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Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20852-7234 [A. W. H.]; Shanghai Cancer Institute, Shanghai, China [J. D., Y-T. G.]; University of Southern California, Los Angeles, California 90033 [F. Z. S.]; University of Rouen, 76031 Rouen, France [J. B.]; Armed Forces Institute of Pathology, Washington, DC 20306 [I. A. S., F. K. M.]; and Department of Urology, Shanghai First Municipal Hospital, Shanghai, China 20032 [T. X.]
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Although the reported incidence in Shanghai is one of the lowest in the world, rates are rising rapidly, increasing 70% between 1972–1977 and 1990–1994 (4) . Reasons for the rapid increase in prostate cancer incidence in China are unclear. However, screening alone is unlikely to explain the rapidly rising rates in this population because clinical prostate cancer is rare there, and screening is relatively uncommon (4) . It is possible that increased westernization and changes in lifestyle may have contributed to some of the rapid rise in incidence.
Westernization has been linked to the increased prevalence of obesity and animal fat intake. Obesity in turn is associated with several hormone-related malignancies and various endocrine and metabolic changes, including lower levels of SHBG2 and higher levels of free estradiol (5, 6, 7) . The role of obesity in prostate cancer, however, is less clear. Results from previous studies have been inconsistent; most reported no association (8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20) , and some reported a positive association with BMI (21, 22, 23, 24, 25, 26) , body weight (27 , 28) , right upper arm circumference (29) , or upper body robustness (i.e., biacromial breadth-to-height ratio and biacromial and bideltoid breadths; Ref 30 ). One prospective study reported an inverse relationship with obesity at age 21 and a positive association with smaller hips and larger WHR for metastatic cancer (31) . Most epidemiological studies to date have focused on adult BMI and few have examined the role of preadult obesity or body fat distribution.
During 1993–1995, we conducted a population-based case-control study in Shanghai, China, to investigate reasons for the extremely low risk of clinical prostate cancer in this population and to identify factors that may help explain the rapid rise in incidence. Using data from this study, herein we report the relationships of obesity as well as body fat distribution with prostate cancer risk.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Information on potential controls was obtained from the personal identification cards maintained at the Shanghai Resident Registry, which contains personal registry cards for all adult residents (>18 years of age) in urban Shanghai. The cards contain name, address, date of birth, gender, and other demographic factors. Those who were deceased, had a history of cancer, or had moved out of the area before the sampling of controls were not eligible for the study. A total of 495 controls were selected randomly from among permanent residents of Shanghai (6.5 million) and frequency-matched to the age distribution (in 5-year age categories) of prostate cancer cases. Study staff visited the home of each selected control to verify his eligibility for the study.
Interview.
An in-person interview was conducted to elicit the following
information: (a) demographic characteristics; (b)
dietary history; (c) consumption of cigarettes and alcohol
and other beverages; (d) medical history; (e)
family history of cancer; (f) physical activity;
(g) body size; and (h) sexual behavior. Cases
were interviewed at the hospital, whereas population controls were
interviewed at home. Of the 268 eligible cases, 243 (91%) were
interviewed. On average, cancer cases were interviewed within 20 days
of diagnosis. Of the 495 eligible controls, 471 (95%) were interviewed
and 313 (66%) underwent digital rectal examination and
prostate-specific antigen testing to identify prostate-related
disorders.
Anthropometric Factors.
Information on self-reports of adult height, usual adult weight, weight
history at various time points in life (at 20–29, 40–49, and 60–69
years of age, and in 1988; hereafter referred to as "the four time
points"), perceived body size at the four time points and at 8–9
years of age, maximum adult weight, and the duration of maximum weight
were elicited during interview. In addition, after interview, standing
height, weight, and circumferences of waist, hip, and right upper arm
were measured. Each measurement was taken twice. If the difference
between two measurements was larger than a predetermined tolerance
(waist, 2.0 cm; hip, 2.0 cm; and right upper arm, 0.8 cm), a third
measurement was taken.
Pathology Review.
Pathology slides of cases were reviewed by Shanghai study pathologists
to confirm the diagnosis and staging of prostate cancer. Subsequently,
all pathology slides were reviewed again independently by two
pathologists from the Armed Forces Institute of Pathology (I. A. S.
and F. K. M.), and a consensus review was held with the Shanghai
pathologists to further confirm the diagnosis. After the consensus
review, five cancer cases were determined to have benign prostatic
hyperplasia and were excluded from the study, leaving 238 cases
for analysis.
Statistical Analysis.
