Results
Demographic and clinical characteristics
There was a significant difference between the three groups in age, F(3,354) = 6.62, p < 0.001. Both the ADHD group (M = 9.8, SD = 1.6 years) and the ASD group (M = 9.6, SD = 1.9 years) were significantly older than the control group (M = 8.7, SD = 2.1 years). A significant between-group difference was found in male:female ratio, with a nearly equal distribution within the control group (51.9% boys) and an overrepresentation of boys in the clinical groups (ADHD, 70.5% boys; ASD, 89.7% boys) (p < 0.001).
Results from the CBCL showed that the three groups differed significantly on the anxious/depressed scale, F(3,344) = 38.15, p < 0.001, internalizing problems, F(3,344) = 40.72, p < 0.001, externalizing problems, F(3,344) = 54.54, p < 0.001 and the Total Behavioral Problems score, F(3,344) = 87.69, p < 0.001. The Anxious/Depressed score was higher in ASD (7.69, SD = 5.04) than in ADHD (5.04, SD = 4.37) (p < 0.001), and both scores were higher than for controls (2.92, SD = 3.13), (both p < 0.001). The ASD group (M = 64.71, SD = 8.63) scored higher on internalizing problems than the ADHD group (M = 57.33, SD = 10.67) (p < 0.001), which scored higher than the control group (M = 50.19, SD = 10.48) (p < 0.001). The ADHD and ASD groups both showed higher scores for externalizing problems (ADHD, M = 62.91, SD = 11.15; ASD, M = 62.47, ASD = 10.24) and the total score of behavioral problems (ADHD, M = 64.30, SD = 8.59; ASD, M = 67.51, SD = 6.82), compared to the control group (externalizing, M = 48.76, SD = 9.47; Total, M = 50.10, SD = 9.63).
Group comparisons
Sleep problems
Significant between group differences were found for DIMS,
F(3,352) = 19.62,
p < 0.001, as well as for DA,
F(3,351) = 3.85,
p = 0.01, SWTD,
F(3,352) = 7.94,
p < 0.001, DES,
F(3,351) = 9.58,
p < 0.001, SHY,
F(3,352) = 4.18,
p < 0.01, and TSP,
F(3,352) = 19.15,
p < 0.001 (Table
2) (all analyses controlled for age and sex). For DA, the ASD group had a significant higher score than the control group. For DIMS, SWTD, DES, SHY, and TSP the ADHD group and the ASD group both had significantly higher scores than the control group. The ADHD and the ASD group did not differ significantly from each other.
Table 2
Differences in sleep problems between ADHD, ASD, and controls
DIMS | 11.05 (4.13) | 12.06 (3.69) | 8.74 (2.78) | ADHD and ASD > Control*** |
SBD | 4.20 (1.46) | 4.25 (1.69) | 3.98 (1.17) | NS |
DA | 4.02 (1.49) | 4.25 (1.52) | 3.70 (1.12) | ASD > Control** |
SWTD | 10.91 (4.01) | 10.62 (3.79) | 9.00 (2.59) | ADHD and ASD > Control*** |
DES | 9.00 (3.20) | 8.91 (2.73) | 7.44 (2.06) | ADHD and ASD > Control*** |
SHY | 3.75 (2.16) | 3.71 (1.94) | 2.97 (1.43) | ADHD > Control* and ASS > Control** |
TSP | 42.93 (10.99) | 43.74 (9.79) | 35.83 (7.22) | ADHD and ASD > Control*** |
Prevalencea
| 28 (63.6%) | 44 (64.7%) | 61 (25.1%) | ADHD and ASD > Control*** |
As for the total SDSC score (TSP), results showed that the ADHD group and the ASD group both had higher scores than the control group, F(3,352) = 15.84, p < 0.001, while the ADHD and ASD group did not differ significantly from each other. Further analyses of sleep problem prevalence rate (score >−39) showed that both the ADHD group (63.6%) and the ASD group (64.7%) had a higher prevalence of children with high sleep disturbance scores compared to controls (25.1%) (p < 0.001).
