It is well established that bone metabolism in African American subjects differs from the Caucasians in several aspects. The mean 25-hydroxyvitamin D levels are lower in African-Americans primarily due to reduced vitamin D production in the skin associated with increased pigmentation as well as reduced intake of vitamin D. As a consequence, African-Americans have relative secondary hyperparathyroidism and resultant higher levels of PTH, and 1, 25 dihydroxyvitamin D, and lower urinary calcium excretion. One would expect that patients with secondary hyperparathyroidism would result in increased bone turnover and decreased bone mass. This is not what is observed in African Americans though. African Americans have higher bone density and lower fracture risk as compared to Caucasians. Moreover, biochemical markers of bone turnover in African-Americans are in general lower than in Caucasians, particularly for bone formation, as measured by osteocalcin. On the other hand, there is normal or increased renal absorption of calcium. Based on these, Dr. Normal Bell proposed that the black skeleton is resistant to the effects of PTH, while renal sensitivity is maintained or even enhanced. This hypothesis is further supported by the observation of significantly lower bone resorption (as measured by cross-linked N-telopeptide of procollagen I (NTx), cross-linked C-telopeptide of type I collagen (CTx), and free deoxypyridinoline (DPD) and normal to low renal excretion of calcium in response to PTH infusion in African American as compared with Caucasian women.