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Study Objectives: Recent studies implicate inadequate sleep duration and quality in metabolic disease. Fewer studies have examined the timing of sleep, which may be important because of its potential impact on circadian rhythms of metabolic function. We examined the association between sleep timing and metabolic risk among Hispanic/Latino adults., Methods: Cross-sectional data from community-based study of 13429 participants aged 18-74 years. People taking diabetic medications were excluded. Sleep timing was determined from self-reported bedtimes and wake times. Chronotype was defined as the midpoint of sleep on weekends adjusted for sleep duration on weekdays. Other measurements included body mass index (BMI), fasting glucose levels, estimated insulin resistance (HOMA-IR), glucose levels 2 hours post oral glucose ingestion, and hemoglobin A1c. Survey linear regression models tested associations between sleep timing and metabolic measures. Analyses were stratified by diabetes status and age-group when significant interactions were observed., Results: Among participants with diabetes, fasting glucose levels were positively associated with bedtime (approximately +3%/hour later, p < .01) and midpoint of sleep (approximately +2%/hour later, p < .05). In participants with and without diabetes combined, HOMA-IR was positively associated with midpoint of sleep (+1.5%/hr later, p < .05), and chronotype (+1.2%/hour later, p < .05). Associations differed by age-group. Among those < 36 years, later sleep timing was associated with lower BMI, lower fasting glucose, and lower HbA1c, but the opposite association was observed among older participants., Conclusions: Later sleep timing was associated with higher estimated insulin resistance across all groups. Some associations between sleep timing and metabolic measures may be age-dependent., (© Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.)

Background: Sleep disordered breathing (SDB) is common in obese adults, but not all obese adults have SDB. The aim of these analyses was to determine what predicted SDB in a sample of obese adults., Methods: We conducted cross-sectional analysis of 139 obese men and women aged 18-50 years who are chronic short sleepers. Habitual sleep duration and sleep efficiency were estimated using two weeks of wrist actigraphy. Respiratory disturbance index (RDI) was assessed by a portable screening device. SDB was defined as RDI ≥15 events h(-1). Subjective sleep quality, sleepiness, and sociodemographic characteristics were evaluated by questionnaires., Results: Increased sleep duration from actigraphy was associated with reduced odds of SDB (OR 0.44 per hour, p=0.043). Neither subjective sleep quality nor sleepiness was associated with SDB. Male sex, older age, and increased waist circumference were associated with increased odds of SDB., Conclusions: In this sample of obese adults, subjective measures of sleep quality and sleepiness were not indicators of SDB. These results suggest that, in obese patients, physicians should not rely on subjective measures to determine who should be referred for a clinical sleep study. A wider use of portable apnea screening devices should be considered in nonsymptomatic, non-Hispanic white males., (Copyright © 2012 Elsevier B.V. All rights reserved.)

The prevalence of obesity is increasing rapidly worldwide, which is cause for concern because obesity increases the risk of cardiovascular disease and diabetes, reduces life expectancy, and impairs quality of life. A better understanding of the risk factors for obesity is therefore a critical global health concern, and human biologists can play an important role in identifying these risk factors in various populations. The objective of this review is to present the evidence that inadequate sleep may be a novel risk factor associated with increased vulnerability to obesity and associated cardiometabolic disease. Experimental studies have found that short-term sleep restriction is associated with impaired glucose metabolism, dysregulation of appetite, and increased blood pressure. Observational studies have observed cross-sectional associations between short sleep duration (generally <6 h per night) and increased body mass index or obesity, prevalent diabetes, and prevalent hypertension. Some studies also reported an association between self-reported long sleep duration (generally >8 h per night) and cardiometabolic disease. A few prospective studies have found a significant increased risk of weight gain, incident diabetes, and incident hypertension associated with inadequate sleep. Given the potential link between inadequate sleep and obesity, a critical next step is to identify the social, cultural, and environmental determinants of sleep, which would help to identify vulnerable populations. Future human biology research should consider variation in sleep characteristics among different populations and determine whether the associations between sleep and obesity observed in Western populations persist elsewhere., (Copyright © 2012 Wiley Periodicals, Inc.)

Previous research in lean subjects has found lower leptin levels associated with shorter sleep duration. Since leptin levels are higher and some of the actions of leptin are impaired in obese individuals, one cannot assume that sleep will be similarly associated with leptin in obese individuals. The aim of this paper was to examine the cross-sectional association between habitual sleep duration and quality and plasma leptin levels in a sample of 80 obese men and premenopausal women aged 18-50 years. Leptin levels (ng/ml) were assayed on a fasting blood sample taken in the morning. We calculated a relative leptin level by dividing leptin by body fat percentage. Sleep duration and sleep efficiency were measured by 2 weeks of wrist actigraphy and respiratory disturbance index (RDI), a measure of sleep disordered breathing, was assessed by a portable screening device on a single night. Mean leptin levels and body fat percentage were higher in women than men (P < 0.001), however, mean RDI was higher in men (P = 0.01). There were no significant associations between relative leptin level and any of the sleep measures, including sleep duration, sleep efficiency, and sleep disordered breathing. There was also no difference between men and women in the association between sleep and leptin. In conclusion, contrary to what has been reported in other studies, measures of sleep duration and quality were not associated with leptin levels in our sample of obese adults.

