52160316 Handbook of Dietary Fiber

DietaryFiber

Handbook of

edited by

Susan Sungsoo ChoKellogg Company

Battle Creek, Michigan

Mark L. DreherMead Johnson Nutritionals/Bristol-Myers Squibb Company

Evansville, Indiana

Copyright 2001 by Taylor & Francis

ISBN: 0-8247-8960-1

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Preface

Since the mid-1970s, dietary ber has been an extremely active area of research because of itscomplexity and wide-ranging biomedical effects. During this time, hundreds of research papers,review articles, and bulletins, and dozens of books have been published on the subject; in addi-tion, scores of seminars and conferences have been held. With active research activities con-ducted over the past two or three decades demonstrating the health benets of dietary ber, theFood and Drug Administration has now mandated that dietary content be declared on foodlabels. In 1984, the Kellogg Company and the National Cancer Institute (NCI) carried out ajoint campaign to educate consumers that wheat bran ber may lower the incidence of certaintypes of cancers, such as colon cancer. This opened a new avenue for nutraceuticals and func-tional foods for consumers throughout the world to lower their risk of chronic diseases byconsuming foods formulated with functional ingredients.

The campaign provoked more active research in linking diet and nutrition to chronic dis-eases to improve public health. Such continuing research efforts have led to health claims madeby food manufacturers to help the public choose foods wisely. Numerous patents have beenled and approved for purposes such as functionality improvement and health benets. Enoughinformation is now available to address the needs of clinicians, dieticians, food scientists, foodregulators, and marketers. Because of the great public interest in dietary ber, there was a needto provide this applied group with a handbook that can bridge the gap between basic researchand applied interest. This handbook will help the audience understand key issues and improvethe consistency and accuracy of the dietary ber information used in their work, such as thedevelopment of new food products, the regulation of these food products, and the dietary berrecommendations to patients by health professionals.

The Handbook of Dietary Fiber has signicantly expanded the scope of dietary ber appli-cations, such as marketing perspectives, health claims, and patent literature. Each chapter offerscontemporary thoughts on dietary ber.

We would like to thank all the dietary ber researchers who designed experiments, col-lected data, and published results that made this book possible.

Susan Sungsoo ChoMark L. Dreher


Contents

PrefaceContributors

I. Dietary Fiber in Health and Disease

1. Dietary Fiber OverviewMark L. Dreher

2. Dietary Fiber and Cardiovascular DiseaseJudith A. Marlett

3. Dietary Fiber and Colon CancerJoanne L. Slavin

4. Dietary Fiber and Breast Cancer RiskSusan Sungsoo Cho, Celeste Clark, and Sharon E. Rickard

5. Dietary Fiber and Breast Cancer EpidemiologyPeter A. Baghurst and Katrine I. Baghurst

6. Dietary Fiber and Prostate CancerEric D. Schwab and Kenneth J. Pienta

7. Dietary Fiber and Glucose Metabolism and DiabetesDavid Cameron-Smith and Gregory R. Collier

8. Resistant OligosaccharidesMarcel Roberfroid and Joanne L. Slavin

9. Resistant Starches, Fermentation, and Large Bowel HealthAnthony R. Bird and David L. Topping


10. Resistant Starches and Lipid MetabolismChristian Demigne, Christian Remesy, and Christine Morand

11. Critical Review of Hydrogen Breath Test Methods in Resistant Starch andDietary Fiber ResearchMerete Olesen

12. Lactulose: A Review on Effects, Clinical Results, and Safety Aspects inRelation to Its Inuence on the Colonic EnvironmentRobert Havenaar and Wim van Dokkum

II. Physicochemical Properties

13. Physicochemical Properties of Dietary Fiber: OverviewDavid Oakenfull

14. Adsorption of Carcinogens by Dietary FiberLynnette R. Ferguson and Philip J. Harris

15. Dietary Fiber and Mineral InteractionBarbara F. Harland and Gurleen Narula

16. The Inuence of Wheat Fiber and Bran on Mineral NutritureSusan Sungsoo Cho, Celeste Clark, and Mazda Jenab

17. Nondigestible Oligosaccharides and Mineral AbsorptionWim van Dokkum and Ellen van den Heuvel

18. Enzymatic Modication of Dietary Fiber SourcesEva Arrigoni

III. Chemistry and Analysis

19. Chemistry, Architecture, and Composition of Dietary Fiber from Plant CellWallsAlistair James MacDougall and Robert Rasiah Selvendran

20. Chemistry and Analysis of LigninRoger Mongeau and Stephen P. J. Brooks

21. High-Performance Liquid Chromatography Techniques Used in Dietary Fiberand Complex Carbohydrates AnalysisAlan Henshall

22. Dietary FiberAssociated Compounds: Chemistry, Analysis, and NutritionalEffects of PolyphenolsFulgencio D. Saura-Calixto and Laura Bravo


IV. Functional Dietary Fiber Ingredients

23. Food Uses of FiberJanette Gelroth and Gur S. Ranhotra

24. Wheat Bran: Physiological EffectsSusan Sungsoo Cho and Celeste Clark

25. Psyllium: Food Applications, Efcacy, and SafetySusan Sungsoo Cho and Celeste Clark

26. Oat Fiber: Production, Composition, Physicochemical Properties,Physiological Effects, Safety, and Food ApplicationsYrjo Malkki

27. Barley FiberChristine E. Fastnaught

28. Rice Bran: Production, Composition, Availability, Healthful Properties,Safety, and Food ApplicationsTalwinder S. Kahlon and Faye I. Chow

29. Sugar Beet Fiber: Production, Composition, Physicochemical Properties,Physiological Effects, Safety, and Food ApplicationsJean-Francois Thibault, C. M. G. C. Renard, and F. Guillon

30. Pectin: Composition, Chemistry, Physicochemical Properties, FoodApplications, and Physiological EffectsMaria Luz Fernandez

31. Classication, Structure, and Chemistry of Polysaccharides of FoodsJames N. BeMiller

32. Guar Gum: Agricultural and Botanical Aspects, Physicochemical andNutritional Properties, and Its Use in the Development of Functional FoodsPeter Rory Ellis, Qi Wang, Phillippa Rayment, Yilong Ren, and Simon B.Ross-Murphy

33. Alginate: Production, Composition, Physicochemical Properties, PhysiologicalEffects, Safety, and Food ApplicationsEdvar Onsyen

34. Gum Arabic: Production, Safety and Physiological Effects, PhysiochemicalCharacterization, Functional Properties, and Food ApplicationsP. A. Williams and G. O. Phillips

35. Gellan GumRaymond C. Valli and Frank J. Miskiel


36. Inulin and OligofructosePaul Coussement and Anne Franck

37. CurdlanFumio Yotsuzuka

V. Worldwide Dietary Fiber Intake and Regulations of Dietary Fiber Foods

38. Dietary Fiber in ChildhoodChristine L. Williams, Laura Boccia Tolosi, and Marguerite C. Bollella

39. Dietary Fiber Intake in Spain: Recommendations and Actual ConsumptionPatternsIsabel Goni Cambrodon

40. Dietary Fiber in Israel: Recommendations, Consumption, and ResearchAliza H. Stark, Zecharia Madar, and Dorit Nitzan Kaluski

41. Dietary Fiber Intake in China: Recommendations and Actual ConsumptionPatternsGuangya Wang

42. Dietary Fiber Intake in Poland: Recommendations and Actual ConsumptionPatternsElzbieta Bartnikowska and Adam Niegodzisz

43. Dietary Fiber Intake in Chile: Recommendations and Actual ConsumptionPatternsNelly Pak

44. Dietary Fiber Intake in Mexico: Recommendations and Actual ConsumptionPatternsJorge L. Rosado

45. Dietary Fiber and Resistant Starch Intake in Brazil: Recommendations andActual Consumption PatternsFranco Maria Lajolo and Elizabete Wenzel de Menezes


Contributors

Eva Arrigoni Institute of Food Science, Swiss Federal Institute of Technology, Zurich, Swit-zerland

Katrine I. Baghurst CSIRO, Adelaide, South Australia, Australia

Peter A. Baghurst Womens and Childrens Hospital, North Adelaide, South Australia, Aus-tralia

Elzbieta Bartnikowska Food Monitoring, Meat and Fat Research Institute, Warsaw, Poland

James N. BeMiller Department of Food Science, Purdue University, West Lafayette, Indiana

Anthony R. Bird Department of Health Sciences and Nutrition, CSIRO, Adelaide, SouthAustralia, Australia

Marguerite C. Bollella Department of Pediatrics, New York Presbyterian Hospital, NewYork, New York

Laura Bravo Department of Metabolism and Nutrition, Instituto del Fro, Consejo Superiorde Investigaciones Cientcas, Madrid, Spain

Stephen P. J. Brooks Nutrition Research Division, Health Protection Branch, Health Canada,Ottawa, Ontario, Canada

Isabel Goni Cambrodon Nutrition Department, Faculty of Pharmacy, University Complu-tense of Madrid, Madrid, Spain

David Cameron-Smith School of Health Sciences, Deakin University, Melbourne, Victoria,Australia

Susan Sungsoo Cho Kellogg Company, Battle Creek, Michigan


Faye I. Chow Cereal Product Utilization, Western Regional Research Center, AgriculturalResearch Service, U.S. Department of Agriculture, Albany, California

Celeste Clark Kellogg Company, Battle Creek, Michigan

Gregory R. Collier School of Health Sciences, Deakin University, Melbourne, Victoria, Aus-tralia

Paul Coussement ORAFTI Active Food Ingredients, Tienen, Belgium

Christian Demigne Laboratoire des Maladies Metaboliques et Micronutriments, INRA deClermont-Ferrand/Theix, Saint-Gene`s-Champanelle, France

Mark L. Dreher Mead Johnson Nutritionals/Bristol-Myers Squibb Company, Evansville,Indiana

Peter Rory Ellis Biopolymers Group, Division of Life Sciences, Kings College London (Uni-versity of London), London, England

Christine E. Fastnaught Castle Dome Foods, Inc., Fargo, North Dakota

Lynnette R. Ferguson Faculty of Medicine and Health Sciences, The University of Auckland,Auckland, New Zealand

Maria Luz Fernandez Department of Nutritional Sciences, University of Connecticut, Storrs,Connecticut

Anne Franck ORAFTI Active Food Ingredients, Tienen, Belgium

Janette Gelroth Nutrition and Analytical Labs, American Institute of Baking, Manhattan,Kansas

F. Guillon Unite de Recherche sur les Polysaccharides, leurs Organisations et Interactions,Institut National de la Recherche Agronomique, Nantes, France

Barbara F. Harland Department of Nutritional Sciences, College of Pharmacy, Nursing, andAllied Health Sciences, Howard University, Washington, D.C.

