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Historically, osteoporosis has not been considered a public health priority for the Hispanic population. However, recent data indicate that Mexican Americans are at increased risk for this chronic condition. Although it is well established that there is heterogeneity in social, lifestyle, and health-related factors among Hispanic subgroups, there are currently few studies on bone health among Hispanic subgroups other than Mexican Americans. The current study aimed to determine the prevalence of osteoporosis and low bone mass (LBM) among 953 Puerto Rican adults, aged 47 to 79 years and living on the US mainland, using data from one of the largest cohorts on bone health in this population: The Boston Puerto Rican Osteoporosis Study (BPROS). Participants completed an interview to assess demographic and lifestyle characteristics and bone mineral density measures. To facilitate comparisons with national data, we calculated age-adjusted estimates for osteoporosis and LBM for Mexican American, non-Hispanic white, and non-Hispanic black adults, aged ≥50 years, from the National Health and Nutrition Examination Survey (NHANES). The overall prevalence of osteoporosis and LBM were 10.5% and 43.3% for participants in the BPROS, respectively. For men, the highest prevalence of osteoporosis was among those aged 50 to 59 years (11%) and lowest for men ≥70 years (3.7%). The age-adjusted prevalence of osteoporosis for Puerto Rican men was 8.6%, compared with 2.3% for non-Hispanic white, and 3.9% for Mexican American men. There were no statistically significant differences between age-adjusted estimates for Puerto Rican women (10.7%), non-Hispanic white women (10.1%), or Mexican American women (16%). There is a need to understand specific factors contributing to osteoporosis in Puerto Rican adults, particularly younger men. This will provide important information to guide the development of culturally and linguistically tailored interventions to improve bone health in this understudied and high-risk population. © 2017 American Society for Bone and Mineral Research.

Osteocalcin (OC) is a vitamin K-dependent protein synthesized during bone formation. Mice injected with the undercarboxylated form of OC (ucOC) had more skeletal muscle mass and less fat mass than sham-treated controls, suggesting a unique metabolic role for ucOC. UcOC decreases in response to vitamin K supplementation. Our objective was to determine the effect of reducing ucOC on change in lean tissue and fat mass in older community-dwelling adults (n = 401, mean ± SD 69 ± 6 years) using data from a randomized controlled trial of vitamin K supplementation. Over 3 years, serum ucOC was reduced by 58% in women and by 61% in men randomized to vitamin K, whereas in the control group, ucOC decreased by 1% in women and 4% in men (supplementation*time p

The acid load accompanying modern diets may have adverse effects on bone and muscle metabolism. Treatment with alkaline salts of potassium can neutralize the acid load, but the optimal amount of alkali is not established. Our objective was to determine the effectiveness of two doses of potassium bicarbonate (KHCO3) compared with placebo on biochemical markers of bone turnover, and calcium and nitrogen (N) excretion. In this double-blind, randomized, placebo-controlled study, 244 men and women age 50 years and older were randomized to placebo or 1 mmol/kg or 1.5 mmol/kg of KHCO3 daily for 3 months; 233 completed the study. The primary outcomes were changes in 24-hour urinary N-telopeptide (NTX) and N; changes in these measures were compared across the treatment groups. Exploratory outcomes included 24-hour urinary calcium excretion, serum amino-terminal propeptide of type I procollagen (P1NP), and muscle strength and function assessments. The median administered doses in the low-dose and high-dose groups were 81 mmol/day and 122 mmol/day, respectively. When compared with placebo, urinary NTX declined significantly in the low-dose group (p = 0.012, after adjustment for baseline NTX, gender, and change in urine creatinine) and serum P1NP declined significantly in the low-dose group (p = 0.004, adjusted for baseline P1NP and gender). Urinary calcium declined significantly in both KHCO3 groups versus placebo (p < 0.001, adjusted for baseline urinary calcium, gender, and changes in urine creatinine and calcium intake). There was no significant effect of either dose of KHCO3 on urinary N excretion or on the physical strength and function measures. KHCO3 has favorable effects on bone turnover and calcium excretion and the lower dose appears to be the more effective dose. Long-term trials to assess the effect of alkali on bone mass and fracture risk are needed. © 2015 American Society for Bone and Mineral Research.

