Rapid Eye Movement Sleep in Relation to Overweight in Children and Adolescents

Department of Psychiatry and Western Psychiatric Institute and Clinic, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
Archives of general psychiatry (Impact Factor: 14.48). 09/2008; 65(8):924-32. DOI: 10.1001/archpsyc.65.8.924
Source: PubMed


Short sleep duration is associated with obesity, but few studies have examined the relationship between obesity and specific physiological stages of sleep.
To examine specific sleep stages, including rapid eye movement (REM) sleep and stages 1 through 4 of non-REM sleep, in relation to overweight in children and adolescents.
A total of 335 children and adolescents (55.2% male; aged 7-17 years) underwent 3 consecutive nights of standard polysomnography and weight and height assessments as part of a study on the development of internalizing disorders (depression and anxiety).
Body mass index (calculated as weight in kilograms divided by height in meters squared) z score and weight status (normal, at risk for overweight, overweight) according to the body mass index percentile for age and sex.
The body mass index z score was significantly related to total sleep time (beta = -0.174), sleep efficiency (beta = -0.027), and REM density (beta = -0.256). Compared with normal-weight children, overweight children slept about 22 minutes less and had lower sleep efficiency, shorter REM sleep, lower REM activity and density, and longer latency to the first REM period. After adjustment for demographics, pubertal status, and psychiatric diagnosis, 1 hour less of total sleep was associated with approximately 2-fold increased odds of overweight (odds ratio = 1.85), 1 hour less of REM sleep was associated with about 3-fold increased odds (odds ratio = 2.91), and REM density and activity below the median increased the odds of overweight by 2-fold (odds ratio = 2.18) and 3-fold (odds ratio = 3.32), respectively.
Our results confirm previous epidemiological observations that short sleep time is associated with overweight in children and adolescents. A core aspect of the association between short sleep duration and overweight may be attributed to reduced REM sleep. Further studies are needed to investigate possible mechanisms underpinning the association between diminished REM sleep and endocrine and metabolic changes that may contribute to obesity.

