ARDIOVASCULAR AND METAbolic risk factors such as hypertension and diabetes have been hypothesized to play a role in the pathogenesis of Alzheimer disease (AD) as well as in development of vascular dementia. [1][2][3][4] The metabolic syndrome, 5 a clustering of several commonly occurring disorders that include (1) abdominal obesity, (2) hypertriglyceridemia, (3) low highdensity lipoprotein (HDL) level, (4) hypertension, and (5) hyperglycemia, has not been specifically investigated as a risk factor for cognitive decline in elderly individuals. The metabolic syndrome may be a risk factor for cognitive decline because it summarizes the joint effects of these risk factors. As obesity and sedentary lifestyle rise in the United States, identification and explication of the role of these modifiable behaviors in increasing risk for developing deleterious outcomes such as cognitive impairment is critical. If the metabolic syndrome is associated with increased risk of developing cognitive impairment, then early identification and treatment of these individuals might offer avenues for disease course modification.High levels of inflammation increase the risk of the development of diabetes and atherosclerosis and are thought to be a possible mechanism for the adverse consequences of the metabolic syndrome. 6,7 Indeed, level of inflammation in the setting of the meta-bolic syndrome may help identify those at especially high risk for adverse outcomes. Furthermore, subclinical inflammation might be an underlying factor for an association between the

Food insecurity may act as a risk factor for diabetes. Among adults with food insecurity, increased consumption of inexpensive food alternatives, which are often calorically dense and nutritionally poor, may play a role in this relationship. Future work should address how primary care clinicians can most effectively assist patients with food insecurity to make healthy dietary changes.

Circulating levels of adiponectin, a hormone produced predominantly by adipocytes, are highly heritable and are inversely associated with type 2 diabetes mellitus (T2D) and other metabolic traits. We conducted a meta-analysis of genome-wide association studies in 39,883 individuals of European ancestry to identify genes associated with metabolic disease. We identified 8 novel loci associated with adiponectin levels and confirmed 2 previously reported loci ( P = 4.5×10 −8 –1.2×10 −43 ). Using a novel method to combine data across ethnicities (N = 4,232 African Americans, N = 1,776 Asians, and N = 29,347 Europeans), we identified two additional novel loci. Expression analyses of 436 human adipocyte samples revealed that mRNA levels of 18 genes at candidate regions were associated with adiponectin concentrations after accounting for multiple testing ( p <3×10 −4 ). We next developed a multi-SNP genotypic risk score to test the association of adiponectin decreasing risk alleles on metabolic traits and diseases using consortia-level meta-analytic data. This risk score was associated with increased risk of T2D ( p = 4.3×10 −3 , n = 22,044), increased triglycerides ( p = 2.6×10 −14 , n = 93,440), increased waist-to-hip ratio ( p = 1.8×10 −5 , n = 77,167), increased glucose two hours post oral glucose tolerance testing ( p = 4.4×10 −3 , n = 15,234), increased fasting insulin ( p = 0.015, n = 48,238), but with lower in HDL-cholesterol concentrations ( p = 4.5×10 −13 , n = 96,748) and decreased BMI ( p = 1.4×10 −4 , n = 121,335). These findings identify novel genetic determinants of adiponectin levels, which, taken together, influence risk of T2D and markers of insulin resistance.

In women with coronary disease, hormone therapy reduced the incidence of diabetes by 35%. This observation provides important insights into the metabolic effects of postmenopausal hormones but is insufficient to recommend the use of hormones for secondary prevention of heart disease.

Larger subcutaneous thigh fat is independently associated with more favourable glucose (in men) and lipid levels (in both sexes) after accounting for abdominal fat depots, which are associated with unfavourable glucose and lipid levels. Anthropometric measures reflect different fat depots at different levels of BMI at the abdomen, and reflect both fat and lean tissue at the thigh. These results emphasise the importance of accurate measures of regional body composition when investigating potential health risks.

Diabetic as well as pre-diabetic women have impaired cognitive performance and greater risk of developing cognitive impairment.

No abstract

The prevalence of diabetes among Hispanic and Asian American subpopulations in the United States is unknown. OBJECTIVE To estimate racial/ethnic differences in the prevalence of diabetes among US adults 20 years or older by major race/ethnicity groups and selected Hispanic and non-Hispanic Asian subpopulations. DESIGN, SETTING, AND PARTICIPANTS National Health and Nutrition Examination Surveys, 2011-2016, cross-sectional samples representing the noninstitutionalized, civilian, US population. The sample included adults 20 years or older who had self-reported diagnosed diabetes during the interview or measurements of hemoglobin A 1c (HbA 1c), fasting plasma glucose (FPG), and 2-hour plasma glucose (2hPG). EXPOSURES Race/ethnicity groups: non-Hispanic white, non-Hispanic black, Hispanic and Hispanic subgroups (Mexican, Puerto Rican, Cuban/Dominican, Central American, and South American), non-Hispanic Asian and non-Hispanic Asian subgroups (East, South, and Southeast Asian), and non-Hispanic other. MAIN OUTCOMES AND MEASURES Diagnosed diabetes was based on self-reported prior diagnosis. Undiagnosed diabetes was defined as HbA 1c 6.5% or greater, FPG 126 mg/dL or greater, or 2hPG 200 mg/dL or greater in participants without diagnosed diabetes. Total diabetes was defined as diagnosed or undiagnosed diabetes. RESULTS The study sample included 7575 US adults (mean age, 47.5 years; 52% women; 2866 [65%] non-Hispanic white, 1636 [11%] non-Hispanic black, 1952 [15%] Hispanic, 909 [6%] non-Hispanic Asian, and 212 [3%] non-Hispanic other). A total of 2266 individuals had diagnosed diabetes; 377 had undiagnosed diabetes. Weighted age-and sex-adjusted prevalence of total diabetes was 12.1% (95% CI, 11.0%-13.4%) for non-Hispanic white, 20.4% (95% CI, 18.8%-22.1%) for non-Hispanic black, 22.1% (95% CI, 19.6%-24.7%) for Hispanic, and 19.1% (95% CI, 16.0%-22.1%) for non-Hispanic Asian adults (overall P < .001). Among Hispanic adults, the prevalence of total diabetes was 24.6% (95% CI, 21.6%-27.6%) for Mexican, 21.7% (95% CI, 14.6%-28.8%) for Puerto Rican, 20.5% (95% CI, 13.7%-27.3%) for Cuban/Dominican, 19.3% (95% CI, 12.4%-26.1%) for Central American, and 12.3% (95% CI, 8.5%-16.2%) for South American subgroups (overall P < .001). Among non-Hispanic Asian adults, the prevalence of total diabetes was 14.0% (95% CI, 9.5%-18.4%) for East Asian, 23.3% (95% CI, 15.6%-30.9%) for South Asian, and 22.4% (95% CI, 15.9%-28.9%) for Southeast Asian subgroups (overall P = .02). The prevalence of undiagnosed diabetes was 3.9% (95% CI, 3.0%-4.8%) for non-Hispanic white, 5.2% (95% CI, 3.9%-6.4%) for non-Hispanic black, 7.5% (95% CI, 5.9%-9.1%) for Hispanic, and 7.5% (95% CI, 4.9%-10.0%) for non-Hispanic Asian adults (overall P < .001). CONCLUSIONS AND RELEVANCE In this nationally representative survey of US adults from 2011 to 2016, the prevalence of diabetes and undiagnosed diabetes varied by race/ethnicity and among subgroups identified within the Hispanic and non-Hispanic Asian populations.