Dual-energy X-ray absorptiometry (DXA) was the first imaging tool widely utilized by clinicians to assess fracture risk, especially in postmenopausal women. The development of DXA nearly coincided with the availability of effective osteoporosis medications. Although osteoporosis in adults is diagnosed based on a T-score equal to or below − 2.5 SD, most individuals who sustain fragility fractures are above this arbitrary cutoff. This incongruity poses a challenge to clinicians to identify patients who may benefit from osteoporosis treatments. DXA scanners generate 2 dimensional images of complex 3 dimensional structures, and report bone density as the quotient of the bone mineral content divided by the bone area. An obvious pitfall of this method is that a larger bone will convey superior strength, but may in fact have the same bone density as a smaller bone. Other imaging modalities are available such as peripheral quantitative CT, but are largely research tools. Current osteoporosis medications increase bone density and reduce fracture risk but the mechanisms of these actions vary. Anti-resorptive medications (bisphosphonates and denosumab) primarily increase endocortical bone by bolstering mineralization of endosteal resorption pits and thereby increase cortical thickness and reduce cortical porosity. Anabolic medications (teriparatide and abaloparatide) increase the periosteal and endosteal perimeters without large changes in cortical thickness resulting in a larger more structurally sound bone. Because of the differences in the mechanisms of the various drugs, there are likely benefits of selecting a treatment based on a patient’s unique bone structure and pattern of bone loss. This review retreats to basic principles in order to advance clinical management of fragility fractures by examining how skeletal biomechanics, size, shape, and ultra-structural properties are the ultimate predictors of bone strength. Accurate measurement of these skeletal parameters through the development of better imaging scanners is critical to advancing fracture risk assessment and informing clinicians on the best treatment strategy. With this information, a “treat to target” approach could be employed to tailor current and future therapies to each patient’s unique skeletal characteristics.

A novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease 2019 [COVID-19]) is now at global pandemic levels causing significant morbidity and mortality. Patients with diabetes are particularly vulnerable and more likely to get severe complications when infected with this virus. Although the information continues to emerge, here we provide our perspective on initial outcomes observed in hospitalized patients with diabetes and the potential role played by the proinflammatory metabolic state in these patients that promotes fertile ground for the virus’ inflammatory surge, resulting in severe insulin resistance and severe hyperglycemia. The rapidly evolving renal failure, hypotension, pressor and steroid use, and variable nutritional support further complicates their management. Thus, timely implementation of glucose management protocols addressing these complex scenarios while also following COVID-19–related trajectories in inflammatory biomarkers and being cognizant of the health care provider exposure may substantially affect morbidity and mortality.

Bone events in patients with thyroid cancer are a poor prognostic indicator. Patients with follicular and medullary thyroid cancers are at especially high risk for skeletal complications.

Background Despite the known links between weakness and early mortality, what remains to be fully understood is the extent to which strength preservation is associated with protection from cardiometabolic diseases such as diabetes. Purpose The purposes of this study were to determine the association between muscle strength and diabetes among adults, and to identify age- and sex-specific thresholds of low strength for detection of risk. Methods A population-representative sample of 4,066 individuals, aged 20–85 years, was included from the combined 2011–2012 National Health and Nutrition Examination Survey datasets. Strength was assessed using a hand-held dynamometer, and the single largest reading from either hand was normalized to body mass. A logistic regression model was used to assess the association between normalized grip strength and risk of diabetes, as determined by hemoglobin A1c (HbA1c) levels (≥6.5% [≥48 mmol/mol]), while controlling for sociodemographic characteristics, anthropometric measures, and television viewing time. Results For every 0.05 decrement in normalized strength, there was a 1.26 times increased adjusted odds for diabetes in men and women. Women were at lower odds of having diabetes (OR: 0.49; 95% CI: 0.29–0.82), whereas age, waist circumference and lower income were inversely associated. Optimal sex- and age-specific weakness thresholds to detect diabetes were 0.56, 0.50, and 0.45 for men, and 0.42, 0.38, and 0.33 for women, for ages 20–39 years, 40–59 years, and 60–80 years. Conclusions and Clinical Relevance We present thresholds of strength that can be incorporated into a clinical setting for identifying adults that are at risk for developing diabetes, and that might benefit from lifestyle interventions to reduce risk.

