Video Abstract

Video Abstract

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OBJECTIVES

Insomnia symptoms are transdiagnostic to physical and mental health disorders. Given the lack of population-based cohorts with objective sleep measures and long-term follow-ups, little is known about the chronicity of childhood insomnia symptoms. We determined the developmental trajectories of insomnia symptoms, their evolution into adult insomnia, and the role of objective sleep duration in the transition to adulthood.

METHODS

A total of 502 children (median 9 years old, 71.7% response rate) were studied 7.4 years later as adolescents (median 16 years old) and 15 years later as adults (median 24 years old). Insomnia symptoms were ascertained as moderate-to-severe difficulties initiating and/or maintaining sleep via parent- or self reports at all 3 time points, adult insomnia via self-report in young adulthood, and objective short-sleep duration via polysomnography in childhood and adolescence.

RESULTS

Among children with insomnia symptoms, the most frequent trajectory was persistence (43.3%), followed by remission (26.9% since childhood, 11.2% since adolescence) and a waxing-and-waning pattern (18.6%). Among children with normal sleep, the most frequent trajectory was persistence (48.1%), followed by developing insomnia symptoms (15.2% since adolescence, 20.7% in adulthood) and a waxing-and-waning pattern (16.0%). The odds of insomnia symptoms worsening into adult insomnia (22.0% of children, 20.8% of adolescents) were 2.6-fold and 5.5-fold among short-sleeping children and adolescents, respectively.

CONCLUSIONS

Early sleep interventions are a health priority because pediatricians should not expect insomnia symptoms to developmentally remit in a high proportion of children. Objective sleep measures may be clinically useful in adolescence, a critical period for the adverse prognosis of the insomnia with short-sleep duration phenotype.

What’s Known on This Subject:

Studies vary in persistence and remission rates, developmental stages, or follow-up length, restricting their findings to specific transitional periods. Reported remission rates for childhood insomnia symptoms by adolescence were high, but subjects were not followed up again in adulthood.

What This Study Adds:

This 15-year longitudinal study unveiled that chronicity of childhood-onset insomnia symptoms is greater than previously believed, indicating 43% of children persist with insomnia symptoms, whereas 20% worsen into adult insomnia, a risk greatest in short-sleeping adolescents.

Difficulties initiating and/or maintaining sleep (DIMS) are the most common parent-reported insomnia symptoms in youth, with a prevalence of 20% to 25% in childhood and 25% to 35% in adolescence.13  In adulthood, these figures increase to 30% to 45%, with 10% of adults reporting insomnia as a disorder.46  Few longitudinal studies have examined the course of insomnia symptoms as the child transitions through adolescence into adulthood,79  which is necessary to understand the long-term prognosis of these prevalent sleep problems encountered in routine clinical practice.

Previous studies suggest the persistence of insomnia symptoms in youth varies depending on the population examined, definition used, and length of follow-up.1016  To shed light on the transitional period between childhood and adolescence, we recently reported in the Penn State Child Cohort the persistence of childhood insomnia symptoms was 56%, with only 30% fully remitting by adolescence,14  a rate similar to previous studies in adolescents15  or in adults.46  Although we identified female sex, racial and ethnic minority, and psychiatric and learning disorders as key risk factors, objective short sleep duration (OSSD) was not a significant determinant of the persistence or incidence of insomnia symptoms in the transition to adolescence.14  This lack of association contrasted with previous evidence showing a link between OSSD and adverse health outcomes, including increased hypothalamic–pituitary–adrenal axis activity; low-grade systemic inflammation; high-frequency cortical activity; internalizing symptoms; and externalizing behaviors in children,17,18  adolescents,1921  and adults22  with insomnia symptoms. OSSD has also been associated with the evolution of insomnia symptoms into adult insomnia; thus, OSSD may be a useful biomarker of the chronicity of insomnia.5,6,23  It remains unknown, however, whether the impact of OSSD in the trajectories of insomnia symptoms is dependent upon the developmental stage in which youth are evaluated and whether it has an impact on the development of insomnia in the transition to adulthood.

