The fact that fracture risk is lower and BMD is higher in blacks compared with whites is surprising in light of what is known about vitamin D status in blacks. Mean 25(OH)D levels are lower in blacks than whites at all stages of life, and a greater proportion of blacks meet criteria for vitamin D deficiency. The racial difference in serum 25(OH)D level is primarily caused by increased pigmentation reducing vitamin D production in the skin. In response to lower 25(OH)D levels and lower average calcium intake, blacks have higher average PTH levels and a higher prevalence of secondary hyperparathyroidism (twice the prevalence compared with whites for both sexes). This is associated with higher average levels of 1,25(OH)2D and lower urinary calcium excretion but not higher biochemical indices of bone turnover. In fact, in general, biochemical indices of bone formation (particularly osteocalcin levels) are lower in blacks. Bone formation rates assessed histomorphometrically are also lower, although wall thickness is maintained. During a 24-h PTH infusion, increments in levels of three different bone resorption markers are significantly lower in blacks than in whites, providing direct confirmation of the thesis that the black skeleton is resistant to the bone-resorbing effects of PTH, whereas renal sensitivity to PTH is maintained or perhaps even enhanced. Vitamin D supplementation studies in black women have shown inconsistent benefits to BMD. Skeletal and renal adaptations to vitamin D deficiency in blacks might be so effective that vitamin D supplementation might not confer any further benefit to the black skeleton. Benefits of vitamin D supplements in blacks may still play a role, however, in the prevention of other chronic diseases.