Obesity is more strongly associated with elevated prostate cancer (PCa) risk among African-American than non-Hispanic white men, according to a new study.

The finding is based on an analysis of data from 22,673 non-Hispanic white (NHW) men and 3,398 African-American (AA) men who participated in the Selenium and Vitamin E Cancer Prevention Trial (SELECT), a prospective randomized clinical trial. Study subjects had a median follow-up of 5.6 years, during which 1,723 were diagnosed with PCa.

Among AA men, subjects with a body mass index (BMI) of 35 kg/m² or higher had a significant 49% increased risk of PCa compared with those who had a BMI less than 25. BMI was not associated with PCa risk in the NHW group. Compared with NHW men, AA men with a BMI less than 25, 25.0 to less than 27.5, 27.5 to less than 30.0, 30 to less than 35.5, and 35.0–50.0 had a significant 28%, 49%, 58%, 75%, and 103% increased risk of PCa, respectively, the researchers reported online in JAMA Oncology.

The study, led by Wendy E. Barrington, PhD, of the University of Washington School of Nursing in Seattle, found that BMI was inversely associated with the risk of low-grade PCa among the NHW men. Those with a BMI of 35 or higher had a significant 20% decreased risk of low-grade PCa compared with subjects who had a BMI below 25. In contrast, among AA men, subjects with a BMI of 35 or higher had a significant 2.2 times increased risk of low-grade PCa compared with those who had a BMI below 25. 

BMI was positively associated with the risk of high-grade PCa in both groups, although the effect was larger in the AA group. AA and NHW men with a BMI of 35 or higher had a significant 81% and 33% increased risk of high-grade PCa compared with their counterparts with a BMI below 25.

The researchers noted that AA men have the highest incidence of PCa of any racial or ethnic group in the United States. “Findings from this study suggest that increased obesity could partially explain the substantially higher risk of prostate cancer among AA men,” they concluded.

The investigators noted that the mechanisms underlying their findings are unknown, but a possible explanation is that the biological effects of obesity differ in AA and NHW men. “Inflammation plays a role in prostate carcinogenesis, and the effect of obesity on systemic inflammation could be stronger in AA than in NHW men,” they wrote. “Similarly, insulin may play a role in prostate carcinogenesis and it is possible that the effect of obesity on insulin secretion is stronger in AA than in NHW men.”

Another possible explanation is that the PCa detection rate in SELECT may be higher among AA compared with NHW men. Additionally, mean PSA levels, adjusted for age and other covariates, are lower among NHW compared with AA men, which may increase the likelihood of diagnostic biopsies among AA men. Moreover, it is well established that obesity is inversely related to PSA concentration.

Strengths of the study include a large sample size, standardized assessment of height and weight, active follow-up for incident PCa, and consideration of bias due to differential detection, Dr. Barrington and her colleagues pointed out. The study also had limitations, such as the use of BMI, which is a nonspecific measure of obesity. It does not discriminate more metabolically active abdominal fat from other body fat, and it does not distinguish whether excess body weight relative to height is due to nonfat tissues, the researchers explained.

“This study reinforces the importance of obesity prevention and treatment among AA men, for whom the health benefits may be comparatively large,” the researchers concluded. “Although obesity is linked to poor health outcomes in all populations, clinicians might consider the unique contribution of obesity prevention and treatment to the health of their AA patients. Such targeted efforts may contribute to reductions in prostate cancer disparities.”

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