Prostate Cancer and Prostatic Diseases (2012) 15, 265272

& 2012 Macmillan Publishers Limited All rights reserved 1365-7852/12

www.nature.com/pcan

ORIGINAL ARTICLE

Body mass index and risk of BPH: a meta-analysis

S Wang, Q Mao, Y Lin, J Wu, X Wang, X Zheng and L Xie

Department of Urology, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China

BACKGROUND: Epidemiological studies have reported conflicting results relating obesity to BPH. A meta-analysis of
cohort and casecontrol studies was conducted to pool the risk estimates of the association between obesity and BPH.

METHODS: Eligible studies were retrieved by both computer searches and review of references. We analyzed abstracted
data with random effects models to obtain the summary risk estimates. Doseresponse meta-analysis was performed for
studies reporting categorical risk estimates for a series of exposure levels.

RESULTS: A total of 19 studies met the inclusion criteria of the meta-analysis. Positive association with body mass index
(BMI) was observed in BPH and lower urinary tract symptoms (LUTS) combined group (odds ratio 1.27, 95% confidence
intervals 1.051.53). In subgroup analysis, BMI exhibited a positive doseresponse relationship with BPH/LUTS in
population-based casecontrol studies and a marginal positive association was observed between risk of BPH and increased
BMI. However, no association between BPH/LUTS and BMI was observed in other subgroups stratified by study design,
geographical region or primary outcome.

CONCLUSIONS: The overall current literatures suggested that BMI was associated with increased risk of BPH. Further
efforts should be made to confirm these findings and clarify the underlying biological mechanisms.

Prostate Cancer and Prostatic Diseases (2012) 15, 265272; doi:10.1038/pcan.2011.65; published online 20 December 2011

