Meta-analysis of observational studies of serum 25-hydroxyvitamin D levels and colorectal, breast and prostate cancer and colorectal adenoma

European Institute of Oncology, Milano, Italy.
International Journal of Cancer (Impact Factor: 5.01). 03/2011; 128(6):1414-24. DOI: 10.1002/ijc.25439
Source: PubMed

ABSTRACT Epidemiological studies have suggested a reduced risk of several cancers associated with high vitamin D status. We performed a systematic review with meta-analyses of observational studies of serum 25-hydroxyvitamin D level and colorectal, breast and prostate cancer and colonic adenoma. The literature of December 2009 was searched without language restriction. The meta-regression analysis was done to compute dose-response effects. Because in case-control studies, serum 25-hydroxyvitamin D level is measured after the diagnosis of cancer, separate analyses for case-control and prospective studies were done. We identified 35 independent studies. The seven studies on colorectal adenomas were heterogeneous in terms of endpoint and control for major confounding factors, and we did not perform a meta-analysis of these data. The summary relative risk (SRR) and (95% confidence interval) for a 10 ng/ml increase in serum 25-hydroxyvitamin D was 0.85 (0.79; 0.91) for colorectal cancer (2,630 cases in 9 studies); 0.89 (0.81;0.98) for breast cancer (6,175 cases in 10 studies); and 0.99 (0.95;1.03) for prostate cancer (3,956 cases in 11 studies). For breast cancer, case-control studies (3,030 cases) had major limitations and obtained SRR of 0.83 (0.79; 0.87) whereas SRR of prospective studies (3,145 cases) was 0.97 (0.92; 1.03). For colorectal and breast cancer, differences between cases and controls in the season of blood draw or in overweight/obesity or physical inactivity could not explain the results. In conclusion, a consistent inverse relationship between serum 25-hydroxyvitamin D levels and colorectal cancer was found. No association was found for breast and prostate cancer.

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Available from: Brian Cox, Jul 31, 2015
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    • "Reduced serum levels of 25(OH)D have been reported correlated with several detrimental health effects [5] [6] [7] [8], including worst prognosis of some cancers [9] [10]. A meta-analysis of 35 independent case-control and cohort studies investigating the association of serum 25(OH)D levels with cancer showed a consistent inverse relationship between circulating 25(OH)D levels and colorectal cancer risk [11]; no similar conclusions could however be drawn for other cancer sites. Notably, so far none of the randomised, controlled trials has shown that vitamin D supplementation can prevent cancer [12] [13] although the increase in vitamin D serum levels achieved in one of these trials, the Women's Health Initiative study, was probably insufficient [14]. "
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    • "This effect is probably partly mediated, at least for some tumours [51], by the increase of vitamin D blood levels, and it could be speculated that the SSR for these tumours would be even higher in its absence. Genetic syndromes have been documented in which mutations at specific genes lead to an increased risk of both melanoma and malignancy at some other site [51] [52] [53] [54], but they are usually rare and can account for only a small part of the results we observed, and only for malignancies at some selected sites. Likewise, adjuvant therapy has a predictably low impact on risk of SPM among melanoma patients, considering the very low percentage of such patients that are treated in this way [55]. "
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    • "Results from studies of serum 25(OH)D levels and breast cancer risk have been inconsistent, which may be due to differences in the timing of serum 25(OH)D measurement relative to cancer diagnosis (Gandini et al. 2011); the inadequacy of a single blood sample in many populations for assessing individuals' usual circulating 25(OH)D levels, which vary by season and possibly over years (Rejnmark et al. 2006); or to the possibility of false-positive findings in some studies. 1,25(OH) 2 D exerts most of its known physiological effects through binding to the vitamin D receptor (VDR) (Krishnan and Feldman 2011). "
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