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Background: Insomnia and eveningness are common and often comorbid conditions in youths. While cognitive behavioural therapy for insomnia (CBT-I) has been suggested as a promising intervention, it remains unclear whether it is sufficient to also address circadian issues in youths. In addition, despite that light has been shown to be effective in phase-shifting one's circadian rhythm, there has been limited data on the effects of bright light therapy and its combination with CBT-I on sleep and circadian outcomes in youths. The current protocol outlines a randomised controlled trial that examines the efficacy of CBT-I and CBT-I plus bright light therapy (BLT) in reducing insomnia severity, improving mood symptoms and daytime functioning (e.g. sleepiness, fatigue, cognitive function), and improving subjective and objective sleep and circadian measures compared to a waitlist control group., Methods: We will carry out a randomised controlled trial (RCT) with 150 youths aged 12-24 who meet the criteria of insomnia and eveningness. Participants will be randomised into one of three groups: CBT-I with bright light therapy, CBT-I with placebo light, and waitlist control. Six sessions of CBT-I will be delivered in a group format, while participants will be currently asked to use a portable light device for 30 min daily immediately after awakening throughout the intervention period for bright light therapy. The CBT-I with light therapy group will receive bright constant green light (506 lx) while the CBT-I with placebo light group will receive the modified light device with the LEDs emitting less than 10 lx. All participants will be assessed at baseline and post-treatment, while the two active treatment groups will be additionally followed up at 1 month and 6 months post-intervention. The primary outcome will be insomnia severity, as measured by the Insomnia Severity Index. Secondary outcomes include self-reported mood, circadian, daytime functioning, and quality of life measures, as well as sleep parameters derived from actigraphy and sleep diary and neurocognitive assessments. Objective measures of the circadian phase using dim-light melatonin onset assessment and sleep parameters using polysomnography will also be included as the secondary outcomes., Discussion: This study will be the first RCT to directly compare the effects of CBT-I and BLT in youths with insomnia and eveningness. Findings from the study will provide evidence to inform the clinical management of insomnia problems and eveningness in youths., Trial Registration: ClinicalTrials.gov NCT04256915. Registered on 5 February 2020., (© 2024. The Author(s).)

Circadian dysregulation and depressed mood commonly co-occur in young people, yet mechanisms linking Delayed Sleep-Wake Phase disorder (DSWPD) with depression are poorly understood. The present study aimed to examine the role of repetitive negative thinking (RNT), by comparing sleep, RNT and depressive symptomology between 40 'good' sleeping young people and 63 with DSWPD, with (n = 30) and without (n = 33) self-reported doctor-diagnosed depression. Secondary analysis from a randomised controlled trial was also undertaken to observe changes in depressive symptoms and RNT as a result of treatment for DSWPD. The 60 young people with DSWPD (mean [SD] age of 15.9 [2.2] years, 63% female) received either short (green) or long (red) wavelength bright light therapy (BLT) over 3 weeks. Cross-sectional baseline comparisons revealed an escalating pattern of worse sleep, more RNT and higher depressed mood scores in the DSWPD young people compared to good sleepers. Across all participants, RNT accounted for the associations between sleep-onset difficulties and depressed mood at baseline. Symptoms of depression, RNT and sleep onset difficulties in DSWPD individuals significantly improved after treatment (d = 0.47-0.65) and at the 1- (d = 0.43-1.00) and 3-month follow-up (d = 0.39-1.38), yet there were no differences between short- and long-wavelength BLT. Results provide preliminary evidence that RNT may link delayed sleep phase with depression. BLT conferred sleep benefits, but also improvements in depressed mood and RNT, and thus represents a potentially cost-effective strategy for young people experiencing delayed sleep phase and low mood., (© 2021 European Sleep Research Society.)

