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Introduction

Sleep problems are increasingly recognized as a significant health concern among youth, with insufficient sleep affecting the majority of adolescents worldwide. Emerging research challenges the traditional view that sleep disturbances are merely symptoms of underlying mental disorders, suggesting instead a bidirectional relationship where sleep issues may also contribute to the development of psychopathology. Despite this growing evidence in adults, the role of sleep disturbances as predictors of mental illness in children and adolescents remains inconclusive. 

Aim

This study aims to systematically review and synthesize existing research to better understand how sleep problems in children and adolescents may predict future mental health issues.

Methods

* Conducted per PRISMA and SYMBALS guidelines, combining active learning machine learning and backwards snowballing.

* Titles and abstracts were screened by multiple authors using ASReview software.

* The databases Embase, MEDLINE, Web of Science and PsychINFO were searched. * Inclusion criteria: Primary studies in English language, Participants 0-18 years at baseline, Sleep disturbance as exposure, Mental illness (diagnosis or symptoms) as outcome, Longitudinal studies with at least 1 month between timepoints.

Results

A total of 136* studies were eligible for inclusion in the systematic review, published between 2000 and 2024.

Of these, 63 concerned adolescents at baseline, 45 school-aged children, and 28 concerned infants, toddlers and pre-school children. 

Some 46 of the studies concerned the broader construct Internalising symptoms, encompassing both depression and anxiety. A total of 59 studies concerned depression as outcome, 26 studies anxiety, 18 studies ADHD, 5 studies GAD, 5 studies social anxiety, 5 studies separation anxiety, and 4 studies psychosis. Rarer outcomes included panic disorder, PTSD, borderline personality disorder, oppositional defiant disorder, mania, OCD, and bipolar disorder. 

A significant association was found in 153 of the analyses (81.8 %), while 34 (18.2 %) did not. The most studied outcome was depression, where 50 studies found an association and 9 did not, followed by internalising symptoms (45 yes, 1 no) and anxiety (24 yes, 2 no). Several additional outcomes were studied, demonstrating more ambiguous results. The information is depicted in Figure 1. 

Conclusions

The preliminary results of this study provide convincing evidence that sleep problems predict later mental illness in children and adolescents: primarily regarding internalising symptoms, anxiety and depression, with more equivocal evidence regarding ADHD, psychosis, GAD, social anxiety and separation anxiety. The majority of studies concern adolescents. More studies on specific mental disorders beyond depression and anxiety are needed.

OBJECTIVES: The purpose of this longitudinal investigation was to examine the association between emotion regulation and future insomnia (incidence and persistence).

DESIGN: A longitudinal study in the general population.

METHODS: A survey was sent out to 5,000 individuals in the community. To those who returned the baseline questionnaire (n = 2,333), two follow-up surveys, 6 and 18 months later, were sent out and then completed by 1,887 and 1,795 individuals, respectively. The survey contained information about demographic factors, insomnia symptomatology, the Difficulties in Emotion Regulation Scale, anxiety, and depression.

RESULTS: The findings suggested that emotion regulation at baseline was not associated with the incidence or persistence of insomnia. Overall, the effect sizes were very small to medium. When examining changes in emotion regulation over time, a different pattern emerged. Partial support was established for the notion that decreases in emotion regulation were related to incident and persistent insomnia, as a decrease in emotion regulation was associated with a higher likelihood of future insomnia. Yet, the effect sizes were very small to small.

CONCLUSION: This study does partly point towards a longitudinal association between emotion dysregulation and insomnia. This might have implications for the conceptualization and management of insomnia as well as for future research.

Statement of contribution:

What is already known on this subject?

• Previous research has indicated that emotion dysregulation might be enhanced in patients with insomnia.
• A number of limitations have however hindered progress in understanding how emotion dysregulation is related to insomnia, such as limited research on the topic and relying solely on cross-sectional data.

What does this study add?

• The current investigation showed that emotion dysregulation is a risk factor for the development of incident and persistent insomnia.
• This study also shows that increased emotion dysregulation over time heightens the risk of incident and persistent insomnia.