Philip J. Harris School of Biological Sciences, The University of Auckland, Auckland, NewZealand

Robert Havenaar Department of Nutritional Physiology, TNO Nutrition and Food Research,Zeist, The Netherlands

Alan Henshall Dionex Corporation, Sunnyvale, California

Mazda Jenab University of Toronto, Toronto, Ontario, Canada

Talwinder S. Kahlon Cereal Product Utilization, Western Regional Research Center, Agricul-tural Research Service, U.S. Department of Agriculture, Albany, California


Dorit Nitzan Kaluski Department of Nutrition, Ministry of Health, Jerusalem, Israel

Franco Maria Lajolo Department of Food and Experimental Nutrition, Faculty of Pharma-ceutical Sciences, University of Sao Paulo, Sao Paulo, Brazil

Alistair James MacDougall Division of Food Materials Science, B. B. S. R. C. Institute ofFood Research, Colney, Norwich, England

Zecharia Madar Faculty of Agricultural, Food and Environmental Quality Sciences, Instituteof Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot,Israel

Yrjo Malkki Cere Ltd., Espoo, Finland

Judith A. Marlett Department of Nutritional Sciences, University of Wisconsin, Madison,Wisconsin

Elizabete Wenzel de Menezes Department of Food and Experimental Nutrition, Faculty ofPharmaceutical Sciences, University of Sao Paulo, Sao Paulo, Brazil

Frank J. Miskiel New Product Development, CP Kelco, San Diego, California

Roger Mongeau Nutrition Consultant, Ottawa, Ontario, Canada

Christine Morand Laboratoire des Maladies Metaboliques et Micronutriments, INRA deClermont-Ferrand/Theix, Saint-Gene`s-Champanelle, France

Gurleen Narula Department of Nutritional Sciences, College of Pharmacy, Nursing, and Al-lied Health Sciences, Howard University, Washington, D.C.

Adam Niegodzisz Meat and Fat Research Institute, Warsaw, Poland

David Oakenfull Ingredient Innovation Program, Food Science Australia, North Ryde, NewSouth Wales, Australia

Merete Olesen Department of Medicine and Gastroenterology, KAS, Gentofte, Copenhagen,Denmark

Edvar Onsyen Pronova Biopolymer a.s., Drammen, Norway

Nelly Pak Center of Nutrition, Faculty of Medicine, University of Chile, Santiago, Chile

G. O. Phillips Centre for Water Soluble Polymers, North East Wales Institute, Wrexham,Wales

Kenneth J. Pienta University of Michigan, Ann Arbor, Michigan

Gur S. Ranhotra Nutrition Research, American Institute of Baking, Manhattan, Kansas


Phillippa Rayment Biopolymers Group, Division of Life Sciences, Kings College London(University of London), London, England

Christian Remesy Laboratoire des Maladies Metaboliques et Micronutriments, INRA deClermont-Ferrand/Theix, Saint-Gene`s-Champanelle, France

Yilong Ren Biopolymers Group, Division of Life Sciences, Kings College London (Univer-sity of London), London, England

C. M. G. C. Renard Unite de Recherche sur les Polysaccharides, leurs Organisations et Inter-actions, Institut National de la Recherche Agronomique, Nantes, France

Sharon E. Rickard University of Toronto, Toronto, Ontario, Canada

Marcel Roberfroid* Department of Pharmaceutical Sciences, Catholic University of Lou-vain, Brussels, Belgium

Jorge L. Rosado Department of Nutritional Physiology, National Institute of Nutrition, Mex-ico City, and School of Natural Sciences, University of Queretaro, Queretaro, Mexico

Simon B. Ross-Murphy Biopolymers Group, Division of Life Sciences, Kings College Lon-don (University of London), London, England

Fulgencio D. Saura-Calixto Department Metabolism and Nutrition, Instituto del Fro, Con-sejo Superior de Investigaciones Cientcas, Madrid, Spain

Eric D. Schwab Section of Urology, Department of Surgery, University of Michigan, AnnArbor, Michigan

Robert Rasiah Selvendran B. B. S. R. C. Institute of Food Research, Colney, Norwich,England

Joanne L. Slavin Department of Food Science and Nutrition, University of Minnesota, St.Paul, Minnesota

Aliza H. Stark Faculty of Agricultural, Food and Environmental Quality Sciences, The He-brew University of Jerusalem, Rehovot, Israel

Jean-Francois Thibault Unite de Recherche sur les Polysaccharides, leurs Organisations etInteractions, Institut National de la Recherche Agronomique, Nantes, France

Laura Boccia Tolosi Division of Nutritional Carcinogenesis, American Health Foundation,Valhalla, New York

*Professor Emeritus.Retired.


David L. Topping Division of Human Nutrition, Department of Health Sciences and Nutri-tion, CSIRO, Adelaide, South Australia, Australia

Raymond C. Valli Food Applications R&D, CP Kelco, San Diego, California

Ellen van den Heuvel Department of Nutritional Physiology, TNO Nutrition and Food Re-search, Zeist, The Netherlands

Wim van Dokkum Department of Nutritional Physiology, TNO Nutrition and Food Research,Zeist, The Netherlands

Guangya Wang Department of Food Chemistry, Institute of Nutrition and Food Hygiene,Chinese Academy of Preventive Medicine, Beijing, China

Qi Wang Biopolymers Group, Division of Life Sciences, Kings College London (Universityof London), London, England

Christine L. Williams Department of Pediatrics and Institute of Human Nutrition, Babiesand Childrens Hospital, Columbia University, New York, New York

P. A. Williams Centre for Water Soluble Polymers, North East Wales Institute, Wrexham,Wales

Fumio Yotsuzuka Marketing Department, Takeda Chemical Industries, Ltd., Tokyo, Japan


1Dietary Fiber Overview

Mark L. DreherMead Johnson Nutritionals/Bristol-Myers Squibb Company, Evansville, Indiana

I. INTRODUCTION

In 1953, Hipsley rst used dietary ber to designate nondigestible plant cell wall constituents.Between 1972 and 1976, dietary bers role was expanded to be used in conjunction with anumber of health-related hypotheses. The dietary ber hypothesis implies that a high intake ofber-containing foods is directly related to, or is associated with, a low incidence of manydisorders and diseases common with a Western lifestyle (e.g., chronic bowel disease, diabetes,coronary heart disease, and colon cancer). Research continues to explore the validity of thehypothesis, and many questions require answers. How much does it explain? Is it overrated?Does it really work in everyday nutrition, especially in interethnic populations? How does itcompare with other well-known disease hypotheses (Walker, 1993)?

The passing years have not lessened the signicance of dietary ber in human health anddisease. There are over a dozen major identiable benecial effects of increased dietary berconsumption on human health and body function. These attributes range from bers contribu-tion to lowering caloric intake to its increase in the water content and mass of human solidwaste. Although there is an enormous database to support the health benets of dietary ber,the data is not without mixed results. Nevertheless, collectively, dietary ber contributes to afascinating story about foods, nutrition, and health which will be examined throughout this book.

While a diet high in ber-containing foods is associated with health benets, the extentof the benets can be enhanced or diminished by the inuence of various nondietary factors(e.g., genetic factors, physical activity, stress), and more needs to be known about the healtheffects of dietary ber in different food forms such as the metabolic effects of high-ber wholefoods (e.g., whole wheat bread), ber concentrates (e.g., modied bran), and bioactive isolates(e.g., pectin).

Increased concern about the relationship between diet and chronic disease has led to anincreased interest in functional food products for risk reduction. This functional food paradigmwas ushered in by the vigorous marketing of bran and ber-enhanced products. It started in themid-1980s with the success of a Kelloggs All-Bran campaign that linked colon cancer riskreduction to increased bran intake. Studies from the scientic community and recommendationsabout dietary ber from the government and consumer organizations have kept dietary beron the radar screen for health promotion. In fact, dietary ber is now a mandatory componentof U.S. food labels. It consists of two major fractionsinsoluble and solublebut reportingthis distribution is only voluntary on food labels. Five food labeling health claims are cur-


rently allowed, which reect the health signicance of dietary ber. Generally stated, these are:(1) ber containing grain products, fruits, and vegetables, help reduce the risk of cancer;(2) fruits, vegetables and grain products that contain ber, particularly soluble ber, help reducethe risk of heart disease; (3) oat bran helps reduce the risk of heart disease; (4) psyllium helpsreduce the risk of heart disease; and (5) whole grains help reduce the risk of heart disease andcertain types of cancers.

