Calorie restriction is promoted to increase longevity, yet this regimen could lead to bone loss and fracture, and therefore affect quality of life. In a recent study [1], 46 individuals were randomized to 4 groups for 6 months: (1) healthy diet (control group); (2) 25% calorie restriction from baseline energy requirements (CR group); (3) 25% energy deficit by a combination of CR and increased aerobic exercise (CR+EX group); and (4) low-calorie diet (890 kcal/d; goal, 15% weight loss) followed by weight maintenance (LCD group). Bone mineral density (total body and hip by dual-energy x-ray absorptiometry) and serum bone markers (bone specific alkaline phosphatase, osteocalcin, cross-linked C-telopeptide of type I collagen, and cross-linked N-telopeptide of type I collagen) were measured at baseline and after 6 months.
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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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Vertebral fractures are the hallmark of osteoporosis. They are the most common osteoporotic fracture, with prevalence estimates of 35% to 50% among women older than 50 years. Women with vertebral fractures experience decreased survival and an increased risk of future vertebral, hip, and other nonspinal fractures. It was previously shown that, over an average follow-up of 3.7 years, low bone mineral density (BMD) is associated with an increased risk of vertebral fracture, and that a prevalent vertebral fracture is associated with a 5-fold increased risk of sustaining a new vertebral fracture. The aim of this study [1] was to examine the absolute risk of incident vertebral fractures by spine and hip BMD and prevalent vertebral fracture status over 15 years of follow-up in a population-based cohort of community-dwelling older women.
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The skeleton is a well-recognized target for sex steroids. Bone fragility is notable when sex steroid levels fall in women after menopause, in elderly males, or after sex organ ablation. In such cases, bone loss follows a release from native constraints on bone resorption that largely result from changes in growth regulators expressed by osteoblasts and from opposing effects on osteoblast and osteoclast activation and apoptosis, leading to an overall increase in bone remodeling. Importantly, imbalances in bone remodeling are restored by sex hormone replacement therapy. Osteoblasts respond in direct and indirect ways to estrogens, and express the estrogen receptor.

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Bone mineral density influences the risk of osteoporosis later in life and is useful in the evaluation of the risk of fracture. A recent study from Iceland [1] aimed to identify sequence variants associated with bone mineral density and fracture. A quantitative trait analysis of data was performed from 5861 Icelandic subjects (the discovery set), testing for an association between 301 019 single-nucleotide polymorphisms (SNPs) and bone mineral density of the hip and lumbar spine. The authors then tested for an association between 74 SNPs (most of which were implicated in the discovery set) at 32 loci in replication sets of Icelandic, Danish, and Australian subjects (4165, 2269, and 1491 subjects, respectively).

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Osteoporosis is diagnosed by the measurement of bone mineral density, which is a highly heritable and multifactorial trait. A recent study [1] aimed to identify genetic loci that are associated with bone mineral density. In this genome-wide association study, the authors identified the most promising of 314 075 single nucleotide polymorphisms (SNPs) in 2094 women in a UK study. They then tested these SNPs for replication in 6463 people from three other cohorts in Western Europe. They also investigated allelic expression in lymphoblast cell lines. They tested the association between the replicated SNPs and osteoporotic fractures with data from two studies.

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Cardiovascular disease and osteoporotic fractures are two major public health problems. Cardiovascular disease and osteoporosis coexist in women: progression of aortic calcifications has been associated with faster bone loss. Low BMD has been shown to predict cardiovascular events and cardiovascular mortality, whereas the association between the extension of aortic calcifications and hip fracture risk is controversial. In contrast to these findings in women, few studies concern the relationship between osteoporosis and cardiovascular disease in men.
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Some studies have reported associations between cardiovascular diseases (CVD) and bone mineral loss. Osteoclast regulatory factors can affect vascular calcifications, and a high blood pressure can induce abnormalities in calcium metabolism and increase bone mineral loss in women. Low bone mineral density is not only an important predictor of osteoporotic fracture, but is also a risk factor for mortality.
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