Association Between Plasma 25-Hydroxyvitamin D and Colorectal Adenoma According to Dietary Calcium Intake and Vitamin D Receptor Polymorphism
– Source: American Journal of Epidemiology, Feb 1, 2012
By T Ymaji, et al.
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 [fifth] 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). [An odds ratio of 1.0 would indicate no difference. The OR of 0.64 indicates cancer risk in highest vitamin D group was 36% less than in the group with least D.]
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 (Pinteraction = 0.03) but not by dietary calcium intake (Pinteraction = 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.
Source: American Journal of Epidemiology, Feb 1, 2012. Yamaji T, Iwasaki M, Sasazuki S, Sakamoto H, Yoshida T, Tsugane S. Epidemiology and Prevention Division, Research Center for Cancer Prevention and Screening, National Cancer Center, Tokyo, Japan [Email: firstname.lastname@example.org]