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From Alert Child to Sleepy Adolescent: Age Trends in Chronotype, Social Jetlag, and Sleep Problems in Youth with Autism

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Title: From Alert Child to Sleepy Adolescent: Age Trends in Chronotype, Social Jetlag, and Sleep Problems in Youth with Autism
Language: English
Authors: Briana J. Taylor (ORCID 0000-0002-9801-3728), Kahsi A. Pedersen (ORCID 0000-0002-0564-3465), Carla A. Mazefsky (ORCID 0000-0001-7467-0902), Martine A. Lamy (ORCID 0000-0001-5873-0813), Charles F. Reynolds (ORCID 0000-0002-2605-7887), William R. Strathmann, Matthew Siegel (ORCID 0000-0003-3457-8532)
Source: Journal of Autism and Developmental Disorders. 2024 54(12):4529-4539.
Availability: Springer. Available from: Springer Nature. One New York Plaza, Suite 4600, New York, NY 10004. Tel: 800-777-4643; Tel: 212-460-1500; Fax: 212-460-1700; e-mail: customerservice@springernature.com; Web site: https://link.springer.com/
Peer Reviewed: Y
Page Count: 11
Publication Date: 2024
Sponsoring Agency: Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) (DHHS/NIH)
Contract Number: K99HD102586
R00HD102586
Document Type: Journal Articles
Reports - Research
Descriptors: Autism Spectrum Disorders, Sleep, Age Differences, Youth, Severity (of Disability), Individual Characteristics, Attention, School Schedules
DOI: 10.1007/s10803-023-06187-0
ISSN: 0162-3257
1573-3432
Abstract: Purpose: Developmental changes in sleep in youth with autism spectrum disorder (ASD) are understudied. In non-ASD youth, adolescents exhibit a "night owl chronotype" (i.e., later sleep/wake timing) and social jetlag (i.e., shifts in sleep timing across school nights and weekends), with corresponding sleep problems. The purpose of this study is to evaluate age trends in chronotype, social jetlag, and sleep problems in high-risk youth with ASD. Methods: Youth with ASD (N = 171), ages 5-21 years old, were enrolled at the time of admission to specialized psychiatric units. Caregivers reported children's demographic information, habitual sleep timing, and sleep problems. Multivariate analyses evaluated the effect of age on chronotype, social jetlag, and sleep problems and the effects of chronotype and social jetlag on sleep problems. Covariates and moderators included sex, race, verbal ability, autism symptom severity, supplemental melatonin, and pubertal status. Results: Older age was associated with later chronotype, more social jetlag, fewer sleep anxiety/co-sleeping problems, fewer night waking and parasomnia problems, and more daytime alertness problems. The effect of age on chronotype was stronger for youth with greater social affective symptom severity. Mediation analyses showed that later chronotype statistically mediated the association between age and daytime alertness problems. Conclusions: Youth with ASD may exhibit night owl chronotype behavior and social jetlag as they enter adolescence. Shifts toward a later chronotype may be exacerbated by autism severity and may contribute to alertness problems and sleepiness during the day. Chronotype is modifiable and may be leveraged to improve daytime functioning in youth with ASD.
Abstractor: As Provided
Entry Date: 2024
Accession Number: EJ1448099
Database: ERIC
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  Value: <anid>AN0180804685;aut01dec.24;2024Nov13.05:17;v2.2.500</anid> <title id="AN0180804685-1">From Alert Child to Sleepy Adolescent: Age Trends in Chronotype, Social Jetlag, and Sleep Problems in Youth with Autism </title> <p>Purpose: Developmental changes in sleep in youth with autism spectrum disorder (ASD) are understudied. In non-ASD youth, adolescents exhibit a "night owl chronotype" (i.e., later sleep/wake timing) and social jetlag (i.e., shifts in sleep timing across school nights and weekends), with corresponding sleep problems. The purpose of this study is to evaluate age trends in chronotype, social jetlag, and sleep problems in high-risk youth with ASD. Methods: Youth with ASD (N = 171), ages 5–21 years old, were enrolled at the time of admission to specialized psychiatric units. Caregivers reported children's demographic information, habitual sleep timing, and sleep problems. Multivariate analyses evaluated the effect of age on chronotype, social jetlag, and sleep problems and the effects of chronotype and social jetlag on sleep problems. Covariates and moderators included sex, race, verbal ability, autism symptom severity, supplemental melatonin, and pubertal status. Results: Older age was associated with later chronotype, more social jetlag, fewer sleep anxiety/co-sleeping problems, fewer night waking and parasomnia problems, and more daytime alertness problems. The effect of age on chronotype was stronger for youth with greater social affective symptom severity. Mediation analyses showed that later chronotype statistically mediated the association between age and daytime alertness problems. Conclusions: Youth with ASD may exhibit night owl chronotype behavior and social jetlag as they enter adolescence. Shifts toward a later chronotype may be exacerbated by autism severity and may contribute to alertness problems and sleepiness during the day. Chronotype is modifiable and may be leveraged to improve daytime functioning in youth with ASD.</p> <p>Keywords: Autism; Sleep; Circadian; Adolescence; Alertness; Sleepiness</p> <p>Copyright comment Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</p> <p>Sleep problems are prevalent in youth with autism spectrum disorder (ASD) with 50–80% experiencing profound sleep problems (Malow et al., [<reflink idref="bib32" id="ref1">32</reflink>]; Richdale & Schreck, [<reflink idref="bib41" id="ref2">41</reflink>]); however, the developmental course of sleep in ASD is underexamined. In typically developing youth, puberty and the transition to adolescence are associated with marked changes in the two processes that regulate sleep: homeostatic sleep drive and the circadian system (Borbely, [<reflink idref="bib5" id="ref3">5</reflink>]). Experimental studies have shown that homeostatic sleep pressure, the drive to fall asleep, builds at a slower rate in non-ASD adolescents at full pubertal maturity relative to younger and less developmentally mature children (Jenni et al., [<reflink idref="bib24" id="ref4">24</reflink>]). In addition, circadian rhythms become delayed in non-ASD adolescents as indicated by later melatonin secretion patterns, resulting in a delayed circadian phase (Crowley et al., [<reflink idref="bib9" id="ref5">9</reflink>]). This delay in circadian rhythms also appears to be tied to the onset of puberty (Hedley et al., [<reflink idref="bib21" id="ref6">21</reflink>]; Jessen et al., [<reflink idref="bib25" id="ref7">25</reflink>]). These developmental changes are associated with altered sleep behavior, the emergence of new sleep problems, and consequences for daytime functioning.