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An assessment of the evidence linking calcium and vitamin D to colon cancer prevention

Authors: Peter W. Parodi


Colorectal cancer is a common form of cancer in both men and women. This review assesses the evidence that calcium and vitamin D protect against colorectal cancer. Although cellular and extracellular calcium levels may be important in carcinogenesis, it is the role of dietary calcium in colonic lumen physiology that has attracted the most attention. Dietary and diet-induced components such as long chain fatty acids and bile acids, which are present in the faecal stream, can be cytotoxic to colonic epithelial cells. Damaged cells are removed by apoptosis. Replacement of these cells causes an increase in the cellular proliferation rate that increases the risk of mutations in oncogenes and tumor suppressor genes, and thus subsequent colorectal cancer. The chemopreventive action of calcium results from the formation of non-toxic insoluble complexes with the cytotoxic lipids. Most animal studies show that dietary calcium can decrease the incidence of chemically induced or bile-acid-promoted cellular proliferation, preneoplastic lesions and colon tumors. However, conflicting results are common with human studies that explore the association between calcium intake and the risk of colorectal adenoma or carcinoma. Although the majority of the studies have demonstrated an inverse association, most did not attain statistical significance. Human intervention studies, where supplemental calcium was used to reduce colonic cell proliferation rate, have also produced conflicting results. This intervention appears to be effective when the initial proliferation rates are high but not when they are normal. There is also limited evidence that calcium supplementation can prevent the recurrence of adenomas in patients who had previously had adenomas resected. Vitamin D3 can likewise help prevent colorectal carcinoma in animals and humans. Moreover, of considerable significance are the studies that suggest vitamin D deficiency can attenuate the beneficial effect of calcium. In this review, reasons for the conflicting outcomes in the various studies are explored in terms of a range of individual, cultural and lifestyle factors. Recent evidence suggests that the effect of calcium on colorectal cancer risk differs according to the molecular nature of the mutated gene. Evaluation of specific types of mutations will need to be included in future studies.

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