Sleep patterns
Group comparisons of bedtime, sleep onset latency, sleep onset time, awake time, and sleep duration during weekdays and weekends can be found in Table
3. On weekdays, sleep onset latency differed significantly between the three groups,
F(3,348) = 11.63,
p < 0.001, as well as sleep onset time,
F(3,348) = 5.00,
p < 0.001, awake time,
F(3,348) = 3.44,
p < 0.05, and sleep duration,
F(3,346) = 8.33,
p < 0.001 (all analyses controlled for age and sex). The ADHD group went to bed (20:36, SD = 0:44) significantly later than the control group (20:15, SD = 0:44) (
p < 0.05). The ASD group woke up (06:52, SD = 0:33) significantly earlier than the control group (07:03, SD = 0:24) (
p < 0.05). Sleep onset time was significantly later in ADHD (21:16, SD = 1:07) and ASD (21:04, SD = 0:55) compared to controls (20:35, SD = 0:48) (
p < 0.001). The ADHD group (584 min, SD = 65) and ASD group (588 min, SD = 54) both showed a significantly shorter sleep duration than the control group (628 min, SD = 48) (
p < 0.001). The ADHD group and the ASD group did not differ from each other on any of the sleep patterns (corrected for differences in age and sex).
Table 3
Differences in sleep patterns between ADHD, ASD, and controls
Week days |
Bedtime | 20:36 (0:44) | 20:30 (0:46) | 20:15 (0:44) | ADHD > Control* |
Sleep onset latency (min) | 40 (42) | 34 (26) | 20 (18) | ADHD and ASD > Control** |
Sleep onset time | 21:16 (1:07) | 21:04 (0:55) | 20:35 (0:48) | ADHD and ASD > Control** |
Awake time | 07:00 (0:31) | 06:52 (0:33) | 07:03 (0:24) | ASD < Control* |
Sleep duration (min) | 584 (65) | 588 (54) | 628 (48) | ADHD and ASD < Control** |
Weekends |
Bedtime | 21:17 (1:08) | 21:04 (1:03) | 21:03 (0:58) | NS |
Sleep onset latency (min) | 32 (20) | 28 (25) | 15 (14) | ADHD and ASD > Control** |
Sleep onset time | 21:49 (1:21) | 21:32 (1:05) | 21:18 (0:58) | ADHD > Control* |
Awake time | 07:38 (1:08) | 07:36 (1:11) | 07:54 (0:57) | NS |
Sleep duration (min) | 589 (58) | 604 (58) | 636 (51) | ADHD and ASD < Control** |
On weekends, sleep onset latency differed significantly for the three groups, F(3,348) = 5.50, p = 0.001, as well as sleep onset time, F(3,348) = 2.97, p < 0.05, and sleep duration, F(3,346) = 6.18, p < 0.001. SOL was significantly longer in the ADHD (32 min, SD = 20) and ASD group (28 min, SD = 25) than in the control group (15 min, SD = 14) (p < 0.001), while sleep duration was shorter in ADHD (589 min, SD = 58) and ASD (604 min, SD = 58) compared to controls (636 min, SD = 51) (p < 0.001). The ADHD group slept in significantly later (21:50, SD = 1:21) than the control group (21:18, SD = 0:58) (p < 0.05). There were no significant differences between the ADHD group and the ASD group.
Chronotype
Total CCTQ score did not differ significantly between the three groups, F(3,347) = 2.04, p = 0.11, after controlling for differences in age and sex: ADHD M = 27.85, SD = 7.37; ASD M = 27.99, SD = 6.79; controls M = 25.90, SD = 5.89.
Sleep hygiene and electronic media use
Sleep hygiene differed significantly between the three groups, F(3,347) = 7.21, p < 0.001, after adjustment for age and sex. The ADHD group (M = 52.53, SD = 10.19) and the ASD group (M = 50.33, SD = 9.46) both showed a significantly higher sleep hygiene score (i.e. worse sleep hygiene) than controls (M = 46.00, SD = 7.48). Group effects at item level are presented as Electronic Supplementary Material.
Group differences in total electronic media were borderline significant,
F(2,351) = 2.58,
p = 0.077. The control group showed a significantly more frequent use of electronic media before bedtime (
M = 12.21, SD = 3.45), than the ASD group (
M = 11.99, SD = 3.73) (
p = 0.024) (Table
4).