</p> <p>Youth with ASD are predisposed to more sleep problems than their non-ASD peers; however, the pathophysiology underlying this predisposition remains unclear. Neurobiological and genetic factors such as abnormalities in neurotransmitter production, endocrine functioning, and circadian-relevant gene expression have been implicated (Tordjman et al., [<reflink idref="bib51" id="ref8">51</reflink>]; Yang et al., [<reflink idref="bib59" id="ref9">59</reflink>]). Common comorbid features of ASD, such as sensory-sensitivities, medical conditions, insistence on sameness, and emotion dysregulation, may also contribute to sleep problems (Souders et al., [<reflink idref="bib48" id="ref10">48</reflink>]). Regardless of etiology, sleep problems have negative repercussions for daytime functioning, particularly with respect to expression of psychiatric symptoms (Moreno et al., [<reflink idref="bib39" id="ref11">39</reflink>]). Understanding the developmental course of sleep behavior and sleep problems in youth with ASD is necessary to identify if sleep should be monitored as a potential intervention target as youth with ASD transition into and across adolescence, a time of heightened risk for those with ASD.</p> <p>In non-ASD adolescents, developmental changes in the regulation of sleep manifest as later bed and wake times. This is referred to as a "night owl" chronotype. The night owl chronotype has a delayed propensity for both falling asleep and waking up which are incompatible with early school start times (Meltzer et al., [<reflink idref="bib37" id="ref12">37</reflink>]). This mismatch between biological and societal timing curtails the window of opportunity for sleep at the beginning and end of the sleep period, contributing to insufficient sleep duration and daytime sleepiness (Carskadon, [<reflink idref="bib6" id="ref13">6</reflink>]). In addition, night owl chronotypes will typically revert to a sleep/wake pattern that is in alignment with their biological rhythms on days when their sleep schedules are not influenced by societal demands such as work and school. As such, night owls with a standard Monday through Friday work/school schedule exhibit dramatic shifts in their sleep/wake timing across weekdays and weekends. This change in sleep/wake timing is akin to traveling across several time zones every week and thus, is referred to as social jetlag. A large and growing body of research suggests that developmental shifts toward a night owl chronotype and increases in social jetlag co-vary with negative psychiatric and behavioral outcomes in non-ASD youth (Karan et al., [<reflink idref="bib27" id="ref14">27</reflink>]; Taylor & Hasler, [<reflink idref="bib50" id="ref15">50</reflink>]).</p> <p>Research on developmental trends in sleep in youth with ASD is quite limited. In one cross sectional study, difficulty falling asleep was greater in children ages 9–12 relative to children ages 6–8 and daytime sleepiness was significantly greater in children ages 9–17 relative to children ages 2–8 (Mayes et al., [<reflink idref="bib35" id="ref16">35</reflink>]). Another study of over 1,800 youth with ASD found that parents of adolescents and older children with ASD reported significantly longer sleep onset latency, shorter sleep duration, and more daytime sleepiness in their children compared to parents of young children and toddlers with ASD (Goldman et al., [<reflink idref="bib17" id="ref17">17</reflink>]). Problems initiating sleep and increased daytime sleepiness in older children may reflect age-related decreases in homeostatic sleep pressure and delays in circadian phase.</p> <p>Two prospective studies have examined changes in sleep in pre-adolescent school-aged children with ASD, ages 10 years old and younger. One study of children ages 2–10 years old found that, over the course of 3–4 years, approximately 20% showed an increase in sleep problems, as measured by the Children's Sleep Habits Questionnaire (Owens et al., [<reflink idref="bib40" id="ref18">40</reflink>]), while approximately 30% showed a decrease (Mazurek et al., [<reflink idref="bib36" id="ref19">36</reflink>]). Another prospective study found that caregiver-reported sleep problems in ASD youth declined over time (Fletcher et al., [<reflink idref="bib13" id="ref20">13</reflink>]). However, the mean ages at the point of follow-up were 10.20 years old (SD = 1.78) and 10.04 (SD = 2.50) for the Mazurek et al. ([<reflink idref="bib36" id="ref21">36</reflink>]) and Fletcher et al. ([<reflink idref="bib13" id="ref22">13</reflink>]), respectively. Therefore, children with ASD in these studies had not reached the developmental stage at which non-ASD youth tend to demonstrate a marked increase in sleep problems (i.e., puberty and/or adolescence).</p> <p>One small prospective study examined changes in actigraphy-measured sleep across the transition into adolescence with mean ages of 11.1 and 13.7 years old at Time 1 and Time 2, respectively (Allik et al., [<reflink idref="bib3" id="ref23">3</reflink>]). This study included 16 youth with ASD and 16 age and sex matched non-ASD controls. Sleep variables measured at each time point included sleep onset latency, number of minutes awake after sleep onset, sleep efficiency, number of night wakings, and sleep duration. There were no differences between ASD and non-ASD youth in terms of change in sleep variables over time and both groups showed a delay in bedtime across the 2–3 year period. Sleep duration on school days decreased by approximately 80 min across this period in both groups. These data seem to suggest that developmental trends in sleep for ASD youth may follow the same pattern as those seen in non-ASD youth, with sleep worsening as children progress into adolescence. However, the roles of chronotype and social jetlag are not examined in the development of increased sleep problems with age.</p> <p>Evaluating age-related trends in chronotype, social jetlag, and sleep problems may elucidate if developmental trends in sleep timing constitute risk factors for adolescents with ASD. For instance, aggression, irritability, and emotional lability are common in youth with ASD at the time of puberty and adolescence (Granana et al., [<reflink idref="bib19" id="ref24">19</reflink>]). In fact, youth with ASD are more likely to develop psychiatric comorbidities in adolescence compared to non-ASD youth (Yeh et al., [<reflink idref="bib60" id="ref25">60</reflink>]), and adolescents with ASD are almost three times more likely to be hospitalized for self-harm than non-ASD adolescents (Widnall et al., [<reflink idref="bib57" id="ref26">57</reflink>]). Sleep problems are known to be associated with challenging behaviors, increased psychiatric symptoms, and even psychiatric hospitalization in youth with ASD (Righi et al., [<reflink idref="bib42" id="ref27">42</reflink>]; Whelan et al., [<reflink idref="bib56" id="ref28">56</reflink>]). However, age-dependent changes in modifiable features of sleep such as chronotype and social jetlag have not been evaluated in youth with ASD.