The goal of the current study was to estimate the developmental trajectories of insomnia symptoms in a population-based sample of children followed-up through adolescence into young adulthood to establish whether it persists or developmentally remits as the child enters adulthood. Furthermore, we sought to identify how many of these children and adolescents worsen into adult insomnia, and whether OSSD is a significant determinant. On the basis of previous studies,5,6,14,23  we hypothesized that the odds of insomnia symptoms evolving into adult insomnia are greater among youth with OSSD, particularly in the transition from adolescence to young adulthood.

The Penn State Child Cohort was designed as a random, population-based study of school-aged children for which details have been previously reported.14,2426  In brief, out of 5740 children (aged 5–12 years), 1000 of them were randomly selected to participate in an in-laboratory polysomnography (PSG) study (visit 1 [V1]) and 700 agreed (70% response rate) at baseline from 2000 to 2005. A total of 421 of these subjects underwent an in-laboratory follow-up study at ages 12 to 23 (visit 2 [V2]; 60.1% response rate) from 2010 to 2013.25  No differences in demographic characteristics at V1 were observed in the 279 subjects lost to follow-up at V2.25  The length between V1 and V2 in the 421 subjects ranged from 5.8 to 13 years (median = 7.4; interquartile range [IQR], 6.8–8.7). A total of 502 subjects (71.7% response rate since V1 and 79.1% since V2) aged 18 to 31 have completed a structured self-reported survey (survey 3 [S3]) from 2018 to 2021. No differences in demographic characteristics at V1 were observed between the 700 subjects and the 502 followed-up at S3, except a lower proportion of males (52.7% vs 48.0%). The length between V1 and S3 in the 502 subjects ranged from 11.4 to 20.3 years (median = 14.8; IQR, 13.4–16.3). The current study focuses on these 502 subjects with S3 data (n = 333 with data at all time points, n = 169 at V1 and S3) (Supplemental Fig 3).

Penn State College of Medicine’s institutional review board approved the study. Written informed consents from the parent or legal guardian and from subjects aged ≥18 years, and assent from those aged <18 years, were obtained.

At V1 and V2, subjects or their parents completed the Pediatric Behavior Scale (PBS)27  and the Pediatric Sleep Questionnaire (PSQ).28  At V1, 118 subjects were identified to have insomnia symptoms, defined as a parent report of “often/moderate” or “very often/severe” DIMS on the PBS1,17,18,29  and/or sleep medication use (over-the-counter or prescription medications for DIMS and not for other medical or sleep issues)4 ; for 3 cases missing PBS data, a positive response to DIMS on the PSQ was used.14  At V2, 120 subjects were identified to have insomnia symptoms, defined as a self report of DIMS on the PSQ28  and/or sleep medication use; for 13 cases missing PSQ data, a parent report of often/moderate or very often/severe DIMS on the PBS was used.14,17,19  Only 1 subject was reclassified as having insomnia symptoms on the basis of their report of sleep medication use and mild DIMS. At S3, 214 subjects were identified as having insomnia symptoms, defined as a self report of “moderate” or “severe” DIMS and/or sleep medication use, on the basis of a structured questionnaire previously developed in the Penn State Adult Cohort.5,6  In addition, 62 subjects who self-reported moderate or severe to the question “Do you have insomnia?” were identified as having adult insomnia at S3. This question has demonstrated adequate reliability and validity in the Penn State Adult Cohort5,6  and further support for its validity in terms of moderate-to-severe daytime functioning impairment and greater nighttime sleep disturbance is shown in Supplemental Table 3. Thus, we use herein the term “insomnia symptoms” to refer to any presence of DIMS,46  and use the term “adult insomnia” to refer to the subset of subjects who specifically reported having insomnia at S3.

At V1 and V2, sleep was monitored with in-laboratory PSG1,2426  from the time of “lights out” (21:00–23:00) until “lights on” (06:00–08:00) to adjust, as much as possible, to the subject’s habitual sleep schedule with 9 hours of time in bed, and was scored according to standard criteria.30,31  Commensurate with previous studies, obstructive sleep apnea (OSA) was defined using pediatric criteria as an apnea hypopnea index of ≥2 per hour,14,25,26  periodic limb movements (PLMS) as a PLM index of ≥5 per hour,14,32,33  and OSSD as a total sleep time (TST) of <7.7 hours, the median of the cohort.14,17,18  This cut-off remains consistent with our previous studies14,17,18  and with other studies using actigraphy data, which provides a measure of habitual sleep duration.34,35 

At S3, all 502 subjects self-reported on their TST for weekdays and weekends. Habitual sleep duration was calculated with the formula: [(weekdays TST × 5) + (weekends TST × 2)]/7 days. Self-reported habitual sleep duration at S3 in the 502 subjects ranged from 3.5 to 11 hours with a mean of 7.1 hours (median = 7.3; IQR, 6.6–7.8).

