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Sleep restriction is associated with increased cardiovascular risk, which is more pronounced in female than male persons. We reported recently first causal evidence that mild, prolonged sleep restriction mimicking “real-life” conditions impairs endothelial function, a key step in the development and progression of cardiovascular disease, in healthy female persons. However, the underlying mechanisms are unclear. In model organisms, sleep restriction increases oxidative stress and upregulates antioxidant response via induction of the antioxidant regulator nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Here, we assessed directly endothelial cell oxidative stress and antioxidant responses in healthy female persons (n = 35) after 6 weeks of mild sleep restriction (1.5 h less than habitual sleep) using randomized crossover design. Sleep restriction markedly increased endothelial oxidative stress without upregulating antioxidant response. Using RNA-seq and a predicted protein–protein interaction database, we identified reduced expression of endothelial Defective in Cullin Neddylation-1 Domain Containing 3 (DCUN1D3), a protein that licenses Nrf2 antioxidant responses, as a mediator of impaired endothelial antioxidant response in sleep restriction. Thus, sleep restriction impairs clearance of endothelial oxidative stress that over time increases cardiovascular risk. Trial Registration: NCT02835261

Purpose of ReviewIn this review, we summarize recent epidemiological data (2014–2019) that examine the association of sleep variability with blood pressure (BP), discuss potential underlying mechanisms, and highlight future research directions.Recent FindingsHigher standard deviations of sleep duration and sleep-onset timing were not related to BP. However, a higher Sleep Regularity Index score was associated with lower odds of hypertension. Studies on social jetlag, a prevalent form of sleep variability, reported null associations. In contrast, lower interdaily stability in circadian rest-activity rhythms, a measure of invariability in sleep-wake cycles between days and synchronization to light and dark cycles, was associated with higher BP and greater hypertension odds, particularly among non-shift workers.SummarySleep variability is consistently associated with risk factors for hypertension. Evidence on sleep variability and BP is limited and varies depending on the measure used to characterize day-to-day variability in sleep. Studies that identify and utilize a standard definition of sleep variability, incorporate a 24-h ambulatory BP monitoring, and ensure coinciding timing of sleep and BP measurements are necessary to disentangle these relationships.

Purpose of ReviewVasomotor symptoms are frequently experienced by women during menopause and have been linked to obesity. Severity of menopausal symptoms is a distinct construct from presence of symptoms, and the relation between severity of symptoms and obesity is less established. The purpose of this brief narrative review was to summarize evidence from recent studies on associations between menopausal symptom severity and measures of obesity.Recent FindingsSixteen articles were identified that specifically assessed and reported on the severity of menopausal symptoms in relation to measures of obesity including body mass index (BMI), waist circumference, and waist-to-hip ratio.SummaryMost studies to date show that greater BMI, waist size, and waist-to-hip ratio are associated with greater severity of menopausal symptoms. Given the large segment of women who will experience symptoms and that severity of symptoms influences treatment decisions, future studies are needed to determine how weight management efforts may reduce the severity of menopausal symptoms.

Blood pressure and cholesterol reduction have proven effective to reduce cardiovascular disease (CVD) risk, yet adherence to medical therapy is suboptimal and contributing factors to non-adherence are not well-established. The purpose of this study was to determine the prevalence and predictors of non-adherence to blood pressure and cholesterol-lowering medications in individuals who participated in an NHLBI-sponsored evaluation of a hospital-based screening and outreach program for high-risk employees and the community. This was a cross-sectional study of 371 adults (mean age 60 years, 57% female, 60% non-white) who were eligible to participate if they were men >40 years, women >50 years, or had established CVD or CVD-risk equivalent. Each participant received a comprehensive standardized CVD screening evaluation; medication non-adherence was defined as missing any pills for high blood pressure or abnormal cholesterol in the past week. Associations between participant demographics, lifestyle and psychosocial risk factors, and non-adherence were assessed using logistic regression to adjust for confounders. The prevalence of taking medication for high blood pressure or abnormal cholesterol in the study population was 48% and 38%, respectively. Among those participants, 14% reported missing high blood pressure pills and 23% reported missing cholesterol pills in the past week. Significant ( p <0.05) univariate predictors of non-adherence to blood pressure medication were smoking, depression, feeling sad or blue for 2 weeks or more, and eating fast food ≥2 times per week. In a multivariable regression model adjusted for confounders, participants who reported missing any blood pressure pills in the past week were 6.6 times more likely to have uncontrolled hypertension (≥140/90 mmHg) compared to those who were adherent (95% CI = 2.1-20.2). Age <65 years and eating outside the home ≥2 times per week were significantly associated with non-adherence to cholesterol medication even after adjusting for measured confounders. Non-adherence to preventive medications was associated with poor blood pressure control and several lifestyle and psychosocial risk factors for CVD. This information may be clinically useful to help identify individuals who may be non-adherent to medical therapy and at increased CVD risk.

