IntroductionMetabolic syndrome is a cluster of cardiometabolic risk factors associated with increased risk of multiple chronic diseases, including cancer and cardiovascular disease. The objectives of this study were to estimate the prevalence of metabolic syndrome overall, by race and sex, and to assess trends in prevalence from 1988 through 2012.MethodsWe analyzed data from the National Health and Nutrition Examination Survey (NHANES) for 1988 through 2012. We defined metabolic syndrome as the presence of at least 3 of these components: elevated waist circumference, elevated triglycerides, reduced high-density lipoprotein cholesterol, high blood pressure, and elevated fasting blood glucose. Data were analyzed for 3 periods: 1988–1994, 1999–2006, and 2007–2012.ResultsAmong US adults aged 18 years or older, the prevalence of metabolic syndrome rose by more than 35% from 1988–1994 to 2007–2012, increasing from 25.3% to 34.2%. During 2007–2012, non-Hispanic black men were less likely than non-Hispanic white men to have metabolic syndrome (odds ratio [OR], 0.77; 95% confidence interval [CI], 0.66–0.89). However, non-Hispanic black women were more likely than non-Hispanic white women to have metabolic syndrome (OR, 1.20; 95% CI, 1.02–1.40). Low education level (OR, 1.56; 95% CI, 1.32–1.84) and advanced age (OR, 1.73; 95% CI, 1.67–1.80) were independently associated with increased likelihood of metabolic syndrome during 2007–2012.ConclusionMetabolic syndrome prevalence increased from 1988 to 2012 for every sociodemographic group; by 2012, more than a third of all US adults met the definition and criteria for metabolic syndrome agreed to jointly by several international organizations.

Sleep-related complaints are widely prevalent in those with alcohol dependence (AD). AD is associated not only with insomnia, but also with multiple sleep-related disorders as a growing body of literature has demonstrated. This article will review the various aspects of insomnia associated with AD. In addition, the association of AD with other sleep-related disorders will be briefly reviewed. The association of AD with insomnia is bidirectional in nature. The etiopathogenesis of insomnia has demonstrated multiple associations and is an active focus of research. Treatment with cognitive behavioral therapy for insomnia is showing promise as an optimal intervention. In addition, AD may be associated with circadian abnormalities, short sleep duration, obstructive sleep apnea, and sleep-related movement disorder. The burgeoning knowledge on insomnia associated with moderate-to-severe alcohol use disorder has expanded our understanding of its underlying neurobiology, clinical features, and treatment options.

Background and ObjectivesBoth genetic and environmental factors contribute to stroke risk. We sought to identify novel metabolites associated with incident stroke in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort and determine whether they reflected genetic or environmental variation.MethodsThis was a stroke case–cohort observational study nested in REGARDS. Cases were defined as incident stroke and metabolomic profiles were compared to a randomly selected control cohort. In baseline plasma samples, 162 metabolites were measured using liquid chromatography–tandem mass spectrometry. Cox proportional hazards models were adjusted for age, sex, race, and age by race in the base model. Fully adjusted models included traditional stroke risk factors. Mediation analyses conducted for these stroke risk factors used the metabolite as mediator. Genome-wide associations with the leading candidate metabolites were calculated using array data. Replication analyses in the Jackson Heart Study (JHS) were conducted using random effects meta-analysis.ResultsThere were 2,043 participants who were followed over an average period of 7.1 years, including 1,075 stroke cases and 968 random controls. Nine metabolites were associated with stroke in the base model, 8 of which were measured and remained significant in meta-analysis with JHS. In the fully adjusted model in REGARDS, guanosine (hazard ratio [HR] 1.34, 95% CI 1.18–1.53; p = 7.26 × 10−6) and pseudouridine (HR 1.28, 95% CI 1.13–1.45; p = 1.03 × 10−4) were associated with incident ischemic stroke following Bonferroni adjustment. Guanosine also partially mediated the relationship between hypertension and stroke (17.6%) and pseudouridine did not mediate any risk factor. Genome-wide association analysis identified loci rs34631560 and rs34631560 associated with pseudouridine, but these did not explain the association of pseudouridine with stroke.DiscussionGuanosine and pseudouridine are nucleosides associated with incident ischemic stroke independently of other risk factors. Genetic and mediation analyses suggest that environmental exposures rather than genetic variation link nucleoside levels to stroke risk.Classification of EvidenceThis study provides Class II evidence that guanosine and pseudouridine are associated with incident stroke.