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Obesity is a major public health problem among US adults. Insufficient sleep and sleep disorders are prevalent and may contribute to the public health problem of obesity. This review addresses several key questions regarding sleep and obesity in adults, including the following: (1) What constitutes adequate sleep in adults? (2) What are the consequences of inadequate sleep in adults? (3) What factors influence sleep in adults? (4) How can adults improve their sleep? (5) How can we implement these in adults? (6) How can these issues be addressed in future research and policy decisions? Although a comprehensive review of all of these is beyond the scope of this article, this review brings these concepts together toward a discussion of the role of sleep in the health of US adults., (Copyright © 2017 National Sleep Foundation. Published by Elsevier Inc. All rights reserved.)

Sleep is increasingly recognized as an important lifestyle contributor to health. However, this has not always been the case, and an increasing number of Americans choose to curtail sleep in favor of other social, leisure, or work-related activities. This has resulted in a decline in average sleep duration over time. Sleep duration, mostly short sleep, and sleep disorders have emerged as being related to adverse cardiometabolic risk, including obesity, hypertension, type 2 diabetes mellitus, and cardiovascular disease. Here, we review the evidence relating sleep duration and sleep disorders to cardiometabolic risk and call for health organizations to include evidence-based sleep recommendations in their guidelines for optimal health., (© 2016 American Heart Association, Inc.)

Purpose of Review: Sleep plays many roles in maintenance of cardiovascular health. This review summarizes the literature across several areas of sleep and sleep disorders in relation to cardiometabolic disease risk factors., Recent Findings: Insufficient sleep duration is prevalent in the population and is associated with weight gain and obesity, inflammation, cardiovascular disease, diabetes, and mortality. Insomnia is also highly present and represents an important risk factor for cardiovascular disease, especially when accompanied by short sleep duration. Sleep apnea is a well-characterized risk factor for cardiometabolic disease and cardiovascular mortality. Other issues are relevant as well. For example, sleep disorders in pediatric populations may convey cardiovascular risks. Also, sleep may play an important role in cardiovascular health disparities., Summary: Sleep and sleep disorders are implicated in cardiometabolic disease risk. This review addresses these and other issues, concluding with recommendations for research and clinical practice.

Objective: Sleep duration is associated with obesity and cardiometabolic disease. It is unclear, though, how these relationship differs across age groups., Methods: Data from 2007 to 2008 National Health and Nutrition Examination Survey (NHANES) were used, including respondents aged 16+ with complete data (N = 5,607). Sleep duration and age were evaluated by self-report, and body mass index (BMI) was assessed objectively. Sleep duration was evaluated continuously and categorically [very short (≤4 h), short (5-6 h), and long (≥9 h) versus average (7-8 h)]. Age was also evaluated continuously and categorically [adolescent (16-17 years), young adult (18-29 years), early middle age (30-49 years), late middle age (50-64 years), and older adult (≥65 years)]., Results: There was a significant interaction with age for both continuous (Pinteraction  = 0.014) and categorical (Pinteraction  = 0.035) sleep duration. A pseudo-linear relationship was seen among the youngest respondents, with the highest BMI associated with the shortest sleepers and the lowest BMI associated with the longest sleepers. This relationship became U-shaped in middle-age, and less of a relationship was seen among the oldest respondents., Conclusions: These findings may provide insights for clinical recommendations and could help to guide mechanistic research regarding the sleep-obesity relationship., (© 2015 The Obesity Society.)

There is increasing awareness of the role of sleep disturbance as an important factor in health and disease. Although sub-clinical sleep disturbances (insufficient sleep duration or inadequate sleep quality) may be difficult to assess with conceptual and/or methodological clarity, this review attempts to summarize and synthesize these findings. First, the concept of sleep disturbance in a public health context is introduced, to provide context and rationale. Second, operational definitions of 'cardiometabolic disease' and 'sleep disturbance' are offered, to address many unclear operationalizations. Third, the extant literature is summarized regarding short or long sleep duration and/or insufficient sleep, insomnia and insomnia symptoms, general (non-specific sleep disturbances), circadian rhythm abnormalities that result in sleep disturbances, and, briefly, sleep-disordered breathing. Fourth, the review highlights the social/behavioural context of sleep, including discussions of sleep and race/ethnicity, socio-economic position, and other social/environmental factors, in order to place these findings in a social-environmental context relevant to public health. Fifth, the review highlights the issue of sleep as a domain of health behaviour and addresses issues regarding development of healthy sleep interventions. Finally, a research agenda of future directions is proposed.