II. WHAT IS DIETARY FIBER?

Dietary ber is an umbrella term for a heterogeneous mixture of plant food components thatare indigestible in the small intestine. The working denition of dietary ber over the last fewdecades is: Dietary ber consists of the remnants of edible plant cell, polysaccharides, lignin,and associated substances resistant to digestion by the alimentary enzymes of humans (Gordon,1999). It is the term generally used to describe the supporting structures of plant cell walls andthe substances intimately associated with them. The typical components of dietary ber includecellulose, hemicellulose, lignins, pectins, and a variety of gums and mucilages. All of theseexcept lignins are polysaccharides. The heterogeneity of dietary ber is the primary reason forthe diversity of its physiological effects.

Is this denition satisfying the consumer, food and health professionals, food processorsand ingredient suppliers, and regulatory agencies (Gordon, 1999)? The American Associationof Cereal Chemists is leading an effort to explore updated changes in what the term dietary berrepresents. Now questions must be addressed: How should synthetic polymers be considered? Isdietary ber only obtained from edible plant cells? Should the denition include both a chemicaland physiological component? Recent surveys show that scientists in the area of dietary berprefer the inclusion of oligosaccharides, which are not recovered with the current Associationof Ofcial Analytical Chemists method for measuring total dietary ber.

Dietary ber is available in the human diet through a wide variety of food sources, suchas both raw and processed cereals, vegetables, legumes, and fruits. The composition of dietaryber varies with the type of plant tissue (Table 1). The proportions of different dietary berconstituents found in plant foods depend on the maturity of the plants. In typical plant cell walls,the percentage of cellulose, lignin, and ash tend to be higher and the percentage of noncellulosicpolysaccharides, waxes, and protein tend to be lower in mature than in immature plants. Theportion of the plant consumed and its relative maturity, as well as storage and ripening, mayinuence the dietary ber composition of plant foods, and food-processing techniques may alsoalter the native ber composition. Vegetables and cereals tend to be good sources of cellulose.Lignin is highest in fruits with edible seeds such as strawberries or in mature vegetables suchas carrots or other root vegetables. Whole grain cereals and bran are rich in hemicellulose.Pectin is found in fruits such as apples and oranges. Oats and dried beans contain a good sourceof soluble dietary ber.

Total dietary ber is the analytical term for dietary ber that includes both water-insolubledietary ber and water-soluble dietary ber. Insoluble ber consists mainly of cell wall compo-nents such as cellulose, lignin, and hemicellulose present mainly in wheat, most grain products,and vegetables. Insoluble ber shortens bowel transit time, increases fecal bulk, and rendersfeces softer. Soluble ber consists of noncellulosic polysaccharides such as pectin, gums, andmucilages found in fruits, oats, barley, and legumes. Soluble ber delays gastric emptying, slowsglucose absorption, enhance immune function and lowers serum cholesterol levels. It is to a largedegree fermented in the colon into short-chain fatty acids, which may inhibit hepatic cholesterol


Table 1 Inuence of Source on Dietary Fiber Composition

Food group Type of tissue Major polymersCereals Endosperm Arabinoxylans

Seed coats -d-GlucansCelluloseLignin

Vegetables and fruit Parenchymatous esh Pectic substancesVascular tissue XyloglucansEpidermal tissue Cellulose

LigninCutinWaxes

Seeds other than cereals Cotyledons Pectic substancesEndosperm walls Galactomannans

XyloglucansCellulose

Polysaccharide food additives Amorphous GumsSoluble Algal polysaccharidesDispersible Sulfated galactans

Cellulose esters/ethers

Source: Pilch, 1987.

synthesis. About 75% of the dietary ber in foods is found in the insoluble fraction. Productsfrequently referred to as soluble or insoluble bers are often sources of both of these types ofbers.

III. HISTORICAL OVERVIEWA. Paleolithic NutritionExperts in paleolithic nutrition have theorized that primitive diets contained high levels of dietaryber (Eaton et al., 1988; Eaton, 1990). This stems from the fact that about 65% of the Stone Agediet was comprised of uncultivated fruits and vegetables. Of course, there were wide regional andsecular variations in the subsistence patterns of Stone Age living conditions, but a number ofsimilar nutritional patterns have been identied (Eaton, 1990). These contrast strikingly withthe nutrition of people living in todays afuent Western culture.

The differences between todays diet and the Stone Age diet are numerous. First, ourancestors ate the meat from wild game. The nutritional composition of wild game is notablydifferent than that of todays domesticated animal products: it has only one fth as much fat,a higher proportion of unsaturated fatty acids, less than half the calories, and more protein.Second, Stone Age humans had not domesticated dairy animals. Dairy products are now a majorcomponent of our diet. Third, Stone Agers consumed uncultivated fruits and vegetables, whichwere high in dietary ber (12.6 g/100 g). Our preagricultural ancestors probably consumed inexcess of 100 grams of dietary ber daily. Fourth, the uncultivated plants consumed by ourancestors contained a high level of micronutrients relative to their calorie content. Fifth, sodiumcontent of the Stone Age diet is estimated to have been about 250 mg daily, which is less thanone twentieth of our current intake.


B. Evolution of Dietary Fiber in the Food SupplyInterest in ber-rich foods has a colorful and long history. In 430 b.c. Hippocrates describedthe laxative effects of whole wheat in comparison with rened wheat. The earliest recordedclinical trial with ber-rich foods is described in the Bible (Daniel 1:816) (Kritchevsky, 1988).The passages explain that Daniel and three of his friends after eating vegetables (pulses) andwater for 10 days appeared healthier than others who had partaken of Nebuchadnezzars feastduring the same period. As for early food patterns, in Mesopotamia, Greece, and Rome and inEuropean countries during the Medieval and Middle Agesindeed, up to the nineteenth cen-turyin general the diet was high in ber-containing cereals, legumes, vegetables, and fruitand relatively low in dairy products and meat; i.e., the typical diet was low in fat and high inber.

At the turn of the century, a marked change took place in the pattern of the Western diet(Walker, 1993). The intake of cereals and of potatoes fell. The intake of fat, sugar, fruit andvegetables, and indulgence items (e.g., ice cream, chocolate) rose. Characteristically, the dietbecame high in fat and low in ber. At about this time, Graham (of graham cracker fame)denounced the harmful effects of rened carbohydrate foods, and the Kellogg and Post cerealsowe their start to an increased interest in the bran content of the diet. In the 1920s, J. H. Kel-logg published extensively on the benets of bran, claiming that it increased stool weight, pro-moted laxation, and prevented disease. Bran was researched throughout the 1930s and thenforgotten.

The modern era of dietary ber research began in the 1950s, and interest in it has steadilygained momentum. In 1956, British Surgeon Captain Cleave hypothesized that most diseasesof civilization were caused by an overconsumption of sugar and a lack of dietary ber. Thishypothesis caught the attention of Drs. Trowell and Burkitt, who are usually credited with pop-ularizing the idea that dietary ber may be protective against the development of Western dis-eases, including diabetes, hypercholesterolemia, heart disease, diverticular disease, and coloncancer. Interest in dietary ber research began slowly. From 1953 to 1968, there was an aver-age of six publications on dietary ber per year. Index Medicus did not include a dietary bersubject category until 1982. Today dietary ber is one of the most widely researched foodcomponents.

Table 2 Dietary Guidelines for Americans (2000)Number of servingsa

Children ages 2 to 6 Older children, teenyears, women, some girls, active women, Teen boys, active

Fiber containing older adults (about most men (about men (about 2,800food groups 1,600 calories) 2,200 calories) calories)Bread, cereal, rice, and pasta 6 9 11

group (grain group) espe-cially whole grain

Vegetable group 3 4 5Fruit group 2 3 4a Dietary Guidelines for Americans (2000).


IV. GENERAL DIETARY GUIDELINES AND RECOMMENDATIONS

The Dietary Guidelines for Americans (2000) calls for Americans to choose a variety of grains,especially whole grains, fruits, and vegetables daily. These food group guidelines are summa-rized in Table 2.

Eating foods with dietary ber is important for proper bowel function and may reducesymptoms of chronic constipation, diverticular disease, and hemorrhoids. Populations with dietslow in dietary ber and complex carbohydrates and high in fat, especially saturated fat, tendto have more heart disease, obesity, and some cancers. Just how dietary ber is involved is stillbeing studied.

Some of the benets from high ber diets come natural from the non-dietary ber compo-nents such as natural antioxidants. For this reason, it is best to get most dietary ber from foods.However, since food consumption of dietary ber tends to be only half the recommended level,the consumption of ber supplements may be benecial when used in moderation.

Dietary ber intake should range from 20 to 35 grams per day or 1013 g per 1000 kcalfor optimal benets but the usual intake in developed countries such as the United States isonly about half this level (Pilch, 1987; Butrum, 1988; Health and Welfare Canada, 1985). Thelower value was selected with special consideration of health benets such as intestinal function,and the upper value was chosen to avoid possible deleterious effects.

V. SOURCES OF DIETARY FIBER

Most dietary ber comes from plant products such as fruits, vegetables, legumes, nuts, andwhole grains. Because of their higher water content, fruits and vegetables provide less dietaryber than the whole grains per ounce consumed. The most concentrated sources of dietary berare whole grains and cereal brans. Rening processes decrease the ber content in grains.

The most common form of dietary ber is insoluble ber. Composed of cellulose, lignin,and some hemicellulose, it promotes regularity and is being studied for its potential to reducethe risk of colon/rectal cancers. In addition to cereal brans and whole grain cereals, other goodsources of insoluble ber are dried beans, peas, vegetables, and nuts.