Breast cancer is a common diagnosis and the majority of women treated will be cured. Women with early stage breast cancer may be at increased risk for osteoporosis due to anticancer therapies. Chemotherapy induced amenorrhea and the use of anti-estrogens can promote bone loss; thus, the management of bone health in women with breast cancer is an important component of survivorship care. Osteoporosis is considered a “silent” disease as there are often no discrete warning signs, until a fracture occurs; therefore, clinicians must be cognizant of the underlying risk for osteoporosis and co-morbid conditions and/or medications that accelerate risk of fracture. Breast cancer therapies that effect bone, screening for bone loss and interventions to mitigate the treatment toxicities are reviewed.

Introduction The management of the hypercholesterolemic patient has evolved tremendously with the introduction of the HMG-CoA Reductase inhibitors, a class of drugs better known as the statins. Statins modify cholesterol metabolism by inhibiting the rate-limiting enzyme of cholesterol biosynthesis, producing greater decreases in plasma cholesterol levels than previously realized with hypolipidemic therapy. With the advent of the classic statin-megatrials such as the Scandinavian Simvastatin Survival Study (4S), WOSCOPS, CARE, and the more recent Heart Protection Study (HPS), the role of statins in both the primary and secondary prevention and ultimate risk reduction of patients with coronary disease has been firmly established. Discussion With an increase in use and popularity, a number of beneficial actions of the statins unrelated to their cholesterol-lowering ability have been reported. These effects have generated greater interest in the possible additional roles and indications for the use of these drugs. Of central focus in this paper is the cholesterol-independent benefit of this group of agents on the cardiovascular system, particularly on the lowering of systemic blood pressure. A number of hypotheses have been proposed for this action and these shall be reviewed within this paper. Conclusion We explore recent data that suggests that statins may provide substantial reduction of blood pressure in the hypertensive, hypercholesterolemic patient independent of their lipid-lowering effect. In addition, we review several notable publications that postulate unique mechanisms for this action and benefit. We also present plausible explanations as to why some of the larger statin trials did not report similar such findings.

These data demonstrate that a simple baseline serum potassium level is independently associated with the presence of multivessel disease, even in the context of clinical CAD risk factors and other established inflammatory markers.

BackgroundThe long-term effect of weight reduction on skeletal health is not well understood. The purpose of this study was to examine the impact of an intensive medical weight loss intervention using very low energy diet (VLED) (~ 800 cal/day) that result in significant changes in body weight, on total body bone mineral density (BMD) over 2 years.MethodsWe examined the impact of VLED-induced weight loss on BMD and FFM (Fat-free Mass) after 3–6 months and again while in weight maintenance at 2 years in 49 subjects. The effects of absolute and relative rate of weight reduction assessed by change in weight in kilograms were assessed using general linear modeling, with baseline BMD (or FFM) as a covariate, and age, sex and changes in body weight as primary model predictors.ResultsAt the end of 2 years, the average weight loss was greater for men (weight: 23.51 ± 12.5 kg) than women (weight: 16.8 ± 19.2 kg) and BMD loss was greater among women (0.03 ± 0.04 g/cm2 vs 0.01 ± 0.04 g/cm2) (all p < 0.05). After adjusting for baseline BMD, age, and sex, there was a small but significant association between total weight loss and 2-year BMD (β = − 0.001 g/cm2; p = 0.01). Similarly, there was a significant independent association between total weight loss and 2-year FFM (β = − 116.5 g; p < 0.01).ConclusionsDespite significant weight loss with VLED, there was only a small loss is BMD.