It is sometimes assumed that dietary fat is required for vitamin D absorption, although the impact of different amounts of dietary fat on vitamin D absorption is not established. This study was conducted to determine whether the presence of a meal and the fat content of the meal influences vitamin D absorption or the 25-hydroxyvitamin D [25(OH)D] response to supplemental vitamin D3. Based on earlier studies in rats we postulated that absorption would be greatest in the low-fat meal group. Sixty-two healthy older men and women were randomly assigned to one of three meal groups: no meal, high-fat meal, or low-fat meal; each was given a monthly 50,000 IU vitamin D3 supplement with the test breakfast meal (or after a fast for the no-meal group) and followed for 90 days. Plasma vitamin D3 was measured by liquid chromatography–mass spectroscopy (LC/MS) before and 12 hours after the first dose; plasma 25(OH)D was measured by radioimmunoassay at baseline and after 30 and 90 days. The mean 12-hour increments in vitamin D3, after adjusting for age and sex, were 200.9 nmol/L in the no-meal group, 207.4 nmol/L in the high-fat meal group, and 241.1 nmol/L in the low-fat meal group (p = 0.038), with the increase in the low-fat group being significantly greater than the increases in the other two groups. However, increments in 25(OH)D levels at 30 and 90 days did not differ significantly in the three groups. We conclude that absorption was increased when a 50,000 IU dose of vitamin D was taken with a low-fat meal, compared with a high-fat meal and no meal, but that the greater absorption did not result in higher plasma 25(OH)D levels in the low-fat meal group.

The relative contributions of calcium and vitamin D to calcium metabolism and bone mineral density (BMD) have been examined previously, but not in a population with very low calcium intake. To determine the relative importance of dietary calcium intake and serum 25-hydroxyvitamin D [25(OH)D] concentration to calcium metabolism and bone mass in a population with low calcium intake, a total of 4662 adults (2567 men and 2095 women) ≥50 years of age from the 2009–2010 Korea National Health and Nutrition Examination Survey (KNHANES) were divided into groups according to dietary calcium intakes (quintiles means: 154, 278, 400, 557, and 951 mg/d) and serum 25(OH)D concentrations ( 75 nmol/L). Serum intact parathyroid hormone (PTH) and femoral neck and lumbar spine BMD were evaluated according to dietary calcium intake and serum 25(OH)D. Mean calcium intake was 485 mg/d; mean serum 25(OH)D concentration was 48.1 nmol/L; PTH was 68.4 pg/mL; femoral neck BMD was 0.692 g/cm2; and lumbar spine BMD was 0.881 g/cm2. Lower dietary calcium intakes were significantly associated with higher serum PTH concentrations and lower femoral neck BMD, not only at lower ( 75 nmol/L) serum 25(OH)D concentrations. Serum PTH was highest and femoral neck BMD was lowest in the group, with a serum 25(OH)D less than 50 nmol/L. In this low-intake population, calcium intake is a significant determinant of serum PTH and BMD at higher as well as lower 25(OH)D levels. This finding indicates that low calcium intake cannot be compensated for with higher 25(OH)D levels alone. As expected, serum 25(OH)D levels were inversely associated with serum PTH and BMD. A calcium intake of at least 668 mg/d and a serum 25(OH)D level of at least 50 nmol/L may be needed to maintain bone mass in this calcium deficient population. © 2013 American Society for Bone and Mineral Research.

We conducted a study to determine whether a recently described restriction fragment length polymorphism in the vitamin D receptor gene (VDR-RFLP) predicts bone mineral density (BMD) in unrelated, premenopausal women as well as to determine the racial contribution to any genotypic influences on BMD. White (n = 83) and black (n = 72) women between 20 and 40 years of age were genotyped based on the presence (b) or absence (B) of a BsmI restriction enzyme site in the VDR gene, and BMD in the lumbar spine and femur neck was determined for each subject. There were 16 BB, 73 Bb, and 66 bb women. No significant difference was observed in genotypic distribution between the racial groups. The interaction of race by genotype on age- and body mass index (BMI)-adjusted BMD was not significant at either site. Age- and BMI-adjusted BMD was higher in black women at the spine (by 7.2%, p = 0.046) and femur neck (7.3% higher, p = 0.004). In the group as a whole, mean BMD in the femur neck was lower in the BB women that the bb (by 8.1%, p = 0.034) or Bb women (by 9.3%, p = 0.015) after controlling for age, BMI, race, and the race by genotype interaction. Adjusted lumbar spine BMD was lower in the BB women than the Bb women (6.4% lower, p = 0.036) in the group as a whole. No difference were detected between Bb and bb women at either site. A similar pattern of low BMD at the femur neck and the lumbar spine was seen in BB women of both races.(ABSTRACT TRUNCATED AT 250 WORDS)