Although soluble ber is less common in foods than insoluble ber, it is believed to haveimportant effects in the digestive and absorptive processes. A growing number of studies showthat soluble ber as part of a low-fat, low-cholesterol diet may help lower blood cholesterol inthose individuals with elevated blood cholesterol levels. It has also been shown to help controlblood glucose levels in individuals with diabetes mellitus. Good sources of soluble ber arewhole grain oats and barley, oat bran, some fruits, dried beans, and other legumes.

When changing from a low-ber diet (typical American diet) to a high-ber diet, it isbest to start by gradually substituting foods with more ber for low ber foods. As a result ofthe diversity of effects of various components of dietary ber, it is important that the dietaryber consumed come from a wide variety of foods that provide a broad spectrum of thesecomponents. Table 3 provides a comprehensive list of the total dietary ber content andinsoluble/soluble levels found in common foods.

The use of dietary ber supplements to achieve an increase in dietary ber intake in thegeneral population should be done prudently (Slavin, 1987; Pilch, 1987). Effects of isolateddietary bers are likely to be different than their effects in native foods.


Table 3 Dietary Fiber Content of Foods

Dietary berMoisture (g/100 g edible portion)(g/100 g

Food edible portion) Total Insoluble SolubleBaked products

Bagels, plain 31.6 2.1 1.5 0.6Biscuits, baking powder 16.7 2.1 1.6 0.5Breads:

Boston brown 47.2 4.7 Bran 39.1 5.4 4.6 0.8Corn 36.1 3.0 2.8 0.2Cracked wheat 35.9 5.3 4.5 0.8French 29.2 2.7 1.9 0.8Hollywood-type, light 37.8 4.8 4.2 0.6Italian:

Plain 26.9 3.8 2.9 0.9Sesame seeds 34.6 3.4 2.5 0.9

Multigrain 38.6 5.6 4.6 1.0Oatmeal 37.8 4.3 3.3 1.0Pita:

White 32.1 1.6 0.8 0.8Whole wheat 30.6 7.4 6.6 0.8

Pumpernickel 38.3 5.9 4.3 1.6Reduced-calorie, high-ber:

Multigrain 39.3 13.6 12.7 0.9White 44.3 12.8 12.3 0.5

Rye (German) 36.8 8.3 6.8 1.5Sourdough 36.4 3.0 2.0 1.0White 37.1 1.9 1.3 0.6

Toasted 2.5 Whole wheat 39.7 8.1 7.0 1.1

Toasted 8.9 Bread crumbs, plain or seasoned 5.7 4.2 3.0 1.2Bread sticks 4.6 3.0 1.8 1.2Bread stufng, avored from dry mix 65.1 2.9 2.0 0.9Cakes, prepared:

Angel food 35.5 0.8 0.5 0.3Chocolate 33.3 2.4 1.8 0.6Coffeecake

Crumb topping 22.3 3.3 2.6 0.7Fruit 31.7 2.5 1.5 1.0

Devils food 30.4 2.5 1.8 0.7Fruitcake 22.0 3.7 2.5 1.2Yellow 26.9 1.4 1.1 0.3

Cheesecake 44.6 2.1 1.5 0.6Cookies:

Brownies 12.8 2.5 1.7 0.8Butter 4.7 2.4 1.6 0.8Chocolate chip 4.1 2.6 1.9 0.7Chocolate sandwich 2.2 2.9 2.2 0.7Fig bar 16.7 4.6 4.0 0.6


Table 3 Continued


Food edible portion) Total Insoluble SolubleFortune 8.0 1.6 1.2 0.4Ginger snaps 4.8 1.8 1.2 0.6Oatmeal 4.9 2.6 1.5 1.1Peanut butter 6.7 1.8 1.3 0.5Shortbread 3.3 1.8 0.9 0.9Sugar 3.3 1.1 0.7 0.4Vanilla wafers 5.5 1.5 0.7 0.8

Crackers:Cheese 3.5 2.5 1.4 1.1Crispbread 7.2 15.9 13.0 2.9Flatbread 4.9 16.5 13.2 3.3Graham 4.4 2.7 1.9 0.8Honey grahams 3.0 3.0 1.7 1.3Melba toast

White 5.1 6.2 4.7 1.5Whole wheat 5.9 8.9 7.1 1.8

Matzo, plain 6.1 2.9 2.2 0.7Saltines 3.0 2.3 1.1 1.2Snack-type 3.3 2.0 1.0 1.0Soda 4.0 2.7 1.3 1.4Wheat 1.7 4.1 3.0 1.1Whole wheat 1.9 10.9 9.1 1.8

Croissants 20.4 2.3 1.4 0.9Croutons 5.6 4.7 4.0 0.7Doughnuts

Cake 19.7 1.7 1.1 0.6Yeast, glazed 26.7 1.2 0.7 0.5

Hamburger buns 35.0 2.6 1.7 0.9Ice cream cone:

Sugar 3.0 4.6 3.4 1.2Wafer 5.3 4.1 3.0 1.1

Mufns:Blueberry 37.3 3.6 3.1 0.5Bran-raisin 26.7 6.3 4.9 1.4English 38.0 3.0 2.4 0.6Oat bran 35.0 7.5 5.0 2.5Plain 27.1 1.5 1.0 0.5Wheat bran 23.3 3.3 2.5 0.8

Pastries:Plain 19.3 1.3 0.9 0.4Fruit 27.6 1.9 1.0 0.9

Pie Crust 14.9 2.3 1.8 0.5Pies:

Apple 44.9 1.6 1.0 0.6Cherry 46.2 0.8 0.5 0.3Pecan 19.8 3.5 3.0 0.5Pumpkin 58.1 2.7 2.1 0.6


Table 3 Continued


Food edible portion) Total Insoluble SolubleRolls:

Brown and serve 23.5 3.0 1.9 1.1Cinnamon 26.4 2.2 1.6 0.6Dinner 30.4 3.8 3.0 0.8French 30.8 3.2 2.2 1.0

Taco shells 4.2 6.3 5.4 0.9Toaster pastries 8.9 1.0 0.6 0.4Tortillas:

Corn 49.0 5.1 4.4 0.7Flour 29.3 2.3 1.3 1.0

Wafes, frozen 45.0 2.4 1.6 0.8

Breakfast cerealsBran 2.9 35.3 32.8 2.5Bran, extra ber 3.1 51.2 48.6 2.6Bran akes

Plain 3.2 19.5 17.5 2.0Raisins 7.6 13.5 15.1 2.4

CornakesPlain 2.8 2.0 1.7 0.3Sugar frosted 1.9 2.2 1.8 0.4

Cream of wheat, 87.9 0.7 0.6 0.1cooked

Crispy rice 2.4 1.9 1.4 0.5Fruit and bran 3.0 14.8 12.0 2.8Granola 3.3 10.5 Grapenuts 3.1 10.4 7.3 3.1Hominy, cooked 85.0 0.6 0.6 0.0Muesli 5.0 12.0 Oat bran, uncooked 7.4 17.0 10.5 6.5Oatmeal, cooked 84.2 1.9 1.2 0.7Psyllium and bran 3.0 21.2 10.6 10.6Puffed wheat 6.9 7.5 5.1 2.4Puffed rice 6.5 1.4 1.0 0.4Shredded wheat 7.1 12.5 9.9 2.6Toasted oats 3.5 7.0 4.2 2.8Wheat akes 2.4 11.4 9.6 1.8

Cereal grainsAmaranth 9.8 15.2 Amaranth our, whole 10.4 10.2

grainArrowroot our 11.4 3.4 Barley 9.4 17.3 Barley, bran 3.5 70.0 67.0 3.0Barley, pearled 10.1 15.6


Table 3 Continued


Food edible portion) Total Insoluble SolubleBulgur, dry 8.0 18.3 Corn, bran 6.5 82.4 80.4 2.0Corn, our, whole grain 10.9 13.4 Cornmeal:

Whole grain 11.0 11.0 Degermed 10.3 5.3

Cornstarch 12.0 0.9 Millet, hulled 8.2 8.5 Oat, bran 10.0 22.2 11.7 10.5Oat, our 7.8 9.6 Oats, rolled, or oatmeal, dry 8.8 10.3 6.5 3.8Rice:

Wild 8.4 5.2 Brown, long-grain:Raw 11.7 3.9 Cooked 73.1 1.7 White:

Long-grain:Dry 8.7 1.3 1.0 0.3Cooked 77.5 0.7 0.7 0.0

Short grain 11.1 2.8 Medium grain 11.7 1.7

Parboiled rice:Dry 10.4 2.2 Cooked 77.0 0.5

Instant:Dry 8.1 1.6 Cooked 76.4 0.8

Rice-a-Roni 71.5 2.5 Rice bran 6.1 21.7 Rice our:

Brown 12.0 4.6 White 11.9 2.4

Rye:Dark 11.1 32.0 Medium 8.8 14.7 Light 10.6 14.6

Semolina 12.7 3.9 Triticale 11.2 18.1 Triticale, our, whole 9.4 14.6

grainWheat, bran 11.6 42.4 40.3 2.1Wheat, our

White, all-purpose 11.2 2.7 1.7 1.0Whole-grain 11.5 12.6 10.2 2.3

Wheat germ 2.9 14.0 12.9 1.1


Table 3 Continued


Food edible portion) Total Insoluble SolubleFruit and fruit products

Apples:Red Delicious:

Unpeeled 83.6 2.0 1.8 0.2Peeled 84.6 1.5 1.3 0.2

Granny Smith, unpeeled 83.8 2.7 2.4 0.3Apple juice,

unsweetened 87.9 0.1 0.1 0.0Applesauce:

