment.59 Lactobacilli thrive at an acidic pH of 3.5to 4.5, levels that are found in the healthy, normalvagina throughout the menstrual cycle. Lacto-bacilli have also been shown to interfere with theadherence and colonization of pathogenic (disease-causing) bacteria.60 In addition, strains of lacto-bacilli that inhabit the vagina produce hydrogenperoxide (H2O2), another well-recognized antago-nist to problematic bacterial populations. Lacto-bacilli also act directly as antibacterials61 and mayfunction as a local immune stimulant in control-ling microbial levels in the vagina.

For these reasons, administering lactobacillusorally and intravaginally is one of the mostimportant aspects of effectively treating and pre-venting yeast and bacterial vaginitis, although thescientific literature has inconsistent results.Women who have hydrogen peroxide–producinglactobacilli in the vagina are less likely to havebacterial vaginosis or candida vaginitis.62 Thesesame lactobacilli are also toxic to Gardnerellavaginalis, the predominant organism in thevagina of women with BV.63 In addition, the bac-teria that cause bacterial vaginosis thrive in ahigher pH of 5.0 to 6.0 and cannot readily sur-vive in the lower pH, more acid environmentthat lactobacilli promotes.

The concept that lactobacilli might be usefulwhen supplemented in the diet or administeredintravaginally dates back to the 1890s. While sci-entists have vacillated on the value of lactobacilliin prevention or in treatment, patients in needhave not. It has been difficult to confirm the “ifs,ands, or buts” in using L. acidophilus in the pre-vention and treatment of infectious vaginitis

because there are few clinical trials. When youconsider the logic, the safety, the affordability,the lack of side effects, the ease, and the researchthat does confirm a benefit, continuing to pro-mote the use of L. acidophilus is a compellingone. Lactobacillus therapy is quite popular bothwith alternative practitioners and with womenwho seek simple self-treatment methods.

A study was done in 1992 on the daily inges-tion of yogurt containing Lactobacillus aci-dophilus in pregnant women with recurrentcandidal vaginitis. The women who ate eightounces daily of the yogurt had a threefolddecrease in infections when compared to thewomen who did not eat the yogurt.64 It is nowalso popular to ingest Lactobacillus acidophilussupplements in oral form in place of or in addi-tion to eating yogurt or to apply lactobacillidirectly into the vagina.

A number of studies have supported the use oflactobacillus in preventing and treating vaginitis.A recently published study on treating BV foundthat both vaginal administration and oral-plus-vaginal administration of lactobacilli were effectiveat reducing the vaginal pH, treating the currentinfection, and preventing recurrence over the sub-sequent three months.65 Another study examinedthe effectiveness of weekly intravaginal Lacto-bacillus acidophilus versus clotrimazole (antifun-gal) tablets in HIV-positive women, a grouphighly susceptible to recurrent yeast vaginitis, andfound the two treatments to be similarly effectiveat preventing candidiasis.66 After any conventionaltreatment with antibiotics, vaginal lactobacilluscan be restored by the coadministration of lacto-bacillus and low-dose vaginal estriol.67 This isespecially important for preventing VVC afterconventional treatment of BV.

A review of lactobacillus treatments for VVCin 200368 found that vaginally administered ororally ingested lactobacillus is able to colonizethe vaginal ecosystem and that most supplemen-tation needed to continue for two to six months


in order to sustain continued colonization. Theauthor also concluded that controlled trials areencouraging but few, and that these trials hadsmall numbers of women, inadequate controls,lack of blinding, high attrition rates, and werenot consistent in the form of lactobacillus used.In addition, they had conflicting results.

Douching used to be a popular method ofadministering lactobacillus, but research hasshown that douching may contribute to infertil-ity and pelvic infections. A safer and more con-venient method is to administer lactobacilluscapsules or tablets intravaginally.69

I believe that lactobacillus, alone or in combi-nation with other vaginal or oral therapies, is thekey to establishing normal vaginal microflora andpreventing recurring infections, as well as treat-ing acute candida and bacterial infections of thevagina. A word to the wise, however, is buyerbeware. There is a great deal of variability in lactobacillus products. For yogurt, make sure thelabel lists lactobacillus, and choose a brand with-out sweeteners. Some yogurts and encapsulatedproducts make claims that they contain L. aci-dophilus but, when tested,70 they did not; more-over, they contained contaminants. When

purchasing encapsulated products, it may beworth requesting product analysis information toassure quality and choosing human strain lacto-bacillus to enhance adherence to the intestinaland vaginal mucosa.

Vaginal Estrogen. One of my most reliabletreatments for chronic or chronic recurring yeastvaginitis or bacterial vaginosis is the use of vaginal estrogen. This is best seen in peri- andpostmenopausal women, but it can be used fordifficult cases in younger women as well. Suffi-cient estrogen promotes the growth of the lacto-bacillus species that maintain the normal vaginalecology. Using this concept as a treatment waswell illustrated in a randomized, placebo-controlled study of 32 premenopausal womenwith bacterial vaginosis71 that used hydrogen peroxide–producing lactobacillus vaginal tabletsdelivered with 0.03 mg of vaginal estriol (a Euro-pean product called Gynoflor). The study foundthat estrogen enhances the acid production of thelactobacilli and assists in their proliferation, inaddition to helping maintain normal vaginaltissue health. At two weeks, a 75 percent curerate occurred in the treatment group comparedwith a 25 percent cure rate in the placebo group.At four weeks, there was an 88 percent cure rateversus a 22 percent placebo rate.

Although this product is not available in theUnited States, vaginal estriol is available by pre-scription from a compounding pharmacy. Yourpractitioner could either request that the phar-macy formulate an estriol/Lactobacillus acidophilussuppository or cream, or a vaginal estriol cream(0.03 mg/g; insert one gram daily for two weeks)and L. acidophilus capsule or suppository (onedaily for two weeks) could be inserted separately.

Boric Acid. The most successful naturaltreatment for VVC that I’ve encountered is boricacid suppositories. Laboratory tests and humantrials support its use for both Candida glabrataand albicans, even in cases of resistance to anti-fungal prescription drugs.72, 73 Several studies

Lactobacillus

Prevention

• Eat 8 oz unsweetened live-culture acidophilusyogurt daily.

• Oral Lactobacillus acidophilus or combinationmultispecies of probiotics daily. Doses mayrange from 2 to 10 billion organisms per dayfor as short as 2 weeks and as high as 24 to48 billion organisms per day for 2 to 6 monthsto maintain vaginal colonization.

Treatment

• For acute infections: intravaginal tablet, gela-tin capsule, or suppository once or twice dailyfor a few days to 2 weeks.


confirm its success, ranging from 64 to 98 per-cent effective.74–76 In one study, 100 women withchronic resistant yeast infections who had failedextensive and prolonged conventional therapywere treated with 600 mg boric acid vaginal suppositories twice a day for two or four weeks;the regimen was effective in curing 98 percent ofthe women.77 Once daily boric acid suppositoriesused for four days per month during the mensesfor four consecutive months was also clearly indi-cated as the treatment of choice for preventingrecurrence.

Clinical effectiveness doesn’t really get anybetter than this. Boric acid works most of thetime, it’s inexpensive, and it’s easy to use. Theonly downside I have observed is that if the tissuehas been irritated by the infection, the boric acidmay burn during urination. Using vitamin E oil,lanolin, or even Vaseline on the external genitaliaprotects the tissue from the boric acid and avertsany significant discomfort. In a study that com-

pared boric acid with the more conventionallyprescribed nystatin, the boric acid cured 92 per-cent after 10 days and 72 percent after 30 days,compared to 64 percent and 50 percent, respec-tively, of nystatin.78

Boric Acid

Acute: 600 mg vaginal suppositories twice a day for3–7 days

Chronic: 600 mg vaginal suppositories twice a day for2–4 weeks

Prevention: 600 mg vaginal suppositories 4 days permonth during menses for 4 consecutive months

Arden’s Powder. A colleague of mine hasbeen using a vaginal douche powder calledArden’s Powder for over 20 years. She attributesits antifungal properties to the essential oils ofeucalyptus, thyme, and boric acid powder. Thementhol crystals in the oils provide quick relieffrom itching and burning even before the infec-

Sample Treatment Plan for Bacterial Vaginosis

Guidelines

• Provide systemic and local immune enhancement.

• Restore vaginal flora and normal vaginal pH.• Use natural antimicrobials.• Relieve symptoms.

2-Week Minimum Regimen

See the Resources section for natural products andformulations used in this regimen.

• Avoid refined foods and simple carbohydrates.• Avoid vaginal sexual activity during course of

treatment to avoid reinfection and reduce irritation.

• Insert one herbal suppository (containingmyrrh, echinacea, slippery elm, golden sealroot, marshmallow, geranium, and yarrow) intovagina every evening, 5 days per week for 2weeks.

• Insert a more potent suppository containinga combination of thuja oil, tea tree oil,bitter orange oil, and vitamin A (as palmi-tate) 2 days per week for the same 2 weeksas the herbal suppositories.

• Follow with vaginal lactobacillus supposi-tory: insert daily for 6 days.

• Oral lactobacillus: take 1 daily for 2 to 6months to restore normal vaginal ecology.

• If there is a recurrence, add boric acid sup-positories; insert 1 daily for 2 weeks.

Other Considerations

• Use boric acid suppositories (600 mg) toacidify the vagina either as a primary treat-ment or after antibiotic regimens.

• Paint the cervix and vagina with povidone-iodine twice each week. (A speculum examwould be the most desirable method ofdoing this.)


Sample Treatment Plan for Candida Vaginitis

Guidelines

• Provide systemic and local immune enhance-ment, especially in chronic cases.

• Restore vaginal flora and maintain normalvaginal pH.

• Natural antifungal agents will be effective inmost cases.

• Relieve symptoms.

Acute Infection

Follow these guidelines for a minimum of 1 week:

• Avoid sugars, refined carbohydrates, and alcohol.

• Eat 8 oz unsweetened acidophilus yogurt daily.• Lactobacillus species capsules: 8 billion or

more organisms per day.• Boric acid powder capsules: insert morning and

evening for 3–7 days in mild cases and up to14 days for resistant cases.

Chronic Infection

• Avoid sugars, refined carbohydrates, alcohol,and fermented foods.

• Eat 8 oz unsweetened acidophilus yogurt daily.• Lactobacillus species capsules: 8–48 billion

organisms per day.• Garlic (allicin) capsules: 1–2 capsules 2 to 4

times daily.

• Boric acid powder capsules: insert morningand evening for 14 days; repeat for an addi-tional 14 days if responding but not com-pletely resolved after the first 2 weeks.

Prophylaxis for Prevention of Recurrence


• Eat 8 oz. unsweetened acidophilus yogurtdaily.

• Lactobacillus species capsules: 8–48 billionorganisms per day.

• Boric acid powder capsules: insert 1 capsuleonce daily at bedtime during menstruationonly for 4 consecutive months.

During Pregnancy

Avoid boric acid suppositories, herbal supposito-ries, and garlic during pregnancy. Consult youralternative and conventional medical practitionerfor safe options. The following guidelines are gen-erally safe for pregnant women:


• Eat 8 oz unsweetened acidophilus yogurtdaily.

• Lactobacillus species capsules: 8 to 48 bil-lion organisms per day.

tion is cleared. Although I have not been a strongproponent of douching, this old-fashionedapproach can most likely be used safely for yeastvaginitis.

Arden’s Powder

Mix 1 tsp Arden’s Powder in 1 pint warm water; douchewith 2 applications daily for the first 2 days, thenreduce to 1 application daily for 5 more days. Avoid dur-ing menstrual period or during pregnancy.

Herbal Combinations. Many different herbscan be prepared in combinations for suppository

use or even douching. In vitro research supportsthe effectiveness of propolis, cayenne, clove, and bergamot oil against a number of Candidaspecies.79 Other in vitro evidence showed berg-amot oil alone and in combination with boricacid to be effective against Candida species, sug-gesting a potential role for topical treatment ofcandida infections.80

Powdered herbal mixes of myrrh, echinacea,usnea, goldenseal, marshmallow, geranium,yarrow, and calendula are often used by herbalistsand naturopathic physicians. Each herb has itsown special feature, whether antimicrobial,


immune enhancing, soothing to the membranes,or antifungal. These suppositories can be made athome with powdered herbs and cocoa butter orcan be purchased from a natural food store oralternative health-care practitioner.

Gentian Violet. Most herbal suppositories,including boric acid and tea tree oil, should beavoided during pregnancy. However, gentianviolet is effective for the mother-to-be and safefor the fetus. In the 1950s, this was the mostcommonly used and favorite treatment of gyne-cologists. It can be painted onto the cervix andthe vaginal wall, but leaves a disconcerting, sig-nature blue stain; moreover, it requires a specu-lum insertion to apply. A gentian violet gel madeup according to the following formula is moredesirable and appropriate for home use: 0.2 per-cent gentian violet; 3.0 percent lactic acid; 1.0percent acetic acid; and polyethylene glycol base.This preparation was proven effective in a 1950study.81 Of 191 cases studied, 78 percent wereconsidered cured, 12 percent were significantly

improved, 3 percent had modest improvement,and 7 percent showed no improvement.

Gentian violet is available only by prescrip-tion in certain states. You may be able to find amilder strength available without a prescription.Put a few drops of the over-the-counter concen-tration onto a tampon if you want to try using iton your own.

Gentian Violet

See a licensed health-care practitioner for a prescrip-tion. Use 1 vaginal applicator daily at bedtime for12 days.

Iodine. Yeast and trichomonal vaginitis infec-tions can often occur simultaneously. Moreover,after treatment for trichomoniasis, a yeast infectionmay flare up. Local therapy that can treat bothwould obviously be desirable. Iodine in the form ofpovidone-iodine preparations is a logical solution.This is another example of an older successful treat-ment that got left behind in the face of more

Sample Treatment Plan for Trichomonas Vaginalis

Guidelines

• Provide systemic and local immune enhancement.

• Restore vaginal flora and normal vaginal pH.• Use natural antimicrobials.• Relieve symptoms.• Treat sexual partner(s).

Treatment

• Avoid sugars, refined carbohydrates, and alcohol.• Tea tree oil: 40% water-miscible emulsified

solution with 40% M. alternifolia oil and 13%isopropyl alcohol.

• Repeat the following treatment once per weekfor up to 6 weeks: Thoroughly wash the vulvaand vagina with pHisoHex followed by a thor-ough water rinse. Dry the area and swab the

vulva and vagina with a 1% solution of thebasic medication (i.e., 0.4% M. alternifoliaoil), using approximately 15 cc. Then inserta tampon that has been saturated with thesolution and keep it in place for 24 hours.

• Douche daily for up to 7 weeks with a solu-tion of 1% of the basic M. alternifolia oilsolution in 1 quart of water (0.4% oil).

• Eat 8 oz unsweetened acidophilus yogurtdaily for 1 month.

• Lactobacillus species capsules: 8 to 48 bil-lion organisms per day.

• Garlic (allicin) capsules: 1–2 capsules 2 to 4times daily.

• Consider goldenseal, echinacea, garlic,licorice, and myrrh for systemic botanicalimmune support.


modern, mass-market pharmaceuticals. In additionto candidiasis and trichomoniasis, povidone-iodinehas been proven effective against potentially patho-genic microorganisms like Gardnerella, Bacteroides,and Enterobacteria without adversely affecting thelactobacillus population.82, 83

One study combined a povidone-iodine solu-tion for swabbing, a povidone-iodine vaginal gelfor application at night, and a povidone-iodinedouche for use in the morning in 93 courses of treatment in 87 patients with yeast or tri-chomonal vaginitis, or a combination of both. Inthe yeast vaginitis cases, symptoms were clearedin one to three weeks in all 74 courses of treat-ment. In four of five patients with trichomonalvaginitis, symptoms were cleared within threeweeks. In 14 courses for combined infections,symptoms were cleared within three weeks in 13patients.84 Another study found that nearly 75percent of cases (trichomoniasis, candidiasis, andnonspecific vaginitis) had complete resolutionwith povidone-iodine treatment.85

Iodine

See licensed health-care practitioner for 6-day regimenusing povidone-iodine preparations.


The accurate diagnosis of vaginitis is critical.Incorrect self-diagnosis or guesswork by the prac-titioner can lead to unnecessary and ineffectivetreatment, thus prolonging the symptoms.

Bacterial Vaginosis

Bacterial vaginosis is more common than can-didiasis and is frequently overlooked or misdiag-nosed. The initial evaluation suggests candidiasis;the candidiasis is treated and the bacterial vagi-nosis is overlooked, left untreated, and continuesto provide a hospitable environment for candida(yeast). Again, an accurate diagnosis is impor-tant, and risk factors for BV should be discussed.

The mainstay of therapy is metronidazole,either orally or in a vaginal gel. Other treatmentregimens involve clindamycin, either orally or ina vaginal cream. Tinidazole, FDA-approved forthe treatment of trichomoniasis, has also beenused for treatment of BV in patients who havefailure of clindamycin and have nausea and vom-iting problems with metronidazole. This shouldnot be used in people who are allergic to metron-idazole because they are members of the sameclass of drugs. Alcohol intake should be avoidedwhile using metronidazole due to a drug interac-tion causing violent vomiting.

Recurrent BV is common and is often associ-ated with high levels of stress. Recommendedprevention regimens include metronidazole(0.75 mg gel, or one full applicator) one to twotimes per week for six months or metronidazolegel for 10 days on the initial treatment. There isno need to treat the sexual partner.

Candida Vaginitis

Uncomplicated, acute candidal infections can betreated with one of a variety of products. Cur-rently, there are over 100 prescription and over-the-counter preparations that are marketed to

Treatment of Acute Bacterial Vaginosis

Recommended Oral Medications

Oral metronidazole: 500 mg twice daily for 7 daysOral metronidazole: 250 mg 3 times daily for 7 daysClindamycin: 300 mg orally twice a day for 7 days

Recommended Vaginal Medications

Metronidazole gel (0.75%): 5 g vaginally once dailyat bedtime for 5 days

Clindamycin cream (2%): 1 full applicator (5 g)intravaginally at bedtime for 7 days

Sustained-release clindamycin (2%): 1 full applicator1 time only (7-day duration)

Clindamycin ovules (100 g): intravaginally once atbedtime for 3 days


deal with this problem. Despite the latest “third-generation” anticandidal preparations, womencontinue to be plagued by the occurrence andrecurrence of candidal vulvovaginal infections.While this is sometimes because of undiagnosedand untreated bacterial vaginosis, chronic yeastinfections do occur. The 2006 CDC recommen-dations for treatment of candidiasis are listed inTable 20.1.

Topical azoles are more effective than nystatinand provide for symptom relief and completetreatment in 80 to 90 percent of patients whofollow recommended treatment guidelines.Creams and suppositories are oil-based and canweaken latex condoms and diaphragms, however,so it is important to be warned of this possibility.For recurrent vulvovaginal candidiasis, extendthe initial topical or oral therapy. The first treat-ment of recurrence would involve a longer 7- to14-day topical therapy regimen or a dose of flu-conazole orally every three days for a total ofthree doses. If this does not work, then consider

oral fluconazole once weekly for six months. Ifthis treatment is not feasible, one can also usetopical clotrimazole (200 mg twice a week) oronce-weekly clotrimazole (500 mg) vaginal sup-positories for six months.

Emergence of azole-resistant candidiasis isincreasing. For non-albicans candidiasis, the recur-rence treatment recommendation is 600 mg ofboric acid in a gelatin capsule vaginally once dailyfor two weeks following the original oral or vaginaltreatment. Sometimes adding oral Lactobacillus aci-dophilus, especially for women who are using oralcontraceptives, daily or every other day helps toreduce recurrences. This is discussed in more detailin the alternative medicine section of this chapter.Instruction in proper hygiene (in terms of alwayswiping from front to back) is also helpful. There isno need to treat the sexual partner.

Trichomoniasis

The treatment of trichomoniasis has not changedvery much over time; it calls for treating the patient

Table 20.1 CDC Guidelines for Intravaginal Treatment of Yeast Vaginitis

Intravaginal Drug Regimen

Butoconazole 2% cream 5 g single intravaginal application

Clotrimazole 1% cream (OTC) 5 g intravaginally for 7–14 days

Clotrimazole 100-mg vaginal tablet 2 per day for 3 days

Miconazole 2% cream (OTC) 5 g intravaginally for 7 days

Miconazole 100-mg vaginal suppository (OTC) 1 per day for 7 days

Miconazole 200-mg vaginal suppository (OTC) 1 per day for 3 days

Miconazole 1200-mg vaginal suppository (OTC) 1 in a single dose

Nystatin 100,000-unit vaginal tablet 1 per day for 14 days

Tioconazole 6.5% ointment (OTC) 5 g intravaginally in a single application

Terconazole 0.4% cream 5 g intravaginally for 7 days

Terconazole 0.8% cream 5 g intravaginally for 3 days

Terconazole 80-mg vaginal suppository 1 per day for 3 days

Oral Drug Regimen

Fluconazole 150-mg oral tablet 1 in a single dose


and her partner with oral metronidazole. Recom-mended medications are metronidazole 2 g orallyin a single dose; the new Tindamax (tinidazole) 2 gorally in a single dose; or metronidazole 500 mgorally twice daily for seven days. For pregnantwomen, metronidazole is the safe treatment ofchoice with 2 g metronidazole in a single oral doseduring pregnancy. Nursing women should with-hold breast-feeding for 12 to 24 hours after thedose of metronidazole. If you are taking Tindamax,practitioners recommend that you interrupt breast-feeding for three days after the dose.


The most appropriate way to assure an accuratediagnosis is to see a licensed health-care practi-tioner (naturopathic doctor; medical doctor;osteopathic doctor; nurse-practitioner, or physi-

cian’s assistant) who is familiar with the clinicalpicture of various forms of vaginitis, can performa physical exam, knows what to test for, and cancollect those samples during your exam. Accuratediagnosis is the most important key to efficientand appropriate treatment, whether the therapiesare natural or pharmaceutical. If you know whatkind of infection you currently have and chooseself-treatment, it is essential to recognize when andif self-treatment isn’t working and to seek profes-sional care at that time. It is most important toseek professional care when infections recur morethan three times per year, if you have a chronicinfection that doesn’t fully resolve, or when youare pregnant. Specific testing can be done, but,more important, a licensed practitioner can helpdetermine if underlying disorders are contributingto the vaginal infection. All the alternative thera-pies discussed in this chapter are generally safe forhome use, except for pregnant women.

359

A P P E N D I X

There is strong and rapidly accumulatingevidence that muscular exertion reduces

cancer risk. The following recommendations arebased on a review of recent scientific literature onphysical exercise and cancer risk reduction:

1. To prevent injuries, begin each exercise ses-sion with Joint Warming Exercises and endeach exercise session with Basic Stretches(see the following pages).

2. Exercise six days a week. Walk or do moder-ate hiking on your day off.

3. Alternate aerobic (cardiovascular) withstrength (weight lifting) exercises.

4. Take one day off each week:

• Forget about your work, your bills, yourproblems. Seek peace in the woods ormountains.

• Refresh your being with pure air, purewater, simple food, and communion withnature.

• Hike moderately, read a good book, liedown and look at the sky or the birds, ortake a nap.

• This is your day of recreation. Let nothinginterfere with it.

5. Calculate your training heart rate (THR) foraerobic exercise. THR is defined as the rangeof heart rates that is safe for your heart andwill strengthen it. To do this, first calculateyour maximum heart rate (MHR):

MHR � 220 � your age (in years)

Next calculate your training heart rate(THR) as a percentage of MHR. If you arejust beginning, multiply MHR by 60 per-

cent and 70 percent to get the bottom andtop of the range:

Bottom THR � MHR � .60

Top THR � MHR � .70

Otherwise, multiply MHR by 70 percentand 85 percent:

Bottom THR � MHR � .70

Top THR � MHR � .85

Divide the results by 6 to calculate THR per10 seconds.

As an example, let us calculate THR fora 50-year-old woman who is beginning toexercise.

MHR � 220 � 50 � 170 beats perminute

Bottom THR � 170 � .60 � 102 beatsper minute

Top THR � 170 � .70 � 119 beats perminute

To calculate THR per 10 seconds:

102 � 6 � 17

119 � 6 � 20

THR range � 17–20 beats per 10 seconds

For this example, the recommendationwould be, after three minutes of aerobicexercise, check your pulse for 10 seconds. Ifit is less than 17, increase your pace. If morethan 20, reduce your pace. Repeat this pro-cedure every three minutes or so throughoutyour exercise session.

AG E N E R A L

E X E R C I S E P R O G R A M


360 A P P E N D I X A

JOINT WARMING EXERCISES

The following exercises are designed to protectthe joints against injury from weight-bearingexercise. These exercises should be performedbefore any cardiovascular or strength workout.

1. NeckRotate neck gently to left 5 times, then toright 5 times.

2. ShouldersRotate shoulders forward 10 times, thenbackward 10 times.

3. Elbows, Wrists, and FingersBegin with arms bent, elbows against thesides of body, hands forming a fist againstshoulders. Then extend arms fully, directlyin front of you, while opening hands andextending fingers. Return to initial position.Repeat 10 times.

Repeat motion, but this time raise yourhands above your head. Don’t forget to openyour hands and your extend fingers as youextend your arms above your head. Repeat10 times.

4. Trunk and WaistBend your trunk at the waist from right toleft and from left to right. Avoid stiffeningyour muscles or applying force as you dothis exercise. Perform the exercise as a gentlerocking movement from side to side. Alter-nate right to left for 20 counts.

5. Hips“Hula-hoop” exercise. Perform full circleswith your hips rotating clockwise 10 times.Repeat rotating counterclockwise 10 times.

6. Hips and KneesBring right knee close to chest by using bothhands around knee and gently pulling withyour arms. Count to 20. Repeat with leftknee.

7. KneesStanding on left leg, gently bend and extendthe right leg 20 times. Repeat exercise with

the left leg, 20 times while standing on rightleg.

8. AnklesStanding on left foot, rotate right ankleinward 10 times and then outward 10 times.Repeat exercise with left ankle while stand-ing on right foot.

BASIC STRETCHES

Here are some general guidelines for stretching:

• Stretch at the end of the exercise session,when muscles are warm.

• Hold stretch steadily—do not bounce.• Accept a bit of discomfort but avoid pain—

do not push.

1. Calves, Hamstrings, Back, Neck• Stand, feet apart about shoulder width,

toes pointing forward, knees straight.• Let head and trunk fall forward and

down. Let arms hang down. Allow gravityto push down your trunk so that your fin-gertips will get closer and closer to yourtoes, without forcing.

• Relax in this position for 30 seconds (overseveral weeks, increase gradually to 60 seconds).

2. Inner Thigh, Low Back• Standing, separate feet as much as possi-

ble, knees straight.• Bend trunk forward at the hips, let arms

and head hang down comfortably.• Relax in this position for 20 seconds.

3. Inner Thigh, Right Side of the Body, LeftHamstrings• Same position as in stretch 2. Rotate

trunk over left leg and let your trunk andarms hang along the left leg with handstrying to reach the left foot.

• Relax in this position for 20 seconds.• Repeat with trunk and arms hanging

along the right leg.• Relax in this position for 20 seconds.

361G E N E R A L E X E R C I S E P R O G R A M

4. Tibialis, Quadriceps, Abdominals, Chest,Front of Neck• Kneel on hands and knees, with thighs

and arms perpendicular to the floor.• Keeping hands and knees in place and

arms extended, move trunk forward untilyour abdomen touches the floor. Thenraise your head up and back so that youcan see the ceiling.

• Hold this position for about 20 seconds.• Keeping hands and knees in place and

arms extended, move trunk backwarduntil your buttocks touch your heels. Lethead down, forehead against the floor.

• Relax in this position for 20 seconds.

PREVENTING EXERCISE INJURIES

Prevention of exercise injuries revolves aroundseveral guidelines:

1. Stretching. Stretching exercises should beengaged in after every exercise session, especiallyconcentrating on the muscle groups that havebeen utilized during the exercise session. For walk-ers and runners, this means concentrating on pos-terior leg muscles, the lower back, and the front ofthe chest. For cyclers, this means the quadriceps,posterior leg muscles, and upper back. For swim-mers, the shoulder joints especially should bestretched as well as the lower back and calves.2. Strengthening. Often muscle imbalances can

create injury problems. For knee problems in run-ners, for example, often the hamstrings are toostrong and the quadriceps are too weak, so pro-gressive resistance exercises for the knee (exten-sion) can be performed, both for prevention andtreatment. If the shin area is giving problems ormight potentially be a future problem, the ante-rior leg muscles can be strengthened through toe-raising resistive exercises (with stretching of thecalf muscle, which is often too strong).3. Warming up and down. Slow aerobic exer-

cises should always precede and follow hard aer-

obic exertion. Five- to ten-minute transitionperiods between rest and exercise and then restare important to help the metabolic, circulatory,and neuromuscular systems adapt withoutinjury or trauma. A recommended warm-up isJoint Warming Exercises (see instructions).4. Proper equipment. Safety equipment and

quality footwear are important for all sports.For the runner this may mean reflective tapeand $50 to $100 shoes; for the cycler, thismeans a hard helmet; for the racquetball player,goggles, etc.5. Gradual progression. The number-one

cause of musculoskeletal problems is overuse—too much, too fast, too soon. A conservativebeginning, with gradual progression, is the mostimportant injury-prevention practice and isreadily available. Many beginner exercisers areoverzealous initially and soon acquire injuriesthat thwart future exercise.6. Moderation. Avoid too much of any one

activity. Engaging in several different activitiescan help prevent overspecialization and resultingmuscle imbalances and overcompulsion.7. Responsibility of the individual. The indi-

vidual’s responsibility is to stay within the toler-ance of her or his own musculoskeletal system.Individual judgment and common sense shouldbe utilized to “listen” to one’s body, makingadjustments when necessary. This can meanavoiding that extra three miles of running orthat extra set of squats, being regular in train-ing, obtaining adequate rest and optimal nutri-tion, and seeking a balanced approach.8. Be willing to rest. An important equation

in exercise is “Exercise plus rest equals fitness.”In other words, it takes both exercise and ade-quate rest to build fitness. Either alone will notdo it. Often beginner exercisers will sacrificesleep time to get up and exercise. Chronicfatigue may result, and the whole purpose ofexercise—to feel better—is negated. It’s impor-tant to get both rest and exercise.


