Evidence has been accumulating over a number of years that phosphate supplements, and possibly dietary phosphate intake, may cause accelerated bone loss. In early studies (Krook & Lowe 1964, Joyce et al. 197i, Draper et al. 1972), predominantly in young animals, high diet iry phosphate levels produced frank secondary hyperparathyroid-ism accompanied by hyperphosphatemia; however, in later studies (Jv'sey & Balasubramaniam 1972, Laflamme & Jowsey 1972) in adult anir, ials, a disease resembling osteoporosis was produced and was characterized by increasing bone porosity and normal serum chemistry values. The suggestion has been made that osteoporosis may be a form of low-grade secondary hyperparathyroidism, and in some patients the osteoporosis was found to be associated with serum parathyroid hormone (PTH) levels above normal (Fujita et al. 1973, Riggs et al.