OBJECTIVE: To evaluate the influence of genetic background as a determinant of peak bone mass. PATIENTS AND METHODS: We compared lumbar spine bone mineral density in 175 girls with a bone age of 16 years or older and in their premenopausal mothers. We also investigated the influence of a family history of osteoporosis on lumbar spine bone mineral density in 275 women and their 559 daughters. RESULTS: In the 175 mother-daughter pairs, heritability (h2) was significantly different from 0 (P < 0.0001) for lumbar spine bone mineral density (h2 = 53%; 95% confidence interval [95% CI] = 28.5-77.6%), bone mineral content (h2 = 62.3%; 95% CI = 37.7-86.8%), bone mineral density adjusted for body mass index (h2 = 56%; CI = 31.5-80.5%), and bone mineral content adjusted for body mass index (h2 = 68.2%; CI = 43.6-92.7%). However, the heritability estimations lacked accuracy, as shown by the wide 95% CIs. Osteopenia and osteoporosis were found in 16.4% and 1% of the mothers, respectively. In the subgroup defined by osteopenia or osteoporosis in the mother, lumbar spine bone mineral density was significantly higher in the daughters than in the mothers (0.994 +/- 0.095 g/cm2 versus 0.895 +/- 0.098 g/cm2; P < 0.0001), whereas the opposite was true in the subgroup defined by normal bone mass in the mothers (1.068 +/- 0.110 g/cm2 versus 1.109 +/- 0.098 g/cm2; P = 0.0003). Nevertheless, lumbar spine bone mineral density was significantly lower in the daughters of low-bone-mass women than in those of normal-bone-mass women (0.994 +/- 0.009 g/cm2 versus 1.069 +/- 0.012 g/cm2; P = 0.0006). These findings suggest a role of genetic factors inherited from the father and also indicate that bone mass gains during adulthood contribute to achievement of the optimal peak bone mass. In the family history study, bone mass was lower in the subjects with a family history of osteoporosis (123 of the 559 daughters, Z-scores normalized for height, weight, and pubertal status: bone mineral density Z-score, -0.054 +/- 1.104; bone mineral content Z-score, -0.014 +/- 1.079; 58 of the 275 mothers: bone mineral density, 1.048 +/- 0.107 g/cm2; bone mineral content, 43.3 +/- 6.8 g) than in those without a family history of osteoporosis (436 daughters, bone mineral density Z-score, 0.006 +/- 0.981; bone mineral content Z-score, -0.007 +/- 0.985; 217 mothers: bone mineral density, 1.070 +/- 0.127 g/cm2; bone mineral content, 43.8 +/- 6.7 g); however, none of these differences were statistically significant. CONCLUSION: Our findings challenge the currently popular concept of marked bone mass heritability but are consistent with early genetic influences on lumbar spine bone mass. Thus, optimization of the peak bone mass acquired during growth may help to prevent osteoporosis.
OBJECTIVE: To evaluate the influence of genetic background as a determinant of peak bone mass. PATIENTS AND METHODS: We compared lumbar spine bone mineral density in 175 girls with a bone age of 16 years or older and in their premenopausal mothers. We also investigated the influence of a family history of osteoporosis on lumbar spine bone mineral density in 275 women and their 559 daughters. RESULTS: In the 175 mother-daughter pairs, heritability (h2) was significantly different from 0 (P < 0.0001) for lumbar spine bone mineral density (h2 = 53%; 95% confidence interval [95% CI] = 28.5-77.6%), bone mineral content (h2 = 62.3%; 95% CI = 37.7-86.8%), bone mineral density adjusted for body mass index (h2 = 56%; CI = 31.5-80.5%), and bone mineral content adjusted for body mass index (h2 = 68.2%; CI = 43.6-92.7%). However, the heritability estimations lacked accuracy, as shown by the wide 95% CIs. Osteopenia and osteoporosis were found in 16.4% and 1% of the mothers, respectively. In the subgroup defined by osteopenia or osteoporosis in the mother, lumbar spine bone mineral density was significantly higher in the daughters than in the mothers (0.994 +/- 0.095 g/cm2 versus 0.895 +/- 0.098 g/cm2; P < 0.0001), whereas the opposite was true in the subgroup defined by normal bone mass in the mothers (1.068 +/- 0.110 g/cm2 versus 1.109 +/- 0.098 g/cm2; P = 0.0003). Nevertheless, lumbar spine bone mineral density was significantly lower in the daughters of low-bone-mass women than in those of normal-bone-mass women (0.994 +/- 0.009 g/cm2 versus 1.069 +/- 0.012 g/cm2; P = 0.0006). These findings suggest a role of genetic factors inherited from the father and also indicate that bone mass gains during adulthood contribute to achievement of the optimal peak bone mass. In the family history study, bone mass was lower in the subjects with a family history of osteoporosis (123 of the 559 daughters, Z-scores normalized for height, weight, and pubertal status: bone mineral density Z-score, -0.054 +/- 1.104; bone mineral content Z-score, -0.014 +/- 1.079; 58 of the 275 mothers: bone mineral density, 1.048 +/- 0.107 g/cm2; bone mineral content, 43.3 +/- 6.8 g) than in those without a family history of osteoporosis (436 daughters, bone mineral density Z-score, 0.006 +/- 0.981; bone mineral content Z-score, -0.007 +/- 0.985; 217 mothers: bone mineral density, 1.070 +/- 0.127 g/cm2; bone mineral content, 43.8 +/- 6.7 g); however, none of these differences were statistically significant. CONCLUSION: Our findings challenge the currently popular concept of marked bone mass heritability but are consistent with early genetic influences on lumbar spine bone mass. Thus, optimization of the peak bone mass acquired during growth may help to prevent osteoporosis.
Authors: Craig C Teerlink; Michael J Jurynec; Rolando Hernandez; Jeff Stevens; Dana C Hughes; Cherie P Brunker; Kerry Rowe; David J Grunwald; Julio C Facelli; Lisa A Cannon-Albright Journal: Ann Hum Genet Date: 2020-10-07 Impact factor: 1.670