Background: The clinical significance of rapid eye-movement (REM)-related obstructive sleep apnea (OSA) is unknown. Moreover, it is unclear what the determinants of sleepiness and quality of life (QoL) are among these patients. Our aim was to identify whether the apnea-hypopnea index during REM sleep (AHI(REM)), AHI during NREM sleep (AHI(NREM)), depressive symptoms, or obesity are independent predictors of excessive daytime sleepiness and reduced QoL in patients with REM-related OSA. We also assessed if these characteristics were predictors of sleepiness and QoL in all patients with OSA (AHI ≥ 5) as well as in non-stage specific OSA., Methods: This was a cross-sectional analysis of a clinic-based population with OSA. In order to minimize the contribution of AHI(NREM), we defined REM-related OSA using the following criteria: an overall AHI ≥ 5, AHI(REM)/AHI(NREM) ≥ 2, AHI(NREM) the lowest quartile of the entire cohort. We examined the predictors of subjective sleepiness using the Epworth Sleepiness Scale (ESS) and QoL using the short-form quality of life questionnaire-12 (SF-12)., Results: Of 1019 consecutive adults that were referred for their first in-laboratory polysomnogram for suspicion of OSA over a 10 month period, 931 had OSA. REM-related OSA was present in 126 patients. In adjusted linear regression models, AHI(NREM) was a significant predictor of sleepiness in the entire cohort of patients with OSA as well as non-stage specific OSA, but not in the REM-related OSA group. AHI(REM) was not a significant predictor of ESS or QoL in any of the three groups. However, greater depressive symptoms and body mass index were significant independent predictors of ESS and reduced QoL in the REM-related OSA group., Conclusion: Higher depression scores and obesity, rather than the severity of OSA (as measured by AHI(NREM) and AHI(REM)), were predictive of sleepiness and QoL scores in patients with REM-related OSA., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Objectives: Although numerous studies have reported negative associations between sleep duration and body size, no studies of this association have focused on Hispanic groups, which was the goal of this work., Methods: Data are from adults in the 1982-1984 Hispanic Health and Nutrition Examination Survey (HHANES), which enrolled Cuban-Americans, Mexican-Americans, and Puerto Ricans. HHANES included self-reported sleep duration and several anthropometric measures. Principle component analysis extracted a single variable to represent body size. Linear regression models stratified by Hispanic group predicted body size from sleep duration adjusting for age, sex, education, income, marital status, household size, and acculturation., Results: Average age was 36-44 years and 52-64% were women. Average sleep duration was 7.3-7.7 h. Shorter sleep duration was associated with larger body size in Mexican-Americans only. The regression coefficient indicated that on average a Mexican-American adult who reported sleeping for 4 h would have a body size that was larger by 0.12 times the standard deviation for body size than a Mexican-American adult reporting 8 h of sleep (all other covariates being equal). This effect was similar to the effect of 10 years of age, which would be associated with an increase in body size by 0.10 times the standard deviation of body size., Conclusions: These results underscore the importance of examining factors associated with obesity in different ethnic groups. It may be inappropriate to combine different Hispanic ethnicities together., (© 2010 Wiley-Liss, Inc.)

Sleep is an important modulator of neuroendocrine function and glucose metabolism in children as well as in adults. In recent years, sleep curtailment has become a hallmark of modern society with both children and adults having shorter bedtimes than a few decades ago. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity. There is rapidly accumulating evidence from both laboratory and epidemiological studies to indicate that chronic partial sleep loss may increase the risk of obesity and weight gain. The present article reviews laboratory evidence indicating that sleep curtailment in young adults results in a constellation of metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, elevated sympathovagal balance, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. We also review cross-sectional epidemiological studies associating short sleep with increased body mass index and prospective epidemiological studies that have shown an increased risk of weight gain and obesity in children and young adults who are short sleepers. Altogether, the evidence points to a possible role of decreased sleep duration in the current epidemic of obesity.

During the past few decades, sleep curtailment has become a very common in industrialized countries. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity and diabetes. Evidence is rapidly accumulating to indicate that chronic partial sleep loss may increase the risk of obesity and diabetes. Laboratory studies in healthy volunteers have shown that experimental sleep restriction is associated with an adverse impact on glucose homeostasis. Insulin sensitivity decreases rapidly and markedly without adequate compensation in beta cell function, resulting in an elevated risk of diabetes. Prospective epidemiologic studies in both children and adults are consistent with a causative role of short sleep in the increased risk of diabetes. Sleep curtailment is also associated with a dysregulation of the neuroendocrine control of appetite, with a reduction of the satiety factor, leptin, and an increase in the hunger-promoting hormone, ghrelin. Thus, sleep loss may alter the ability of leptin and ghrelin to accurately signal caloric need, acting in concert to produce an internal misperception of insufficient energy availability. The adverse impact of sleep deprivation on appetite regulation is likely to be driven by increased activity in neuronal populations expressing the excitatory peptides orexins that promote both waking and feeding. Consistent with the laboratory evidence, multiple epidemiologic studies have shown an association between short sleep and higher body mass index after controlling for a variety of possible confounders.