Subjects and parents completed a standard questionnaire with demographic information at V1, V2, and S3, with information including date of birth, sex, race, and ethnicity, as well as any psychiatric or learning disorders and psychotropic medication use.24,25  At V1 and V2, height and weight were measured in the laboratory,24,25,29  BMI percentile for sex and age was calculated using standard growth curves, and the presence of overweight was defined as a BMI percentile ≥85%. At S3, subjects reported on their height and weight, self-reported BMI was calculated using the standard formula, and the presence of overweight was defined as a BMI ≥25.

Descriptive statistics were used to report the demographic characteristics of the overall sample (Table 1). Our analytic approach examined the transitional probabilities of insomnia symptoms, their developmental trajectories and, thereafter, the associated risk of adult insomnia.

TABLE 1

Demographic Characteristics of the Sample

V1 (n = 502)V2 (n = 333)S3 (n = 502)
Female sex 261 (52.0) 167 (50.2) 261 (52.0) 
Non-Hispanic White 389 (77.5) 258 (77.5) 389 (77.5) 
Age, y, mean (SD) 8.6 (1.7) 16.5 (2.2) 24.0 (2.6) 
Overweight 161 (32.1) 111 (33.3) 245 (49.2) 
Psychiatric/learning disorder 110 (21.9) 115 (34.5) 231 (46.0) 
Psychotropic medication 42 (8.4) 50 (15.0) 109 (21.7) 
OSSD 261 (52.0) 164 (49.2) n/a 
OSA 68 (13.5) 126 (37.8) n/a 
PLMS 18 (3.6) 78 (23.4) n/a 
Insomnia symptoms 118 (23.5) 120 (36.0) 214 (42.6) 
 Adult insomnia n/a n/a 62 (12.4) 
Length of follow-up    
 Since V1, y, mean (SD) — 7.8 (1.4) 14.9 (1.9) 
 Since V2, y, mean (SD) — — 6.9 (1.0) 
V1 (n = 502)V2 (n = 333)S3 (n = 502)
Female sex 261 (52.0) 167 (50.2) 261 (52.0) 
Non-Hispanic White 389 (77.5) 258 (77.5) 389 (77.5) 
Age, y, mean (SD) 8.6 (1.7) 16.5 (2.2) 24.0 (2.6) 
Overweight 161 (32.1) 111 (33.3) 245 (49.2) 
Psychiatric/learning disorder 110 (21.9) 115 (34.5) 231 (46.0) 
Psychotropic medication 42 (8.4) 50 (15.0) 109 (21.7) 
OSSD 261 (52.0) 164 (49.2) n/a 
OSA 68 (13.5) 126 (37.8) n/a 
PLMS 18 (3.6) 78 (23.4) n/a 
Insomnia symptoms 118 (23.5) 120 (36.0) 214 (42.6) 
 Adult insomnia n/a n/a 62 (12.4) 
Length of follow-up    
 Since V1, y, mean (SD) — 7.8 (1.4) 14.9 (1.9) 
 Since V2, y, mean (SD) — — 6.9 (1.0) 

All values provided as n (%) unless otherwise indicated. n/a, not available. —, not applicable

First, we examined the transitional probabilities of insomnia symptoms between each time point (ie, V1 to V2, V1 to S3, and V2 to S3) among the 502 subjects with V1 and S3 data and the 333 subjects with V1, V2, and S3 data.

