Obesity rates have reached alarming levels in the developed world, particularly among youth and adolescent populations. Roughly one-third of adolescents in the United States are overweight or obese [1], which can have significant implications for overall health later in life [2]. While numerous factors such as diet and activity affect the risk of obesity, mounting evidence suggests that poor sleep and circadian misalignment are key contributors to poorer cardiometabolic outcomes [3]. Though extreme misalignments, such as what occurs with overnight or rotating shift work, have been well-established to impair health, there has been growing interest in identifying health consequences associated with acute but recurring circadian disruptions arising from a phenomenon known as social jetlag. Social jetlag is defined as the discrepancy between the sleep timing imposed by external/social obligations (i.e. work–school schedules) and the biologically preferred sleep timing on obligation-free days, thereby causing a misalignment between the external environment and the internal biological clock akin to that experienced when flying rapidly across time zones (i.e. jetlag) [4]. While global prevalence rates of social jetlag are unknown, it is estimated that up to 70% of individuals experience at least 1-hour of social jetlag per week [5–9] and nearly one-third of the general adult population experiences ≥2-hour of social jetlag [5, 8]. Because adolescents on average have a delayed (i.e. later) circadian phase relative to adults [10] they are more likely to go to sleep and awaken at a later clock hour, even when these events conflict with the timing of school and other commitments, making them a vulnerable population to high levels of social jetlag [11]. Moreover, light exposure patterns, which partially contribute to adolescent circadian phase [12, 13], can also further delay circadian phase. Since light during the solar night is easily obtainable in a multitude of ways (e.g. overhead lighting, television, and personal electronic devices) [14] typical delayed bedtimes can further aggravate the tendency towards delayed circadian phase via light exposure in the early portion of the biological night. Importantly, these recurrent circadian disruptions have consequences; social jetlag increases the risk of unfavorable cardiometabolic profiles, increased adiposity and body mass index (BMI) [5, 15–17], particularly in individuals with overweight/obesity [5]. And while there are investigations into the cross-sectional associations between social jetlag and obesity in adolescent populations [18, 19], there is limited information on the longitudinal effects of social jetlag on BMI trajectories in adolescence.
In this issue of SLEEP, Chang and colleagues present compelling longitudinal evidence on developmental social jetlag trajectories throughout adolescence and the association with BMI in young males and females [20]. Data were analyzed from two independent longitudinal studies conducted in Taiwan. Social jetlag was tracked in 4287 participants (aged 11–22 years) and quantified as the absolute difference in hours between the midpoint of sleep on free days and the midpoint of sleep on weekdays based on self-reported bedtimes and wake-up times. Participants were stratified as having either ≥2 or <2 hours of social jetlag and the association between the social jetlag across adolescence and BMI at age 23 was assessed. After controlling for confounding factors such as stressful life events, insomnia, and substance abuse, four social jetlag trajectory patterns were observed: (1) low-stable, with a low likelihood of having ≥2 hours social jetlag at most time points (42%), (2) low-increasing, with an initial low likelihood of social jetlag that progressively increased through adolescence, peaking at 18 years (22%), (3) moderate-decreasing, being a moderate probability of social jetlag initially that exhibited a downward trend over time (19%), and (4) chronic social jetlag persisting throughout the study period (17%). Notably, authors report sex differences in the associations between social jetlag trajectories and BMI. Compared to the low-stable trajectory, males in the low-increasing trajectory had an increased risk of both underweight and obesity while females with low-increasing and chronic trajectories were more likely to have obesity.
The present study is an innovative longitudinal study that tracks trajectories in social jetlag and its sex-dependent association with BMI in a large cohort of adolescents. In adults, McMahon et al examined social jetlag over a 2-year period (n = 390, ages 22–35) and found no differences in BMI between low and high social jetlag groups [21]; however, participants in the high group only had an average social jetlag of 1.4 hours. Thus, these discrepant findings likely underscore the vulnerability of children and adolescents to experiencing a greater degree of social jetlag and the importance of the present study. The internal circadian clock governs 24-hour rhythms in physiological processes and behaviors, but as mentioned previously, the use of electrical lighting and portable electronic devices can disrupt circadian mechanisms and contribute to poorer sleep outcomes [22, 23]. Consequently, the differences in sleep duration between school days and weekend days become more drastic in adolescence as the average sleep duration decreases considerably, with up to 25% of adolescents getting <6 hours of sleep on school nights [5, 24]. Short sleep duration and circadian misalignment have been shown to be associated with insulin resistance in overweight and obese adolescents [25], which may be in part mediated by the effects of social jetlag on BMI and obesity. Additional mechanistic pathways may include a later timing of food intake [26], more variable total sleep durations [27, 28], and poorer diet habits [29] in those with greater social jetlag.
The present investigation by Chang and colleagues is a potential pivotal step in identifying the effects of social jetlag on other cardiometabolic health outcomes and developing intervention strategies that improve circadian alignment and sleep outcomes in adolescents. This may be of particular importance as this time of life is a critical developmental time period for establishing long-term healthy-weight behaviors [30]. Examples of interventions could include public health campaigns to promote reducing variability in sleep timing between school and free days or changes to imposed schedules that alter sleep–wake timing. Later school start times are not only associated with more sleep and better academic performance, but also lower BMIs [31, 32]. It is also important to note that additional work in this topic area is needed, as the investigation by Chang and colleagues is limited to self-report of sleep–wake timing and BMI, utilized a study population that may not be generalizable, and because the use of BMI alone could be misleading in this aged population due to body composition (e.g. high percentage of muscle vs. fat) or developmental stage [33].
Quantifying social jetlag could be a useful tool to not only assess the magnitude of circadian disruptions in adolescent populations, but also to identify individuals who may be at greater risk of adverse metabolic outcomes and obesity in adulthood. The findings from Chang and colleagues highlight the urgent need to develop interventions that promote better circadian alignment in adolescents, particularly during the high school years when degree of social jetlag notably increases. The ability to improve BMI outcomes among adolescents by targeting social jetlag would be of great benefit on the individual level and to society as a whole. As obesity has a substantial global economic impact [34, 35], the effect of social jetlag on long-term health outcomes merits a greater focus in the sleep health field.
Contributor Information
Brooke M Shafer, Sleep, Chronobiology, and Health Laboratory, School of Nursing, Oregon Health and Science University, Portland, OR, USA.
Kathryn E McAuliffe, Sleep, Chronobiology, and Health Laboratory, School of Nursing, Oregon Health and Science University, Portland, OR, USA.
Andrew W McHill, Sleep, Chronobiology, and Health Laboratory, School of Nursing, Oregon Health and Science University, Portland, OR, USA; Oregon Institute of Occupational Health Sciences, Oregon Health and Science University, Portland, OR, USA.
Funding
This work was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health (NIH) T32 HL083808, the NIH K01HL146992, R01HL156948, R01HL169317 and the OHSU School of Nursing PhD Student Scholarship Award.
Disclosure Statements
Financial Disclosure: AWM consults for Pure Somni Corporation. The remaining authors have no conflicts of interest to declare. Nonfinancial Disclosure: None.
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