The association between increased risk of hip fracture and low vitamin D status has long been recognized. However, the level of vitamin D required to maintain bone strength is controversial. In this study[1], the authors used a rodent model of vitamin D depletion to quantify the 25-hydroxyvitamin D (25D) levels required for normal mineralization. Six groups of 10-wk-old male Sprague-Dawley rats (n = 42) were fed a diet containing 0.4% calcium and various levels of dietary vitamin D3 for 4 months to achieve stable mean serum 25D levels ranging between 10 and 115 nmol/L. At 7 months of age, animals were killed, and the histomorphometry of distal and proximal femora and L2 vertebra was analyzed. Total RNA was extracted from whole femora for real-time RT-PCR analyses.
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Clinical studies have shown that total body fat mass is related to both bone density and fracture risk and that fat ingestion reduces bone turnover. These effects are at least partially mediated by endocrine mechanisms, but it is possible that lipids might act directly on bone. This study [1] assessed the effects of broad fractions of milk lipids in osteoblasts, bone marrow, and neonatal mouse calvariae.
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Recent data suggest that vitamin K plays an important role in bone metabolism. Vitamin K is the essential cofactor for the carboxylation of glutamate to gamma-carboxyglutamic acid (Gla), which confers functionality to vitamin K–dependent Gla-containing proteins synthesized by osteoblasts such as osteocalcin. Vitamin K has been widely promoted as a supplement for decreasing bone loss in postmenopausal women, but the long-term benefits and potential harms are unknown. This study [1] was conducted to determine whether daily high-dose vitamin K1 supplementation safely reduces bone loss, bone turnover, and fractures. This single-center study was designed as a 2-y randomized, placebo-controlled, double-blind trial, extended for earlier participants for up to an additional 2 y because of interest in long-term safety and fractures. A total of 440 postmenopausal women with osteopenia were randomized to either 5 mg of vitamin K1 or placebo daily. Primary outcomes were changes in BMD at the lumbar spine and total hip at 2 y. Secondary outcomes included changes in BMD at other sites and other time points, bone turnover markers, height, fractures, adverse effects, and health-related quality of life.
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For more than 15 years, 5-α reductase inhibitors, which block the conversion of testosterone to dihydrotestosterone, have been used in the treatment of benign prostatic hyperplasia (BPH). Short-term studies show no effects of these agents on bone metabolism, but long-term data are not available. This study [1] aimed to assess the association between use of 5-α reductase inhibitors (eg, finasteride) for BPH and occurrence of hip fracture. It is a population-based case-control study using data from Kaiser Permanente Southern California, a managed care organization with more than 3 million members. Case patients included 7076 men 45 years and older with incident hip fracture from 1997-2006. Control patients were 7076 men without incident hip fracture, optimally matched at a 1:1 ratio to case patients on age and medical center. Electronic information on pharmaceutical use was used to identify use of finasteride from 1991 forward.
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