Sleep curtailment is accompanied by increased intake of calories from snacks

Department of Medicine, The University of Chicago, Chicago, IL 60637, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 01/2009; 89(1):126-33. DOI: 10.3945/ajcn.2008.26574
Source: PubMed


Short sleep is associated with obesity and may alter the endocrine regulation of hunger and appetite.
We tested the hypothesis that the curtailment of human sleep could promote excessive energy intake.
Eleven healthy volunteers [5 women, 6 men; mean +/- SD age: 39 +/- 5 y; mean +/- SD body mass index (in kg/m(2)): 26.5 +/- 1.5] completed in random order two 14-d stays in a sleep laboratory with ad libitum access to palatable food and 5.5-h or 8.5-h bedtimes. The primary endpoints were calories from meals and snacks consumed during each bedtime condition. Additional measures included total energy expenditure and 24-h profiles of serum leptin and ghrelin.
Sleep was reduced by 122 +/- 25 min per night during the 5.5-h bedtime condition. Although meal intake remained similar (P = 0.51), sleep restriction was accompanied by increased consumption of calories from snacks (1087 +/- 541 compared with 866 +/- 365 kcal/d; P = 0.026), with higher carbohydrate content (65% compared with 61%; P = 0.04), particularly during the period from 1900 to 0700. These changes were not associated with a significant increase in energy expenditure (2526 +/- 537 and 2390 +/- 369 kcal/d during the 5.5-h and 8.5-h bedtime periods, respectively; P = 0.58), and we found no significant differences in serum leptin and ghrelin between the 2 sleep conditions.
Recurrent bedtime restriction can modify the amount, composition, and distribution of human food intake, and sleeping short hours in an obesity-promoting environment may facilitate the excessive consumption of energy from snacks but not meals.