Second, we estimated the developmental trajectories of insomnia symptoms among the 118 subjects with childhood insomnia symptoms (V1) and the developmental trajectories of normal sleep among the 384 subjects with normal sleep in childhood (V1). To fully use the data set, missing values for insomnia symptoms at V2 for 169 subjects were imputed on the basis of a logistic regression model built on the 333 subjects with complete data and under the missing-at-random assumption. The outcome of this regression model was the probability of insomnia symptoms at V2, and the predictors were insomnia symptoms at V1, insomnia symptoms at S3, and previously identified key risk factors (ie, sex, race and ethnicity, and psychiatric or learning disorders at V1).1,14  Multiple imputations were performed and the SD and IQR among the 1000 imputations for each trajectory are reported; demographics and trajectories based on complete data can be found in Supplemental Table 4 and Supplemental Fig 4.

Third, we examined the percentage of subjects with normal sleep and insomnia symptoms at V1 or V2 who worsened into adult insomnia at S3. Logistic regression models were used to test if insomnia symptoms at V1 or at V2 were associated with increased odds of adult insomnia at S3 among subjects with or without OSSD at V1 or V2, on the basis of previous findings in youth and adults.5,6,1721  Covariates considered for inclusion for adjustment included sex, race and ethnicity, age (V1 or V2), overweight (V1 or V2), OSA (V1 or V2), PLMS (V1 or V2), psychiatric or learning disorder (V1 or V2), psychotropic medication use (V1 or V2), self-reported habitual sleep duration (S3), and time to follow-up (ie, from V1 to S3 or from V2 to S3). Stepwise regression procedures were used to select a subset for inclusion in the final model.

Analyses were conducted using SPSS version 26 and R version 4.1.0. P values ≤.05 were considered statistically significant.

As shown in Table 1, there were no significant differences in the sex, race, or ethnicity distribution between the 502 subjects with V1 and S3 data and the subset of 333 subjects who also had V2 data. The mean age at each time point was commensurate with the developmental stages of childhood (V1), adolescence (V2), and young adulthood (S3).

The prevalence of insomnia symptoms at V1 (23.5%) and at V2 (36.0%) did not significantly deviate from our previous cross-sectional studies,1,14  whereas its prevalence at S3 (42.6%) was commensurate with that reported in other cross-sectional studies in young adults.2 

Table 2 presents the transitional probabilities of insomnia symptoms and normal sleep across all three time points. Among subjects with insomnia symptoms at V1, 53.7% persisted with insomnia symptoms at V2 and 61.9% did at S3, whereas 46.3% and 38.1% remitted during those periods. Among subjects with insomnia symptoms at V2, 57.5% persisted with insomnia symptoms at S3 and 42.5% remitted from insomnia symptoms at S3 (Table 2). A total of 44 subjects reported insomnia symptoms at both V1 and V2, of whom 81.8% persisted with insomnia symptoms at S3 and only 18.2% remitted by S3. Among the 38 subjects with insomnia symptoms at V1 who had remitted by V2, 60.5% remained remitted and 39.5% relapsed into insomnia symptoms at S3.

TABLE 2

Transitional Probabilities of Insomnia Symptoms from Childhood to Adolescence, from Childhood to Young Adulthood, and from Adolescence to Young Adulthood

V2OR (95% CI)S3OR (95% CI)
Insomnia SymptomsNormal SleepInsomnia SymptomsNormal Sleep
V1       
 Insomnia symptoms 53.7% (44/82) 46.3% (38/82) 2.67 (1.60-4.44) 61.9% (73/118) 38.1% (45/118) 2.80 (1.83-4.28) 
 Normal sleep 30.3% (76/251) 69.7% (175/251)  36.7% (141/384) 63.3% (243/384)  
V2       
 Insomnia symptoms — —  57.5% (69/120) 42.5% (51/120) 3.22 (2.02-5.14) 
 Normal sleep — —  29.6% (63/213) 70.4% (150/213)  
V2OR (95% CI)S3OR (95% CI)
Insomnia SymptomsNormal SleepInsomnia SymptomsNormal Sleep
V1       
 Insomnia symptoms 53.7% (44/82) 46.3% (38/82) 2.67 (1.60-4.44) 61.9% (73/118) 38.1% (45/118) 2.80 (1.83-4.28) 
 Normal sleep 30.3% (76/251) 69.7% (175/251)  36.7% (141/384) 63.3% (243/384)  
V2       
 Insomnia symptoms — —  57.5% (69/120) 42.5% (51/120) 3.22 (2.02-5.14) 
 Normal sleep — —  29.6% (63/213) 70.4% (150/213)  

