Baseline selenium status and effects of selenium and vitamin E supplementation on prostate cancer risk - Abstract

BACKGROUND: The Selenium and Vitamin E Cancer Prevention Trial found no effect of selenium supplementation on prostate cancer (PCa) risk but a 17% increased risk from vitamin E supplementation.

This case-cohort study investigates effects of selenium and vitamin E supplementation conditional upon baseline selenium status.

METHODS: There were 1739 total and 489 high-grade (Gleason 7-10) PCa cases and 3117 men in the randomly selected cohort. Proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for effects of supplementation within quintiles of baseline toenail selenium. Cox proportional hazards models were used to estimate hazard ratios, and all statistical tests are two-sided.

RESULTS: Toenail selenium, in the absence of supplementation, was not associated with PCa risk. Selenium supplementation (combined selenium only and selenium + vitamin E arms) had no effect among men with low selenium status (< 60th percentile of toenail selenium) but increased the risk of high-grade PCa among men with higher selenium status by 91% (P = .007). Vitamin E supplementation (alone) had no effect among men with high selenium status (≥40th percentile of toenail selenium) but increased the risks of total, low-grade, and high-grade PCa among men with lower selenium status (63%, P = .02; 46%, P = .09; 111%, P = .008, respectively).

CONCLUSIONS: Selenium supplementation did not benefit men with low selenium status but increased the risk of high-grade PCa among men with high selenium status. Vitamin E increased the risk of PCa among men with low selenium status. Men should avoid selenium or vitamin E supplementation at doses that exceed recommended dietary intakes.

Written by:
Kristal AR, Darke AK, Morris JS, Tangen CM, Goodman PJ, Thompson IM, Meyskens FL Jr, Goodman GE, Minasian LM, Parnes HL, Lippman SM, Klein EA.   Are you the author?
Cancer Prevention Program and SWOG Statistical Center, Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Epidemiology and Department of Environmental Health, University of Washington, Seattle, WA; University of Missouri, Research Reactor Center, Columbia, MO; Harry S. Truman Memorial Veterans Hospital, Columbia, MO; Department of Urology, University of Texas Health Science Center at San Antonio, San Antonio, TX; Chao Family Comprehensive Cancer Center, University of California Irvine, Irvine, CA; Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, MD; Moores Cancer Center, University of California San Diego, San Diego, CA; Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, OH.

Reference: J Natl Cancer Inst. 2014 Feb 22. Epub ahead of print.
doi: 10.1093/jnci/djt456


PubMed Abstract
PMID: 24563519

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