Dietary calcium does not reduce experimental colorectal carcinogenesis after small bowel resection despite reducing cellular proliferation.

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Abstract
It has been proposed that colorectal carcinogenesis is accompanied by increased mucosal cell proliferation and that the converse may also apply. To examine this thesis, the crypt cell production rate (CCPR) was measured in eight groups of rats (n = 187) that had received 1,2 dimethylhydrazine, 70% small bowel resection, supplemental dietary calcium, or a combination of these. Analysis of variance showed the following: (1) the CCPR decreased between the ileum and distal colon; (2) the CCPR decreased between 16 and 32 weeks; (3) 1,2 dimethylhydrazine and small bowel resection increased the CCPR and calcium decreased the CCPR independently of one another; (4) the CCPR interacted with 1,2 dimethylhydrazine x small bowel resection, calcium x 1,2 dimethylhydrazine and interacted between the site of bowel and calcium, 1,2 dimethylhydrazine, small bowel resection, and 1,2 dimethylhydrazine x small bowel resection (p = 0.014 to p < 0.001). The tumour yield was reduced by calcium in 1,2 dimethylhydrazine treated animals (chi 2 = 14.1, df = 3, p < 0.01) but was unaffected by calcium in 1,2 dimethylhydrazine and small bowel resection treated animals despite significant differences in the CCPR. An increase of the CCPR both preceded and accompanied colorectal carcinogenesis but reduction of the CCPR was not invariably accompanied by reduced carcinogenes.