9. Exercise technique. Various aerobic activi-ties require special techniques to avoid injury.Flexibility exercises demand stretching belowthe pain threshold. Regarding aerobic activitiessuch as running or jogging, it is important tokeep the body in an upright posture and thearms at a 90-degree angle, swinging from theshoulder. The feet should land almost flat-footed with the weight well back toward theheel. Only sprinters should run on their toes.Breathing should be through the mouth andnose in a regular fashion. Overall, the bodyshould be loose, natural, and poised. Each sport should be studied to ensure adequate technique.

ABBREVIATED GENERAL EXERCISE PROGRAM

Aerobic Exercise

Beginner

• Allow at least 6 weeks for conditioning ofyour heart: exercise very moderately.

• Exercise at a training heart rate (THR) thatis 60–70 percent of your maximum heartrate (MHR).

• Walk for 15 minutes. Increase time of exer-cise gradually to 30 minutes over the 6-weekperiod.

More Advanced

• For 10 weeks, increase THR to 65–75 per-cent of MHR.

• Walk for 30–45 minutes.

Advanced

• Increase THR to 70–85 percent of MRH.• Walk for 45–60 minutes.• Introduce variations in program. For exam-

ple, do interval training: walk fast for 5 min-utes and then jog for 30 seconds. Repeatcombination three times during workout.

Strength Exercise

Beginner

• Follow program of exercise planned for youby an exercise specialist.

• Allow at least 8 weeks for conditioning ofyour muscles and joints: exercise very mod-erately and increase weight gradually everyweek as you get stronger.

More Advanced

• For 6 weeks, do 10 reps, 2 sets.• Keep increasing weight every week,

gradually.

Advanced

• Divide workout into upper body exerciseson alternate days.

• Do 10 reps, 3 sets of each exercise.

Preventing Injury from Strength Training

• Work with an exercise specialist who canshow you the safe way to use weights.

• Do not compete with anyone but yourself.• Begin with very light weight, so that you

can perform 12–15 repetitions of the exer-cise easily. Increase weight very gradually.

• Avoid holding your breath while lifting.Breathe in during relaxing part of exerciseand breathe out during effort part of exercise.

• Rest and take a mouthful of pure waterbetween exercises.

• Warm up for 3–5 minutes before weight lift-ing exercises and stretch the muscles usedduring the exercise session after the workout.

SPEAK PREGNANCY EXERCISES

These exercises for pregnant women are adaptedfrom Health magazine (December 1993: 28–30).

1. Cobbler’s Pose. This exercise helps the pelvicorgans by promoting circulation of blood in this

363G E N E R A L E X E R C I S E P R O G R A M

area. It also helps to assure the correct position ofthe pelvis. This exercise can be done as often asyou like and can be used in general as a sittingposition. When sitting in this position, youshould be able to feel a stretch on the inside ofyour thighs, vagina, and hip joints. You may alsofeel stretching in your knees and ankles.

• Sit on the floor with your back straight andlegs stretched out in front. You can sitagainst a wall to support the lower back.

• Bend your knees and let your knees relaxaway from each other to each side, bringingthe bottom of your feet together. The solesof your feet should now be touching withthe outside ankle region resting on the floor.

• Pull your pressed-together feet as close tothe opening of your vagina as possible.Open out your thighs and let your kneeslower toward the floor. Breathe deeply.

2. Kneeling with Knees Apart. This positionhelps to alleviate low back pain and decreasetension in the pelvis and pelvic joints. Thepelvic joints open and the muscles are able torelax and lengthen in the low back and pelvis.Stretch only as far as you can without bendingyour back, and then hold this position whilebreathing deeply. You should be able to feel thestretch in the vaginal region and in the kneesand ankles.

• Kneel on the floor with knees as wide apart aspossible, the top of your feet on the floor, andyour toes pointing in toward each other. Tryto sit between your feet with your buttockson the floor or sit on top of your heels.

• Move slowly forward from the hips, keepingyour buttocks down as much as possible andthen lean forward and place your palms onthe floor in front of you with both armsstraight. Try resting on your arms, keepingyour back straight. You should feel a stretchin the vagina.

• Try a gently rocking movement, shiftingyour weight from your arms to your legs.

• Breathe deeply while trying to stay in thisposition for a minute or longer, and thencome up and resume a normal sitting position.

3. Pelvic Floor Exercises. This exercise willhelp your pelvic floor muscles relax if you do itoften enough. This will prove to be helpful inthe second stage of labor, and it may prevent atear when giving birth. This exercise should bedone daily, especially in the third trimester.

• Stand with your feet about two feet apart.Squat down and end up squatting on theballs of your feet. Lean forward onto yourhands, keeping your arms and back straight,and open your knees wide apart, pointingthem to the outside.

• Tighten your pelvic floor muscles, pullingthem in as if you are trying to stop yourselffrom urinating. Hold for several seconds, andthen slowly let go. Repeat three to five times.

• Repeat the exercise again, but this time letgo in four stages, a little at a time.

• Repeat the exercise again, and this time pic-ture your baby’s head passing through yourpelvis during the second stage of labor. Eachtime you breathe out, imagine that yourbaby is continuing to pass through yourvagina as you release your pelvic muscles.

4. Pelvic Tuck-In. One of the health problemsduring pregnancy can be strain on the lowerback due to the extra weight. This exercisestrengthens the buttocks muscles, increases sup-port to the lower back, and stabilizes the pelvis,which can help prevent back pain. A gentlerocking movement added to the exercise can begood practice for labor and lessen pain and easethe passage of the baby through the birth canal.

• Position yourself on the floor on your handsand knees. Your knees should be about onefoot apart.


• Pull in and tighten your buttocks, pullingyour pelvis so that your back arches like acat’s back when it’s afraid or angry. Hold thisfor 10 to 15 seconds, and then let go.

• Repeat this at least six times, and then dothe exercise a little bit faster, rocking yourpelvis gently up and down along with yourback motion.

More Advanced Strength Training: Weeks 9–16

To continue with strength training, it is probably bestto join a health club, fitness club, gymnasium, or asimilar organization.

Divide your workouts into body parts and do twosets per exercise. Begin each workout by warming upfor 5 to 10 minutes and end each workout with 5 to10 minutes of Basic Stretches.

ExerciseDay Part (2 sets each) RepsDay 1 Chest Bench press 8–10

Biceps Arm curl 8–10Abdominals Easy crunches 8–10

Day 2 Back Pull-down to chest 8–10Triceps Arm extension 8–10Abdominals Easy crunches 8–10

Day 3 Legs Squat or leg press 8–10Calves Heel raise 8–10Shoulders Press behind neck 8–10

Weight Lifting Guidelines

1. Work out on alternate days.2. Take a mouthful of water between sets.3. For each repetition, breathe out during the

effort phase of the repetition, breathe in duringthe relaxation phase.

4. If, after a workout, the exercised muscles aresore for more than 48 hours, reduce the weightand/or the number of repetitions.

5. Most injuries from exercise result from doing“too much, too fast, too soon.”

6. Warm up for 5 to 10 minutes before the work-out. Joint mobility exercises are excellent forthis purpose.

7. From week to week increase weight slightly sothat you can continue to perform the samenumber of repetitions per exercise as in the pre-vious week.

8. After 16 weeks of this conditioning program,you may

Increase the number of sets per exerciseModify your routine to include other exercisesConcentrate on body areas that need extra work

Sample Conditioning Exercise Program: 8 Weeks

Aerobic (Sunday, Tuesday, and Thursday)

• Joint Warming Exercises (see instructions).• Walk briskly for 15 minutes. Gradually increase

to 30, 45, or 60 minutes over a period of 4 to6 weeks. (Other possibilities: Jog, run, swim,cycle, row, play a sport such as tennis, skate,ski, or water exercise.)

• Basic Stretches (see instructions).• Friction entire body, from feet up (30 sec-

onds), with dry washcloth.• Shower.

Strength (Monday, Wednesday, and Friday)

• Joint Warming Exercises (see instructions).• Walk briskly for 15 minutes.• Dumbbell exercises:

Week 1: begin with a weight that allows you todo 10–12 repetitions (reps) of each exerciseeasily.

Week 2: increase weight, 10 reps.Week 3: 10 reps, 2 sets per exercise.Week 4: increase weight, 10 reps, 2 sets.Week 5: increase weight, 10 reps, 2 sets.Week 6: increase reps to 12, 2 sets.Week 7: increase weight, 12 reps, 2 sets.Week 8: increase weight, 12 reps, 2 sets.

• Basic Stretches (see instructions).• Friction entire body, from feet up (30 sec-

onds), with dry washcloth.• Shower.

Rest (Saturday)

• See item 4 on page 359.

365

A P P E N D I X BB O D Y M A S S

I N D E X

Healthy Weight Overweight Obese

BMI 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36

Ht (in) Body weight (lb)

58 91 95 100 105 110 114 119 124 129 133 138 143 148 152 157 162 167 172

59 94 99 104 109 114 119 124 129 134 139 144 149 154 159 164 169 174 179

60 97 102 107 112 117 122 127 132 138 143 148 153 158 163 168 173 178 183

61 101 106 111 117 122 127 132 138 143 148 154 159 164 169 175 180 185 191

62 103 109 114 120 125 130 136 141 147 152 158 163 168 174 179 185 190 196

63 107 113 119 124 130 135 141 147 152 158 164 169 175 181 186 192 198 203

64 111 117 123 129 135 141 146 152 158 164 170 176 182 187 193 199 205 211

65 114 120 126 132 138 144 150 156 162 168 174 180 186 192 198 204 210 216

66 118 124 131 137 143 149 156 162 168 174 180 187 193 199 205 212 218 224

67 121 127 134 140 147 153 159 166 172 178 185 191 198 204 210 217 223 229

68 125 132 139 145 152 158 165 172 178 185 191 198 205 211 218 224 231 238

69 128 135 142 149 155 162 169 176 182 189 196 203 209 216 223 230 236 243

70 133 140 147 154 161 168 175 182 189 196 203 210 217 224 231 237 237 244

71 136 143 150 157 164 171 179 186 193 200 207 214 221 229 236 243 250 257

72 140 148 155 162 170 177 185 192 199 207 214 221 229 236 244 251 258 266

73 143 151 158 166 174 181 189 196 204 211 219 226 234 241 249 257 264 272

74 148 156 164 171 179 187 195 203 210 218 226 234 242 249 257 265 273 281

75 151 159 167 175 183 191 199 207 215 223 231 239 247 255 263 271 279 287

76 156 164 172 181 189 197 205 214 222 230 238 246 255 263 271 279 287 296



367

H O R M O N E R E P L A C E M E N T

T H E R A P Y P R E S C R I P T I O N SA P P E N D I X C

The following has been adapted from The 2004Guide to Hormone Therapy Products by NayahmkaMcGriff-Lee, Pharm.D., GlaxoSmithKline; andKarim Anton Calis, Pharm.D., M.P.H., Depart-ment of Health and Human Services, NationalInstitutes of Health (Ob/Gyn Special EditionSpring 2004: North American Menopause Society).

ORAL ESTROGENS

Cenestin 9 synthetic plant-derived conjugatedestrogens; slow-release tablet0.3 mg, 0.45 mg, 0.625 mg, 0.9mg, 1.25 mg

Enjuvia Synthetic conjugated estrogens0.3 mg, 0.45 mg, 0.625 mg, 1.25mg

Estratab Esterified estrogens0.3 mg, 0.625 mg, 1.25 mg, 2.5mg

Estrace 17 beta-estradiol; most active formof endogenous estrogen; up to 90%of the oral dose is converted toestrogen by the gut and liver0.5 mg, 1.0 mg, 2.0 mg

Femtrace Estradiol acetate0.45 mg, 0.9 mg, 1.8 mg

Gynediol 17 beta-estradiol; micronized for-mulation; 2 mg tablet contains tar-trazine (dye) that may cause allergyin patients with a sensitivity toaspirin0.5 mg, 1.0 mg, 1.5 mg; 2.0 mg

Menest Esterified estrogens (syntheticplant-derived)0.3 mg, 0.625 mg, 1.25 mg, 2.5 mg

Ogen Estropipate; 0.625 mg tablet con-tains 0.75 mg estropipate; 1.25 mg

tablet contains 1.5 mg estropipate;2.5 mg tablet contains 3 mgestropipate0.625 mg, 1.25 mg, 2.5 mg

Ortho-Est Estropipate; 0.625 mg tablet con-tains 0.75 mg estropipate; 1.25 mgtablet contains 1.5 mg estropipate0.625 mg, 1.25 mg

Premarin Conjugated equine estrogens;50–60% estrone sodium sulfate;20–35% equilin sodium sulfate and17 beta-dihydroequilin; smallamounts of 17 beta-estradiol andequilenin; contains over 200 com-pounds, including androgenic com-pounds0.3 mg, 0.45 mg, 0.625 mg, 0.9mg, 1.25 mg

Indications

Moderate to severe vasomotor symptomsVulvar and vaginal atrophyOsteoporosis prevention

Note: Cenestin and Menest are not FDA-approved for the prevention of osteoporosis;Cenestin 0.3 mg is indicated only for vasomotorsymptoms; Menest is indicated for atrophicvaginitis.

Adverse Effects

Common: breakthrough bleeding, breast ten-derness, nausea, bloating, abdominal cramps,vomiting, headache, dizziness, depression,peripheral edema, weight changes, rash, intoler-ance to contact lenses, migraine, libido changesRare: thromboembolism, stroke, endometrialcancer, breast cancer (when used with a proges-


368 A P P E N D I X C

togen), hepatic adenoma, gallbladder disease,increased blood pressure, myocardial infarction

Dosing

Continuous or cyclic (21 days on, 7 days off )Add a progestogen 10–14 days of month forwomen with uterus.

Drug Interactions

Drugs affected by oral estrogens: cortico-steroids (increased), levothyroxine (decrease),theophylline (increase), warfarin (decrease),antibiotics (decrease), androgens (decrease),nicotine (eliminates more rapidly)Drugs that affect oral estrogens: barbiturates(decrease), rifampin (decrease)

TRANSDERMAL ESTROGENS

Alora 17 beta-estradiol (2x/week); 0.05mg/24-hour patch0.025 mg, 0.05 mg, 0.075 mg, 0.1 mg

Climara 17 beta-estradiol (1x/week); 0.05mg/24-hour patch0.025 mg, 0.0375 mg, 0.05 mg,0.06 mg, 0.075, 0.1mg

Esclim 17 beta-estradiol (2x/week); 0.05mg/24-hour patch0.025 mg, 0.0375 mg, 0.05 mg,0.075 mg, 0.1 mg

Estraderm 17 beta-estradiol (2x/week);0.05mg/24-hour patchIncludes a drug reservoir of estradiol and alcohol and a copoly-mer membrane that controls the rate of drug diffusion0.05 mg, 0.1 mg

Estrasorb Topical emulsion of estradiol hemihydrate1 g emulsion � 2.5 mg estradiol;each foil-laminated pouch contains1.74 g (4.35 mg estradiol hemihy-drate); nominal estradiol deliveryrate of 0.05 mg/day

Estrogel 17 beta-estradiol; nonaerosol,metered-dose pump; gel dries in as little as 2–5 minutes1.25 g (0.75 mg estradiol) 1x/day; 1 pump � 0.05 patch

FemPatch 17 beta-estradiol0.025 mg (2x/week)

Menostar 17 beta-estradiolOne patch provides 14 mcg of estradiol per day (1x/week)

Vivelle or 17 beta-estradiol (2x/week); 0.05Vivelle-Dot mg/24-hour patch

0.025 mg, 0.0375, 0.05 mg, 0.075 mg, 0.1 mg

Indications

Moderate to severe vasomotor symptomsVulvar and vaginal atrophy

Note: Alora and Vivelle-Dot are also indicatedfor the prevention of osteoporosis; Estrasorb isindicated only for moderate to severe vasomotorsymptoms.

Adverse Effects

Common: Erythema and skin irritation occurs in10–17% of patients using reservoir-type patchescompared to approximately 5% with newermatrix-type patches, breakthrough bleeding,breast tenderness, nausea, abdominal cramps,headache, peripheral edema, migraineRare: rash, thromboembolism, stroke, endome-trial cancer, breast cancer (when used with aprogestogen), increased blood pressure

Dosing and Administration

Discontinue oral therapy for 1 week before ini-tiating transdermal estrogen.Patch should be applied to the trunk of the body.Avoid application on the breasts.Rotate application site weekly to minimize irri-tation.Patch may be worn while showering or swimming.

369H O R M O N E R E P L A C E M E N T T H E R A P Y P R E S C R I P T I O N S

Drug Interactions

See oral estrogens (except antibiotics and nicotine).

VAGINAL ESTROGENS

Estrace 17 beta-estradiol; 0.01% cream;cream 1 g 1–3x/week 0.1 mg per g

Consider starting with 2–4 g everyday intravaginally for 2–4 weeks,and then 1–2 g for 1–2 weeks;maintenance dose usually 1 g1–3x/week

Estring Alpha estradiol; biologically inertliquid polymer matrix with purecrystalline estradiol; releases 7.5mcg/24 hours over 90 days2 mg delivered over 90 days;replace ring every 90 days

Femring Estradiol acetate; device contains12.4 mg or 24.8 mg estradiol ac-etate, which releases 0.05 mg/24hours or 0.1 mg/24 hours; replaceevery 3 months

Ogen cream Estropipate; 2–4 g 1–3x/ week1.5 mg per g of cream

Premarin Conjugated equine estrogenscream (CEE)

0.625 mg per g of cream; 0.5–2 g1–3x/week; applicator marked in0.5 g intervals; absorbed slowerthan other estrogen preparationsand therefore a longer duration ofaction

Vagifem Estradiol hemihydrate vaginaltablets; a gel forms when thetablet comes in contact with thevagina; initial dose of 1 tablet1x/day for 2 weeks, and thenmaintenance of 2x/week25 mcg in single use applicator; 1tablet 2x/week

Indications

Vulvar and vaginal atrophy

Note: Premarin and Vagifem are indicated foratrophic vaginitis; Femring is also indicated formoderate to severe vasomotor symptoms.

Adverse Effects

Common: headache, nausea, vaginal discom-fort, vaginal candidiasisRare: vaginal trauma from the applicator ifpatient has severe atrophy


Daily dosing will achieve systemic concentrations.Low dose, 1–3x/week, will achieve predomi-nantly local effects.

Drug Interactions

See oral estrogens (except antibiotics and nico-tine); interactions are based on extent of systemicabsorption.

ORAL ESTROGEN-PROGESTINCOMBINATIONS

Activella 1 mg 17 beta-estradiol/0.5 mgnorethindrone acetateContinuous combined regimen, 1pill daily

Angeliq 1 mg 17 beta-estradiol � 0.5 mgdrospirenone

Femhrt 5 mcg ethinyl estradiol/1 mgnorethindrone acetateContinuous combined regimen, 1pill daily

Prefest 1 mg 17 beta-estradiol � 1 mg 17beta-estradiol/.09 mg norgestimate3 days estradiol tablet, and then 3days norgestimate tablet, alternat-ing continuously; packaged as 2separate tablets


Premphase 0.625 conjugated equine estrogen(CEE) days 1–14 days and a combotablet of 0.625 mg CEE/5.0 mgmedroxyprogesterone acetate (MPA) days 15–28Packaged as 2 separate tablets

Prempro 0.625 mg CEE/2.5 mg MPA; or0.625 mg CEE/5.0 mg MPA; or0.3 mg CEE/1.5 mg MPA; or 0.45 mg CEE/1.5 mg MPAA single tablet contains one of thefour dosing options; continuouscombined regimen

Indications

Combination therapy is indicated for womenwith an intact uterus

Adverse Effects

See oral estrogens and oral progestins.


Addition of a progestin for at least 10–12 daysper month protects against the increased risk ofendometrial hyperplasia that occurs with unop-posed estrogen use.Continuous combined therapy is an alternativeregimen that reduces and often eliminates with-drawal bleeding when compared to a cyclic regi-men.

Potential Drug Interactions

See oral estrogens (except antibiotics and nico-tine) and oral progestins.

TRANSDERMAL ESTROGEN-PROGESTIN COMBINATIONS

CombiPatch .05 mg 17 beta-estradiol/0.14 mgnorethindrone acetate; 2 patches/week.05 mg 17 beta-estradio/0.25 mgnorethindrone acetate; 2patches/week

ClimaraPro 0.045 estradio/0.015 mg lev-onorgestrel; 1 patch/week

Indications

Moderate to severe vasomotor symptoms

Note: CombiPatch is also indicated for vulvarand vaginal atrophy.

Adverse Effects

See transdermal estrogens and oral progestins.


Complete the current cycle of therapy beforeinitiating combination transdermal therapy.Apply to lower abdomen.


See oral estrogens (except antibiotics and nico-tine) and oral progestins.

ORAL PROGESTINS

Amen Medroxyprogesterone acetate 5.0 mg, 10 mg

Aygestin Norethindrone acetate 5 mg

Cycrin Medroxyprogesterone acetate2.5 mg, 5 mg, 10 mg

Megace Megestrol acetate 20 mg, 40 mg

Micronor Norethindrone acetate 5 mg

Nor-QD Norethindrone .35 mg

Ovrette Norgestrel 0.075 mg; 19-nor deriv-ative of testosterone with progesto-genic, estrogenic, androgenic, andantiestrogenic effects

Provera Medroxyprogesterone acetate2.5 mg, 5 mg, 10 mg; usual main-tenance dose of 5–10 mg daily for12–14 days per month

371H O R M O N E R E P L A C E M E N T T H E R A P Y P R E S C R I P T I O N S

Indications

To reduce the incidence of endometrial hyper-plasia in nonhysterectomized women receivingestrogen

Adverse Effects

Common: breast tenderness, nausea, irritability,weight change, fluid retention, sleep disturbanceRare: thromboembolism, edema, rash; increasedrisk of breast cancer when used with estrogens


Use for 12–14 consecutive days.Start on day 16 or 21 of cycle when used incombination with estrogen.


Drugs affected by oral progestins: warfarin(decrease), digoxin (decrease)Drugs that affect oral progestins: rifampin(decrease)

PROGESTERONE

Prometrium Oral micronized progesterone100 mg, 200 mg; 200 mg dailyfor 12–14 days, or 100 mgdaily

Prochieve 4% vaginal progesterone

Note: Progesterone is generally associated withless nuisance effects than progestins. It is unclearif progesterone has a better safety profile for moreserious side effects. Natural progesterone may beused as a sleep aid.

INTRAUTERINE PROGESTINS

Mirena 20 mcg/day approximaterelease rate52 mg IU has 5-year use

VAGINAL PROGESTERONE GEL

Prochieve 4% progesterone; 45-mg applicator

ESTROGEN/TESTOSTERONE

Estratest h.s. 0.625 esterified estrones/1.25methyltestosterone

Estratest 1.25 esterified estrones/2.5methyltestosterone

TESTOSTERONE

Androgel 10 mg/g (formulated for men)1% gelTestoderm 1 patch delivers 4 mg over 24

hours (formulated for men)1 patch delivers 6 mg over 24hours

Androderm 1 patch delivers 2.5 mg over 24hours (formulated for men)1 patch delivers 5 mg over 24hours

Female 300 mcg patch (not commer-testosterone cially available yet)patch

Indications

Treatment of vasomotor symptoms in patientswho do not respond to estrogen aloneAndrogens may improve libido, energy, andoverall well-being

Adverse Effects

Common: virilization, changes in libido(increased or decreased), nausea, abdominalcramps, headache, breakthrough bleeding,breast tenderness, edemaRare: increased liver function tests, poly-cythemia, cholestatic hepatitis, jaundice, hyper-calcemia, thromboembolism, stroke,endometrial cancer, breast cancer, hepatic ade-noma, gallbladder disease, increased blood pressure


Cycle 21 days on, 7 offCan be used continuously



Drugs affected by oral estrogens-androgens:warfarin (increase), cyclosporine (increase)Drugs that affect oral estrogens-androgens:barbiturates, phenytoin

373

P R O C E D U R E S

A N D P R A C T I C E SA P P E N D I X

BREAST SELF-EXAM

The breast self-exam should be done in three steps:*

1. The first step is a visual exam in front of amirror: Look at your breasts with your arms atyour sides, then hold your arms overhead, clasp-ing your hands behind your head. Next placeyour hands on your hips, roll your shouldersforward, and bow forward slightly as you pullyour shoulders and elbows forward. Inspectboth breasts for swelling, changes in skin (dim-pling, puckering, discoloration, or scaling ofskin), or changes in your nipples, includingretraction or discharge.2. The second step is to lie down and place a

small pillow or folded towel under your rightshoulder and your right arm behind your head.Press firmly with the pads of your fingers andmove your left hand over all parts of your rightbreast in an up-and-down motion as if you aretracking vertical lines in rows next to eachother. Pay extra attention to the area betweenthe breast and the armpit, including the armpititself. Gently squeeze the nipple to check fordischarge. Check the left breast with your righthand in the same way.3. The third step is standing. With your left arm

behind your head, use your right hand to examineyour left breast. Move your fingers up and downin vertical rows pressing firmly with the pads ofyour fingers. Repeat this on the right breast.

ALTERNATING SITZ BATHS

Obtain two large tubs that you are able to sit in.Fill one half full with hot water (bath water tem-

perature). Fill the other one half full with ice coldwater. Sit in the hot water for three minutes andthen quickly sit in the cold for 30 seconds.Repeat this three times in succession. Quickly getdressed or put on a robe or blankets so as not tobecome chilled. The room where you are doingthe treatment should be comfortable and warm.

CASTOR OIL PACK

Materials needed:

1. Wool flannel cloth2. Plastic sheet (medium thickness)3. Bath towel4. Two safety pins5. Bowl6. Castor oil7. Plastic wrap8. Baking soda9. Large resealable plastic bag

Instructions

Fold a piece of wool or cotton flannel to make apack three layers thick and approximately 12inches square. This size is recommended forabdominal and pelvic applications. Pour castoroil into the bowl. Place the cloth in the bowl tosaturate the flannel; wring it out so it is not drip-ping. Place the plastic sheet on the bed whereyou will be lying down. Apply the cloth to thedesignated bodily area and cover it with a pieceof plastic wrap. Wrap a towel around the entirearea and fasten it with safety pins. Lie down andavoid becoming chilled. The pack should stay inplace for a minimum of one hour but may beworn longer. After removing the castor oil pack,clean the skin with soda water (two teaspoons ofbaking soda added to a quart of warm water).

D

*Adapted from the American Cancer Society, September2006, cancer.org.


374 A P P E N D I X D

The castor oil pack may be saved in a reseal-able plastic bag or container for future use. It canbe used repeatedly for a number of treatments.

INFUSIONS

An infusion is a simple tea made with one or moreherbs steeped in boiled water. To make an infusion,

weigh out one ounce of dry herbs. Add one pint(two cups) of boiling water to the herbs. Someherbs will taste better if you use more than twocups of water. Steep the herbs for ten to twentyminutes. Herbs that are steeped longer will becomestronger. Strain the tea through a metal-wire orbamboo tea strainer. Drink throughout the day.

375

R E C O M M E N D E D S C R E E N I N G

T E S T S A N D I M M U N I Z AT I O N SA P P E N D I X

health-care needs. The charts are based on therecommendations of the National Women’sHealth Information Center, U.S. Department ofHealth and Human Services, Office on Women’sHealth as of October 2006.

The following charts list recommended screen-ings and immunizations for women at averagerisk for most diseases and for women with vari-ous risk factors. These are guidelines only. Yourhealth-care provider will personalize the timingof each test and immunization to best meet your

E

Recommended Screening Tests and Immunizations for Women at Average Risk

Screening Tests Ages 18–39 Ages 40–49 Ages 50–64 Ages 65 and Older

Full checkup, Discuss with your Discuss with your Discuss with your Discuss with yourincluding weight doctor or nurse. doctor or nurse. doctor or nurse. doctor or nurse.and height

Thyroid test Start at age 35, and Every 5 years Every 5 years Every 5 years(TSH) then every 5 years

Blood pressure At least every At least every At least every At least every test 2 years 2 years 2 years 2 years

Cholesterol test Start at age 20; discuss Discuss with your Discuss with your Discuss with yourwith your doctor or nurse. doctor or nurse. doctor or nurse. doctor or nurse.

Bone mineral Discuss with your Discuss with your At least once; talk density test doctor or nurse. doctor or nurse. to your doctor

or nurse about repeat testing.

Blood glucose Discuss with your Start at age 45, and Every 3 years Every 3 yearstest doctor or nurse. then every 3 years

Mammogram Every 1–2 years; Every 1–2 years; Every 1–2 years;discuss with your discuss with your discuss with yourdoctor or nurse. doctor or nurse. doctor or nurse.

Pap test and Get this test if you have Every 1–3 years Every 1–3 years Discuss with yourpelvic exam been sexually active doctor or nurse.

or are older than 21.

Chlamydia test Yearly until age 25 if Get this test if you Discuss with your Discuss with yoursexually active; older have new or doctor or nurse. doctor or nurse.than age 25, get this multiple partners. test if you have new All pregnant women or multiple partner. should have this All pregnant women test.should have this test.

(continued)


376 A P P E N D I X E

Recommended Screening Tests and Immunizations for Women at Average Risk (continued)

Screening Tests Ages 18–39 Ages 40–49 Ages 50–64 Ages 65 and Older

Sexually transmitted Both partners Both partners Both partners Both partnersinfection (STI) tests should get tested should get tested should get tested should get tested

for STIs, including for STIs, including for STIs, including for STIs, includingHIV, before HIV, before HIV, before HIV, beforeinitiating sexual initiating sexual initiating sexual initiating sexualintercourse. intercourse. intercourse intercourse.

Fecal occult blood test Yearly Yearly

Flexible sigmoidoscopy Every 5 years Every 5 years(with fecal occult (if not having a (if not having ablood test) colonoscopy) colonoscopy)

Double contrast Every 5–10 years Every 5–10 yearsbarium enema (DCBE) (if not having a (if not having a

colonoscopy or colonoscopy orsigmoidoscopy) sigmoidoscopy)

Colonoscopy Every 10 years Every 10 years

Rectal exam Discuss with your Discuss with your Every 5–10 years Every 5–10 yearsdoctor or nurse. doctor or nurse. (with (with

sigmoidoscopy, sigmoidoscopy,colonoscopy, colonoscopy, or DCBE) or DCBE)

Eye exam Get your eyes Every 2–4 years Every 2–4 years Every 1–2 yearschecked if you haveproblems or visualchanges.

