Are men with low selenium levels at increased risk of prostate cancer?

Department of General Practice, Maastricht University, Maestricht, Limburg, Netherlands
European Journal of Cancer (Impact Factor: 5.42). 11/2006; 42(15):2463-71. DOI: 10.1016/j.ejca.2006.02.027
Source: PubMed


A meta-analysis was undertaken to quantitatively determine if men with low selenium levels were at increased risk of prostate cancer. PubMed, EMBASE and current contents were searched to identify relevant studies. The effect size was calculated by pooling the mean difference for serum, plasma and toenail selenium levels (95% confidence intervals) separately and combined using a random effects model. Meta-regression analysis explored possible sources of heterogeneity. Twenty epidemiologic studies were selected. Mean differences were: -5.55 microg/l (-9.82; -1.27; p=0.01), -0.01 microg/g (-0.03; 0.006; p=0.19), -0.52 microg/l (-4.63; 3.58; p=0.80) for serum, toenail and plasma studies, respectively. Overall, the pooled standardized mean difference between cases and controls was; -0.23 (-0.40; -0.05; p=0.01) indicating a possible inverse association between selenium levels and risk of prostate cancer. Differences in selenium levels between populations, a possible threshold effect and the relationship between selenium and the different stages of prostate cancer require further investigation.

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Available from: Raoul Reulen, Feb 23, 2015
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    • "There has been considerable interest in its antioxidant properties and potential as a chemopreventive agent since a large randomised control trial in the 1990’s found it to be protective against the development of many cancers [62]. This led to many epidemiological studies, 21 of which were included in a meta-analysis by Brinkman et al. whom demonstrated an increase in prostate cancer in men with lower selenium levels [63]. Many in vitro studies have found Selenium to induce apoptosis, inhibit cellular proliferation and inhibit angiogenesis [64]. "
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    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
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    • "Anticancer properties of selenium are of particular interest. Although the mechanisms of its activities are not fully understood, a clear correlation between the increased morbidity of cancer and the deficiencies of selenium in the diet was noted [1, 2]. Several investigations on populations from selenium-poor areas give statistically proven evidence that the selenium deficit increases cancer appearance, when compared to the areas rich in this element [3]. "
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    ABSTRACT: The aim of this study was to evaluate the biological and chemical response of Allium cepa L. exposed to inorganic selenium compounds. Besides the investigation of the total content of selenium as well as its chemical speciation, the Allium test was used to evaluate the growth of onion roots and mitotic activity in the roots’ meristem. The total content of selenium was determined by inductively coupled plasma mass spectrometry (ICP MS). High-performance liquid chromatography (HPLC), coupled to ICP MS, was used for the selenium chemical speciation. Results indicated that A. cepa plants are able to biotransform inorganic selenium compounds into their organic derivatives, e.g., Se-methylselenocysteine from the Se(IV) inorganic precursor. Although the differences in the biotransformation of selenium are due mainly to the oxidation state of selenium, the experiment has also shown a fine effect of counter ions (H+, Na+, NH4+) on the response of plants and on the specific metabolism of selenium. Figure ᅟ
    Analytical and Bioanalytical Chemistry 03/2014; 406(15). DOI:10.1007/s00216-014-7742-7 · 3.44 Impact Factor
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    • "For cancer studies, ULSAM is comparatively small and modest or weak associations may go undetected: our data indicate an overall modest inverse relation of serum selenium level with prostate cancer risk, which we could not substantiate. The serum selenium levels and co- variates were measured at a median of 23 years before diagnosis, a disadvantage, which however is shared with the other studies in the field [10,11,16]. In a Swedish population the range of selenium exposure is limited, with few high serum selenium level values. "
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    ABSTRACT: Serum selenium level (s-Se) has been associated with prostate cancer (PrCa) risk. We investigated the relation between s-Se, smoking and non-screening detected PrCa and explored if polymorphisms in two DNA repair genes: OGG1 and MnSOD, influenced any effect of s-Se. ULSAM, a population based Swedish male cohort (n = 2322) investigated at age 50 for s-Se and s-Se influencing factors: serum cholesterol, erythrocyte sedimentation rate and smoking habits. At age 71 a subcohort, (n = 1005) was genotyped for OGG1 and MnSOD polymorphisms. In a 34-year-follow-up, national registries identified 208 PrCa cases further confirmed in medical records. Participants with s-Se in the upper tertile had a non-significantly lower risk of PrCa. Smokers with s-Se in the two lower tertiles (≤80 μg/L) experienced a higher cumulative incidence of PrCa than smokers in the high selenium tertile (Hazard Ratio 2.39; 95% CI: 1.09-5.25). A high tertile selenium level in combination with non-wt rs125701 of the OGG1 gene in combination with smoking status or rs4880 related variation of MnSOD gene appeared to protect from PrCa. S-Se levels and smoking habits influence long-term risk of PrCa. Smoking as a risk factor for PrCa in men with low s-Se is relevant to explore further. Exploratory analyses of variations in OGG1 and MnSOD genes indicate that hypotheses about patterns of exposure to selenium and smoking combined with data on genetic variation in genes involved in DNA repair can be valuable to pursue.
    BMC Cancer 10/2011; 11(1):431. DOI:10.1186/1471-2407-11-431 · 3.36 Impact Factor
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