Fractional Whole-Body Retention Of 47Ca (retention fraction) in 58 healthy postmenopausal women participating in a calcium supplementation trial was examined for seasonal variation and for relationships to rates of bone loss and plasma vitamin D levels. Retention fraction was measured after 18 months in the trial. Bone mineral densities of the radius, femoral neck, and lumbar spine were measured at baseline, 12 months, and 24 months in the trial, and plasma 1,25-dihydroxyvitamin D [1,25-(OH)2D] and 25-hydroxyvitamin D (25-OHD) at 12, 18, and 24 months. The adjusted retention (retention fraction adjusted for total calcium intake, smoking status, and log years since menopause) was significantly higher in women evaluated in the months of August through October (mean ± SD, 19.8 ± 4.1%, n = 13) than in March through May (mean ± SD, 17.0 ± 4.7%, n = 18, p = 0.05). Plasma 25-OHD was associated with retention fraction only in women with low calcium intakes (partial r = 0.69 controlling for total calcium intake and log body mass index, n = 14, p = 0.01). Plasma 1,25-(OH)2D was not related to retention fraction. Adjusted retention, independent of total calcium intake, log years since menopause, smoking status, and season, explained 8% of the variability in the annual change in radius density (partial r = 0.29, p < 0.05). No significant associations were seen at the spine and femur. These results indicate there is seasonal variation in calcium retention, that calcium retention is positively correlated with plasma 25-OHD levels in women with low calcium intakes, and that an increased level of retained calcium is associated with a lower rate of bone loss from the radius.

Serum parathyroid hormone (PTH) and low-normal serum phosphorus (P) concentrations have well-known trophic effects on renal 1-hydroxylase. A role for serum ionized calcium (Ca2+) in the day-to-day regulation of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] has not been identified in normal humans. The associations between serum Ca2+, PTH, P, and plasma 1,25-(OH)2D3 were evaluated in a cross-sectional study of 275 healthy postmenopausal women. Partial correlations of Ca2+, PTH, and P (each controlled for the other two) with 1,25-(OH)2D3 were sought within quintiles of Ca2+. At low-normal concentrations (less than 1.26 mmol/liter, quintile 1) Ca2+ was inversely correlated with 1,25-(OH)2D3 (rp = -0.30, p = 0.028). At mid-normal concentrations Ca2+ was not significantly correlated with 1,25-(OH)2D3. At high-normal concentrations (greater than 1.32 mmol/liter, quintile 5) Ca2+ attenuated the positive associations of both PTH and low-normal P with 1,25-(OH)2D3. In quintile 5 Ca2+, PTH, and P together accounted for none of the variability in 1,25-(OH)2D3 (R2 = 0.03, p = 0.671). Women with Ca2+ below 1.32 mmol/liter were next examined by quintile of P. As expected, at low-normal concentrations (less than 1.03 mmol/liter, quintile 1) P was significantly correlated with 1,25-(OH)2D3 (rp = -0.32, p = 0.047). The association between PTH and 1,25-(OH)2D3 was statistically significant only at mid-normal concentrations of P (rp = 0.52, p = 0.001, quintile 3). We conclude that Ca2+, along with PTH and P, is associated with the plasma concentration of 1,25-(OH)2D3 in normal postmenopausal women.

A higher calcium intake is still the primary recommendation for the prevention of osteoporosis, whereas vitamin D deficiency is often not addressed. To study the relative importance of dietary calcium intake and serum 25-hydroxyvitamin D [25(OH)D] status in regard to hip BMD, 4958 community-dwelling women and 5003 men ≥20 yr of age from the U.S. NHANES III population-based survey were studied. Calcium supplement users and individuals with a prior radius or hip fracture were excluded. We calculated standardized means for BMD by quartiles of sex-specific calcium intake for three 25(OH)D categories (566 mg/d) was not significantly associated with BMD at 25(OH)D concentrations >50 nM. Among men, there was no significant association between a higher calcium intake beyond the upper end of the lowest quartile (626 mg/d) and BMD within all 25(OH)D categories. Among both sexes, BMD increased stepwise and significantly with higher 25(OH)D concentrations (