Hearing test Starting at age 18, Every 10 years Every 3 years Every 3 yearsand then every 10 years

Mole exam Monthly mole Monthly mole Monthly mole Monthly moleself-exam; by a self-exam; by a self-exam; by a self-exam; by adoctor every 3 years, doctor every year doctor every year doctor every yearstarting at age 20

Dental exam One to two times One to two times One to two times One to two timesevery year every year every year every year

Mental health Discuss with your Discuss with your Discuss with your Discuss with yourscreening doctor or nurse. doctor or nurse. doctor or nurse. doctor or nurse.

377R E C O M M E N D E D S C R E E N I N G T E S T S A N D I M M U N I Z A T I O N S

The following chart lists screenings or tests you might need more often or earlier due to havinghigh-risk factors or things in your life that increase your chances of developing a condition or disease.

Immunizations Ages 18–39 Ages 40–49 Ages 50–64 Ages 65 and Older

Influenza vaccine Discuss with your Discuss with your Yearly Yearlydoctor or nurse. doctor or nurse.

Pneumococcal vaccine One time only

Human papillomavirus Discuss with your Discuss with your Discuss with yourvaccine (HPV) doctor or nurse. doctor or nurse. doctor or nurse.

Meningococcal vaccine Discuss with yourdoctor or nurse ifattending college.

Tetanus-diphtheria Every 10 years Every 10 years Every 10 years Every 10 yearsbooster vaccine

Recommended Screening Tests and Immunizations for Women with High-Risk Factors

Does your family history include? You may need these tests more often or at a younger age

High blood pressure Blood pressure test

High cholesterol Cholesterol test

Heart disease, premature heart disease, Blood pressure test, cholesterol test, exercise stress testor heart attack

Diabetes Blood glucose test

Breast cancer Mammogram, ovarian cancer tests

Cervical, uterine, or vaginal cancer Pap test, pelvic exam, ovarian cancer tests, colon screening

Ovarian cancer Pelvic exam, ovarian cancer tests, colon screening, clinicalbreast exam

Osteoporosis, bone fracture in adulthood Bone mineral density test

Thyroid disease or thyroid cancer Thyroid test and/or genetic counseling

Gum (periodontal) disease Oral exam

Are you? You may need these tests or vaccines more often or at ayounger age

African-American Blood pressure test, cholesterol test, blood glucose test, visionexam, colonoscopy, genetic counseling for sickle cell anemia

Alaska Native or Pacific Islander Blood glucose test

Ashkenazi Jewish descent Genetic counseling for Tay-Sachs disease if you want to becomepregnant

(continued)


Recommended Screening Tests and Immunizations for Women with High-Risk Factors (continued)

Are you? You may need these tests or vaccines more often or at ayounger age

Ashkenazi Jewish with family history Genetic counseling for possible BRCA1⁄2 mutation of breast or ovarian cancer

Asian-American Blood glucose test

Hispanic American Blood pressure test, cholesterol test, blood glucose test,colonoscopy

Native American Blood glucose test

Age 65 or older Bone mineral density test, flu vaccine, pneumococcal vaccine

Between the ages of 60 and 64, Bone mineral density test weigh less than 154 lbs., and not taking estrogen

College age MMR vaccine, varicella vaccine, human papillomavirus (HPV) vaccine, meningococcal vaccine

Postmenopausal Bone mineral density test

Pregnant Blood pressure test, blood glucose test, urine test, HIV test, STItests, MMR vaccine, hepatitis B antigen test

A nonpregnant woman of MMR vaccine, varicella vaccinechildbearing age

A smoker Blood pressure test, cholesterol test, bone mineral density test,oral exam, vision exam

Overweight Blood pressure test, blood glucose test, weight checked

Living in prison Tuberculosis (TB) test, HIV test, STI tests, hepatitis A and B vaccines

Living in long-term care TB test, influenza vaccine, pneumococcal vaccine

A health-care worker TB test, influenza vaccine, pneumococcal vaccine, MMR vaccine,varicella vaccine, hepatitis B vaccine with post-vaccination testing,HIV test, hepatitis test, hepatitis B vaccine if exposed to blood

Do you have or have you had? You may need these tests or vaccines more often or at ayounger age

High blood pressure Blood pressure test, cholesterol test, blood glucose test

High cholesterol Blood pressure test, cholesterol test, blood glucose test

Heart disease Blood pressure test, cholesterol test, blood glucose test, influenzavaccine, pneumococcal vaccine

Diabetes Blood pressure test, cholesterol test, blood glucose test, visionexam, urine sugar test

Gestational diabetes Blood glucose test

A baby weighing more than 9 lbs. Blood glucose test

(continued)

379R E C O M M E N D E D S C R E E N I N G T E S T S A N D I M M U N I Z A T I O N S

Do you have or have you had? You may need these tests or vaccines more often or at a younger age

Breast cancer Mammogram, ovarian cancer tests

Dense breasts Mammogram, clinical breast exam

Cervical, uterine, vaginal cancer Pap test, pelvic exam, ovarian cancer tests, colon screening

Ovarian cancer Pelvic exam, ovarian cancer tests, mammogram, colon screening

Previous abnormal Pap tests Pap test, pelvic exam, human papillomavirus (HPV) vaccine

Early menopause (natural or surgical), Bone mineral density testabsent or infrequent menstrual periods, bone fracture in adulthood, low calcium intake, little physical activity, low bodyweight (under 154 lbs.), an eating disorder such as anorexia nervosa

An autoimmune disease (lupus, Thyroid test, TB test, influenza vaccine, MMR vaccine, rheumatoid arthritis, scleroderma, pneumococcal vaccine, autoimmune screening test, bone mineral multiple sclerosis, psoriasis) density test

Chronic lung disease Influenza vaccine, pneumococcal vaccine

Chronic liver disease Hepatitis A and B vaccines

Thyroid disease Thyroid test, influenza vaccine, pneumococcal vaccine, bone (if hyperthyroid) mineral density test

Gum (periodontal) disease Oral exam

Colon polyps or inflammatory Colonoscopybowel disease

A developmental delay Vision exam, hearing test

Eye injury or disease Vision exam

Ear injury or prolonged exposure Hearing test to loud noise

HIV/AIDS Oral exam, vision exam, Pap test, pelvic exam, TB test, thyroid test, STI tests, influenza vaccine, pneumococcal vaccine, hepatitis screening, hepatitis A and B vaccines

A blood transfusion or organ Hepatitis C testtransplant before 1992 or receivedclotting factor concentrates madebefore 1987

A blood transfusion before 1985 HIV test

Multiple sex partners or a partner who STI tests, HIV test, hepatitis B vaccine, Pap test, pelvic exam,has or has had multiple sex partners human papillomavirus (HPV) vaccine

Alcoholism Pneumococcal vaccine, TB test, psychological screening, liver tests

Injection drug use (IDU) or addiction Hepatitis A and B vaccines, hepatitis C test, TB test, STI tests,HIV test, psychological screening

(continued)


Recommended Screening Tests and Immunizations for Women with High-Risk Factors (continued)

Do you have or have you had? You may need these tests or vaccines more often or at a younger age

A sexually transmitted infection (STI) STI tests, HIV test, Pap test, pelvic exam, hepatitis B vaccine,human papillomavirus (HPV) vaccine

Lived or worked with someone exposed TB testto tuberculosis (TB)

A serious injury (cut or laceration) Tetanus-diphtheria booster vaccine

A baby within the last few months Postpartum depression screening

381

R E S O U R C E S

Horse Chestnut Varicose veins, lymphedema

HRT Companion Companion to HRTIC Blend Interstitial cystitisImmune Symmetry Infections, immune

supportIron Extra Iron-deficient anemiaIpriflavone Bone supportLactationBlend Breast-feeding supportLuminous Hair, skin, nailsLysine Extra Herpes infectionsMaternal Symmetry Prenatal multivitaminMindblend Memory, focus,

concentrationNausea Ease Nausea—pregnancy

and otherOC Companion Companion to oral

contraceptivesOpti-Recovery Surgery supportOsteoblend Osteoporosis

preventionOsteoDrink Osteoporosis

preventionPCOS Blend Polycystic ovarian

syndromePhytoEstrogen Phytoestrogen powderHerbalPregnancy Prep Fertility enhancementRed Clover Hot flashesRhodiola Fatigue, memory,

stressSenior Symmetry Multiple vitamin-

mineral 65+Sleepblend InsomniaSlow Flow Menstrual flow

reductionSoy Choice Hot flashes, elevated

cholesterol

HERBAL AND NUTRITIONALPRODUCTS

Vitanica Formulations Developed by Dr. Tori Hudson

Product Purpose

Adrenal Assist Adrenal support,fatigue

Black Cohosh Menopause symptomsBreastblend Breast cancer

preventionButterbur Extra Migraine headachesCandidaStat Systemic candida

syndromeCardioblend Heart disease

preventionChaste Tree Berry Abnormal uterine

bleedingCholestblend High cholesterolCoQ10 Heart diseaseCramp Bark Extra Menstrual crampsCranStat Extra Urinary tract

infectionsFem Rebalance Irregular menses,

hormonal balanceFibroblend Fibrocystic breastsGABA Ease AnxietyGinger Extract Plus Nausea, high choles-

terol, crampingGingko Extract Plus MemoryGreen Tea Breast health, immune

supportHBP Blend High blood pressureHepaFem Liver support, liver

detoxHerbal Symmetry Multiherb dailyHerpblend Herpes simplex


382 R E S O U R C E S

St. John’s Wort DepressionThyro Fem HypothyroidUplift DepressionVeinoblend Varicose veinsWoman’s Passage Menopause symptoms

supportWomen’s Phase I Premenstrual

syndromeWomen’s Phase II Menopause symptoms

supportWomen’s Symmetry Multiple vitamin-

mineralYeast Arrest Yeast vaginitis

Companion Products to ConventionalCancer Treatments. The following Vitanicaproducts are available only through licensedpractitioners:

AC BlendTX BlendR BlendBase Blend

Environmental Products. The followingVitanica products are available only throughlicensed practitioners:

Endocrine Disruptor ReliefNeuro Disruptor ReliefWomen’s Detox Co-Factors

Vaginal Suppositories. The following Vitan-ica products are available only through licensedpractitioners, except Yeast Arrest:

Green TeaHerbal-CPapilloVag PakVita-AYeast Arrest

CLINICAL GUIDE TO VITANICA PRODUCT USAGE

Abnormal Uterine Bleeding: Heavy Bleeding

Slow Flow Acute: 3 caps every 3 hoursduring heavy flowChronic recurring: 2 capsdaily (up to 6 caps dailyfor 3 months, and then 1cap daily and/or ChasteTree Berry 1–2 caps/daily)

Abnormal Uterine Bleeding: Irregular Bleeding

Chaste Tree Berry 1–2 caps daily

Amenorrhea

Rhodiola 100 mg 2 to 3 times dailyChaste Tree Berry 1 cap dailyOsteoblend 2 caps twice daily to

prevent osteoporosisIpriflavone 1 cap 3 times daily to

prevent osteoporosis

Anemia (Iron Deficiency)

Iron Extra 1–4 caps daily

Anxiety

GABA Ease 2 caps twice daily

Bladder Infections

CranStat Extra Acute: 2 caps every 2 hoursfor the first 2 days, andthen 2 caps 3–4 timesdaily for 7–14 days oruntil resolution; for bestresults, add 1,000 mg vitamin C to each doseChronic recurring: 2 capsdaily

383R E S O U R C E S

Breast-feeding

LactationBlend 1 to 2 caps twice daily

Breast Cancer Prevention

Breastblend 2 caps twice dailyGreen Tea 1–3 caps dailyPhytoEstrogen 1 tbs 1–2 times dailyHerbalSoy Choice 1–4 caps dailyCoQ10 1 cap daily

Cholesterol

Cardioblend 2 caps twice dailyCholestblend 1 cap 3 times dailyCoQ10 1 cap dailyGinger Extract Plus 1–2 caps dailyPhytoEstrogen 1 tbs 1–2 times dailyHerbalSoy Choice 1–4 caps daily

Depression

Rhodiola 100 mg 1 to 3 timesdaily

St. John’s Wort 1 cap 3 times dailyUplift 1 cap 3 times daily

Detoxification

Women’s Detox 4 caps twice dailyCo-factorsEndocrine 2 caps twice dailyDisruptor ReliefNeuro 2 caps twice dailyDisruptor Relief

Fibrocystic Breasts

Fibroblend 2–4 caps daily through-out cycle; or 2 caps twicedaily from day 15 untilonset of menstrual flow

General Health

Women’s Symmetry General: 1–2 caps daily

Chronic health problem:3–4 caps dailySerious chronic healthproblem, high stress, orheavy exerciser: 2 caps 3times daily

Senior Symmetry Same regimen as withWomen’s Symmetry

Herbal Symmetry 2 caps daily

Hair, Skin, Nails

Luminous 2–6 caps daily

Heart Disease

Cardioblend 2 caps twice daily forgeneral prevention

CoQ10 1 cap dailyGinger Extract Plus 1 cap twice dailySoy Choice 1–4 caps daily

Hemorrhoids

Horse Chestnut 1 cap twice daily

Herpes (Oral or Genital)

Lysine Extra Acute: 2 caps 2–3 timesdaily for up to 10 daysChronic: 2 caps per day

High Blood Pressure

HBP Blend 1 cap 1–3 times dailyCoQ10 1 cap daily

Hormonal Balance

Fem Rebalance 2 caps daily

Infections

Immune Symmetry Acute infections: 2 capsevery 2 hours for 2 days,and then 2 caps 3 timesdaily for 1–2 weeksChronic immune prob-lems: 2 caps 1–3 timesdaily as needed


Infertility

Pregnancy Prep 2 caps dailyChaste Tree Berry 1–2 caps dailyRhodiola 100–300 mg daily

Insomnia

Sleepblend 1–2 caps 30–60 minutesbefore bed

Interstitial Cystitis

IC Blend 3 caps 3 times daily

Liver Support

HepaFem 2 caps daily

Lymphedema

Horse Chestnut 1 cap twice daily

Migraines

Butterbur Extra 2 caps twice daily for 1–2months, and then 2 capsdaily

Memory

Mindblend 2 caps dailyGinkgo Extract Plus 1 cap 3 times dailyRhodiola 100 mg 1 to 3 times

daily

Menopause Symptoms

Black Cohosh 1–2 caps 1–2 times dailyPhytoEstrogen 1 tbs 1–2 times dailyHerbalRed Clover 1 cap dailySoy Choice 1–4 caps dailyWoman’s Passage 1 cap dailyWomen’s Phase II 2–6 caps daily

Also see Abnormal Uterine Bleeding, Depres-sion, Insomnia, and Memory.

Menstrual Cramps

Cramp Bark Extra Acute: 1–3 caps every 3hours up to 4 times dailyduring mensesTo prevent recurringcramps: 2 caps daily;increase to 2 caps twicedaily the week beforemenses

Ginger Extract Plus 1–3 caps daily, for acuteor for prevention

Nausea

Nausea Ease 1–2 caps dailyGinger Extract Plus 1–4 caps as needed

throughout the day

Osteoarthritis

Ginger Extract Plus 1–4 caps as neededthroughout the day

Osteoporosis

Ipriflavone 1 cap 3 times dailyOsteoblend 2 caps twice dailyOsteoDrink 1 scoop dailyPhytoEstrogen 1 tbs 1–2 times dailyHerbalSoy Choice 1–2 caps daily

PMS

Ginkgo Extract Plus 1 cap 2–3 times dailySt. John’s Wort 1 cap 3 times dailyUplift 1 cap 3 times dailyChaste Tree Berry 1–2 caps dailyWomen’s Phase I Mild symptoms: 2 caps

daily throughout cycleModerate to severe symp-toms: 2 caps twice dailythroughout cycle


Polycystic Ovarian Syndrome

Green Tea 1–3 caps dailyPCOS Blend 3–6 caps dailyPhytoEstrogen 1–2 tbs dailyHerbal

Pregnancy

Maternal Symmetry 2–6 caps daily

Stress

Rhodiola 100 mg 1–3 times daily

Surgery Recovery

Opti-Recovery 1 cap twice daily

Thyroid (Hypo)

ThyroFem 2 caps daily

Vaginitis (Yeast)

Yeast Arrest Acute: 1 suppository invagina morning andevening for 3–14 daysChronic: 1 cap twice dailyfor 2–4 weeks, and then1 cap daily duringmenses for 4 months

CandidaStat 2 caps 1–2 times daily

Varicose Veins

Veinoblend 1 cap 3 times dailyHorse Chestnut 1 cap twice daily

Weight Loss

Green Tea 2 caps with breakfast,2 caps with lunch

VITANICA SPECIALTY LINES FOR PROFESSIONALS ONLY

Cancer Support for Cancer Adjunctive Care

AC Blend 4 caps twice daily withadriamycin/cytoxin

TX Blend 5 caps twice daily with

taxane familyBase Blend 4 caps twice daily with

any chemotherapeuticregimen

R Blend 3 caps twice daily withradiotherapy

Environmental Medicine and Women’s Health

Women’s Detox 4 caps twice dailyCo-FactorsEndocrine 2 caps twice dailyDisruptor ReliefNeuro 2 caps twice dailyDisruptor Relief

Suppositories for Infections, ASCUS, Cervical Dysplasias, HPV

All suppositories are to be inserted vaginally. Foruse in escharotic treatments, insert two supposito-ries after each treatment. Can also be used forvaginal infections and as part of an overall treat-ment plan for abnormal Pap smears. See clinicalindications listed for each suppository in “ProductKnowledge” manual for infections, condyloma,cervical dysplasia, and ACUS; also see Encyclope-dia of Natural Medicine by Tori Hudson, N.D.Suppositories may require use of panty liner dueto leakage when suppository dissolves.

Green TeaHerbal-CPapilloVag PackVita-AYeast Arrest

MORE PRODUCT SOURCES

Bio-Identical Hormone Creams Company

Progest Emerita/Transitions forHealth

Proganol Bezwecken (available


through professionals)Ostaderm Bezwecken (available

through professionals)Ostaderm V Bezwecken (available

through professionals)Compounded Women’s Internationalhormones Pharmacy

Fish Oils

Nordic Naturals

Greens Drink

Wellness Naturals

Homeopathic Medicines

Boiron

Standardized Herbal Extracts by Vitanica

Black CohoshChaste Tree BerryGinger Extract PlusGingko Extract PlusGreen TeaHorse ChestnutRed CloverRhodiolaSt. John’s Wort

Other Reputable Suppliers of Standardized Herbal Extracts

Enzymatic Therapies (Retail)Integrative Therapeutics (Professionals)

Herbal Tinctures

Eclectic InstituteHerb PharmWise Woman Herbals

Probiotics Formulations

Pharmax

Uterine Fibroid Herbal Formulations from Gaia Herbs

Scudder’s AlterativeEchinacea/Red Root CompoundFraxinus/Ceonothus CompoundGelsemium/Phytolacca Compound

(Turska Formula)

NUTRITIONAL AND HERBAL COMPANIES

Vitanica (Dr. Tori Hudson’s women’s healthproduct line)P.O. Box 1285Sherwood, OR 97140800-572-4712vitanica.com

Bezwecken15495 SW Millikan WayBeaverton, OR 97006800-743-2256

Boiron USA98c West Cochran StreetSimi Valley, CA 93065805-582-9091

Eclectic Institute14385 SE Lusted RoadSandy, OR 97055800-332-4372

Emerita/Transitions for Health621 SW AlderPortland, OR 97205800-888-6814emerita.com

Emerson Ecologics (distributor of professionalproducts)7 Commerce DriveBedford, NH 03110603-656-9778emersonecologics.com


Enzymatic Therapies825 Challenger DriveGreenbay, WI 54311800-783-2286enzymatictherapy.com

Gaia Herbs108 Island Ford RoadBrevard, NC 28712800-831-7780

Herb PharmP.O. Box 116Williams, OR 97544800-599-2392herb-pharm.com

Natural Factors1550 United BoulevardCoquitlam, BC V3K 6Y7Canada604-415-4155

Natural Partners (distributor of professionalproducts)7949 E. Acoma, Suite 103Scottsdale, AZ 85260888-633-7620naturalpartners.com

Nordic Naturals94 Hangar WayWatsonville, CA 95076800-662-2544nordicnaturals.com

Pharmax (for professionals)1233 120th Avenue NEBellevue, WA 98005800-538-8274pharmaxllc.com

Vital Nutrients (for professionals)45 Kenneth Dooley DriveMiddletown, CT 06457888-328-9992vitalnutrients.com

Wise WomanP.O. Box 279Creswell, OR 97426800-532-5219

COMPOUNDING PHARMACIES

International Academy of CompoundingPharmacistsP.O. Box 1365Sugarland, TX 77487713-933-8400900-927-4227

Women’s International Pharmacy12012 N. 111th AvenueYoungtown, AZ 85363800-699-8143

Lloyd Center Pharmacy1302 Lloyd CenterPortland, OR 97232800-358-8974

LABORATORY TESTING

Metametrix Clinical Laboratory4855 Peachtree Industrial BoulevardNorcross, GA 30092800-221-4640, ext. 373Fax: 770-441-2237metametrix.com

SKIN CARE PRODUCTS FORWOMEN

Emerita/Transitions for Health621 SW AlderPortland, OR 97205800-888-6814emerita.com


SPECIALTY FOODS

Hemp Seeds, Hemp Protein, Hemp Oil

Living HarvestP.O. Box 4407Portland, OR 97208503-274-0755livingharvest.com

Organic Dairy Foods and Meats

Organic ValleyOne Organic WayLa Rarge, WI 54639608-625-2666organicvalley.coop

Whole-Grain Breads

French Meadow Bakery2610 Lyndale Avenue SouthMinneapolis, MN 55408612-870-4740

CLINICS, NATUROPATHICCOLLEGES, AND ORGANIZATIONS

A Woman’s Time, P.C.Tori Hudson, N.D.2067 NW LovejoyPortland, OR 97209503-222-2322awomanstime.comE-mail: [email protected]: torihudson.com

Institute of Women’s Health and IntegrativeMedicine (postgraduate training in women’shealth and natural therapies)Dr. Tori Hudson2067 NW LovejoyPortland, OR 97209503-222-2322instituteofwomenshealth.com

National College of Naturopathic Medicine049 SW PorterPortland, OR 97201503-499-4343

Bastyr University14500 Juanita Drive NEBothell, WA 98011425-602-3100

Southwest College of Naturopathic Medicineand Health Sciences2140 East BroadwayTempe, AZ 85282602-990-7424

Bridgeport University126 Park AvenueBridgeport, CT 06601203-576-4552

Canadian College of Naturopathic Medicine2300 Yonge StreetP.O. Box 2431Toronto, ON M4P1E4416-486-8584

American Association of Naturopathic Physicians4435 Wisconsin Avenue NW, Suite 403Washington, DC 20016202-895-1392

American Holistic Medical Association6728 Old McLean Village RoadMcLean, VA 22101703-556-9728

American College of Obstetricians and GynecologistsResource Center409 12th Street SWWashington, DC 20024202-863-2518


The American Herbalists GuildP.O. Box 746555Arvada, CO 80006303-423-8800

American Botanical CouncilP.O. Box 12006Austin, TX 78711512-331-8868

American Herb AssociationP.O. Box 1673Nevada City, CA 95959530-265-9552

Herb Research Foundation1007 Pearl StreetBoulder, CO 80302303-449-2265

ADDITIONAL PUBLICATIONS,ARTICLES, AND TAPES BY DR.TORI HUDSON

Dr. Tori Hudson’s blogtorihudson.com

Women’s Health Update, The Complete Collection of Townsend Letter Columns1992–2005, Volumes I, II, and IIITori Hudson, N.D.TK Publications2067 NW LovejoyPortland, OR 97209503-222-2322

Institute of Women’s Health and IntegrativeMedicine (audiotapes and lecture series of post-graduate seminars for licensed health-care prac-titioners)2067 NW LovejoyPortland, OR 97209instituteofwomenshealth.com503-222-2322

Emerson Ecologics800-654-4432emersonecologics.com

Holistic Primary CareP.O. Box 953Peck Slip StationNew York, NY212-406-8957

Townsend Letter for Doctors and Patients360-385-6021

Herbal Educational Services (tapes)P.O. Box 3427Ashland, OR 97520800-252-0688

Tree Farm Communications (tapes)800-468-0464


391

R E F E R E N C E S

CHAPTER 1: ABNORMAL UTERINE BLEEDING

1. Phipps W, Martini M, Lampe J, Slavin J,Kurzer M. “Effect of flaxseed ingestion onthe menstrual cycle.” J Clin EndocrinMetab 1993; 77 (5): 1215–19.

2. Cassidy A, Bingham S, Setchell K. “Bio-logical effects of a diet of soy protein richin isoflavones on the menstrual cycle ofpremenopausal women.” Am J Clin Nutr1994; 60:333–40.

3. Olsson H, Landin-Olsson M, Gullberg B.“Retrospective assessment of menstrualcycle length in patients with breastcancer, in patients with benign breast dis-ease, and in women without breast dis-ease.” J Natl Canc Inst 1983; 70:17–20.

4. Juneja H, Murthy S, Ganguly J. “Theeffect of vitamin A deficiency on thebiosynthesis of steroid hormones in rats.”J Biochem 1966; 99 (1): 138–45.

5. Lithgow D, Politzer W. “Vitamin A inthe treatment of menorrhagia.” SAMJ1977; 51:191–93.

6. Biskind M. “Nutritional deficiency in theetiology of menorrhagia, metrorrhagia,cystic mastitis and premenstrual tension:treatment with vitamin B complex.” JClin Endocrin Metab 1943; 3:227–34.

7. Lusher JM. “Systemic causes of excessiveuterine bleeding.” Semin Hematol 1999Jul; 36 (3 Suppl 4): 10–20.

8. Cohen J, Rubin H. “Functional menorrhagia:treatment with bioflavonoids and vitamin C.”Curr Therap Res 1960; 2 (11): 539.

9. Weiss RF, Fintelmann, V. Herbal Medicine,2nd ed. New York: Thieme, 2000.

10. Amann W. “Removing an obstipationusing Agnolyt.” Ther Gegenew 1965; 104(9): 1263–65.

11. Sliutz G, Speiser P, et al. “Agnus castusextracts inhibit prolactin secretion of ratpituitary cells.” Horm Metab Res 1993;25:253–55.

12. Probst V, Roth O. “On a plant extractwith a hormonelike effect.” Dtsch MeWschr 1954; 79 (35): 1271–74.

13. Bleier W. “Phytotherapy in irregular men-strual cycles or bleeding periods and othergynecological disorders of endocrineorigin.” Zentralblatt Gynakol 1959; 81(18): 701–9.

14. Milewica A, Gejdel E, et al. “Vitex agnuscastus extract in the treatment of lutealphase defects due to hyperprolactinemia:results of a randomized placebo-controlled double-blind study.” Arzneim-Forsch Drug Res 1993; 43:752–56.

15. Wuttke W, Jarry H, Christoffel V, Spen-gler B, Seidlova-Wuttke D. “Chaste tree(Vitex agnus-castus)—pharmacology andclinical indications.” Phytomedicine 2003May; 10 (4): 348–57.

16. Daniele C, Thompson Coon J, PittlerMH, Ernst E. “Vitex agnus castus: a sys-tematic review of adverse events.” DrugSaf 2005; 28 (4): 319–32.

17. Macalo N, Jain R, Jain S, et al.“Ethnopharmacologic investigations ofginger (Zingiber officinale).” J Ethnopharm1989; 27:129–40.

18. Kim SO, Chun KS, Kundu JK, Surh YJ.“Inhibitory effects of [6]-gingerol onPMA-induced COX-2 expression and


392 R E F E R E N C E S

activation of NF-kappaB and p38 MAPKin mouse skin.” Biofactors 2004; 21(1–4): 27–31; Surh YJ. “Anti-tumor pro-moting potential of selected spice ingredi-ents with antioxidative and anti-inflammatory activities: a short review.”Food Chem Toxicol 2002 Aug; 40 (8):1091–97; Tjendraputra E, Tran VH, Liu-Brennan D, Roufogalis BD, Duke CC.“Effect of ginger constituents and syn-thetic analogues on cyclooxygenase-2enzyme in intact cells.” Bioorg Chem2001 Jun; 29 (3): 156–63.

19. Kelly R, Lumsden M, et al. “The rela-tionship between menstrual blood lossand prostaglandin production in thehuman: evidence for increased availabil-ity of arachidonic acid in women suffer-ing from menorrhagia.” Prostaglandinsand Leukotrienes in Medicine 1984;16:69–77.

20. Skibola CF. “The effect of Fucus vesiculo-sus, an edible brown seaweed, upon men-strual cycle length and hormonal status inthree pre-menopausal women: a casereport.” BMC Complement Altern Med2004 Aug 4; 4 (1): 10.

21. Mowrey D. The Scientific Validation ofHerbal Medicine. New York: McGraw-Hill, 1986; 188.

22. Kuroda K, Takagi K. “Physiologicallyactive substances in Capsella bursa-pastoris.” Nature 1968; 220 (5168):707–8.

23. Yang T, Jia M, Mei Q, Shang P. “Effectsof Angelica polysaccharide on blood coag-ulation and platelet aggregation.” ZhongYao Cai 2002 May; 25 (5): 344–45.

24. Saarikoski S, Yliskoski M, Penttila I. “Sequential use of norethisterone and nat-ural progesterone in pre-menopausalbleeding disorders.” Maturitas 1990 Jun;12 (2): 89–97.

CHAPTER 2: AMENORRHEA

1. Wabisch M, Hauner H, et al. “Body fatdistribution and steroid hormone concen-trations in obese adolescent girls beforeand after weight reduction.” J Clin En-docrin Metab 1995; 80 (12): 3469–75.

2. Castillo-Martinez L, Lopez-Alvarenga JC,Villa AR, Gonzalez-Barranco J. “Men-strual cycle length disorders in 18- to 40-year-old obese women.” Nutrition 2003Apr; 19 (4): 317–20.

3. Butzow TL, Lehtovirta M, Siegberg R, etal. “The decrease in luteinizing hormonesecretion in response to weight reductionis inversely related to the severity of in-sulin resistance in overweight women.” J Clin Endocrinol Metab 2000 Sep; 85(9): 3271–75.

4. Crosignani PG, Colombo M, Vegetti W,Somigliana E, Gessati A, Ragni G. “Over-weight and obese anovulatory patientswith polycystic ovaries: parallel improve-ments in anthropometric indices, ovarianphysiology and fertility rate induced bydiet.” Hum Reprod 2003 Sep; 18 (9):1928–32.

