Vitamin and Mineral Use and Risk of Prostate Cancer: The Case-Control Surveillance Study Editorial Comment

Clinical Epidemiology Research and Training Unit, School of Medicine, Boston University, Boston, MA, USA.
Cancer Causes and Control (Impact Factor: 2.74). 07/2009; 20(5):691-8. DOI: 10.1007/s10552-008-9282-y
Source: PubMed


Many studies have evaluated the association between vitamin and mineral supplement use and the risk of prostate cancer, with inconclusive results.
The authors examined the relation of use of multivitamins as well as several single vitamin and mineral supplements to the risk of prostate cancer risk among 1,706 prostate cancer cases and 2,404 matched controls using data from the hospital-based case-control surveillance study conducted in the United States. Odds ratios (OR) and 95% confidence intervals (CI) for risk of prostate cancer were estimated using conditional logistic regression model.
For use of multivitamins that did not contain zinc, the multivariable odds ratios of prostate cancer were 0.6 for 1-4 years, 0.8 for 5-9 years, and 1.2 for 10 years or more, respectively (p for trend = 0.70). Men who used zinc for ten years or more, either in a multivitamin or as a supplement, had an approximately two-fold (OR = 1.9, 95% CI: 1.0, 3.6) increased risk of prostate cancer. Vitamin E, beta-carotene, folate, and selenium use were not significantly associated with increased risk of prostate cancer.
The finding that long-term zinc intake from multivitamins or single supplements was associated with a doubling in risk of prostate cancer adds to the growing evidence for an unfavorable effect of zinc on prostate cancer carcinogenesis.

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Available from: Yuqing Zhang, Feb 24, 2014
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    • "Epidemiological data indicate that selenium status is inversely connected with cancer risk, and the results of some, but not all, nutritional studies show that high selenium intakes greatly reduce the risk of mammary, prostate, lung, colon, and liver cancers (Zeng et al., 2009). Numerous case– control studies have verified a negative correlation between a low serum selenium concentration and the risk of developing PCa (Nomura et al., 1987, 2000; Brooks et al., 2001; Zhang et al., 2009; Zeng et al., 2009). Various in vitro studies have suggested that the possible mechanisms of the antiproliferative effect of selenium formulations in PCa cells are caused by cell cycle arrest and the induction of programmed cell death. "
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    ABSTRACT: Epidemiological data indicate that selenium status is inversely connected with cancer risk. Animal and human studies have demonstrated that most inorganic and organic forms of selenium compounds have an anticancer action. This work investigated the impact of organic selenium on the multiple signalling pathways involved in the inhibition of the viability of prostate cancer cells. Prostate adenocarcinoma cells (PC-3) were incubated with seleno-l-methionine (SeMet) at four concentrations and cell viability and programmed cell death were determined by the WST-1, BrdU assays and Tali image based cytometer. The expression of chosen cell-cycle regulatory genes was determined by real-time RT-PCR analysis and confirmed at the protein level. SeMet treatment of PC-3 cells resulted in an inhibition of cell proliferation in a dose- and time-dependent manner. The inhibition of proliferation correlated with the up-regulation of gene expression and the protein levels of CCNG1, CHEK1, CDKN1C and GADD45A, whereas SeMet down-regulated the expression of CCNA1 and CDK6 genes. Therefore SeMet inhibits the proliferative activity of prostate cancer cells by a direct influence on the expression of genes involved in the regulation of cell cycle progression.
    Full-text · Article · Apr 2014 · Journal of applied biomedicine
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    • "We observed no gene-environment interaction between the MTHFR C677T polymorphism and folate intake. Our findings for the effects of folate intake on prostate cancer risk are consistent with five case-control studies (Vlajinac et al., 1997; Weinstein et al., 2003; Johansson et al., 2008; Zhang et al., 2009; Collin et al., 2010b) and three cohort studies (Stevens et al., 2006; Weinstein et al., 2006; Beilby et al., 2010). Our results are inconsistent with two case-control studies reporting decreased risk with higher dietary folate intake (Pelucchi et al., 2005; Shannon et al., 2009), and a prospective study and randomized clinical trial both finding increased risk with higher intakes (Hultdin et al., 2005; Figueiredo et al., 2009). "
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    ABSTRACT: Purpose: Folate is essential to DNA methylation and synthesis and may have a complex dualistic role in prostate cancer. Alcohol use may increase risk and epigenetic factors may interact with lifestyle exposures. We aimed to characterize the independent and joint effects of folate intake, alcohol consumption, and the MTHFR C677T gene polymorphism on prostate cancer risk, while accounting for intakes of vitamins B(2), B(6), B(12), methionine, total energy, and confounders. Methods: A case-control study was conducted at Kingston General Hospital of 80 incident primary prostate cancer cases and 334 urology clinic controls, all with normal age-specific PSA levels (to exclude latent prostate cancers). Participants completed a questionnaire on folate and alcohol intakes and potential confounders prior to knowledge of diagnosis, eliminating recall bias, and blood was drawn for MTHFR genotyping. Joint effects of exposures were assessed using unconditional logistic regression and significance of multiplicative and additive interactions using general linear models. Results: Folate, vitamins B(2), B(6), B(12), methionine, and the CT and TT genotypes were not associated with prostate cancer risk. The highest tertile of lifetime alcohol consumption was associated with increased risk (OR = 2.08; 95% CI: 1.12-3.86). Consumption of >5 alcoholic drinks per week was associated with increased prostate cancer risk among men with low folate intake (OR = 2.38; 95% CI: 1.01-5.57), and higher risk among those with the CC MTHFR genotype (OR = 4.43; 95% CI: 1.15-17.05). Increased risk was also apparent for average weekly alcohol consumption when accounting for the multiplicative interaction between folate intake and MTHFR C677T genotype (OR = 3.22; 95% CI: 1.36-7.59). Conclusion: Alcohol consumption is associated with increased prostate cancer risk, and this association is stronger among men with low folate intake, with the CC MTHFR genotype, and when accounting for the joint effect of folate intake and MTHFR C677T genotype.
    Full-text · Article · Aug 2012 · Frontiers in Oncology

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