Colon Cancer
As just described, unabsorbed dietary calcium forms complexes with unabsorbed fatty acids and bile acids that would otherwise serve as mucosal irritants (and hence cancer promoters). Such complexation effectively renders these irritants harmless, thereby breaking one of the chains of potential colon cancer development. Early epidemiological studies noted a strong inverse relationship between calcium intake and colon cancer risk, with several studies indicating that the risk was minimal at intakes in the range of 45 mmol (1800 mg)/d or higher. As with observational studies in most disorders, the evidence implicating calcium intake is mixed, and even when positive, the results could not by themselves be used to establish a causal connection.
However, animal carcinogenesis studies followed the observational data, showing that unabsorbed fatty acids and bile acids serve as cancer promoters in systems using potent carcinogens, and that a high calcium intake complexed (and hence effectively neutralized) both types of promoter. More importantly, calcium reduced the numbers of cancers that developed. Similarly, studies in humans with a familial cancer tendency showed lower levels of cellular atypia and reduced mitotic indices in those whose calcium intakes were high. At least two randomized trials of calcium supplementation have been recently reported.
Neither used actual cancer as the endpoint, but in one, adenoma recurrence was £ignificantly reduced in calcium-supplemented individuals and in the other, various indices of mucosal hyperplasia were significantly reduced. Thus, although the bulk of the evidence points :0 protection, fmal proof is still not available. This may be because sample size requirements a or cancer endpoint" are large, and no controlled trials to date have involved the requisite number of subject-years of observation. In summary, the epidemiological data, the animal odels, the chemistry of the chyme, and the still limited clinical trials are all concordant, pointing to a protective effect of high calcium intakes for colon cancer risk.