There is sufficient evidence showing that greater sleep quality improves weight loss outcomes achieved through dietary modifications; however, the effects of dietary modifications such as caloric restriction on sleep outcomes is less established. Caloric restriction is a commonly recommended weight-loss method, yet it may result in short-term weight loss and subsequent weight regain, known as “weight cycling”, which has recently been shown to be associated with both poor sleep and worse cardiovascular health. The purpose of this brief narrative review was to summarize the evidence from recent studies of the effects of caloric restriction on sleep. Six articles were identified that specifically measured effects of a caloric restriction-based intervention on aspects of sleep as primary or secondary outcomes. Most research to date indicates that caloric restriction improves sleep outcomes including sleep quality and sleep onset latency. However, the relation between caloric restriction and sleep duration is less clear. Given the mixed results and the potential for severe caloric restriction to lead to weight cycling, future studies are needed to clarify how caloric restriction affects sleep and the potential implications for weight-management efforts.

Purpose of ReviewNight-to-night variability in sleep patterns leads to circadian disruption and, consequently, could increase cardiometabolic risk. The purpose of this review is to summarize findings from studies published between 2015 and 2020 examining various measures of night-to-night variability in sleep in relation to metabolic syndrome (MetS), type 2 diabetes (T2D), and their risk factors. We illustrate a potential causal pathway between irregular sleep patterns and T2D, highlighting knowledge gaps along the way.Recent FindingsAcross different measures of sleep variability, irregular sleep patterns were associated with poorer cardiometabolic outcomes. Higher standard deviations (SD) across nights of sleep duration and onset or midpoint of sleep were associated with increased odds of having MetS and clusters of metabolic abnormalities as well as greater adiposity and poorer glycemic control. Conversely, greater regularity of rest-activity patterns related to lower risk for T2D. Social jetlag was associated with glycemic dysregulation, adiposity, T2D, and MetS. These associations are often observed in both metabolically healthy and unhealthy individuals; both higher SD of sleep duration and social jetlag relate to poorer glucose regulation in individuals with diabetes.SummaryThere is consistent evidence of associations of sleep variability with increased risk for adiposity, glucose dysregulation, T2D, and MetS. Although experimental evidence is needed to determine causation, there is support to recommend stabilizing sleep patterns for cardiometabolic risk prevention.

Residing in lower socioeconomic status (SES) neighborhoods is associated with increased risk of morbidity and mortality. Few studies have examined this association for cardiovascular disease (CVD) outcomes in a treated population in New York City (NYC). The purpose of this study was to determine the relationship between neighborhood level poverty and 1-year clinical outcomes (rehospitalization and/or death) among hospitalized patients with CVD. Data on rehospitalization and/or death at 1-year were collected from consecutive patients admitted at a university medical center in NYC from November 2009 to September 2010. NYC residents totaled 2,198. U.S. Census 2000 zip code data was used to quantify neighborhood SES into quintiles of poverty (Q1 = lowest poverty to Q5 = highest poverty). Univariate analyses were used to determine associations between neighborhood poverty and baseline characteristics and comorbidities. A logistic regression analysis was used to calculate odds ratios for the association between quintiles of poverty and rehospitalization/death at 1 year. Fifty-five percent of participants experienced adverse outcomes. Participants in Q5 (9 %) were more likely to be female [odds ratio (OR) = 0.49, 95 % confidence interval (CI) 0.33–0.73], younger (OR = 0.50, 95 % CI 0.34–0.74), of minority race/ethnicity (OR = 18.24, 95 % CI 11.12–29.23), and have no health insurance (OR = 4.79, 95 % CI 2.92–7.50). Living in Q5 was significantly associated with increased comorbidities, including diabetes mellitus and hypertension, but was not a significant predictor of rehospitalization/death at 1 year. Among patients hospitalized with CVD, higher poverty neighborhood residence was significantly associated with a greater prevalence of comorbidities, but not of rehospitalization and/or death. Affordable, accessible resources targeted at reducing the risk of developing CVD and these comorbidities should be available in these communities.

Background Medication non-adherence is a significant contributor to suboptimal control of blood pressure and lipids. Purpose This study determined if having a paid and/or family caregiver was associated with medication adherence in patients hospitalized for cardiovascular disease. Methods Consecutive patients admitted to the cardiovascular service at a university medical center who completed a standardized questionnaire about medication adherence and caregiving (paid/professional or family member/friend) were included in this analysis ( N  = 1,432; 63 % white; 63%male). Results Among cardiac patients, 39 % reported being prescribed ≥7 different medications, and one in four reported being non-adherent to their medication(s). Participants who reported having/planning to have a paid caregiver were 40 % less likely to be non-adherent to their medications compared to their counterparts. The association remained significant after adjustment for demographic confounders and comorbid conditions (OR = 0.49; 95 %CI = 0.29–0.82). Conclusion Cardiac patients with a paid caregiver were half as likely to be non-adherent to medications as those without caregivers.