CALCIUM-PHOSPHATE SUPPLEMENTATION RESULTS IN LOWER RAT FECAL BILE-ACID CONCENTRATIONS AND A MORE QUIESCENT COLONIC CELL-PROLIFERATION PATTERN THAN DOES CALCIUM LACTATE

Although there is general agreement that dietary calcium is protective against colon carcinogenesis, considerable controversy exists on the relative efficacy of the counterion in calcium supplements We therefor e conducted a comparative study in rats of four forms of calcium suppl ementation (calcium phosphate, casein, lactate, and a 50:50 phosphate- carbonate combination). The relative effects of these supplements on m easurements of colon physiology, in vivo pH, fecal fat, individual bil e acids, and in vivo cell proliferation were measured in the same anim als. In contrast to results when amounts of calcium are varied, there was no effect of form of supplement on total fecal output or output of fecal fat. Calcium phosphate resulted in the most acidified cecal con tents. Calcium phosphate and calcium casein resulted in lower fecal co ncentrations of lithocholate and lower amounts of total fecal bile aci ds than supplementation with the calcium lactate or combination diets. In addition, rats fed calcium phosphate had lower concentrations of f ecal beta-muricholate than rats provided with the calcium combination supplement. In the proximal colon, calcium phosphate resulted in a sig nificantly lower number of cells per crypt column and a lower labeling index than the calcium lactate diet. The position of the highest labe led cell was lower with calcium phosphate supplementation than with su pplementation from the calcium combination or the calcium lactate diet . There was a highly significant correlation between the pH of cecal c ontents and labeling index in the proximal colon (r = 0.98, p = 0.003) . The results suggest that calcium phosphate may inhibit colon tumor i ncidence more effectively than calcium lactate, because the calcium ph osphate group had a lower colonic proliferative status than the calciu m lactate group. Changes in the proliferative status of colonocytes ar e known to precede and accompany neoplasia.