A prime risk factor for the development of osteoporosis is low peak bone mass, which most investigators believe is under genetic control. However, the genetic determinants of bone mineral quantity are poorly understood, and the candidate genes thus far identified are controversial. One problem with human studies of the inheritance of bone mass is their reliance on twin and other pedigree data that are confounded by shared familial environment, so that estimates of heritability tend to be inflated. We therefore investigated the heritability of bone mass by applying segregation analysis to a large macaque pedigree. The advantage of the macaque model is that many of the familial and environmental factors confounding human studies can be controlled. In addition, bone metabolism in macaques is so similar to that in humans that macaques are widely used in experimental studies of osteoporosis. Bone mass was measured by dual energy X-ray absorptiometry in 234 animals <12 ye ars of age. Their degrees of relatedness were calculated from the RPRC's breeding colony pedigree of 11,857 animals that extended back to 1960. High heritabilities in the range of those reported for humans were found for body size, total body mineral and spinal bone density. Adjustment of total body mineral for several measures of body size reduced or eliminated heritability. On the other hand, adjusting spinal bone mineral density for body size did not reduce its highly significant heritability. Further analysis showed that both total bone mineral and spinal density could be accounted for by a single factor, suggesting that a few genes may determine both the acquisition of body size and bone quantity. If so, the search for genes that control bone quantity should focus on agents with general growth-promoting effects. Data from this study were presented at an international symposium organized by Dr. Newell in 1998. FUNDING NIH grants RR00166 and AR40813, and a grant from the UW Royalty Research Fund.
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