Article

Association Between Vitamin D and Risk of Colorectal Cancer: A Systematic Review of Prospective Studies

The Sixth People's Hospital affiliated with Shanghai Jiao Tong University, 600 Yishan Rd, Shanghai 200233, People's Republic of China.
Journal of Clinical Oncology (Impact Factor: 18.43). 08/2011; 29(28):3775-82. DOI: 10.1200/JCO.2011.35.7566
Source: PubMed

ABSTRACT To conduct a systematic review of prospective studies assessing the association of vitamin D intake or blood levels of 25-hydroxyvitamin D [25(OH)D] with the risk of colorectal cancer using meta-analysis.
Relevant studies were identified by a search of MEDLINE and EMBASE databases before October 2010 with no restrictions. We included prospective studies that reported relative risk (RR) estimates with 95% CIs for the association between vitamin D intake or blood 25(OH)D levels and the risk of colorectal, colon, or rectal cancer. Approximately 1,000,000 participants from several countries were included in this analysis.
Nine studies on vitamin D intake and nine studies on blood 25(OH)D levels were included in the meta-analysis. The pooled RRs of colorectal cancer for the highest versus lowest categories of vitamin D intake and blood 25(OH)D levels were 0.88 (95% CI, 0.80 to 0.96) and 0.67 (95% CI, 0.54 to 0.80), respectively. There was no heterogeneity among studies of vitamin D intake (P = .19) or among studies of blood 25(OH)D levels (P = .96). A 10 ng/mL increment in blood 25(OH)D level conferred an RR of 0.74 (95% CI, 0.63 to 0.89).
Vitamin D intake and blood 25(OH)D levels were inversely associated with the risk of colorectal cancer in this meta-analysis.

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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. "
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    ABSTRACT: Vitamin D is formed mainly in the skin upon exposure to sunlight and can as well be taken orally with food or through supplements. While sun exposure is a known risk factor for skin cancer development, vitamin D exerts anti-proliferative and pro-apoptotic effects on melanocytes and keratinocytes in vitro. To clarify the role of vitamin D in skin carcinogenesis, we performed a review of the literature and meta-analysis to evaluate the association of vitamin D serum levels and dietary intake with cutaneous melanoma (CM) and non-melanoma skin cancer (NMSC) risk and melanoma prognostic factors. Twenty papers were included for an overall 1420 CM and 2317 NMSC. The summary relative risks (SRRs) from random effects models for the association of highest versus lowest vitamin D serum levels was 1.46 (95% confidence interval (CI) 0.60-3.53) and 1.64 (95% CI 1.02-2.65) for CM and NMSC, respectively. The SRR for the highest versus lowest quintile of vitamin D intake was 0.86 (95% CI 0.63-1.13) for CM and 1.03 (95% CI 0.95-1.13) for NMSC. Data were suggestive of an inverse association between vitamin D blood levels and CM thickness at diagnosis. Further research is needed to investigate the effect of vitamin D on skin cancer risk in populations with different exposure to sunlight and dietary habits, and to evaluate whether vitamin D supplementation is effective in improving CM survival.
    European journal of cancer (Oxford, England: 1990) 07/2014; 50(15). DOI:10.1016/j.ejca.2014.06.024 · 4.82 Impact Factor
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    • "However, results were rather inconsistent both within and across various forms of cancer. Evidence for an inverse association of serum 25(OH)D concentration with cancer is the most consistent for breast cancer (Chen et al., 2013), colorectal cancer (Gandini et al., 2011; Lee et al., 2011; Ma et al., 2011; Touvier et al., 2011; Yin et al., 2009a), colorectal adenoma (Wei et al., 2008; Yin et al., 2011b), uncertain for ovarian cancer (Yin et al., 2011a), and absent for prostate cancer (Yin et al., 2009b). For other forms of cancer, only single or very few studies have been published to date, some of which even point to a possibly increased cancer risk at very high Fig. 1. "
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    ABSTRACT: To conduct a systematic review and meta-analysis of longitudinal studies on the association of 25(OH)D with total cancer incidence and mortality. Relevant longitudinal observational studies were identified by systematically searching Ovid Medline, EMBASE, and ISI Web of Knowledge databases. Due to the heterogeneity across studies in categorizing 25(OH)D concentration, all results were recalculated for an increase of 25(OH)D by 50 nmol/L. In meta-analyses with random effects models, the summary risk ratios and confidence intervals (RRs (95% CI)) for the association of an increase of 25(OH)D by 50 nmol/L with total cancer incidence (5 studies) and mortality (13 studies) were 0.89 (0.81, 0.97) and 0.83 (0.71, 0.96), respectively. In sex-specific analyses no significant association with total cancer incidence was observed among men or women. A clear inverse association with total cancer mortality was observed among women (0.76 (0.60, 0.98)) but not among men (0.92 (0.65, 1.32)). Large heterogeneity was observed for studies on total cancer mortality (p<0.01) but not for studies on cancer incidence (p=0.41). No publication bias was found. The meta-analysis suggests a moderate inverse association of 25(OH)D concentration with total cancer incidence and mortality.
    Preventive Medicine 09/2013; 57(6). DOI:10.1016/j.ypmed.2013.08.026 · 2.93 Impact Factor
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    • "Calcium metabolism is under control through the coordinated actions of parathyroid hormone (PTH) and activated vitamin D, and the most common cause of hypocalcemia in primary care is vitamin D deficiency [3]. Vitamin D deficiency is increasing worldwide [4] [5] [6] [7] [8], and it has been drawing much attention in the association of various diseases including cancer, cardiovascular disease, endocrine and metabolic diseases, and infectious and autoimmune diseases [9] [10] [11] [12] [13]. In addition, it has been more recently suggested that vitamin D deficiency is associated with Graves' disease [14] [15] [16]. "
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    ABSTRACT: We herein report the case of a 41-year-old Japanese female office worker who developed symptomatic hypocalcemia with severe vitamin D deficiency following treatment for Graves' disease with methimazole. The patient's hypocalcemia was mainly caused by vitamin D deficiency due to unbalanced diets and inadequate exposure to sunlight in addition to the resolution of hyperthyroidism. Vitamin D deficiency is increasing worldwide, and it has been more recently shown to relate to the pathogenesis of Graves' disease. However, vitamin D deficiency as a cause of hypocalcemia has received little attention. Taken together, this case suggests that we should take more care in calcium kinetics and vitamin D status during treatment for Graves' disease with antithyroid drugs.
    04/2013; 2013:512671. DOI:10.1155/2013/512671
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