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Association Between Plasma 25-Hydroxyvitamin D and Colorectal Adenoma According to Dietary Calcium Intake and Vitamin D Receptor Polymorphism
Author(s) -
Taiki Yamaji,
Motoki Iwasaki,
Shizuka Sasazuki,
Hiromi Sakamoto,
Teruhiko Yoshida,
Shoichiro Tsugane
Publication year - 2011
Publication title -
american journal of epidemiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.33
H-Index - 256
eISSN - 1476-6256
pISSN - 0002-9262
DOI - 10.1093/aje/kwr295
Subject(s) - colorectal adenoma , taqi , calcitriol receptor , vitamin d and neurology , odds ratio , medicine , foki , endocrinology , adenoma , gastroenterology , confidence interval , colorectal cancer , calcium , polymorphism (computer science) , biology , genetics , genotype , cancer , gene
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 FokI and TaqI 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 TaqI 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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