This study is the largest prospective study to examine the association of meat and HCA intake on prostate cancer risk in African-American men to date. There was no association found for total red, white, or processed meat consumption; however, those consuming a lot of red meats cooked at high temperatures and DiMeIQx had an increased risk of nonadvanced prostate cancers. We found that African-American men in the highest intake quantile of red meat cooked at high temperatures had a 22% higher risk of prostate cancer over a 10-year period than men in the lowest-consumption quantile. There was no increase risk seen for advanced prostate cancers.
The majority of previous prospective studies examining the relation between meat and prostate cancer have been in primarily Caucasian populations, and results have been inconsistent (7
). Rodriguez et al
. (2006) examined meat consumption among black and white men separately in the Cancer Prevention Study II (CPS-II) Nutrition Cohort (21
), and found a significant increased risk for prostate cancer for men whose consumption of cooked processed meat was in the highest quartile. Researchers did not examine risks associated with HCAs and due to the small number of cases (85 total prostate cases) in the CPS-II cohort, were unable to examine risk of advanced or metastatic disease among blacks. In our study, 1,089 African-American men developed prostate cancer, 108 of whom had advanced disease.
We have previously shown in the full, predominantly Caucasian NIH-AARP study that high consumption of red or processed meat is associated with increased risk of total and advanced prostate cancer (7
). Our mean meat intake values were within the range of those reported for the full study. In the present study, however, we did not observe an increased risk with total red or processed meats or with heme iron, nitrite/nitrate, or B[a]P. Instead, in the present sub-cohort of African-American men, we observed associations with red meat cooked at high temperatures and subsequent risk of prostate cancer, which was supported by the finding that risk was also increased for men with higher intakes of DiMeIQx. We did not observe significant associations for advanced disease, which may be due in part to the small number of cases (n=108) in our sub-cohort of African-American men.
Multiple mechanisms have been proposed to explain the association between increased meat intake and subsequent cancer risk. One proposed mechanism is that the contents of red meat are involved in the development of carcinogens that may increase the risk of disease, such as heme iron, which may cause oxidative biochemical and cellular damage(22
), as well as increase endogenous formation of N
-nitroso compounds (Cross 2003). In addition, meats cooked at high temperatures (e.g., barbecuing, grilling, and frying) form HCAs, which are genotoxic and carcinogenic compounds thought to increase cancer risk (23
). The carcinogenicity of HCAs have been demonstrated in experimental studies (28
). Also, PhIP, which has estrogenic activity, has been shown to induce cancer specifically in the prostate of rats(29
). Although the exact biological effect of these compounds remains unclear, DiMeIQx and MeIQx are thought to be more potent mutagens than PhIP(30
). In the present study, we observed an association between increased DiMeIQx, but not PhIP, and risk of prostate cancer.
Among the inherent strengths of the present study is the prospective design in which diet and other health risk factors were measured prior to development of disease. Extensive data collection of information on lifestyle and medical history allowed us to control for possible confounding on a wide set of characteristics and lifestyle factors. Further, the large size of the NIH-AARP Diet and Health Study allowed us to examine potential associations among a high-risk population.
A limitation of our study is that the cohort consisted of predominantly older, upper-to-middle class participants; therefore, results may not apply to other African-American populations. The FFQ used here was not specifically developed for African-Americans and therefore may not capture unique dietary patterns not reflected in the general U.S. population diet. The lack of specific ethnic/minority foods may have led to misclassification of dietary intakes for this analytic cohort, resulting in a bias of observed associations. The FFQ was assessed at study baseline and did not assess early life exposure; therefore we were unable to examine changes in diet. Our findings may reflect incomplete adjustment for other health risk factors not available in our study cohort, although the NIH-AARP Diet and Health study did collect a wide range of characteristics and lifestyle factors, which we adjusted for in our analyses that are typically not available in other study populations. However, NIH-AARP Study did not assess PSA screening on the baseline questionnaire; therefore, we were unable to adjust the observed associations between meat intake and prostate cancer for screening. The number of advanced prostate cancer cases was small (n=108), which may in part explain why we did not observe significant associations for advanced disease.
For African-American men, reducing and/or avoiding eating red meats cooked at high temperature may reduce one's risk for developing prostate cancer. If confirmed, our results suggest that African-Americans may be able to decrease their risk of prostate cancer by dietary modification. Further studies are needed to replicate these associations.