5. Jeghers H. “Skin changes of nutritionalorigin.” N Engl J Med 1943; 228:678–86.

6. Almond S, Logan R. “Carotenemia.” NEngl J Med 1942; 2:239–41.

7. Robboy M, Sato A, Schwabe A. “The hypercarotenemia in anorexia nervosa: acomparison of vitamin A and carotenelevels in various forms of menstrual dys-function and cachexia.” Amer J Clin Nutr1974; 27:362–67.

8. Pops M, Schwabe A. “Hypercarotenemiain anorexia nervosa.” JAMA 1968;205:533–34.

9. Frumar A, Medrum D, Judd H. “Hyper-carotenemia in hypothalamic amenor-rhea.” Fertil Steril 1979; 32:261–64.

393R E F E R E N C E S

10. Page S. “Golden ovaries.” Aust N Z JObstet Gynaecol 1971; 11:32–36.

11. Richards S, Chang F, et al. “Serumcarotene levels in female long-distance run-ners.” Fertil Steril 1985; 43 (1): 79–81.

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18. Jarry H, Leonhardt S, Wuttke W. “Agnuscastus as dopaminergous effective princi-ple in mastodynon N.” Zeitschrift Phy-tother 1991; 12:77–82.

19. Milewica A, Gejdel E, et al. “Vitex agnuscastus extract in the treatment of lutealphase defects due to hyperprolactinemia.Results of a randomized placebo-controlled double-blind study.” Arzneim-Forsch Drug Res 1993; 43:752–56.

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21. Liske E, Hanggi W, Henneicke-vonZepelin H, Boblitz N, et al. “Physiologicinvestigation of a unique extract of blackcohosh (Cimicifugae racemosae rhizome): a6-month clinical study demonstrates nosystemic estrogenic effect.” J Women’s

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33. De Souza MJ, Williams NI. “Physiologicalaspects and clinical sequelae of energy defi-ciency and hypoestrogenism in exercisingwomen.” Hum Reprod Update 2004Sep–Oct; 10 (5): 433–48. Epub 2004 Jul 1.

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36. DeSouza, M, et al. “Adrenal activationand the prolactin response to exercise ineumenorrheic and amenorrheic runners.”J Appl Physiol 1991; 70:2378.

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38. Bonen A. “Recreational exercise does notimpair menstrual cycles: a prospectivestudy.” Int J Sports Med 1992; 13:110.

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23. Newfield L, Goldsmith A, Bradlow H,Auborn K. “Estrogen metabolism andhuman papillomavirus-induced tumors ofthe larynx: chemo-prophylaxis withindole-3-carbinol.” Anticancer Res 1993;13:337–41.

24. Palan P, Mikhail M, Basu J, Romeny S.“Beta-carotene levels in exfoliated cervico-vaginal epithelial cells in cervical intraep-ithelial neoplasia and cervical cancer.” AmJ Obstet Gynecol 1992 Dec; 167 (6):1899–1903.

25. Van Enwik J, Davis F, Bowen P. “Dietaryand serum carotenoids and cervicalintraepithelial neoplasia.” Int J Canc1991; 48:34–38.

26. Palan P, Romney S, Mikhail M, Basu J.“Decreased plasma beta-carotene levels inwomen with uterine cervical dysplasiasand cancer.” J Nat Canc Inst 1988; 80(6): 454–55.

27. Nagata C, Shimizu H, Yoshikawa H, etal. “Serum carotenoids and vitamins andrisk of cervical dysplasia from a case-control study in Japan.” Br J Cancer 1999Dec; 81 (7): 1234–37.

28. Sedjo RL, Papenfuss MR, Craft NE, Giuliano AR. “Effect of plasma micronu-trients on clearance of oncogenic humanpapillomavirus (HPV) infection (UnitedStates).” Cancer Causes Control 2003May; 14 (4): 319–26.


29. Sedjo RL, Roe DJ, Abrahamsen M, et al.“Vitamin A, carotenoids, and risk of per-sistent oncogenic human papillomavirusinfection.” Cancer Epidemiol BiomarkersPrev 2002 Sep; 11 (9): 876–84.

30. Hudson T. “Consecutive case studyresearch of carcinoma in situ of cervixemploying local escharotic treatmentcombined with nutritional therapy.” J Nat Med 1991; 2:6–10, 19.

31. Hudson T. “Escharotic treatment for cer-vical dysplasia and carcinoma in situ.” J Nat Med 1993; 4 (1): 23.

32. Wylie-Rosett J, Seymour L, Romney N,et al. “Influence of vitamin A on cervicaldysplasia and carcinoma in situ.” Nutrand Canc 1984; 6 (1): 49–57.

33. Shannon J, Thomas DB, Ray RM, et al.“Dietary risk factors for invasive and in-situ cervical carcinomas in Bangkok,Thailand.” Cancer Causes Control 2002Oct; 13 (8): 691–99.

34. Yeo AS, Schiff MA, Montoya G, MasukM, van Asselt-King L, Becker TM. “Serummicronutrients and cervical dysplasia inSouthwestern American Indian women.”Nutr Cancer 2000; 38 (2): 141–50.

35. Nagata C, Shimizu H, Higashiiwai H, etal. “Serum retinol level and risk of subse-quent cervical cancer in cases with cervi-cal dysplasia.” Cancer Invest 1999; 17 (4):253–58.

36. Shannon J, Thomas DB, Ray RM, et al.“Dietary risk factors for invasive and in-situ cervical carcinomas in Bangkok,Thailand.” Cancer Causes Control 2002Oct; 13 (8): 691–99.

37. Gasowska-Giszczak U, Darmochwal-Kolarz D, Kwasniewska A, et al. “Apopto-sis of HeLa cell lines incubated withretinol.” Eur J Obstet Gynecol Reprod Biol2005 Mar 1; 119 (1): 119–22.

38. Ding Z, Green AG, Yang X, et al.“Retinoic acid inhibits telomerase activity

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39. Yokoyama M, Nakao Y, Iwasaka T, PaterA, Sugimori H. “Retinoic acid and interferon-alpha effects on cell growthand differentiation in cervical carcinomacell lines.” Obstet Gynecol 2001 Aug; 98(2): 332–40.

40. Meyskens F, Surwit E, et al. “Enhance-ment of regression of cervical intraepithe-lial neoplasia II (moderate dysplasia) withtopically applied all-trans-retinoic acid: arandomized trial.” J Natl Canc Inst 1994;86 (7): 539–43.

41. Graham W, Surwite E, Weiner S, MeyskensF. “Phase II trial of beta-all-trans-retinoicacid for cervical intraepithelial neoplasiadelivered via a collagen sponge and cervicalcap.” West J Med 1986; 145:192–95.

42. Ruffin M, Bailey J, Normolle D, et al.“Low-dose topical delivery of all-trans-retinoic acid for cervical intraepithelialneoplasia II and III.” Cancer EpidemiolBiomarkers Prev 2004 Dec; 13 (12):2148–52.

43. Palan PR, Woodall AL, Anderson PS,Mikhail MS. “Alpha-tocopherol andalpha-tocopheryl quinone levels in cervi-cal intraepithelial neoplasia and cervicalcancer.” Am J Obstet Gynecol 2004 May;190 (5): 1407–10.

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45. Yeo AS, Schiff MA, Montoya G, et al.“Serum micronutrients and cervical dys-plasia in Southwestern American Indian


women.” Nutr Cancer 2000; 38 (2):141–50.

46. Ho GY, Palan PR, Basu J, et al. “Viralcharacteristics of human papillomavirusinfection and antioxidant levels as riskfactors for cervical dysplasia.” Int J Cancer1998 Nov 23; 78 (5): 594–99.

47. Lehtinen M, Luostarinen T, YoungmanLD, Anttila T, Dillner J, Hakulinen T,Koskela P, Lenner P, Hallmans G. “Lowlevels of serum vitamins A and E in bloodand subsequent risk for cervical cancer:interaction with HPV seropositivity.”Nutr Cancer 1999; 34 (2): 229–34.

48. Mason B, Ghanee N, Haigh WG, et al.“Effect of vitamins A, C and E on normaland HPV-immortalized human oralepithelial cells in culture.” Anticancer Res1999 Nov–Dec; 19 (6B): 5469–74.

49. Palan PR, Woodall AL, Anderson PS,Mikhail MS. “Alpha-tocopherol andalpha-tocopheryl quinone levels in cervi-cal intraepithelial neoplasia and cervicalcancer.” Am J Obstet Gynecol 2004 May;190 (5): 1407–10.

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54. Wassertheil-Smoller S, Romney S, Wylie-Rosett J, et al. “Dietary vitamin C and

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55. Romney S, Duttagupta C, Basu J, et al.“Plasma vitamin C and uterine cervicaldysplasia.” Am J Obstet Gynecol 1985April 1; 151 (7): 976–80.

56. Butterworth C, Hatch K, Gore H, et al.“Improvement in cervical dysplasia associ-ated with folic acid therapy in users oforal contraceptives.” Am J Clin Nutr1982; 35:73–82.

57. Weinstein SJ, Ziegler RG, Frongillo EAJr, et al. “Low serum and red blood cellfolate are moderately, but nonsignificantlyassociated with increased risk of invasivecervical cancer in U.S. women.” J Nutr2001 Jul; 131 (7): 2040–48.

58. Piyathilake CJ, Henao OL, Macaluso M, etal. “Folate is associated with the natural his-tory of high-risk human papillomaviruses.”Cancer Res 2004 Dec 1; 64 (23): 8788–93.

59. Whitehead N, Reyner F, Lindenbaum J.“Megaloblastic changes in the cervicalepithelium: association with oral contra-ceptive therapy and reversal with folicacid.” JAMA 1973; 226:1421–24.

60. Streiff R. “Folate deficiency and oral contraceptives.” JAMA 1970; 214:105–8.

61. Weinstein SJ, Ziegler RG, Selhub J, et al.“Elevated serum homocysteine levels andincreased risk of invasive cervical cancerin US women.” Cancer Causes Control2001 May; 12 (4): 317–24.

62. Thomson SW, Heimburger DC, Corn-well PE, et al. “Effect of total plasmahomocysteine on cervical dysplasia risk.”Nutr Cancer 2000; 37 (2): 128–33.

63. Shikany JM, Heimburger DC, Piyathi-lake CJ, Desmond RA, Greene PG.“Effect of folic acid fortification of foodson folate intake in female smokers withcervical dysplasia.” Nutrition 2004 May;20 (5): 409–14.


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65. Sedjo RL, Inserra P, Abrahamsen M, et al.“Human papillomavirus persistence andnutrients involved in the methylationpathway among a cohort of youngwomen.” Cancer Epidemiol BiomarkersPrev 2002 Apr; 11 (4): 353–59.

66. Weinstein SJ, Ziegler RG, Selhub J, et al.“Elevated serum homocysteine levels andincreased risk of invasive cervical cancerin US women.” Cancer Causes Control2001; 12 (4): 317–24.

67. Thomson SW, Heimburger DC, CornwellPE, Turner ME, Sauberlich HE, Fox LM,Butterworth CE. “Effect of total plasmahomocysteine on cervical dysplasia risk.”Nutr Cancer 2000; 37 (2): 128–33.

68. Ahn WS, Huh SW, Bae SM, et al. “Amajor constituent of green tea, EGCG,inhibits the growth of a human cervicalcancer cell line, CaSki cells, throughapoptosis, G (1) arrest, and regulation ofgene expression.” DNA Cell Biol 2003Mar; 22 (3): 217–24.

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CHAPTER 4: CONTRACEPTION

1. Lader L. The Margaret Sanger Story andthe Fight for Birth Control, 1st ed. GardenCity, NY: Country Life Press, 1955.

2. Brown S, Eisenberg L, eds. Committeeon Unintended Pregnancy, Division of


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8. Shojania A, Hornady G. “The effect oforal contraceptives on folate metabolism.”Am J Obstet Gynecol 1971; 111 (6):782–91.

9. Webb J. “Nutritional effects of oral con-traceptive use: a review.” J Reprod Med1980 Oct; 25 (4): 150–56.

10. Alan P, Mikhail M, Basu J, Romeny S.“Beta-carotene levels in exfoliated cervicov-aginal epithelial cells in cervical intraepithe-lial neoplasia and cervical cancer.” Am JObstet Gynecol 1992; 167 (6): 1899– 1903.

11. Palan P, Romney S, Mikhail M, Basu J.“Decreased beta-carotene levels in women

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16. Jobst KA, McIntyre M, St. George D, et al.“Safety of St John’s wort (Hypericum perfo-ratum).” Lancet 2000; 355 (9203): 575.

17. Gorski JC, Hamman MA, Wang Z, et al.“The effect of St. John’s Wort on the effi-cacy of oral contraception.” American Soci-ety for Clinical Pharmacology andTherapeutics Annual Meeting, Atlanta, GA,March 24–27, 2002. Abstract MPI-80.

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CHAPTER 5: CYSTITIS

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20. Carlsson S, Wiklund N, Engstrand L.“Effects of pH, nitrite, and ascorbic acidon nonenzymatic nitric oxide generationand bacterial growth in urine.” NitricOxide 2001; 5 (6): 580–86.

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22. Larsson B, Jonasson A, Fianu S. “Prophy-lactic effect of UVA-E in women withrecurrent cystitis: a preliminary report.”Curr Ther Res 1993; 53:441–43.

23. Amin A, Subbaiah T, Abbasi K. “Berber-ine sulfate: antimicrobial activity, bioas-say, and mode of action.” Can JMicrobiology 1969; 15:1067–76.

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25. Hahn F, Ciak J. “Berberine.” Antibiotics1976; 3:577–88.

26. Raz R, Stamm WE. “A controlled trial ofintravaginal estriol in postmenopausalwomen with recurrent urinary tract infec-tions.” N Engl J Med 1993; 329 (11):753–56.

CHAPTER 6: ENDOMETRIOSIS

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3. Simpson J, Elias S, Malinak L, ButtramV. “Heritable aspects of endometriosis.”Am J Obstet Gynecol 1980 June;137:327–31.

4. Cramer D, Wilson E, et al. “The relationof endometriosis to menstrual characteris-tics, smoking, and exercise.” JAMA 1986;255 (14): 1904–8.

5. Woodworth S, Singh M, et al. “A prospec-tive study on the association between redhair color and endometriosis in infertilepatients.” Fertil Steril 1995 Sept; 64 (3):651–52.

6. D’Hooghe T, Bambra C, et al. “Theprevalence of spontaneous endometriosisin the baboon (Papio anubis, Papio cyno-cephalus) increases with the duration ofcaptivity.” Acta Obstet Gynecol Scand1996 Feb; 75 (2): 98–101.

7. Harrop-Griffiths J, Katon W, et al. “Theassociation between chronic pelvic pain,psychiatric diagnoses, and childhoodsexual abuse.” Obstet Gynecol 1988 Apr;71:589–94.

8. Koninckx P, Oosterlynck D, et al.“Deeply infiltrating endometriosis is adisease whereas mild endometriosis could

be considered a non-disease.” Ann N YAcad Sci 1994 Sept; 333–41.

9. Lanzone A, Marana R. “Serum CA-125levels in the diagnosis and managementof endometriosis.” J Repro Med 1991Aug; 36:603–7.

10. Gould S, Shannon J, Cunha G. “Nuclearestrogen binding sites in human endome-triosis.” Fertil Steril 1983:520–24.

11. Sampson J. “Peritoneal endometriosis dueto the menstrual dissemination of endome-trial tissue into the peritoneal cavity.” Am JObstet Gynecol 1927 Oct; 14:422–69.

12. Dmowski W, Steele R, et al. “Deficientcellular immunity in endometriosis.” AmJ Obstet Gynecol 1981 Oct; 141:377–83.

13. Noble L, Simpson E, et al. “Aromataseexpression in endometriosis.” J Clin EndoMetab 1996; 81:174–79.

14. Dmowski W, Steele R, et al. “Deficientcellular immunity in endometriosis.” AmJ Obstet Gynecol 1981 Oct; 141:377–83.

15. Peterson N, Hasselbring B. “Endometri-osis reconsidered.” Med Self Care 1987May–June; 52–55.

16. Rier S, Martin D, et al. “Immunorespon-siveness in endometriosis: implications ofestrogenic toxicants.” Envir Health Per-spect 1995; 103 (Suppl 7): 151–56.

17. Koninckx P, Meuleman C, et al. “Sugges-tive evidence that pelvic endometriosis isa progressive disease, whereas deeply infiltrating endometriosis is associatedwith pelvic pain.” Fertil Steril 1991 Apr;55 (4): 759–65.

18. Koninckx P, Martin D. “Treatment ofdeeply infiltrating endometriosis.” CurrOpin Obstet & Gynec 1994 June; 6 (3):231–41.

19. Kennedy S, Mardon H, Barlow D.“Familial endometriosis.” J Assist ReprodGenet 1995; 12:32–34.

20. Stefansson H, Geirsson R, Steinthorsdot-tir V, et al. “Genetic factors contribute to


the risk of developing endometriosis.”Hum Reprod 2002; 17:555–59.

21. Moen M. “Endometriosis in monozygotictwins.” Acta Obstet Gynecol Scand 1994;73:59–62.

22. Hadfield R, Mardon H, Barlow D,Kennedy S. “Endometriosis in monozy-gotic twins.” Fertil Steril 1997; 68:941–42.

23. Treloar S, O’Connor D, O’Connor V,Martin N. “Genetic influences on endo-metriosis in an Australian twin sample.”Fertil Steril 1997; 71:701–10.

24. Wang Y, Guo S. “Statistical methods fordetecting genomic alterations througharray-based comparative genomichybridization (CGH).” Front Biosci 2004;9:540–549.

25. Ranton J, Golden J. “Radiation-inducedendometriosis in Maccaca mulatta.”Radiat Res 1991; 126:141–46.

26. Rier S, Martin D, Bowman R, et al.“Endometriosis in rhesus monkeys (Mac-caca mulatta) following chronic exposureto 2,3,7,8 tetrachlorodibenzo-p-dioxin.”Fundam Appl Toxicol 1993; 21:431–41.

27. Koninckx P, Braet P, Kennedy S, et al.“Dioxin pollution and endometrisis inBelgium.” Hum Reprod 1994; 9:1001–2.

28. Pauwels A, Schepens P, D’Hooghe T, etal. “The risks of endometriosis and expo-sure to dioxons and polychlorinatedbiphenyls: a case-controlled study ofinfertile women.” Hum Reprod 2001;16:2050–55.

29. Eskenazi B, Mocarelli P, Warner M, et al.“Serum dioxin concentrations and endo-metriosis: a cohort sudy in Seveso, Italy.”Environ Health Perspect 2002; 110:629–34.

30. Myers J, Guillette L Jr, Palanza P, et al.“The emerging science of endocrine dis-ruption.” Science and Culture Series,International Seminar on Nuclear Warand Planetary Emergencies, 28th Session,Erice, Italy, 2003.

31. Davis D, Bradlow H. “Can environmen-tal estrogen cause breast cancer?” Sci Am1995 Oct: 166–72.

32. Sotkstad E. “Pollution gets personal.” Sci-ence 2004; 304:1892–94.

33. Leibovic D, Mueller M, Taylor R.“Immunobiology of endometriosis.” FertilSteril 2001; 75:1–10.

34. D’Hooghe T, Bambra C, et al. “Theeffects of immunosuppression on devel-opment and progression of endometriosisin baboons (Papio anubis).” Fertil Steril1995 Jul; 64 (1): 172–78.

35. Nomiyama M, Hachisuga T, et al. “Localimmune response in infertile patientswith minimal endometriosis.” Gynecoland Obstet Invest 1997; 44:32–37.

36. Halme J, Becker S. “Increased activationof pelvic macrophages in infertile womenwith mild endometriosis.” Am J ObstetGynecol 1983 Feb; 145:333–37.

37. Muscato J, Haney A, et al. “Spermphagocytosis by human peritoneal macro-phages: a possible cause of infertility inendometriosis.” Am J Obstet Gynecol1982; 144:503–10.

38. Wilson T, Hertzog P, et al. “Decreasednatural killer cell activity in endometriosispatients: relationship to disease pathogen-esis.” Fertil Steril 1994 Nov; 62 (5):1086–88.

39. Oosterlynick D, Meuleman C, et al.“Immunosuppressive activity of peri-toneal fluid in women with endometri-osis.” Obstet Gynecol 1993 Aug; 82 (2):206–11.

40. Garzetti G, Ciavattini A, et al. “Naturalkiller cell activity in endometriosis: corre-lation between serum estradiol levels andcytotoxicity.” Obstet Gynecol 1993 May;81 (5): 665–68.

41. Gleicher, N, El-Roeiy A, et al. “Is endo-metriosis an autoimmune disease?” ObstetGynecol 1987 July; 70:115–22.


42. Gleicher N, Pratt D. “Abnormal(auto)immunity and endometriosis.” Int JGynaecol Obstet 1993; 40 (Suppl): S21–27.

43. Mathur S, Peress M, et al. “Autoimmu-nity to endometrium and ovary in endo-metriosis.” Clin Exp Immunol 1982;50:259–66.

44. Oosterlynck D, Cornillie F, Waer M, etal. “Women with endometriosis show adefect in natural killer activity resulting ina decreased cytotoxicity to autologousendometrium.” Fertil Steril 1991;56:45–51.

45. Chegini N. “Peritoneal molecular envi-ronment, adhesion formation, and clini-cal implication.” Front Biosci 2002;1:e91–115.

46. Bazvani R, Templeton A. “Peritonealenvironment, cytokines and angiogenesisin the pathophysiology of endometriosis.”Reproduction 2002; 123:217–26.

47. Galle P. “Clinical presentation and diag-nosis of endometriosis.” Obstet GynecolClin North Am 1989 Mar; 16 (1): 29–42.

48. Baron J. “Beneficial effects of nicotineand cigarette smoking: the real, the possi-ble and the spurious.” Br Med Bull 1996Jan; 52 (1): 58–73.

49. McCann S, Freudenheim J, et al. “Endo-metriosis and body fat distribution.”Obstet Gynecol 1993 Oct; 82:545–49.

50. Malinak R. “ACOG technical bulletin.”Endomet 1993 Sept: 1–6.

51. Pauci A, Braunwald E, et al. Harrison’sPrinciples of Internal Medicine. New York:McGraw-Hill, 1998.

52. Hill M, Goddard P, et al. “Gut bacteriaand etiology of cancer of the breast.”Lancet 1971 Aug; 472–73.

53. Portz D, Elkins T. “Oxygen free radicalsand pelvic adhesion formation: I. block-ing oxygen free radical toxicity to preventadhesion formation in an endometriosismodel.” Int J Fertil 1991; 36 (1): 39–42.

54. Goldin B, Adlercreutz H, et al. “Effect ofdiet on excretion of estrogens in pre- andpostmenopausal women.” Canc Res 1981Sept; 41:3771–73.

55. Parazzini F, Chiaffarino F, Surace M, etal. “Selected food intake and risk of endo-metriosis.” Hum Reprod 2004 Aug; 19(8): 1755–59. Epub 2004 Jul 14.

56. Murray M, Pizzorno J. “Digestion andelimination.” In Encyclopedia of NaturalMedicine, rev. 2nd ed. Roseville, CA:Prima Publishing, 1998.

57. Kappas A, Anderson K, et al. “Nutrition-endocrine interactions: induction ofreciprocal changes in the delta-5alpha-reduction of testosterone and thecytochrome P-450-dependent oxidationof estradiol by dietary macronutrients inman.” Proc Natl Acad Sci 1983 Dec;80:7646–49.

58. Nagata C, Takatsuka N, Kawakami N,Shimizu H. “Soy product intake and pre-menopausal hysterectomy in a follow-upstudy of Japanese women.” Eur J ClinNutr 2001 Sep; 55 (9): 773–77.

59. Mathias JR, Franklin R, Quast DC, FragaN, Loftin CA, Yates L, Harrison V. “Rela-tion of endometriosis and neuromusculardisease of the gastrointestinal tract: newinsights.” Fertil Steril 1998 Jul; 70 (1):81–88.

60. Michnovicz J, Bradlow H. “Altered estro-gen metabolism and excretion in humansfollowing consumption of indol-3-carbinol.” Nutr & Cancer 1991; 16:59–66.

61. Leibovitz B, Mueller J. “Bioflavonoidsand polyphenols: medical applications.”Ins for the Study of Opt Nutr 1993; 2 (1):17–35.

62. Leung A. Encyclopedia of Common Nat-ural Ingredients Used in Food, Drugs andCosmetics. New York: Wiley & Sons,1980; 17.


63. Yudkin J, Elisa O. “Dietary sucrose andoestradiol concentration in young men.”Ann Nutr Metab 1988; 32:53–55.

64. Grodstein F, Goldman M. “Relation offemale infertility to consumption of caffeinated beverages.” Am J Epidemiol1993; 137:1353–60.

65. Tremblay L. “Reproductive Toxins Con-ference—Pollution Prevention Network.”Endomet Assoc Newsletter 1996; 17 (5–6):13–15.

66. Anderson R. “The immunostimulatory,anti-inflammatory and anti-allergic prop-erties of ascorbate.” Adv Nut Res 1984;6:19–45.

67. Leibovitz B, Siegel B. “Ascorbic acid andthe immune response.” Adv Exp Med Biol1981; 135:1–25.

68. Sawatsri S, Desai N, Rock JA, Sidell N.“Retinoic acid suppresses interleukin-6production in human endometrial cells.”Fertil Steril 2000 May; 73 (5): 1012–19.

69. Alexander M, et al. “Oral beta-carotenecan increase the number of OKT4 cells inhuman blood.” Immunol Lett 1985; 9:221–24.

70. Gerster H. “Anticarcinogenic effect ofcommon carotenoids.” Internat J Vit NutrRes 1993; 63:93–121.

71. Ongsakul M, et al. “Impaired bloodclearance of bacteria and phagocyticactivity in vitamin A deficient rats.” ProcSoc Exp Biol Med 1985; 178 (2): 204–8.

72. Watson R. “Effect of b-carotene on lym-phocyte subpopulations in elderlyhumans; evidence for a dose-responserelationship.” Am J Clin Nutr 1991;53:90–94.

73. Foyouzi N, Berkkanoglu M, Arici A,Kwintkiewicz J, Izquierdo D, Duleba AJ.“Effects of oxidants and antioxidants onproliferation of endometrial stromalcells.” Fertil Steril 2004 Oct; 82 (Suppl3): 1019–22.

74. Murphy AA, Santanam N, ParthasarathyS. “Endometriosis: a disease of oxidativestress?” Semin Reprod Endocrinol 1998; 16(4): 263–73. Review.

75. London R, Sundaram G, et al. “Endo-crine parameters and alpha-tocopheroltherapy of patients with mammary dys-plasia.” Canc Res 1981 Sept; 41:3811–13.

76. Butler E, McKnight E. “Vitamin E in thetreatment of primary dysmenorrhea.”Lancet 1955; 1:844–47.

77. Moncada S, et al. “Leucocytes and tissueinjury; the use of eicosapentaenoic acid in the control of white cell activation.”Wien Klin Wochenschr 1986; 98 (4):104–6.

78. Gazvani MR, Smith L, Haggarty P,Fowler PA, Templeton A. “High omega-3:omega-6 fatty acid ratios in culturemedium reduce endometrial-cell survivalin combined endometrial gland and stro-mal cell cultures from women with andwithout endometriosis.” Fertil Steril 2001Oct; 76 (4): 717–22.

79. Covens AL, Christopher P, Casper RF.“The effect of dietary supplementationwith fish oil fatty acids on surgicallyinduced endometriosis in the rabbit.”Fertil Steril 1988 Apr; 49 (4): 698–703.

80. Biskind M, Biskind G. “Effect of vitaminB complex deficiency on inactivation ofestrone in the liver.” Endocr 1942; 31:109–14.

81. Kiremidjian-Schumacher, Stotsky G.“Selenium and immune responses.” Envi-ron Res 1987; 42:277–303.

82. Spallholtz, et al. “Immune response ofmice fed diets supplemented with sele-nium.” Proc Soc Exper Biology & Med143:685–869.

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85. Xiao YH, Chen DP, Yan JH, Yokoyama Y.“Mechanism of action of TripterygiumWilfordii polyglycoside on experimentalendometriosis.” Eur J Gynaecol Oncol2002; 23 (1): 63–67.

86. Decapite L. “Histology, anatomy andantibiotic properties of vitex agnus castus.”Ann Fac Agr Univ Studi Perugi 1967;22:109–26.

87. Baba K, Abe S, et al. “Antitumor activityof hot water extract of dandelion, Tarax-acum officinale—correlation between antitumor activity and timing of adminis-tration.” Yakugaku Zasshi 1981 June; 101(6): 538–643.

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CHAPTER 7: FIBROCYSTICBREASTS

1. Love S, et al. “Fibrocystic ‘disease’ of thebreast: a nondisease.” N Engl J Med 1982;307:1010.

2. Page D, Dupont W. “Indicators ofincreased breast cancer risk in humans.” J Cell Biochem Suppl 1992; 16G:175.

3. Devitt J, et al. “Risk of breast cancer inwomen with breast cysts.” Can Med Assoc J 1992; 147:45.

4. Sterns E. “The natural history of macro-scopic cysts in the breast.” Surg GynObstet 1992; 174:36.

5. Hentes D. “Does diet influence humanfecal microflora composition?” Nutr Rev1980; 38:329–36.

6. Wu C, Ray RM, Lin MG, et al. “A case-control study of risk factors for fibrocysticbreast conditions: Shanghai Nutritionand Breast Disease Study, China,

1995–2000.” Am J Epidemiol 2004 Nov15; 160 (10): 945–60.

7. Fleming RM. “What effect, if any, doessoy protein have on breast tissue?” IntegrCancer Ther 2003 Sep; 2 (3): 225–28.

8. Rohan TE, Jain M, Miller AB. “Alcoholconsumption and risk of benign prolifera-tive epithelial disorders of the breast: acase-cohort study.” Public Health Nutr1998 Sep; 1 (3): 139–45.

9. Minton J, Foeking M, Webster D,Matthews R. “Caffeine, cyclicnucleotides, and breast disease.” Surg1979; 86:105.

10. Ernster V, Mason L, Goodson W, et al.“Effects of caffeine-free diet on benignbreast disease: a randomized trial.” Surg1982; 912:263–67.

11. Lubin F et al. “A case-control study ofcaffeine and methylxanthine in benignbreast disease.” JAMA 1985; 253 (16):2388–92.

