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

CHILDHOOD OBESITY HAS BEcome a major public health concern. During the past 3 decades, the childhood obesity rate has more than tripled for children aged 6 to 11 years1,2; currently, approximately 17% of US adolescents are overweight or obese as defined by having a body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) greater than or equal to the 95th percentile for age and sex.3 Obesity is associated with various short-term and long-term psychosocial, behavioral, and physical health problems.4-6 Multiple psychosocial, lifestyle, nutritional, and familial or genetic factors are associated with childhood obesity.7,8 Obesity results from impaired balance between energy intake (food calories) and expenditure (physical activity), but little is known about what factors alter the balance.9 Recent epidemiological and laboratory studies suggest that shortened sleep duration may be one of the risk factors that alters the energy balance in ways that are contributing to the obesity pandemic in modern society.9-11 A number of cross-sectional epidemiological studies have demonstrated a link between short self-reported sleep duration and obesity in adults and children.9,10 It has been shown that adults who report sleeping on average less than 5 hours per night tend to have elevated BMIs.12 A dose-response relationship between short sleeping hours and obesity has been observed in a large sample of Japanese children (n=8274).13 Several longitudinal studies have identified short sleep duration or inadequate sleep as a risk factor for weight gain or obesity in the future.6,12,14-16 Interestingly, a longitudinal study of UK children has shown that short sleep duration at an early age of 30 months predicts obesity at age 7 years.6 Using objective sleep measures, several studies have confirmed the short sleep-obesity association. For example, Gupta et al17 used 24-hour wrist actigraphy to assess sleep in 383 adolescents and found that 1 hour of sleep loss increased the odds of obesity by 80%. In one comparative study of 60 overweight adolescents and 20 control subjects, Beebe et al18 reported that obese participants as compared with control subjects slept shorter (469 minutes vs 507 minutes, respectively) and had lower sleep efficiency (80% vs 87%, respectively) as assessed by 5-night actigraphy. However, total sleep duration and percentage of stages 1, 2, 3, 4, and rapid eye movement (REM) sleep as assessed by 1 overnight polysomnography (PSG) sleep in the laboratory did not significantly differ between the 2 groups. Sleep loss has been hypothesized to contribute to overweight and obesity through endocrine changes, such as decreased levels of leptin (an adipocyte-derived hormone that suppresses appetite), increased levels of ghrelin (a stomach-derived peptide that stimulates appetite), and compromised insulin sensitivity.14,19-21 Importantly, one experimental study22 reported that sleep restriction in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. These findings have been confirmed by a large population-based study21 (Wisconsin Sleep Cohort Study) that shows a significant association of sleep duration with leptin and ghrelin levels, independent of age, sex, sleepdisordered breathing, and self-reported exercise. The combination of growing epidemiological and laboratory studies points to a conclusion that there is a potential causal relationship between short sleep duration and obesity mediated by endocrine and metabolic changes. However, many questions remain to be answered.21 One of the questions is whether there is a significant interaction effect between sleep and obesity pertaining to specific sleep stage(s). During the course of a night, a person's sleep is divided into non-REM (NREM) sleep and REM sleep. The NREM sleep is further divided into 4 stages. However, it is unknown what sleep stage loss uniquely contributes to overweight and whether the association between short sleep time and overweight differs across sleep stages. Human studies have shown that the sleeping metabolic rate is higher in REM sleep and electrophysiological alterations are sleep stage dependent.23,24 Specifically, glucose utilization during REM sleep is higher than during NREM sleep.25,26 In addition, brain glucose metabolic changes during sleep occur independent of slow-wave sleep stages but brain metabolism increases during REM sleep.26 Research has also shown that children with short sleep duration (<6 hours) spend proportionally less time in REM sleep.27 Thus, it is possible to speculate that the association between short sleep duration and obesity may also be sleep stage dependent. Specifically, REM-related sleep may be associated with obesity. The goal of the current study was to examine whether the association between short sleep duration and BMI or overweight differs across sleep stages with a large clinical sample of children and adolescents who underwent 3 consecutive nights of standard polysomnography and weight and height assessments. Based on previous studies,23,25-27 we hypothesized that REM sleep time and activity are negatively related to BMI and that overweight children are more likely to have reduced REM sleep than normal-weight peers.