Abstract 623: Prostate cancer and B-vitamins

Abstract

Abstract BACKGROUND. Recent reports suggest that excess of nutrients involved in the one-carbon metabolism pathway increases PC risk, however empirical data are lacking. Our hypothesis was to examine whether excessive intake of one carbon nutrients was associated with PC risk and whether this association was similar in LG vs. HG prostate cancer. METHODS. Veteran American men (272 controls and 144 PC cases) who attended the Durham Veteran American Medical Center, between 2004-2011, were enrolled into a case-control study. Intake of folate, vitamin B12, B6 and methionine were measured using a food frequency questionnaire. Regression models were used to evaluate the association among one-carbon cycle nutrients, MTHFR genetic variants and prostate cancer. RESULTS. Higher methionine intake was positively associated with PC risk, OR=2.1 95%CI 1.1-3.9, p=0.02; a risk which increased for low grade PC or Gleason <7, OR=2.75 (95%CI 1.32-5.73), p=0.007. These associations did not vary by MTHFR C677T genotype, however the cross-product term for the association of MTHFR A1298C variant and methionine was statistically significant, compared to non-carriers (p=0.045). Evidence for associations between B vitamins (folate, B12 and B6) and PC risk were less clear. CONCLUSIONS. Our results suggest that high methionine intake increases PC risk. Higher intakes of folate and vitamin B6 may be protective against advanced prostate cancer- however the associations were weak, while vitamin B12 higher intakes showed a trend for significance for higher PC risk. Individuals carrying MTHFR A1298C variants, and consuming more than the recommended levels of methionine, may be at higher risk for PC. Key words: Prostate cancer (PC), folate, vitamins B6, B12, methionine, methylenetetrahydrofolate reductase (MTHFR). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 623. doi:1538-7445.AM2012-623