Background Short sleep is associated with obesity and may alter the endocrine regulation of hunger and appetite. Objective To test the hypothesis that the curtailment of human sleep could promote excessive energy intake. Design Eleven healthy volunteers (5F/6M; mean ± SD age 39 ± 5y; BMI 26.5 ± 1.5 kg/m2) completed in random order two 14-day stays in the sleep laboratory with ad lib access to palatable food and 5.5- or 8.5-hour bedtimes. The primary endpoints were the calories from meals and snacks consumed during each bedtime condition. Additional measures included total energy expenditure and 24-hour profiles of serum leptin and ghrelin. Results Sleep was reduced by 122 ± 25 min/night during the 5.5-hour bedtime condition. While meal intake remained similar (P=0.51), sleep restriction was accompanied by increased consumption of calories from snacks (1087 ± 541 vs. 866 ± 365 kcal/day; P=0.026) with higher carbohydrate content (65 vs. 61%; P=0.04), particularly during the period from 19:00 to 7:00. These changes were not associated with a significant increase in energy expenditure during the 5.5-h (2526 ± 537 kcal/d) vs. 8.5-h bedtime period (2390 ± 369 kcal/d, P=0.58) and there were no significant differences in serum leptin and ghrelin between the two sleep conditions. Conclusions The results indicate that recurrent bedtime restriction can modify the amount, composition, and distribution of human food intake, and support the notion that sleeping short hours in an obesity-promoting environment may facilitate the excessive consumption of energy from snacks, but not meals.
Background Sleep loss can modify energy intake and expenditure. Objective To determine whether sleep restriction attenuates the effect of reduced-calorie diet on excess adiposity. Design Randomized two-period two-condition crossover study. Setting University clinical research center and sleep laboratory. Patients 10 overweight nonsmoking adults (3F/7M); mean (SD) age 41 (5) y; body mass index 27.4 (2.0) kg/m2. Intervention 14 days of moderate caloric restriction with 8.5 or 5.5-hour nighttime sleep opportunity. Measurements Primary: loss of fat and fat-free body mass. Secondary: changes in substrate utilization, energy expenditure, hunger, and 24-h metabolic hormone concentrations. Results Sleep curtailment decreased the fraction of weight lost as fat by 55% (1.4 vs. 0.6 kg with 8.5 vs. 5.5-h sleep opportunity, P=0.043) and increased the loss of fat-free body mass by 60% (1.5 vs. 2.4 kg, P=0.002). This was accompanied by markers of enhanced neuroendocrine adaptation to caloric restriction, increased hunger, and a shift in relative substrate utilization towards oxidation of less fat. Limitations The nature of the study limited its duration and sample size. Conclusions The amount of human sleep contributes to the maintenance of fat-free body mass at times of decreased energy intake. Lack of sufficient sleep may compromise the efficacy of typical dietary interventions for weight loss and related metabolic risk reduction.
Experimental bedtime restriction, designed to approximate the short sleep times experienced by many individuals in Westernized societies, may facilitate the development of insulin resistance and reduced glucose tolerance.
Background: Sleep exerts important modulatory effects on neuroendocrine function and glucose regulation. During the past few decades, sleep curtailment has become a very common behavior in industrialized countries. This trend toward shorter sleep times has occurred over the same time period as the dramatic increases in the prevalence of obesity and diabetes. Aims: This article will review rapidly accumulating laboratory and epidemiologic evidence indicating that chronic partial sleep loss could play a role in the current epidemics of obesity and diabetes. Conclusions: Laboratory studies in healthy young volunteers have shown that experimental sleep restriction is associated with a dysregulation of the neuroendocrine control of appetite consistent with increased hunger and with alterations in parameters of glucose tolerance suggestive of an increased risk of diabetes. Epidemiologic findings in both children and adults are consistent with the laboratory data.
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. Resent findings Epidemiological studies have established an association between decreased self-reported sleep duration and an increased incidence of type 2 diabetes (T2D), obesity, and cardiovascular disease. Experimental laboratory studies have demonstrated that decreasing either the amount or quality of sleep decreases insulin sensitivity and decreases glucose tolerance. Experimental sleep restriction also causes physiological and behavioral changes that promote a positive energy balance. While sleep restriction increases energy expenditure due to increased wakefulness, it can lead to a disproportionate increase in food intake, decrease in physical activity, and weight gain. Summary Sleep disruption has detrimental effects on metabolic health. These insights may help in the development of new preventative and therapeutic approaches against obesity and T2D based on increasing the quality and/or quantity of sleep.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.