Table 4
Differences in social media use between ADHD, ASD, and controls
Before bedtime | 12.92 (3.97) | 11.99 (3.73) | 12.21 (3.45) | ASD < Control* |
In bed | 3.48 (1.83) | 3.13 (0.62) | 3.36 (1.45) | NS |
Total | 16.40 (5.18) | 15.12 (3.92) | 15.57 (4.26) | ASD < Control* |
Predicting sleep problems in ADHD, ASD and controls
Linear regression analyses were used to investigate the predictive value of chronotype, sleep hygiene, and electronic media use on sleep problems, over age and sex. As can be seen in Table
5, the second model in ADHD explained 28.6% of the variance [
R
2 = 0.286,
F(5,48) = 3.84,
p = 0.005]. In ADHD, evening chronotype of the child significantly predicted more sleep problems, Beta = 0.471,
p = 0.002. For ASD, the second model explained 15.6% of the variance [
R
2
= 0.156,
F(5,64) = 2.36,
p = 0.05]. Worse sleep hygiene predicted more sleep problems in ASD, Beta = 0.362,
p = 0.01. The second model for the typically developing controls explained 18.3% of the variance [
R
2 = 0.183,
F(5,232) = 10.4,
p < 0.001]. Results showed that evening chronotype, Beta = 0.317,
p < 0.001, inadequate sleep hygiene, Beta = 0.312,
p < 0.001, and electronic media use, Beta = 0.151,
p < 0.05, predicted more sleep problems in the controls.
Table 5
Hierarchical regression analysis for variables predicting sleep problems in ADHD, ASD, and controls
Age | −0.138 | 0.823 | −0.023 | −1.37 | 0.871 | −0.226 | −1.32 | 0.848 | −0.218 |
Sex | 4.96 | 2.87 | 0.235 | 0.144 | 2.85 | 0.007 | 0.136 | 2.74 | 0.006 |
Chronotype | | | | 0.615 | 0.185 | 0.471** | 0.638 | 0.188 | 0.488** |
Sleep hygiene | | | | 0.187 | 0.128 | 0.190 | 0.161 | 0.124 | 0.163 |
Electronic media | | | | −0.135 | 0.260 | −0.072 | −0.156 | 0.250 | −0.083 |
Anx/depr | | | | | | | 0.637 | 0.259 | 0.292* |
Chronotype × anx/depr | | | | | | | −0.006 | 0.036 | −0.023 |
R
2
| | 0.056 | | | 0.286 | | | 0.369 | |
F for change in R
2
| | 1.51 | | | 5.14** | | | 3.03 | |
Age | −0.612 | 0.647 | −0.117 | −0.646 | 0.699 | −0.123 | −0.574 | 0.686 | −0.110 |
Sex | 0.101 | 4.06 | 0.003 | 0.755 | 3.85 | 0.023 | 0.527 | 3.78 | 0.016 |
Chronotype | | | | 0.150 | 0.189 | 0.101 | 0.181 | 0.185 | 0.121 |
Sleep hygiene | | | | 0.379 | 0.142 | 0.362** | 0.174 | 0.174 | 0.166 |
Electronic media | | | | 0.278 | 0.355 | 0.111 | 0.293 | 0.354 | 0.117 |
Anx/depr | | | | | | | 0.416 | 0.262 | 0.208 |
Sleep hygiene × anx/depr | | | | | | | 0.022 | 0.024 | 0.154 |
R
2
| | 0.014 | | | 0.156 | | | 0.218 | |
F for change in R
2
| | 0.468 | | | 3.59* | | | 2.46 | |
Age | 0.157 | 0.224 | 0.046 | −0.434 | 0.273 | −0.127 | −0.599 | 0.256 | −0.175* |
Sex | −0.164 | 0.950 | −0.011 | −0.684 | 0.872 | −0.047 | −0.431 | 0.817 | −0.030 |
Chronotype | | | | 0.389 | 0.090 | 0.317** | 0.358 | 0.083 | 0.292** |
Sleep hygiene | | | | 0.307 | 0.065 | 0.312** | 0.201 | 0.070 | 0.204** |
Electronic media | | | | 0.253 | 0.124 | 0.151* | 0.129 | 0.129 | 0.077 |
Anx/depr | | | | | | | 0.886 | 0.137 | 0.382** |
Chronotype × anx/depr | | | | | | | −0.016 | 0.018 | −0.057 |
Sleep hygiene × anx/depr | | | | | | | 0.010 | 0.022 | 0.032 |
Electronic media × anx/depr | | | | | | | 0.005 | 0.034 | 0.010 |
R
2
| | 0.002 | | | 0.183 | | | 0.313 | |
F for change in R
2
| | 0.276 | | | 17.05** | | | 10.782** | |
Subsequent analyses in ADHD [model 3, R
2 = 0.369, F(7,46) = 3.84, p = 0.05] revealed a significant and positive main effect of chronotype, Beta = 0.488, p = 0.001, and anxiety/depression, Beta = 0.292, p = 0.018. There was no significant chronotype × anxiety/depression interaction in ADHD. Analyses for the ASD group showed neither a main effect of anxiety/depression, nor an interaction of sleep hygiene × anxiety/depression. In typically developing controls [model 3, R
