Oral calcium supplementation is thought to be a useful interventional agent to decrease colon cancer risk. This is supposedly due, at least in part, to the binding of bile acids and fatty acids by calcium in the colon, thus prohibiting the damaging effects of these substances to the epithelium. To determine the effects of calcium supplementation on fecal fat excretion, 24 subjects kept a fat and calcium constant diet for one week and were supplemented with either 0, 2 or 4 g elemental calcium as calcium carbonate in a double-blind fashion. At the end of the week 72-hour feces was collected, and total fat, neutral fat, fatty acids and the ratio of polyunsaturated and saturated fatty acids (P/S ratio) were measured. Calcium dose-dependently increased the percentual excretion of total fat as related to fat intake: 6.8 ± 0.9% during Og, 7.4 ± 1.0% during 2 g and 10.2 ± 1.4% during 4 g, r = 0.44, p = 0.03. This was due to increased fatty acid excretion, excretion of neutral fat was not affected, nor was the P/S ratio. It is concluded that calcium supplementation modestly increases fecal fatty acid excretion. No adverse metabolic effects are to be expected from this in case of long-term calcium supplementation in subjects at increased risk for colon cancer.

An increased colonic epithelial proliferation rate and an increase of the cryptal proliferative zone are probable markers of increased susceptibility to colonic cancer. In this study an immunohistochemical method using 5-bromodeoxyuridine (BrdUrd) In this study we describe our methodology to measure the proliferation rate of colonic mucosa in vitro using immunohistochemistry in normal controls and patients with colonic neoplasms. This study was performed using normal looking colonic mucosa, which is especially important in view of the potential use of this method for identification of high risk patients and in dietary intervention studies. MethodsBiopsy specimens of endoscopically normal looking colonic mucosa were taken at 30 cm from 10 healthy subjects (six men, four women, mean age 44-5 years, range 17 to 75 years) who underwent diagnostic sigmoidoscopy and who were found not to have organic colonic disorders. In all these patients a barium enema and histological examination of the biopsy specimens yielded normal results. Biopsy specimens of endoscopically normal looking colonic mucosa were taken at 30 cm from 14 patients (nine men, five women, mean age 68-7 years, range 47 to 85 years) who had one or more adenomatous colonic polyps or a colon carcinoma, or who had undergone surgery for colon carcinoma in the recent past. The polyps were located in the sigmoid colon and the tumours were localised throughout the whole colon and in the sigmoid. The size of the polyps ranged from 3 to 45 mm.

Calcium has been proposed to prevent colon cancer in subjects at risk for this tumour. This effect is supposed to be due at least in part to binding the bile acids to calcium, making them insoluble and harmless. To evaluate the effects of oral calcium supplementation on intestinal bile acids, 19 patients with adenomatous colonic polyps were supplemented with 35.5 mmol Ca2+ daily for 12 weeks. Duodenal bile, 24-h feces and 24-h urine were collected before and at the end of the 12-week period. In duodenal bile proportional concentration of cholic acid increased (38 +/- 4 vs. 51 +/- 3%, P < 0.001), whereas that of chenodeoxycholic acid decreased (35 +/- 3 vs. 25 +/- 2%, P < 0.01). Total fecal bile acid excretion increased (950 +/- 126 vs. 1218 +/- 137 mumol 24 h-1, P < 0.01), with proportional concentrations of the main primary and secondary bile acids remaining the same. Cytolytic activity of fecal water, measured by the degree of lysis of erythrocytes by the water, decreased (45 +/- 8 vs. 30 +/- 7%, P < 0.05). Total excretion of calcium increased as expected from the supplementary dose. It is concluded that calcium supplementation markedly affects intestinal bile acids and lytic activity of fecal water and that, in view of similar results during 1-week calcium supplementation in young healthy subjects, these effects remain constant over at least 3 months and occur both in healthy persons and in patients at increased risk for colon cancer.

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