Hypoparathyroid patients have for decades been subjected to vitamin D therapy, in varying pharmacologic doses, with widely discrepant responses. They have been hypocalcemic on extremely large doses of the vitamin and hypercalcemic on doses that are not toxic to normal persons. The resistance to conventional forms of vitamin D and calcium supplementation therapy has produced a need for other therapeutic preparations. Dihydrotachysterol (DHT), 25-(OH)D₃ and 1⍺-(OH)D have been tried in short-term studies, often with limited success. More detailed analyses of long-term results of therapy with 25-(OH)D, 1,25-(OH)₂D or 1⍺-(OH)D are warranted before their superiority over vitamin D and DHT therapy can be established. Until such time that these substances are available in sufficient quantities for these studies, a rational approach to vitamin D therapy should include a more definitive analysis of the factors leading to the hypocalcemic hyperphosphatemic state. This knowledge should be combined with an appreciation of the effects of emotion and psychologic stress, estrogens, oral contraceptives, tranquilizers, anticonvulsants, magnesium deficiency, dietary indiscretions and diuretics on calcium homeostasis. Measurements of circulating PTH levels and para-thyroid reserve, and reservations about accepting urinary values as estimates of circulating calcium levels in treated patients would add additional sophistication to planned therapeutic approaches with vitamin D. The final result of these combined endeavors may ultimately lead to better control and a much happier patient.