</p> <p>In the current cross-sectional study, we evaluate age-related trends in chronotype, social jetlag, and sleep problems in a large sample of youth with ASD at the time of admission to psychiatric inpatient units, a representative sample of the most at-risk youth with ASD. Here, we seek to: (<reflink idref="bib1" id="ref29">1</reflink>) evaluate age-related differences in chronotype, social jetlag, and sleep problem in ASD youth, (<reflink idref="bib2" id="ref30">2</reflink>) evaluate if chronotype and/or social jetlag are associated with sleep problems in ASD youth, and (<reflink idref="bib3" id="ref31">3</reflink>) evaluate if chronotype and social jetlag mediate associations between age and sleep problems in ASD youth. Finally, we will examine if patterns in the data vary by demographic (e.g., race and sex) and phenotypic characteristics (e.g., verbal ability and high vs. low Autism severity).</p> <hd id="AN0180804685-2">Methods</hd> <p></p> <hd id="AN0180804685-3">Participants</hd> <p>Participants were all recruits of a larger study known as the Autism Inpatient Collection (AIC) (Siegel et al., [<reflink idref="bib46" id="ref32">46</reflink>]), a multi-site study of youth with ASD in psychiatric inpatient units specially designed for the care and treatment of the population. All participants enrolled in the AIC had a clinical diagnosis of ASD, confirmed by a research-reliable administration of the Autism Diagnostic Observation Schedule-2 (ADOS-2) (Gotham et al., [<reflink idref="bib18" id="ref33">18</reflink>]). Methods for the broader AIC protocol are described in Siegel et al., [<reflink idref="bib46" id="ref34">46</reflink>]. Participants in the current study reflect a subset for whom caregiver-reported sleep data were collected. A total of 208 participants were enrolled in the sleep research arm of this study. Twenty-one participants had incomplete CSHQ questionnaires and 11 were missing sleep timing data resulting in a sample for analysis of 171 participants. An additional 26 participants were missing ADOS-2 comparison scores because comparison scores cannot be calculated for children who are beyond the age cut off for their respective modules (e.g., a participant over the age of 14 receiving Module 1). To minimize missing data, the social affect and restricted and repetitive behavior subscales were used in place of the comparison scores. Participants with and without missing data did not differ on any variable except for the Daytime Alertness Problem subscale. Those with complete data had significantly higher scores on this subscale relative to those with incomplete data (N = 31). Descriptive statistics on the sample of 171 are included in Table 1.</p> <p>Table 1 Sample demographics (N = 171)</p> <p> <ephtml> <table frame="hsides" rules="groups"><thead><tr><th align="left"><p>Demographic and Phenotypic Characteristics</p></th><th align="left"><p>Mean or N</p></th><th align="left"><p>SD or %</p></th></tr></thead><tbody><tr><td align="left"><p>Age, Mean ± SD</p></td><td align="left"><p>12.8</p></td><td align="left"><p>± 3.8</p></td></tr><tr><td align="left"><p>Male, N (%)</p></td><td align="left"><p>141</p></td><td align="left"><p>82.5%</p></td></tr><tr><td align="left"><p>White, N (%)</p></td><td align="left"><p>153</p></td><td align="left"><p>89.5%</p></td></tr><tr><td align="left"><p>Fluently Verbal, N (%)</p></td><td align="left"><p>88</p></td><td align="left"><p>51.5%</p></td></tr><tr><td align="left"><p>Comorbid Intellectual Disability (N = 142), N (%)</p></td><td align="left"><p>66</p></td><td align="left"><p>38.6%</p></td></tr><tr><td align="left"><p>Social Affect Severity, Mean ± SD</p></td><td align="left"><p>13.5</p></td><td align="left"><p>± 3.9</p></td></tr><tr><td align="left"><p>Restricted Repetitive Behavior, Mean ± SD</p></td><td align="left"><p>4.2</p></td><td align="left"><p>± 2.3</p></td></tr><tr><td align="left"><p>ADOS Comparison Score (N = 149), Mean ± SD</p></td><td align="left"><p>7.9</p></td><td align="left"><p>± 1.5</p></td></tr><tr><td align="left"><p>Pubertal Status (N = 129)</p></td><td align="left" /><td align="left" /></tr><tr><td align="left"><p> Pre-pubertal, N (%)</p></td><td align="left"><p>37</p></td><td align="left"><p>28.7%</p></td></tr><tr><td align="left"><p> Early pubertal, N (%)</p></td><td align="left"><p>21</p></td><td align="left"><p>16.3%</p></td></tr><tr><td align="left"><p> Mid-pubertal, N (%)</p></td><td align="left"><p>25</p></td><td align="left"><p>19.4%</p></td></tr><tr><td align="left"><p> Late pubertal, N (%)</p></td><td align="left"><p>25</p></td><td align="left"><p>19.4%</p></td></tr><tr><td align="left"><p> Post-pubertal, N (%)</p></td><td align="left"><p>21</p></td><td align="left"><p>16.3%</p></td></tr><tr><td align="left"><p>Sleep Statistics</p></td><td align="left" /><td align="left" /></tr><tr><td align="left"><p>School Day Bedtime</p></td><td align="left"><p>8:39 pm</p></td><td align="left"><p>± 1.18 h</p></td></tr><tr><td align="left"><p>School Day Wake Time</p></td><td align="left"><p>6:24 am</p></td><td align="left"><p>± 1.17 h</p></td></tr><tr><td align="left"><p>School Day Sleep Duration</p></td><td align="left"><p>9.76 h</p></td><td align="left"><p>± 1.53 h</p></td></tr><tr><td align="left"><p>Weekend Bedtime</p></td><td align="left"><p>9:09 pm</p></td><td align="left"><p>± 1.33 h</p></td></tr><tr><td align="left"><p>Weekend Wake Time</p></td><td align="left"><p>7:19 am</p></td><td align="left"><p>± 1.70 h</p></td></tr><tr><td align="left"><p>Weekend Sleep Duration</p></td><td align="left"><p>10.18 h</p></td><td align="left"><p>± 1.89 h</p></td></tr><tr><td align="left"><p>Chronotype (minutes from midnight)</p></td><td align="left"><p>146.07 min</p></td><td align="left"><p>± 93.86 min</p></td></tr><tr><td align="left"><p>Social Jetlag</p></td><td align="left"><p>42.82 min</p></td><td align="left"><p>± 48.96 min</p></td></tr><tr><td align="left"><p>Sleep Initiation & Sleep Duration</p></td><td align="left"><p>15.38</p></td><td align="left"><p>± 5.38</p></td></tr><tr><td align="left"><p>Sleep Anxiety & Co-sleeping</p></td><td align="left"><p>8.96</p></td><td align="left"><p>± 5.10</p></td></tr><tr><td align="left"><p>Night Waking & Parasomnias</p></td><td align="left"><p>14.72</p></td><td align="left"><p>± 4.10</p></td></tr><tr><td align="left"><p>Daytime Alertness Problems</p></td><td align="left"><p>16.45</p></td><td align="left"><p>± 