The goal of our study was to estimate the prevalence of osteoporosis and low bone mass based on bone mineral density (BMD) at the femoral neck and the lumbar spine in adults 50 years and older in the United States (US). We applied prevalence estimates of osteoporosis or low bone mass at the femoral neck or lumbar spine (adjusted by age, sex, and race/ethnicity to the 2010 Census) for the non-institutionalized population age 50 years and older from the National Health and Nutrition Examination Survey 2005–2010 to 2010 US Census population counts to determine the total number of older US residents with osteoporosis and low bone mass. There were over 99 million adults 50 years and older in the US in 2010. Based on an overall 10.3% prevalence of osteoporosis, we estimated that in 2010 10.2 million older adults had osteoporosis. The overall low bone mass prevalence was 43.9%, from which we estimated that 43.4 million older adults had low bone mass. We estimated that 7.7 million non-Hispanic White, 0.5 million non-Hispanic Black, and 0.6 million Mexican American adults had osteoporosis and another 33.8, 2.9, and 2.0 million had low bone mass, respectively. When combined, osteoporosis and low bone mass at the femoral neck or lumbar spine affected an estimated 53.6 million older US adults in 2010. Although most of the individuals with osteoporosis or low bone mass were non-Hispanic White women, a substantial number of men and women from other racial/ethnic groups also had osteoporotic BMD or low bone mass.

Lean body mass, consisting mostly of skeletal muscle, is important for healthy aging. We performed a genome-wide association study for whole body (20 cohorts of European ancestry with n = 38,292) and appendicular (arms and legs) lean body mass (n = 28,330) measured using dual energy X-ray absorptiometry or bioelectrical impedance analysis, adjusted for sex, age, height, and fat mass. Twenty-one single-nucleotide polymorphisms were significantly associated with lean body mass either genome wide (p < 5 × 10−8) or suggestively genome wide (p < 2.3 × 10−6). Replication in 63,475 (47,227 of European ancestry) individuals from 33 cohorts for whole body lean body mass and in 45,090 (42,360 of European ancestry) subjects from 25 cohorts for appendicular lean body mass was successful for five single-nucleotide polymorphisms in/near HSD17B11, VCAN, ADAMTSL3, IRS1, and FTO for total lean body mass and for three single-nucleotide polymorphisms in/near VCAN, ADAMTSL3, and IRS1 for appendicular lean body mass. Our findings provide new insight into the genetics of lean body mass.

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Hip fracture incidence has declined among whites in the United States since 1995, but data on recent trends in racial and ethnic minorities are limited. The goal of this analysis was to investigate hip fracture incidence trends in racial/ethnic subgroups of older Medicare beneficiaries. We conducted a cohort study to determine annual hip fracture incidence rates from 2000 through 2009 using the Medicare national random 5% sample. Beneficiaries were eligible if they were !65 years of age and had 90 days of consecutive full feefor-service Medicare coverage with no hip fracture claims. Race/ethnicity was self-reported. The incidence of hip fracture was identified using hospital diagnosis codes or outpatient diagnosis codes paired with fracture repair procedure codes. We computed agestandardized race/ethnicity-specific incidence rates and assessed trends in the rates over time using linear regression. On average, 821,475 women and 632,162 men were included in the analysis each year. Beneficiaries were predominantly white (88%), with African, Hispanic, and Asian Americans making up 8%, 1.5%, and 1.5% of the population, respectively. We identified 102,849, 4,119, 813, and 1,294 hip fractures in white, black, Asian, and Hispanic beneficiaries over the 10 years. A significant decreasing trend (p < 0.05) in hip fracture incidence from

Objectives To determine associations between postmenopausal change in body weight and incidence of fracture and associations between voluntary and involuntary weight loss and risk of fracture.Design Post hoc analysis of data from the Women’s Health Initiative Observational Study and Clinical Trials.Setting 40 clinical centers in the United States.Participants 120 566 postmenopausal women, aged 50-79 at baseline (1993-98), followed through 2013 (mean fracture follow-up duration 11 years from baseline).Exposures Annualized percentage change in measured body weight from baseline to year 3, classified as stable (<5% change), weight loss (≥5%), or weight gain (≥5%). Self assessment of whether weight loss was intentional or unintentional. Cox proportional hazards regression models were adjusted for age, race/ethnicity, baseline body mass index (BMI), smoking, alcohol intake, level of physical activity, energy expenditure, calcium and vitamin D intake, physical function score, oophorectomy, hysterectomy, previous fracture, comorbidity score, and drug use.Main outcomes Incident self reported fractures of the upper limbs, lower limbs, and central body; hip fractures confirmed by medical records.Results Mean participant age was 63.3. Mean annualized percent weight change was 0.30% (95% confidence interval 0.28 to 0.32). Overall, 79 279 (65.6%) had stable weight; 18 266 (15.2%) lost weight; and 23 021 (19.0%) gained weight. Compared with stable weight, weight loss was associated with a 65% higher incidence rates of fracture in hip (adjusted hazard ratio 1.65, 95% confidence interval 1.49 to 1.82), upper limb (1.09, 1.03 to 1.16), and central body (1.30, 1.20 to 1.39); weight gain was associated with higher incidence rates of fracture in upper limb (1.10, 1.05 to 1.18) and lower limb (1.18, 1.12 to 1.25). Compared with stable weight, unintentional weight loss was associated with a 33% higher incidence rates of hip fracture (1.33, 1.19 to 1.47) and increased incidence rates of vertebral fracture (1.16, 1.06 to 1.26); intentional weight loss was associated with increased incidence rates of lower limb fracture (1.11, 1.05 to 1.17) and decreased incidence of hip fracture (0.85, 0.76 to 0.95).Conclusions Weight gain, weight loss, and intentional weight loss are associated with increased incidence of fracture, but associations differ by fracture location. Clinicians should be aware of fracture patterns after weight gain and weight loss.

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The plateau in age-adjusted hip fracture incidence rate resulted in more than 11,000 additional estimated hip fractures over the time periods 2013, 2014, and 2015. We recommend further study to assess all factors contributing to this remarkable change in hip fracture rate and to develop strategies to reduce the osteoporosis treatment gap.