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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    • "Selenium, an essential trace element and antioxidant, is known to be used in the prevention of various cancers (Clark et al, 1991, 1996; Zhuo et al, 2004; Brinkman et al, 2006; Amaral et al, 2010). Specific types of selenium, such as MSC, potentiated the therapeutic efficacy of a variety of chemotherapeutic agents against various human tumour xenografts (Cao et al, 2004). "
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    ABSTRACT: Background: Identification and development of drugs that can effectively modulate the therapeutic efficacy and toxicity of chemotherapy remain an unmet challenge. We evaluated the effects of Se-methylselenocysteine (MSC) on the toxicity and antitumour activity of cyclophosphamide, cisplatin, oxaliplatin, and irinotecan in animal models. Methods: Cyclophosphamide, cisplatin, and oxaliplatin were administered by a single i.v. injection and irinotecan by i.v. weekly × 4 schedules. For the combination, MSC was administered daily via the oral route for 7 days in mice and daily for 14 days in rats before and concurrent with drug administration. Results: Se-methylselenocysteine significantly protected against organ-specific toxicity induced by lethal doses of cyclophosphamide, cisplatin, oxaliplatin, and irinotecan. These include diarrhoea, stomatitis, alopecia, bladder, kidney, and bone marrow toxicities. Protection from lethal toxicity by MSC was associated with enhanced antitumour activity in rats bearing advanced Ward colorectal carcinoma and in nude mice bearing human squamous cell carcinoma of the head and neck, FaDu, and A253 xenografts. Conclusions: Se-methylselenocysteine offers selective protection against organ-specific toxicity induced by clinically active agents and enhances further antitumour activity, resulting in improved therapeutic index. These data provided the rationale for the need to clinically evaluate MSC as selective modulator of the antitumour activity and selectivity of anticancer drugs.
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