2 = 0.313, F(9,228) = 11.52, p < 0.001], significant main effects were found for chronotype, Beta = 0.292, p < 0.001, sleep hygiene, Beta = 0.204, p = 0.004, and anxiety/depression, Beta = 0.382, p < 0.001, however, interaction effects of anxiety/depression with either chronotype, sleep hygiene, or electronic media use were not significant.
Discussion
This study aimed to compare sleep problems and sleep patterns of children with ADHD, ASD, and typically developing controls, and to investigate within those groups the association of sleep problems with sleep hygiene and chronotype. As expected we found significant differences in sleep patterns between both clinical groups and the typically developing controls. Sleep onset during weekdays was around 30–45 min later in ADHD and ASD than in controls. ASD youth woke up earlier than controls despite a later sleep onset time, which is in line with previous reports of frequent early morning awakenings [
48], but which contradicts findings in other studies [
6]. Whether the early rise times are due to biological differences in sleep patterns and/or environmental constraints on sleep related to the diagnosis (e.g., awoken earlier to allow more time for morning routines) remains unknown. Sleep duration was significantly shorter—around 45 min—in ADHD and ASD compared to controls. Along this line, parents indicated that children with ADHD and ASD both suffered more frequently than controls from sleep problems. That was the case for all types of sleep problems in our study, except for sleep breathing disorders. Furthermore, disorders of arousal were more prevalent in ASD, but not in ADHD, compared to controls. Importantly, sleep problems were present in nearly two-third of the children with ADHD (64%) and ASD (65%), compared to 25% in controls. Those high prevalence rates correspond to previous findings [
5,
6], and underline the importance of this issue in ADHD and ASD. Importantly, we found no differences in sleep patterns or sleep problems between the clinical groups. Thus, our results demonstrate that both psychiatric disorders are characterized by equally high prevalence rates and a broad spectrum of sleep problems.
As for the prediction of sleep problems, we found that sleep disturbances were differentially predicted by eveningness and sleep hygiene within the various groups. As expected, in normal controls both eveningness and sleep hygiene were associated with sleep disturbances. However, sleep disturbances in children with ADHD were only related to increased eveningness and not to sleep hygiene. Moreover, eveningness was of more predictive value for sleep problems in ADHD than in typically developing controls. That is in line with our hypotheses, since eveningness is associated with circadian rhythm markers [
49,
50], and those markers have been found delayed in ADHD [
15,
34,
51]. Furthermore, genetic studies showed Clock gene aberrances in ADHD [
52,
53] and an absence of rhythmic expression in BMAL1 and PER2 clock gene products [
15]. Higher prevalence rates of evening chronotype were also previously found in childhood ADHD [
20] and adult ADHD [
15‐
17]. Intriguingly, although we were able to replicate the association of sleep problems with increased eveningness in ADHD, and although sleep onset was delayed in ADHD, we did not find differences in chronotype scores between ADHD, ASD, and controls. It remains unknown how a delayed sleep onset in ADHD can be reconciled with the lack of chronotype findings. Possibly, delayed sleep onset was due to behavior differences in ADHD versus controls such as bedtime resistance [
54], limit-setting problems or inadequate enforcement of bedtimes by caregivers [
55], or staying up later due to finishing homework that took longer because of distractibility, rather than biological rhythm differences.
