UNLABELLED: The effect of weight gain in late adolescence on bone is not clear. Young women who consistently gained weight (n = 23) from 17 to 22 yr of age had increased BMD but a lack of subperiosteal expansion compared with stable weight peers (n = 48). Bone strength increased appropriately for lean mass in both groups but decreased relative to body weight in weight gainers, suggesting increased bone fragility in weight gainers. INTRODUCTION: Weight gain leading to obesity often starts in adolescence, yet little is known about its effects on bone. We used longitudinal data to examine the effects of weight gain in late adolescence (from 17 to 22 yr of age) on proximal femur BMD, geometry, and estimates of bending strength. MATERIALS AND METHODS: Participants were classified as either weight gainers (WG, n = 23) or stable weight (SW, n = 48) using a random coefficients model. Weight gainers had positive increases in weight (p < 0.05) at each clinic visit from age 17 onward. Proximal femur DXA scans (Hologic QDR 2000) taken annually from 17 to 22 yr of age were analyzed for areal BMD (g/cm(2)), subperiosteal width (cm), and bone cross-sectional area (CSA) at the proximal femoral shaft. Cortical thickness was measured, and section modulus (Z, cm(3)) was calculated as a measure of bone bending strength. Total body lean (g) and fat (g) mass were measured from DXA total body scans. RESULTS: Over ages 17-22, height remained stable in both groups. Weight remained static in the SW group but increased 14% on average in the WG group (p < 0.05). After controlling for age 17 baseline values, WG had higher BMD (+2.6%), thicker cortices (+3.6%), and greater bone CSA (+2.3%). Increased BMD did not translate to greater increases in bone bending strength (Z). The SW group achieved similar gains in Z by greater subperiosteal expansion. Bone strength index (SI = Z/height) normalized for body weight remained constant in the SW group but decreased significantly in the WG group. In contrast, SI normalized to lean mass did not change over time in either group. Other variables including physical activity, nutrition, and hormone levels (estradiol, testosterone, cortisol) did not differ significantly between groups. CONCLUSIONS: These data suggest that weight gain in late adolescence may inhibit the periosteal expansion known to normally occur throughout life in long bones, resulting in decreased bone strength relative to body weight.
UNLABELLED: The effect of weight gain in late adolescence on bone is not clear. Young women who consistently gained weight (n = 23) from 17 to 22 yr of age had increased BMD but a lack of subperiosteal expansion compared with stable weight peers (n = 48). Bone strength increased appropriately for lean mass in both groups but decreased relative to body weight in weight gainers, suggesting increased bone fragility in weight gainers. INTRODUCTION:Weight gain leading to obesity often starts in adolescence, yet little is known about its effects on bone. We used longitudinal data to examine the effects of weight gain in late adolescence (from 17 to 22 yr of age) on proximal femur BMD, geometry, and estimates of bending strength. MATERIALS AND METHODS:Participants were classified as either weight gainers (WG, n = 23) or stable weight (SW, n = 48) using a random coefficients model. Weight gainers had positive increases in weight (p < 0.05) at each clinic visit from age 17 onward. Proximal femur DXA scans (Hologic QDR 2000) taken annually from 17 to 22 yr of age were analyzed for areal BMD (g/cm(2)), subperiosteal width (cm), and bone cross-sectional area (CSA) at the proximal femoral shaft. Cortical thickness was measured, and section modulus (Z, cm(3)) was calculated as a measure of bone bending strength. Total body lean (g) and fat (g) mass were measured from DXA total body scans. RESULTS: Over ages 17-22, height remained stable in both groups. Weight remained static in the SW group but increased 14% on average in the WG group (p < 0.05). After controlling for age 17 baseline values, WG had higher BMD (+2.6%), thicker cortices (+3.6%), and greater bone CSA (+2.3%). Increased BMD did not translate to greater increases in bone bending strength (Z). The SW group achieved similar gains in Z by greater subperiosteal expansion. Bone strength index (SI = Z/height) normalized for body weight remained constant in the SW group but decreased significantly in the WG group. In contrast, SI normalized to lean mass did not change over time in either group. Other variables including physical activity, nutrition, and hormone levels (estradiol, testosterone, cortisol) did not differ significantly between groups. CONCLUSIONS: These data suggest that weight gain in late adolescence may inhibit the periosteal expansion known to normally occur throughout life in long bones, resulting in decreased bone strength relative to body weight.
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