Snedeker et al., 1982). For this reason, as well as because trace mineral status may be low for many reasons, it was not considered feasible to use trace mineral status as an indicator of excess phosphorus intake. Nevertheless, given the trend toward increased use of phosphate additives in a variety of food products (Calvo and Heath, 1988; Calvo and Park, 1996), it would be well to be alert to the possibility of some interference in individuals with marginal trace mineral status.
Most of the studies that describe harmful effects of phosphorus intake used animal models. In extrapolating these data to humans, it is important to note that the phosphorus density of human diets represents the extreme low end of the continuum of standard diets for pets and laboratory animals. The median human dietary phosphorus density in the 1994 CSFII was very close to 62 mg (2.0 mmol)/100 kcal for all adults and for both sexes (Cleveland et al., 1996). By contrast, the diets of standard laboratory rats and mice have phosphorus densities ranging from 124 to 186 mg (4 to 6 mmol)/100 kcal. Cats and dogs have diets with densities close to 279 mg (9 mmol)/100 kcal, and laboratory primate diets average about 155 mg (5 mmol)/100 kcal.
As noted earlier, Pi is not, strictly speaking, regulated. Thus, a high phosphorus diet produces a higher level of plasma Pi, especially during the absorptive phase after eating. High Pi levels reduce urine calcium loss, reduce renal synthesis of 1,25(OH) 2D, reduce serum ionized calcium, and lead to increases in PTH release (Portale et al., 1989; Wood et al., 1988). These effects reflect adjustments in the control system that regulates the calcium economy and are not in themselves necessarily adverse. As already noted, the reduction in 1,25(OH)2D synthesis may slightly mitigate the hyperphosphatemia by a small reduction in phosphorus absorption from the intestine.
It is known that added dietary phosphate loads of 1.5 to 2.5 g of inorganic phosphorus (as phosphate) in humans lead acutely to very slight drops in ECF [Ca2+] and to correspondingly elevated PTH concentrations (Calvo and Heath, 1988; Silverberg et al., 1986). It has been proposed that these adjustments in circulating calcium regulating hormones (associated with any elevation of serum Pi, even though within the usual normal range) could have adverse effects on the skeleton (Calvo and Heath, 1988; Calvo et al., 1988, 1990; Krook et al., 1975). The increase in PTH is often pre-