As for sleep hygiene, our results were in line with earlier findings in ADHD. Van der Heijden and colleagues [
47] showed that children with ADHD and sleep onset insomnia did not differ in sleep hygiene from children with ADHD without sleep disturbances. Although the current data revealed no significant prediction of sleep problems by sleep hygiene in ADHD, we did find a reduced sleep hygiene level in ADHD compared to controls. This suggests that poorer levels of sleep hygiene in families with ADHD might be an epiphenomenon of a disorganized home environment, partly resulting from parental problems with inhibition of impulses, sustained attention, and consistency [
56]. Another explanation is that the effects of sleep hygiene in ADHD are masked or suppressed by eveningness. In other words, because of the detrimental effects of chronotype on sleep problems in ADHD, the additional effects of inadequate sleep hygiene might appear insignificant.
As expected, and consistent with previous findings, higher levels of anxiety and depression problems predicted more sleep problems both in ADHD and in typically developing controls [
38]. The negative effect of eveningness on sleep problems in ADHD was not moderated by anxiety and depression problems. In other words, the findings demonstrate that evening types among children with ADHD have a higher risk of sleep problems, irrespective of the presence of comorbid anxiety and depression problems. Similarly, the results showed that the negative effects of evening chronotype and inadequate sleep hygiene in typically developing controls were not moderated by anxiety and depression problems. Interestingly, sleep problems in ASD were not associated with anxiety and depression problems. A possible explanation is that a relatively strong positive association of sleep hygiene with anxiety/depression in ASD (
r = 0.34,
p = 0.002), led to a mutually diminishing effect in the final model. A recent study demonstrated a contradicting finding that children with ASD and comorbid anxiety were particularly predisposed to sleep problems [
57]. More future research on the interplay of sleep hygiene, anxiety/depression, and sleep disturbances in ASD is needed.
As for ASD, the results revealed that sleep problems were not related to eveningness and that there were no differences in eveningness scores between ASD and normal controls. Those results indicate that although ASD might be associated with disturbances in melatonin production and rhythm [
24], those melatonin disturbances may not affect sleep wake rhythm. That is in accordance with a recent study showing that children with ASD and insomnia who were responsive to a low dose of melatonin had relatively normal profiles of baseline endogenous melatonin and normal pharmacokinetic melatonin profiles after supplemental melatonin administration [
26]. Thus, apparently, melatonin did not improve sleep problems in ASD through replacing endogenous melatonin or acting on the circadian system. It remains unknown what the behavioral correlates of the endogenous melatonin disturbances in ASD are, but evidence suggests that sleep problems in ASD are not associated with a delayed circadian system, but might be due to an inadequate sleep hygiene. Sleep hygiene intervention studies in the ASD population are scarce so far [
36], however the current findings suggest that sleep hygiene improvement might be an effective intervention strategy in children with ASD. Nevertheless, the results showed that negative effects of inadequate sleep hygiene disappeared when the predictive model included anxiety and depressive problems. This contradicts the possible role of sleep hygiene, and emphasizes the importance for future studies to control for anxiety and depressive problems.
There was a significant association of access to electronic media with sleep problems in typically developing controls, but there were no significant differences in electronic media use between the psychiatric populations and the typically developing children, except for a more frequent use of electronic media before bedtime in the control group compared to the ASD group. Previous studies in children have found a frequent use of electronic media, particularly in ASD, and demonstrated associations of sleep and media use in ADHD, ASD and typically developing children [
32,
33], however, those studies were conducted in adolescents. Of note, there are recent suggestions of a higher sensitivity for light in the ADHD population which might impact on the circadian system and therefore affect sleep wake rhythm [
58]. We conclude that electronic media use might play a significant role in the etiology of sleep problems in elementary school aged children, however, more research is needed in children with ADHD and ASD.
