rus, and then even sharply reduced phosphorus diets may still be excessive as they lead to hyperphosphatemia.

Although metastatic calcification can occur in patients with endstage renal disease in whom ECF Pi levels are not adequately controlled, it is not known to occur from dietary sources alone in persons with adequate renal function. For that reason, calcification in previously normal kidneys produced by high phosphorus intakes has been studied mainly in rats and mice (Craig, 1959; Hamuro et al., 1970; McFarlane, 1941; NRC, 1995). Production of calcification has required very high phosphate loads over and above the animals' already high basal phosphate intakes and in several reports has required partial reduction of renal tissue mass, as well.

Skeletal Porosity

Skeletal lesions associated with high phosphorus intakes have been described in rabbits (Jowsey and Balasubramaniam, 1972) and bulls (Krook et al., 1975). As with kidney toxicity, the bony lesions required extremely large phosphate intakes (in rabbits, about 40-fold typical human intakes on a body weight basis, and in bulls, feeding of a ration designed to support milk production in cows). None of these situations has any evident direct relevance to human nutrition or to human dietary intake of phosphate. Krook et al. (1975) also noted that bone loss develops in household pets and zoo animals fed human table scraps and meat. Despite acknowledging that such foods are poor in calcium, they attribute the bone loss to the high phosphorus content of such diets. Lacking evidence that phosphorus would produce this effect with diets adequate in calcium, this conclusion seems unwarranted. Finally, given the evidence cited above that high phosphorus intakes in humans do not lead to negative calcium balance or to increased bone resorption, it seems likely that the bone disease in other animals is more a consequence of low effective calcium intake than of high phosphorus intake per se.

Interference with Calcium Absorption

As noted, some concerns have been expressed that a high phosphorus intake could interfere with calcium nutrition by complexing calcium in the chyme and reducing its absorption (Calvo and Heath, 1988; Calvo and Park, 1996). Given the relative absorption efficiencies of calcium and phosphorus, there would not be a stoichiometric excess of phosphorus relative to calcium in the chyme until the Ca:P intake ratio fell below 0.375:1. However, even this is a purely theoretical concern. In the studies of Spencer et al. (1978a), in

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