Article

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: 4.28). 04/2007; 32(3):210-6. DOI: 10.1016/j.amepre.2006.11.004
Source: PubMed

ABSTRACT 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.

Download full-text

Full-text

Available from: William Burgess Grant, Aug 22, 2015
1 Follower
 · 
125 Views
  • Source
    • "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). "
    [Show abstract] [Hide abstract]
    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
  • Source
    • "A 19 year prospective study found a significant inverse association between the risk of CRC and dietary intake of vitamin D and calcium, even when adjusted for age, BMI, cigarette and alcohol consumption (Garland et al., 1985). In a quantitative meta-analysis, a 25[OH]D concentration greater than 33 ng/mL was associated with a 50% lower risk of developing CRC in comparison to a value of less than 12 ng/mL, and a linear relationship between 25[OH]D values and the risk of CRC was noted (Gorham et al., 2007). In a more recent systematic review of prospective studies comprising approximately 1,000,000 patients, vitamin D intake and serum 25[OH]D concentration were inversely associated with the risk of developing CRC (Grau et al., 2003). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Diabetes and cancer are common diseases that may co-exist in the same individual. There is significant evidence that patients with diabetes have increased risk of developing certain cancers, especially colorectal, pancreatic and primary hepatic cancer. There is also good evidence that low levels of vitamin D are associated with increased risk of diabetes and increased risk of colorectal, and possibly other, cancers. In this article we propose that low levels of vitamin D may increase the risk of cancer in people with diabetes and describe potential molecular pathways. We suggest that large scale randomised trials of vitamin D supplementation in patients at risk of diabetes, and in patients with established diabetes to examine the effect on cancer risk, are required.
    Journal of diabetes and its complications 11/2012; DOI:10.1016/j.jdiacomp.2012.10.005 · 1.93 Impact Factor
  • Source
    • "Higher 25(OH)D levels are associated with a lower risk of incident left-sided colorectal adenomas [135]. Multiple meta-analyses , and large prospective and retrospective observational studies have established that vitamin D deficiency is associated with an increased risk of colon [136] [137] [138] [139], breast [140] [141] [142], and prostate cancer [143] [144]. Furthermore, increased sunlight exposure is associated with a reduced risk of non-Hodgkin's lymphoma [145] and VDR polymorphisms are associated with adenocarcinoma in the colon [146], ovary [147], breast, prostate, renal cell carcinoma, and melanoma [148]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Vitamin D is synthesized predominantly in the liver and functions as an important secosteroid hormone with pleiotropic effects. While its key regulatory role in calcium and bone homeostasis is well established, recently there is increasing recognition that vitamin D also regulates cell proliferation and differentiation, and has immunomodulatory, anti-inflammatory and anti-fibrotic properties. These non-skeletal effects are relevant in the pathogenesis and treatment of many causes of chronic liver disease. Vitamin D deficiency is frequently present in chronic liver disease and may predict non-response to antiviral therapy in chronic hepatitis C. Small studies suggest that vitamin D supplementation improves sustained viral response rates, while 1α-hydroxylase polymorphisms and vitamin D-binding protein are also implicated in therapeutic outcomes. Vitamin D deficiency also closely relates to the severity of non-alcoholic fatty liver disease (NAFLD) and is implicated in the pathogenesis of insulin resistance, a key factor in the development of NAFLD. In preclinical studies, phototherapy and vitamin D supplementation ameliorate NAFLD histopathology, while vitamin D is a powerful anti-fibrotic against thioacetamide liver injury. In liver transplant recipients severe vitamin D deficiency predicts, and vitamin D supplementation prevents, acute cellular rejection. The role of vitamin D in the activation and regulation of both innate and adaptive immune systems may explain its importance in the above liver diseases. Further prospective studies are therefore warranted to investigate the therapeutic impact of vitamin D supplementation in chronic liver disease.
    Journal of Hepatology 05/2012; 57(4):897-909. DOI:10.1016/j.jhep.2012.04.033 · 10.40 Impact Factor
Show more