Background: Cardiometabolic diseases, which include obesity, diabetes, hypertension, and cardiovascular disease, are associated with reduced quality of life and reduced life expectancy. Unfortunately, there are racial/ethnic and socioeconomic disparities associated with these diseases such that minority populations, such as African Americans and Hispanics, and those of lower socioeconomic status, experience a greater burden. Several reports have indicated that there are differences in sleep duration and quality that mirror the disparities in cardiometabolic disease. The goal of this paper is to review the association between sleep and cardiometabolic disease risk because of the possibility that suboptimal sleep may partially mediate the cardiometabolic disease disparities.Methods: We review both experimental studies that have restricted sleep duration or impaired sleep quality and examined biomarkers of cardiometabolic disease risk, including glucose metabolism and insulin sensitivity, appetite regulation and food intake, and immune function. We also review observational studies that have examined the association between habitual sleep duration and quality, and the prevalence or risk of obesity, diabetes, hypertension, and cardiovascular disease.Conclusion: Many experimental and observational studies do support an association between suboptimal sleep and increased cardiometabolic disease risk. [ABSTRACT FROM AUTHOR]

Abstract: Sleep is a biological imperative associated with cardiometabolic disease risk. As such, a thorough discussion of the sociocultural and demographic determinants of sleep is warranted, if not overdue. This paper begins with a brief review of the laboratory and epidemiologic evidence linking sleep deficiency, which includes insufficient sleep and poor sleep quality, with increased risk of chronic cardiometabolic diseases such as obesity, diabetes and hypertension. Identification of the determinants of sleep deficiency is the critical next step to understanding the role sleep plays in human variation in health and disease. Therefore, the majority of this paper describes the different biopsychosocial determinants of sleep, including age, gender, psychosocial factors (depression, stress and loneliness), socioeconomic position and race/ethnicity. In addition, because sleep duration is partly determined by behavior, it will be shaped by cultural values, beliefs and practices. Therefore, possible cultural differences that may impact sleep are discussed. If certain cultural, ethnic or social groups are more likely to experience sleep deficiency, then these differences in sleep could increase their risk of cardiometabolic diseases. Furthermore, if the mechanisms underlying the increased risk of sleep deficiency in certain populations can be identified, interventions could be developed to target these mechanisms, reduce sleep differences and potentially reduce cardiometabolic disease risk. [Copyright &y& Elsevier]

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]

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]

Aim: To test the association between cardiometabolic risk factors and subjective sleep quality assessed by the Pittsburgh sleep quality index (PSQI), independent of obstructive sleep apnea (OSA) and sleep duration.Methods: A total of 573 participants from the Baependi Heart Study, a rural cohort from Brazil, completed sleep questionnaires and underwent polygraphy for OSA evaluation. Multivariable linear regression analysis tested the association between cardiovascular risk factors (outcome variables) and sleep quality measured by PSQI, adjusting for OSA and other potential confounders (age, sex, race, salary/wage, education, marital status, alcohol intake, obesity, smoking, hypertension, and sleep duration).Results: The sample mean age was 43 ± 16 years, 66% were female, and mean body mass index (BMI) was 26 ± 5 kg/m2. Only 20% were classified as obese (BMI ≥30). Overall, 50% of participants reported poor sleep quality as defined by a PSQI score ≥5. A high PSQI score was significantly associated with higher very-low-density lipoprotein (VLDL) cholesterol levels (beta = 0.392, p = 0.012) and higher triglyceride levels (beta = 0.017, p = 0.006), even after adjustments, including the apnea-hypopnea index. Further adjustments accounting for marital status, alcohol intake, and medication use did not change these findings. No significant association was observed between PSQI scores and glucose or blood pressure. According to PSQI components, sleep disturbances (beta = 1.976, p = 0.027), sleep medication use (beta = 1.121, p = 0.019), and daytime dysfunction (beta = 1.290, p = 0.024) were significantly associated with higher VLDL serum levels. Only the daytime dysfunction domain of the PSQI components was significantly associated with higher triglyceride levels (beta = 0.066, p = 0.004).Conclusion: Poorer lipid profile was independently associated with poor sleep quality, assessed by the PSQI questionnaire, regardless of a normal sleep duration and accounting for OSA and socio-economic status. [ABSTRACT FROM AUTHOR]

The article highlights a report from the American Heart Association (AHA), in conjunction with the National Institutes of Health and other government agencies, on statistics related to heart disease, stroke, and the cardiovascular risk factors which include health behaviors and health factors that contribute to cardiovascular health. Topics include statistical update representing a critical resource for policy makers, clinicians, healthcare administrators, researchers, and health advocates.

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]