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Obesity and Benign Prostatic Hyperplasia: Clinical Connections,Emerging Etiological Paradigms and Future Directions

J. Kellogg Parsons,*,† Aruna V. Sarma, Kevin McVary‡ and John T. Wei§

From the Division of Urologic Oncology, Moores Cancer Center, University of California, San Diego and Section of Surgery, San Diego

Veterans Affairs Medical Center (JKP), La Jolla, California, Departments of Epidemiology (AVS) and Urology (AVS, JTW), Ann Arbor,

Michigan, and Department of Urology, Northwestern University (KM), Chicago, Illinois

Abbreviations

and Acronyms

BLSA Baltimore Longitudinal

Study of Aging

BMI body mass index

BPH benign prostatic

hyperplasia

HPS Health Professionals

Follow-up Study

I-PSS International Prostate

Symptom Score

LUTS lower urinary tract

symptoms

NHANES National Health and

Nutrition Examination Survey

PCPT

Prostate CancerPrevention Trial

* Correspondence: Division of Urology, Univer-

sity of California-San Diego, 200 West Arbor Dr.,

No. 8897, San Diego, California 92103-8897 (tele-

phone: 619-543-2630; FAX: 619-543-6573; e-mail:

[email protected]).

† Financial interest and/or other relationship

with American Medical Systems.

‡ Financial interest and/or other relationship

with GlaxoSmithKline, Pfizer, Lilly/ICOS, Sanofi-

Aventis, Allergan and National Institute of Dia-

betes and Digestive and Kidney Diseases.

§ Financial interest and/or other relationship

with Sanofi, American Medical Systems, Envi-

sioneering, Gen-Probe and Beckman.

Purpose: Benign prostatic hyperplasia is a highly prevalent disease in older menwith substantial adverse effects on public health. Classic etiological paradigmsfor benign prostatic hyperplasia focus on nonmodifiable risk factors. However,obesity also potentially promotes benign prostatic hyperplasia.

Materials and Methods: We performed a structured, comprehensive literaturereview to identify studies of obesity, benign prostatic hyperplasia, lower urinarytract symptoms and physical activity.Results: A preponderance of published evidence suggests strong positive associ-ations of obesity with benign prostatic hyperplasia and lower urinary tractsymptoms. This evidence encompasses most established metrics of adiposity,including body mass index, waist circumference and waist-to-hip ratio, and fallsunder 3 general categories, including prostate volume, clinical benign prostatichyperplasia and lower urinary tract symptoms. 1) Prior studies consistentlyshowed that increased adiposity is positively associated with radiographicallydetermined prostate volume and enlargement, suggesting that obesity promotesprostate growth. 2) Most studies revealed that obesity increases the risk of

clinical benign prostatic hyperplasia by several measures, including the initiationof benign prostatic hyperplasia medical treatment, noncancer prostate surgery,physician diagnosed benign prostatic hyperplasia, histological diagnosis andurinary flow rate. 3) Prior studies demonstrated that obesity increases the risk of lower urinary tract symptoms, as measured by a validated questionnaire. Also,most studies showed that physical activity significantly decreases the risk of benign prostatic hyperplasia.Conclusions: Obesity markedly increases the risk of benign prostatic hyperpla-sia. Since physical activity decreases the risk of benign prostatic hyperplasia,these observations support the development of novel prevention strategies andtreatment targeted toward adiposity, weight loss and lifestyle.

Key Words: prostate, prostatic hyperplasia, urination disorders, obesity,

metabolic syndrome X

BENIGN prostatic hyperplasia is a highlyprevalent disease in older men withsubstantial adverse effects on publichealth since 3 of 4 men 60 to 69 yearsold in the United States are affected, 21to 38 million hours of productivity arelost annually and more than $1 billion

per year in direct health care expendi-tures are consumed exclusive of outpa-tient medication.1 The primary clinicalmanifestation of BPH is the LUTS com-plex. As a result, BPH and LUTS re-main inextricably interconnected inthe contemporary study of and treat-

S102 www.jurology.com

Please cite this article as J Urol 2013;189: S102-S106. DOI: http://dx.doi.org/10.1016/j.juro.2012.11.029

0022-5347/13/1891-0102/0 http://dx.doi.org/10.1016/j.juro.2012.11.029

THE JOURNAL OF UROLOGY ® Vol. 189, S102-S106, January 2013© 2013 by AMERICAN UROLOGICAL A SSOCIATION EDUCATION AND R ESEARCH, INC. Printed in U.S.A.