Data are percentage (number of cases/denominator) for 502 children (V1) followed-up in young adulthood (S3), of whom 333 were also followed-up through adolescence (V2), as well as odds ratio and their 95% confidence interval. Results based on cases with complete data, odds ratio not adjusted for any covariates. CI, confidence interval; OR, odds ratio. —, not applicable

As shown in Fig 1A, among subjects with insomnia symptoms at V1 (n = 118), the most frequent predicted developmental trajectory was that of persistence (43.3% ± 1.6%, IQR, 42.4%–44.9% for 1000 imputations), followed by that of remission (26.9% ± 1.4%, IQR, 26.3%–28.0% since V1 and 11.2% ± 1.4%, IQR, 10.2%–11.9% since V2) and that of a waxing-and-waning pattern (18.6% ± 1.6%, IQR, 16.9%–19.5%).

FIGURE 1

Developmental trajectories of insomnia symptoms from childhood through adolescence and into young adulthood. Lines depict the eight potential trajectories and data are the percentage of each predicted trajectory among 118 subjects with insomnia symptoms in childhood (A) and among 384 subjects with normal sleep during childhood (B). Missing data for insomnia symptoms in adolescence (V2) in 169 subjects was imputed under the missing-at-random assumption on the basis of a logistic model with predictors for insomnia symptoms in childhood (V1); insomnia symptoms in young adulthood (S3); and sex, race and ethnicity, and psychiatric or learning disorders in childhood (V1).1,14  Multiple (1000) imputations were performed.

FIGURE 1

Developmental trajectories of insomnia symptoms from childhood through adolescence and into young adulthood. Lines depict the eight potential trajectories and data are the percentage of each predicted trajectory among 118 subjects with insomnia symptoms in childhood (A) and among 384 subjects with normal sleep during childhood (B). Missing data for insomnia symptoms in adolescence (V2) in 169 subjects was imputed under the missing-at-random assumption on the basis of a logistic model with predictors for insomnia symptoms in childhood (V1); insomnia symptoms in young adulthood (S3); and sex, race and ethnicity, and psychiatric or learning disorders in childhood (V1).1,14  Multiple (1000) imputations were performed.

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Among subjects with normal sleep at V1, 69.7% remained with normal sleep at V2 and 63.3% did at S3, whereas 30.3% and 36.7% developed insomnia symptoms during those transitional periods. Similarly, among subjects with normal sleep at V2, 70.4% remained with normal sleep at S3 and 29.6% developed insomnia symptoms at S3 (Table 2). A total of 175 subjects reported normal sleep at both V1 and V2, of whom 72.6% continued to report normal sleep and 27.4% developed insomnia symptoms at S3. Among the 76 subjects with normal sleep at V1 who had developed insomnia symptoms at V2, 43.4% persisted with insomnia symptoms and 56.6% remitted into normal sleep at S3.

As shown in Fig 1B, among subjects with normal sleep at V1 (n = 384), the most frequent predicted developmental trajectory was remaining a normal sleeper (48.1% ± 0.9%, IQR, 47.7%–48.7%), followed by newly developing insomnia symptoms at S3 (20.7% ± 1.0%, IQR, 20.0%–21.3%), a waxing-and-waning pattern (16.0% ± 1.0%, IQR, 15.4%–16.7), and persisting with insomnia symptoms since V2 into S3 (15.2% ± 0.9%, IQR, 14.6%–15.6%).

The prevalence of adult insomnia at S3 was 12.3% (n = 62). A total of 22.0% and 20.8% of subjects with insomnia symptoms at V1 or at V2, respectively, reported adult insomnia at S3, whereas only 9.4% and 6.6% of subjects with normal sleep at V1 or at V2, respectively, reported adult insomnia at S3 (both P < .001).

As shown in Fig 2, multivariable-adjusted regression models indicated that insomnia symptoms at V1 were associated with 2.6-fold significantly increased odds of adult insomnia at S3 among those with OSSD at V1 (P = .039), whereas insomnia symptoms at V2 were associated with 5.5-fold significantly increased odds of adult insomnia at S3 among those with OSSD at V2 (P = .001). The odds of adult insomnia at S3 associated with insomnia symptoms among those with normal sleep duration either at V1 (P = .265) or at V2 (P = .749) were not significantly increased.