5.78</p></td></tr></tbody></table> </ephtml> </p> <p>N = sample size; SD = standard deviation; ADOS = Autism Diagnostic Observation Schedule; Chronotype = midpoint of sleep on weekends adjusted for oversleep on the weekends; Social Jetlag = midpoint of sleep on weekends minus midpoint of sleep on school days</p> <hd id="AN0180804685-4">Procedure</hd> <p>Caregivers were informed about the study at the time of their child's admission. Caregivers who chose to sign written informed consent were administered a battery of questionnaires, including those that measure their child's recent habitual sleep behavior and sleep problems at home, prior to admission. During the child's treatment, those participating in the research study were evaluated using gold standard diagnostic and testing tools. Specifically, Autism severity was measured using the ADOS-2 and non-verbal IQ was assessed using the Leiter International Performance Scale (3rd edition). This study was approved by the institutional review boards of the AIC institutions: MaineHealth, the University of Pittsburgh Medical Center, and the University of Cincinnati.</p> <hd id="AN0180804685-5">Materials</hd> <p></p> <hd id="AN0180804685-6">Demographic and Phenotypic Variables</hd> <p> <uline>Demographic Characteristics</uline> – At the time of admission, caregivers provided demographic information. Sex and race were included as covariates in the statistical analyses performed in this study and evaluated as potential moderators of associations between age and sleep variables.</p> <p> <uline>Pubertal Status</uline> – Caregivers completed a pubertal development scale (Carskadon & Acebo, [<reflink idref="bib7" id="ref35">7</reflink>]) at the time of admission. The scale was designed for self-report but given the level of impairment and crisis among our participants, the scale was administered to caregivers. The scale asks about the status of development across secondary sex characteristics and, in girls, menarche. The scale divides participants into five puberty categories: pre-pubertal, early pubertal, mid-pubertal, late pubertal, and post-pubertal.</p> <p> <uline>Autism Diagnostic Observation Schedule, 2nd Edition (ADOS-2)</uline> (Gotham et al., [<reflink idref="bib18" id="ref36">18</reflink>]) – The ADOS-2 is an interactive activity-based diagnostic tool to determine the presence of ASD and measure Autism severity across two core domains: social affect symptoms and restricted/repetitive behaviors. Social affect symptoms reflect deficits in social communication. Restricted/repetitive behavior reflects a narrow range of interests as well as stereotyped behaviors. The subscales were used instead of the comparison score due to 26 comparison scores being incalculable. The diagnostic test can be administered using one of four different modules, each of which is designed to accommodate verbal ability (i.e., non-verbal to fluently verbal) and ages. Modules 1–2 are used for non-verbal/minimally verbal individuals while modules 3–4 are used for fluently verbal children and fluently verbal adolescents and adults, respectively. Please see Siegel et al. ([<reflink idref="bib46" id="ref37">46</reflink>]) for a thorough description of the ADOS-2 and protocol for training clinicians to conduct research-reliable ADOS-2 assessments.</p> <p> <uline>Verbal Ability</uline> – Clinicians administering the ADOS-2 chose the most appropriate module based on the age and verbal ability of each child as recorded in their medical records and reported by their caregivers at the time of admission. The choice of ADOS-2 module was used in this analysis as abroad indicator of verbal ability. Those receiving modules 1 or 2 were categorized as non-verbal/minimally verbal and those who received modules 3 or 4 were categorized as fluently verbal.</p> <p> <uline>Melatonin Use</uline> – Research assistants recorded medications from each child's medical chart. While many medications can be prescribed to help with sleep in children and adolescents with ASD, the only sleep-specific medication participants were taking was melatonin. Melatonin use was controlled for and examined as a moderator in analyses.</p> <hd id="AN0180804685-7">Sleep Behavior</hd> <p>Sleep behavior metrics were derived from a single set of items asking caregivers to report their child's average bed and wake times on school nights and on weekends. Average bed and wake times were used to estimate average sleep duration (not accounting for time spent awake after sleep onset) on school nights and weekends as well as the midpoint between bedtime and wake time (i.e., sleep midpoint) on school nights and weekends. Sleep durations and sleep midpoint values were then used to calculate chronotype and social jetlag. Definitions and calculations are described below.</p> <p> <uline>Chronotype</uline> – Chronotype reflects an individual's preference for night versus morning hours (i.e., the extent to which one is a night owl versus an early bird). Chronotype can be measured via self-report questionnaires to assess preferred timing for exerting mental and/or physical effort (e.g., the Morningness-Eveningness Questionnaire (Horne & Ostberg, [<reflink idref="bib22" id="ref38">22</reflink>]), the Composite Scale of Morningness (Smith et al., [<reflink idref="bib47" id="ref39">47</reflink>]), etc.). Chronotype can also be estimated from sleep timing using the Munich Chronotype Questionnaire (MCTQ) (Roenneberg et al., [<reflink idref="bib43" id="ref40">43</reflink>]). Because the MCTQ is brief and does not require the subjective opinion of the child, caregivers reported on their child's chronotype using the MCTQ which quantified chronotype as sleep midpoint on free (non-school/non-work days) corrected for over-sleeping on the weekends. Sleep midpoint is halfway between sleep onset clock-time and sleep offset clock-time. Sleep midpoint on free days (i.e., when sleep/wake timing is not dictated by social obligations such as work or school) is a behavioral indicator of chronotype (Roenneberg et al., [<reflink idref="bib44" id="ref41">44</reflink>]). For students with a traditional Monday through Friday school schedule, free days are weekends and are considered a better reflection of endogenous circadian rhythms, when individuals tend to have more autonomy over their schedules. Sleep midpoint is clock time, measured as minutes from midnight and corrected for the difference in sleep duration between school days and weekends (a.k.a., sleep debt) (Jessen et al., [<reflink idref="bib25" id="ref42">25</reflink>]). Specifically, half of one's sleep debt is subtracted from sleep midpoint. The resulting value is a way to quantify chronotype with larger values reflecting later chronotype (e.g., more night owl tendencies). Those with later chronotypes have been shown to have later circadian phases per biological markers. For instance, endogenous melatonin production is the gold standard measure of circadian phase. Those with late chronotypes have been shown to begin melatonin production later in the evening than earlier chronotypes (Kantermann et al., [<reflink idref="bib26" id="ref43">26</reflink>]).