Keywords: body mass index; BPH; meta-analysis

Introduction as body mass index (BMI) with less interest in waist

BPH and concomitant lower urinary tract symptoms
(LUTS) are the most common non-malignant medical
conditions of the prostate occurring in middle aged and
older men.1 BPH is an enlargement of the prostate gland
tissue and narrowing of the urethra characterized by
overgrowth of the transitional and periurethral area
resulting from proliferation of stromal and glandular
elements. LUTS, generally regarded as primary clinical
manifestation of BPH, encompasses disorders of bladder
storage or emptying. According to the recent epidemio-
logical study,2 BPH affects 70% of men 6069 years old
and 80% of those X70 years old. Identification of
potentially modifiable factors contributing to its cause
may help reduce the burden of this disease.
Body size and composition have long been hypothe-
sized to influence the risk of prostate hyperplasia.
Scientific interest in anthropometric measurements and
prostate hyperplasia has mainly been focused on height,
weight and measures of weight adjusted for height, such
Correspondence: Dr L Xie, Department of Urology, First Affiliated
Hospital, School of Medicine, Zhejiang University, Qingchun,
Hangzhou 310003, China.
E-mail: xielp@zjuem.zju.edu.cn
Received 25 July 2011; revised 14 October 2011; accepted 5 November
2011; published online 20 December 2011
circumference and its ratio to hips circumference.
Although a cluster of published epidemiological evi-
dence demonstrates that obesity may increase the risks of
BPH and LUTS,35 it still lacks the quantitative evidence
to certify this association. To provide a comprehensive
summary of the relation between obesity and BPH risk,
we use the BMI as the measure of obesity to summarize
the evidence from the epidemiological literature on this
issue. We also sought to address the sources of
heterogeneity including study design and geographic
distribution.
Materials and methods
Search strategy
A literature search of MEDLINE database using
PubMed, Web of Science and the Cochrane Library was
conducted to identify potential epidemiological studies
up to December 2010. The following key words were
used to search the published literature: BPH, LUTS and
obesity. References in the retrieved publications, as well
as those in previous systematic review, were checked for
any other pertinent studies. For inclusion in this analysis,
eligible studies had to fulfill all the following inclusion
criteria: (a) casecontrol or cohort study published as an
 BMI and risk of BPH
S Wang et al
266 original article; (b) papers reported in English between
1980 and December 2010; and (c) papers providing odds
ratio (OR) or relative risk (RR) with corresponding 95%
confidence intervals (CI) (95%) adjusted at least for age
or sufficient information allowing us to compute them.
In studies with overlapping patients or controls, only the
latest or the most complete was included. Any study
with inconsistent or erroneous data was excluded.
Meeting abstracts with insufficient data or unpublished
reports were not considered.
Data extraction
Two investigators (SW and QM) independently extracted
data from all potentially relevant studies. Conflicting
evaluations were resolved by either discussion or third-
party resolution. Data extracted from these articles
included the name of the first author, year of publication,
study design, outcomes definition, sample size, geogra-
phical region, exposure assessment and the covariates
included in the final adjusted models. For studies that
reported separate adjusted ORs for several BMI strata,
we abstracted the adjusted OR comparing the highest
category of BMI with the lowest category (reference
group).
Statistical analysis
We performed all statistical analyses utilizing Stata/SE
11.0 (Stata Corporation, College Station, TX, USA)
commercial software with the most recent updates for
meta-analysis commands. The OR was used as a
measure of the RR for all studies, and the RR estimates
were log-transformed. The data from individual studies
was pooled utilizing the random-effect model with the
DerSimonian-Laird method6 in our analysis, which
consider both within-study and between-study variation.
We performed subgroup analyses based on likely sources
of between-study heterogeneity, such as study design,
geographical region and primary outcome of BPH.
For the doseresponse meta-analysis, we included
studies considering at least three levels of BMI, and
