Short sleep duration and obesity: mechanisms and future perspectives (original) (raw)
Related papers
Short Sleep Duration, Glucose Dysregulation and Hormonal Regulation of Appetite in Men and Women
SLEEP, 2000
Epidemiologic studies report an association between selfreported sleep duration and obesity. 1 In fact, obesity and self-reported sleep duration show inverse trends with obesity prevalence increasing over the past decades and sleep duration decreasing. 2 Moreover, there is increasing evidence from clinical studies showing that reducing sleep leads to greater food intake relative to habitual sleep. 3-6 Data on the role of physical activity and energy expenditure on the relationship between sleep duration and obesity are controversial. We 5 and others 4 have found no effect of reducing sleep on energy expenditure, whereas Schmid et al. 7 found that sleep restriction decreased physical activity and Jung et al. 8 found greater energy expenditure during total sleep deprivation relative to habitual sleep.
Metabolic effects of sleep disruption, links to obesity and diabetes
Purpose of the review-To highlight the adverse metabolic effects of sleep disruption and to open ground for research aimed at preventive measures. This area of research is especially relevant given the increasing prevalence of voluntary sleep curtailment, sleep disorders, diabetes, and obesity.
Sleep–obesity relation: underlying mechanisms and consequences for treatment
Obesity Reviews, 2017
SummaryShort sleep duration has been associated with obesity in numerous epidemiological studies. However, such association studies cannot establish evidence of causality. Clinical intervention studies, on the other hand, can provide information on a causal effect of sleep duration on markers of weight gain: energy intake and energy expenditure. Herein is an overview of the science related to the impact of sleep restriction, in the context of clinical intervention studies, on energy intake, energy expenditure and body weight. Additionally, studies that evaluate the impact of sleep restriction on weight loss and the impact of sleep extension on appetite are discussed. Information to date suggests that weight management is hindered when attempted in the context of sleep restriction, and the public should be made aware of the negative consequences of sleep restriction for weight regulation.
Diabetes, 2015
Recent increases in the prevalence of obesity and type 2 diabetes mellitus (T2DM) in modern societies have been paralleled by reductions in the time their denizens spend asleep. Epidemiological studies have shown that disturbed sleep-comprising short, low-quality, and mistimed sleep-increases the risk of metabolic diseases, especially obesity and T2DM. Supporting a causal role of disturbed sleep, experimental animal and human studies have found that sleep loss can impair metabolic control and body weight regulation. Possible mechanisms for the observed changes comprise sleep loss-induced changes in appetite-signaling hormones (e.g., higher levels of the hunger-promoting hormone ghrelin) or hedonic brain responses, altered responses of peripheral tissues to metabolic signals, and changes in energy intake and expenditure. Even though the overall consensus is that sleep loss leads to metabolic perturbations promoting the development of obesity and T2DM, experimental evidence supporting...
Short Sleep Duration Increases Metabolic Impact in Healthy Adults: A Population-Based Cohort Study
Sleep, 2017
Objectives: The metabolic impact of inadequate sleep has not been determined in healthy individuals outside laboratories. This study aims to investigate the impact of sleep duration on five metabolic syndrome components in a healthy adult cohort. Methods: A total of 162 121 adults aged 20-80 years (men 47.4%) of the MJ Health Database, who were not obese and free from major diseases, were recruited and followed up from 1996 to 2014. Sleep duration and insomnia symptoms were assessed by a self-administered questionnaire. Incident cases of five metabolic syndrome components were identified by follow-up medical examinations. Cox proportional hazard ratios (HRs) were calculated for three sleep duration categories "< 6 hours/day (short)," "6-8 hours/day (regular)," and "> 8 hours/day (long)" with adjustment for potential confounding factors. Analyses were stratified by insomnia symptoms to assess whether insomnia symptoms modified the association between sleep duration and metabolic syndrome. Results: Compared to regular sleep duration, short sleep significantly (p < .001) increased the risk for central obesity by 12% (adjusted HR 1.12 [1.07-1.17]), for elevated fasting glucose by 6% (adjusted HR 1.06 [1.03-1.09]), for high blood pressure by 8% (adjusted HR 1.08 [1.04-1.13]), for low high-density lipoprotein-cholesterol by 7% (adjusted HR 1.07 [1.03-1.11]), for hypertriglyceridemia by 9% (adjusted HR 1.09 [1.05-1.13]), and for metabolic syndrome by 9% (adjusted HR 1.09 [1.05-1.13]). Long sleep decreased the risk of hypertriglyceridemia (adjusted HR 0.89 [0.84-0.94]) and metabolic syndrome (adjusted HR 0.93 [0.88-0.99]). Insomnia symptoms did not modify the effects of sleep duration. Conclusions: Sleep duration may be a significant determinant of metabolic health.
Annals of Medicine, 2014
Epidemiological data have identifi ed an association • between short sleep duration and overweight and/or obesity. Th is association is more consistent in children than in adults. Sleep restriction results in metabolic and endocrine • alterations (e.g. increased levels of ghrelin, decreased levels of leptin, increased hunger and appetite, decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol). Insuffi cient sleep is associated with increased food • intake, snacking, and poor diet quality. Short sleep duration has been shown to be associated with elevated body mass index (BMI) in many epidemiological studies. Several pathways could link sleep deprivation to weight gain and obesity, including increased food intake, decreased energy expenditure, and changes in levels of appetite-regulating hormones, such as leptin and ghrelin. A relatively new factor that is contributing to sleep deprivation is the use of multimedia (e.g. television viewing, computer, and internet), which may aggravate sedentary behavior and increase caloric intake. In addition, shift-work, long working hours, and increased time commuting to and from work have also been hypothesized to favor weight gain and obesity-related metabolic disorders, because of their strong link to shorter sleep times. This article reviews the epidemiological, biological, and behavioral evidence linking sleep debt and obesity.
Review The metabolic burden of sleep loss
In parallel with the increasing prevalence of obesity and type 2 diabetes, sleep loss has become common in modern societies. An increasing number of epidemiological studies show an association between short sleep duration, sleep disturbances, and circadian desynchronisation of sleep with adverse metabolic traits, in particular obesity and type 2 diabetes. Furthermore, experimental studies point to distinct mechanisms by which insufficient sleep adversely affects metabolic health. Changes in the activity of neuroendocrine systems seem to be major mediators of the detrimental metabolic effects of insufficient sleep, through favouring neurobehavioural outcomes such as increased appetite, enhanced sensitivity to food stimuli, and, ultimately, a surplus in energy intake. The effect of curtailed sleep on physical activity and energy expenditure is less clear, but changes are unlikely to outweigh increases in food intake. Although long-term interventional studies proving a cause and effect association are still scarce, sleep loss seems to be an appealing target for the prevention, and probably treatment, of metabolic disease.