FIGURE 2

Odds of adult insomnia in young adulthood associated with insomnia symptoms in childhood or adolescence: role of objective sleep duration. Data are multivariable-adjusted odds ratios (95% confidence interval) for the association of insomnia symptoms in childhood (V1) or adolescence (V2), with adult insomnia (S3) stratified by the presence of normal sleep duration (PSG-measured total sleep time ≥7.7 hours) and short sleep duration (PSG-measured total sleep time <7.7 hours) at each developmental stage. *P < .05. **P < .01

FIGURE 2

Odds of adult insomnia in young adulthood associated with insomnia symptoms in childhood or adolescence: role of objective sleep duration. Data are multivariable-adjusted odds ratios (95% confidence interval) for the association of insomnia symptoms in childhood (V1) or adolescence (V2), with adult insomnia (S3) stratified by the presence of normal sleep duration (PSG-measured total sleep time ≥7.7 hours) and short sleep duration (PSG-measured total sleep time <7.7 hours) at each developmental stage. *P < .05. **P < .01

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This is the first long-term cohort study to date to describe the developmental trajectories of childhood insomnia symptoms through young adulthood, as well as their evolution into adult insomnia by including PSG measures. The most common developmental trajectory for insomnia symptoms was that of persistence from childhood through young adulthood. Of those who persisted with childhood insomnia symptoms in the transition to adolescence, only 11% remitted by young adulthood. Additionally, nearly 20% of youth with insomnia symptoms worsened into adult insomnia, an incidence rate similar to adult studies with long follow-ups.4,5  The odds of insomnia symptoms worsening into adult insomnia were 2.6-fold and 5.5-fold among children and adolescents, respectively, who slept objectively short in the laboratory, although were not significantly increased among those who had normal sleep duration. Thus, these 15-year longitudinal findings across 3 developmental stages indicate that insomnia symptoms should not be expected to developmentally remit in at least 40% of children and that adolescence is a critical developmental period for the adverse prognosis of the insomnia with short sleep duration phenotype.

Previous longitudinal studies examining insomnia symptoms across developmental stages have predominantly relied on self- and parent reports.12,15,16  The current study used a combination of longitudinal parent- and self-reported data and in-laboratory PSG to determine the developmental trajectory of insomnia symptoms from childhood to young adulthood. Although the persistence of childhood insomnia symptoms has been reported at 30% to 56%,1416  a previous study found that remission, by early adolescence (26.2%) or by late adolescence (20.9%), was the most frequent trajectory of childhood insomnia symptoms, whereas 32.6% of children persisted with insomnia symptoms across adolescence.15  More recently, adolescent insomnia symptoms had a higher persistence rate (50%) in the transition to early adulthood.16  These seminal studies examined the transition from ages 7 to 9 through 11 to 13 into 16 to 19, restricting their findings to childhood and adolescence,15  or the transition from ages 16 to 18 to 22 to 25, limiting their findings to adolescence and young adulthood.16  The current study expanded upon this work by examining 3 developmental transitions and found that 27% of children with insomnia symptoms experience remission already in the transition to adolescence and confirms the high persistence (43%) and waxing-and-waning rates (18%) of insomnia symptoms using a within-subjects approach with longer follow-ups across these developmental stages.

Our novel data also indicated that PSG-measured short sleep, as typically assessed in sleep laboratories with fixed-time recordings, may be a useful assay for identifying youth with insomnia symptoms at greatest risk of worsening into adult insomnia, independent of OSA and PLMS. Previous studies have shown that youth who report insomnia symptoms and sleep objectively short differ from those with normal sleep duration in their association with neuroendocrine, inflammatory and cortical biomarkers, and adverse behavioral health outcomes.1721  However, we previously failed to demonstrate that children with OSSD were more likely to persist with insomnia symptoms in the transition to adolescence.14  Such finding suggested the persistence of childhood insomnia symptoms in the transition to adolescence is either mostly determined by behavioral factors18,3643  or by the strong homeostatic sleep drive present in children,44  which may preclude the expression of increased biological vulnerability during that developmental period.14  The current study indicates that the odds of worsening into adult insomnia were greatest (5.5-fold) in adolescents who reported insomnia symptoms and slept objectively short, adding to previous data on their increased inflammation, cortical hyperarousal and depression risk,1921  and role of OSSD in the evolution of insomnia symptoms into insomnia disorder.5  These findings suggest that adolescence is a critical period for expression of the greater vulnerability underlying insomnia with short sleep duration, a more biologically severe phenotype associated with an unremitting course and cardiovascular and neurocognitive risk in adults.22  Given that in-laboratory PSG is cumbersome and expensive, future studies should examine these associations using ambulatory PSG and/or actigraphy devices to obtain habitual estimates of sleep duration.34,35 