ORs and 95% CIs for prostate cancer in relation to
anthropometric variables were estimated using multiple logistic
regression analysis (34)
. In the standard model, age at
interview, education (none, primary-junior high, 
senior high),
marital status (currently married or other), and total calories were
included as potential confounding factors. Total caloric intake was
included because it was found to be related to both body size and
prostate cancer risk in this study population (the dietary results are
reported separately). BMI, expressed as weight divided by the square of
height (kg/m2
), was developed as a measure of
overall obesity, whereas WHR was used as a measure for abdominal
obesity (or upper-body fat). Because waist or hip circumference was
related to height and weight, we included BMI in the regression models
to estimate the net effect of these two anthropometric factors. In
selected analyses, cases were additionally divided into localized and
regional/remote categories to evaluate the effect of cancer on these
anthropometric factors and to assess whether body size is related to
progression of prostate cancer. Smoking, use of alcohol, and other
dietary or lifestyle factors were also included in additional analyses.
We derived population-attributable risk estimates for the study population by an approach based on logistic regression (35 , 36) to control for age, education, marital status, BMI, and total caloric intake, as was done to estimate ORs.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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compared with controls, cases were slightly older, were less likely to
be currently married, had a higher level of education, or were less
likely to use alcohol. Age, education, and marital status were included
in subsequent analyses as covariates. About two-thirds of the cases
were diagnosed as having advanced (regional/remote stages) cancer, and
most tumors were moderately or poorly differentiated. Most cases were
symptomatic at diagnosis, with 77% of the cases having serum
prostate-specific antigen levels greater than 10 ng/ml (median
levels were 87 ng/ml for total cases, 48 ng/ml for cases with regional
cancer, and 205 ng/ml for those with remote cancer).
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shows the mean anthropometric
characteristics in cases and controls. To evaluate the potential
disease effect on certain anthropometric factors for cases, results are
shown for total cases and separately for localized and advanced cases.
Among controls, the mean height and weight were 167.5 cm (65.9 inches)
and 61.5 kg (135.3 pounds), respectively, and the average BMI and waist
and hip circumferences were 21.9, 82.5 cm (32.4 inches), and 92.5 cm
(36.4 inches), respectively. There were no significant differences
between groups for height, usual adult weight, measured adult weight
(measured at interview), BMI at various ages, usual BMI (based on
self-reports of usual adult weight and height), BMI based on weight and
height measured at interview, and right upper arm circumference
(measured at interview) between cases (all stages) and controls. Cases
(all stages), however, had smaller hip circumferences and larger WHRs
than controls. Compared with cases with localized cancer, those with
advanced cancer (regional/remote) had slightly lower mean levels of
measured weight, measured BMI, and measured waist, hip, and right upper
arm circumferences but not usual adult weight or usual BMI, suggesting
a slight change in body weight among advanced cases. In addition, for
these advanced cases, weight measured at interview was slightly lower
(2%) than self-report of usual adult weight. Such a difference,
however, was not observed for controls and localized cases.
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presents risk in
relation to selected anthropometric characteristics for total cases and
by stage of diagnosis. No significant associations were found for
height, usual adult weight, or BMI. Increased right upper arm
circumference was associated with a reduced risk for advanced cancer.
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. As
shown, no strong or consistent risk patterns emerged for reported
weight histories or BMI at the four time points. A slight excess risk
was associated with a higher BMI in all age groups, although none of
the trends was significant. In addition, perceived body size (relative
to others in the same age groups) at these four time points plus at age
8–9, maximum weight, duration of maximum weight, and weight changes
over time (between 20 and 60 years of age) were evaluated, but no
significant associations were found (data not shown).
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. The risk patterns for waist
circumference were inconsistent, with excess risk found for localized
cancer and reduced risk for advanced cancer. In contrast, large hip
circumference was associated with a significantly reduced risk,
with men in the highest quartile having a 54% reduction in risk (OR,
0.46; 95% CI = 0.29–0.74; Ptrend =
0.001). When the analysis was stratified by stage of cancer, the
reduced risks were more pronounced for advanced cancer.
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Table 6
presents prostate cancer risks in
relation to WHR and BMI. In the first model, using tertiles of BMI and
WHR as the cutoffs, increasing levels of WHR were associated with an
elevated risk of prostate cancer, regardless of levels of BMI. The
excess risk was more pronounced among men in the first (<20.5) and
second (20.5–22.8) tertile of BMI. In addition, the excess risk
associated with WHR was much less evident among those with a BMI >25.
