Attempts have been made to utilize vitamin D for prevention and treatment of hypocalcemia in postpartum dairy cows since the discovery that vitamin D was required for calcium homeostasis. A few initial experiments established that feeding 10,000 to 20,000 IU of vitamin D₃ was adequate for maintaining blood Ca concentrations in lactating dairy cows. Hypocalcemia, however, is not necessarily a vitamin D nutrition problem but, rather, the inability of Ca homeostatic mechanisms to account for irreversible mammary loss with the onset of lactation. The failure to maintain Ca homeostasis, in part, is due to inadequate synthesis of 1,25-dihydroxyvitamin D₃ from 25-hydroxyvitamin D₃ in response to parathyroid hormone and decreased sensitivity of tissues to 1,25-dihydroxyvitamin D₃. Feeding acidogenic diets prepartum to induce a compensated metabolic acidosis is a proven strategy to minimize postpartum hypocalcemia. A diet with negative DCAD increases concentrations of 1,25-dihydroxyvitamin D₃ in serum in response to parathyroid hormone and, perhaps more important, it increases Ca flux from intake and skeletal stores to urine which can be rapidly diverted to the mammary gland at the onset of lactation. Increasing supplemental vitamin D₃ above current practices (30,000 to 50,000 IU/d) does little to augment a prepartum diet with negative DCAD because cows seem to have a limited capacity to convert vitamin D₃ to 25-hydroxyvitamin D₃. However, dose titration experiments with supplemental vitamin D₃ in combination with a negative DCAD are needed. In contrast, feeding 25-hydroxyvitamin D₃ in combination with a diet with negative DCAD is a promising approach to improving Ca homeostasis and performance of transition cows on the basis of ouctomes from recent experiments. Parental administration of 1,25-dihydroxyvitamin D₃ at, or soon after, parturition also results in a sustained increase in serum Ca. In summary, vitamin D is required for Ca homeostasis, but vitamin D nutrition is not the sole solution to hypocalcemia. A prepartum diet with negative DCAD is effective at reducing the risk of hypocalcemia and may benefit from nutritional or therapeutic use of vitamin D metabolites.