Eating frequency and colon cancer risk.

Increased exposure of the colon to bile acids, as a result of increased eating frequency, might promote the development of colon cancer. Our aim was to evaluate the association between eating frequency and colon cancer. We used data from a population-based case-control study of colon cancer in North Carolina. Eating frequency (a combination of meals and snacks) was categorized as fewer than three, three or four, or more than four eating episodes per day. Multivariate logistic regression was used to calculate odds ratios (ORs) for the association between eating frequency and colon cancer, adjusting for confounders. We also performed stratified analyses to evaluate for differences by sex, coffee intake, or tumor site. Six hundred thirty-six participants with colon cancer and 1,048 control participants were included. The effect of eating frequency on colon cancer differed by sex. Among men, participants in the lowest group of eating frequency had approximately half the risk of colon cancer compared with the middle group (adjusted OR = 0.53; 95% confidence interval, CI = 0.30-0.92). Compared with the middle group, men in the highest group had no greater risk of cancer (adjusted OR = 1.03; 95% CI = 0.74-1.44). No significant associations were detected among women. Decreased eating frequency was associated with a lower risk of colon cancer among men but not women.

Vitamin C intake and apoptosis in normal rectal epithelium.

Apoptosis, or programmed cell death, may lower the risk of neoplasia by removing genetically damaged or mutated cells. A high rate of apoptosis has been linked to a reduced risk of colorectal adenomas; therefore, it is important to understand factors that impact apoptosis. Antioxidants (e.g., vitamin C) protect cells from harmful oxidation processes but may interfere with apoptosis by protecting genetically damaged cells from reactive oxygen species-dependent cell death. The objective of this study was to evaluate the association between vitamin C intake and apoptosis in normal rectal mucosa. Study participants were part of a large, cross-sectional study, the Diet and Health Study III. Participants were recruited from consecutive, consenting patients who underwent colonoscopy at University of North Carolina Hospitals between August 1, 1998 and March 4, 2000. Vitamin C intake, obtained from a food frequency questionnaire, included both dietary sources and vitamin supplements. Apoptosis was measured by morphological evaluation of H&E-stained sections obtained from pinch biopsy samples of normal rectal mucosa in consenting participants (n = 503). The relationship between vitamin C and apoptosis varied by adenoma status. Among individuals with adenomas, there was an inverse linear association between apoptosis and total vitamin C intake. Similarly, individuals with adenomas in the highest quintile of total vitamin C intake were substantially less likely than those in the lowest quintile to have increased colonic apoptosis (odds ratio, 0.05; 95% confidence interval, 0.01-0.46). Vitamin C was not significantly associated with apoptosis in adenoma-free patients. High vitamin C intake was associated with reduced colorectal apoptosis among individuals with adenomas in this study population. Given that high apoptosis may lower colorectal cancer risk, vitamin C supplements may be contraindicated for patients with a history of adenomas.