Background: Self-reported short or long sleep duration has been associated with adverse cardiometabolic health outcomes in laboratory and epidemiologic studies, but interpretation of such data has been limited by methodologic issues., Methods: Adult respondents of the 2007-2008 US National Health and Nutrition Examination Survey (NHANES) were examined in a cross-sectional analysis (N=5649). Self-reported sleep duration was categorized as very short (<5 h), short (5-6 h), normal (7-8 h), or long (≥9 h). Obesity, diabetes mellitus (DM), hypertension, and hyperlipidemia were objectively assessed by self-reported history. Statistical analyses included univariate comparisons across sleep duration categories for all variables. Binary logistic regression analyses and cardiometabolic factor as outcome, with sleep duration category as predictor, were assessed with and without covariates. Observed relationships were further assessed for dependence on race/ethnicity., Results: In adjusted analyses, very short sleep was associated with self-reported hypertension (odds ratio [OR], 2.02, [95% confidence interval {CI},1.45-2.81]; P<0.0001), self-reported hyperlipidemia (OR, 1.96 [95% CI, 1.43-2.69]; P<0.0001), objective hyperlipidemia (OR, 1.41 [95% CI, 1.04-1.91]; P=0.03), self-reported DM (OR, 1.76 [95% CI, 1.13-2.74]; P=0.01), and objective obesity (OR, 1.53 [95% CI, 1.03-1.43]; P=0.005). Regarding short sleep (5-6 h), in adjusted analyses, elevated risk was seen for self-reported hypertension (OR, 1.22 [95% CI, 1.02-1.45]; P=0.03) self-reported obesity (OR, 1.21 [95% CI, 1.03-1.43]; P=0.02), and objective obesity (OR, 1.17 [95% CI, 1.00-1.38]; P<0.05). Regarding long sleep (≥9 h), no elevated risk was found for any outcomes. Interactions with race/ethnicity were significant for all outcomes; race/ethnicity differences in patterns of risk varied by outcome studied. In particular, the relationship between very short sleep and obesity was strongest among blacks and the relationship between short sleep and hypertension is strongest among non-Hispanic whites, blacks, and non-Mexican Hispanics/Latinos., Conclusions: Short sleep duration is associated with self-reported and objectively determined adverse cardiometabolic outcomes, even after adjustment for many covariates. Also, these patterns of risk depend on race/ethnicity., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Existing research has demonstrated associations between sleep duration and obesity, diabetes, cardiovascular disease and mortality. Sleep disorders research has shown that sleep apnoea, insomnia and other sleep disorders confer risk for cardiometabolic disease, particularly in the presence of reduced sleep duration. The aim of the present study was to examine the associations between general sleep disturbance, operationalized as 'difficulty falling asleep, staying asleep, or sleeping too much' as measured in a large, nationally representative sample, and self-reported history of myocardial infarction, stroke, coronary artery disease, diabetes and obesity. Data from the Behavioral Risk Factor Surveillance System were analysed. Complete data were available for 138,201 individuals. A hierarchical logistic regression analysis examined associations before and after adjustment for demographic, socioeconomic, medical and psychological factors. After adjusting for demographic, socioeconomic and health risk factors, sleep duration was associated with obesity [odds ratio (OR)=1.18, P<0.0005), diabetes (OR=1.18, P<0.005), myocardial infarction (OR=1.36, P<0.0005), stroke (OR=1.22, P<0.05) and coronary artery disease (OR=1.59, P<0.0005). In fully adjusted models that included physical health, significant relationships remained for obesity (OR=1.14, P<0.0005), myocardial infarction (OR=1.23, P<0.005) and coronary artery disease (OR=1.43, P<0.0005). Sleep disturbance is a significant risk factor for obesity, diabetes, myocardial infarction, stroke and coronary artery disease, and effects for obesity, myocardial infarction and coronary artery disease are the most robust after adjustment. This study demonstrates that sleep disturbance is a novel risk factor that is potentially modifiable. Future research should determine whether sleep intervention could reduce the cardiometabolic consequences of sleep disturbance., (© 2011 European Sleep Research Society.)

A workshop was held at the National Institute for Diabetes and Digestive and Kidney Diseases with a focus on the impact of sleep and circadian disruption on energy balance and diabetes. The workshop identified a number of key principles for research in this area and a number of specific opportunities. Studies in this area would be facilitated by active collaboration between investigators in sleep/circadian research and investigators in metabolism/diabetes. There is a need to translate the elegant findings from basic research into improving the metabolic health of the American public. There is also a need for investigators studying the impact of sleep/circadian disruption in humans to move beyond measurements of insulin and glucose and conduct more in-depth phenotyping. There is also a need for the assessments of sleep and circadian rhythms as well as assessments for sleep-disordered breathing to be incorporated into all ongoing cohort studies related to diabetes risk. Studies in humans need to complement the elegant short-term laboratory-based human studies of simulated short sleep and shift work etc. with studies in subjects in the general population with these disorders. It is conceivable that chronic adaptations occur, and if so, the mechanisms by which they occur needs to be identified and understood. Particular areas of opportunity that are ready for translation are studies to address whether CPAP treatment of patients with pre-diabetes and obstructive sleep apnea (OSA) prevents or delays the onset of diabetes and whether temporal restricted feeding has the same impact on obesity rates in humans as it does in mice.

