Rohsen man saver post pounder2/22/2023 ![]() ![]() Vitamin D deficiency enhances the risk of osteoporotic fractures and is associated with many diseases. These findings point to a need for continued ongoing and future basic and clinical studies to better define whether vitamin D status can be optimized to improve many aspects of human health. Results of randomized controlled trials and Mendelian randomization studies are supportive of vitamin D supplementation in reducing the incidence of some diseases, but, globally, conclusions are mixed. From observational studies in human subjects, poor vitamin D status is associated with nearly all diseases predicted by these extraskeletal actions. These include regulation of cell proliferation, immune and muscle function, skin differentiation, and reproduction, as well as vascular and metabolic properties. Numerous genetic, molecular, cellular, and animal studies strongly suggest that vitamin D signaling has many extraskeletal effects. VDR and vitamin D metabolic enzymes are widely expressed. These risks can be reduced by 800 IU of vitamin D together with an appropriate calcium intake, given to institutionalized or vitamin D–deficient elderly subjects. ![]() Vitamin D deficiency (serum 25-hydroxyvitamin D <50 nmol/L) accelerates bone turnover, bone loss, and osteoporotic fractures. Rickets and osteomalacia can be prevented by daily supplements of 400 IU of vitamin D. The effects of the vitamin D endocrine system on bone and its growth plate are primarily indirect and mediated by its effect on intestinal calcium transport and serum calcium and phosphate homeostasis. ![]() Vitamin D is the precursor of 25-hydroxyvitamin D and other metabolites, including 1,25(OH) 2D, the ligand for the vitamin D receptor (VDR). The etiology of endemic rickets was discovered a century ago. ![]()
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