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Available from: Jennifer M Kilkus, Jul 09, 2014
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    • "Findings from epidemiologic studies indicate that disturbed-and short periods of sleep are a risk factor for obesity (Moraes et al., 2013), diabetes (Togeiro et al., 2013), cardiovascular disease (Rod et al., 2014) and metabolic syndrome (Drager et al., 2013). Controlled laboratory studies have also shown several behavioral and physiological alterations that seem to favor the induction of metabolic syndrome (Chaput et al., 2008; Van Cauter et al., 2008), including reduction of leptin and increase of ghrelin levels (Spiegel et al., 1999, 2004), which may explain the augmented caloric intake (Beebe et al., 2013; Hogenkamp et al., 2013) and craving for carbohydrate-and fat-rich foods observed in volunteers (Nedeltcheva et al., 2009; Spiegel et al., 2004), possibly reflecting a homeostatic and hedonic response to this situation (Taheri et al., 2004). In addition , increased cortisol levels and sympathetic tonus (Spiegel et al., 1999), reduced glucose clearance and increased insulin resistance (Donga et al., 2010) have been found in short-term sleep restriction laboratory studies. "
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    ABSTRACT: Chronic sleep restriction in human beings results in metabolic abnormalities, including changes in the control of glucose homeostasis, increased body mass and risk of cardiovascular disease. In rats, 96h of REM sleep deprivation increases caloric intake, but retards body weight gain. Moreover, this procedure increases the expression of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which may be involved with the molecular mechanism proposed to mediate insulin resistance. The goal of the present study was to assess the effects of a chronic protocol of sleep restriction on parameters of energy balance (food intake and body weight), leptin plasma levels and its hypothalamic receptors and mediators of the immune system in the retroperitoneal adipose tissue (RPAT). Thirty-four Wistar rats were distributed in control (CTL) and sleep restriction groups; the latter was kept onto individual narrow platforms immersed in water for 18h/day (from 16:00h to 10:00h), for 21days (SR21). Food intake was assessed daily, after each sleep restriction period and body weight was measured daily, after the animals were taken from the sleep deprivation chambers. At the end of the 21day of sleep restriction, rats were decapitated and RPAT was obtained for morphological and immune functional assays and expression of insulin receptor substrate 1 (IRS-1) was assessed in skeletal muscle. Another subset of animals was used to evaluate blood glucose clearance. The results replicated previous findings on energy balance, e.g., increased food intake and reduced body weight gain. There was a significant reduction of RPAT mass (p<0.001), of leptin plasma levels and hypothalamic leptin receptors. Conversely, increased levels of TNF-α and IL-6 and expression of phosphorylated NFκ-β in the RPAT of SR21 compared to CTL rats (p<0.01, for all parameters). SR21 rats also displayed reduced glucose clearance and IRS-1 expression than CTL rats (p<0.01). The present results indicated that 21days of sleep restriction by the platform method induced metabolic syndrome-related alterations that may be mediated by inflammation of the RPAT. Copyright © 2014. Published by Elsevier Inc.
    Full-text · Article · Dec 2014 · Brain Behavior and Immunity
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    • "Spiegel et al. (2004) reported increased rates of hunger and appetite in subjects submitted to two nights of 4 h of sleep, compared to two subsequent nights of 10 h of sleep. In addition, volunteers sleep-restricted for 14 days (5.5 h in bed) increased their preference for high-carbohydrate foods during the night, compared to 14 days of 8.5 h of sleep (Nedeltcheva et al., 2009). Similar to what is observed in humans, rats subjected to sleep deprivation also display increased food intake (Galvão et al., 2009; Koban et al., 2008; Martins et al., 2010; Rechtschaffen and Bergmann, 1995). "
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    ABSTRACT: Studies have shown a gradual reduction of sleep time in the general population, accompanied by increased food intake, representing a risk for developing obesity, type II diabetes and cardiovascular disease. Rats subjected to paradoxical sleep deprivation (PSD) exhibit feeding and metabolic alterations, both of which are regulated by the communication between peripheral signals and the hypothalamus. This study aimed to investigate the daily change of 96 h of PSD-induced food intake, body weight, blood glucose, plasma insulin and leptin concentrations and the expression of their receptors in the hypothalamus of Wistar rats. Food intake was assessed during the light and dark phases and was progressively increased in sleep-deprived animals, during the light phase. PSD produced body weight loss, particularly on the first day, and decreased plasma insulin and leptin levels, without change in blood glucose levels. Reduced leptin levels were compensated by increased expression of leptin receptors in the hypothalamus, whereas no compensations occurred in insulin receptors. The present results on body weight loss and increased food intake replicate previous studies from our group. The fact that reduced insulin levels did not lead to compensatory changes in hypothalamic insulin receptors, suggests that this hormone may be, at least in part, responsible for PSD-induced dysregulation in energy metabolism.
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    • "Some recent studies have examined the relationship between reported sleep and food intake and obesity (Baron et al., 2011; Hairston et al., 2010; Patel et al., 2006) both from a qualitative (Brondel et al, 2010; St-Onge et al, 2011) and quantitative (Brondel et al., 2010; Garaulet et al., 2011; St-Onge et al., 2011) point of view. Nedeltcheva et al. (2009) found that a reduction of sleep time led to an increase in the number of calories being obtained from snacks, compared to the amount of calories greater after the sleep period (p ¼ 0.02), with higher carbohydrate content (p ¼ 0.04). Similar results were found by St-Onge et al. (2011), who found that the energy consumption was higher during conditions of sleep deprivation TABLE 2. Correlation between work/sleep factors and sociodemographic, anthropometric, physical activity and metabolic parameters. "
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    ABSTRACT: Shift work and long hours of work are common in medical training and have been associated with a higher propensity for developing nutritional problems and obesity. Changes in leptin and ghrelin concentrations - two hormones that contribute importantly to the central regulation of food intake - are poorly described in this population. The aim of this study was to identify possible negative associations between sleep patterns, nutritional status and serum levels of adipokines. The study included 72 resident physicians (52 women and 20 men) who underwent the following assessments: nutritional assessment (3-day dietary recall evaluated by the Adapted Healthy Eating Index), anthropometric variables, fasting metabolism, physical activity level, sleep quality and sleepiness. Resident physicians with poor sleep quality reported greater weight gain after the beginning of residency (5.1 and 3.0 kg, respectively; p = 0.01) and higher frequency of abnormal waist circumference (44.2 and 17.6%, respectively; p = 0.04) than those with better sleep quality. Mean ghrelin concentration was greater in volunteers with poor sleep quality (64.6 ± 67.8 and 26.2 ± 25.0 pg/mL, respectively; p = 0.04). Women identified as having excessive daytime sleepiness had lower levels of leptin (9.57 ± 10.4 ng/mL versus 16.49 ± 11.4 ng/mL, respectively; p = 0.03) than those without excessive sleepiness. Furthermore, correlations were found between hours of additional work per week and: intake of cereals, bread and pasta (r = 0.22, p = 0.01); intake of servings of fruits (r = -0.20; p = 0.02) and beans (r = -0.21; p = 0.01); and global score for Adapted Healthy Eating Index (r = -0.23; p = 0.008; Table 3). The sleep quality total score correlated with servings of beans (r = -0.22; p = 0.01) and servings of oils (r = 0.23; p = 0.008). Significant correlations were found between mean of time of sleep and servings of cereals, bread and pasta (r = 0.20; p = 0.02), servings of meat (r = -0.29; p = 0.02) and cholesterol levels (r = 0.27; p = 0.03). These observations indicate that sleep patterns and long working hours of resident physicians are negatively associated with biological markers related to central food control, the lipid profile, cholesterol levels and eating healthy foods. These factors may predispose these shift workers to become overweight and develop metabolic disorders.
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