Background: Sleep duration and morningness/eveningness (circadian preference) have separately been associated with cardiovascular risk factors (i.e. tobacco use, physical inactivity). Interactive effects are plausible, resulting from combinations of sleep homeostatic and circadian influences. These have not been examined in a population sample. Methods: Multivariable regression models were used to test the associations between combinations of sleep duration (short [-6 h], adequate [7-8 h], long [≥9 h]) and morning/evening preference (morning, somewhat morning, somewhat evening, evening) with the cardiovascular risk factors of tobacco use, physical inactivity, high sedentary behaviour, obesity/overweight and eating fewer than 5 daily servings of fruit and vegetables, in a cross- sectional sample of 439 933 adults enrolled in the United Kingdom Biobank project. Results: Participants were 56% female, 95% white and mean age was 56.5 (SD= 8.1) years. Compared with adequate sleep with morning preference (referent group), long sleep with evening preference had a relative odds of 3.23 for tobacco use, a 2.02-fold relative odds of not meeting physical activity recommendations, a 2.19-fold relative odds of high screen-based sedentary behaviour, a 1.47-fold relative odds of being obese/overweight and a 1.62-fold relative odds of <5 fruit and vegetable daily servings. Adequate sleep with either morning or somewhat morning preference was associated with a lower prevalence and odds for all cardiovascular risk behaviours except fruit and vegetable intake. Conclusions: Long sleepers with evening preference may be a sleep phenotype at high cardiovascular risk. Further work is needed to examine these relationships longitudinally and to assess the effects of chronotherapeutic interventions on cardiovascular risk behaviours. [ABSTRACT FROM AUTHOR]

Short sleep duration is increasingly recognized as a risk factor for obesity. Sleep is now considered 1 of the 3 lifestyle behaviors, along with diet and exercise, which are closely associated with health. If sleep duration is a causal factor in the etiology of obesity, it must affect energy intake and/or energy expenditure to create a positive energy balance. The preponderance of evidence to date points to an effect of sleep restriction on energy intake that exceeds the added energy costs of maintaining longer wakefulness. Observational studies describe greater intakes of energy, fat, and possibly carbohydrates in short sleepers and this is corroborated by clinical interventions. These intervention studies further provide mechanistic explanations, via alterations in hormonal and neuronal controls of food intake, for an association between short sleep and obesity. [ABSTRACT FROM PUBLISHER]

Abstract: Short sleep duration is associated with weight gain and obesity, diabetes, cardiovascular disease, psychiatric illness, and performance deficits. Likewise, long sleep duration is also associated with poor physical and mental health. The role of a healthy diet in habitual sleep duration represents a largely unexplored pathway linking sleep and health. This study evaluated associations between habitual sleep parameters and dietary/nutritional variables obtained via the National Health and Nutrition Examination Survey (NHANES), 2007–2008. We hypothesized that habitual very short (<5h) short (5–6h) and long (9+h) sleep durations are associated with intake of a number of dietary nutrient variables. Overall, energy intake varied across very short (2036kcal), short (2201kcal), and long (1926kcal) sleep duration, relative to normal (2151kcal) sleep duration (p =0.001). Normal sleep duration was associated with the greatest food variety (17.8), compared to very short (14.0), short (16.5) and long (16.3) sleep duration (p <0.001). Associations between sleep duration were found across nutrient categories, with significant associations between habitual sleep duration and proteins, carbohydrates, vitamins and minerals. In stepwise analyses, significant contributors of unique variance included theobromine (long sleep RR=0.910, p <0.05), vitamin C (short sleep RR=0.890, p <0.05), tap water (short sleep RR=0.952, p <0.001; very short (<5h) sleep RR=0.941, p <0.05), lutein+zeaxanthin (short sleep RR=1.123, p <0.05), dodecanoic acid (long sleep RR=0.812, p <0.05), choline (long sleep RR=0.450, p =0.001), lycopene (very short (<5h) sleep RR=0.950, p <0.05), total carbohydrate (very short (<5h) sleep RR=0.494, p <0.05; long sleep RR=0.509, p <0.05), selenium (short sleep RR=0.670, p <0.01) and alcohol (long sleep RR=1.172, p <0.01). Overall, many nutrient variables were associated with short and/or long sleep duration, which may be explained by differences in food variety. Future studies should assess whether these associations are due to appetite dysregulation, due to short/long sleep and/or whether these nutrients have physiologic effects on sleep regulation. In addition, these data may help us better understand the complex relationship between diet and sleep and the potential role of diet in the relationship between sleep and obesity and other cardiometabolic risks. [Copyright &y& Elsevier]