Sweetened 79.6 1.2 1.0 0.2Unsweetened 88.4 1.5 1.3 0.2

Apricots, dried 31.1 7.8 6.0 1.8Apricot nectar 84.9 0.6 0.5 0.1Bananas 75.7 1.7 1.2 0.5Blueberries:

Fresh 85.4 2.7 2.4 0.3Frozen 83.5 3.2 2.5 0.7

Cherries, canned 78.8 1.0 0.4 0.6Figs, dried 28.4 9.3 Fruit cocktail 1.5 Grapefruit:

Fresh 87.8 1.8 0.7 1.1Juice 90.1 0.5 0.0 0.5

Grapes 80.6 1.2 0.7 0.5Kiwifruit 83.0 3.4 Melons 90.1 0.7 0.4 0.3Nectarine 89.7 1.2 0.8 0.4Oranges:

Fresh 86.0 1.8 0.7 1.1Juice 89.4 0.4 0.1 0.3

Peaches:Fresh 87.1 1.9 1.0 0.9Canned 83.0 1.2 0.7 0.5

Pears:Fresh 84.5 3.0 2.0 1.0Canned 84.1 2.3 1.5 0.8

Pineapple, canned 84.2 0.9 0.7 0.2Plums:

Fresh 85.4 1.6 0.7 0.9Canned 75.8 2.4 1.1 1.3

Prunes, dried 26.2 7.3 3.1 4.2Prune juice 81.2 1.0 Raisins, seedless 12.6 3.7 2.4 1.3Strawberries:

Fresh 90.5 2.2 1.3 0.9Frozen 75.0 1.6 0.9 0.7Jam 31.8 0.9 0.7 0.2


Table 3 Continued


Food edible portion) Total Insoluble SolubleTangerine:

Fresh 85.1 1.8 1.4 0.4Canned 84.5 0.4 0.1 0.3

Watermelon 90.1 0.4 0.3 0.1

Legumes and pulsesBaked beans, canned:

B-BQ 5.8 Sweet or tomato sauce:

Plain 72.6 7.7 With franks 69.3 6.9

Black-eyed peas, canned 65.0 3.9 3.5 0.4Lentils:

Dried, raw 9.9 11.4 10.3 1.1Dried, cooked 66.5 5.3 4.7 0.6

Garbanzo beans, canned 65.6 3.5 3.1 0.4Lima beans, canned 74.5 4.2 3.8 0.4Kidney beans, canned 70.4 6.3 4.7 1.6Peas, black-eyed, canned 78.6 3.1 2.7 0.4Peas, green:

Canned 81.5 4.3 4.0 0.3Frozen 82.3 3.5 3.2 0.3

Pinto beans:Dried, raw 8.2 19.5 12.1 7.4Dried, cooked 71.2 8.0 5.8 2.2Canned 73.3 5.2 4.0 1.2

Soybeans:Dry 8.0 15.0 Tofu 84.6 1.2

White beans:Dried, raw 3.6 17.7 13.4 4.3Dried, cooked 71.2 5.4 3.9 1.5Canned 73.6 5.6 3.9 1.7

Nuts and seedsAlmonds, roasted 3.3 11.2 Cashews, oil-roasted 5.4 6.0 Coconut:

Raw 47.0 9.0 8.5 0.5Shredded 18.5 6.6 6.2 0.4

Hazelnuts, oil-roasted 1.2 6.4 Peanuts:

Dry-roasted 1.6 8.0 7.5 0.5Oil-roasted 2.0 8.8 8.0 0.8

Peanut butter:Chunky 1.1 6.6 6.0 0.6Smooth 1.4 6.0 5.5 0.5


Table 3 Continued


Food edible portion) Total Insoluble SolublePecans 4.8 6.5 Pistachio nuts 3.9 10.8 Sesame seeds:

Dry 24.6 15.4 Roasted 5.8 11.6

Walnuts 3.5 3.8 3.7 0.1

MiscellaneousAvocado 77.3 3.9 2.6 1.3Beer 92.3 0.5 Candy:

Caramels, vanilla 7.6 1.2 Milk chocolate 0.8 2.8

Carob powder 1.2 32.8 Chili powder 9.1 34.2 Chocolate, baking 0.7 15.4 Cocoa, baking 1.3 29.8 Curry powder 8.7 33.2 Jelly, apple 32.3 0.6 Pancake mix 8.3 4.5 3.5 1.0Pepper, black 9.4 25.0 Pickles 93.4 1.1 0.7 0.4Preserves:

Peach 32.4 0.7 Strawberry 31.7 1.2

Olives:Black 80.5 2.2 2.1 0.1Green, with pimento 76.5 2.0 1.8 0.2

Soup:Chicken noodle 86.5 0.5 Vegetable 84.9 1.3

Yeast, active, dry 6.8 31.6

PastaMacaroni

Dry 8.5 4.3 4.1 0.2Cooked 69.6 2.0 1.7 0.3

Noodles:Dry:

Spinach 8.5 6.8 Chow-mein 0.7 3.9 Somen 11.3 4.3 Egg 9.5 4.0 Cooked 67.3 1.8 1.3 0.5


Table 3 Continued


Food edible portion) Total Insoluble SolubleSpaghetti:

Dry:Regular 9.2 3.6 2.1 1.5Whole wheat 7.1 11.8 Spinach 8.7 10.6

Cooked 60.7 1.5 1.1 0.4

SnacksCorn chips 1.1 4.3 3.9 0.4Corn puffs 1.5 1.0 Granola bars, crunchy:

Chocolate chip 4.4 Cinnamon 5.0

Popcorn:Air-popped 15.1 Oil-popped 10.0

Potato chips 2.4 3.8 1.9 1.9Pretzels

Hard 3.5 3.7 2.8 0.9Soft 32.7 2.5 1.6 0.9

Tortilla chips 2.0 6.5

Vegetables and vegetable productsArtichoke 84.4 7.6 4.4 3.2Artichoke, globe 82.5 7.9 4.7 3.2Asparagus

Fresh, cooked 90.5 2.1 1.6 0.5Canned 93.3 1.6 1.2 0.4

Bamboo shoots, canned 97.4 1.5 1.4 0.1Beans, green

Canned 91.8 2.1 1.4 0.7Boiled 91.8 2.5 1.5 1.0

Bean sprouts 96.2 1.2 1.1 0.1Beets, canned 92.4 1.7 1.3 0.4Broccoli:

Raw 88.5 3.3 3.0 0.3Cooked 90.2 3.5 3.1 0.4

Brussels sprouts 87.2 4.1 3.6 0.5Cabbage:

Raw 90.9 1.8 1.1 0.7Boiled 94.0 1.7 1.1 0.6

Carrots:Raw 88.5 2.4 1.1 1.3Cooked 90.5 2.7 1.2 1.5


Table 3 Continued


Food edible portion) Total Insoluble SolubleCauliower:

Raw 92.6 1.8 1.1 0.7Cooked 93.3 1.8 1.1 0.7

Celery:Raw 94.6 1.5 1.0 0.5Cooked 95.2 1.4 0.9 0.5

Chives 92.0 3.2 Corn, sweet:

Canned:Whole 76.7 2.1 1.8 0.3Cream style 75.6 1.3 1.1 0.2

Fresh:Raw 76.0 3.2 3.0 0.2Cooked 69.6 3.7 3.5 0.2

Frozen, whole 75.8 2.1 2.0 0.1Cucumbers:

Peeled 96.2 0.6 0.5 0.1Unpeeled 95.8 0.9 0.8 0.1

Eggplant 6.6 5.3 1.3Leek 90.3 2.9 2.0 0.9Lettuce:

Iceberg 96.0 0.7 0.5 0.2Romaine 94.9 1.7

Mushrooms, canned 90.9 2.8 2.6 0.2Onions, raw:

Green 92.7 2.2 2.2 0.0Yellow 90.3 1.7 1.6 0.1

Parsley 88.3 4.4 Peas, green:

Canned 80.7 4.5 3.6 0.9Boiled 76.9 6.7 5.0 1.7Frozen, boiled 81.6 4.4 3.2 1.2

Peppers, green, raw 93.5 1.9 1.2 0.7Potatoes:

Baked, skin 73.3 2.5 1.9 0.6Boiled,

without skin 79.5 1.3 1.0 0.3French fried 48.6 3.0 1.5 1.5

Pumpkin, canned 90.2 2.9 2.4 0.5Radish, red 94.2 1.4 1.3 0.1Rutabagas:

Raw 89.0 2.4 1.2 1.2Boiled 92.3 2.1 1.2 0.9

Spinach:Raw 91.6 2.6 2.1 0.5Cooked 93.7 2.2 1.8 0.4


Table 3 Continued


Food edible portion) Total Insoluble SolubleSquash:

Summer:Raw 93.7 1.2 Cooked 93.7 1.4

Winter:Raw 88.7 1.8 Cooked 89.0 2.8

Zucchini, raw 94.5 0.9 0.8 0.1Sweet potatoes:

Cooked 72.8 3.0 2.5 0.5Canned 75.6 1.7 1.3 0.4

Tomatoes:Raw 94.5 1.2 0.8 0.4Boiled 93.2 1.5 1.0 0.5Canned 93.3 1.0 0.7 0.3Sauce 90.9 1.4 0.8 0.7Paste 74.1 4.3 Catsup 66.7 1.2 0.9 0.3Juice 94.1 0.7 0.4 0.3

Turnip greens:Frozen 92.9 2.5 2.4 0.1Cooked 93.2 3.1 2.9 0.2

Turnips 94.7 2.0 1.5 0.5Water chestnuts 87.9 2.2

Based on published values: Am. Assoc. of Cereal Chemists, 1987; Dreher, 1987; Anderson and Bridges, 1988; Cardozoand Eitenmiller, 1988; Del Toma et al., 1988; Mongeau et al., 1989; USDA, 1989; Toma and Curtis, 1989; Ranhotraet al., 1990; Prosky and DeVries, 1992; and Marlett 1991.

