In T2DM, TBS is lower and associated with poor glycemic control. Abnormal trabecular microarchitecture may help explain the paradox of increased fractures at a higher BMD in T2DM. Further studies are needed to better understand the relationship between glycemic control and trabecular bone quality.

Free serum 25(OH)D is the same across races despite the lower total serum 25(OH)D in black women. Results comparing VDBP between races using a monoclonal vs a polyclonal assay were discordant.

Context Increased bone fragility and reduced energy absorption to fracture associated with type 2 diabetes (T2D) cannot be explained by bone mineral density alone. This study, for the first time reports on alterations in bone tissue's material properties obtained from individuals with diabetes and known fragility fracture status. Objective To investigate the role of T2D in altering biomechanical, microstructural and compositional properties of bone in individuals with fragility fracture. Design Femoral head bone tissue specimens were collected from patients who underwent replacement surgery for fragility hip fracture. Trabecular bone quality parameters were compared in samples of two groups: non-diabetic (n=40) and diabetic (n=30), with a mean duration of disease 7.5±2.8 years. Results No significant difference was observed in aBMD between the groups. Bone volume fraction (BV/TV) was lower in the diabetic group due to fewer and thinner trabeculae. The apparent-level toughness and post-yield energy were lower in those with diabetes. Tissue-level (nanoindentation) modulus and hardness were lower in this group. Compositional differences in diabetic group included lower mineral:matrix, wider mineral crystals, and bone collagen modifications - higher total fAGEs, higher non-enzymatic-cross-link-ratio (NE-xLR), and altered secondary structure (Amide bands). There was a strong inverse correlation between NE-xLR and post-yield-strain, fAGEs and post-yield energy, and, fAGEs and toughness. Conclusion Current study is novel in examining bone tissue in T2D following first hip fragility fracture. Our findings provide evidence of hyperglycemia’s detrimental effects on trabecular bone quality at multiple scales leading to lower energy absorption and toughness-indicative of increased propensity to bone fragility.

Context X-linked hypophosphatemia (XLH) is an inherited skeletal disorder that can lead to lifelong deleterious musculoskeletal and functional consequences. Although often perceived as a childhood condition, children and adults both experience the negative effects of XLH. Adolescents and young adults (AYAs) benefit from effective health care transition (HCT) preparation to support the transfer from pediatric- to adult-focused care. Whereas transition timelines, milestones, and educational tools exist for some chronic conditions, they do not meet the unique needs of patients with XLH. Evidence Acquisition To produce the first expert recommendations on HCT preparation for AYAs with XLH developed by clinical care investigators and transition experts, a formal literature search was conducted and discussed in an advisory board meeting in July 2020. A modified Delphi method was used to refine expert opinion and facilitate a consensus position. Evidence Synthesis We identified the need for psychosocial and access-related resources for disease education, genetic counseling, family planning, and AYA emancipation from caregiver-directed care. Additionally, we recognized that it is necessary to facilitate communication with patients through channels familiar and accessible to AYAs and teach patients to advocate for their health care/access to specialists. Conclusion Clear HCT preparation guidelines and treatment-related goals are defined. Individualized timelines and practical strategies for HCT preparation are proposed to optimize health outcomes resulting from continuous clinical care throughout the patient lifecycle. We provide an expert consensus statement describing a tailored HCT preparation program specifically for AYAs with XLH to aid in the effective transfer from pediatric- to adult-focused health care.

OBJECTIVES To examine the effect of 25‐hydroxyvitamin D (25(OH)D) levels recommended by Endocrine Society guidelines (>30 ng/mL) on cognition in healthy older African‐American women over 3 years. DESIGN Randomized, double‐blind, placebo‐controlled clinical trial. SETTING Bone Mineral Research Center at New York University Winthrop Hospital. PARTICIPANTS Healthy postmenopausal African American women aged 65 and older (N=260; mean age 68.2 ± 4.9; 46% college education or higher). INTERVENTION Half of the women were randomized to receive vitamin D (adjusted to achieve a serum level > 30 ng/mL) with calcium (diet and supplement total of 1,200 mg), and half were randomized to receive placebo with calcium (1,200 mg). MEASUREMENTS Cognitive assessments every 6 months using the Mini‐Mental State Examination (MMSE) to detect cognitive decline. Mean MMSE scores were calculated over time for both groups. Those with MMSE scores less than 21 at baseline were excluded. RESULTS The average dose of vitamin D3 was 3,490 ± 1,465 IU per day, and average serum 25(OH)D at 3 years was 46.8 ± 1.2 ng/mL in the active group and 20.7 ± 1.1 ng/mL in the placebo group. Serum 25(OH)D concentration was maintained at greater than 30 ng/mL in 90% of the active group. Over the 3‐year period, MMSE scores increased in both groups (p < .001), although change over time was not significantly different between the groups. No adverse events associated with vitamin D were observed. CONCLUSION There was no difference in cognition over time between older African‐American women with serum concentrations of 25(OH)D of 30 ng/mL and greater than those taking placebo. There is no evidence to support vitamin D intake greater than the recommended daily allowance in this population for preventing cognitive decline. J Am Geriatr Soc 67:81–86, 2019.

Fasting PTH declines with vitamin D supplementation. PTH declines after calcium intake. Supplementation of the diet with 1200 mg calcium/d reduces bone turnover markers, whereas supplementation with up to100 μg vitamin D3/d does not.

There was no advantage from measuring free over total 25(OH)D in assessing the response of calcium absorption, PTH, and markers of bone turnover to vitamin D. Free 25(OH)D responded to increasing doses of vitamin D in a similar fashion to total 25(OH)D.

No evidence of a threshold of calcium absorption was found with a serum 25(OH)D range from 40 to 130 nmol/L. Calcium absorption in this range is not a useful biomarker to determine nutritional recommendations for vitamin D.