The effect of dietary calcium supplementation on intestinal lipid metabolism

Population studies in man and experimental animal work support the contention that dietary supplementation with calcium may prevent the development of colorectal cancer. The mechanism of action is postulated to be bile acid chelation in the small-bowed forming non-toxic calcium soap compounds but such substances have yet to be isolated and quantified. In this 2-part study faecal concentrations of acidic lipids and neutral sterols were measured in 93 Sprague-Dawley rats whose calcium intake was modulated by enriching the chow and adding calcium lactate (24 g/l) to the drinking water. In study-1 (dietary calcium intake doubled from 0.4–0.8%) small bowel resection was used to manipulate colonic lipid concentration for comparison with control rats who had undergone transection with immediate restoration of bowel continuity at an equivalent point. Faecal concentrations of free bile acids were 53–67% less in animals receiving added calcium [1.76 ± 1.33 vs 0.82 ± 0.65 mg/g (transection); 2.74 ± 3.73 vs 1.03 ± 1.27 mg/g (small bowel resection): P < 0.001]. In study-2 (dietary calcium intake trebled to 1.21%) faecal bile acid concentration was reduced by 32% (1.86 ± 0.57 vs 1.27 ± 0.34 mg/g: NS) whereas long chain fatty acid concentrations were increased by 117% (6.77 ± 2.39 vs 14.67 ± 4.82 mg/g: P < 0.001) in animals receiving added calcium. Serum calcium levels remained unchanged in these animals. Calcium soaps of the bile acids were not detected in faeces and therefore contrary to popular theory these results indicate that conditions within the intestinal lumen favour calcium chelation of long chain fatty acids rather than bile acids.