</p> <p> <uline>Social Jetlag</uline> – Social jetlag is calculated as the difference between sleep midpoint on free and non-free days, or weekends and school days, respectively. Social jetlag refers to weekly systematic shifts in sleep timing that are akin to traveling across one-to-two time zones each week. Social jetlag reflects circadian misalignment, or a mismatch between one's biological and social rhythms (Wittmann et al., [<reflink idref="bib58" id="ref44">58</reflink>]). Greater social jetlag has been associated with psychiatric problems such as increased anxiety in adolescents (Mathew et al., [<reflink idref="bib34" id="ref45">34</reflink>]). For reference, the average social jetlag in North American and European countries is approximately 1.5 h for adolescents (Gariepy et al., [<reflink idref="bib15" id="ref46">15</reflink>]) and greater than 1 h of social jetlag has been associated with numerous problems such as increased anxiety problems and cardiometabolic risk factors in neurotypical children and adolescents (Mathew et al., [<reflink idref="bib34" id="ref47">34</reflink>]; Stoner et al., [<reflink idref="bib49" id="ref48">49</reflink>]).</p> <hd id="AN0180804685-8">Sleep Problems</hd> <p> <uline>Children's Sleep Habits Questionnaire – Modified for Autism (CSHQ-ASD) (</uline>Katz et al., [<reflink idref="bib28" id="ref49">28</reflink>]) - The CSHQ-ASD is a 23-item, caregiver-reported retrospective measure of sleep problems in children with ASD. This is a modified version of the original 33-item questionnaire (Owens et al., [<reflink idref="bib40" id="ref50">40</reflink>]) that produces four sleep problem domain subscales: sleep initiation and duration, sleep anxiety and co-sleeping, night waking and parasomnias, and daytime alertness. The subscales demonstrated acceptable to good internal consistency in this sample (Cronbach's α = 0.71–0.83).</p> <hd id="AN0180804685-9">Statistical Analysis</hd> <p>Multivariate analyses were used to evaluate the effect of age on chronotype, social jetlag, and sleep problems (CSHQ subscales: Sleep Initiation and Duration Problems, Sleep Anxiety and Co-Sleeping, Night Wakings and Parasomnias, and Daytime Alertness Problems) while controlling for Type I error. Covariates including sex, race, verbal ability, dimensions of Autism severity (i.e., social affect symptoms, and restricted/repetitive behaviors), and melatonin use were included in the multivariate models and explored as moderators of age effects. A second multivariate analysis assessed if chronotype and social jetlag were associated with sleep problems. Again, age sex, race, verbal ability, and Autism severity were included as covariates and examined as moderators. Exploratory analyses evaluated the role of puberty both as a predictor chronotype, social jetlag, and sleep problems, as well as a moderator of other evaluated predictor variables. Analyses including pubertal status were considered exploratory due to substantial missing data for this variable. Adjusted values from multivariate analyses were saved and regressed onto age to visualize associations after adjusting for covariates.</p> <hd id="AN0180804685-10">Results</hd> <p>Participants were predominantly male and white with a mean age of 12.8 ± 3.8 years old (Table 1). Approximately half of the participants were minimally verbal and 38.6% of participants had comorbid intellectual disability (NVIQ < 70). Of 171 participants, 62 (36.3%) were taking melatonin. On average, caregivers reported that on school days, their children went to bed at 8:39pm ± 1.2 h and woke up at 6:24am ± 1.2 h. On weekends, children went to bed at 9:09pm ± 1.33 h and woke up at 7:19am ± 1.7 h. Mean sleep durations were 9.8 ± 1.5 h on school days and 10.2 ± 1.9 h on weekends. Chronotype (operationalized as sleep midpoint on free days, corrected for sleeping-in on weekends) was on the earlier side of average (i.e., approximately 2:24 am) with the sample demonstrating great variability with a standard deviation of approximately 1.5 h. The mean social jetlag was approximately 43 min (± 49 min).</p> <hd id="AN0180804685-11">Is Age Associated with Chronotype, Social Jetlag, and Sleep Problems in Children with ASD?</hd> <p>There was a significant and large multivariate effect of age on sleep variables before and after adjusting for sex, race, verbal ability, dimensions of autism severity, and melatonin use (Pillai's Trace = 0.23, F = 7.68, p < 0.001). In fully adjusted models, older age was associated with later chronotype (F = 18.09, p < 0.001), more social jetlag (F = 14.89, p < 0.001), fewer Sleep Anxiety/Co-sleeping problems (F = 19.66, p < 0.001), fewer Night Waking/Parasomnia problems (F = 5.52, p = 0.02), and more Daytime Alertness Problems (F = 5.77, p = 0.02) (Fig. 1). Age was unrelated to the Sleep Initiation/Sleep Duration subscale.</p> <p>Graph: Fig. 1 Adjusted sleep variable and age with adjusted β coefficients</p> <p>Social affective symptoms of ASD moderated the effect of age on chronotype (Pillai's Trace = 0.09, F = 2.59, p = 0.02) (Fig. 2). The strength of the association between age and chronotype was significantly higher for those with higher SA symptom severity (F = 8.15, p = 0.005). No other variables moderated the effect of age on chronotype, social jetlag, or any sleep problems. Verbal ability was the only other significant predictor of sleep variables (Pillai's Trace = 0.10, F = 2.93, p = 0.01). Minimally verbal participants had higher scores on the Night Waking and Parasomnia subscale (F = 10.02, p = 0.002) and the Daytime Alertness Problem subscale (F = 3.95, p = 0.05).</p> <p>Graph: Fig. 2 The association between age and chronotype is stronger for those with higher social affective symptom severity</p> <p>The multivariate effect of age was robust to adjustment for pubertal status (Pillai's Trace = 0.16, F = 3.53, p = 0.003). When pubertal status was added to the model, positive associations with age remained significant for chronotype (F = 5.80, p = 0.02), social jetlag (F = 4.56, p = 0.04), and Sleep Anxiety/Co-sleeping problems (F = 9.47, p = 0.003). There were no multivariate effects of pubertal status on sleep variables in fully adjusted models.</p> <hd id="AN0180804685-12">Are Chronotype and/or Social Jetlag Associated with Sleep Problems?