Sleep trends in children and potential associations with obesity
Although sleep assessments of children have largely relied on parental reports,1–7 it has become apparent that children are highly unlikely to obtain sufficient sleep on a stable and regular schedule. Polls by the National Sleep Foundation1,2 show that parents routinely overestimate their children's sleep duration, and that in fact children sleep much less than what is deemed appropriate for their age. At the society level, and likely across all pediatric ages, children sleep less than what they did one century ago.8 Despite the compelling evidence supporting a vital role for healthy sleep in brain maturation, somatic growth, information processing, memory consolidation, learning, and other important neurobehavioral functions, parents and professionals instead focus their attention on children's accomplishments (e.g., first steps, first words, school grades, extracurricular activity performances), and often treat sleep as a tradable commodity.
Clearly, disturbed sleep patterns can lead to multidimensional adverse effects. For example, 43% of school-aged children and 57% of adolescents have a TV in their bedroom;1,2,9 and as many as 42% have mobile phones in their bedroom and many other electronic devices, such as computers, video games, and other electronic gadgetry are also frequently present in bedrooms.9,10 These devices account for multiple intrusion patterns that can curtail or disrupt sleep in children and may result in the development of decreased opportunities for sleep in children over time—put differently, it could be said that modern life has “polluted” the opportunity to sleep because of a variety of intrusions, which may further lead to reduced sleep duration or sleep disruption.
In the last 20 years, a large number of studies have been published on sleep duration in children, and most have aimed to evaluate the potentially adverse impact of poor sleep on health outcomes. Although these studies are heterogeneous in their methodology and scope, they all point to the critical need for urgent large-scale representative and longitudinal studies on objective sleep–wake patterns in children, particularly to explore the impact of sleep on health and body weight in a valid ecological and contextual setting. For example, the family domain, important with respect to sleep–wake patterns,11,12 influences food and health-related behaviors in the developing child. Not surprisingly, the presence of parental beliefs about being overweight and nutrition can have significant impact on the risk of childhood obesity.13,14 Because daily activities and sleep patterns evolve in a circadian continuum, parenting feeding styles15 may interact with sleep. For instance, when U.S. preschoolers were exposed to three household routines, namely, evening family meal for more than 5 nights per week, sleeping ≥10.5 h/night on weekdays, and ≤2 h/day television, video, or other screen-viewing behavior, obesity prevalence decreased by 40% compared with when no such simple routines were present.16
The estimated dose–response relationship between sleep and obesity is highly variable,17 with pooled odd ratios ranging from 1.15 to 11.0, which likely represents heterogeneities in methodologies and the diversity of contributing factors (Fig. 1).18 In a recent study in which sleep and weight were carefully monitored using objective assessments, we found that irregular and shorter sleep is a significant risk factor for the occurrence of weight problems in children, and that a nonlinear trend between sleep and weight was present.19 We further found that obese children are less likely to catch-up in their sleep “debt” during weekends, and that the combination of shorter sleep duration and more variable sleep patterns was associated not only with increased weight risk but also with adverse metabolic outcomes (i.e., insulin resistance, elevated serum lipids, and increased high-sensitivity C reactive protein levels).
The biological correlates of the association between sleep patterns and body mass index (BMI) have been partially elucidated and would support the assumption that either inadequate amounts of sleep or disrupted sleep architecture lead to alterations in some of the neuropeptides that regulate appetite, such as increased levels of ghrelin, reduced levels of leptin, and reduced central biological activity of orexin, with the anticipated cumulative effect of promoting increased food intake (Fig. 1).20,21
The association between short sleep duration and increased risk for obesity is, as mentioned, somewhat conflictive, whereby discrepancies also emerge in relation to age. For example, although a significant contribution of sleep duration to obesity risk is present in adults, the associations are, as indicated above, highly variable and could reflect a multitude of possible confounders that may be operational in early life.22–28 Furthermore, in an elegant and important cross-sectional and longitudinal study, Chaput and colleagues reported that only those adults manifesting short sleep duration, highly disinhibited eating behaviors, and/or low dietary calcium intake had significantly higher BMI compared with corresponding controls. Indeed, over the six-year follow-up period, such high-risk adults were significantly more likely to gain weight and develop obesity.18
Notwithstanding these considerations, a recent meta-analysis of the literature appears to support the conclusion that the strength of the association between sleep duration and obesity is actually stronger in children and adolescents, and that it declines over time.29 Furthermore, some degree of predisposition for the existence of such association has been proposed in light of the findings that sleep-associated changes in BMI appear to be primarily occurring in children whose BMI was already elevated.30
We should emphasize that the majority of these studies have, as mentioned above, relied on subjective, parentally reported estimates of sleep duration,31–33 and that the effects of variability of sleep schedules on BMI has not been explored. Also, parental reports generally overestimate sleep duration of children.32–36 In addition, we are unaware of experimental studies that aim to characterize the effect of sleep manipulations on metabolic homeostasis in children. Indeed, the definition of what constitutes “short sleep” is arbitrary and highly variable across different people and across various studies, further adding to the complexity of the critical assessment of the association between sleep and BMI. A given “sleep duration” over a relatively large range may in fact be considered long and sufficient sleep in one child, although short and insufficient sleep in another.
Regardless of the aforementioned limitations, the association of sleep duration with BMI generally exhibits about a 1.5- to twofold increase in the likelihood of being a short sleeper when obesity is present.37–39 And although interventional studies aiming to modify sleep patterns in children are clearly needed, they may be fraught with substantial failure rates, particularly considering that both sleep regularity and sleep duration are maintained across long periods of time during childhood; and thus any intervention will likely need to be initiated very early in life if the effect is to be measurable.39 Accordingly, identification of particular young children at high risk and prospective interventions aiming to prolong and regularize sleep in these children will provide more definitive evidence regarding the role of sleep in BMI and metabolic regulation. Even if such studies are conducted, it will take a long time before their findings can be incorporated into clinical practice. Accordingly, based on the current, albeit deficient level of knowledge, we feel that it might be worth advocating for implementing educational campaigns aimed at families and health professionals, campaigns that target the promotion of longer and regular sleep habits among toddlers and beyond.
Although not exactly within the scope of this paper, it is worthwhile mentioning that strong evidence supporting the biological plausibility of a strong link between sleep, appetite regulation, and adiposity has been made over the last few years. For example, circadian clocks are integral regulators of cellular metabolism that also modulate both appetite and food intake in both animals and humans.40–42 Perturbations of the endogenous global or organ-specific circadian cycle, or alterations in the integrity of sleep homeostatic mechanisms, therefore increases the risk of altered energy intake and disposition, which may ultimately lead to increased propensity for developing obesity and metabolic disturbances.