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8/19/2019 Pi is 0022534712054948


ment for urinary symptoms in older men. LUTSaffects 15% to 60% of males older than 40 years andis associated with an increased risk of falls, signifi-cantly decreased quality of life, sadness, depression,impaired instrumental activity of daily life and de-creased SF-12® scores.2–5

Classic causal paradigms for BPH concentratedon relatively nonmodifiable etiological stimuli, in-cluding sex steroid hormones, genetic predispositionand age related detrusor changes. However recentobservations indicate that systemic metabolic dis-turbances may also contribute substantially to BPHpathogenesis.6 These data intimate that many of themetabolic disturbances associated with cardiovascu-lar disease and the lifestyle factors that modulatethese disturbances are associated with BPH onsetand progression. In this context accumulating evi-dence suggests that obesity promotes BPH. We re-

viewed published data on obesity, BPH, LUTS andphysical activity.

MATERIALS AND METHODS

We performed a structured, comprehensive literaturereview to identify studies of obesity, BPH, LUTS andphysical activity. We completed separate searches of theMEDLINE® database (January 1966 to April 2009), TheCochrane Library Central Search and the EMBASE™database (1980 to 2009). Initial search terms were benignprostatic hyperplasia, lower urinary tract symptoms andobesity. Subsequent search terms were physical activity

and exercise. To maximize inclusion of the most recentpertinent data we also examined reference sections inpublished articles, abstracts presented at the annualmeeting of the American Urological Association (2002 to2007) accessed on the American Urological Associationwebsite (www.auanet.org ) and unpublished data to whichwe had access.

RESULTS

This review revealed a number of subjective andobjective clinical definitions of BPH. Some entailed

validated questionnaires for LUTS combined withprostate examination and urinary flow rate, andothers entailed medical or surgical treatment, pa-tient reported history, physician diagnosis and his-tological diagnosis.

Also, obesity is a component of metabolic syn-drome, a clinical constellation of metabolic abnor-malities that increases the risk of cardiovasculardisease. In the several published definitions of met-abolic syndrome there is no consensus about whichanthropometric measures should be used to defineobesity, that is BMI, waist circumference or waist-to-hip ratio.7

Overall published evidence supports strong asso-ciations of obesity with BPH. This evidence encom-

passes most established metrics of adiposity, includ-ing BMI, waist circumference and waist-to-hip ratio,and involves 3 general categories of outcome, that isprostate volume, BPH and LUTS (see table).

Obesity and Increased Prostate Volume

Prior studies consistently showed that increased ad-iposity, as determined by most anthropometric mea-sures, is positively associated with ultrasound andmagnetic resonance imaging measured prostate vol-ume. The greater the adiposity, the greater the pros-tate volume. Increased prostate volume is clini-cally relevant, in that it strongly predicts adverseclinical outcomes associated with BPH, including acute urinary retention and renal failure.8,9 Bodyweight,10,11 BMI11–15 and waist circumference11,13

were positively associated with prostate volume inmultiple study populations. In the BLSA cohorteach 1 kg/m2 increase in BMI corresponded to a0.41 cc (95% CI 0.15– 0.84) increase in prostate

volume (p-trend 0.06).11

Moreover, obesity is associated with prostate en-largement. In BLSA obese (BMI 35 kg/m2 or greater)participants were at 3.5-fold increased risk for pros-tate enlargement, defined as magnetic resonance im-aging determined prostate volume 40 cc or greater,compared to nonobese (BMI less than 25 kg/m2) par-ticipants.11 A recent analysis of more than 16,000radical prostatectomy specimens validated thesefindings (Parsons et al, unpublished data). Multivar-iate adjusted analysis revealed that each 1 kg/m2

increase in preoperative BMI was associated with a0.45 gm (95% CI 0.35–0.55) increase in total pros-tate weight (p-trend 0.001). Moreover, there was a41% increased risk of prostate enlargement, definedas total prostate weight 40 gm or greater, in obese(BMI 35 kg/m2 or greater) compared to nonobese(BMI less than 25 kg/m2) men (OR 1.41, 95% CI1.01–1.95). These observations suggest that adipos-ity is linked to prostate growth.

