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In recent years, strong evidence has emerged suggesting that insufficient duration, quality, and/or timing of sleep are associated with cardiovascular disease (CVD), and various mechanisms for this association have been proposed. Such associations may be related to endophenotypic features of the sleep homeostat and the circadian oscillator, or may be state-like effects of the environment. Here, we review recent literature on sleep, circadian rhythms and CVD with a specific emphasis on differences between racial/ethnic groups. We discuss the reported differences, mainly between individuals of European and African descent, in parameters related to sleep (architecture, duration, quality) and circadian rhythms (period length and phase shifting). We further review racial/ethnic differences in cardiovascular disease and its risk factors, and develop the hypothesis that racial/ethnic health disparities may, to a greater or smaller degree, relate to differences in parameters related to sleep and circadian rhythms. When humans left Africa some 100,000 years ago, some genetic differences between different races/ethnicities were acquired. These genetic differences have been proposed as a possible predictor of CVD disparities, but concomitant differences in culture and lifestyle between different groups may equally explain CVD disparities. We discuss the evidence for genetic and environmental causes of these differences in sleep and circadian rhythms, and their usefulness as health intervention targets. [ABSTRACT FROM AUTHOR]

Laboratory studies have found that short-term sleep restriction is associated with impairments in glucose metabolism, appetite regulation and blood pressure regulation. This chapter reviews the epidemiologic evidence for an association between habitual sleep duration and quality and risk of cardiometabolic diseases including obesity, diabetes and hypertension. Multiple studies observed a cross-sectional association between short sleep duration (generally <6 h per night) and increased body mass index or obesity, prevalent diabetes and prevalent hypertension. Many studies also reported an association between self-reported long sleep duration (generally >8 h per night) and cardiometabolic disease. There have been a few prospective studies and several, but not all, have found an association between short sleep and incident diabetes, hypertension and markers of cardiovascular disease. Future prospective epidemiologic studies need to include objective measures of sleep, and intervention studies are needed in order to establish a causal link between impaired or insufficient sleep and cardiometabolic disease risk. [ABSTRACT FROM AUTHOR]

Objective: To examine bed times and wake times in US adolescents aged 15 to 17 years using time diaries to determine whether adolescent sleep has changed in recent years and what factors determine bed times and wake times. Study design: Time diary analysis using 2 national probability samples: 1981 Time Use Longitudinal Panel Study (n = 130) and 2003-2006 American Time Use Survey (n = 2978). Results: Average time in bed on school days was about 8 hours and was 1 to 2 hours longer on non-school days. Bed times and wake times were similar in 1981 and 2003-2006. Sociodemographic factors and daytime activities, specifically computer use and social activities, predicted bed time. On school days, school start time was the strongest predictor of wake time. Every hour earlier that school started, wake time was about 25 minutes earlier. Conclusions: Adolescents spent less than the recommended 9 hours in bed on school days. There is no evidence that this is a recent change in bed times and wake times, however. Although many factors influence bed time, school start time is the strongest determinant of wake time on school days. Increased computer use and earlier school days may be contributing to insufficient sleep in adolescents. [Copyright &y& Elsevier]

Background: Recent epidemiologic studies have found that self-reported duration of sleep is associated with obesity, diabetes, hypertension, and mortality. The extent to which self reports of sleep duration are similar to objective measures and whether individual characteristics influence the degree of similarity are not known.Methods: Eligible participants at the Chicago site of the Coronary Artery Risk Development in Young Adults Study were invited to participate in a 2003-2005 ancillary sleep study; 82% (n = 669) agreed. Sleep measurements collected in 2 waves included 3 days each of wrist actigraphy, a sleep log, and questions about usual sleep duration. We estimate the average difference and correlation between subjectively and objectively measured sleep by using errors-in-variables regression models.Results: Average measured sleep was 6 hours, whereas the average from subjective reports was 6.8 hours. Subjective reports increased on average by 34 minutes for each additional hour of measured sleep. Overall, the correlation between reported and measured sleep duration was 0.47. Our model suggests that persons sleeping 5 hours over-reported their sleep duration by 1.2 hours, and those sleeping 7 hours over-reported by 0.4 hours. The correlations and average differences between self-reports and measured sleep varied by health, sociodemographic, and sleep characteristics.Conclusion: In a population-based sample of middle-aged adults, subjective reports of habitual sleep are moderately correlated with actigraph-measured sleep, but are biased by systematic over-reporting. The true associations between sleep duration and health may differ from previously reported associations between self-reported sleep and health. [ABSTRACT FROM AUTHOR]

Summary: The prevalence of diabetes and obesity is increasing at an alarming rate worldwide, and the causes of this pandemic are not fully understood. Chronic sleep curtailment is a behavior that has developed over the past 2–3 decades. Laboratory and epidemiological studies suggest that sleep loss may play a role in the increased prevalence of diabetes and/or obesity. Current data suggest the relationship between sleep restriction, weight gain and diabetes risk may involve at least three pathways: (1) alterations in glucose metabolism; (2) upregulation of appetite; and (3) decreased energy expenditure. The present article reviews the current evidence in support of these three mechanisms that might link short sleep and increased obesity and diabetes risk. [Copyright &y& Elsevier]

Objective: To determine whether an association between short sleep duration and increased body mass index (BMI) exists in a sample of U.S. adolescents. Study design: Public-use dataset of the National Longitudinal Study of Adolescent Health. Final sample included 4486 adolescents (51% female). Main outcome was BMI transformed into z-scores for age and sex using reference values from the Centers for Disease Control/National Center for Health Statistics. Overweight was defined as ≥95th percentile. Linear and logistic regression models were calculated. Sleep duration was self-reported in hours. A quadratic term for sleep was added to test curvilinear association. Covariates included age, race, parental education, activity and inactivity scores. Results: Among males, linear regression indicated that sleep duration significantly predicted BMI z-score (Beta = −0.08, 95% CI: −0.12, −0.03). Logistic regression indicated that sleep duration predicted risk of overweight among males (OR = 0.90, 95% CI: 0.82, 1.00). Sleep duration was not a significant predictor among females in either regression model. Quadratic term for sleep was not significant for either sex. Conclusions: Longer sleep duration was weakly associated with lower BMI and risk of overweight among male adolescents only. This sex-related difference may be due to differences in the physiology of puberty or in sleep characteristics. [Copyright &y& Elsevier]