This study has several limitations. First, measures of OSSD, OSA, and PLMS were collected via 1-night, 9-hour PSG, which may be affected by the first-night effect and may not be representative of habitual sleep timing and duration at home; however, our methods are translatable to current clinical practice where pediatric sleep studies are typically performed in-laboratory with fixed-time recordings. Second, the lack of PSG measures at S3 precluded controlling or examining the role of objective sleep and its trajectory into adulthood and only self-reported habitual sleep duration could be controlled for at S3. Third, while we collected data on the presence of a complaint of adult insomnia at S3 by relying on a previously validated epidemiologic method,4549  its presence as per strict diagnostic criteria could not be ascertained at any time point with the available self-reported data.

This study unveiled that the chronicity of childhood-onset insomnia symptoms is greater than previously believed, indicating that 43% of children with insomnia symptoms persist through young adulthood. Furthermore, this study revealed that 20% of children with insomnia symptoms worsen into adult insomnia, and that this increased risk is very high (5.5-fold) among adolescents who sleep objectively short. Pediatricians should consider adolescence a critical period for the adverse prognosis of insomnia symptoms, particularly for the insomnia with short sleep duration phenotype. Early sleep interventions are a priority, as clinicians should not expect insomnia symptoms to developmentally remit in a high proportion of children, and objective sleep measures may be indicated in adolescence to identify those with poorer long-term prognosis.

We thank the staff at the Clinical Research Center of Penn State College of Medicine, where this study was performed.

Dr Fernandez-Mendoza conceptualized and designed the study, drafted the initial manuscript, reviewed and critically revised the manuscript for important intellectual content, collected data and contributed to data interpretation, supervised the statistical analyses, and acquired funding; Ms Ricci and Dr Lenker contributed to data acquisition, drafted the initial manuscript, and critically revised the manuscript for important intellectual content; Drs Bourchtein and Vgontzas interpreted the data and critically revised the manuscript for important intellectual content; Ms Qureshi contributed to data acquisition, drafted the initial manuscript, and critically revised the manuscript for important intellectual content; Drs Jiangang Liao and Duanping Liao and Mr. He conducted the statistical analyses, contributed to data interpretation, and critically revised the manuscript for important intellectual content; Drs Calhoun and Bixler contributed to data acquisition and data interpretation and critically revised the manuscript for important intellectual content; and all authors approved the final manuscript as submitted and agreed to be accountable for all aspects of the work.

FUNDING: Research in this article was supported in part by the National Heart, Lung, and Blood Institute, National Institute of Mental Health, and the National Center for Advancing Translational Sciences of the National Institutes of Health under award numbers R01HL136587 (Dr Fernandez-Mendoza), R01MH118308 (Dr Fernandez-Mendoza), R01HL097165 (Drs Bixler and D. Liao), R01HL063772 (Dr Bixler), and UL1TR000127 (Penn State University). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

     
  • DIMS

    difficulty initiating and/or maintaining sleep

  •  
  • IQR

    interquartile range

  •  
  • OSA

    obstructive sleep apnea

  •  
  • OSSD

    objective short sleep duration

  •  
  • PBS

    Pediatric Behavior Scale

  •  
  • PLMS

    periodic limb movements

  •  
  • PSG

    polysomnography

  •  
  • PSQ

    pediatric sleep questionnaire

  •  
  • S3

    survey 3

  •  
  • TST

    total sleep time

  •  
  • V1

    visit 1

  •  
  • V2

    visit 2

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Competing Interests

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