Background: Delayed sleep-wake phase disorder (DSWPD) during adolescence has been linked to impaired health and poor functioning. However there is a dearth of knowledge about DSWPD in young adulthood. We seek to contribute knowledge on the prevalence and correlates of DSWPD in this age group., Methods: Data were drawn from a 2018 national survey of students in higher education in Norway (the SHoT-study). All 162,512 fulltime students in Norway were invited to participate and 50,054 students (69.1% women) aged 18-35 years were included (response rate = 30.8%). DSWPD was assessed by self-report, and was operationalized according to the criteria for DSWPD in the most recent edition of the International Classification of Sleep Disorders. Correlates of DSWPD were examined by validated self-report instruments covering a wide range of demographic and health domains., Results: The overall prevalence of DSWPD was 3.3%, and significantly higher in male (4.7%) than female (2.7%) students. DSWPD was associated with being single, having financial difficulties, having divorced parents, being overweight/obese, and physical inactivity. Students with DSWPD had more sleep problems during weekdays, and higher levels of somatic and mental health problems. Students with DSWPD also had an elevated risk of self-harm-related thoughts and behaviors as well as suicidality., Conclusion: DSWPD remains a significant problem among young adults, and the high symptom load across health domains indicates that suggests a need for existing evidence-based approaches to be scaled for college students who present with DSWPD., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Difficult early morning awakening is one of the defining symptoms of delayed sleep-wake phase disorder. It is accompanied by low cognitive arousal and drowsiness resulting in difficulty concentrating and focusing attention upon awakening. We designed the current study to quantitate cognitive performance (i.e. omissions, commissions, reaction time [average and variability]) and cognitive domains (i.e. focused attention, sustained attention, impulsivity and vigilance) with Conners' Continuous Performance Test II during both habitual and conventional (00:00-07:00 hr) sleep-wake schedule in young adult patients with delayed sleep-wake phase disorder (n = 20, mean age = 24.8 years, SD = 3.0) and controls (n = 16, mean age = 24.4 years, SD = 3.4). Conners' Continuous Performance Test II was administered after awakening and in the afternoon during both habitual and conventional conditions. In-laboratory polysomnography was performed for 2 nights. We assessed sleep, tiredness, chronotype and depression using questionnaires. Saliva was sampled for dim light melatonin onset measurements. Repeated-measures ANOVAs were applied for the Conners' Continuous Performance Test II measures with group (patient/control), time (afternoon/morning) and condition (habitual/conventional schedule) as fixed factors. Patients with delayed sleep-wake phase disorder had reduced reaction times, especially in the morning, greater response speed variability, and made more omission and commission errors compared with controls. Patients with delayed sleep-wake phase disorder also had reduced focused attention, especially upon forced early awakening. The short total sleep time of patients with delayed sleep-wake phase disorder could not statistically explain this outcome. In conclusion, we observed a state-dependent reduced ability to focus attention upon early morning awakening in patients with delayed sleep-wake phase disorder. Patients also had more omissions, longer reaction time and increased RT variability after habitual sleep, suggesting a possible small cognitive trait dysfunction in delayed sleep-wake phase disorder., (© 2018 European Sleep Research Society.)

