Selenium and Prostate Cancer Prevention: Insights from the Selenium and Vitamin E Cancer Prevention Trial (SELECT)

Cancer Prevention Fellowship Program, Nutritional Science Research Group, Division of Cancer Prevention, National Cancer Institute, 9609 Medical Center Dr, Rockville, MD 20850, USA. .
Nutrients (Impact Factor: 3.27). 04/2013; 5(4):1122-48. DOI: 10.3390/nu5041122
Source: PubMed


The Selenium and Vitamin E Cancer Prevention Trial (SELECT) was conducted to assess the efficacy of selenium and vitamin E alone, and in combination, on the incidence of prostate cancer. This randomized, double-blind, placebo-controlled, 2 × 2 factorial design clinical trial found that neither selenium nor vitamin E reduced the incidence of prostate cancer after seven years and that vitamin E was associated with a 17% increased risk of prostate cancer compared to placebo. The null result was surprising given the strong preclinical and clinical evidence suggesting chemopreventive activity of selenium. Potential explanations for the null findings include the agent formulation and dose, the characteristics of the cohort, and the study design. It is likely that only specific subpopulations may benefit from selenium supplementation; therefore, future studies should consider the baseline selenium status of the participants, age of the cohort, and genotype of specific selenoproteins, among other characteristics, in order to determine the activity of selenium in cancer prevention.

9 Reads
  • Source
    • "Worryingly, an elevated risk with vitamin E was found [65]. A possible explanation for these null findings include the agent formulation and dose, the baseline characteristics of the cohort and the study design, which suggests that it is likely that only specific subpopulations may benefit from selenium supplementation [66]. Furthermore, a recent phase III studies of selenium vs placebo in patients with HGPIN found no benefit in the prevention of progression to prostate cancer and suggested higher intake might increase the risk of cancer [67]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Prostate cancer is the second most common cause of cancer worldwide after lung cancer. There is increasing evidence that diet and lifestyle plays a crucial role in prostate cancer biology and tumourigenesis. Prostate cancer itself represents a good model of cancer in which to look for chemopreventive agents due to the high disease prevalence, slowly progressive nature, and long latency period. Dietary agents have gained considerable attention, often receiving much publicity in the media. To review the key evidence available for potential chemopreventive nutrients. The methodology for this review involved a PubMed search from 1990 to 2013 using the key-words “diet and prostate cancer”, “nutrition and prostate cancer”, “dietary factors and prostate cancer”, “prostate cancer epidemiology”, “prostate cancer prevention”, “prostate cancer progression”. Red meat, dietary fat and milk intake should be minimised as they appear to increase the risk of prostate cancer. Fruit and vegetables and polyphenols may be preventive in prostate cancer, but further studies are needed to draw more solid conclusions and to clarify their role in patients with an established diagnosis of prostate cancer. Selenium and vitamin supplements cannot be advocated for the prevention of prostate cancer and indeed higher doses may be associated with a worse prognosis. There is no specific evidence regarding benefits of probiotics or prebiotics in prostate cancer. From the wealth of evidence available, many recommendations can be made although more randomised control trials are required. These need to be carefully designed due to the many confounding factors and heterogeneity of the population.
    Nutrition & Metabolism 06/2014; 11(1):30. DOI:10.1186/1743-7075-11-30 · 3.26 Impact Factor
  • Source
    • "Another example is that vitamin E had been recommended as a way to slow the progress of Alzheimer's disease (Sano et al., 1997). However, vitamin E not only has no proven effectiveness but also increases the risk of cancer in men (Nicastro and Dunn, 2013). A recent study of older Iowa women showed that taking any nutritional supplement was risky. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The knowledge base of nutrition and the brain is steadily expanding. Much of the research is aimed at ways to protect the brain from damage. In adults, the major causes of brain damage are aging and dementia. The most prominent dementia, and the condition that grabs the most public attention, is Alzheimer's disease. The assumption in the field is that possibly some change in nutrition could protect the brain and prevent, delay, or minimize Alzheimer's disease damage. Presented here is a framework for understanding the implications of this research. There is a gap between publishing research results and change in public nutrition behavior. Several influencing elements intervene. These include regulatory agencies and all the organizations and people who advise the public, all with their own perspectives. In considering what advice to give, advisors may consider effectiveness, research model, persuasiveness, and risks, among other factors. Advice about nutrition and Alzheimer's disease today requires several caveats.
    Neurobiology of Aging 05/2014; 35. DOI:10.1016/j.neurobiolaging.2014.02.029 · 5.01 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Dietary selenium is an essential micronutrient. To study the effect of increasing dietary selenium on malignant mesothelioma (MM) progression, we cultured four different MM cell lines in media containing increasing amounts of sodium selenite (30, 50, and 80 nmol/L). Increasing the amounts of selenium increased density-dependent proliferation and mobility for CRH5 and EKKH5, but not AB12 and AK7. Comparison of these cell lines showed that extracellular regulated kinase (ERK) phosphorylation was sensitive to a selenium increase in CRH5 and EKKH5, but not AB12 and AK7 cells. Stable expression of a dominant-negative mutant ERK eliminated the effects of increasing selenium. Because ERK is redox sensitive, we compared the MM cell lines in terms of glutathione levels and the capacity to reduce exogenous hydrogen peroxide. Increasing selenium levels led to higher glutathione and reducing capacity in CRH5 and EKKH5, but not AB12 and AK7. The reducing agent N-acetylcysteine eliminated the effects of selenium on ERK activation, proliferation, and mobility. Mice fed diets containing increasing levels of selenium (0.08, 0.25, and 1.0 ppm) showed increased tumor progression for CRH5, but not AB12, MM cells, and in vivo N-acetylcysteine treatment eliminated these effects. Data suggest that the effects of dietary selenium on MM tumor progression depend on the arising cancer cells' redox metabolism, and the tumors able to convert increased selenium into a stronger reducing capacity actually benefit from increased selenium intake.
    American Journal Of Pathology 01/2014; 184(4). DOI:10.1016/j.ajpath.2013.12.008 · 4.59 Impact Factor
Show more


9 Reads
Available from