REFERENCES

American Association of Cereal Chemists. (1987). Dietary ber guide. Cereal Foods World. 32(8):555570.

Anderson, J. W. and Bridges, S. R. (1998). Dietary ber content of selected foods. Am. J. Clin. Nutr. 47:440447.

Block, G., Patterson, B., and Subar, A. (1991). Fruit, vegetables, and cancer prevention: a review of theepidemiological evidence. Nutr. Cancer 18(1):1.

Butrum, R. R., Clifford, C. K., and Lanza, E. (1988). NCI dietary guidelines: rationale. Am. J. Clin. Nutr.48:888895.

Cardozo, M. S. and Ettenmiller, R. R. (1988). Total dietary ber analysis of selected baked and cerealproducts. Cereal Foods World. 33(5):414418.

Dietary Guidelines for Americans (2000). Aim for Fitness, Build a Healthy Base, and Choose Sensiblyfor Good Health. USDA and DHHS. Home and Garden Bulletin No. 232.

DeCosse, J. J., Miller, N. H., and Lesser, M. L. (1989). Effect of wheat ber and vitamins C and E onrectal polyps in patients with familial adenomatous polyposis. J. Natl. Cancer Inst. 81:12901294.


Del Toma, E., Celemnti, A., Marcelli, M., Cappelloni, M., and Lintas, C. (1988). Food ber choices fordiabetic diets. Am. J. Clin. Nutr. 47:243246.

Dreher, M. L. (1987). Dietary ber content of food sources. Handbook of Dietart Fiber: An Applied Ap-proach. Marcel Dekker, Inc., New York.

Eaton, S. B. (1990). What did our late paleolithic preagricultural ancestors eat? Nutr. Rev. 48(5):227228.Eaton, S. B., Konner, M. J., and Shostak, M. (1988). Stone agers in the fast lane: chronic degenerative

disease in evolutionary perspective. Am. J. Med. 84:739749.Gordon, D. T. (1999). Dening dietary bera progress report. Cereal Foods World. 44(5):336.Health and Welfare Canada. (1985). Report of the Expert Advisory Committee on Dietary Fibre to the

Health Protection Branch. Health and Welfare Canada, Ottawa.International Food Information Council. (1991). How Americans are making food choices. IFIC Review,

Washington, DC.Kritchevsky, D. (1988). Dietary ber. Ann. Rev. Nutr. 8:301328.Marlett, J. A. (1992). Content and composition of dietary ber in 177 frequently consumed foods. J. Am.

Diet. Assoc. 92:175186.Mongeau, R., Brassard, R., and Verdier, P. (1989). Measurement of dietary ber in a total diet study. J.

Food Comp. Anal. 2:317326.Pilch, S. M. (1987). Physiological Effects and Health Consequences of Dietary Fiber, Life Sciences Re-

search Ofce. Federation of American Societies for Experimental Biology. Bethesda, Maryland.Contract Number FDA 223-84-2059, pp. 162, 163.

Prosky, L. and DeVries, J. (1992). Controlling Dietary Fiber in Food Products. Van Nostrand Reinhold,New York.

Ranhotra, G. S., Gelroth, J. A., and Astroth, K. (1990). Total and soluble ber in selected bakery andother cereal products. Cereal Chem. 67(5):499501.

Siegal, S. W. (1968). Biochemistry of the plant cell wall. Comprehensive Biochemistry. M. Florkin andE. H. Stotz (Eds.). Elsevier Publishing Company, Amsterdam, pp. 151.

Slavin, J. L. (1987). Dietary ber: classication, chemical analysis, and food sources. J. Am. Diet. Assoc.87(9):11641171.

Walker, A. R. P. (1993). Does the dietary ber hypothesis really work? Cereal Foods World. 38(3):128134.


2Dietary Fiber and Cardiovascular Disease

Judith A. MarlettUniversity of Wisconsin, Madison, Wisconsin

I. INTRODUCTION

The foundation of the recognition of a relationship between diet and cardiovascular disease(CVD) was the demonstration that different fats have signicantly different effects on bloodlipid levels. These seminal observations were made during two series of classic experimentsconducted nearly 35 years ago by Keys et al. (1) and Hegsted et al. (2). These ndings havebeen duplicated often, but rarely with the same rigor shown by these two eminent scientists,and the outcome of all further studies is fundamentally unchanged (3). In the intervening time,several other aspects of dietary fats (e.g., different types of unsaturated and saturated fats andoxidized lipids) were and are being studied for their effects on blood lipid levels (47).

Specic nutrients, such as (a) vitamins E and C, cobalamin, pyridoxine, and folate; (b) theminerals potassium, calcium, magnesium, and selenium; (c) specic characteristics of nutrients,(e.g. antioxidants); (d) specic foods, herbs, and spices and other botanical agents; (e) bacteria;and (f) specic components of foods, such as saponins, phytosterols and terpenes, have beenexplored for their effects on blood lipid levels (8,9). In some cases, unrealistic amounts of thesecomponents have been tested. But in many other instances, the component has been shown tolower undesirable concentrations of blood lipids. These nutrients and components in food aregenerally consumed as part of an incredibly complex mix of chemicals we call a varied diet.

Within this complex milieu, it is surprising that any benecial response to dietary berconsumption was identied, particularly since dietary ber is not a single entity but rather acomplex mixture of polysaccharides and lignin (10). In addition, accurate measurement of beris difcult (10,11), and interpretation of bers effects are confounded by other lipid-alteringfood components that frequently are part of the ber source (12).

The role of dietary ber in the modulation of blood lipid concentrations was initiallyexplored in the 1960s. In fact, one of the earliest demonstrations of the hypocholesterolemicresponse to dietary ber was made by Keys et al. (13) in a series of experiments designed toexplain why serum cholesterol levels were lower in Italian than in North American populations.They reported that ingestion of 15 g/d of pectin, along with a constant diet, reduced bloodcholesterol concentrations by about 5% in healthy adult men. Trowell (14) presented a perspec-tive in nutrition in 1972 to support his hypothesis that high consumption of natural starchycarbohydrates, taken with their full complement of ber, is protective against hyperlipidemiaand ischemic heart disease.

It is now well established that certain sources of dietary ber, independent of the fat or


carbohydrate content of the diet, can lower serum cholesterol concentrations. Fiber specicallyaffects the concentration of the major fraction of cholesterol in blood, that carried by low-densitylipoproteins (LDL). Blood concentrations of triacylglycerols and high-density lipoproteins areunaffected by these bers.

The purpose of this chapter is threefold. First, the effects of dietary bers and high-berdiets on serum cholesterol levels are reviewed. Second, the kinds and properties of serum choles-terollowering sources of dietary ber are summarized. Third, data are presented to support theconclusion that bers lower blood cholesterol level only if they are viscous; this viscosity be-comes concentrated in the ileum, interfering with bile acid absorption and subsequently stimulat-ing bile acid synthesis from LDL-derived cholesterol (12). This review is based on the generallyaccepted premise that measuring blood cholesterol levels provides an indication of likely impacton cardiovascular disease. When data are available, the focus is primarily on the results ofhuman studies.

II. EPIDEMIOLOGICAL ASSOCIATIONS

Humble (15) and Anderson (16) summarized the evidence supporting an inverse relationship be-tween CVD and dietary ber. Interest in this association grew out of the initial observations inAfrica byWalker (17), Trowell (14), and Burkitt (18) that Western diseases were not prevalentamong native Africans who consumed high-ber, low-fat diets and who had very different life-styles. The results of prospective studies since that time have been variable. In the majority (veof eight) of the prospective studies, the initial inverse correlation between some measure of CVDand dietary ber intake was retained, although sometimes weakened, after data were adjusted toaccount for other diet factors (1923). In three other prospective studies the statistical signicanceof the associationsbetweenCVDanddietaryberwas lostwhendietarydatawere adjusted, usuallyfor energy (2426).Results of epidemiological studies using ecological case comparisons or cross-sectional population surveys also have not yielded uniform results (16).

III. DIET AND CVD PREVENTION OR REGRESSION

Results of studies that used multiple diet changes to achieve lower fat and higher carbohydrateintakes suggest that diet can have a signicant, favorable impact on the incidence and progres-sion of cardiovascular disease. While a reduction in fat intake has a more pronounced effecton blood lipid levels, the higher carbohydrate aspect of these diets undoubtedly increased berintake. Such diets resulted in signicantly less CVD (27), inhibited progression of CVD (28),and induced actual regression of CVD (29) in clinical trials. Severe changes in diet and lifestylealso induced regression of cardiovascular lesions (30). One study was not able to demonstratea uniform reduction in mortality rates using a diet expected to lower the frequency of CVDevents (31). In one carefully conducted, 8-month study, pectin, compared to cellulose, signi-cantly increased aortic sudanophilia in vervet monkeys (32). It is unlikely that consumption ofan isolated ber supplement without substantial changes in dietary fat intake would affect theresults seen when both dietary components are changed.

IV. HYPOCHOLESTEROLEMIC DIETARY FIBER SOURCES

Many sources of dietary ber have been evaluated for their effects on serum lipid concentrations.The details of most of these studies have been admirably summarized in table form in other


Table 1 Puried and Food Sources ofHypocholesterolemic Dietary Fibers

Puried sources Food sources

Beet ber ApplesGuar gum BarleyGum arabic Beans and other legumesKaraya gum Fruits and vegetablesKonjac mannan Oatmeal and oat branLocust bean gum Rice hullsPectinPsyllium seed huskSoy polysaccharideXanthan gum

reviews (3338). Fibers reported to lower serum cholesterol concentrations signicantly in morethan one human study are listed in Table 1. Fiber sources having no effect on serum cholesterollevels in humans include puried wood pulp cellulose, wheat bran, and oat hulls.

