Bone
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Polymorphisms of methylenetetrahydrofolate reductase (MTHFR) have been well documented to cause hyperhomocysteinemia, and recent studies suggest an association of C677T mutation of methylenetetrahydrofolate reductase with low bone mineral density (BMD). In this study, the association of plasma total homocysteine (Hcy), plasma folate, and vitamin B12 as well as methylenetetrahydrofolate reductase C667T polymorphism with bone mineral density at neck of femur and lumbar spine in 271 postmenopausal Iranian women was investigated. Bone mineral density was measured by dual-energy X-ray absorptiometry. ⋯ Methylenetetrahydrofolate reductase polymorphism, however, was not associated with plasma folate (r = 0.086, P = 0.17) or vitamin B12 (r = 0.05, P = 0.4). Plasma folate was one of the main predictors explaining 3.0% and 1.7% of variance of the bone mineral density at femoral neck and lumbar spine, respectively. Results from this study suggest hyperhomocysteinemia as a result of folate deficiency, but not methylenetetrahydrofolate reductase polymorphism, is independently associated with low bone mineral density and may contribute to the pathogenicity of osteoporosis in postmenopausal Iranian women.
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Comparative Study
Body composition changes with age have gender-specific impacts on bone mineral density.
Body weight, smoking, alcohol, physical activity, and diet have been proven to affect bone mineral density (BMD) directly or indirectly. Of these, body weight is perhaps best known to affect BMD. However, there is some debate as to whether lean body mass (LBM) or fat mass (FM), the two components of body weight, most determines BMD. ⋯ LBM was an important contributor for BMD in men, but both LBM and FM were equally important contributors in female to BMD. This stems from the fact that body composition changes with age differ in men and women. Thus, the augmentation of muscle mass in men and the maintenance of an optimal weight in women act to prevent osteoporosis.