</hd> <p>In fully adjusted models, there was a multivariate effect of chronotype (Pillai's Trace = 0.12, F = 5.46, p < 0.001) but not social jetlag (Pillai's Trace = 0.04, F = 1.42, p = 0.23) on sleep problems. Later chronotype was associated with more Sleep Anxiety and Co-sleeping (F = 6.99, p = 0.009) and more Daytime Alertness Problems (F = 11.83, p < 0.001) (Fig. 3).</p> <p>Graph: Fig. 3 Adjusted CSHQ subscale and age with β coefficients</p> <hd id="AN0180804685-13">Does Chronotype Statistically Account for the Association Between Age and Sleep Problems?</hd> <p>The association between age and Daytime Alertness Problems was mediated by chronotype (Sobel test statistic = 3.63, SE = 0.06, p < 0.001), controlling for sex, race, verbal ability, autism severity, and melatonin use. Chronotype did not help to explain associations between age and either Sleep Anxiety and Co-sleeping or Night Waking and Parasomnias.</p> <hd id="AN0180804685-14">Discussion</hd> <p>The cross-sectional evidence presented here demonstrates that sleep profiles in ASD youth may follow the same developmental trajectory of sleep seen in non-ASD youth, with chronotype becoming later and social jetlag increasing with age. This suggests that youth with ASD may experience typical developmental shifts in the circadian and homeostatic regulation of sleep as they transition into adolescence. Age-related decreases in sleep problems such as sleep anxiety, co-sleeping, night waking, and parasomnias was evident in our data and consistent with longitudinal sleep data in non-ASD youth (Furet et al., [<reflink idref="bib14" id="ref51">14</reflink>]; Laberge et al., [<reflink idref="bib29" id="ref52">29</reflink>]). Likely due to the variance accounted for by age, pubertal status had no independent effect on sleep variables. Importantly, our data show that later chronotype may contribute to or exacerbate sleep problems such as sleep anxiety and daytime sleepiness, and that age-related changes in chronotype may be intensified in those with higher social affective symptom severity. Our results fill an important gap in understanding the developmental course of chronotype, social jetlag, and sleep problems in ASD and couches these data in the context of individual differences.</p> <hd id="AN0180804685-15">Age, Chronotype, and Autism Severity</hd> <p>The night owl chronotype is typified by progressively later sleep midpoints on free days when sleep timing is not dictated by social obligations such as school. Sleep midpoint is seen as a behavioral indicator of an individual's circadian phase is correlated with the time at which melatonin is secreted from the pineal gland, acting as a circadian messenger to organs throughout the body that it is no longer daytime, increasing the propensity for sleep. The night owl chronotype is manifested by later bed and wake times and is known to have a cascading effect on sleep problems such as chronic sleep restriction on school days and increased variability in sleep timing and duration due to fluctuating sleep/wake behavior across school days and weekends. As a result, sleep timing systematically shifts every week to the extent that, for many adolescents, transitioning from the weekend to the school week is akin to traveling across multiple time zones (i.e., social jetlag).</p> <p>In this sample, higher social affective symptom severity moderated the association between age and chronotype such that positive associations between age and later chronotype were stronger when social affective symptom severity was high. Social affective symptom severity indicates the extent to which an individual struggles with social interactions, the forming and maintaining of social relationships, and reciprocal communication. Difficulties in this area can also manifest as a lack of interest in social interactions. Lower social motivation may decrease responsivity to unstructured social pressures to wake up on the weekends (e.g., joining friends and family for leisure activities). As such, individuals with higher social affective symptoms severity, may be less inclined to override their biological clocks and align their behavioral rhythms with those who have earlier chronotypes. Thus, heightened social affect symptoms may exacerbate age-related shifts toward the behavioral profile of the night owl chronotype.</p> <hd id="AN0180804685-16">The Effects of Chronotype on Sleep Problems</hd> <p>Later chronotype was associated with more sleep problems, as indicated by higher scores on the Sleep Anxiety/Co-sleeping and Daytime Alertness Problem subscales. This is consistent with the extant literature on chronotype and sleep quality in pediatric samples with daytime sleepiness as the most common correlate (Becker et al., [<reflink idref="bib4" id="ref53">4</reflink>]; Chan et al., [<reflink idref="bib8" id="ref54">8</reflink>]; Durmus et al., [<reflink idref="bib10" id="ref55">10</reflink>]; Jafar et al., [<reflink idref="bib23" id="ref56">23</reflink>]; Moreno et al., [<reflink idref="bib39" id="ref57">39</reflink>]). While night owl chronotypes frequently demonstrate increased anxiety (Taylor & Hasler, [<reflink idref="bib50" id="ref58">50</reflink>]), this is the first study to show an association between later chronotype and increase sleep-specific anxiety and co-sleeping.</p> <p>Few studies have examined chronotype in youth with ASD, let alone the relevance of chronotype for sleep in ASD. One study compared associations between chronotype, sleep problems, and anxiety/depression symptoms in a sample of typically developing children, children with attention-deficit hyperactivity disorder (ADHD), and children with ASD, ages 6–12 years old (van der Heijden et al., [<reflink idref="bib53" id="ref59">53</reflink>]). Interestingly, later chronotype was associated with more sleep problems in the typically developing and ADHD groups but not the ASD group. Another study used a sample of ASD youth across a broader age-range, 4–17 years old (Türkoğlu et al., [<reflink idref="bib52" id="ref60">52</reflink>]). This study found that later chronotype predicted increases in sleep problems and increased autism severity during the COVID-19 lockdown conditions.</p> <hd id="AN0180804685-17">Strengths, Limitations, and Future Directions</hd> <p>Our sample consists of youth with ASD at the time of admission to psychiatric hospital units. This sample is enriched for more severely affected individuals, with approximately 50% being minimally-verbal and all being in a state of crisis requiring inpatient treatment. Little is known about this more severely affected subpopulation of youth with ASD, including how developmental changes in the biological processes that regulate sleep impact health and functioning. Our sample reflects an understudied and highly vulnerable population. The data presented here suggest that children with ASD requiring psychiatric hospitalization may show normative developmental trends in sleep and circadian functioning with consequences for features of sleep quality and daytime functioning.