12. Shawer C, Brinton L, Hoover R.“Methylxanthine and benign breast dis-ease.” Am J Epidemiol 1986; 124 (4):603–11.

13. Marshall J, Graham S, Swanson M. “Caffeine consumption and benign breastdisease: a case-control comparison.” AmerJ Public Health 1982; 72 (6): 610–12.

14. La Vecchia C, et al. “Benign breast dis-ease and consumption of beverages con-taining methylxanthines.” JNCI 1985; 74(5): 995–1000.

15. Boyle C, et al. “Caffeine consumptionand fibrocystic breast disease: a case-control epidemiologic study.” JNCI 1984;72 (5): 1015–19.

16. Boyd N, McGuire V, Shannon P, et al.“Effect of a low-fat high-carbohydrate dieton symptoms of cyclical mastopathy.”Lancet 1988 July 16; 2 (8603): 128–32.

17. Rose D, et al. “Effect of a low-fat diet onhormone levels in women with cystic


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18. Abrams A. “Use of vitamin E in chroniccystic mastitis.” N Engl J Med 1965;272:1080.

19. Solomon D, Strummer D, Nair P. “Rela-tionship between vitamin E and urinaryexcretion of ketosteroid fractions in cysticmastitis.” Ann N Y Acad Sci 1972; 203:103.

20. London R, et al. “Clinical response andurinary excretion of 11-desoxy-17 keto-steroids and pregnanediol following alpha-tocopherol therapy.” Breast 1978; 4:19.

21. London R, et al. “Mammary dysplasia:endocrine parameters and tocopheroltherapy.” Nutr Res 1982; 7:243.

22. Meyer E, et al. “Vitamin E and benignbreast disease.” Surg 1990; 107 (5): 549–51.

23. London R, et al. “The effect of vitamin Eon mammary dysplasia: a double-blindstudy.” Obstet Gynecol 1985; 65 (1): 104–6.

24. London R, et al. “Endocrine parametersand alphatocopherol therapy of patientswith mammary dysplasia.” Canc Res1981; 41:3811–13.

25. Pye J, et al. “Clinical experience of drugtreatment for mastalgia.” Lancet 1985;2:373–77.

26. Pashby N, et al. “A clinical trial ofevening primrose oil in mastalgia.” Br JSurg 1981; 68:801–24.

27. Pasquali D, Bellastella A, Valente A, et al.“Retinoic acid receptors alpha, beta andgamma, and cellular retinol binding protein-I expression in breast fibrocysticdisease and cancer.” Eur J Endocrinol1997 Oct; 137 (4): 410–14.

28. Band P, et al. “Treatment of benign breastdisease with vitamin A.” Prev Med 1984;13:549.

29. Estes N. “Mastodynia due to fibrocysticdisease of the breast controlled with thyroidhormone.” Amer J Surg 1981; 142:102.

30. Eskin B, Bartushka D, Dunn M, et al.“Mammary gland dysplasia in iodine defi-ciency.” JAMA 1967; 200:691–95.

31. Ghent W, et al. “Iodine replacement infibrocystic disease of the breast.” Can JSurg 1993 Oct; 35 (5): 453–60.

32. Lee, J. What Your Doctor May Not Tell Youabout Menopause. New York: WarnerBooks, 1996.

CHAPTER 8: GENITAL HERPES

1. American Medical Association. GenitalHerpes: A Clinician’s Guide to Diagnosisand Treatment. Chicago: American Med-ical Association, 2001.

2. Centers for Disease Control and Preven-tion. “Tracking the Hidden Epidemics.Trends in STDs in the United States2000.”cdc.gov/nchstp/dstd/stats_trends/trends2000.pdf. Corrected April 6, 2001.

3. Handsfield HH. Genital Herpes. NewYork: McGraw-Hill Medical PublishingDivision, 2001.

4. Fleming D, et al. “Herpes simplex virustype 2 in the United States, 1976–1994.”N Engl J Med 1997; 337:1105–11.

5. Wild D, Patrick D, Johnson E, Berzon R,Wald A. “Measuring health-related qual-ity of life in persons with genital herpes.”Qual Life Res 1995; 4:532–39.

6. Langenberg A, et al. “A prospective studyof new infections with herpes simplexvirus type 1 and type 2.” N Engl J Med1999; 341:1432–38.

7. Griffith R, DeLong D, Nelson J. “Rela-tion of arginine-lysine antagonism toherpes simplex growth in tissue culture.”Chemo 1981; 27 (3): 209–13.

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CHAPTER 10: INFERTILITY

1. “2000 assisted reproductive technologysuccess rates.” National Summary and Fer-tility Clinic Reports. Atlanta, GA: Depart-ment of Health and Human


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3. Norman R, Noakes M, Wu R, et al.“Improving reproductive performance inoverweight/obese women with effectiveweight management.” Hum ReprodUpdate 2004 May–Jun; 10 (3): 267–80.

4. Moran L, Norman R. “The obese patientwith infertility: a practical approach todiagnosis and treatment.” Nutr Clin Care2002 Nov–Dec; 5 (6): 290–97.

5. Morris S, Missmer S, et al. “Effects oflifetime exercise on the outcome of invitro fertilization.” Obstet Gynecol 2006Oct; 108 (4): 938–45.

6. Cannavo S, Curto L, Trimarchi F. “Exercise-related female reproductive dysfunction.” J Endocrinol Invest 2001;24 (10): 823–32.

7. Warren MP, Perlroth NE. “The effects ofintense exercise on the female reproduc-tive system.” J Endocrinol 2001; 170 (1):3–11.

8. Zenzes M. “Cigarette smoking as a causeof delay in conception.” Reprod Med Rev1995; 4:189–205.

9. Practice Committee of the AmericanSociety for Reproductive Medicine.“Smoking and infertility.” Fertil Steril2004; 81 (4): 1181–86.

10. Baird D, Wilcox A. “Cigarette smokingassociated with delayed conception.”JAMA 1985; 253 (20): 2979–83.

11. Hughes E, Young Lai E, Ward S. “Ciga-rette smoking and outcomes of in-vitrofertilization and embryo transfer: aprospective cohort study.” Hum Reprod1992 Mar; 7 (3): 358–61.

12. El-Nemr A, Al-Shawaf T, Sabatini L, etal. “Effect of smoking on ovarian reserveand ovarian stimulation in in-vitro fertil-ization and embryo transfer.” HumReprod 1998; 12 (8): 2192–98.

13. Zenzes M. “Smoking and reproduction:gene damage to human gametes andembryos.” Hum Reprod Update 2000; 6(2): 122–131.

14. Paszkowski T, Clarke R, Hornstein M.“Smoking induces oxidative stress insidethe graafian follicle.” Hum Reprod 2002;17 (4): 921–25.

15. Domar A, Clapp D, Slawsby E, Dusek J,Kessel B, Freizinger M. “Impact of grouppsychological interventions on pregnancyrates in infertile women.” Fertil Steril2000; 73 (4): 805–811.

16. Jensen T, Hjollund N, Henriksen T, et al.“Does moderate alcohol consumptionaffect fertility? Follow up study amongcouples planning first pregnancy.” Br MedJ 1998; 317 (7157): 505–10.

17. Hakim R, Gray R, Zacur H. “Alcohol andcaffeine consumption and decreased fertil-ity.” Fertil Steril 1998; 70 (4): 632–37.

18. Fernandes O, Sabharwal M, et al. “Mod-erate to heavy caffeine consumptionduring pregnancy and relationship tospontaneous abortion and abnormal fetalgrowth: a meta-analysis.” Reprod Toxicol1998; 12 (4): 435–44.

19. Barbieri R. “The initial fertility consulta-tion in couples planning pregnancy:lifestyle factors.” Available at uptodateonline.com. Accessed May 7, 2004.

20. Peaslee M, Einhellig F. “Reduced fecun-dity in mice on tannic acid diet.” CompGen Pharmacol 1973; 4 (16): 393–97.

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22. Cassidy A, Bingham S, Setchell K. “Bio-logical effects of a diet of soy protein rich


in isoflavones on the menstrual cycle ofpremenopausal women.” Am J Clin Nutr1994; 60:333–40.

23. Phipps W, Martini M, Lampe J, et al.“Effect of flax seed ingestion on the men-strual cycle.” J Clin Endocrinol Metab1993; 77:1215–19.

24. Stamets K, Taylor DS, et al. “A random-ized trial of the effects of two types ofshort-term hypocaloric diets on weight lossin women with polycystic ovary syn-drome.” Fertil Steril 2004 Mar; 81 (3):630–37.

25. Katsuki A, Sumida Y, Ito K, et al. “A caseof obesity, diabetes and hypertensiontreated with very low calorie diet (VLCD)followed by successful pregnancy withintrauterine insemination (IUI).” Endocr J2000 Dec; 47 (6): 787–91.

26. Choy C, Lam C, et al. “Infertility, bloodmercury concentrations and dietaryseafood consumption: a case-controlstudy.” BJOG 2002 Oct; 109 (10):1121–25.

27. McGuinness B, Buck G, et al. “Infecun-dity and consumption of polychlorinatedbiphenyl-contaminated fish.” Arch EnvironHealth 2001 May–Jun; 56 (3): 250–53.

28. Rice R. “Fish and healthy pregnancy:more than just a red herring!” Prof CareMother Child 1996; 6 (6): 171–73.

29. Bayer R. “Treatment of infertility withvitamin E.” Int J Fertil 1960; 70–78.

30. Tarin J, et al. “Effects of maternal agingand dietary anti-oxidant supplementationon ovulation, fertilization and embryodevelopment in vitro in the mouse.”Reproduction, Nutrition, Development1998; 38 (5): 499–508.

31. Hurley L. “Teratogenic aspects of man-ganese, zinc and copper.” Nutrition Physi-ological Reviews 1991; 61:249–95.

32. Battaglia C, Salvatori M, Maxia N, et al.“Adjuvant L-arginine treatment for in-vitro

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33. Sieve B. “The clinical effects of a new Bcomplex factor, para-aminobenzoic acid,on pigmentation and fertility.” South MedSurg 1942; 104:135–39.

34. Czeizel A, Metneki J, Dudas I. “The effectof preconceptional multivitamin supple-mentation on fertility.” Int J Vitam NutrRes 1996; 66:55–58.

35. Sanfilippo J, Liu Y. “Vitamin B12 defi-ciency and infertility: report of a case.” J Int J Fertil 1991; 36 (1): 36–38.

36. Gulden K. “Pernicious anemia, vitiligo,and infertility.” Am Board Fam Pract 1990;3 (3): 217–20.

37. Mackay G. “Pregnancy following treat-ment for pernicious anaemia.” Practitioner1972; 208 (246): 509–10.

38. Howard J, Davies S, Hunnisett A. “Redcell magnesium and glutathione peroxidasein infertile women—effects of oral supple-mentation with magnesium and selenium.”Magnes Res 1994 Mar; 7 (1): 49–57.

39. Amann W. “Removing an ostipationusing Agnolyt.” Ther Gegenew 1965; 104(9): 1263–65.

40. Milewicz A, Gehdel E, et al. “Vitex agnuscastus extract in the treatment of lutealphase defects due to hyperprolactinemia:results of a randomized placebo-controlled double-blind study.” Arzneim-Forsch Drug Res 1993; 43:752–56.

41. Jarry H, et al. “Studies on the endocrineeffects of the contents of Cimicifuga race-mosa, 1: in vitro binding of compounds toestrogen receptors.” Planta Med 1985;1:46–49.

42. Jarry H, et al. “Studies on the endocrineeffects of the contents of Cimicifuga race-mosa, 2: influence on the serum concen-tration of pituitary hormone in ovari-ectomized rats.” Planta Medica 1985;1:46–49.


43. Gerasimova H. “Effect of Rhodiola roseaextract on ovarian functional activity.” Procof Scientific Conference on Endocrinologyand Gynecology. Sverdlovsk, Russia: Siber-ian Branch of the Russian Academy of Sciences, 1970 Sept 15–16; 46–48.

44. Saratikov A, Krasnov E. “The influence ofRhodiola on endocrine glands and theliver.” Chapter VI in Saratikov A, KrosnovE, eds, Rhodiola Rosea Is a Valuable Medici-nal Plant (Golden Root). Tomsk, Russia:Tomsk State University, 1987; 180–93.

45. Zhu D. “Dong Quai.” Am J Chinese Med1986; XV (3–4): 117–25.

46. Zhiping H, et al. “Treating amenorrhea invital energy-deficient patients with Angel-ica sinensis.” J Trad Chin Med 1986; 6 (3):187–90.

47. Darymov, LV. “On the gonadotrophiceffect of Eleutherococcus glycosides.” LekSrd Dalinego Vostioka 1972; 11:939–44.

48. Unfer V, Casini L, et al. “Phytoestrogensmay improve the pregnancy rate in invitro fertilization–embryo transfer cycles:a prospective, controlled, randomizedtrial.” Fertil Steril 2004; 82 (6): 1509–13.

49. Unfer V, Casini M, et al. “High dose ofphytoestrogens can reverse the anti-estrogenic effects of clomiphene citrate onthe endometrium in patients undergoingintrauterine insemination: a randomizedtrial.” J Soc Gynecol Investig 2004 Jul; 11(5): 323–28.

50. Tabakova P, Dimitrov M, Ognyanov K,Popvassilev N. “Clinical study ofTribestan in females with endocrine steril-ity.” Unpublished. tribestan.com.

51. Belinda F, Wurn P, et al. “Pregnancy rateswith a manual physical therapy tech-nique.” medscape.com/viewarticle/480429_1. Accessed June 2004.

52. Stazi A, Trinti B. “Reproductive aspects ofceliac disease.” Ann Ital Med Int 2005Jul–Sep; 20 (3): 143–57.

53. Stazi A, Mantovani A. “A risk factor forfemale fertility and pregnancy: celiac dis-ease.” Gynecol Endocrinol 2000 Dec; 14(6): 454–63.

54. Hin H, Ford F. “Celiac disease and infer-tility: making the connection and achiev-ing a successful pregnancy.” J Fam HealthCare 2002; 12 (4): 94–97.

55. Zaffaroni L, Costa P, Vinci G. “Topicalprogesterone as support for the lutealphase in induced cycles.” Minerva Ginecol1997 Jul–Aug; 49 (7–8): 361–64.

56. Palagiano A, Bulletti C, et al. “Effects ofvaginal progesterone on pain and uterinecontractility in patients with threatenedabortion before twelve weeks of preg-nancy.” Ann N Y Acad Sci 2004 Dec;1034: 200–210.

57. Wong W, Zielhuis GA, et al. “New evi-dence of the influence of exogenous andendogenous factors on sperm count inman.” Eur J Obstet Gynecol Reprod Biol2003 Sep 10; 110 (1): 49–54.

58. Wong W, Merkus H, et al. “Effects offolic acid and zinc sulfate on male factorsubfertility: a double-blind, randomized,placebo-controlled trial.” Fertil Steril2002 Mar; 77 (3): 491–98.

59. Geva E, Bartoov B, et al. “The effect ofantioxidant treatment on human sperma-tozoa and fertilization rate in an in vitrofertilization program.” Fertil Steril 1996Sep; 66 (3): 430–34.

60. Dawson E, et al. “Effect of ascorbic acidon male fertility.” Ann N Y Acad Sci1987; 498:812–28.

61. Geva E, et al. “The effect of anti-oxidanttreatment on human spermatozoa andfertilization rate in an in vitro fertilizationprogram.” Fertil Steril 1996; 66 (3):430–34.

62. Greco E, Iacobelli M, et al. “Reduction ofthe incidence of sperm DNA fragmenta-


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64. Sandler B, Faragher B. “Treatment ofoligospermia with vitamin B12.” Infertility1984; 7:133–38.

65. Kumamoto Y, et al. “Clinical efficacy ofmecobalamin in treatment of oligosper-mia: Results of a double-blind compara-tive clinical study.” Acta Urol Japan 1988;34:1109–32.

CHAPTER 11: INTERSTITIAL CYSTITIS

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2. Whitmore K. “Self-care regimens forpatients with interstitial cystitis.” UrolClin North Am 1994; 21:121–30.

3. Parsons C, Stein P, Bidair M, Lebow D.“Abnormal sensitivity to intravesicalpotassium in interstitial cystitis and radia-tion cystitis.” Neurourol Urodynamics1994; 13:515.

4. Parsons C, Greenberger M, Gabal L,Bidair M, Barme G. “The role of urinarypotassium in the pathogenesis and diag-nosis of interstitial cystitis.” J Urol 1998;159:1862.

5. Parsons C, Lilly J, Stein P. “Epithelialdysfunction in nonbacterial cystitis (inter-stitial cystitis).” J Urol 1991; 145:732.

6. Chelsky M, Rosen S, Knight L, MaurerA, Hanno P, Ruggieri M. “Bladder per-meability in interstitial cystitis is similarto that of healthy volunteers: direct meas-urement by transvesical absorption oftechnetium-diethylenetriaminepentaaceticacid.” J Urol 1994; 151:346.

7. Hurst R, Roy J, Min K, et al. “A deficit ofchondroitin sulfate proteoglycans on thebladder uroepithelium in interstitial cysti-tis.” Urology 1996; 48:817.

8. Erickson D, Mast S, Ordille S, Bhavanan-dan V. “Urinary epitectin in the men-strual cycle and in interstitial cystitis.” J Urol 1996; 156:938.

9. Moskowitz M, Byrne D, Callahan H, etal. “Decreased expression of a glycopro-tein component of bladder surface mucinin interstitial cystitis.” J Urol 1994;151:343.

10. Parsons C, Hurst R. “Decreased urinaryuronic acid levels in individuals withinterstitial cystitis.” J Urol 1990; 143:690.

11. Hurst R, Parsons C, Roy J, Young J.“Urinary glycosaminoglycan excretion asa laboratory marker for interstitial cysti-tis.” J Urol 1993; 149:31.

12. Erickson D, Ordille S, Martin A, Bha-vanadan V. “Urinary chondroitin sulfates,heparan sulfate and total sulfated gly-cosaminoglycans in interstitial cystitis.” J Urol 1997; 157:61.

13. Parsons C, Schimdt J, Pollen J. “Success-ful treatment of interstitial cystitis withsodium pentosanpolysulfate.” J Urol1983; 130:51.

14. Hanno P. “Analysis long-term Elmirontherapy for interstitial cystitis.” Urology1997; 49 (Suppl 5A): 93.

15. Fritjofsson A, Fall M, Johlin R, PerssonB, Ruutu M. “Treatment of ulcer andnonulcer interstitial cystitis with sodiumpentosanpolysulfate: a multicenter trial.”J Urol 1987; 138:508.

16. Parsons C, Mulholland S. “Successfultherapy of interstitial cystitis with pen-tosanpolysulfate.” J Urol 1987; 138:513.

17. Mulholland S, Hanno P, Parsons C, et al.“Pentosanpolysulfate sodium for therapyof interstitial cystitis.” Urology 1990;35:552.


18. Parsons C, Benson G, Childs S, et al. “Aquantitatively controlled method to studyprospectively interstitial cystitis anddemonstrate the efficacy of pentosanpoly-sulfate.” J Urol 1993; 150:845.

19. Holm-Bentzen M, Jacobsen F, NerstromB, et al. “A prospective double-blind clin-ically controlled multicenter trial ofsodium pentosanpolysulfate in the treat-ment of interstitial cystitis and relatedpainful bladder disease.” J Urol 1987;138:503.

20. Perez-Marrero R, Emerson L, et al. “Pro-longation of response to DMSO byheparin maintenance.” Urology 1993; 41(Suppl): 64.

21. Morales A, Emerson L, Mickel J, LundieM. “Intravesical hyaluronic acid in thetreatment of refractory interstitial cysti-tis.” J Urol 1996; 156:45.

22. Slobodov G, Feloney M, Gran C, Kyker K,Hurst R, Culkin D. “Abnormal expressionof molecular markers for bladder imperme-ability and differentiation in the uroepithe-lium of patients with interstitial cystitis.” J Urol 2004 Apr; 171 (4): 1554–58.

23. Wiedermann U, Chen XJ, Enerback L,Hanson L, Kahu H, Dahlgren U. “Vita-min A deficiency increases inflammatoryresponses.” Scand J Immunol 1996 Dec;44 (6): 578–84.

24. Alexandrakis M, Kyriakou D, SeretakisD, et al. “Inhibitory effect of retinoic acidon proliferation, maturation and tryptaselevel in human leukemic mast cells(HMC-1).” Int J Immunopathol Pharma-col 2003; 16 (1): 43–47.

25. Lesser R, Brodie S, Sugin S. “Mastocytosis-induced nyctalopia.” J Neuroopthalmol 1996; 16 (2): 115–19.

26. Eichelberg D, Schmutzler W. “Syntheticretinoids inhibit histamine release fromisolated human mast cells.” Arch Derma-tol Res 1988; 280 (3): 155–57.

27. Reifen R. “Vitamin A as an anti-inflammatory agent.” Proc Nutr Soc 2002;61 (3): 397–400.

28. Reifen R, Nur T, Ghebermeskel K, et al.“Vitamin A deficiency exacerbates inflam-mation in a rat model of colitis throughactivation of nuclear factor-kappa B andcollagen formation.” J Nutr 2002; 132(9): 2743–47.

29. Myata Y, Nakatsuka T, Arai M, et al.“Inhibition by an aromatic retinoid ofDNA damage induced by the bladdercarcinogen N-butyl-N- (3-carboxypropyl)nitrosamine.” Gann 1980; 71 (3):341–48.

30. Chew B, Park J. “Carotenoid action onthe immune response.” J Nutr 2004; 134(1): 257S–261S.

31. MacKay D, Miller A. “Nutritional sup-port for wound healing.” Altern Med Rev2003; 8 (4): 359–77.

32. Varani J, Inman D, Perone P, et al.“Retinoid toxicity for fibroblasts andepithelial cells is separable from growthpromoting activity.” J Invest Dermatol1993; 101 (6): 839–42.

33. Koussoulakos S, Sharma K, Anton H.“Effect of vitamin A on wound epidermisduring forelimb regeneration in adultnewts.” Int J Dev Biol 1990; 34 (4):433–39.

34. Albers R, Bol M, Bleumink R, et al.“Effects of supplementation with vitaminsA, C, and E, selenium, and zinc onimmune function in a murine sensitizationmodel.” Nutrition 2003; 19 (11–12):940–46.

35. Schwartz E, Mezick J, Gendimenico G,Kilgman L. “In vivo prevention of corticosteroid-induced skin atrophy bytritinoin in the hairless mouse is accompa-nied by modulation of collagen, glycosaminoglycans, and fibronectin.” J Invest Dermatol 1994; 102 (2): 241–46.


36. Salvemini D, Misko T, Masferrer J, et al.“Nitric oxide activates cyclooxygenaseenzymes.” Proc Natl Acad Sci USA 1993;90 (15): 7240–44.

37. Fathian-Sabet B, Bloch W, Klotz T, et al.“Localization of constitutive nitric oxidesynthase isoforms and the nitric oxidetarget enzyme soluble guanylyl cyclase inthe human bladder.” J Urol 2001; 165(5): 1724–29.

38. Wheeler M, Smith S, Saito N, et al.“Effect of long-term oral L-arginine onthe nitric oxide synthase pathway in theurine from patients with interstitial cysti-tis.” J Urol 1997; 158 (6): 2045–50.

39. Ehren I, Hosseini A, Lundberg J, Wicklund N. “Nitric oxide: a useful gasin the detection of lower urinary tractinflammation.” J Urol 1999; 162 (2):327–29.

40. Lundberg J, Ehren I, Jansson O, et al.“Elevated nitric oxide in the urinary blad-der in infectious and noninfectious cysti-tis.” Urology 1996; 48 (5): 700–702.

41. Smith S, Wheeler M, Foster H Jr, WeissR. “Improvement in interstitial cystitissymptom scores during treatment withoral L-arginine.” J Urol 1997; 158 (3 Pt1): 703–8.

42. Logadottir YR, Ehren I, Fall M, WiklundNP, Peeker R, Hanno PM. “Intravesicalnitric oxide production discriminatesbetween classic and nonulcer interstitialcystitis.” J Urol 2004 Mar; 171 (3):1148–50.

43. Appleton J. “Arginine: clinical potentialof a semi-essential amino.” Altern MedRev 2002 Dec; 7 (6): 512–22.

44. Erickson D. “Urine markers of interstitialcystitis.” Urology 2001; 57 (6 Suppl 1):15–21.

45. Cartledge J, Davies A, Eardley I. “A ran-domized double-blind placebo-controlledcrossover trial of the efficacy of L-arginine

in the treatment of interstitial cystitis.” BJUInt 2000; 85 (4): 421–26.

46. Korting G, Smith S, Wheeler M, et al. “A randomized double-blind trial of oral L-arginine for treatment of interstitial cystitis.” J Urol 1999; 161 (2): 558–65.

47. Parsons C, Greenberger M, Gabal L, et al.“The role of urinary potassium in thepathogenesis and diagnosis of interstitialcystitis.” J Urol 1998; 159 (6): 1862–66;discussion 1866–67.

48. Martin H, McCallum M, Stofer W,Eichinger M. “Kavain attenuates vascularcontractility through inhibition of calciumchannels.” Planta Med 2002; 68 (9):784–89.

49. Theoharides T, Cochrane D. “Critical roleof mast cells in inflammatory diseases andthe effect of acute stress.” J Neuroimmunol2004; 146 (1–2): 1–12.

50. Lutgendorf S, Latini J, Rothrock N, et al.“Autonomic response to stress in interstitialcystitis.” J Urol 2004; 172 (1): 227–31.

51. Weissman M, Gross R, Fyer A, et al.“Interstitial cystitis and panic disorder: apotential genetic syndrome.” Arch GenPsychiatry 2004; 61 (3): 273–79.

52. Cairney S, Maruff P, Clough A. “The neu-robehavioural effects of kava.” Aust N Z JPsychiatry 2002; 36 (5): 657–62.

53. Bauer O, Razin E. “Mast cell-nerve inter-actions.” News Physiol Sci 2000 Oct;15:213–18.

54. Theoharides T, Kempuraj D, Sant G.“Mast cell involvement in interstitial cysti-tis: a review of human and experimentalevidence.” Urology 2001; 57 (6 Suppl 1):47–55. Review.

55. Penissi AB, Rudolph MI, Piezzi RS. “Roleof mast cells in gastrointestinal mucosaldefense.” Biocell 2003 Aug; 27 (2):163–72. Review.

56. Kimata M, Shichijo M, Miura T, SerizawaI, Inagaki N, Nagai H. “Effects of luteolin,


quercetin and baicalein on immunoglobu-lin E-mediated mediator release fromhuman cultured mast cells.” Clin ExpAllergy 2000 Apr; 30 (4): 501–8.

57. Lee E, Choi EJ, Cheong H, Kim YR, RyuSY, Kim KM. “Anti-allergic actions of theleaves of Castanea crenata and isolation ofan active component responsible for theinhibition of mast cell degranulation.” ArchPharm Res 1999 Jun; 22 (3): 320–23.

58. Martin MW, O’Sullivan AJ, GompertsBD. “Inhibition by cromoglycate andsome flavonoids of nucleoside diphos-phate kinase and of exocytosis from per-meabilized mast cells.” Br J Pharmacol1995 Jul; 115 (6): 1080–86.

59. Bronner C, Landry Y. “Kinetics of theinhibitory effect of flavonoids on hista-mine secretion from mast cells.” AgentsActions 1985 Apr; 16 (3–4): 147–51.

60. Osiecki H. “The role of chronic inflam-mation in cardiovascular disease and itsregulation by nutrients.” Altern Med Rev2004; 9 (1): 32–53.

61. Teixeira S. “Bioflavonoids: proantho-cyanidins and quercetin and their poten-tial roles in treating musculoskeletalconditions.” J Orthop Sports Phys Ther2002; 32 (7): 357–63.

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63. Kim TS, Kang BY, Cho D, Kim SH.“Induction of interleukin-12 production inmouse macrophages by berberine, a benzo-dioxoloquinolizine alkaloid, deviates CD4�

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64. Kang BY, Chung SW, Cho D, Kim TS.“Involvement of p38 mitogen-activatedprotein kinase in the induction of

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65. Huang CG, Chu ZL, Wei SJ, Jiang H, JiaoBH. “Effect of berberine on arachidonicacid metabolism in rabbit platelets andendothelial cells.” Thromb Res 2002 May15; 106 (4–5): 223–27.

66. Habtemariam S. “Extract of corn silk(stigma of Zea mays) inhibits the tumournecrosis factor-alpha- and bacteriallipopolysaccharide-induced cell adhesionand ICAM-1 expression.” Planta Med 1998May; 64 (4): 314–18.

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CHAPTER 12: MENOPAUSE

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3. Katz E, McClamrock H, Adashi E. “Ovar-ian failure including menopause, prema-ture menopause, and resistant ovariansyndrome, and hormonal replacement.”Cur Opin Obstet Gynecol 1990; 2 (3):392–97.

4. Keshavarz H, Hillis S, Kieke B, March-banks P. “Morbidity and Mortality WeeklyReport.” MMWR 2002 July 12; 51(SS05): 1–8.

5. Williamson M. “Sexual adjustment afterhysterectomy.” JOGNN 1991; 21 (1): 42.

6. Nathorst-Boos J, von Schoultz B. “Psychological reactions and sexual lifeafter hysterectomy with and withoutoophorectomy.” Gynecol Obstet Invest1992; 34:97.


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8. McKinlay S, Brambilla D, Posner J. “Thenormal menopause transition.” Maturitas1992; 14:103–15.

9. Kronenberg, F. “Hot flashes: epidemiologyand physiology.” Ann N Y Acad Sci 1990;592:52–86.

10. Lock M. “Ambiguities of aging: Japaneseexperience and perceptions of meno-pause.” Cult Med Psychiatry 1986;10:23–46.

11. Beyene Y. “Cultural significance and physi-ological manifestations of menopause: abiocultural analysis.” Cult Med Psychiatry1986; 10:47–71.

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13. Chakravarti S, Collins W, Thom M, StuddJ. “Relation between plasma hormone pro-files, symptoms, and responses to oestro-gen treatment in women approaching themenopause.” Br Med J 1979; 1:983–85.

14. Shoupe D, Lobo R. “Endogenous opioidsin the menopause.” In Speroff L, Lobo R,eds., Role of Opioid Peptides in Reproduc-tive Endocrinology. Seminars in Reproduc-tive Endocrinology. New York: ThiemeMedical Publishers, Inc., 1987; 5 (2):199–206.