providing the number of case patients and control
subjects in each exposure category. For results reported
in categories of BMI, these were transformed to an
estimate per unit increase in BMI. To treat BMI as a
continuous exposure variable, we assigned the level of
BMI from each study to these categories based on the
calculated midpoint of BMI. For open-ended categories
the approximate midpoint was set at double the distance
between the midpoint and upper bound of the closest
category. The log RR, as well as the BMI, for the reference
category was set to zero (corresponding to a RR of one).
We subtracted the midpoint BMI of this category from
the midpoint BMI of all other categories. A weighted
regression was then fit through the origin where
the exposure was at the reference level with log RR
zero. The regression was weighted by the inverse
variance of the log RR for each category. The correlation
between categories was estimated using method of
Greenland et al.7
Between-study heterogeneity across the eligible com-
parisons was quantitatively assessed using the w2-based
Q statistical test and I2 score.8,9 Heterogeneity was
considered statistically significant when a two-sided
Prostate Cancer and Prostatic Diseases
Po0.05. Meta-regression analysis was used to explore
the influence of publication year, sample size, geogra-
phical region and method of BMI assessment in the
heterogeneity. Publication bias assessment was per-
formed using the Egger regression asymmetry test10
and the Begg adjusted rank correlation test.11 Po0.05
was considered indicative of significant publication bias.
Result
We identified 188 potentially relevant abstracts in our
initial search. Of these, 154 were unrelated or not original
research articles. Upon closer examination, 15 studies
were excluded for the following reasons: 4 studies1215
were not casecontrol or cohort studies, 9 studies did not
provide sufficient information to estimate a summary OR
and its 95% CI1623 or a summary OR adjusted for age.24
One study25 evaluated OR and its 95% CI with weight
and height, respectively, but no BMI. One study26
researched the relationship between BPH and BMI in
the form of annual growth rates.
The remaining 19 articles2745 that examined the risk
of BPH and LUTS with BMI were chosen for
detailed review. The finally selected studies included
7 cohort studies27,28,30,32,36,39,42 and 12 casecontrol stu-
dies29,31,3335,37,38,40,4345 (Table 1). Nine of these studies
were conducted in the United States,27,28,30,32,34,36,39,41,43
four were in Europe,31,35,38,44 four in East Asia,37,40,42,45
one in Middle East29 and one in Australia.33 Of the 19
studies, 15 used BPH2740,45 and 4 used LUTS4144 as the
primary outcome. Four studies28,30,32,41 provided ORs,
respectively, with different outcomes but no total OR. So,
we defined prostate volume 430 cm3,28 prostate volume
440 cm3,32 surgery30,41 as BPH, and AUASI score47,28
AUASI score414,32 frequent urinary obstructive
symptoms without surgery30,41 as LUTS. Thus, we
pooled the ORs of these four studies mentioned above
separately when subgroup analyses were performed
according to BPH or LUTS alone.
BPH and LUTS combined
Fifteen studies were included in the meta-analy-
sis.27,29,31,3340,4245 When BPH and LUTS were com-
bined, we observed that the BMI was associated with
BPH or LUTS (Figure 1, OR 1.23, 95% CI 1.031.48) and
the summary OR were similar in population-based case
control study, whereas the summary OR in cohort study
and hospital-based casecontrol study showed no asso-
ciation between BMI and BPH/LUTS. Heterogeneity was
detected (Po0.05) among all studies and in the subgroup
of population-based casecontrol studies. On the con-
trary, there was no evidence of heterogeneity in cohort
and hospital-based casecontrol studies. To explore the
source of the heterogeneity, we pooled the OR estimates
by geographical region (United States, Europe, East Asia,
Middle East and Austrian). As shown in Table 2, the OR
estimates from subgroups of the United States, Europe,
East Asia and Austrian showed that BMI was not
associated with the likelihood of BPH/LUTS when
analyzed by geographical regions. A positive relation-
ship between BMI and risk of BPH/LUTS was observed
in the Middle East, although it only included one study.
 Table 1 Study characteristics of published cohort and casecontrol studies on BMI and BPH
References Study design Geographical Sample size Outcome Definition of outcome Adjusted variables BMI assessment
region