</p> <p>This sample is not representative of the broader ASD population and, therefore, the results cannot be generalized to broader groups of youth with ASD. Additionally, sleep data used here is based on parent-reports of their child's sleep prior to admission, which may be subject to retrospection bias. The severity of the population may also bias our data. Caregivers of severely affected children may be more vigilant regulating a child's sleep/wake schedule as more severely affected children with ASD tend to have less autonomy (Roquette Viana et al., [<reflink idref="bib45" id="ref61">45</reflink>]; Ventola et al., [<reflink idref="bib54" id="ref62">54</reflink>]). This may be reflected in the early weekend bed and wake times we see in this sample (e.g., 9:09 pm ± 1.33 h and 7:19 am ± 1.70 h for bed and wake times, respectively). In addition, social jetlag is markedly lower in this sample (i.e., approximately 43 ± 49 min), relative to the average amount of social jetlag seen in adolescents in North America and Europe (i.e., 1.5 h) (Gariepy et al., [<reflink idref="bib15" id="ref63">15</reflink>]).</p> <p>Studies using larger and more representative samples of children with ASD are needed to substantiate the findings reported here. Additionally, previous research shows that youth with ASD and sleep problems are more likely to be hospitalized relative to children with ASD and no sleep problems (Righi et al., [<reflink idref="bib42" id="ref64">42</reflink>]). Prospective studies using objective sleep monitoring and experience sampling are needed to evaluate if developmental changes in sleep and circadian functioning precede increased problems in sleep (e.g., sleep anxiety and daytime alertness problems), and may contribute to daytime functioning problems that ultimately necessitate hospitalization.</p> <p>Chronotype and social jetlag are modifiable. Chronotherapeutic interventions such as melatonin administration and morning bright light therapy have been shown to advance circadian timing, resulting in earlier sleep midpoints (Lack et al., [<reflink idref="bib30" id="ref65">30</reflink>]; Moon et al., [<reflink idref="bib38" id="ref66">38</reflink>]) and reduced social jetlag (Geerdink et al., [<reflink idref="bib16" id="ref67">16</reflink>]). In addition, while not impacting chronotype, delaying school start times has been shown to reduce social jetlag, increase sleep duration, and reduce daytime sleepiness in adolescents (Alfonsi et al., [<reflink idref="bib2" id="ref68">2</reflink>]; Evanger et al., [<reflink idref="bib11" id="ref69">11</reflink>]). Structural changes that accommodate biological shifts in sleep among youth diminish the incompatibility between biological timing (e.g., delays in circadian phase) and behavioral timing (e.g., waking up early on school days) with collateral benefits for health and functioning. Studies that examine pre-post treatment and/or school start time delays may provide experimental evidence for the roles of circadian phase and social jetlag in the sleep problems of youth with ASD.</p> <p>Comparative clinical effectiveness trials with long-term monitoring are also needed to compare the costs and benefits of policy changes relative to chronotherapeutic interventions to promote sleep in adolescents (i.e., delaying school start times). For instance, delayed school start times are associated with improvements in sleep, mental health, and academic performance (Wheaton et al., [<reflink idref="bib55" id="ref70">55</reflink>]); however, there are many barriers (e.g., resistance from teachers, transportation challenges, etc.) that prevent school districts from implementing later school start time policies (Albrecht et al., [<reflink idref="bib1" id="ref71">1</reflink>]; Fitzpatrick et al., [<reflink idref="bib12" id="ref72">12</reflink>]). On the other hand, while most research suggests that long-term use of synthetic melatonin is safe for children and adolescents (Mantle et al., [<reflink idref="bib33" id="ref73">33</reflink>]), melatonin use is associated with increased risk for so called, "non-serious adverse events" (e.g., nausea, headaches, eye problems, etc.) (Händel et al., [<reflink idref="bib20" id="ref74">20</reflink>]) and the effect of long-term use of synthetic melatonin on endogenous melatonin production is unclear (Liampas et al., [<reflink idref="bib31" id="ref75">31</reflink>]). Assessing the long-term gains and losses associated with policy and/or pharmacological approaches to address age-related sleep problems is essential for our most vulnerable youth.</p> <hd id="AN0180804685-18">Conclusion</hd> <p>The current study suggests that, similar to typically developing youth, chronotype may indeed delay with age in children with ASD as they approach and enter adolescence. Age-related delays in chronotype may also be exacerbated by heightened autism severity, particularly in the social affective symptom domain. The shift toward the evening chronotype, as indicated by later sleep midpoints, likely contributes to increased daytime alertness problems. Moreover, sleep anxiety, co-sleeping, night waking, and the presence of parasomnias show a decline with age, consistent with longitudinal trends in non-ASD youth. Future prospective studies using objective measures are needed to understand the developmental course of sleep profiles and sleep problems in youth with ASD and the extent to which sleep may be leveraged to improve daytime functioning in this at-risk population.</p> <hd id="AN0180804685-19">Acknowledgements</hd> <p>The funding for this research was provided by a grant from The Simons Foundation (SFARI 296318, 618037), The Nancy Lurie Marks Family Foundation, and The National Institute of Child Health and Human Development (K99 HD102586 and R00 HD102586). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Data were collected in partnership with the Autism and Developmental Disorders Inpatient Research Collaborative (ADDIRC) during the Autism Inpatient Collection (AIC) study. We thank the study staff for their time and energy in this work. Special thanks also to the AIC research participants and their families who made this research possible.</p> <hd id="AN0180804685-20">Declarations</hd> <p></p> <hd id="AN0180804685-21">Conflicts of Interest</hd> <p>The authors have no conflicts of interest to disclose.</p> <hd id="AN0180804685-22">Publisher's Note</hd> <p>Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.</p> <ref id="AN0180804685-23"> <title> References </title> <blist> <bibl id="bib1" idref="ref29" type="bt">1</bibl> <bibtext> Albrecht JN, Werner H, Yaw ML, Jenni OG, Huber R. Teachers' preference for later school start times. Journal of Sleep Research. 2022; 31; 4: e13534. 10.1111/jsr.13534. 34923707</bibtext> </blist> <blist> <bibl id="bib2" idref="ref30" type="bt">2</bibl> <bibtext> Alfonsi, V, Scarpelli, S, D'Atri, A, Stella, G, & De Gennaro, L. (2020). 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Items – Name: Title