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    • "This indicates that daytime REM sleep might impair energy metabolism. Studies demonstrate an association between elevated body weight and decreased nocturnal total sleep and REM sleep in humans (36). Also it was suggested that endocrine changes like reduced leptin and increased ghrelin were more sensitive to reduced REM sleep during the rest phase (36). "
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    ABSTRACT: Objective Sleep-restriction in humans increases risk for obesity, but previous rodent studies show weight loss following sleep deprivation, possibly due to stressful-methods used to prevent sleep. Obesity-resistant (OR) rats exhibit consolidated-sleep and resistance to weight-gain. We hypothesized that sleep disruption by a less-stressful method would increase body weight, and examined effect of partial sleep deprivation (PSD) on body weight in OR and Sprague-Dawley (SD) rats. Design and Methods OR and SD rats (n=12/group) were implanted with transmitters to record sleep/wake. After baseline recording, six SD and six OR rats underwent 8 h PSD during light-phase for 9 d. Sleep was reduced using recordings of random noise. Sleep/wake states were scored as wakefulness (W), slow-wave-sleep (SWS) and rapid-eye-movement-sleep (REMS). Total number of transitions between stages, SWS-delta-power, food intake and body weight were documented. Results Exposure to noise decreased SWS and REMS time, while increasing W time. Sleep-deprivation increased number of transitions between stages and SWS-delta-power. Further, PSD during the rest phase increased recovery-sleep during active phase. The PSD SD and OR rats had greater food intake and body weight compared to controls Conclusions PSD by less-stressful means increases body weight in rats. Also, PSD during rest phase increases active period sleep.
    Obesity 07/2013; 21(7). DOI:10.1002/oby.20182 · 3.73 Impact Factor
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    • "In addition, studies demonstrated that elevated body weight was associated with decreased nocturnal total sleep and REM sleep in humans (Dixon et al., 2005, Liu et al., 2008) and suggested that endocrine changes such as reduced leptin and increased ghrelin mediated the association between sleep and obesity (Liu et al., 2008). These endocrine changes are suggested to be more sensitive to reduced REM sleep at night (Liu et al., 2008). "
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    ABSTRACT: The rapid rise in obesity prevalence in the modern world parallels a significant reduction in restorative sleep (Agras et al., 2004; Dixon et al., 2007, 2001; Gangwisch and Heymsfield, 2004; Gupta et al., 2002; Sekine et al., 2002; Vioque et al., 2000; Wolk et al., 2003). Reduced sleep time and quality increases the risk for obesity, but the underlying mechanisms remain unclear (Gangwisch et al., 2005; Hicks et al., 1986; Imaki et al., 2002; Jennings et al., 2007; Moreno et al., 2006). A majority of the theories linking human sleep disturbances and obesity rely on self-reported sleep. However, studies with objective measurements of sleep/wake parameters suggest a U-shaped relationship between sleep and obesity. Studies in animal models are needed to improve our understanding of the association between sleep disturbances and obesity. Genetic and experimenter-induced models mimicking characteristics of human obesity are now available and these animal models will be useful in understanding whether sleep disturbances determine propensity for obesity, or result from obesity. These models exhibit weight gain profiles consistently different from control animals. Thus a careful evaluation of animal models will provide insight into the relationship between sleep disturbances and obesity in humans. In this review we first briefly consider the fundamentals of sleep and key sleep disturbances, such as sleep fragmentation and excessive daytime sleepiness (EDS), observed in obese individuals. Then we consider sleep deprivation studies and the role of circadian alterations in obesity. We describe sleep/wake changes in various rodent models of obesity and obesity resistance. Finally, we discuss possible mechanisms linking sleep disturbances with obesity.
    Neuroscience & Biobehavioral Reviews 03/2012; 36(3):1015-29. DOI:10.1016/j.neubiorev.2012.01.001 · 8.80 Impact Factor
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    • "Stress can also reduce the amount of REM sleep (Cui et al., 2008), so stress could also be a plausible explanation for the lower percentage of REM sleep in patients with PCOS. A reduction of REM sleep is associated with overweight in children and adolescents (Liu et al., 2008), and overweight and obesity, again, is associated with PCOS (Ehrmann, 2005). Therefore, perhaps, a complex relationship between stress, overweight, PCOS and reduction of REM sleep exists. "
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    ABSTRACT: The aim of this study was to compare polysomnographic variables of obese adolescents with polycystic ovarian syndrome (PCOS) to those of healthy controls and to analyse whether polysomnographic variables correlate to parameters of body weight/body composition, to serum androgens and to parameters of glucose metabolism. Thirty-one obese adolescents with PCOS (15.0 years ± 1.0, body mass index 32.7 kg per m(2) ± 6.2) and 19 healthy obese adolescents without PCOS (15.2 years ± 1.1, body mass index 32.4 kg per m(2) ± 4.0) underwent polysomnography to compare apnoea index, hypopnoea index, apnoea-hypopnoea index, the absolute number of obstructive apnoeas, percentage sleep Stages 1, 2, 3 and 4 of non-rapid eye movement (NREM) sleep, percentage of REM sleep, TIB, total sleep time (TST), sleep-onset latency, total wake time (TWT), wakefulness after sleep onset (WASO) and sleep efficiency. Furthermore, we correlated polysomnographic variables to parameters of body weight/body composition, to serum androgens and to parameters of glucose metabolism. We found no differences between the two groups concerning the respiratory indices, percentage sleep Stages 2, 3 and 4 of NREM sleep, TIB and sleep-onset latency. The girls with PCOS differed significantly from the controls regarding TST, WASO, TWT, sleep efficiency, percentage Stage 1 of NREM sleep and percentage of REM sleep. We found a weak significant correlation between insulin resistance and apnoea index and between insulin resistance and apnoea-hypopnoea index. Concerning the respiratory variables, adolescents with PCOS do not seem to differ from healthy controls; however, there seem to be differences concerning sleep architecture.
    Journal of Sleep Research 12/2010; 20(3):472-8. DOI:10.1111/j.1365-2869.2010.00902.x · 3.35 Impact Factor
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