The purpose with the investigation was to examine whether improvements in pre-sleep cognitive arousal, unhelpful beliefs about sleep, and maladaptive sleep behaviors mediate the outcomes in in-person CBT-I. Fifty-eight participants with insomnia were administered either cognitive behavioral therapy or belonged to a waitlist. At pre- and post-treatment, participants completed questionnaires and sleep diaries assessing cognitive arousal, unhelpful beliefs about sleep, maladaptive sleep behaviors, insomnia severity, dysfunction, and subjective sleep parameters. Outcome measures were re-administered at a 3-month follow-up. Decreases in cognitive arousal mediated the effect on dysfunction. Reductions in unhelpful beliefs mediated the treatment effect on insomnia severity and dysfunction. Decreases in bedtime variability mediated the outcome on insomnia severity, and reductions in time in bed had a mediating effect on total wake time. Neither rise time variability nor napping mediated the improvements. A reversed model, in which the outcomes were used as mediators, showed less fit with the current data, indicating that change in the psychological processes as mediators of improvement in the outcomes was the most plausible conclusion. These findings are clearly supportive of cognitive-behavioral models of insomnia by highlighting cognitive arousal, unhelpful beliefs about sleep, and maladaptive sleep behaviors as mediators in the treatment of insomnia. The results are also important for clinical work and for testing new approaches in future research.

Aim: To investigate the effects of group CBT for insomnia (CBT-I) on insomnia and depressive symptomatology in a comorbid sample through a randomised controlled trial with a 6 month follow-up.

Methods: 64 participants were recruited through advertisements and randomised to receive CBT-I or an active control (relaxation training: RT) during four group sessions. Insomnia Severity Index and BDI-II were the primary outcome measures, assessed pre-treatment, post-treatment and at 6 month follow-up. Insomnia and depressive diagnoses, and functional impairment were assessed before and after treatment, whereas sleep diary data was gathered continuously from one week before treatment until after treatment.

Results: CBT-I was more efficient than RT in reducing insomnia severity and equally effective in reducing depressive symptoms, although CBT-I was associated with a higher proportion of remitted persons than RT, regarding both insomnia and depression diagnoses. Also, CBT-I was associated with less functional impairment, shorter sleep onset latency and wake after sleep onset but both treatments had equal improvements of sleep quality, early morning awakenings and total sleep time.

Conclusion: Group CBT-I is an efficient form of insomnia-treatment for people with insomnia comorbid with depressive symptomatology. The mixed results regarding depression outcomes warrants replication and further studies into treatment mechanisms. (C) 2015 Elsevier Ltd. All rights reserved.

Aim: Insomnia is a common health problem that affects about 10% of the population. The purpose of this investigation was to examine the association between cognitive processes and the persistence and remission from insomnia in the general population.

Methods: In a longitudinal design, 2333 participants completed a survey on night time and daytime symptoms, and cognitive processes. Follow-up surveys were sent out six months and 18 months after the first assessment. Participants were categorised as having persistent insomnia, being in remission from insomnia or being a normal sleeper.

Results: Cognitive processes distinguished between people with persistent insomnia and normal sleepers. Specifically, worry, dysfunctional beliefs, somatic arousal, selective attention and monitoring, and safety behaviours increased the likelihood of reporting persistent insomnia rather than normal sleep. For people with insomnia, more worry about sleep at baseline predicted persistent insomnia but not remission later on. Lower selective attention and monitoring, and use of safety behaviours over time increased the likelihood of remission from insomnia. In general, these results remained, when psychiatric symptoms and medical complaints were added to the models.

Conclusions: The findings support that certain cognitive processes may be associated with persistence and remission of insomnia. Clinical implications are discussed.

Background: Dysfunction is an integral part of chronic insomnia. Despite this, very little effort has yet been made to design and psychometrically validate an insomnia-specific measure of dysfunction.

Aims: The purpose was to examine the psychometric properties of the Work and Social Adjustment Scale (WSAS) as a measure of dysfunction in chronic insomnia.

Method: Seventy-three patients with chronic insomnia from three subsamples participated. All the patients completed the WSAS, the Insomnia Severity Index (ISI), and sleep diaries over one week.

Results: An exploratory factor analysis suggested a one-factor solution for the WSAS, determining dysfunction, accounting for 73.7% of the variance. The internal consistency of the WSAS was α = .91. The test-retest reliability for the WSAS items was high at .90-.99 and for the entire scale .99. A cut-off at 17 points was established, discriminating those with subclinical versus moderate or severe clinical insomnia (88% sensitivity and 78% specificity). Evidence of convergent and criterion validity was documented via (1) a significant, positive association between the WSAS and ISI and (2) a higher WSAS score among those with severe clinical insomnia, relative to those with moderate clinical and subthreshold insomnia, as well as a higher WSAS score among those with moderate clinical insomnia relative to those with subthreshold insomnia. The WSAS was also shown to be a treatment-sensitive measure for insomnia patients.

Conclusions: The WSAS appears as a reliable and valid measure of dysfunction in chronic insomnia. Additional advantages are its shortness, easiness, and treatment-sensitivity.