Responses in humans have been variable after ingestion of a few bers, such as puriedlignin, carrots, corn bran or maize, and diets containing large amounts of fruits and vegetables.For example, blood cholesterol levels signicantly decreased in one study when an atypical dietcontaining less than 20% energy as fat and over 24 g/1000 kcal dietary ber was modied tocontain about one third of the ber as soluble ber, compared to 17% soluble in the controldiet (39). In another study in which the constant diet was more typical, containing 34% of energyas fat, increasing dietary ber intake using a mix of foods, from about 5 to 14 g/1000 kcal,which produced a 2.7-fold increase in soluble ber, had no effect on serum cholesterol concentra-tions (40). The diet used in the latter study was consistent with the guideline set by the USFood and Drug Administration for adequate dietary ber intakes, of 12 g total ber/1000 kcal.

Single reports of lower blood cholesterol concentration after ingestion of a ber source(e.g., prunes, rhubarb stalk), have not been conrmed (41,42). Much has been written aboutresistant starch as a dietary ber source, but few studies have examined its effect on bloodcholesterol levels. Asp (43) has concluded that data are too limited to formulate a conclusionabout its hypocholesterolemic potential. The variable results from different studies may be ex-plained in part by the use of very different sources of the starch.

The hypocholesterolemic potential of many other bers have been evaluated in animalmodels (44,45). Because of the wide range and varying rigor of the experimental designs usedin human and animal studies, conrmation of human studies and testing in humans of agentsobserved to be hypocholesterolemic in animals are important components of developing a hypo-lipidemic prole for a food or food component.

V. HOW DOES DIETARY FIBER LOWER BLOOD CHOLESTEROLLEVELS?

A. Changing Diet IntakeSources of dietary ber may displace some hyperlipidemic agent in the diet or alter the bodyssterol pool (Table 2). Human experiments involving a dietary ber source usually have beenconducted in one of two ways. In some studies a metabolic diet is followed, that is, a dietthat is constant in composition and in which intake is rigidly controlled. In other instances


Table 2 Effects of IncreasedDietary Fiber Intake

Change of diet compositionReduced cholesterol absorptionReduced bile acid absorptionChange of bile acid synthesisReduced cholesterol biosynthesis

subjects are counseled to follow specic dietary guidelines, and food intake is assessed one ormore times, usually by written questionnaire, during the course of the study to determine whetherintake has changed. Clearly, a study using a metabolic diet will generate more accurate results,because sources of diet and nondiet variation have been reduced to a minimum. However, meta-bolically controlled experiments are costly. When diet is not constant, monitoring adherence todiet guidelines is of critical importance. A good deal of the variation among the studies ofhypocholesterolemia with ber consumption is likely a consequence of subtle changes in theunderlying diet which are not detected by most currently used methods of monitoring nutrientintake. This is particularly true for fat and energy intakes, because small changes in both ofthese diet variables could confound blood lipid responses but not be detected as signicantchanges in the mean intakes of the study population.

B. Altering Dietary Cholesterol AbsorptionCarefully conducted studies that have been repeatedly conrmed have established that a beris hypocholesterolemic because it alters the bodys total sterol pool. The hypothesis that berslower blood cholesterol levels by interfering with absorption of dietary cholesterol is attractivebecause of its simplicity. However, it is unlikely that ber-induced hypocholesterolemia is aresult primarily of decreased exogenous cholesterol absorption. This is because exogenous cho-lesterol represents only a quarter to a third of the bodys cholesterol, and a substantial changein the proportion absorbed would still represent only a relatively small amount. Some bersmay decrease absorption of dietary cholesterol by altering the composition of the bile acid pool.Pectin (46) and oat bran (47) increased the portion of the total bile acid pool that was deoxycholicacid (DCA). DCA has been reported to decrease the absorption of exogenous cholesterol from46 to 28 mol/h during intestinal perfusion in humans (48).

C. Altering Cholesterol BiosynthesisDemonstrating a reduction in endogenous cholesterol biosynthesis, the major source of thebodys cholesterol, is difcult in humans. Many of the data to support such a change are indirector come from animal experiments. However, data that are available do indicate that endogenouscholesterol synthesis may be affected. Hydroxymethylglutaryl-CoA (HMG CoA) reductase, therate-limiting enzyme in the cholesterol biosynthesis pathway, is signicantly inhibited by DCA,compared to cholic acid (CA) or chenodeoxycholic acid (CDCA) (49). The increase in theproportion of the bile acid pool that was DCA produced by oat bran (47) and pectin (46) supportsthe hypothesis that part of the hypocholesterolemic action of ber is a consequence of its inhibi-tory effect on endogenous cholesterol synthesis. However, cholesterol biosynthesis increasedfollowing supplementation of low-cholesterol diets with psyllium (50) or large amounts (4050 g/d) of pectin (51). When the diet contained typical amounts of cholesterol, psyllium supple-


mentation had no effect on cholesterol synthesis (52). The relative hydrophobicity of the bileacid pool may indicate the extent of the effect on cholesterol metabolism (53,54).

D. Increasing Bile Acid SynthesisCholesterol carried by LDL is quantitatively the most important substrate for bile acid synthesis(55). It is estimated that 4050% of cholesterol is eliminated daily through bile acid synthesis(49,56). Beginning in the early 1970s, Kritchevsky and Story (45,57,58) focused interest on thispossible sink for blood cholesterol with a series of studies in which the in vitro binding ofdifferent bile acids by various ber sources was examined. Although not all of the in vitrondings have been consistent with subsequent in vivo observations, these important experimentswere insightful and ahead of their time.

Two laboratories have unambiguously demonstrated, using stable isotope-labeled bileacids to study bile acid kinetics, that at least two hypocholesterolemic dietary bers, psyllium(52) and oat bran (47), stimulate bile acid synthesis and alter the composition of the bile acidpool. Oat bran signicantly decreased pool size of CA and doubled DCA pool size, whereaspsyllium increased CDCA pool size but had no effect on pool sizes of CA or DCA. Neitherber changed the size of the total bile acid pool (47,52). These studies also revealed that turnoverof one or both primary bile acids was increased when bile acid kinetics during ber supplementa-tion were compared to what was measured during a low-ber diet control period. The differingeffects on the composition of the bile acid pool could be due to the ber source or to the useof different study populationsnormocholesterolemic in the oat bran study and hypercholester-olemic in the psyllium study.

E. Increasing Bile Acid ExcretionBile acid synthesis reects fecal losses when total pool size does not change and sterol balanceis in steady state. These conditions were met in both of the bile acid kinetic studies (47,52),and thus, it would be predicted from the increased synthesis measured during these studies thatfecal sterol excretion also would increase during ber supplementation. Fecal sterol excretionwas increased signicantly during the oat bran study (47) but not during the psyllium study(52). Failure to detect a signicant increase in fecal excretion when serum cholesterol concentra-tions are lowered by dietary ber supplementation has been reported in about half of the studiesin which both parameters were measured (36). Forty to fty percent of bile acids in excreta aremicrobially produced derivatives, which are not quantitated during gas chromatographic analysis(59,60). It is likely that the inability to account for these bile acid derivatives is responsible forinsignicant fecal losses of the bile acids in studies in which serum cholesterol concentrationsare signicantly lowered by ber. Increases in ileal bile acid excretion of 4050% during oatbran (61) or psyllium (62) consumption supports the contention that fecal steroid excretion isan insensitive measure of bile acid loss or synthesis.

VI. HOW DOES FIBER INCREASE BILE ACID EXCRETION?

Two mechanisms have been proposed to explain the hypocholesterolemic properties of somedietary bers. One is that increased amounts of propionate are produced during microbial fer-mentation of these bers and that the propionate inhibits cholesterol biosynthesis (34). The otherproposed mechanism is that the viscosity of these bers becomes concentrated in the ileum andinterferes with bile acid absorption (12).


A. Short-Chain Fatty Acids and FermentationMost hypocholesterolemic dietary bers are rapidly fermented and would be expected to createan acute inux of SCFA into the blood. Nonetheless, a wide variety of data from human andanimal studies do not consistently support a role for SCFA in the cholesterol-lowering activityof dietary ber. In vitro hepatic cholesterol biosynthesis from labeled acetate is inhibited bypropionate at concentrations of 1.0 mmol (63). However, in the same set of experiments, 2.5mmol of propionate was needed to inhibit cholesterol biosynthesis from tritiated water or labeledmevalonate (63). These inhibitory effects on cholesterol biosynthesis were not reproduced whenphysiological concentrations of propionate or acetate were incubated with isolated hepatocytesin the presence of tritiated water (64). Oral propionate had no effect on the blood cholesterollevels in both a rat (65) and a human (66) study, although the activity of HMG CoA reductaseactivity was slightly depressed in the rat study.

An increase in the concentration of propionate in the cecum occurring with oral -cyclo-dextrin was accompanied by increased bile acid excretion and microsomal HMG CoA reductaseactivity, responses that would be consistent with induction of cholesterol biosynthesis (65).However, body weight gain of the test animals was signicantly less than that of the controlgroup (65). Surgical removal of the cecum or cecum and colon (67), but not the prevention ofcoprophagy (68), did negate the hypocholesterolemic response to a beet ber preparation or oatbran.

