Dietary Phosphorus and Bone Disease

The intake of phosphorus from foods, both inorganic and organic sources, may exert an adverse effect on the homeostatic regulation of calcium as well as of phosphate if it is too high or too low. This effect is especially true when the ratio of dietary calcium to dietary phosphorus is below 0.5–1 or greater than 1.5–1. These skewed dietary ratios stimulate hormonal responses of parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23) that result from altered serum concentrations of ionic calcium (Ca2+) and ionic phosphate (Pi2−). Skeletal responses to these hormones result in changes in bone, both cortical and cancellous, that may contribute to suboptimal structure and function. When phosphorus intake is too high, phosphate-induced bone loss may if the abnormal dietary intake pattern becomes prolonged; these conditions are referred to as hyperparathyroid-induced osteopenia or osteoporosis. High phosphorus intakes are of less concern in those individuals with reasonably healthy renal function because of the normal responses of FGF-23 and PTH that promptly act following meals. In those with declining renal function, as well as in chronic renal failure, concerns of bone loss from high phosphate intakes remain.