The rising prevalence of obesity in both adults and children is among the most important current public health issues worldwide. Lifestyle modifications involving increased exercise and dietary modifications for maintenance of healthy weight are frequently promoted by pediatricians, but there is limited evidence to show efficacy.1 This makes the identification of other modifiable factors to prevent childhood obesity of great importance. Recent studies in diverse populations and various age groups have confirmed associations between shorter sleep duration or poor sleep quality and increased risk of obesity.2–13 Furthermore, recent data document an inverse correlation between sleep duration in children and risk markers for type 2 diabetes that persists after adjusting for differences in adiposity and differences in physical activity.14
Given the increasing evidence linking sleep habits and obesity, it is essential to understand the nature of this association. Theories suggesting both causative and noncausative associations might be proposed. It is possible that obesity and inadequate sleep might jointly reflect the effects of other influences such as excess screen time, inadequate exercise, or less vigilance overall about health habits on the part of the family.15 Alternatively, reduced or altered sleep and obesity might both represent manifestations of altered hypothalamic functions controlling sleep and controlling neuroendocrine regulation of appetite and insulin sensitivity. The circadian locomotor output cycles protein kaput gene and several related genes form the foundation for the brain’s circadian system.16,17 Alterations in the circadian locomotor output cycles protein kaput gene and related genes have been found to influence both sleep and weight gain and affect metabolic processes that contribute to type 2 diabetes and the metabolic syndrome.16,17 Furthermore, several brain regions involved in regulating sleep and wake cycles also are involved in regulating fasting and feeding, and these neural systems are influenced by the same hormones and neurotransmitters.16,17 Sleep and body weight regulation are therefore intricately intertwined on multiple levels.
Although a clinical trial comparing weight gain in children randomly assigned to different sleep conditions could address the question of a causal relation between insufficient sleep and obesity, such a trial would involve substantial logistic and ethical hurdles. In the absence of such a trial, it is essential to collect other types of evidence to characterize the association between sleep and obesity. In this issue of Pediatrics, Xiu et al18 longitudinally followed children 2 to 6 years of age with yearly objective measurements of sleep and adiposity. They found that more frequent late sleep was associated with greater increases in measures of adiposity and that this association was more pronounced in children of parents with overweight or obesity. This study increases the evidence for a causal relation between sleep and obesity because the findings were similar (although of lesser magnitude) in children not genetically predisposed to obesity, and there were no significant differences in sleep patterns at baseline on the basis of obesity risk. In addition, children were young and of normal weight at enrollment, so obesity-related factors that could interfere with sleep (ie, sleep apnea) were less likely to be present. The study unfortunately involved a relatively small sample size, and therefore statistical power to detect differences was somewhat limited. It is possible that differences in some sleep measures may have been significant had the sample size been larger. A more robust picture of associations between sleep and adiposity could be gained by following a larger sample for a longer time period.
The data from Xiu et al18 make an important contribution to the accumulating evidence supporting a link between decreased sleep and adiposity. Whether this association is causal, and therefore amenable to intervention, will be a far more difficult question to answer. Future studies, using interventions to increase sleep duration and sleep quality, will be needed to address this weighty question.
Opinions expressed in these commentaries are those of the authors and not necessarily those of the American Academy of Pediatrics or its Committees.
FUNDING: No external funding.
COMPANION PAPER: A companion to this article can be found online at www.pediatrics.org/cgi/doi/10.1542/peds.2019-1420.
POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.
FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.