  Label: Title
  Group: Ti
  Data: From Alert Child to Sleepy Adolescent: Age Trends in Chronotype, Social Jetlag, and Sleep Problems in Youth with Autism
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  Label: Language
  Group: Lang
  Data: English
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AR" term="%22Briana+J%2E+Taylor%22">Briana J. Taylor</searchLink> (ORCID <externalLink term="http://orcid.org/0000-0002-9801-3728">0000-0002-9801-3728</externalLink>)<br /><searchLink fieldCode="AR" term="%22Kahsi+A%2E+Pedersen%22">Kahsi A. Pedersen</searchLink> (ORCID <externalLink term="http://orcid.org/0000-0002-0564-3465">0000-0002-0564-3465</externalLink>)<br /><searchLink fieldCode="AR" term="%22Carla+A%2E+Mazefsky%22">Carla A. Mazefsky</searchLink> (ORCID <externalLink term="http://orcid.org/0000-0001-7467-0902">0000-0001-7467-0902</externalLink>)<br /><searchLink fieldCode="AR" term="%22Martine+A%2E+Lamy%22">Martine A. Lamy</searchLink> (ORCID <externalLink term="http://orcid.org/0000-0001-5873-0813">0000-0001-5873-0813</externalLink>)<br /><searchLink fieldCode="AR" term="%22Charles+F%2E+Reynolds%22">Charles F. Reynolds</searchLink> (ORCID <externalLink term="http://orcid.org/0000-0002-2605-7887">0000-0002-2605-7887</externalLink>)<br /><searchLink fieldCode="AR" term="%22William+R%2E+Strathmann%22">William R. Strathmann</searchLink><br /><searchLink fieldCode="AR" term="%22Matthew+Siegel%22">Matthew Siegel</searchLink> (ORCID <externalLink term="http://orcid.org/0000-0003-3457-8532">0000-0003-3457-8532</externalLink>)
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  Data: <searchLink fieldCode="SO" term="%22Journal+of+Autism+and+Developmental+Disorders%22"><i>Journal of Autism and Developmental Disorders</i></searchLink>. 2024 54(12):4529-4539.
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  Data: Springer. Available from: Springer Nature. One New York Plaza, Suite 4600, New York, NY 10004. Tel: 800-777-4643; Tel: 212-460-1500; Fax: 212-460-1700; e-mail: customerservice@springernature.com; Web site: https://link.springer.com/
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  Data: Y
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  Label: Page Count
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  Data: 11
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  Label: Publication Date
  Group: Date
  Data: 2024
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  Label: Sponsoring Agency
  Group: SrcSuprt
  Data: Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) (DHHS/NIH)
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  Label: Contract Number
  Group: NumCntrct
  Data: K99HD102586<br />R00HD102586
– Name: TypeDocument
  Label: Document Type
  Group: TypDoc
  Data: Journal Articles<br />Reports - Research
– Name: Subject
  Label: Descriptors
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22Autism+Spectrum+Disorders%22">Autism Spectrum Disorders</searchLink><br /><searchLink fieldCode="DE" term="%22Sleep%22">Sleep</searchLink><br /><searchLink fieldCode="DE" term="%22Age+Differences%22">Age Differences</searchLink><br /><searchLink fieldCode="DE" term="%22Youth%22">Youth</searchLink><br /><searchLink fieldCode="DE" term="%22Severity+%28of+Disability%29%22">Severity (of Disability)</searchLink><br /><searchLink fieldCode="DE" term="%22Individual+Characteristics%22">Individual Characteristics</searchLink><br /><searchLink fieldCode="DE" term="%22Attention%22">Attention</searchLink><br /><searchLink fieldCode="DE" term="%22School+Schedules%22">School Schedules</searchLink>
– Name: DOI
  Label: DOI
  Group: ID
  Data: 10.1007/s10803-023-06187-0
– Name: ISSN
  Label: ISSN
  Group: ISSN
  Data: 0162-3257<br />1573-3432
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Purpose: Developmental changes in sleep in youth with autism spectrum disorder (ASD) are understudied. In non-ASD youth, adolescents exhibit a "night owl chronotype" (i.e., later sleep/wake timing) and social jetlag (i.e., shifts in sleep timing across school nights and weekends), with corresponding sleep problems. The purpose of this study is to evaluate age trends in chronotype, social jetlag, and sleep problems in high-risk youth with ASD. Methods: Youth with ASD (N = 171), ages 5-21 years old, were enrolled at the time of admission to specialized psychiatric units. Caregivers reported children's demographic information, habitual sleep timing, and sleep problems. Multivariate analyses evaluated the effect of age on chronotype, social jetlag, and sleep problems and the effects of chronotype and social jetlag on sleep problems. Covariates and moderators included sex, race, verbal ability, autism symptom severity, supplemental melatonin, and pubertal status. Results: Older age was associated with later chronotype, more social jetlag, fewer sleep anxiety/co-sleeping problems, fewer night waking and parasomnia problems, and more daytime alertness problems. The effect of age on chronotype was stronger for youth with greater social affective symptom severity. Mediation analyses showed that later chronotype statistically mediated the association between age and daytime alertness problems. Conclusions: Youth with ASD may exhibit night owl chronotype behavior and social jetlag as they enter adolescence. Shifts toward a later chronotype may be exacerbated by autism severity and may contribute to alertness problems and sleepiness during the day. Chronotype is modifiable and may be leveraged to improve daytime functioning in youth with ASD.
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  Label: Entry Date
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  Data: 2024
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  Label: Accession Number
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  Data: EJ1448099
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    PhysicalDescription:
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        PageCount: 11
        StartPage: 4529
    Subjects:
      – SubjectFull: Autism Spectrum Disorders
        Type: general
      – SubjectFull: Sleep
        Type: general
      – SubjectFull: Age Differences
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      – SubjectFull: Youth
        Type: general
      – SubjectFull: Severity (of Disability)
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      – TitleFull: From Alert Child to Sleepy Adolescent: Age Trends in Chronotype, Social Jetlag, and Sleep Problems in Youth with Autism
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