15. McKinlay J, McKinlay S, Brambilla D.“The relative contributions of endocrinechanges and social circumstances todepression in mid-aged women.” J HealthSoc Behav 1987; 28:345–63.

16. Avis N, Brambilla D, McKinlay S, Vass K.“A longitudinal analysis of the associationbetween menopause and depression: resultsfrom the Massachusetts Women’s HealthStudy.” Ann Epidemiol 1994; 4:214–20.

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23. Kingsberg S. “The impact of aging onsexual function in women and their part-ners.” Arch Sex Behav 2002; 31 (5):431–37.

24. Gracia C, Sammel M, Freeman E, et al.“Predictors of decreased libido in womenduring the later reproductive years.”Menopause 2004; 11 (2): 144–50.

25. McCoy N, Davidson J. “A longitudinalstudy of the effects of menopause on sex-uality.” Maturitas 1985; 7 (3): 203–10.

26. Bachmann G, Leiblum S, Kemmann E,et al. “Sexual expression and its determi-nants in the post-menopausal women.”Maturitas 1984; 6:19–29.

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29. Huntley A, Ernst E. “Soy for the treatmentof perimenopausal symptoms—a system-atic review.” Maturitas 2004; 47:1–9.

30. Krebs E, Ensrud K, MacDonald R, WiltT. “Phytoestrogens for treatment ofmenopausal symptoms: a systematicreview.” Obstet Gynecol 2004; 104:824–36.

31. North American Menopause Society.“The role of isoflavones in menopausalhealth: consensus opinion of the NorthAmerican Menopause Society.” Meno-pause 2000; 7:215–29.

32. Anderson J, Johnstone B, Cook-NesellM. “Meta-analysis of the effects of soyprotein intake on serum lipids.” N Engl JMed 1995; 333 (5): 276–82.

33. Messina M, Persky V, Setchell K, BarnesS. “Soy intake and cancer risk: a review ofthe in vitro and in vivo data.” NutrCancer 1994; 21:113–31.

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36. Messina M, Loprinzi C. “Soy for breastcancer survivors: a critical review of the literature.” J Nutrition 2001; 131:3095S–3108S.

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50. Russ C, Hendricks T, et al. “Vitamin B6

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51. Wynn V, et al. “Tryptophan, depressionand steroidal contraception.” J SteroidBiochem 1975; 6:965–70.

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54. Pye J, et al. “Clinical experience of drugtreatments for mastalgia.” Lancet 1985;II:373–77.

55. Gately C, et al. “Drug treatments formastalgia: 17 years experience in theCardiff mastalgia clinic.” J Roy Soc Med1992; 85:12–15.

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CHAPTER 13: MENSTRUALCRAMPS

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123. Firooznia H, Golimbi C, Rafii M,Schwartz M. “Rate of spinal trabecularbone loss in normal perimenopausalwomen: CT measurement.” Radiol 1986;161:735–38.

124. Riggs B, Wahner H, Melton L, et al.“Rates of bone loss in the appendicularand axial skeleton of women: evidence ofsubstantial vertebral bone loss beforemenopause.” J Clin Invest 1986; 77:1487–91.

125. Krohner B, Nielson S. “Bone mineralcontent of the lumbar spine in normaland osteoporotic women: cross-sectionaland longitudinal studies.” Clin Sci 1982;62:329–36.

126. Marcus R, Kosek J, Plefferbaum A,Homing S. “Age-related loss of trabecularbone in premenopausal women: a biopsystudy.” Calc Tiss Int 1983; 35:406–9.

127. Baran D, Sorensen A, Grimes J, et al.“Dietary modification with dairy prod-ucts for preventing vertebral bone loss inpremenopausal women: a three-yearprospective study.” J Clin Endocr Metab1990; 70:264–70.

128. Prior J, Vigna Y, Schechter M, Burgess A.“Spinal bone loss and ovulatory distur-bances.” N Engl J Med 1990; 323:1221–27.

129. Prior J. “Progesterone as a bone-trophichormone.” Endocr Rev 1990; 11 (2):386–98.

130. Adachi J, Anderson C, Murray T, Prior J.“Effect of progestins on bone.” J SocObstet Gynecol of Can 1991; 13:7.

131. Prior J. “Trabecular bone loss is associatedwith abnormal luteal phase length:endogenous progesterone deficiency maybe a risk factor for osteoporosis.” Int ProcJ 1989; 1:70–73.

132. Prior J, Vigna Y, Lentle B, et al. “Cyclicprogestin and calcium increase spinalbone density in women athletes withmenstrual cycle disturbances.” EndocrinolSoc Abst 1991; 73:450.

133. Wren B, Champion S, Willetts K, et al.“Transdermal progesterone and its effecton vasomotor symptoms, blood lipidlevels, bone metabolic markers, moods,and quality of life for postmenopausal.”Menopause 2003; 10 (1): 13–18.

134. Burry K, Patton P, Hermsmayer K. “Percutaneous absorption of progesteronein postmenopausal women treated withtransdermal oestrogen.” Am J ObstetGynecol 1999; 180:1504–11.

135. Carey B, Carey A, Patel S, Carter G,Studd J. “A study to evaluate serum andurinary hormone levels following shortand long term administration of two regi-mens of progesterone cream in postmenopausal women.” BJOG 2000; 107:722–26.


136. Leonetti H, Longo S, Anasti J. “Transder-mal progesterone cream for vasomotorsymptoms and post menopausal boneloss.” Obstet Gynecol 1999; 94:225–28.

137. Writing group for the PEPI Trial. “Effectsof hormone therapy on bone mineraldensity. Results from the PEPI Trial.”JAMA 1996; 276 (17): 1389–96.

138. Souza M, Prestwood K, et al. “A compari-son of the effect of synthetic andmicronized hormone replacement therapyon bone mineral density and biochemicalmarkers of bone metabolism.” Menopause:The J North Amer Meno Soc 1996; 3 (3):140–48.

139. Ettinger B, Genent H, Steiger P, MadvigP. “Low-dosage micronized 17 beta-estradiol prevents bone loss in postmeno-pausal women.” Am J Obstet Gynecol1992; 166:479–88.

140. Minaguchi H, Usmura T, Shirasu K, et al.“Effect of estriol on bone loss in post-menopausal Japanese women: a multicen-ter prospective open study.” J Obstet GynRes 1996; 22:259–65.

141. Nozaki M, Hashimoto K, Inoue Y, et al.“Usefulness of estriol for the treatment ofbone loss in postmenopausal women.”Nippon Sanka Fujinka Gakkai Zasshi1996; 48:83–88.

142. Nishibe A, Morimoto S, Hirota K, et al.“Effect of estriol and bone mineral den-sity of lumbar vertebrae in elderly andpostmenopausal women.” Nippon RonenIgakkai Zasshi 1996; 33:353–59.

143. Lindsay R, Hart D, Maclean A, et al. “Boneloss during oestriol therapy in postmeno-pausal women.” Maturitas 1979; 1:279–85.

144. Heaney R. “Bone mass, nutrition, andother lifestyle factors.” Nutr Rev 1996;54:53.

145. Bassey E. “Exercise in primary preventionof osteoporosis in women.” Ann Rheum Dis1995; 54:861.

146. “American College of Sports Medicine:ACSM position on osteoporosis and exer-cise.” Med Sci Sports Exerc 1995; 27:i–vii.

147. Suominen H. “Bone mineral density andlong-term exercise: an overview of cross-sectional athlete studies.” Sports Med1993; 16:316.

148. Chow R, Harrison J, Notarius C. “Effectof two randomised exercise programmeson bone mass in healthy postmenopausalwomen.” Br Med J 1987; 295:1441.

149. Pruitt L, Taaffe D, Marcus D. “Effects ofa one-year high-intensity versus low-intensity resistance training program onbone mineral density in older women.” J Bone Miner Res 1995; 10:1788.

150. Dook J, et al. “Exercise and bone mineraldensity in mature female athletes.” MedSci Sports Exerc 1997; 29:291.

151. Cassel C, Benedict M, Specker B. “Bonemineral density in elite 7 to 9 yr-oldfemale gymnasts and swimmers.” Med Sci Sports Exerc 1996; 28:1243.

152. Dyson K, et al. “Gymnastic training andbone density in pre-adolescent females.”Med Sci Sports Exerc 1997; 29:443.

153. McCartney N, et al. “Long-term resist-ance training in the elderly: effects ondynamic strength, exercise capacity,muscle, and bone.” J Gerontol 1995;50A:B97.

154. Rockwell J, et al. “Weight trainingdecreases vertebral bone density in pre-menopausal women: a prospective study.”J Clin Endocrinol Metab 1990; 71:988.

155. Gunnes M, Lehmann E. “Physical activ-ity and dietary constituents as predictorsof forearm cortical and trabecular bonepain in healthy children and adolescents:a prospective study.” Acta Paediata 1996;85:19.

156. Hirota T, et al. “Effect of diet and lifestyleon bone mass in Asian young women.”Am J Clin Nutr 1992; 55:1168.


157. Recker R, et al. “Bone gain in youngadult women.” JAMA 1992; 268:2403.

158. Prince R, et al. “The effects of calciumsupplementation (milk powder or tablets)and exercise on bone density in post-menopausal women.” J Bone Miner Res1995; 10:1068.

159. Grove K, Londeree B. “Bone density inpostmenopausal women: high impact vslow impact exercise.” Med Sci Sports Exerc1992; 24:1190.

160. Bloomfield S, et al. “Non-weightbearingexercise may increase lumbar spine bonemineral density in healthy postmenopausalwomen.” Am J Phys Med Rehab 1993;72:204.

161. Suleiman S, et al. “Effect of calcium intakeand physical activity on bone mass andturnover in healthy, white, postmenopausalwomen.” Am J Clin Nutr 1997; 66:937.

162. Campbell A, et al. “Randomised controlledtrial of a general practice programme onhome based exercise to prevent falls in eld-erly women.” Br Med J 1997; 315:1065.

163. Bouxsein M, Marcus R. “Overview of exer-cise and bone mass.” Rheum Dis ClinicsNorth Am: Osteoporosis 1994 Aug; 20 (3):787–802.

164. Erickson S, Sevier T, Christie D. “Osteo-porosis in active women.” Phys Sports Med1997; 25:61.

165. Johnson T. “Age-related differences in iso-metric and dynamic strength andendurance.” Phys Ther 1982; 62:985.

166. Rutherford O, Jones D. “The relationshipof muscle and bone loss and activity levelswith age in women.” Age Ageing 1992;21:286.

167. Lane N, et al. “Long-distance running,bone density, and osteoarthritis.” JAMA1986; 255:1147.

168. Cooper C, et al. “Childhood growth, phys-ical activity, and peak bone mass inwomen.” J Bone Miner Res 1995; 10:940.

169. Jaglal S, Kreiger N, Carlington G. “Postand recent physical activity and risk of hipfractures.” Am J Epidemiol 1993; 138:107.

170. Vuori I. “Peak bone mass and physicalactivity: a short review.” Nutr Rev 1996; 54:S11.

171. Snow-Harter C, Bouxsein M, Lewis B, etal. “Effects of resistance and endurance exercise on bone mineral status of youngwomen: a randomized exercise interventiontrial.” J Bone Miner Res 1992; 18:761–69.

172. Kelley G, Kelley K, Tran Z. “Exercise andlumbar spine bone mineral density inpostmenopausal women: a meta-analysisof individual patient data.” J Gerontol ABiol Sci Med Sci 2002; 57:599–604.

173. Notelovitz M, Martin D, Tesar R, et al.“Estrogen therapy and variable-resistanceweight training increase bone mineral insurgically menopausal women.” J BoneMiner Res 1991; 6:583–90.

174. Robertson M, Campbell A, Gardner M,Devlin N. “Preventing injuries in olderpeople by preventing falls: a meta-analysisof individual-level data.” J Am Geriatr Soc2002; 50:905–11.

CHAPTER 15: PELVIC INFLAMMATORY DISEASE

1. Washington A, Aral S, Wolner-Hanssen P,et al. “Assessing risk for pelvic inflamma-tory disease and its sequelae.” JAMA1991; 266:2581.

2. Grimes D. “Intrauterine devices andpelvic inflammatory disease: recent devel-opments.” Contraception 1987; 36:97.

3. Ness R, Keder L, Soper D, et al. “Oralcontraception and the recognition ofendometritis.” Am J Obstet Gynecol 1997;176:580.

4. Wolner-Hanseen P, Eschenback D,Paavonen J, et al. “Association betweenvaginal douching and acute pelvic inflam-matory disease.” JAMA 1990; 263:1936.


5. Bauer R, Wagner H. “Echinacea speciesas potential immunostimulatory drugs.”Econ Med Plant Res 1991; 5:253–321.

CHAPTER 16: PREGNANCY

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30. Laurence K, et al. “Double-blind ran-domized controlled trial of folate treat-ment before conception to preventrecurrence of neural-tube defects.” BrMed J 1981; 282:1509.

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32. Editorial staff. “Excessive folic acid.”Amer Fam Phys 1985; 32 (4): 290–91.

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35. Heller S, et al. “Riboflavin status duringpregnancy.” Am J Clin Nutr 1974; 27:1225–30.

36. Heller S, et al. “Vitamin B1 status in preg-nancy.” Am J Clin Nutr 1974; 27:1221–24.

37. Heller S, et al. “Vitamin B6 status in preg-nancy.” Am J Clin Nutr 1973; 26 (12):1339–48.

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45. Klieger JA, et al. “Abnormal pyridoxinemetabolism in toxemia of pregnancy.”Ann N Y Acad Sci 1969; 166:288–96.

46. Kirby PN, Molloy AM, Daly LE, et al.“Maternal plasma folate and vitamin B12

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47. Martinez-Frias ML, Salvador J. “Megadosevitamin A and teratogenicity.” Letter.Lancet 1988; 1:236.

48. Smithell RW. “Spina bifida and vitamins.”Br Med J 1983; 286:388–89.

49. Rothman KJ, Moore LL, Singer MR, et al.“Teratogenicity of high vitamin A intake.”N Engl J Med 1995; 333:1369–73.

50. Fell D, Steele RD. “Modification ofhepatic folate metabolism in rats fed excessretinol.” Life Sci 1986; 38:1959–65.

51. Kubler W. “Nutritional deficiencies inpregnancy.” Bibl Nutr Dieta 1981;30:17–29.

52. Hustead V, et al. “Relationship of vitaminA (retinol) status to lung disease in thepreterm infant.” J Pediat 1984; 105 (4):610–15.

53. Jendryczko A, Drozdz M. “Plasma retinol,beta-carotene and vitamin E levels in rela-tion to the future risk of preeclampsia.”Zent bl Gynakol 1989; 111:1121–23.

54. Czeizel AE, Dudas I. “Prevention of thefirst occurrence of neural-tube defects bypericonceptional vitamin supplementa-tion.” N Engl J Med 1992; 327:1832–35.

55. Kizer K, Fan A, Bankowska J, et al. “Vitamin A—a pregnancy hazard alert.”West J Med 1990; 152:78–81.

56. Lark S. Women’s Health Companion. Berke-ley, CA: Celestial Arts, 1995.

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58. Hammar M, et al. “Calcium and magne-sium status in pregnant women: a compar-ison between treatment with calcium andvitamin C in pregnant women with legcramps.” Int J Vit Nutr Res 1987; 57 (2):179–83.

59. Mino M, Nagamatu M. “An evaluation ofnutritional status of vitamin E in preg-nant women with respect to red bloodcell tocopherol level.” Int J Vit Nutr Res1986; 56:149–53.

60. Shah R, et al. “Vitamin E status of thenewborn in relation to gestational age,birth weight, and maternal vitamin Estatus.” Br J Nutr 1987; 58:191–98.

61. Marks J. “Critical appraisal of the thera-peutic value of alpha-tocopherol.” VitHorm 1962; 20:573–98.

62. Golding J, et al. “Childhood cancer,intramuscular vitamin K, and pethidinegiven during labour.” Br Med J 1992Aug; 305 (6849): 341–46.

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69. Hemminkl E, Rimpelü U. “A randomizedcomparison of routine versus selectiveiron supplementation during pregnancy.”J Am Coll Nutr 1991; 10 (1): 3–10.

70. Franz KB. “Correlation of urinary mag-nesium excretion with blood pressure ofpregnancy.” Magnesium Bull 1983;4:73–78.

71. Weaver K. Magnesium in Health and Dis-ease. Jamaica, NY: Spectrum Publications,1980; 833.

72. Kurzel R. “Serum magnesium levels inpregnancy and preterm labor.” Am J Peri-natol 1991; 8:119–27.

73. Conradt A. “Pathophysiology and clinicalaspects of pre-eclampsia.” Z GeburtshilfePerinatol 1985; 189 (4): 149–61.

74. Spatling L, Spatling G. “Magnesium sup-plementation in pregnancy. A double-blind study.” Br J Obstet Gynaecol 1988;95:120–25.

75. Sjögren A, et al. “Reduced concentrationsof magnesium, potassium and zinc inskeletal muscle from women duringnormal pregnancy or eclampsia.” Abstract.J Am Coll Nutr 1988; 7 (5): 408.

76. Argemi J, et al. “Serum zinc bindingcapacity in pregnant women.” Ann NutrMetab 1988; 32:121–26.

77. Apgar J, Evertt G. “Low zinc intakeaffects maintenance of pregnancy inguinea pigs.” J Nutr 1991; 121:192–200.

78. Lazebnik N, et al. “Zinc status, preg-nancy complications and labor abnormal-ities.” Am J Obstet Gynecol 1988; 158 (1):161–66.

79. Mukherjee M, et al. “Maternal zinc, iron,folic acid, and protein nutriture and out-come of human pregnancy.” Am J ClinNutr 1984; 40 (3): 496–507.

80. Buamah P, et al. “Maternal zinc status: adeterminant of central nervous systemmalformation.” Br J Obstet Gynaecol1984; 91:788–90.

81. Bergmann K, et al. “Abnormalities of hairzinc concentration in mothers of new-born infants with spina bifida.” Am J ClinNutr 1980; 33:2145.

82. Malhotra A, et al. “Placental zinc innormal and intrauterine growth-retardedpregnancies.” Br J Nutr 1990;63:613–21.

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123. Ernhart C, Sokol R, Martier S, et al.“Alcohol teratogenicity in the human: adetailed assessment of specificity, criticalperiod, and threshold.” Am J ObstetGynecol 1987; 156 (1): 33–39.

124. U.S. Department of Health and HumanServices. The Health Consequences ofSmoking: A Report of the Surgeon General—2004. Atlanta, GA: Centers for DiseaseControl and Prevention, Office on Smok-ing and Health, May 2004.

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129. Berger A. “Effects of caffeine consump-tion on pregnancy outcome. A review.” J Reprod Med 1988; 33 (12): 945–56.

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140. Weed S. Wise Woman Herbal for theChildbearing Years. Woodstock, NY:Ashtree Publishing, 1986.

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CHAPTER 17: PREMENSTRUALSYNDROME

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16. Wurtman J. “Carbohydrate craving. Rela-tionship between carbohydrate intake anddisorders of mood.” Drugs 1990; 39(Suppl 3): 49–52.

17. Moller SE. “Serotonin, carbohydrates, andatypical depression.” Pharmacol Toxicol1992; 71 (Suppl 1): 61–71.

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19. Rossignol AM, Bonnlander H. “Preva-lence and severity of the premenstrualsyndrome. Effects of foods and beveragesthat are sweet or high in sugar content.” J Reprod Med 1991 Feb; 36 (2): 131–36.

20. Puder JJ, Blum CA, Mueller B, DeGeyter CH, Dye L, Keller U. “Menstrualcycle symptoms are associated withchanges in low-grade inflammation.” EurJ Clin Invest 2006 Jan; 36 (1): 58–64.

21. Jakubowica D. “The significance of pro-staglandins in the premenstrual syndrome.”In Taylor R, ed., Premenstrual Syndrome.London: Medical New-Tribune, 1983; 16.

22. Danis R, Newton N, Keith L. “Pregnancyand alcohol.” Curr Prob Obstet Gynecol1981; 4:5.

23. Belfer M, Shader R, Carroll M, et al. “Alco-holism in women.” Arch Gen Psych 1971;25:540.

24. Rossignol AM, Bonnlander H. “Prevalenceand severity of the premenstrual syndrome.Effects of foods and beverages that aresweet or high in sugar content.” J ReprodMed 1991 Feb; 36 (2): 131–36.

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27. Stewart A. “Clinical and biochemicaleffects of nutritional supplementation onthe premenstrual syndrome.” J ReprodMed 1987; 32:435–40.


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29. Chuong C, Dawson E, Smith E. “Vita-min E levels in premenstrual syndrome.”Am J Obstet Gynecol 1990; 163:1591–95.

30. Chuong J, Dawson E. “Critical evaluationof nutritional factors in the pathophysiol-ogy and treatment of premenstrual syn-drome.” Clin Obstet Gynecol 1992; 35:3.

31. Chakmakjian Z, Higgins C, Abraham G.“The effect of a nutritional supplement,Optivite for women, on premenstrualtension syndrome: effect of symptomatol-ogy, using a double blind crossoverdesign.” J Appl Nutr 1985; 37:12.

32. London R, Bradley L, Chiamori N.“Effect of a nutritional supplement onpremenstrual symptomatology in womenwith premenstrual syndrome: a double-blind longitudinal study.” J Am Coll Nutr1991; 10 (5): 494–99.

33. Adams P, et al. “The effect of pyridoxinehydrochloride (vitamin B6) upon depres-sion associated with oral contraception.”Lancet 1973; 1:897–904.

34. Kleijnen J, ter Jtiet G, Knipschild P. “Vitamin B6 in the treatment of the pre-menstrual syndrome—a review.” Br JObstet Gynaecol 1990; 97:847–52.

35. Ebadi M, Govitrapong P. “Pyrodoxalphosphate and neurotransmitters in thebrain.” In Tryfiates G, ed., Vitamin B6

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37. Doll H, Brown S, Thurston A, Vessey M.“Pyridoxine (vitamin B6) and the pre-menstrual syndrome: a randomized

crossover trial.” J R Coll Gen Pract 1989Sep; 39 (326): 364–68.

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41. Thys-Jacobs S. “Vitamin D and calciumin menstrual migraine.” Headache 1994Oct; 34 (9): 544–46.

42. London R, et al. “The effect of alpha-tocopherol on premenstrual symptoma-tology: a double-blind study. II.Endocrine correlates.” J Am Coll Nutr1984; 3:351–56.

43. Callender K, McGregor M, Kirk P,Thomas C. “A double-blind trial ofevening primrose oil in the premenstrualsyndrome: nervous symptom subgroup.”Hum Psychopharmacol 1988; 3:57–61.

44. Khoo S, Munro C, Battistutta D.“Evening primrose oil and treatment ofpremenstrual syndrome.” Med J Aust1990; 153:189–92.

45. Collins A, Cerin A, Coleman G, Land-gren B. “Essential fatty acids in the treat-ment of premenstrual syndrome.” ObstetGynecol 1993; 81:93–98.

46. Puolakka J, et al. “Biochemical and clini-cal effects of treating the premenstrualsyndrome with prostaglandin synthesisprecursors.” J Rep Med 1985; 30 (3):149–53.


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48. Massil H, et al. “A double blind trial ofEfamol evening primrose oil in premen-strual syndrome.” Second InternationalSymposium on PMS, Kiawah Island, Sept1987.

49. Casper R. “A double blind trial ofevening primrose oil in premenstrual syn-drome.” Second International Sympo-sium on PMS, Kiawah Island, Sept 1987.

50. Sampalis F, Bunea R, Pelland MF, Kowal-ski O, Duguet N, Dupuis S. “Evaluationof the effects of Neptune Krill Oil on themanagement of premenstrual syndromeand dysmenorrhea.” Altern Med Rev 2003May; 8 (2): 171–79.

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53. Facchinetti F, Borella P, Sances G, et al.“Oral magnesium successfully relievespremenstrual mood changes.” ObstetGynecol 1991 Aug; 78 (2): 177–81.

54. Abraham GE, Lubran MM. “Serum andred cell magnesium levels in patients withpremenstrual tension.” Am J Clin Nutr1981 Nov; 34 (11): 2364–66.

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56. Shamberger RJ. “Calcium, magnesium,and other elements in the red blood cellsand hair of normals and patients withpremenstrual syndrome.” Biol Trace ElemRes 2003 Aug; 94 (2): 123–29.

57. Thys-Jacobs S. “Micronutrients and thepremenstrual syndrome: the case for cal-cium.” J Am Coll Nutr 2000 Apr; 19 (2):220–27.

58. Muneyvirci-Delale O, Nacharaju VL,Altura BM, Altura BT. “Sex steroid hor-mones modulate serum ionized magne-sium and calcium levels throughout themenstrual cycle in women.” Fertil Steril1998 May; 69 (5): 958–62.

59. Ward MW, Holimon TD. “Calcium treat-ment for premenstrual syndrome.” AnnPharmacother 1999 Dec; 33 (12):1356–58.

60. Thys-Jacobs, et al. “Calcium carbonate andthe premenstrual syndrome: effects on pre-menstrual and menstrual symptoms.” Am J Obstet Gynecol 1998 Aug: 444–52.

61. Eriksson O, Wall A, Marteinsdottir I, et al.“Mood changes correlate to changes inbrain serotonin precursor trapping inwomen with premenstrual dysphoria.” Psy-chiatry Res 2006 Mar 31; 146 (2): 107–16.

62. Bond A, Wingrove J, Critchlow D. “Tryp-tophan depletion increases aggression inwomen during the premenstrual phase.”Psychopharmacology (Berl) 2001 Aug; 156(4): 477–80.

63. Steinberg S, Annable L, Young SN, Liyan-age N. “A placebo-controlled clinical trialof L-tryptophan in premenstrual dyspho-ria.” Biol Psychiatry 1999 Feb 1; 45 (3):313–20.

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66. Haller J. “The influence of plant extractsin the hormonal exchange betweenhypophysis and ovary. An experimentalendocrinological animal study.” ZGeburtsh Gynakol 1961; 156:274–302.

67. Loch E. “Diagnosis and therapy of hor-monal bleeding disturbances.” TWGynakol 1989; 2:379–85.

68. Wuttke W. “Cell biological investigationswith Agnolyt preparations.” HN 246,NH 247 Report 1992; 8:7.

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76. Dittmar F. “Das pramenstruelle Span-nungssyndrom.” Jiatros Gynakologie 1989;5 (6): 4–7.

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78. Tamborini A, Taurelle R. “Value of stan-dardized Ginkgo biloba extract in themanagement of congestive symptoms ofpremenstrual syndrome.” Rev Fr GynecolObstet 1993; 88:447–57.

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80. Huang K, Tsai S. “St. John’s wort (Hyper-icum perforatum) as a treatment for pre-menstrual dysphoric disorder: casereport.” Int J Psychiatry Med 2003; 33(3): 295–97.

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86. Prior J, et al. “Conditioning exercisedecreases premenstrual symptoms: aprospective, controlled 6-month trial.”Fertil Steril 1987; 47:402.

87. Aganoff J, Boyle G. “Aerobic exercise,mood states and menstrual cycle symp-toms.” J Psychosom Res 1994; 38:183.

88. Choi P, Salmon P. “Stress responsivity inexercisers and non-exercisers during dif-ferent phases of the menstrual cycle.” SocSci Med 1995; 41:769.

89. Gannon L. “The potential role of exercisein the alleviation of menstrual disordersand menopausal symptoms: a theoreticalsynthesis of recent research.” Women &Health 1988; 14:105.

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CHAPTER 18: SEXUALLY TRANS-MITTED DISEASES

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2. Majeroni B. “Chlamydial cervicitis: com-plications and new treatment options.”Am Fam Phys 1994; 49:1825–29.

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6. Quinn T, Gaydos C, Shepherd M, et al.“Epidemiologic and microbiologic corre-lates of Chlamydia trachomatis in sexualpartnerships.” JAMA 1996; 276:1737.


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10. Rein M. “Vulvovaginitis and cervicitis.”In Mandell G, Bennett J, Dolin R, eds.,Principles and Practice of InfectiousDiseases, 4th ed. New York: ChurchillLivingstone, 1995; 1074–90.

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12. Bauer R, Wagner H. “Echinacea species aspotential immunostimulatory drugs.”Econ Med Plant Res 1991; 5:253–321.

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15. Zheng H, Cao J, Jin H, Wang J. “Prelim-inary examination of a LB-H2O2 sub-stance that inhibit Neisseria gonorrheagrowth.” Zhongguo Yi Xue Ke Xue YuanXue Bao 1999 Oct; 21 (5): 379–83.

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CHAPTER 19: UTERINE FIBROIDS

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6. Wilson E, Yang F, Rees E. “Estradiol andprogesterone binding in uterine leiomy-omata and in normal uterine tissues.”Obstet Gynecol 1980; 5:20.

7. Puuka M, Kontula K, Kauppila A, JanneO, Vihdo R. “Estrogen receptor inhuman myoma tissue.” Mol CellEndocrinol 1976; 6:35.

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11. Haney A. “Clinical decision makingregarding leiomyomata: what we need inthe next millennium.” Environ HealthPerspect 2000; 108:835–39.

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14. Vollenhoven B, Lawrence A, Healy D.“Uterine fibroids: a clinical review.” Br J Obstet Gynaecol 1990; 97:285–98.

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16. Carter J. “Combined hysteroscopic andlaparoscopic findings in patients withchronic pelvic pain.” J Am Assoc GynecolLaparosc 1994; 2:43–47.

17. Tay S, Bromwich N. “Outcome of hys-terectomy for pelvic pain in premeno-pausal women.” Aust N Z J ObstetGynaecol 1998; 38:72–76.

18. Kjerulff K, Langenberg P, Seidman J, etal. “Uterine leiomyomas: racial differencesin severity, symptoms and age at diagno-sis.” J Reprod Med 1994; 41:483–90.

19. Buttram V Jr, Reiter R. “Uterine leiomy-omata: etiology, symptomatology, andmanagement.” Fertil Steril 1981;36:433–45.

20. Lippman S, Warner M, Samuels S, et al.“Uterine fibroids and gynecologic painsymptoms in a population-based study.”Fertil Steril 2003; 80:1488–94.

21. Exacoustos C, Rosati P. “Ultrasound diag-nosis of uterine myomas and complica-tions in pregnancy.” Obstet Gynecol 1993;82:97–101.

