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Prostate cancer will be diagnosed in approximately 180,890 men and account for 26,129 deaths in the United States in 2016, making prostate cancer the most commonly diagnosed and third leading cause of cancer death for American men [1]. Mortality related to prostate cancer has declined by more than 50% since 1990 [2]. In the last 25 years, annual PSA screening was both widely implemented and subsequently disproven as an effective prevention strategy and numerous chemoprevention clinical trials have failed to show a benefit; therefore, most experts attribute decreased prostate cancer mortality to improvements in treatment options [2]. While treatment options for prostate cancer are improving, treatments are both expensive and have adverse effects: urinary, sexual, and bowel-related adverse effects are common [3]. Given the prevalence, cost of treatment and associated adverse effects, primary prevention of prostate cancer remains an attractive option. Preclinical and epidemiologic evidence supporting a role for selenium and vitamin E in prostate cancer risk reduction led to the implementation of a prospective randomized trial, the Selenium and Vitamin E Cancer Prevention Trial (SELECT) [4] unfortunately demonstrating that vitamin E supplementation increased the risk of prostate cancer. The findings of SELECT are in contrast to those of the Alpha-Tocopherol, Beta Carotene (ATBC) trial [5], which reported a 35% risk reduction for prostate cancer in men taking 50mg daily of Vitamin E for a median of 6.1 years, as well as the Physicians Health Study [6] which showed no difference. Given that all the participants of ATBC were long term smokers compared to 43% never smokers and 8% current smokers in SELECT, this may suggest a differential benefit of vitamin E in smokers.

journal of pharmacology and clinical research

Quantification of ï ¡-Tocopherol in Smokers and Non-Smokers Before and After Supplementation: Mechanism of Failure for Vitamin E in Prostate Cancer Prevention?