Within the same level of WHR, increases in BMI had a relatively small
impact on risk.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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BMI, reflecting both lean and fat body mass, is the most common measure of overall adiposity. Although eight studies did report a positive association between BMI and prostate cancer (20, 21, 22, 23, 24, 25, 26) , most epidemiological studies have not found significant effects for BMI and prostate cancer (7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20 , 27, 28, 29, 30) . We too did not find BMI to be associated with prostate cancer risk. We may not be able to evaluate the effect of overall obesity fully, inasmuch as only 4% of our study subjects were considered overweight (BMI >27.8) versus 24% in men in the United States (37 , 38) . BMIs in our study subjects ranged from 19.8 to 35.1, with an average of 21.9, which was even smaller than the cutoff point for the baseline category (BMI <23) in a prospective study of United States health professionals (31) .
Several studies have reported that body weight at birth or BMI at an early age was related to an excess prostate cancer risk, especially for advanced disease (39, 40, 41) . We evaluated the role of obesity in early life by examining BMI at four time points (using self-reports of height and weight at these time points) and self-perceived body size at these four time points and at age 8–9, but we were unable to confirm the hypothesis that preadult obesity was associated with an inverse risk (31) . In fact, in our study, BMI in later years (60–69 years of age) was associated with higher risk than that at younger ages (20–29 or 40–49 years of age). Although long-term recall of past weight is difficult, several validation studies conducted in Western men have reported a high reproducibility of self-reports of past weight and high correlations between recall of recorded and past weight (42, 43, 44) . In our study, self-reports of body height, usual adult weight, and weight in both 1988 and at 60–69 years of age were similar to measurements taken at interview, suggesting some level of consistency in the recall of body weight among Chinese men. In addition, among the 471 controls, values for BMI at various time points in life correlated well with each other.
Few studies have investigated the role of body fat distribution in prostate cancer. Despite the very low prevalence (4%) of overall obesity in our study subjects, we found that, independent of BMI, a greater WHR is an important risk factor for prostate cancer. When the analysis was further stratified by BMI, higher levels of WHR, but not BMI, were strongly related to risk. The risk associated with WHR was more pronounced among men with a low level of BMI (<25), suggesting that lean people with upper-body fat may be at greater risk of prostate cancer. We did not have enough obese subjects in the study to evaluate fully the effect of abdominal adiposity among obese subjects and the combined effect of abdominal and overall obesity.
In one prospective study among men in the United States, higher levels of WHR and smaller hips were associated with an increased risk of metastatic prostate cancer (31) , trends were not statistically significant. Relative to our study subjects, these Western men had much higher levels of BMI and WHR. In our study, 4% of the study subjects were considered overweight (BMI >27.8) versus 25% of the Western subjects, and 26% were considered to have abdominal obesity with a WHR >0.92 (versus 60% in men in the United States; Ref. 31 ). For both waist and hip circumferences, cutoff points for the highest quartile (75th percentile) in our study were similar to those for the 40th percentile in Western men (31) .
The WHR is a standard measure for abdominal adiposity, which has been linked to hormonal changes, metabolic aberrations (such as insulin resistance, glucose intolerance, hyperinsulinemia, and hyperlipidemia), and certain morbidities, including diabetes mellitus, cardiovascular disease, and cancers of the breast and endometrium (45 , 46) . In men, abdominal obesity is associated with higher circulating levels of cortisol, insulin, leptin, and free fatty acids but with lower levels of free testosterone and SHBG (47, 48, 49, 50, 51) , although the precise hormonal mechanism is unclear. The WHR is a measure of both visceral and subcutaneous fat; most of the metabolic changes are linked more closely to visceral fat in the intra-abdominal area. We have no data on visceral fat. Future studies are needed to confirm the finding regarding upper-body fat and to elucidate further the role of visceral fat. Whether WHR among lean subjects better reflects hormonal status also needs to be investigated further.
It has been suggested that waist circumference alone is also a good indicator of abdominal obesity and perhaps a better predictor of cardiovascular risk than WHR. In our study, however, the association with waist circumference was less consistent. Large waist circumference was associated with a nonsignificant increased risk of localized prostate cancer. However, the reduced risk for advanced cases associated with a large waist may be attributable, in part, to minor weight loss in advanced cases. On the basis of self-reported usual adult weight and measured weight at interview, we estimated that, on average, cases with advanced cancer may have lost up to 2.9 pounds, with two cases and three controls reporting a weight loss of more than 5 pounds. Exclusion of subjects with weight loss more than 2 pounds did not materially change the results. The minor weight loss in cases with advanced tumors might have resulted in their smaller measured circumferences of waist, hip, and right upper arm (0.3–1.3 inches smaller than those for men with localized cancer). Previous data suggest that among men, weight loss could result in more reduction in waist than in hip circumference (52) , resulting in a lower WHR. Thus, weight loss in cases with advanced tumors, but not in controls, should lead to lower WHRs in cases and result in an underestimate of the true risk. The risk estimates for localized cancer were higher than those for advanced cancer, suggesting that the overall risks for all cases combined may have been even higher than those reported here.