Demographic differences may produce interstate variation in the burden of osteoporosis. We estimated the burden of fragility fractures by race/ethnicity, age, sex, and service site across five diverse and populous states. State inpatient databases for 2000 were used to describe hospital fracture admissions, and a Markov decision model was used to estimate annual fracture incidence and cost for populationsor=50 yr of age for 2005-2025 in Arizona (AZ), California (CA), Florida (FL), Massachusetts (MA), and New York (NY). In 2000, mean hospital charges for incident fractures varied 1.7-fold across states. For hip fracture, mean charges ranged from $16,700 (MA) to $29,500 (CA), length of stay from 5.3 (AZ) to 8.9 days (NY), and discharge rate to long-term care from 43% (NY) to 71% (CA). In 2005, projected fracture incidence rates ranged from 199 (CA) to 266 (MA) per 10,000. Total cost ranged from $270 million (AZ) to $1,434 million (CA). Men accounted for 26-30% of costs. Across states, hip fractures constituted on average 77% of costs; "other" fractures (e.g., leg, arm), 10%; pelvic, 6%; vertebral, 5%; and wrist, 2%. By 2025, Hispanics are projected to represent 20% of fractures in AZ and CA and Asian/Other populations to represent 27% of fractures in NY. In conclusion, state initiatives to prevent fractures should include nonwhite populations and men, as well as white women, and should address fractures at all skeletal sites. Interstate variation in service utilization merits further evaluation to determine efficient and effective disease management strategies.

This study predicts the burden of incident osteoporosis-related fractures and costs in the United States, by sex, age group, race/ethnicity, and fracture type, from 2005 to 2025. Total fractures were >2 million, costing nearly $17 billion in 2005. Men account for >25% of the burden. Rapid growth in the disease burden is projected among nonwhite populations. Introduction: The aging of the U.S. population will likely lead to greater prevalence of osteoporosis. Policy makers require precise projections of the disease burden by demographic subgroups and skeletal sites to effectively target osteoporosis intervention and treatment programs. Materials and Methods: A state transition Markov decision model was used to estimate total incident fractures and costs by age, sex, race/ethnicity, and skeletal site for the U.S. population ≥50 years of age for 2005–2025. Results: More than 2 million incident fractures at a cost of $17 billion are predicted for 2005. Total costs including prevalent fractures are more than $19 billion. Men account for 29% of fractures and 25% of costs. Total incident fractures by skeletal site were vertebral (27%), wrist (19%), hip (14%), pelvic (7%), and other (33%). Total costs by fracture type were vertebral (6%), hip (72%), wrist (3%), pelvic (5%), and other (14%). By 2025, annual fractures and costs are projected to rise by almost 50%. The most rapid growth is estimated for people 65–74 years of age, with an increase >87%. An increase of nearly 175% is projected for Hispanic and other subpopulations. Conclusions: Osteoporosis prevention, treatment, and education efforts should address all skeletal sites, not just hip and vertebral, and appropriate attention is warranted for men and diverse race/ethnicity subgroups.

There is a lack of substantial data on changes in calciotropic hormones and bone markers in elderly subjects living in North America. Parathyroid hormone (PTH), serum 25-hydroxyvitamin D (25(OH)D) and bone markers (serum osteocalcin and urine N-telopeptide), were measured in 735 Caucasian subjects (235 men and 500 women) aged 65-87 years. There was a significant increase in serum osteocalcin and urine N-telopeptide with age in men, and a significant increase in serum osteocalcin with age in women. Serum PTH and 25(OH)D showed no significant change with age in men or women. After adjusting for age, calcium intake, serum creatinine, season, and weight, mean serum PTH (p = 0.01), serum osteocalcin (p = 0.0001) and 24 h urine N-telopeptide (p = 0.0001) were higher in women than men, and mean serum 25(OH)D (p = 0.0001) and 24 h urine calcium (p = 0.0001) were higher in men than women. Serum PTH was correlated with serum osteocalcin in men and women, r = 0.24, r = 0.17, p < 0.001, but not with urine N-telopeptide. Serum PTH was inversely correlated with serum 25(OH)D (r = -0.25, r = -034,p < 0.001), and positively correlated with serum creatinine (r = 0.14, r = 0.17,p < 0.01) in men and women. The prevalence of serum 25(OH)D levels below 12 ng/ml was only 33% in females and 0.4% in men. Thus vitamin D deficiency was very uncommon in the U.S.A. compared with Europe. Although mean serum PTH was increased in the elderly, only 4-6% had PTH levels above the normal range. In summary, the increase in serum PTH in the elderly can be explained more by changes in vitamin D status than by declining renal function. These data also show significantly higher (p = 0.001) bone remodeling markers in women.