Optimal Vitamin D Status for Colorectal Cancer Prevention. A Quantitative Meta Analysis

Section of Endocrinology, Diabetes, Nutrition, Boston University, Boston, Massachusetts, United States
American Journal of Preventive Medicine (Impact Factor: 4.53). 04/2007; 32(3):210-6. DOI: 10.1016/j.amepre.2006.11.004
Source: PubMed


Previous studies, such as the Women's Health Initiative, have shown that a low dose of vitamin D did not protect against colorectal cancer, yet a meta-analysis indicates that a higher dose may reduce its incidence.
Five studies of serum 25(OH)D in association with colorectal cancer risk were identified using PubMed. The results of all five serum studies were combined using standard methods for pooled analysis. The pooled results were divided into quintiles with median 25(OH)D values of 6, 16, 22, 27, and 37 ng/mL. Odds ratios were calculated by quintile of the pooled data using Peto's Assumption-Free Method, with the lowest quintile of 25(OH)D as the reference group. A dose-response curve was plotted based on the odds for each quintile of the pooled data. Data were abstracted and analyzed in 2006.
Odds ratios for the combined serum 25(OH)D studies, from lowest to highest quintile, were 1.00, 0.82, 0.66, 0.59, and 0.46 (p(trend)<0.0001) for colorectal cancer. According to the DerSimonian-Laird test for homogeneity of pooled data, the studies were homogeneous (chi(2)=1.09, df=4, p=0.90. The pooled odds ratio for the highest quintile versus the lowest was 0.49 (p<0.0001, 95% confidence interval, 0.35-0.68). A 50% lower risk of colorectal cancer was associated with a serum 25(OH)D level > or =33 ng/mL, compared to < or =12 ng/mL.
The evidence to date suggests that daily intake of 1000-2000 IU/day of vitamin D(3) could reduce the incidence of colorectal with minimal risk.

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    • "A preliminary analysis of the WHI RCT does not indicate that vitamin D supplements reduce the risk of CRC after a seven-year follow-up period.51 A re-evaluation of these data consistently shows an interaction with estrogens, to the extent that vitamin D amends the effect in relation to the CRC risk depending on whether estrogens were administered concomitantly or not.52 "
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    ABSTRACT: Cancer is a worldwide problem as it will affect one in three men and one in four women during their lifetime. Colorectal cancer (CRC) is the third most frequent cancer in men, after lung and prostate cancer, and is the second most frequent cancer in women after breast cancer. It is also the third cause of death in men and women separately, and is the second most frequent cause of death by cancer if both genders are considered together. CRC represents approximately 10% of deaths by cancer. Modifiable risk factors of CRC include smoking, physical inactivity, being overweight and obesity, eating processed meat, and drinking alcohol excessively. CRC screening programs are possible only in economically developed countries. However, attention should be paid in the future to geographical areas with ageing populations and a western lifestyle.19,20 Sigmoidoscopy screening done with people aged 55-64 years has been demonstrated to reduce the incidence of CRC by 33% and mortality by CRC by 43%.
    Clinical Medicine Insights: Gastroenterology 07/2014; 7:33-46. DOI:10.4137/CGast.S14039
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    • "cit.) and adenoma recurrence [16–18]. Lower dietary intakes of vitamin D have been associated with a higher risk of developing colonic neoplasia [12, 19–21]. Some have suggested that vitamin D insufficiency, which increases with advancing age, is a factor contributing to sporadic CRC, which is also associated with aging [22]. "
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    ABSTRACT: Disparities in both colorectal cancer (CRC) incidence and survival impact African Americans (AAs) more than other US ethnic groups. Because vitamin D is thought to protect against CRC and AAs have lower serum vitamin D levels, genetic variants that modulate the levels of active hormone in the tissues could explain some of the cancer health disparity. Consequently, we hypothesized that genetic variants in vitamin D-related genes are associated with CRC risk. To test this hypothesis, we studied 39 potentially functional single-nucleotide polymorphisms (SNPs) in eight genes (CYP2R1, CYP3A4, CYP24A1, CYP27A1, CYP27B1, GC, DHCR7, and VDR) in 961 AA CRC cases and 838 healthy AA controls from Chicago and North Carolina. We tested whether SNPs are associated with CRC incidence using logistic regression models to calculate p values, odds ratios, and 95 % confidence intervals. In the logistic regression, we used a log-additive genetic model and used age, gender, and percent West African ancestry, which we estimated with the program STRUCTURE, as covariates in the models. A nominally significant association was detected between CRC and the SNP rs12794714 in the vitamin D 25-hydroxylase gene CYP2R1 (p = 0.019), a SNP that has previously been associated with serum vitamin D levels. Two SNPs, rs16847024 in the GC gene and rs6022990 in the CYP24A1 gene, were nominally associated with left-sided CRC (p = 0.015 and p = 0.018, respectively). Our results strongly suggest that genetic variation in vitamin D-related genes could affect CRC susceptibility in AAs.
    Cancer Causes and Control 02/2014; 25(5). DOI:10.1007/s10552-014-0361-y · 2.74 Impact Factor
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    • "In 1980, Garland and Garland hypothesized that lower concentrations of vitamin D, resulting from much weaker UV-B radiation at higher latitudes, may account for the striking geographical pattern of cancer mortality (Garland and Garland, 1980). This hypothesis has remained subject to ongoing debate and further investigation (Armstrong, 2006; Boscoe and Schymura, 2006; Giovannucci, 2006; Gorham et al., 2007; Kampman et al., 2000). "
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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 · 3.09 Impact Factor
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