Obesity and BPH

Most studies showed that obesity increases the risk

of BPH, as defined by several measures. Of almost26,000 male participants in HPS those with an obesewaist circumference (greater than 109 cm) were 38%(OR 1.38, 95% CI 1.01–1.95) more likely to undergoBPH surgery than those with a nonobese waist cir-cumference (less than 89 cm).16 In a case-controlstudy of 500 Chinese men those with the highestwaist-to-hip ratio were 41% more likely (OR 1.41,95% CI 1.01–1.95) to undergo BPH surgery thanthose with the lowest waist-to-hip ratio.17 Finally, in5,700 American men participating in the PCPT theincidence of BPH, defined as consistently severe uri-nary symptoms on the I-PSS, initiation of medicaltherapy or surgery, increased 10% for each 0.05increase in the waist-to-hip ratio.18 Also, a BMI of 30

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to 34 kg/m2 was associated with a 30% increasedrisk of BPH relative to a BMI of less than 25 kg/m2

(OR 1.30, 95% CI 1.08–1.57). Notably the PCPTtracked incident BPH for up to 7 years and to ourknowledge is the largest incident analysis of obesityand BPH to date.

Results in a case-control study of 3,000 Italianmen also showed a link between obesity and BPHbut were somewhat more equivocal.19 Men with alowest lifelong BMI of 23.7 kg/m2 or greater were56% more likely to have histological BPH than menwith a lowest lifelong BMI of 20.7 kg/m2 or less butBMI and waist circumference at evaluation wereinversely associated with BPH risk, as defined byhistological diagnosis. Furthermore, 2 smaller stud-ies showed no links between obesity and BPH. An

analysis of 475 American men enrolled in the Olm-sted County cohort showed no associations of obesitywith peak urinary flow rate or acute urinary reten-tion,20 while a case-control study in 870 Western

Australian men revealed no associations of obesitywith BPH surgery.21 Although a cohort analysis of United States Air Force veterans did not demon-strate any linear associations of BMI with physiciandiagnosed BPH, this study did not present data onBPH and obesity.22

Obesity and LUTS

Several studies showed that obesity increases therisk of LUTS, as measured by a questionnaire.Obese men in the HPS were 100% more likely (OR2.00, 95% CI 1.01–1.95) to report LUTS, defined asresponses to a questionnaire encompassing storageand voiding symptoms, compared to men with anonobese waist circumference.16 In 2,800 men inNHANES III an increase in BMI during adulthoodand obese waist circumference were associated withincreased LUTS, defined as at least 3 of certainsymptoms, including nocturia, incomplete emptying,weak stream and hesitancy.23 In the second Nord-Trøndelag Health Study in 21,700 Norwegian menobese BMI and an increased waist-to-hip ratio wereassociated with increased LUTS, as measured by

I-PSS.24 In a cohort of 1500 Austrian men there wasa trend toward higher I-PSS with increased waistcircumference but not with increased BMI.25 Therewere no associations of BMI determined obesity withLUTS in a cohort of black American men26 or in acohort of Chinese men.27

Physical Activity, BPH and LUTS

Obesity is strongly associated with a lack of physicalactivity. Accordingly increased physical activity hasbeen linked to a decreased risk of BPH surgery,28,29

clinical BPH,30,31 histological BPH32 and LUTS.29,33

A meta-analysis of 11 published studies indicatedthat moderate to vigorous physical activity de-creased the risk of BPH or LUTS by as much as 25%relative to a sedentary lifestyle.34 The strength of

the protective effect appeared to be greater at higheractivity levels but there was a nonsignificant trendtoward a protective effect with even light physicalactivity. Adjusting for multiple confounders under-scored the independence of the protective effect of physical activity toward BPH.

A decreased risk of BPH with increased physicalactivity provides further evidence of a link betweenobesity and BPH. Moreover, this observation inti-mates that lifestyle changes may alter the naturalhistory of BPH.

DISCUSSION

Thus, obesity increases the risk of BPH by multipleoutcome measures. The public health import of thisobservation is considerable. The prevalence of obe-sity continues to increase and obesity now affectsmore than a third of American men.35 BPH alsoaffects a broad swath of the older male population,which (like obesity) grows larger each year. By 2030,20% of the American population will be 65 years oldor older, including more than 20 million men.36 Theconfluence of these 3 trends, that is an increasedBPH risk with obesity, the obesity epidemic and therapid aging of the population, suggests the gather-ing of a perfect storm that will markedly swell the

Select studies of obesity, BPH and LUTS

Study Population (outcome measure) Risk Factor Referent OR (95% CI)

