S rySeventy-nine patients with colorctal adenomata were randomised to receve calcium carbonate (3,000 mg) or plaebo in a double-blnd randomised trial to assms the short-and long-term effects on rectal mucosal proiferation mesued by the in vitro aas arrt technique crypt cell producton rate (CCPR). There was no signifkant difference in mean CCPR between the groups before treatment or after 3 or 12 months. In those paients randonised to calcium, CCPR fel at both 3 months [9.0 (2.8) It is becoming clear that while genetic changes play an important part in the genesis of colorectal cancer the major influences are likely to be dietary (Armstrong, 1975;Fearon and Vogelstein, 1990;Willett et al., 1990). Diet is complex in most societies, and identifying those constituents which substantially influence the risk of colorectal cancer is the subject of much study (Armstrong, 1975;Willett et al., 1990;Thun et al., 1993). The results of such studies are not as yet clear and are often conflicting, but it would appear that a diet which is high in animal fat and low in fibre is associated with a high risk; conversely, a diet low in fat and high in fibre appears to be protective (Armstrong, 1975;Willett et al., 1990).An attempt to modify diet in order to reduce cancer risk is seen as a possible goal. However, there are two major difficulties in determining efficacy in diet intervention. The first is deciding which element of the diet to modify and the second is the end point required. Clarly the best end point is the reduction in mortality from colorectal cancer. However, this would require very large numbers of individuals to be recruited and studied over decades. Intermediate end points have therefore been sought, the most obvious of which is the adenoma, widely held as the benign precursor of most cancers (Morson, 1974). The incidence of new adenomas or the change in size of existing adenomas may be useful, since intervention may cause either a reduction in the number of new adenomas formed in a 'clean colon' or reduction in growth or regression of existing adenomas. Fmally, one can utilise changes in rectal mucosal proliferation. An increase in mucosal proliferation is thought to be an early step in the genesis of colorectal neoplasia (Fearon and Vogelstein, 1990). We have previously shown that individuals at increased risk of colorectal cancer have elevated mucosal proliferation (Rooney et al., 1993a), and this finding has been confirmed by others (Terpstra et al., 1987; Anti et al., 1993). Reduction of rectal mucosal proliferation by an intervention may be evidence of an effect on reduction of risk of colorectal cancer and perhaps a modification of the progression to cancer.A number of investigators have studied the effect of calcium on the risk of colorectal cancer. There is some epidemiological evidence that diets high in calcium may be protective for colorectal cancer (Garland et al., 1985;Sorenson et al., 1988). There is no ckar mechanism of action, but much of its action is thought to be by binding faecal bile acids ...