Seitter and Barrett- Cohort United States 929 BPH Surgery Age Researcher
Connor39 measured
Porta et al.35 Pop c/c Europe 1063 BPH Prostatic disorders (no detail) Age Interview
Giovannucci et al.30 Cohort Europe 25 892 BPH Surgery or obstructive symptoms Age, smoking and waist circumference Questionnaire
without surgery
Gann et al.34 Pop c/c United States 640 BPH Surgery Age, diastolic blood pressure, exercise and Questionnaire
alcohol
31
Signorello et al. Hosp c/c Europe 430 BPH Surgery Age, height and years of schooling Interview
Meigs et al.27 Cohort United States 1019 BPH Clinical diagnosis or an interim TURP Age, marital status, waist-to-hip ratio, Researcher
hypertension, alcohol consumption, heart measured
disease and medication use
Dahle et al.40 Hosp c/c East Asia 502 BPH Surgery Age, education and waist-to-hip ratio Interview
Rohrmann et al.41 Pop c/c United States 2797 LUTS 3/4 Symptoms from AUA symptom Age, race, waist circumference, cigarette Interview
score with correlation to AUA index smoking and physical activity
or non-cancer surgery
Zucchetto et al.38 Hosp c/c Europe 2820 BPH Histologically confirmed Age, center, education and physical activity Interview
Rohrmann et al.43 Pop c/c United States 3446 LUTS IPSS48 Age and zygosity Interview
Seim et al.44 Pop c/c Europe 21 694 LUTS IPSS48 Age Researcher
measured
S Wang et al