BLSA11 (prostate vol 40 cc or greater) BMI greater than 35 mg/kg2 BMI less than 25 kg/m2 3.52 (1.45–8.56)

HPS:16 Waist circumference greater than 109 cm Waist circumference less than 89 cm

BPH surgery 2.38 (1.42–3.99)

LUTS 2.00 (1.47–2.72)

Nord-Trøndelag Health Study 224 (LUTS) BMI 40 mg/kg2 or greater BMI less than 25 mg/kg2 1.79 (0.90–3.56)PCPT18 (incident BPH*) BMI 30–35 mg/kg2 BMI less than 25 mg/kg2 1.30 (1.08–1.57)

Shanghai case-control17 (BPH surgery) Waist-to-hip ratio greater than 0.923 Waist-to-hip ratio less than 0.856 1.41 (1.01–1.95)

NHANES III23 (LUTS) Waist circumference greater than 102 cm Waist circumference less than 94 cm 1.48 (0.87–2.54)

Flint Men’s Health Study26 (LUTS) BMI 30 mg/kg2 or greater BMI less than 25 mg/kg2 1.13 (0.75–1.70)

Hong Kong cohort27 (LUTS) BMI 25 mg/kg2 or greater BMI less than 23 mg/kg2 1.08 (0.84–1.38)

* Defined as consistently severe urinary symptoms on I-PSS, initiation of medical therapy or BPH surgery.

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ranks of men with BPH in the near future and placeever greater burdens on finite health care resources.

These observations are also important becausethey intimate the existence of modifiable pathwaysfor BPH that represent novel targets for preventionand treatment by modulating adiposity. Also, the

robust, significant inverse association of physicalactivity with BPH justifies the design and imple-mentation of clinical trials using weight loss, exer-cise and lifestyle alterations. To our knowledgethere are no published studies to date of the effect of such interventions on BPH or LUTS. Further stud-ies should determine optimum physical activity lev-els and the relative importance of targeting adipos-ity vs overall body weight to achieve a therapeuticeffect.

These data are observational and, thus, shouldserve primarily as a guide to inform the design of

future clinical trials. However, there is little if anynegative side to promoting healthy lifestyle inter-

ventions, specifically increased physical activity andweight loss, in obese older men to prevent or atten-uate BPH, particularly since such interventionshave proven benefits to overall and cardiovascularhealth.

To our knowledge the physiological mechanisms bywhich obesity promotes BPH remain to be described. A potential explanation is systemic inflammation. Obe-sity is a component of metabolic syndrome,7 and obe-sity and metabolic syndrome are associated with sys-

temic inflammation and oxidative stress.37

There aremultiple lines of evidence connecting BPH with in-flammation. 1) BPH in surgical specimens is associ-ated with inflammation,38–40 and the extent and se-

verity of inflammation correspond to the amount of prostate enlargement.41 2) In NHANES III higher se-rum C-reactive protein was associated with an in-creased risk of LUTS.42 3) In the Olmsted county co-hort daily nonsteroidal anti-inflammatory use was

associated with a 27%, 49% and 47% decreased risk of LUTS, low urinary flow rate and enlarged prostate,respectively.43 Thus, it is possible that BPH representsa nonmalignant pathway of unregulated prostategrowth promoted by oxidative stress and inflamma-tory mediators.

The extent to which obesity may influence BPHindependent of sex steroid hormones is also unclear.Since increased adiposity promotes increased aro-matization of circulating testosterone into estrogen,alterations in the balance between testosterone andestrogen in prostate tissue may possibly contributeto BPH pathogenesis. However, the BLSA controlledfor serum total and free testosterone, suggesting that obesity may influence prostate growth throughmechanisms other than sex steroid growth path-ways.11

While these data are compelling, they are primar-

ily cross-sectional. Moreover, it is unclear as to howobesity interacts with other components of metabolicsyndrome, including glucose insensitivity, dyslipide-mia and hypertension. Additional longitudinal anal-yses of incident BPH and LUTS may be needed toelucidate these pathways. These analyses shouldexplore correlations among variables and incorpo-rate evaluations of prevalent and incident healthconditions that could confound associations of obe-sity with BPH and LUTS. Such analyses would fa-cilitate the development and implementation of ef-ficacious prevention strategies.

CONCLUSIONS

Obesity substantially increases the risk of BPH.Since physical activity decreases BPH risk, theseobservations support the development of novel strat-egies for BPH prevention and treatment targetedtoward adiposity, weight loss and lifestyle interven-tions.

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