Dietary phosphorus, calcium metabolism and bone

Abstract

Many American women consume diets high in phosphorus and low in calcium. Concern about this dietary pattern stems from studies that show high phosphorus, low calcium intake causes secondary hyperparathyroidism and bone loss in several animal models. Recent studies in young adults have shown that a high phosphorus, moderately low calcium intake results in mild secondary hyperparathyroidism that persisted over 4 wk. However, plasma concentrations of the active form of vitamin D did not change in these subjects, despite stimulatory changes in parathyroid hormone and serum ionized calcium. Studies in normal adult men have shown that dietary phosphorus at levels within the observed normal range of intake can finely regulate the renal production and serum concentration of 1,25-dihydroxycholecalciferol. Thus, prolonged high phosphorus intake may impair the usual homeostatic mechanisms that are evoked when dietary calcium is limited. The current dietary patterns of high phosphorus, low calcium consumption result in persistent changes in the calcium regulating hormones that are not conductive to optimizing peak bone mass or slowing the rate of bone loss.