4.6 Article

Association Between Plasma 25-Hydroxyvitamin D and Colorectal Adenoma According to Dietary Calcium Intake and Vitamin D Receptor Polymorphism

期刊

AMERICAN JOURNAL OF EPIDEMIOLOGY
卷 175, 期 3, 页码 236-244

出版社

OXFORD UNIV PRESS INC
DOI: 10.1093/aje/kwr295

关键词

adenoma; calcium; case-control studies; intestine, large; Japan; polymorphism, single nucleotide; vitamin D

资金

  1. Ministry of Health, Labor, and Welfare of Japan
  2. Ministry of Education, Culture, Sports, Science, and Technology of Japan [17015049, B-22790579]
  3. National Institute of Biomedical Innovation of Japan
  4. Grants-in-Aid for Scientific Research [22790579, 221S0001] Funding Source: KAKEN

向作者/读者索取更多资源

The anticarcinogenic potential of vitamin D might be mediated by not only calcium metabolism but also other mechanisms initiated by vitamin D receptor (VDR). The authors measured plasma 25-hydroxyvitamin D in healthy volunteer examinees who underwent total colonoscopy in Tokyo, Japan, 2004-2005, and evaluated its influence on colorectal adenoma, both alone and in interaction with VDR polymorphisms, which correspond to the Fold and Taql restriction sites. The main analysis of plasma 25-hydroxyvitamin D included 737 cases and 703 controls. Compared with the lowest quintile of plasma 25-hydroxyvitamin D, only the highest was related to a significantly decreased odds ratio of colorectal adenoma (odds ratio = 0.64,95% confidence interval: 0.45, 0.92). In contrast, all but the lowest quintile of dietary calcium intake presented similarly reduced odds ratios (odds ratio for the highest = 0.67, 95% confidence interval: 0.47, 0.95). Of note, the association between plasma 25-hydroxyvitamin D levels and colorectal adenoma was modified by the Taql polymorphism of the VDR gene (P-interaction = 0.03) but not by dietary calcium intake (P-interaction = 0.93). These observations highlight the importance of vitamin D in colorectal tumorigenesis. Vitamin D might protect against colorectal neoplasia, mainly through mechanisms other than the indirect mechanism via calcium metabolism.

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