Summary: Existing data from laboratory studies suggest a number of negative consequences of acute reductions in sleep time. Also, epidemiological data suggest links between shorter self-reported sleep duration and negative health outcomes. These bodies of work are growing, revealing several key points of convergence and opportunities for future exploration. In addition, they begin to highlight possible problems experienced by “short sleepers,” who sleep approximately 6h or less per night. While it is likely that this group is heterogeneous, comprised both of individuals with less need for sleep and those not sleeping enough, the laboratory and epidemiological findings point towards directions that can be more fully explored in verified short sleepers. This paper discusses problems associated with the terminology used to describe “short sleep,” summarizes laboratory studies exploring neurobehavioral performance, metabolism and obesity, and psychological health and epidemiological studies exploring mortality risk, obesity and metabolism, cardiovascular disease, and general health/psychosocial stress, describes studies of verified short sleepers and explores areas of convergence, laying out possible future directions. [Copyright &y& Elsevier]

Abstract: Objective: To describe which dietary nutrient variables are related to subjective and objective habitual sleep and subjective and objective napping. Methods: Participants were 459 post-menopausal women enrolled in the Women’s Health Initiative. Objective sleep was estimated using one week of actigraphy. Subjective sleep was prospectively estimated with a daily sleep diary. Dietary nutrients were calculated from food frequency questionnaires. Results: The most significant correlations were with subjective napping, including (from strongest to weakest): total fat, calories, saturated fat, monounsaturated fat, trans fat, water, proline, serine, tyrosine, phenylalanine, valine, cholesterol, leucine, glutamic acid, ash, isoleucine, histidine, sodium, tryptophan, protein, threonine, cystine, methionine, phosphorous, polyunsaturated fat, animal protein, aspartic acid, arginine, lysine, alanine, caffeine, riboflavin, gamma-tocopherol, glycine, retinol, delta-tocopherol, Vitamin D, and selenium. Actigraphic nocturnal sleep duration was negatively associated with total fat, monounsaturated fat, trans fat, saturated fat, polyunsaturated fat, calories, gamma-tocopherol, cholesterol, and alpha-tocopherol-eq. Conclusions: Actigraphic total sleep time was negatively associated with intake of fats. Subjective napping, which may be a proxy for subjective sleepiness, was significantly related to fat intake as well as intake of meat. [Copyright &y& Elsevier]

Abstract: Objective: The objective of the present study was to investigate the relationship between sleep insufficiency and sleep duration, particularly regarding negative cardiometabolic health outcomes already considered to be affected by reduced sleep time. Methods: A total of N =30,934 participants from the 2009 Behavioural Risk Factor Surveillance System (BRFSS) answered questions about their sleep duration as well as subjective feelings of sleep insufficiency. Outcomes included body mass index (BMI), obesity (BMI⩾30kgm−2) and history of hypertension, diabetes, hypercholesterolaemia, heart attack and stroke. Linear and logistic regression models examined whether cardiometabolic outcomes were associated with (1) sleep duration alone, (2) sleep insufficiency alone and (3) the combined effect of sleep duration and sleep insufficiency. Results: Results indicated that, when examined alone, sleep duration <5h (versus 7h) was related to BMI (B =2.716, p <0.01), obesity (B =2.080, p <0.000001), diabetes (B =3.162, p <0.000001), hypertension (B =2.703, p <0.000001), hypercholesterolaemia (B =1.922, p <0.00001), heart attack (B =4.704, p <0.000001) and stroke (B =4.558, p< 0.000001), and sleep insufficiency (days per week, continuous) was related to BMI (B =0.181, p <0.01), obesity (B =1.061, p <0.000001) and hypercholesterolaemia (B =1.025, p <0.01). All of these relationships remained significant after adjustment for covariates, except for diabetes and sleep duration. Also, after adjustment, a significant relationship between insufficient sleep and hypertension emerged (B =1.039, p <0.001). When evaluated together, after adjustment for covariates, significant relationships remained between sleep duration <5h (versus 7h) and BMI (B =1.266, p <0.05), obesity (B =1.389, p <0.05), hypertension (B =1.555, p <0.01), heart attack (B =2.513, p <0.01) and stroke (B =1.807, p <0.05). It should be noted that relationships between sleep duration >9h (versus 7h) were seen for heart attack (B =1.863, p <0.001) and stroke (B =1.816, p <0.01). In these models, sleep insufficiency was associated with hypercholesterolaemia (B =1.031, p <0.01) and hypertension (B =1.027, p <0.05). Conclusions: These analyses show that both sleep duration and insufficiency are related to cardiometabolic health outcomes, and that when evaluated together, both variables demonstrate unique effects. [Copyright &y& Elsevier]