1.
Relation of Vitamin E and Selenium Exposure to Prostate Cancer Risk by Smoking Status: A Review and Meta-Analysis.
Kim, Y, Wei, J, Citronberg, J, Hartman, T, Fedirko, V, Goodman, M
Anticancer research. 2015;(9):4983-96
Abstract
BACKGROUND Epidemiological studies of selenium and vitamin E, two antioxidants hypothesized to reduce prostate cancer risk, have shown no discernible benefit. It has been proposed, however, that tobacco smoking may modify the effect of these nutrients. MATERIALS AND METHODS We performed a meta-analysis of studies evaluating the relation of vitamin E and selenium exposure to prostate cancer risk in never smokers vs. ever smokers and, when feasible, former and current smokers. Overall and stratum-specific meta-risk ratios (meta-RRs) and 95% confidence intervals (CIs) were calculated using random-effects models. RESULTS A total of 21 studies have met the inclusion criteria. Meta-RR (95% CI) estimates of prostate cancer associated with vitamin E use were 1.03 (0.95-1.11) in never smokers and 0.98 (0.90-1.07) in ever-smokers. For selenium, meta-RRs were 1.09 (0.78-1.52 and 0.76 (0.60-0.96) for never and ever-smokers, respectively; however, results for current smokers were weaker than those for former smokers. Sub-analyses according to different exposure assessment methods and outcome definitions produced similar results across strata. CONCLUSION The association between vitamin E and prostate cancer is not modified by smoking. Selenium exposure is associated with lower prostate cancer risk among ever-smokers; however, the lack of an association for current smokers indicates that this finding needs to be interpreted with caution.
2.
Coffee consumption and risk of prostate cancer: a meta-analysis of epidemiological studies.
Park, CH, Myung, SK, Kim, TY, Seo, HG, Jeon, YJ, Kim, Y, ,
BJU international. 2010;(6):762-9
Abstract
OBJECTIVE To evaluate the association between coffee consumption and the risk of prostate cancer. METHODS We searched PubMed, EMBASE, and the bibliographies of relevant articles in August 2009. Two evaluators independently reviewed and selected articles based on predetermined selection criteria. RESULTS Twelve epidemiological studies (eight case-control studies and four cohort studies) were included in the final analysis. In a meta-analysis of all included studies, when compared with the lowest level of coffee consumption, the overall relative risk (RR) of prostate cancer for the highest level of coffee consumption was 1.16 (95% confidence interval [CI] 1.01-1.33). In subgroup meta-analyses by study design, there was a significant positive (harmful) association between coffee consumption and prostate cancer risk in seven case-control studies using both crude and adjusted data (RR 1.20, 95% CI 1.02-1.40; and RR 1.21, 95% CI 1.03-1.43, respectively), whereas there was no significant association in four cohort studies using crude or adjusted data (RR 0.97, 95% CI 0.68-1.38; and RR 1.06, 95% CI 0.83-1.35, respectively). CONCLUSION Given that a cohort study gives a higher level of evidence than a case-control study, there is no evidence to support a harmful effect of coffee consumption on prostate cancer risk. Further prospective cohort studies are required.