Coffee, beer, and wine consumption and PhIP-DNA adducts in black and white men with prostate cancer

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Coffee, beer and wine consumption and PhIP-DNA adducts in black and white men with prostate cancer
 Background
 Prostate cancer incidence and mortality is significantly higher in black men compared to white men in the U.S. and racial differences in diet may play a role in this disparity. The predominant heterocyclic amine in cooked meats, 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP), has been shown to be carcinogenic in rat prostate and likely derives its carcinogenic potential through the formation of DNA adducts. Blacks have been shown to have higher levels of PhIP in their diet and urine. In addition, a recent prospective cohort study of black men showed PhIP intake was positively associated with PSA blood levels. Coffee, beer and red wine have been shown to affect PhIP metabolizing enzymes. Therefore, we tested whether consumption of these beverages was associated with prostate PhIP-DNA adduct levels in black and white men with prostate cancer.
 Methods
 The study population included 105 black and 161 white men who underwent radical prostatectomy treatment for prostate cancer. Beverage consumption and meat intake information was based on food frequency questionnaires. PhIP-DNA adducts in tumor and adjacent non-tumor cells were measured using immunohistochemical methods. Data were analyzed using ANCOVA and stepwise linear regression.
 Results
 In tumor and adjacent non-tumor prostate tissue of all subjects, significantly lower mean PhIP-DNA adduct levels were found among beer (mean optical density units, tumor: 0.101 vs. 0.108, p=0.01, non-tumor: 0.162 vs. 0.174, p=0.03) and red wine (tumor: 0.097 vs. 0.108, p< 0.01, non-tumor: 0.157 vs. 0.174, p<0.01) drinkers as compared to non-drinkers after adjusting for income, smoking, meat consumption, prostate volume and tumor volume. In race-stratified analyses, black men who consumed beer (tumor: 0.100 vs. 0.110, p= 0.01, non-tumor: 0.160 vs. 0.174, p= 0.04) or coffee (tumor: 0.102 vs.0.119, p< 0.01, adjacent non-tumor: 0.162 vs. 0.187, p<0.01) had significantly lower mean adduct levels than blacks who did not consume these beverages. Among whites, only red wine consumers (tumor: 0.096 vs. 0.107, p< 0.01, non-tumor: 0.157 vs. 0.173, p= 0.03) had significantly lower PhIP adducts. In stepwise regression models, which included coffee, beer and wine, red wine remained a significant predictor of lower PhIP adduct levels among all subjects and among whites. Coffee was the only beverage to remain a significant predictor of PhIP adduct levels in blacks. Nearly 23% of black men did not consume the beverages that were related to lower PhIP adducts, as compared to only 5% of white men who were non-coffee-beer-and-wine drinkers. Interestingly, in stepwise regression analyses that included beverages, meat consumption was a significant predictor of PhIP adduct levels in whites but not blacks.
 Conclusions
 Although our previous work has shown that black and white men with prostate cancer did not differ quantitatively in PhIP-DNA adduct levels, the PhIP adducts in these two race/ethnic groups may result from different dietary exposures and therefore, may differ in mutagenic potential. More work is needed to identify dietary and genetic factors that impact PhIP-DNA adducts and their carcinogenic potential in diverse populations.