Burke et al.28 Cohort Europe 2064 BPH AUASI score 47, Prostate volume Age Researcher
430 cm3 measured
Lee et al.45 Hosp c/c East Asia 146 BPH Prostate volume 4 20 cm3 Age and waist circumference Researcher
BMI and risk of BPH

measured
32
Parsons et al. Cohort United States 422 BPH Prostate volume 4 40 cm3, AUASI Age, waist circumference, fasting glucose and Researcher
score 414 diabetes measured
Wong et al.42 Pop c/c East Asia 1738 LUTS IPSS48 Age, CHD, HTN, b-blocker, physical activity Researcher
and alcohol consumption measured
33
Fritschi et al. Pop c/c Australia 869 BPH Surgical treatment Age Questionnaire
Xie et al.37 Pop c/c East Asia 649 BPH Prostate volume 420 cm3 Age Interview
Kristal et al.36 Cohort United States 4770 BPH Surgery, medical treatment, repeat Age, race/ethnicity and baseline IPSS Researcher
IPSS 14 or greater measured
Safarinejad29 Pop c/c Middle East 8466 BPH IPSS47, maximum flowo15 ml s1, Age and race Interview
prostate size 430 gm
Abbreviations: AUA, American Urological Association; AUASI, American Urological Association Symptom Index; BMI, body mass index; CHD, coronary heart disease; Hosp c/c, Hospital based casecontrol study;
HTN, hypertension; IPSS, International Prostate Symptom Score; LUTS, lower urinary tract symptoms; Pop c/c, population based casecontrol study.
267

Prostate Cancer and Prostatic Diseases

 BMI and risk of BPH
S Wang et al
268

Figure 1 A forest plot showing risk estimates from casecontrol and cohort studies, estimating the association between BMI and risk for
BPH/LUTS. BMI, body mass index; Hosp c/c, Hospital based casecontrol study; LUTS, lower urinary tract symptoms; Pop c/c, population
based casecontrol study.

Table 2 Summary of pooled odds ratios of BPH by geographical region and outcome
Subgroup Number of studies Pooled OR Q-test for heterogeneity Eggers test Beggs test
(95% CI) P-value (I2 score) P-value P-value

All studies 15 (refs 27,29,31,3340,4245) 1.23 (1.031.48) o0.001 (74.0%) 0.21 0.43

Geographical region
United States 9 (refs 27,34,36,39,43) 1.09 (0.891.32) 0.066 (54.6%) 0.64 0.62
Europe 4 (refs 31,35,38,44) 1.09 (0.751.57) 0.173 (39.8%) 0.40 0.50
East Asia 4 (refs 37,40,42,45) 1.37 (0.981.92) 0.203 (34.9%) 0.14 0.50
Middle East 1 (ref. 29) 2.7 (1.963.72)
Australia 1 (ref. 33) 0.88 (0.571.35)

Primary outcome
BPH 16 (refs 2741,45) 1.21 (1.001.46) o0.001 (74.5%) 0.24 0.21
LUTS 7 (ref. 28,30,32,4144) 1.11 (0.841.47) 0.004 (68.3%) 0.13 0.45
Abbreviation: LUTS, lower urinary tract symptoms.

The results from subgroups analyses above were non-
heterogeneous except the group of United States. We also
used meta-regression analysis to explore the influence of
publication year, sample size and method of BMI
assessment on the heterogeneity. However, none was
identified as a possible source of heterogeneity among all
the included studies. No publication bias was found
among all studies (P 0.21 by Eggers test) or in any
subgroup either with the Eggers or Beggs test (Table 2).
We also performed sensitivity analysis by sequentially
excluding one study in each turn to examine the
influence of a single study on the overall estimate or in
any strata. The results showed that none of the study
could considerably affect the summary of risk estimates
in our meta-analysis (data not shown). It confirmed the
stability of our results.
BPH alone
To further explore the association of BMI with BPH
alone, we excluded the four studies from analysis that
used LUTS as the primary outcome and added four
studies28,30,32,41 mentioned before, and then repeated the
pooled analyses. The summary OR of BPH was 1.21
(Figure 2, 95% CI 1.001.46) for subjects in the highest
category of BMI compared with those in the lowest
category. The result was heterogeneous and there was no
evidence of significant publication bias either with the
Eggers or Beggs test in this subgroup.
LUTS alone
Of the studies that used LUTS as the primary outcome
one demonstrated an increased likelihood of LUTS43 and