In humans, plasma cholesterol levels actually increased when acetate was intrarectallyinfused (69,70) or rapidly fermented lactulose was consumed (71). Co-infusion of propionatewith acetate reduced acetate incorporation into cholesterol, although the small number of sub-jects prevented the effect from reaching statistical signicance (70).

B. Viscosity of Hypocholesterolemic Dietary FibersMost viscous dietary bers are also rapidly fermented to SCFA. Thus, if an independent rolefor viscosity is to be demonstrated, it is necessary to separate viscosity from SCFA production.Viscosity and SCFA production have been separated by (a) conducting experiments using vis-cous bers that are not fermented, (b) using a fermented viscous ber that has been modiedto reduce the viscosity, and (c) employing germfree animals in the experiment.

3-Hydroxylpropyl methylcellulose, a cellulose ether, is not fermented (72). Using this non-fermented synthetic product at three different viscosities, Gallaher et al. (73) demonstrated thatthe viscosity of the diet or of small bowel digesta was inversely proportional to blood cholesterollevels in hamsters. Lumenal viscosity produced by 3-hydroxypropyl methylcellulose also hasbeen inversely correlated with cholesterol absorption in hamsters (74). In another experiment,methylcelluloses of differing viscosities had no effect on rat blood cholesterol levels (75). Bloodcholesterol levels are difcult to perturb in the rat unless they are rst elevated (76), which mayexplain why Topping et al. (75) did not observe a response to the viscous cellulose ester.

Reducing the viscosity of a hypocholesterolemic ber does appear to lower its effective-ness. Partially hydrolyzed guar gum is not as effective a hypocholesterolemic agent as the unhy-drolyzed, more viscous product (77). Isolating some viscous bers reduces the molecular weightand viscosity, which probably explains why -glucan isolated from oat bran did not lower bloodcholesterol concentrations in one human study (78). Hydrolysis of -glucans in oat bran elimi-nated the increased ileal excretion of bile acids that was observed when the unhydrolyzed oatbran was ingested by human ileostomates (79).

Germ-free animals will have no microora and, thus, do not ferment dietary ber (80).Guar gum still lowered LDL cholesterol and plasma and hepatic total cholesterol concentrations


when germ-free animals were used (81), indicating that SCFA production is not necessary toachieve cholesterol lowering by ber.

VII. CONFOUNDERS IN HYPOCHOLESTEROLEMIC DIETARY FIBERS

Many natural constituents in plants are being examined for their effects on human metabolism,including lipid metabolism. These botanicals are frequently present in dietary ber sources.With few exceptions, there has been little research to distinguish the effects of the ber fromthose that could be attributed to some other component in the ber source. Two componentsof ber sources that have been studied for their hypocholesterolemic potential are protein andtocotrienols.

A. Plant ProteinIngestion of soy protein has an established history of lowering blood cholesterol levels in bothhumans and animal models (8285). The response differs from that observed when ber isconsumed, as blood triglycerides as well as cholesterol concentrations are usually affected (85).Although the active agent has not been dened, the failure to induce hypolipidemia in femaleprimates fed soy from which the estrogens had been extracted suggest that phytoestrogens, andnot the ber per se, is the active agent (86). Several phytosterols have been shown to lowerserum cholesterol levels (87). Three different soy protein preparations had no effect on ilealbile acid or cholesterol excretion in a short-term study in human ileostomates, suggesting thatsterol excretion is not involved as the mechanism (88).

Kritchevsky (83) published data from an experiment in rabbits to support his hypothesisthat higher ratios of lysine to arginine were more hypercholesterolemic. The experiment usedthree sources of proteinsh, casein, and whole milknone of which are known to containestrogenic compounds. Casein is frequently used as the protein source in the control diets ofthese experiments, and its hypercholesterolemic effect, at least in rabbits, may be dependent ona high-cholesterol diet (89). As a different approach to exploring the role of protein, doublingprotein intake primarily with animal sources, from about 10 to 25% of energy, did reduce serumcholesterol levels in normolipidemic and moderately hyperlipidemic adults when total fat intakewas low (25% of energy) (90).

B. TocotrienolsTocotrienols are naturally occurring farnesylated analogs of the tocopherols that have been foundin the lipophilic fractions of whole oats, oat bran, barley, and rice bran and in palm oil (9193). Tocotrienols reduce HMG CoA reductase activity and protein levels in HepG2 cells andappear to modulate the mevalonate pathway by suppressing the enzyme posttranscriptionally(94). In humans following the American Heart Association Step I diet, a tocotrienol concentratefrom palm oil providing about 250 mg/d of tocos signicantly lowered total plasma and LDLcholesterol concentrations and levels of ApoB (95). However, in another study in which oat bransignicantly lowered serum cholesterol at one month, no indication of a change in cholesterolbiosynthesis could be detected when cholesterol synthesis precursors were measured in theblood (96).

Toco dietary supplements have not uniformly reduced blood cholesterol levels (92,95,97,98), in part because little attention has been paid to the composition of the supplement. Inseveral experiments, toco mixtures have been used that would not be expected to be effective,


had the composition been determined. For example, -tocotrienol is the most effective inhibitorof cholesterol biosynthesis, being 30 times more effective than the -analog (99). Yet, -toco-trienol is usually the dominant tocotrienol in cereal grains or concentrates (91,100,101). In addi-tion, -tocopherol, which can be present in grains in signicant amounts, has been demonstratedto attenuate the hypocholesterolemic effect of tocotrienols (102).

The concentration of the different toco isomers varies greatly among different genotypesof the same grain (101) and can be further modied by growing (101), storage (103,104), andprocessing (105) conditions. A third reason for the inability to induce hypocholesterolemia withtocos in animals is the design of the experiment. Available evidence indicates the tocos downreg-ulate endogenous cholesterol synthesis. Many animal models used to study blood cholesterollevels are fed diets supplemented with cholesterol to elevate the normally low blood levels.This exogenous cholesterol overwhelms any effect of the tocos by inhibiting their likely site ofaction.

VIII. ANALYTICAL MEASUREMENT TO PREDICTHYPOCHOLESTEROLEMIC PROPERTYOF DIETARY FIBER

The most common descripter of hypocholesterolemic bers is that they are soluble. In reality,not all soluble bers lower blood cholesterol levels. The data generated over the past 20 yearsargue convincingly that only those soluble bers that are also viscous perturb whole body sterolbalance. Measuring the active fraction of ber analytically instead of biologically remains elu-sive. Many of the viscous bers are non-Newtonian, making it very difcult and expensive tomeasure viscosity. The proportion of total ber measured as the soluble fraction can vary by100% using methodologies accepted by countries throughout the world (11). Even if viscosityand the proportion of total ber that is soluble can be accurately measured, few studies havecompared analytical results with the biological behavior of the analyzed ber in the gastrointesti-nal lumen.

IX. CONCLUSIONS: MECHANISMS OF ACTION FORHYPOCHOLESTEROLEMIC DIETARY FIBERS

Fiber is the grandparent of the current wave of interest in functional foods and food components.An adequate ber diet has a variety of specic healthful benets, the major one of which isoptimizing gastrointestinal physiological function. In addition, several therapeutic roles for spe-cic bers have been identied.

With respect to CVD, only soluble dietary bers that are also viscous lower blood choles-terol concentrations. Available data support a role for the viscosity in the ileum where it becomesconcentrated after most food has been digested and absorbed (12). This lumenal viscosity inter-feres with bile acid absorption. Actual binding or chelation is probably not required. The re-sulting loss of bile acids is not always detected, because up to half of fecal steroids are microbi-ally produced metabolites that are not quantitated during fecal steroid analysis (59,60). Theincreased loss in bile acids stimulates bile acid synthesis, which uses LDL cholesterol as asubstrate (47,52).

Bile acid pool size need not be changed, but its composition may be. Though more dataare needed, available evidence suggests that increasing the hydrophobicity of the bile acid poolwill suppress endogenous cholesterol synthesis (53,54). Suppressing endogenous cholesterol


synthesis also promotes lower blood cholesterol levels. Fermentation and its primary product,SCFA, probably have only a minor role, if any, in producing hypocholesterolemia. In fact, arapid inux of SCFA that would occur with the fermentation of a highly soluble ber providessubstrate for cholesterol synthesis.

Efforts to measure analytically the hypocholesterolemic potential of a ber remain prob-lematic. It appears that the ber must be not only soluble, but also viscous.

Because of differences in analytical methodologies, the proportion of a ber that is ana-lyzed as the soluble component ranges from 15 to 50% of the total ber (11). Standardizationof the methodology for ber analysis is not really a solution, as the critical measurement is thesolubility behavior in the lumen of the gastrointestinal tract.

Similarly, accurate measurement of the hypocholesterolemic property, viscosity, is dif-cult and expensive if the material is non-Newtonian, as most foodstuffs are. Again, retentionof this viscosity in the gut lumen needs to be veried to label the material as hypocholesterol-emic. Problems are exacerbated when a ber fraction is isolated for more denitive studies andanalyses. Isolation decreases molecular weight, molecular interaction, and viscosity; the neteffect is diminishing hypocholesterolemia.

A diet that prevents CVD or slows its progression is one that is lower in fat (2530%of energy) and higher in complex carbohydrate (60% of energy). A higher ber intake is anatural outgrowth of such a food intake pattern, although the proportion of soluble ber remainsabout 2535% of the total ber (40). Southgate (106) and Jenkins (107) both recently discussedprotective or optimal diets to reduce risk for degenerative diseases. Such diets composed ofminimally processed foods undoubtedly also will include other hypocholesterolemic compo-nents, including those such as phytoestrogens, vegetable protein, and tocotrienols that haveconfounded studies of dietary ber.

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