Hip circumference reflects gluteo-femoral adipose tissue, a major component of peripheral obesity. We found that larger hips were associated with a reduced risk of prostate cancer independent of WHR. This inverse relationship has been reported previously (31) , and an earlier clinical study reported an inverse correlation between free testosterone and larger hips (53) . Because of small numbers and the high correlation between waist and hip circumference (r = 0.7), we were unable to evaluate the role of hip circumference independent of abdominal adiposity. Because WHR is a ratio estimator, in an additional analysis, we included both WHR and hip circumference in the same model, and results were materially unchanged. Additional studies are needed to elucidate the independent protective effect of large hips on prostate cancer.
Of all of the lifestyle factors examined in the study to date, WHR is the strongest, with the most consistent patterns and dose-response relationship. The strong and consistent dose-response relationship suggests that the observed association may be real. Future studies are needed to confirm this association, especially in prospective studies in which the anthropometric measurements are taken before the diagnosis of disease and in Western populations where the risk of prostate cancer and the prevalence of abdominal obesity are much higher. International trends in prostate cancer suggest that westernization may increase the risk of prostate cancer (4) . Westernization in developing countries is related to an improved socioeconomic status, an increase in animal fat and red meat intake, reduced levels of physical activity, and an increase in the incidence of obesity and diabetes mellitus. Most of these factors have been linked to higher WHRs (54) . However, the observed WHR association in this study is independent of socioeconomic status, overall obesity, physical activity, intake of animal fat and red meat, and total calories. Although possible, it is unlikely that some unknown factors related to westernization may be confounding the observed association.
It has been shown that lean muscle mass, but not fat mass, in the arm area was associated with testosterone and an increased risk of prostate cancer in a prospective study among Japanese-American men (29) . In our study, we found that larger right upper arm circumference was associated with a reduced risk of advanced cancer even after adjustment for BMI or WHR. This result needs to be interpreted with caution, because such a reduction in risk was found only for advanced cancer but not for localized cancer, suggesting that the reduced circumference related to weight loss among cases with advanced cancer could have potentially biased the results. Right upper arm circumference in our study correlated strongly and positively with hip circumference (more than with waist circumference and WHR), and when the model was further adjusted for hip circumference, the ORs were >1. The arm circumference in our study reflects both fat and lean muscle mass; we have no information on lean muscle mass in the arm area.
Adult height has been reported in several studies to be associated with an increased prostate cancer risk (13 , 17 , 19 , 31 , 55 , 56) . In a recent study showing a positive association with height, substantial risk (22–68% excess) was found only for men who were taller than 72 inches (56) . We were unable to evaluate the risk in relation to height fully, because the variation in height is limited and because very few study subjects (2%) were taller than 72 inches. In our study, men in the highest quartile were only taller than 172 cm (67.7 inches), which is usually the baseline group in Western studies.
In summary, our findings suggest that abdominal adiposity, especially among nonobese men, is a strong risk factor for prostate cancer. Assuming that the abdominal adiposity association is causal, we estimated that 24% (95% CI = 14–33%) of the cases in Shanghai can be attributed to abdominal obesity (WHR > 0.92). Additional research is needed to confirm this finding in Western populations, where the prevalence of abdominal obesity is much higher, and to clarify the underlying hormonal mechanisms involved.
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Acknowledgments |
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Footnotes |
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1 To whom requests for reprints should be
addressed, at Division of Cancer Epidemiology and Genetics, National
Cancer Institute, 6120 Executive Boulevard, Executive Plaza South, MSC
7234, Room 7058, Bethesda, MD, 20852-7234. Fax: (301) 402-0916;
E-mail: hsinga{at}exchange.nih.gov 
2 The abbreviations used are: SHBG, sex
hormone-binding globulin; BMI, body mass index; OR, odds ratio; CI,
confidence interval; WHR, waist-to-hip ratio.
3 A. W. Hsing, Y-T. Gao, G. Wu, X. Wang, A.
Chokkcalingam, J. Deng, J. Cheng, I. A. Sesterhenn, F. K. Mostofi, J.
Benchiou, and C. Chang. Polymorphic CAG repeat lengths in the
AIB1 gene and prostate cancer risk: a population-based
case-control study in China, submitted for publication.
Received 7/12/00; revised 8/16/00; accepted 10/ 9/00.
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