Prostate Cancer and Prostatic Diseases


Figure 2 Forest plots showing the risk estimates of each study and the pooled risk estimates for BPH and LUTS, respectively. LUTS, lower
urinary tract symptoms.
one a decreased30 likelihood of LUTS with increased
BMI. In this pooled subgroup analysis, the BMI was not
significantly associated with the likelihood of LUTS
(Figure 2, OR 1.11, 95% CI 0.841.47). There was some
evidence of heterogeneity among all these studies. No
publication bias was detected among this subgroup.
Doseresponse analysis
As in the population-based casecontrol group, the BMI/
LUTS was associated with increased risk of BPH; we
further performed the doseresponse analysis for this
group. The doseresponse meta-analysis included seven
studies.3335,37,4244 An increase in BMI of 1 kg m2 was
statistically significantly associated with a 4.7% ((95% CI
1.5, 8.0%), Pheterogenityo0.001). In meta-regression analy-
sis, we explored the influence of publication year,
geographical region, sample size, method of BMI
assessment and primary outcome in the heterogeneity.
However, none of these above was identified as a
possible source of heterogeneity among all the included
studies.
Discussion
In this pooled analysis of published cohort and case
control studies, elevated BMI could increase the risk of
BPH or LUTS. Similar risk was seen among population-
based casecontrol studies group. We also noted a
marginal positive association between risk of BPH and
BMI and risk of BPH
S Wang et al
269
increased BMI. Thus, our results may reflect the trend
toward increased risk of BPH with increased BMI.
Interestingly, the significant association did not extend
to LUTS. This observation likely reflects inherent
differences between BPH and LUTS as distinct condi-
tions. LUTS is a relatively recent term describing a
particular phenotype, that is, a quantifiable manifesta-
tion of a group of disorders affecting the prostate and
bladder that share a common clinical outcome. The term
includes the BPH component but acknowledges that
other factors, primarily those related to the bladder,
may contribute to the genesis of these symptoms.
Thus, the symptom severity does not correlate with
prostate volume. Obesity exerts several systemic effects,
including increased intra-abdominal pressure which in
turn increased bladder pressure and intravesical pres-
sure, with the potential to exacerbate bladder directed
LUTS.
The world has globally seen a dramatic rise in the levels
of obesity and obesity-related disorders, including hyper-
tension, diabetes mellitus and dyslipidemia.46 Together
these entities comprise the metabolic syndrome, which
as defined by the Adult Treatment Panel III includes
three or more of the following findings, central obesity
(waist circumference 4102 cm), triglycerides more than
150 mg dl1, high-density lipoprotein less than 40 mg dl1,
BP more than 135/85 mm Hg and fasting plasma glucose
more than 110 mg dl1.47 There has been a conceptual
model posits that to a large extent systemic metabolic
disturbances may drive BPH pathogenesis.3 A growing
body of evidence has demonstrated increased adiposity,
disruptions in glucose homeostasis, lower high-density
Prostate Cancer and Prostatic Diseases
 BMI and risk of BPH
S Wang et al
270 lipoprotein cholesterol and higher low-density lipopro-
tein cholesterol have a strong and independent link with
an increased likelihood of BPH.3,4 In addition, basic
science researches demonstrate physiological connec-
tions of metabolic disturbances with BPH. In an animal
model, rats fed a high-fat diet, leading to hyperlipidemia,
are found to develop prostatic enlargement and bladder
overactivity.48
Obesity has been hypothesized to be associated with
BPH because of the endocrine changes in men that occur
with age. Abdominal obesity increases the estrogen to
androgen ratio and may increase sympathetic nervous
activity, both known to influence the development of
BPH and the severity of urinary obstructive symptoms.30
An alternative mechanism for BPH may be related to
association of obesity with inflammation and oxidative
stress.49 Analyses of surgical specimens have shown that
is usually associated with inflammation50 and that the
extent and severity of the inflammation corresponds to
the amount of prostate enlargement.51 Thus, it is possible
that obesity promotes microvascular disease and inflam-
mation, which in turn contribute to ischemia, oxidative
stress and an intraprostatic environment favorable to
BPH.
In our analysis, further quantitative assay stratified by
regional information yielded null results in most
subgroups. However, it should still be interpreted with
caution considering the limited number of primary
studies. The null results could possibly be due to an
inadequate number of primary studies to detect the
strength of the postulated associations. Also, there
existed a possibility that the complex etiology of BPH,
which included genetic susceptibility, culture and life-
styles, would probably mask the positive association,
whereas a single study in our analysis could not provide
sufficient information. But a positive relationship be-
tween BMI and risk of BPH/LUTS was observed in
Middle East. This difference may, in part, be due to
differences in diet, environment and ethic background in
this region.
The results of the studies included in this analysis
were heterogeneous, likely reflecting differences among
study populations, model selection, analytic methodol-
ogy, exposure assessment and operational definitions of
BPH/LUTS. We conducted a meta-regression analysis to
assess the effect of publication year, geographical region,
study design, primary outcome, sample size and BMI
assessment on the heterogeneity. However, none of
the confounding factors could explain heterogeneity
between the individual studies. Our results from
subgroup analysis also could not demonstrate any
stratified association. We speculated the variations in
extent of adjustment for confounding variables such as
dietary or lifestyle characteristics, and uniform outcome
assessment may be the source of heterogeneity, but
it cannot be verified by meta-regression analysis
or subgroup analysis. The presence of heterogeneity
indicates the need for consensus definitions for BPH and
LUTS in future population-based studies.
As a meta-analysis of previously published observa-
tional studies, our study has several limitations that need
to be taken into account when considering its contribu-
tions. First, because we did not attempt to uncover
unpublished observations and not include studies with
insufficient information to estimate an adjusted OR, this
Prostate Cancer and Prostatic Diseases
could have brought a publication bias even though no
significant evidence of publication bias was observed in
Eggers and Beggs test. Second, the limited number of
studies and the heterogeneity in the doseresponse meta-
analysis could possibly result in inaccurate estimates.
Third, the BMI levels in the lowest and highest categories
and the range of BMI varied across studies. These
differences may have contributed to the heterogeneity
among studies in the analysis of the highest versus the
lowest categories.
Some articles5253 had hypothesized the reason of
inconsistent results for BMI in obesity-related diseases. It
was that BMI was an imperfect measure of obesity that
combines adipose and non-adipose body components.
However, we still used BMI as the measure because there
was no feasible variable that could address this issue
well in most studies. So it left some problems still in
vague. Is the risk of BPH due to increased BMI largely
driven by adipose or non-adipose mass or both? Does
distribution of adipose mass matter? Future research to
confirm these conclusions is warranted.
Conclusions
In summary, this study applied a detailed meta-analytic
approach for combining OR estimates from studies on
the relationship between BPH and LUTS incidence and
BMI. Although we cannot reject the possibility that our
estimates were distorted because of residual confound-
ing, the overall current literature suggests significant
association on the risk of BPH and obesity; and a further
exploration of population-based casecontrol study in
doseresponse manner indicated that BMI could increase
risk for BPH. However, when the including studies were
stratified by study design, geographical region and
primary outcome, most of the subgroups shows BMI is
not associated with BPH/LUTS.
While this meta-analysis helps resolve some of the
inconsistencies with obesity and BPH risk, some do
remain. Future researches are needed to confirm these
findings and resolve the remaining problems. A greater
understanding of what influences risk and progression
of BPH would lead to a greater understanding of the
likely biological mechanisms for this disease.
Conflict of interest
The authors declare no conflict of interest.
Acknowledgements
This study was supported by grants from the National
Natural Science Foundation of China (Grant No.
30801370).
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