22. Rice J, Kay H, Mahony B. “The clinicalsignificance of uterine leiomyomas inpregnancy.” Am J Obstet Gynecol 1989;160:1212–16.

23. Sahin K, Ozercan R, Onderci M, et al.“Lycopene supplementation prevents thedevelopment of spontaneous smoothmuscle tumors of the oviduct in Japanesequail.”Nutr Cancer 2004; 50 (2): 181–89.

24. Chiaffarino F, Parazzini F, La Vecchia C,Chatenoud L, Di Cintio E, Marsico S.“Diet and uterine myomas.”ObstetGynecol 1999 Sep; 94 (3): 395–98.

25. Golden B, et al. “Estrogen excretion pat-terns and plasma levels in vegetarian andomnivorous women.” N Engl J Med1982; 307:1542–47.

26. Goodman M, Wilkens L, et al. “Associa-tion of soy and fiber consumption withthe risk of endometrial cancer.” Am J Epi-demiol 1997; 146 (4): 294–306.

27. Xu WH, Zheng W, Xiang YB, Ruan ZX,et al. “Soya food intake and risk ofendometrial cancer among Chinesewomen in Shanghai: population basedcase-control study.” Br Med J 2004;328:1285–88.

28. Unfer V, Casini ML, Costabile L,Mignosa M, et al. “Endometrial effects oflong-term treatment with phytoestrogens:a randomized, double-blind, placebo-controlled study.” Fertil Steril 2004;82:145–48.

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32. Sang H. “Clinical and experimentalresearch into treatment of hysteromyomawith promoting qi flow and blood circu-lation, softening and resolving hardlump.” J Tradit Chin Med 2004 Dec; 24(4): 274–79.

33. Dean D, Exley D, Goodwin T. “Steroidoestrogens in plants: re-estimation ofoestrone in pomegranate seeds.” Phy-tochem 1971; 10:2215–16.

34. Verdeal R, Ryan D. “Naturally-occurringoestrogens in plant foodstuffs—a review.”J Food Protec 1979; 42:577–83.

35. Price K, Fenwick G. “Naturally occurringoestrogens in foods—a review.” FoodAddit Contam 1985; 2:73–106.

36. Miksicek R. “Estrogenic flavonoids: struc-tural requirements for biological activity.”Proceed Soc Exper Biol Med 1995;208:44–50.

37. Bennetts H, Underwood E, Shier F. “Abreeding problem of sheep in the south-west division of Western Australia.” J Dept Agric West Aust 1946; 23:1–12.

38. Saloniemi H, Wahala K, Nykanen-KurkiP, Saastamoinen I. “Phytoestrogen con-tent and effect of legume fodder.”PSEBM 1995; 208:13–17.

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40. Adams N. “Cervical mucus and repro-ductive efficiency in ewes after exposureto oestrogenic pastures.” Aust J Agric Res1977; 28:481–89.

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42. Shutt D, Cox R. “Steroid and phyto-oestrogen binding to sheep uterine recep-tors in vitro.” J Endocrin 1972; 52:299–310.

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44. Messina M, Persky V, Setchell K, BarnesS. “Soy intake and cancer risk: a review ofthe in vitro and in vivo data.” Nutr andCanc 1994; 21 (2): 113–31.

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48. Lipschutz A. “Experimental fibroids andthe antifibromatogenic action of steroidhormones.” JAMA 1942; 120:71.

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50. Lee J. What Your Doctor May Not Tell YouAbout Menopause. New York: WarnerBooks, 1996.

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CHAPTER 20: VAGINITIS

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the sexual partner.” Br J Obstet Gynaecol1988; 95:920.

8. Vutyavanich T, Pongsuthirak P,Vannareumol P, et al. “A randomizeddouble-blind trial of tinidazole treatmentof the sexual partners of females with bac-terial vaginosis.” Obstet Gynecol 1993;82:550.

9. Barbone F, Austin H, Louv W, AlexanderW. “A follow-up study of methods ofcontraception, sexual activity, and rates oftrichomoniasis, candidiasis and bacterialvaginosis.” Am J Obstet Gynecol 1990;75:1028.

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11. Berger B, Kolton S, Zenilman J, et al.“Bacterial vaginosis in lesbians: a sexuallytransmitted disease.” Clin Infect Dis 1995;21:1402.

12. Goldenberg R, Klebanoff M, Nugent R,Krohn M, Hillier S, Andrews W. “Bacter-ial colonization of the vagina during preg-nancy in four ethnic groups.” Am J ObstetGynecol 1996; 174:1618–24.

13. Martin J, Richardson B, Nyange P, et al.“Vaginal lactobacilli, microbial flora, andrisk of human immunodeficiency virustype 1 and sexually transmitted diseaseacquisition.” J Infect Dis 1999;180:1863–68.

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20. Watts D, Eschenbach D, Kenn G. “Earlypostpartum endometritis: the role of bacte-ria, genital mycoplasmas, and chlamydiatrachomatis.” Obstet Gynecol 1989; 73:52.

21. Blackwell A, Fox A, Phillips I, Barlow D.“Anaerobic vaginosis (nonspecific vaginitis):clinical, microbiological, and therapeuticfindings.” Lancet 1983; 2: 1279–1382.

22. Foxman B, Barlow R, D’Arcy H, GilespieB, Sobel J. “Candida vaginitis: self-reportedincidence and associated costs.” Sex TransmDis 2000; 27 (4): 230–35.

23. Spinillo A, Capuzzo E, Gulminetti R, et al.“Prevalence of and risk factors for fungalvaginitis caused by non-albicans species.”Am J Obstet Gynecol 1997; 176:138–41.

24. Odds F. “Resistance of yeasts to azole-derivative antifungals.” J AntimicrobChemother 1993; 31:463–71.

25. Ledger W, Monif G. “A growing concern:inability to diagnose vulvovaginal infec-tions correctly.” Obstet Gynecol 2004;103: 782–84.

26. Odds F. “Candidosis of the genitalia.” InOdds F, ed., Candida and Candidosis, 2nded. London: Balliere Tindall, 1988; 124.

27. Faro S. “Systemic vs. topical therapy forthe treatment of vulvovaginal candidia-

sis.” Infect Dis Obstet Gynecol 1994; 1:202–8.

28. Horowitz B. “The role on non-albicansCandida in vulvovaginal candidiasis.” J Clin Pract Sexuality 1991; 7 (specialissue): 16–20.

29. O’Connor M, Sobel J. “Epidemiology ofrecurrent vulvovaginal candidiasis: identi-fication and strain differentiation of Can-dida albicans.” J Infect Dis 1986; 54:358–63.

30. Horowitz B, Edelson S, Lippman L.“Sexual transmission of Candida.” ObstetGynecol 1987; 69 (6): 883–86.

31. Miles MR, Olsen L, Rogers A. “Recur-rent vaginal candidiasis. Importance of anintestinal reservoir.” JAMA 1977 Oct 24;238 (17): 1836–37.

32. Horowitz B, Giaquinta D, Ito S. “Evolv-ing pathogens in vulvovaginal candidiasis:implications for patient care.” J ClinPharmacol 1992; 32 (3): 248–55.

33. Donders GG, Prenen H, Verbeke G, Rey-brouck R. “Impaired tolerance for glucosein women with recurrent vaginal candidi-asis.” Am J Obstet Gynecol 2002 Oct; 187(4): 989–93.

34. Elegbe I, Botu M. “A preliminary studyof dressing patterns and incidence of can-didiasis.” Am J Public Health 1982; 72:176–77.

35. Heidrich F, Berg A, Bergman J. “Clothingfactors and vaginitis.” J Family Practice1984; 19 (4): 491–94.

36. Gerbase A, Rowley J, Heymann D, et al.“Global prevalence and incidence esti-mates of curable STDs.” Sex Transm InfectSuppl 1998; 74:512–17.

37. Cates W. “Estimates of the incidence andprevalence of sexually transmitted diseasesin the United States.” Sex Transm Dis1999; 26 (Suppl): 52–57.

38. Lossick J. “Epidemiology of urogenitaltrichomoniasis.” In Honinberg B, ed.,


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39. Rein M, Muller M. “Trichomonas vagi-nalis and trichomiasis.” In Holmes K, ed.,Sexually Transmitted Diseases. New York:McGraw-Hill, 1990; 481–92.

40. Heine P, McGregor J. “Trichomonas vagi-nalis: a reemerging pathogen.” Clin ObstetGynecol 1993; 36:137–44.

41. Levine G. “Sexually transmitted parasiticdiseases.” Prim Care 1991; 18:101–28.

42. Wolner-Hanssen P, et al. “Clinical mani-festations of vaginal trichomonas.” JAMA1989; 264:571–76.

43. Ohlemeyer C, Hornberger L, Lynch D,Swierkosz E. “Diagnosis of Trichomonasvaginalis in adolescent females: InPouchTV culture versus wet-mount micro-scopy.” J Adolesc Health 1998; 22:205–8.

44. Doderlein A. “Die Scheidensekretunter-suchugen.” Zentralbl Gynakol 1894;18:10–14.

45. Ant M. “Diabetic vulvovaginitis treatedwith vitamin E suppositories.” Am JObstet Gynecol 1954; 67 (2): 407–9.

46. Petersen EE, Magnani P. “Efficacy andsafety of vitamin C vaginal tablets in thetreatment of non-specific vaginitis. A ran-domised, double blind, placebo-con-trolled study.” Eur J Obstet GynecolReprod Biol 2004 Nov 10; 117 (1):70–75.

47. Adetumbi M, Javor G, Lau B. “Alliumsativum (garlic) inhibits lipid synthesis byCandida albicans.” Antimicrob Agents andChemother 1986; 30 (3): 499–501.

48. Hronek M, Vachtlova D, Kudlackova Z,Jilek P. “Antifungal effect in selected natu-ral compounds and probiotics and theirpossible use in prophylaxis of vulvovagini-tis.” Ceska Gynekol 2005 Sep; 70 (5):395–99.

49. Moore G, Atkins R. “The fungicidal andfungistatic effects of an aqueous garlic

extract on medically important yeastlikefungi.” Mycologia 1977; 15:466–68.

50. Cavallito C, Bailey J. “Allicin, the anti-bacterial principle of Allium sativum. Iso-lation, physical properties andantibacterial action.” J Am Chem Soc1944; 66:1950–51.

51. Amin AH, Subbaiah TV, Abbasi KM.“Berberine sulfate: antimicrobial activity,bioassay, and mode of action.” Can JMicrobiology 1969; 15:1067–76.


53. Hammer KA, Carson CF, Riley TV.“Melaleuca alternifolia (tea tree) oilinhibits germ tube formation by Candidaalbicans.” Med Mycol 2000 Oct; 38 (5):355–62.

54. Hammer KA, Carson CF, Riley TV. “In-vitro activity of essential oils, in particularMelaleuca alternifolia (tea tree) oil and teatree oil products, against Candida spp.” J Antimicrob Chemother 1998 Nov; 42(5): 591–95.

55. Ergin A, Arikan S. “Comparison ofmicrodilution and disc diffusion methodsin assessing the in vitro activity of flu-conazole and Melaleuca alternifolia (teatree) oil against vaginal Candida isolates.”J Chemother 2002 Oct; 14 (5): 465–72.

56. Mondello F, De Bernardis F, Girolamo A,Salvatore G, Cassone A. “In vitro and invivo activity of tea tree oil against azole-susceptible and -resistant human patho-genic yeasts.” J Antimicrob Chemother2003 May; 51 (5): 1223–29.

57. Pena E. “Melaleuca alternifolia oil: its usefor trichomonal vaginitis and other vagi-nal infections.” Obstet Gynecol 1962; 19(6): 793–95.


58. Williams L, Home V. “A comparativestudy of some essential oils for potentialuse in topical applications for the treat-ment of the yeast Candida albicans.” AustJ Med Herbal 1995; 7 (3): 57–62.

59. Reid G. “Probiotics for urogenitalhealth.” Nutr Clin Care 2002; 5:3–8.

60. Chan R, Bruce A, Reid G. “Adherence ofcervical, vaginal and distal urethralnormal microbial flora to human uroep-ithelial cells and the inhibition of adher-ence of gram-negative uropathogens bycompetitive exclusion.” J Urol 1984;131:596–601.

61. Andersson R, Daeschel M, Hassan H.“Antibacterial activity of plantaricin SIK-83, a bacteriocin produced by Lacto-bacillus plantarum.” Biochimie 1988;70:381–90.

62. Hillier S, Krohn M, Klebanoff S, Eschen-bach D. “The relationship of hydrogenperoxide–producing lactobacilli to bacter-ial vaginosis and genital microflora inpregnant women.” Obstet Gynecol 1992;79 (3): 369–72.

63. Klebanoff S, Hillier S, Eschenbach D,Waltersdorph A. “Control of the microbial flora of the vagina by H2O2-generating lactobacilli.” J Infec Dis 1991;164:94–100.

64. Hilton E, Isenberg H, Alperstein P,France K, Borenstein M. “Ingestion ofyogurt containing Lactobacillus aci-dophilus as prophylaxis for candidalvaginitis.” Ann Intern Med 1992;116:353–57.

65. Delia A, Morgante G, Rago G, et al.“Effectiveness of oral administration ofLactobacillus paracasei subsp. paracaseiF19 in association with vaginal supposito-ries of Lactobacillus acidofilus in the treat-ment of vaginosis and in the preventionof recurrent vaginitis.” Minerva Ginecol2006 Jun; 58 (3): 227–31.

66. Williams AB, Yu C, Tashima K, Burgess J,Danvers K. “Evaluation of two self-caretreatments for prevention of vaginal candidiasis in women with HIV.” J AssocNurses AIDS Care 2001 Jul–Aug; 12 (4):51–57.

67. Ozkinay E, Terek MC, Yayci M, Kaiser R,Grob P, Tuncay G. “The effectiveness oflive lactobacilli in combination with lowdose oestriol (Gynoflor) to restore the vagi-nal flora after treatment of vaginal infec-tions.” BJOG 2005 Feb; 112 (2): 234–40.

68. Jeavons H. “Prevention and treatment ofvulvovaginal candidiasis using exogenousLactobacillus.” J Obstet Gynecol NeonatalNurs 2003; 32 (3): 287–96.

69. Hilton E, Rindos P, Isenberg H. “Lacto-bacillus GG vaginal suppositories andvaginitis.” J Clin Microbiol 1995; 33 (5):1433.

70. Hughes V, Hillier S. “Microbiologic char-acteristics of lactobacillus products usedfor colonization of the vagina.” ObstetGynecol 1990; 75 (2): 244–48.

71. Parent D, Bossens M, Bayot D, et al.“Therapy of bacterial vaginosis usingexogenously applied Lactobacilusi aci-dophilus and a low dose of estriol: aplacebo-controlled multicentric clinicaltrial.” Arneimittelforschung 1996;46:68–73.

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74. Keller Van Slyke K, Michel V, Rein M.“Treatment of vulvovaginal candidiasis


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75. Jovanovic R, Congema E, Nguyen H.“Antifungal against versus boric acid fortreating chronic mycotic vulvovaginitis.”Journal of Reproductive Medicine 1991; 36(8): 593–97.

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481

I N D E X

Abortion, 61–62, 295Abraham, Guy, 252Acne, 184–85Activella, 369. See also Hormone replacement

therapy (HRT)Acupuncture, 162Adrenal Assist, 381Adrenal glands, 177Age factors

bone density, 243cervical dysplasia, 33menopause, 175–76osteoporosis, 237, 238screening tests for risk factors, 378

AIDS infectionscreening tests risk factors, 379

Alcohol, 126infertility and, 158osteoporosis and, 247pelvic inflammatory disease (PID) and, 268pregnancy and, 290screening tests risk factors, 380

Alfalfa (Medicago sativa), 23Allicin extract, 322Aloe vera, 105–6Alora, 368. See also Hormone replacement

therapy (HRT)Alpha-linolenic acid (ALA), 120Alternative treatments, 388–89

for amenorrhea, 18–27for cervical dysplasia, 34–47for cystitis, 67–72definitions, xviifor endometriosis, 79–85for fibrocystic breasts, 90–96for genital herpes, 102–7for heart disease, 114–48

for infertility, 157–64for interstitial cystitis (IC), 168–72for menopause, 187–219for menstrual cramps, 226–34for osteoporosis, 243–63for pelvic inflammatory disease (PID),

269–71for pregnancy, 275–90for premenstrual syndrome (PMS), 304–13for sexually transmitted infections (STIs),

321–23for uterine bleeding, 4–13for uterine fibroids, 330for vaginitis, 348–55

Amen, 370. See also Hormone replacementtherapy (HRT)

Amenorrhea, 15–30, 382alternative treatments, 18–27conventional treatment, 27–30diagnosis, 17–18licensed primary health-care practitioners

and, 30physical exercise and, 25–27prevention, 17sample treatment plans, 27–28

American College of OB/GYN (ACOG), 219

American Heart Association recommendations,128, 150–51

Amylases, 333Androderm, 371. See also Hormone

replacement therapy (HRT)Androgel, 371. See also Hormone replacement

therapy (HRT)Androgens, 213–14

osteoporosis and, 265Anemia, 382


482 I N D E X

Angeliq, 369. See also Hormone replacementtherapy (HRT)

Anorexia nervosa, 19Anti-atherosclerosis, 143Antibiotics

for pelvic inflammatory disease (PID), 270

for sexually transmitted infections, 323–24

Antihypertensives, 143Antioxidant combinations

for heart disease, 130Antiviral herpes treatments, 107Anxiety, 181–82, 382Aqueous iodine, 95Archer, David, 222Arden’s powder, 353–54Aromatase inhibitors (AI), 164–65Ashwagandha, 218Astringent herbs, 10Atherosclerosis, 123Atypia, 33Atypical glandular cells of undetermined

significance (AGUS), 33–34, 385Autoimmune disease, screening tests risk

factors, 379Autoimmune theories of interstitial cystitis

(IC), 168Aygestin, 370. See also Hormone replacement

therapy (HRT)

Backache, 296Bacterial vaginosis (BV), 341–44, 356–57. See

also VaginitisBastyr, John, xixBee propolis, 105Beta-carotene

for endometriosis, 82for fibrocystic breasts, 94for vaginitis, 349

Bio-identical testosterone, 215Biofeedback, 228

Bioflavonoids, 171, 193for abnormal uterine bleeding, 8for genital herpes, 103–4for pregnancy, 285

Birthfootling breech, 299frank breech infant, 299screening tests risk factors, 379, 380vaginal, 299

Birth control pills (BCPs), 55–60, 62. See alsoOral contraceptives

Bisphosphonates, 266Bitter melon (Momordica charantia), 24, 106Black cohosh (Cimicifuga racemosa), 197–98,

232–33, 381, 384, 386for amenorrhea, 21–22for infertility, 161

Black haw (Viburnum prunifolium), 232root, 295

Black tea, 139Bladder epithelial permeability, 168, 169Bladder infection, 66, 296–97, 382. See also

CystitisBladderwrack (Fucus vesiculosus), 9–10Blood clots, 202–3Blood glucose test, 375Blood pressure, 150. See also High blood

pressurepregnancy and, 298–99tests for, 375

Blood transfusionscreening tests risk factors, 379

Bloodroot (Sanguinaria canadensis), 23Blue cohosh (Caulophyllum thalictroides), 23,

233for infertility, 161

Body weight, 242. See also Weight gain;Weight loss

body mass index, 365pregnancy and, 277, 294screening tests for risk factors, 378

Boiron, 386

483I N D E X

Bone density, 222bone mineral density (BMD), 243, 375estriol and, 207osteoporosis, 237–66peak ages, 243

Bone health, 192bone remodeling, 238–39osteoporosis, 237–66

Bone imaging, 242–43Boniva, 264Boric acid, 353Boron, 252–53Botanicals

for amenorrhea, 21–24for cervical dysplasia, 39–41for cystitis, 70–72for endometriosis, 83–85for fibrocystic breasts, 95–96for genital herpes, 104–7for heart disease, 138–43for infertiliy, 161–62for interstitial cystitis (IC), 171–72for menopause, 194–201for menstrual cramps, 231–33for osteoporosis, 256–60for pregnancy, 288–90for premenstrual syndrome (PMS),

310–11for sexually transmitted infections (STIs),

322–23for uterine bleeding, 8–11for uterine fibroids, 334–37for vaginitis, 350–56

Breast cancerbirth control pills and, 56–57estriol and, 207–8hormone replacement therapy (HRT) and,

203, 211–13prevention, 383self-exam for, 373

Breast-feeding, 383Breast nodularity, 89

Breasts, densescreening tests risk factors, 379

Breasts, painful. See Fibrocystic breasts;Mastalgia

Bromocriptine, 97

C-reactive protein, 306Caffeine, 91–92, 124–25

content in foods, 159infertility and, 158, 159pregnancy and, 291premenstrual syndrome (PMS) and, 306

Calcitonin, 265Calcium, 133, 192

for amenorrhea, 20excretion in urine, 245for menstrual cramps, 230for osteoporosis, 241, 245, 248–50, 265for pregnancy, 283premenstrual syndrome (PMS) and, 309recommendations of intake, 248

Calcium glycerophosphate (Prelief ), 171Canadian fleabane (Erigeron canadensis),

11Cancer, 385. See also Specific types

companion products, 382screening tests risk factors, 379

Cancer Research Center (University ofHawaii), 331

Candida vaginitis, 344–46, 356–57. See alsoVaginitis

Canola oil, 117Carbohydrates, 123Cardiac imaging tests, 113Cardiovascular disease (CVD). See Heart

diseaseCarotenes, 20, 36–37, 121Carotenoids, 322Castor oil pack, 373–74Celiac disease, 162Cenestin, 367. See also Hormone replacement

therapy (HRT)

484 I N D E X

Centers for Disease Control (CDC)guidelines for treatment of yeast vaginitis,

357Ceonothus compound, 334Cervical cancer, 2, 31Cervical cap, 53–54, 63Cervical dysplasia, 31–50, 385

alternative treatments, 34–47conventional medical treatments, 47–50licensed primary health-care practitioners

and, 50preventative medicine, 34–35psychological factors, 47risk factors, 33sample treatment plans, 42, 43, 44, 45, 46,

48Chamomile, 217Chapparal (Larrea tridentate), 106Chaste tree (Vitex agnus castus), 23, 199, 310,

334, 384for amenorrhea, 21berry, 381, 382, 384, 386for endometriosis, 83for infertility, 161for uterine bleeding, 8–9

Chlamydia trachomatis (CT), 269, 317–18,322

cervical dysplasia and, 33sample treatment plan, 322test, 375

Chocolate, 126–27Choice, xixCholesterol, 118–19, 383. See also HDL

cholesterol; LDL cholesterolcaffeine and, 124heart disease and, 111, 116screening tests, 378test, 375

Choline, 95Chromium, 24, 283Chronic anovulation, 29–30Cinnamon (Cinnamomum verum), 11

Circulation aids, 142Citrus bioflavonoids, 139Cleavers (Galium aparine), 95Climara, 368. See also Hormone replacement

therapy (HRT)ClimaraPro, 370. See also Hormone

replacement therapy (HRT)Clinics, 388Clomiphene citrate (CC), 164Cobalamin, 281Cobalt, 284Coconut oil, 117Coenzyme Q10, 132–33, 287Cognitive-behavioral therapy (CBT),

314Cognitive decline, 203Colon disease

screening tests risk factors, 379Colonoscopy, 376Colposcopy, 40CombiPatch, 370. See also Hormone

replacement therapy (HRT)Comfrey (Symphytum officinale), 172Computed tomography (CT), 113Concentration, 182. See also MemoryCondoms, 53–54, 63Condyloma, 31Conization, 41, 47, 49Constipation, 296Contraception. See also Oral contraceptives

barrier methods, 53–54basal body temperature, 53birth control pills (BCPs), 55–60, 62calendar methods, 52cervical mucus, 52–53emergency, 60fertility awareness, 51–53hormonal, 55–61patches, 61pelvic inflammatory disease (PID) and,

268for premenstrual syndrome (PMS), 315

485I N D E X

Conventional medical treatments, xxi–xxiifor amenorrhea, 27–31for cervical dysplasia, 47–50for cystitis, 73for endometriosis, 85–87for fibrocystic breasts, 96–97for genital herpes, 107–8for heart disease, 148–51for infertility, 164–65for interstitial cystitis (IC), 172–73for menopause, 219–23for menstrual cramps, 234–36for osteoporosis, 264–66for pelvic inflammatory disease (PID),

271–72for pregnancy, 297–98for premenstrual syndrome (PMS), 314–15for sexually transmitted infections (STIs),

323–24for uterine bleeding, 13–14for uterine fibroids, 337–40for vaginitis, 356–58

Copper, 253, 284Corn oil, 117Corn silk (Zea mays), 172Cortical bone, 238Coumestrol, 335Crampbark (Vibernum opulus), 172, 232

for infertility, 161Cranberry, 68–69Cryotherapy, 47, 49Curcumin, 40

for pelvic inflammatory disease (PID), 270Cuts

screening tests risk factors, 380Cycrin, 370. See also Hormone replacement

therapy (HRT)Cystitis, 65–73

alternative treatments, 67–72botanicals, 70–72diagnosis, 66–67diet, 68

licensed primary health-care practitionersand, 73

nutrition, 67–70sample treatment plans, 71

Cytology methods, 34

D-mannose, 69–70Dalton, Katharina, 312Damiana, 218Dandelion leaf, 95, 288–89Dandelion root (Taraxacum officinale), 83, 288,

334DASH diet, 124, 125Deep vein thrombosis (DVT), 265Dehydroepiandrosterone (DHEA), 215Dementia, 203Dental issues

changes with menopause, 185exam, 376

Depo-Provera, 60–61, 86Depression, 181–82, 383

sample treatment plan, 199Detoxification, 383Developmental delay

screening tests risk factors, 379Diabetes, 123

heart disease and, 111–12screening tests, 378–79

Diabetes mellitushormone replacement therapy (HRT) and,

203Diagnostic and Statistical Manual of Mental

Disorders (DSM-IV), 303Diaphragm, 53–54, 63Diet

for abnormal uterine bleeding, 6cholesterol and, 119for cystitis, 68DASH diet, 124, 125for endometriosis, 80–81for fertility, 158, 159fiber and, 120–22

486 I N D E X

for fibrocystic breasts, 91–92genital herpes and, 102–3heart and, 116–29high-fiber, 331for hypertension, 124for interstitial cystitis (IC), 169for menopause, 192for menstrual cramps, 228–29for premenstrual syndrome (PMS), 306vegan, 92, 248vegetarian, 245

Dietary fat, 92Dilation and curettage (D&C), 14Diuretics, 95, 142Docahexaenoic acid (DHA), 120, 137,

285–86Dong quai (Angelica sinensis), 23, 194

infertility and, 161Double contrast barium enema (DCBE), 376Drug use, illegal

pelvic inflammatory disease (PID) and, 268pregnancy and, 292–93screening tests risk factors, 380

Drugs, over-the-counterpregnancy and, 292

Drugs, prescriptionpregnancy and, 292

Dysfunctional uterine bleeding (DUB), 1,3–14

alternative treatments, 4–14diagnosis, 3–4prevention, 4sample treatment plans, 12

Dysmenorrhea, 225, 226. See also Menstrualcramps

Dysuria, 167

Ear injuryscreening tests risk factors, 379

Echinacea, 106, 334sexually transmitted infections (STIs), 322

Eclampsia, 295–96

Ectopic pregnancy, 267Eicosapentanoic acid (EPA), 119, 120Electrocardiogram (ECG), 113Embolization, 338Endoctrine disorders

osteoporosis and, 241Endometrial ablation, 14Endometrial cancer, 2–3, 330

estriol and, 207Endometrial hyperplasia, 2–3Endometrial polyps, 2Endometriosis, 75–87

alternative treatments, 79–85botanicals, 83–85conventional medical treatments, 85–87diet, 80–81environmental factors, 77genetic factors, 77hormone metabolism, 78–79immune connection, 77–78licensed primary health-care practitioners

and, 87nutrition, 80–83preventative medicine, 79research, 75–77sample treatment plan, 84stress and, 75

Endometritis, 267Enjuvia, 367. See also Hormone replacement

therapy (HRT)Environmental factors, 385

endometriosis and, 77infertility and, 158–59pregnancy and, 290–91, 292

Ernster, Virginia, 91Escharotic treatment, 41, 48Esclim, 368. See also Hormone replacement

therapy (HRT)Essential fatty acids, 93–94

endometriosis and, 82–83heart disease and, 116–17, 119–20, 137–38osteoporosis and, 254–56

487I N D E X

pregnancy and, 285–87premenstrual syndrome (PMS) and, 308

Essure, 61Estrace, 367. See also Hormone replacement

therapy (HRT)Estrace cream, 369. See also Hormone

replacement therapy (HRT)Estraderm, 368. See also Hormone replacement

therapy (HRT)Estradiol, 13Estrasorb, 368. See also Hormone replacement

therapy (HRT)Estratab, 367. See also Hormone replacement

therapy (HRT)Estratest, 371. See also Hormone replacement

therapy (HRT)Estring. See Hormone replacement therapy

(HRT)Estriol, 206–7Estrogel, 368. See also Hormone replacement

therapy (HRT)Estrogen, 13, 86, 220–21, 302

bio-identical, 146–49, 206–8, 260–61combination products, 221conjugated equine estrogens (CEE),

213natural, 146–49, 260–61oral, 367–68for osteoporosis, 260–61selective estrogen receptor modulator

(SERM), 264, 265transdermal, 368–69vaginal, 221–22, 369

Estrogen dominance, 304Estrogen-progestin

oral combinations, 369–70transdermal combinations, 370

Estrogen-progestogen therapy (EPT), 201

Estrogen/testosterone, 371Estrogen therapy (ET), 201, 264. See also

Hormone replacement therapy (HRT)

Ethnicityscreening tests for risk factors, 377–78

Evening primrose oil, 94, 138, 193, 231, 287premenstrual syndrome (PMS) and, 308

Exercise. See Physical exerciseEye issues

changes with menopause, 185exam, 376screening tests risk factors for injury, 379

Facial hair, 184–85Falling risks, 241False unicorn, 288

infertility, 161False unicorn root (Chamaelirium luteum),

233, 295Family history. See also Genetic factors

cervical dysplasia and, 33screening tests for risk factors, 377

Fastingsexually transmitted infections (STIs),

322Fats, 116–120. See also Essential fatty acids

monounsaturated, 117polyunsaturated fatty acids (PUFAs), 117saturated, 117unsaturated, 117