There are several methodological strengths of this study. The inclusion of both an ADHD and ASD group enabled a comparison of clinical groups which provided the possibility to infer about the specificity of the various findings. As our data demonstrated, predictors of sleep problems varied for the different clinical and nonclinical groups. Other strengths are the diagnostic procedures of ADHD and ASD which were carried out by trained psychologists and psychiatrists according to DSM-IV and based on multidisciplinary consultation. Furthermore, well validated instruments were used to assess sleep, eveningness, and sleep hygiene.
However, our study also has several limitations. First, assessments were based on subjective parent reports. Although the instruments are well validated and commonly used in research, objective assessments of behavioral problems, sleep, and chronotype would have strengthened our findings. For instance, the assessment of electronic media use took place through parent report, however we cannot assure that parents were fully aware of the use of electronic media in bed by their children. Objective registration of electronic media use was not feasible in the current study, but is recommended for future studies. Furthermore, assessments of chronotype by means of objective measures such as actigraphy or dim light melatonin onset would have strengthened our study.
Second, this study includes only one single assessment. In order to infer conclusions about the etiological role of sleep hygiene and chronotype long term cohort studies are required. Third, we assessed chronotype through a questionnaire which usually shows high correspondence with objective circadian measures such as with endogenous melatonin, cortisol, or body temperature [
59], however, the measures are not interchangeable. Where markers of circadian rhythm inform about the time of the circadian system, chronotype reflects the subjective individual experience of circadian preference and includes also the impact on daily life. The subjective nature of this measure therefore entails high ecological validity, but also requires caution as to conclusions about circadian disturbances. Fourth, we cannot exclude with certainty the presence of ADHD or ASD in the typically developing control group. Although 4.5% of the control group was excluded based on parental reports of a diagnosis of ADHD, and 3% of ASD, it is possible that there were children with ADHD or ASD in the control group who had not been formally assessed or diagnosed previously. A rigorous screening procedure with validated instruments would have provided more certainty that all children in the control group were indeed ‘typically developing’.
Finally, we cannot exclude the influence of medication use on the findings. Psychostimulants exert a negative effect on sleep and circadian rhythms [
12], although this cannot explain the absence of differences in chronotype in the present study. Possibly, deteriorating effects on sleep and circadian rhythm taking place after commencement with stimulants were opposed by alleviating effects of melatonin treatment started because of the sleep disturbances.
To conclude, this study aimed to shed light on the potential role of chronotype and sleep hygiene in the etiology of sleep problems in ADHD, ASD and typical developing children. The study shows that both chronotype and sleep hygiene are associated with sleep problems in typically developing children, whereas in children with ADHD sleep problems are related to chronotype and in children with ASD only to inadequate sleep hygiene. Furthermore, the deteriorating role of anxiety and depressive problems in childhood sleep problems was corroborated in this study, however, negative effects of evening chronotype and inadequate sleep hygiene were not moderated by the presence of anxiety or depression.
The findings have implications for the clinical field since they corroborate that intervention and prevention programs of sleep disturbances should be tailored to different psychiatric diagnoses. As this study reveals, treatment strategies in ASD should contain a strong focus on sleep hygiene improvements, while interventions in ADHD should include methods to shift circadian preference, such as bedtime fading [
60,
61], melatonin treatment [
62], or early morning light therapy [
63]. We do not suggest that sleep hygiene improvements are not relevant for children with ADHD. Individuals with ADHD who present with inadequate sleep hygiene might certainly profit from sleep hygiene improvements. This is particularly relevant since a great deal of children with ADHD have traits of ASD and vice versa. Sleep hygiene interventions should always be the first step in the management of sleep disturbances. Also, certain aspects of sleep hygiene interventions, such as a reduction of bright light in the late evening or avoidance of sleeping in over weekends, can have beneficial (phase-advancing) effects on evening chronotypes. Similarly, methods to shift circadian preference should be considered in children with ASD and traits of ADHD, particularly when sleep hygiene interventions do not seem to be sufficiently effective. Further replication studies are necessary to validate the findings of this association study.