Fatty acids. See Essential fatty acidsFecal occult blood test, 376Female testosterone patch, 371. See also

Hormone replacement therapy (HRT)FemCap. See Cervical capFemhrt, 369. See also Hormone replacement

therapy (HRT)FemPatch, 368. See also Hormone replacement

therapy (HRT)Femring, 369. See also Hormone replacement

therapy (HRT)Femtrace, 367. See also Hormone replacement

therapy (HRT)Fenugreek (Trigonella foenumgraecum), 23,

24

488 I N D E X

Fertility. See also Infertilityawareness, 51–53diet, 159male, 163menopause and, 180–81nutrition, 159–62

Feverfew (Tanacetum parthenium), 172Fiber, 120–22

research and, 121Fibrins, 338Fibrocystic breasts, 89–97, 383

alternative treatments, 90–96botanicals, 95–96conventional medical treatments, 96–97diet, 91–92dominant masses, 90licensed primary health-care practitioners

and, 97nondominant masses, 90nutrition, 91–95research, 91sample treatment plan, 96

Fish oil, 119, 120, 138, 159–60, 386. See alsoEssential fatty acids

for menstrual cramps, 230–315-hydroxytryptophan (5-HTP), 217Flavonoids, 121, 138–39, 335–36Flax oil, 117Flaxinus, 334Flaxseed (Linum usitatissimum), 23, 24,

192oil, 95, 138powder, 6

Flexible sigmoidoscopy, 376Folic acid

cervical dysplasia and, 38heart disease and, 136osteoporosis and, 253pregnancy and, 279

Follicle-stimulating hormone (FSH), 176, 178,181

tests, 186

Gamma-linolenic acid (GLA), 93–94, 120premenstrual syndrome (PMS) and, 308

Gamma-oryzanol, 193Garlic (Allium sativum), 139–40

for pelvic inflammatory disease (PID), 270for vaginitis, 350

Gas, 296Gastrointestinal disease

osteoporosis and, 241Genetic factors

endometriosis, 77infertility, 158osteoporosis, 239–40, 241

Genital herpes, 99–108alternative treatments, 102–7botanicals, 104–7conventional medical treatments, 107–8diagnosis, 99, 100–102diet, 102–3licensed primary health-care practitioners

and, 108nutrition, 102–4preventative medicine, 102, 108research, 99, 101, 104sample treatment plan, 106symptoms, 99–100

Genital warts, 31Gentian violet, 355German chamomile (Matricaria chamomilla),

233Ghent, William, 95Ginger (Zingiber officinale), 140, 232, 288–89,

381, 383, 386abnormal uterine bleeding and, 9root, 334

Ginkgo (Ginko biloba), 195, 310–11, 381,384, 386

Ginseng (Panax ginseng), 23, 162, 195,217–18

Globe artichoke (Cynara scolymus), 140Glucosamine sulfate, 170Glucose tolerance, 111

489I N D E X

Glycosaminoglycans (GAGs), 169–70GnRH agonists, 86, 97Golden root. See RhodiolaGoldenseal (Hydrastis canadensis), 70–71, 106,

334, 350for pelvic inflammatory disease (PID),

270root, 334

Gonorrhea. See Neisseria gonorrhoeae (GC)Gonzalez, Nicholas, 333Green, Raymond, 312Green leafy vegetables, 245Green tea, 24, 39, 139, 385, 386Greens drink, 386Gugulipid (Commiphora mukul), 140–41Gum disease

screening tests risk factors, 379Gurevich, Maria, 301Gynediol, 367. See also Hormone replacement

therapy (HRT)

Hair, 383loss, 184–85

Hawthorn (Crataegus oxyacantha), 141HDL cholesterol, 111, 116, 119, 142

fiber and, 120–21niacin and, 134soy and, 122

Headachesmenopause, 185

Hearing test, 376Heart disease, 109–53, 186, 192, 383

alternative treatments, 114–48botanicals, 138–43conventional medical treatments,

148–51definitions, 111diagnosis, 112–13estriol, 207genetic factors, 111hormone replacement therapy (HRT),

111–12, 138, 202

licensed primary health-care practitionersand, 151–53

lifestyle changes, 114–16nutrition, 116–38obesity, 109physical exercise, 143–44risk factors, 109, 111–14, 149–50sample treatment plan, 147screening, 113, 378stress and, 144women compared to men, 109

Heart palpitationsmenopause and, 185–86

Heart tonics, 142Heartburn, 296Helonias (Chamaelerium luteum), 161Hemorrhoids, 383Hepatitis B (HBV), 320–21Herbs. See also Botanicals

to avoid during pregnancy, 289companies, 386–87high mineral herbs, 257for menstrual cramps, 233nonphytoestrogen, 197–200for pelvic inflammatory disease (PID), 270for polycystic ovarian syndrome, 23–24for premenstrual syndrome (PMS), 311products, 380–87progesterone precursors, 23tinctures, 386uterine stimulants, 23for vaginitis, 354–55

Herpes simplex 2 (HSV-2), 99–108, 383HERS study, 148High blood pressure, 383

heart disease and, 111, 150–52screening tests, 378

Hip fracture, 238HIV infection, 346

cervical dysplasia and, 33screening tests risk factors, 379

Homeopathic medicines, 386

490 I N D E X

Homocysteine levels, 125Hops (Humulus lupulus), 23, 201, 217, 233Hormonal changes, 275Hormone creams, 385–86Hormone metabolism, 78–79Hormone replacement therapy (HRT),

144–48, 186, 187–88, 201–15, 219–20benefits of, 204blood clots from, 202–3breast cancer and, 203, 211–13diabetes mellitus and, 203dosing of, 204evaluation of, 202friendly versus less-friendly, 213–15heart disease and, 111–12, 138, 153, 202hot flashes and, 202non-oral hormones and, 204prescriptions, 367–71risks of, 204stroke and, 203studies of, 148vaginal symptoms and, 202

Hormones, bio-identical, xx–xxi, 205–15for abnormal uterine bleeding, 11–13for amenorrhea, 24–25

Hormones, natural, 205–15Horse chestnut, 386Hot flashes, 179–80

hormone replacement therapy (HRT), 202symptom relief, 215

Human papillomavirus (HPV), 31, 35, 385vaccine, 50, 377

Hunner’s ulcers, 167Hydrogenated oils, 118Hypergonadotropic hypogonadism, 17, 28Hyperlipidemia, 147Hyperparathyroidism, 237Hyperprolactinemia, 17, 27, 28–29Hypertension

diet, 124heart disease, 111sample treatment plan, 148

Hypoestrogenic states, 27Hypogonadotropic hypogonadism, 17–18, 29Hypothalamic amenorrhea, 27–28Hysterectomy, 14, 41, 176–77, 338

endometriosis and, 86

Ice packs, 321, 322Immunity issues

endometriosis and, 77–78pelvic inflammatory disease (PID) and, 270

Immunizations, 375–80high risk factors, 377–80

Implanon, 60–61Incontinence, 167Indole-3-carbinol/diindolylmethane (DIM), 39Infections, 383

suppositories for, 385Infertility, 155–65, 340, 384

alternative treatments, 157–64botanicals, 161–62causes, 156conventional medical treatments, 164–65definition, 155diet, 158laboratory testing, 156–57licensed primary health-care practitioners

and, 165lifestyle factors, 157–59medical history, 155preventative medicine, 157resources, 165sample treatment plan, 163statistics, 155uterine fibroids and, 329

Influenza vaccine, 377Infusions, 374Insomnia, 181, 222, 384

menopause and, 216–17Insulin, 123Interstitial cystitis (IC), 167–73, 384

alternative treatments, 168–72botanicals, 171–72

491I N D E X

causes, 168diagnostic tests, 167diet, 169foods to avoid, 169licensed primary health-care practitioners

and, 173nutrition, 169–71preventative medicine, 168sample treatment plan, 172

Intestine, hormone metabolism and, 78–79Intima-media thickness (IMT), 113Intrauterine devices (IUDs), 2, 54–55, 63Intrauterine insemination (IUI), 164Intravaginal estriol, 71–72Iodine, 355–56

fibrocystic breasts and, 94–95Ipriflavones, 257, 382, 384Iron

for abnormal uterine bleeding, 6deficiency, 382for pregnancy, 283–84

Irritability, 199Isoflavones, 332–33

Joint pain, 186

Kava (Piper methysticum), 171, 172, 200, 217Kelley, William, 333Keloids, 338Kelp, dietary (Fucus vesiculosus), 9–10Kemp, Harvey, 112Krill oil, 309

L-arginineheart disease and, 135–36infertility and, 160interstitial cystitis (IC) and, 170

L-carnitineheart disease and, 136infertility and, 163–64

L-lysinegenital herpes and, 103

Laboratories, 387Lactobacilli, 69

Lactobacillus acidophilus, 69, 270, 321, 322sexually transmitted infections (STIs) and,

322vaginitis and, 348, 350–53

Laparoscopic surgery, 86, 269, 330LDL cholesterol, 111, 116, 119, 142

alcohol and, 126fiber and, 120–21niacin and, 134soy and, 122

Lecithin, 287Lee, John, 336LEEP, 41, 47, 49Lemon balm (Melissa officinalis), 104, 217Leuprolide acetate, 337Licensed primary health-care practitioners

for abnormal uterine bleeding, 14for amenorrhea, 30for cervical dysplasia, 50for cystitis, 73for endometriosis, 87for fibrocystic breasts, 97for genital herpes, 108for heart disease, 151–53for infertility, 165for interstitial cystitis (IC), 173for menopause, 223for menstrual cramps, 236for osteoporosis, 266for pelvic inflammatory disease (PID),

272–73for pregnancy, 298–99for premenstrual syndrome (PMS), 315for sexually transmitted infections (STIs),

324–25for uterine fibroids, 339–40for vaginitis, 358

Licorice (Glycyrrhiza glabra), 23, 24, 104–5,172, 195–96

Life root (Senecio aureus), 11

492 I N D E X

Lifestyle. See also Preventative medicinecervical dysplasia and, 42–47heart-healthy diets, 127–29infertility and, 157–59osteoporosis and, 239–40premenstrual syndrome (PMS) and, 314

Linoleic acid (LA), 120Lipases, 333Lipids, 123. See also Cholesterol; HDL

cholesterol; LDL cholesterolLipotropics, 333

endometriosis and, 83Liver, 331, 384

detoxification, 304estrogen clearance, 91hormone metabolism, 78–79screening tests risk factors for disease,

379Love, Susan, 177Lung disease

screening tests risk factors, 379Lupron, 337–38Lymphedema, 384

Maca (Lepidium peruvianum), 218amenorrhea and, 22–23

Magnesiumheart disease and, 133–34osteoporosis and, 250–52pregnancy and, 284premenstrual syndrome (PMS) and, 309

Magnetic resonance imaging (MRI), 113Mammogram, 375Manganese, 252Manual soft-tissue therapy, 162Marshmallow (Althea officinalis), 172Mast cell activation, 168Mastalgia, 89Meditation, 228Mediterranean diet, 129Megace, 370. See also Hormone replacement

therapy (HRT)

Melatonin, 217, 231Memory, 182, 384Menest, 367. See also Hormone replacement

therapy (HRT)Meningococcal vaccine, 377Menometrorrhagia, 1Menopause, 175–223


219–23diet, 192evaluation, 186–87induced, 176–77licensed primary health-care practitioners

and, 223naturopathic approach, 188–89nutrition, 189–94osteoporosis and, 239sample treatment plans, 199, 215, 216screening tests risk factors, 379stages, 175–76statistics, 175–76symptoms, 178–86, 384temporary, 176transition, 177–78

Menorrhagia, 1, 12Menostar, 368. See also Hormone replacement

therapy (HRT)Menstrual cramps, 225–36, 384


234–36diet, 228–29licensed primary health-care practitioners

and, 236nutrition, 228–31physical exercise, 233–34, 235preventative medicine, 227–28sample treatment plan, 234stress and, 228

493I N D E X

Menstruationabsence of menstrual bleeding (amenorrhea),

15–30benign abnormal bleeding, 1normal cycle, 15–16

Mental health screening, 376Methionine (SAM), 95, 287Methylxanthines, 91Metrorrhagia, 1, 328Micronor, 370. See also Hormone replacement

therapy (HRT)Migraines, 384Minerals

amenorrhea and, 20–21high mineral herbs, 257infertility and, 161

Minton, John, 91Mirena IUD, 220, 371. See also Hormone

replacement therapy (HRT)Miscarriage, 295Mojzisova method therapy, 162Mole exam, 376Molimina, 302Monoglycerides, 116Monounsaturated fats, 117Mood swings, 181

sample treatment plan, 199Morning sickness, 294–95Motherwort (Leonurus cardiaca), 83–84,

201Mugwort (Artemisia vulgaris),

23Mushrooms, 106Myomas, 2Myomectomies, 338Myrrh, 106

Nails, 383National Health and Nutrition Examination

Survey (NHANES), 212Nature, healing power of, xvii–xviiiNaturopathic colleges, 388–89

Naturopathic medicine. See also Alternativetreatments

college, xviieclectic traditions of, xxhistory of, xviiprinciples of, xvii–xviiiroots of, xvii

Naturopathic organizations, 388–89Nausea, 384Neisseria gonorrhoeae (GC), 269, 318–20, 322

quinolone-resistant gonorrhea, 324Nervines, 143Nettle (Urtica dioica), 289, 334

root, 24Niacin, 134, 280

for menstrual cramps, 229Nicotinic acid, 280Nielsen, Forrest, 252Night sweats, 179–80Nitric oxide (NO), 170Nonsteroidal anti-inflammatory drugs

(NSAIDs), 234–36abnormal uterine bleeding and, 13–14

Normogonadotropic anovulation, 18Nor-QD, 370. See also Hormone replacement

therapy (HRT)North American Menopause Society (NAMS),

201, 214, 219Nurses’ Health Study, 212Nutrition

amenorrhea and, 18–21birth control pill users and, 58–59cervical dysplasia and, 33, 36–39cystitis and, 67–70endometriosis and, 80–83fertility and, 159–62fibrocystic breasts and, 91–95genital herpes and, 102–4heart disease and, 116–38interstitial cystitis (IC) and, 169–71menopause and, 189–94menstrual cramps and, 228–31

494 I N D E X

osteoporosis and, 239–40, 241, 243–56pregnancy and, 276–88premenstrual syndrome (PMS) and, 305–10sexually transmitted infections (STIs) and,

322supplements, 129–38uterine bleeding, abnormal, and, 5–8uterine fibroids and, 330–33vaginitis and, 349–50

Nuts, 118

Oat (Avena sativa), 172Oat straw, 217Obesity

amenorrhea and, 18cervical dysplasia and, 33heart disease and, 109infertility and, 157

Obstetrics, 298Ogen, 367. See also Hormone replacement

therapy (HRT)Ogen cream, 369. See also Hormone

replacement therapy (HRT)Oleic acid, 117Oligomenorrhea, 1, 12Olive oil, 117, 118Omega-3 fatty acids, 120, 254–56

menstrual cramps and, 230–31pregnancy and, 285–87

Omega-6 fatty acids, 93–94, 120, 254–56Omega-9 oil, 117Oophorectomy, 176Oral contraceptives, 55–60, 234. See also

Contraceptionbirth control pills (BCPs), 55–60, 62cervical dysplasia and, 33, 45–47for premenstrual syndrome (PMS), 315

Oral micronized progesterone (OMP), 211Oregon grape root (Berberis aquifolium),

70–71, 171, 334, 350for pelvic inflammatory disease (PID),

270

Organ transplantscreening tests risk factors, 379

Organic foods, 388Ornish, Dean, 114, 129Ornish Lifestyle Modification Program, 129Ortho-Est, 367. See also Hormone replacement

therapy (HRT)Osteoarthritis, 384Osteopenia

definition, 243Osteoporosis, 186, 237–66, 384

alternative treatments, 243–63assessing risk, 240–43bone effects, 238–39botanicals, 256–60conventional medical treatments, 264–66definition, 237, 243diagnosing, 240–43fracture sites, 238heredity and, 239–40hormone replacement therapy, 203licensed primary health-care practitioners

and, 266lifestyle and, 239–40menopause and, 239nutrition and, 239–40, 243–56preventative medicine, 244, 263sample treatment plan, 263severe, 243statistics, 237

Ovarian abscess, 272Ovrette, 370. See also Hormone replacement

therapy (HRT)

Pancreatic enzymes, 333Pantehine

heart disease and, 135Pap smears, 31, 33, 375

new technologies, 34recommendations, 35reporting, 34screening tests risk factors, 379

495I N D E X

Para-aminobenzoic acid (PABA)infertility and, 160–61

Partridgeberry (Mitchella repens), 289Passionflower (Passiflora incarnata), 233Pelvic exam, 375Pelvic inflammatory disease (PID), 267–73,

321, 346alternative medicine, 269–71conventional medical treatments, 271–72diagnosis, 268–69, 273licensed primary health-care practitioners

and, 272–73preventative medicine, 269risk factors, 267–68statistics, 267types, 267vaginitis and, 341

Pelvic peritonitis, 267Pennyroyal (Mentha pulegium), 23Perimenopause, 178Periwinkle, greater (Vinca major), 11Pesticides

pregnancy and, 291–92Pharmacies, 387Phosphatidylcholine (PC), 287Physical exercise, 359–64

amenorrhea and, 25–26basic stretches, 360–61conditioning, 364endometriosis and, 80heart disease and, 115, 143–44infertility and, 158joint warming exercises, 360menopause and, 215–16menstrual cramps and, 233–34, 235osteoporosis and, 261–63pregnancy and, 293–94, 362–64premenstrual syndrome (PMS) and, 311–12preventing injuries, 361–62strength exercises, 362, 364

Phytoestrogens, 23, 162, 189–92, 194herbal, 335–36

Phytosterols, 141–42Placenta abruption, 299Placenta previa, 299Plant stanols, 141–42Plant sterols, 141–42Pneumococcal vaccine, 377Poke root (Phytolacca americana), 95Policosanol, 142Polycystic ovarian syndrome (PCOS), 23–24,

28, 29–30, 162, 385chronic anovulation and, 28

Polymenorrhea, 1, 12Polyunsaturated fatty acids (PUFAs), 117Postmenopause urinary discomfort, 66Potassium, 123–24

heart disease and, 135pregnancy and, 284

Preeclampsia, 295–96, 299Prefest, 369. See also Hormone replacement

therapy (HRT)Pregnancy, 275–99, 385

abnormal uterine bleeding and, 1alternative medicine, 275–90bleeding and, 298–99botanicals, 288–90common complaints, 293–97conventional medical treatments, 297–98ectopic, 267, 272, 291genital herpes and, 108hormonal changes, 275licensed primary health-care practitioners

and, 298–99nutrition, 276–88physical exercise, 293–94, 362–64postnatal period, 279preventative medicine for complications, 276substances to avoid, 289, 290–93urinary discomfort and, 66with uterine fibroids, 340weight gain, 277–78, 293

Premarin, 367. See also Hormone replacementtherapy (HRT)

496 I N D E X

Premarin cream, 369. See also Hormonereplacement therapy (HRT)

Premature ovarian failure (POF), 27, 176,203–4

Premenstrual dysphoric disorder (PMDD),303

Premenstrual syndrome (PMS), 301–15, 384

alternative treatments, 304–13botanicals, 310–11classifications systems, 303, 307conventional medicine approach, 314–15definition, 301diet, 306licensed primary health-care practitioners

and, 315lifestyle, 314liver and, 303medications, 314–15nutrition, 305–10physical exercise, 311–12preventative medicine, 303sample treatment plan, 314statistics, 301–2symptoms, 301–2

Premphase, 370. See also Hormonereplacement therapy (HRT)

Prempro, 370. See also Hormone replacementtherapy (HRT)

Preventative medicinefor cervical dysplasia, 34–35, 43–47for endometriosis, 79for fibrocystic breasts, 91for genital herpes, 102, 108for heart disease, 115for infertility, 157for interstitial cystitis (IC), 168for menstrual cramps, 227–28for osteoporosis, 244, 263for pelvic inflammatory disease (PID), 269for pregnancy complications, 276for premenstrual syndrome (PMS), 303

for sexually transmitted infections (STIs),320

for uterine fibroids, 329for vaginitis, 343, 346, 347

Prickly ash (Xanthoxylum americanum), 83Prochieve, 371. See also Hormone replacement

therapy (HRT)Procyanidolic oligomers (PCO), 140Progesterone, 24–25, 219–20, 371

for abnormal uterine bleeding, 11–13bio-identical, 145–46, 208–13, 257–60,

312–13, 335–36creams, 96, 209–10, 233, 313, 337for endometriosis, 85gel, 371natural, 85, 95, 145–46, 208–13, 233,

257–60, 312–13, 335–36oral, 210–11oral micronized, 313for osteoporosis, 257–60for premenstrual syndrome (PMS), 312–13precursors, 23sublingual, 211

Progestins, 86intrauterine, 371oral, 370–71therapy, 264

Progestogens, 202, 221combination products, 221

Prometrium, 371. See also Hormonereplacement therapy (HRT)

Propolis, 105Prostaglandin (PG) synthesis, 305–6Proteases, 333Protein, 245Provera, 370. See also Hormone replacement

therapy (HRT)Prozac, 302Psychological factors

cervical dysplasia and, 47infertility and, 158

Pyridoxine, 280

497I N D E X

Quercetin, 139, 171

Rapkin, Anita, 302Reaven, Gerald, 112Reaven’s syndrome, 112Rectal exam, 376Red clover (Trifolium pratense), 23, 196, 381,

384, 386for osteoporosis, 256–57

Red raspberry (Rubus idaeus), 290Red root compound, 334Red yeast rice, 142Reflex sympathetic dystrophy, 168Rein, Mitchell, 336Relaxation techniques, 228Rhodiola (Rhodiola rosea), 218, 383, 384, 385,

386for amenorrhea, 22for infertility, 161

Riboflavin, 280Rose, 231Rutin, 229–30

Safflower oil, 117Saint John’s wort (Hypericum perforatum), 106,

199–200, 311, 382, 383, 384, 386Salpingitis, 267Salt, 123–24Sarsaparilla (Smilax officinalis), 23Savin (Sabrina officinalis), 11Saw palmetto, 24Scalzo, Rick, 334Screening tests, 375–80

high risk factors, 377–80Scudder’s Alterative, 334Scutellaria barbata, 334Selenium

for endometriosis, 83for infertility, 160

SERMS (selective estrogen receptormodulators), 332

osteoporosis and, 264, 265

Serotonin, 302Sesame oil, 117Sexual practices, 217–19, 222

cervical dysplasia and, 33, 42–44female arousal, 218–19genital herpes and, 108lubrication, 218menopause and, 183–84screening tests risk factors, 379trauma during intercourse, 2

Sexually transmitted infections (STIs), 66,315–25

alternative medicine, 321–22antibiotics, 323–24botanicals, 322–23cervical dysplasia and, 35Chlamydia trachomatis (CT), 269, 317–18conventional medical treatments, 323–24genital herpes, 99–108licensed primary health-care practitioners

and, 324–25Neisseria gonorrhoeae (GC), 269, 318–20nutrition, 322pelvic inflammatory disease (PID) and, 267preventative medicine, 320sample treatment plan, 322screening tests risk factors, 380testing for, 319–20, 376vaginitis and, 341–58

Shepherd’s purse (Capsella bursa-pastoris), 11Siberian ginseng (Eleutherococcus senticosus),

105Sitz baths, 373Skin, 383

changes during menopause, 185products for, 387

Skullcap, 217Sleep disturbance, 181Slippery elm (Ulmus fulva), 172Smoking, 24

cervical dysplasia and, 33, 44–45heart disease and, 114–15

498 I N D E X

infertility and, 158organizations to help quit, 292osteoporosis and, 240, 247pelvic inflammatory disease (PID) and, 268pregnancy and, 291screening tests for risk factors, 378

Socioeconomic status, cervical dysplasia and,33

Sodium, 123–24Soy foods, 24, 122–23, 189–92, 383

for abnormal uterine bleeding, 6–7for osteoporosis, 246–47for premenstrual syndrome (PMS), 306research, 122–23for uterine fibroids, 332

Soy oil, 117Specialty food companies, 388Spermicides, 53–54, 63–64Squamous intraepithelial lesions (SIL), 31Squaw vine (Mitchella repens), 23

for infertility, 161Sterilization, 61Stress, 385

endometriosis and, 75heart disease and, 115, 144infertility and, 158menstrual cramps and, 228uterine bleeding, abnormal, and, 4, 5

Stroke, hormone replacement therapy (HRT)and, 203

Sugar, 123, 245, 305Surgery recovery, 385Syndrome X, 112

Tamoxifen, 97Tannins, 10Taurine, 287–88Tea, 139. See also Green teaTea tree (Melaleuca alternifolia), 350

oil, 350Testoderm, 371. See also Hormone

replacement therapy (HRT)

Testosterone, 371–72Tetanus-diphtheria booster vaccine, 377Thermal ablation treatment techniques, 338Thiamine, 229, 280ThyroFem, 385Thyroid disease, 385

screening tests risk factors, 379Thyroid hormone

fibrocystic breasts and, 94–95Thyroid test, 375Tissue tonification

uterine bleeding, abnormal, and, 5TLC diet, 127–28Toxemia, 295–96Trabecular bone, 238Trans fats, 118Transvaginal ultrasound, 156Tribulus (Tribulus terrestris), 162Trichomonas vaginalis, 346–48, 357–58. See

also VaginitisTriglycerides, 111, 118

niacin and, 134Tryptophan

premenstrual syndrome (PMS) and, 309–10

Tubal ligation, 61Tuberculosis

screening tests risk factors, 380Tubo-ovarian abscess, 267Turska’s formula, 84–85, 334

Ultrasound, 338Underweight issues

infertility and, 157Urinary problems, 183

urinary discomfort, 65, 267urinary tract infection, 65–73 (See also

Cystitis)Uterine bleeding, abnormal, 1–14, 339–40,

382alternative treatments, 4–14benign, 1–2, 3–4

499I N D E X

in children, 1irregular menses, 180licensed primary health-care practitioners

and, 14malignant, 2–3menses and, 1nutrition, 5–8during pregnancy, 1sample treatment plans, 12during sexual intercourse, 2

Uterine fibroids, 2, 327–40alternative medicine, 330bleeding, 339–40botanicals, 334–37, 337diagnosis, 329–30herbs for, 386infertility and, 340licensed primary health-care practitioners

and, 339–40nutrition, 330–33pregnancy and, 339–40preventative medicine, 329sample treatment plan, 337statistics, 327symptoms, 328–29

Uterine tonicsfor abnormal uterine bleeding, 10–11

Uva-ursi (Arctostaphylos uva-ursi), 70, 95

Vaccines. See ImmunizationsVagifem, 369. See also Hormone replacement

therapy (HRT)Vaginal cancer, 2Vaginal dryness, 182–83Vaginal estrogen treatments, 66Vaginal flora, 341, 348Vaginal suppositories, 382Vaginal symptoms

hormone replacement therapy (HRT) for,202

Vaginal thinning, 182–83

Vaginitis, 341–58, 385alternative medicine, 348–56botanicals, 350–56Centers for Disease Control (CDC)

guidelines, 357diagnosis, 341–48herbs for, 354–55licensed primary health-care practitioners

and, 358nutrition, 349–50preventative medicine, 343, 346, 347sample treatment plans, 353, 354, 355symptoms, 341

Vaginosis organisms, 267Valerian (Valeriana officinalis), 172, 201, 217,

231–32Varicose veins, 296, 385Vasectomy, 61Vasomotor symptoms, 222Venous thromboembolism, 202–3Vertebral fracture, 238, 242Viracea, 106Visualization, 228Vitamin A

abnormal uterine bleeding and, 7amenorrhea and, 20cervical dysplasia and, 37fibrocystic breasts and, 94interstitial cystitis (IC) and, 170pregnancy and, 281sexually transmitted infections (STIs) and,

322vaginitis and, 349

Vitamin B complexabnormal uterine bleeding and, 7–8fibrocystic breasts and, 95

Vitamin Bs, 193cervical dysplasia and, 38–39endometriosis and, 83heart disease and, 136–37menstrual cramps and, 229osteoporosis and, 253

500 I N D E X

pregnancy and, 280–81premenstrual syndrome (PMS) and,

307–8Vitamin C, 24

abnormal uterine bleeding and, 8cervical dysplasia and, 38cystitis and, 69–70endometriosis and, 81–82genital herpes and, 103–4heart disease and, 129, 132infertility and, 163menstrual cramps and, 229–30osteoporosis and, 253pregnancy and, 282sexually transmitted infections (STIs) and,


Vitamin D, 192osteoporosis and, 237, 239, 241, 250–51,

265pregnancy and, 282premenstrual syndrome (PMS) and, 308

Vitamin E, 193–94abnormal uterine bleeding and, 7cervical dysplasia and, 37–38endometriosis and, 82fibrocystic breasts and, 92–93genital herpes and, 104heart disease and, 130–32infertility and, 160, 163menstrual cramps and, 230pregnancy and, 282premenstrual syndrome (PMS) and,


Vitamin K, 253–54abnormal uterine bleeding and, 8pregnancy and, 282–83

Vitamins. See also Specific typesinfertility and, 161

Vivelle, 368. See also Hormone replacementtherapy (HRT)

Vivelle-Dot, 368. See also Hormonereplacement therapy (HRT)

Von Willebrand’s disease, 1Vulvovaginal candidiasis (VVC), 344–46,

356–57. See also Vaginitis

Water pepper (Polygonnum hydropiper), 23Weight gain, 185. See also Body weight

pregnancy and, 277, 294Weight loss, 159, 385. See also Body weight

amenorrhea and, 18–19WIC (supplemental food program), 277Wild yam (Dioscorea villosa), 23, 172, 233,

290root, 295

Women, modern, xxchoice, xixas consumers of health care, xxiparticipation in health care, xxi

Women’s Health Initiative (WHI), 148, 201,213, 219

World Health Organization, 243

Yarrow (Achillea millefolium), 11, 23, 95Yeast infection, 385. See also VaginitisYucca (Yucca spp), 23

Zincgenital herpes and, 104infertility and, 160osteoporosis and, 253pregnancy and, 284–85sexually transmitted infections (STIs) and,

322

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WOMEN’S - noblogs.org...years to treat the kind of women’s health problems that I was seeing every day, ranging from irregular periods and menstrual cramps to hot ﬂashes. As