Objectives: Recent evidence indicates that adolescents' motivation to change sleep-wake patterns is low, despite significant impact of adolescent sleep problems on many areas of daytime functioning. The aim of the present study is to evaluate components of adolescents' motivation, and subsequent changes in behaviour., Methods: Fifty-six adolescents, aged 13-23 (M = 15.8 ± 2.3 y; 38% m) diagnosed with Delayed Sleep-Wake Phase Disorder (DSWPD) underwent three therapy sessions involving bright light therapy to phase advance sleep patterns. Adolescents were instructed to advance wake-up times by 30-min daily. Motivation ratings of desire, ability, reason, need and commitment to change sleep patterns were taken at baseline. Sleep diaries were taken at the end of treatment session 1, with sequentially earlier wake-up times in 30-min intervals indicating compliance., Results: At the outset of therapy, adolescents indicated strong desire, reasons and need, yet moderate ability and commitment to advance their sleep-wake patterns. Following therapy, sleep-onset times were significantly advanced, total sleep time increased and sleep latency decreased (all p < 0.05). Therapy lasted 6-27 days (M = 13.9 ± 4.5) and clients complied for approximately half the time (between 3 and 15 days; M = 8.8 ± 2.7). Commitment was associated with ability (r = 0.66, p < 0.001) but not desire, reason or need (all p > 0.05). Adolescents' desire to change (r = 0.30, p = 0.03) and commitment (r = 0.30, p = 0.03) were positively correlated with behaviour change, but their need, ability and reasons were not. A mediation analysis showed that ability and desire were important in predicting behaviour change, by total effects through commitment (ie, indirectly and directly)., Conclusion: Our findings suggest that the total effects of ability (ie, confidence) and desire to change are the best predictors of behavioural changes, thus clinicians should focus on these components of the readiness to change model when undertaking treatments with sleep-disordered adolescents., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Objective: To systematically investigate whether cognitive "insomnia" processes are implicated in adolescent Delayed Sleep-Wake Phase Disorder (DSWPD) and to examine whether these processes are responsive to chronobiological treatment., Method: Sixty-three adolescents (M = 15.8 ± 2.2 years, 63.5% f) diagnosed with DSWPD and 40 good sleeping adolescents (M = 15.9 ± 2.4 years, 75% f) completed baseline measures of sleep, daytime functioning and cognitive "insomnia" processes (i.e., repetitive negative thinking, physiological hyperarousal, distress, sleep-related attention and monitoring, sleep misperception). Sixty DSWPD adolescents (M = 15.9 ± 2.2 y, 63% f) entered a treatment trial and received 3 weeks of light therapy. Sleep, daytime functioning, and insomnia were measured again post-treatment and at 3-month follow-up., Results: Adolescents with DSWPD had significantly later sleep timing (d = 0.99-1.50), longer sleep latency (d = 1.14), and shorter total sleep time (d = 0.85) on school nights, compared with the good sleeping adolescents. There was evidence of cognitive "insomnia" symptoms, with the DSWPD group reporting more repetitive negative thinking (d = 0.70-1.02), trait hyperarousal (d = 0.55), distress (d = 2.19), sleep associated monitoring (d = 0.76), and sleep onset misperception (d = 1.29). Across treatment and follow-up, adolescents with DSWPD reported advanced sleep timing (d = 0.54-0.62), reduced sleep latency (d = 0.53), increased total sleep time (d = 0.49), and improved daytime functioning (d = 0.46-1.00). Repetitive negative thinking (d = 0.64-0.96), physiological arousal (d = 0.69), distress (d = 0.87), and sleep onset misperception (d = 0.37) also showed improvement., Conclusions: Cognitive "insomnia" processes may be implicated in the development and maintenance of DSWPD in adolescents. Many of these processes are amendable to chronobiological treatment; however, residual symptoms may place adolescents at risk of poor treatment outcome or relapse. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

A randomised controlled trial evaluated bright light therapy and morning activity for the treatment of Delayed Sleep-Wake Phase Disorder (DSWPD) in young people. 60 adolescents and young adults (range = 13-24 years, mean = 15.9 ± 2.2 y, 63% f) diagnosed with DSWPD were randomised to receive three weeks of post-awakening Green Bright Light Therapy (∼507 nm) and Sedentary Activity (sitting, watching TV), Green Bright Light Therapy and Morning Activity (standing, playing motion-sensing videogame), Red Light Therapy (∼643 nm) and Sedentary Activity or Red Light Therapy and Morning Activity. Sleep (ie sleep onset time, wake up time, sleep onset latency, total sleep time) and daytime functioning (ie morning alertness, daytime sleepiness, fatigue, functional impairment) were measured pre-treatment, post-treatment and at one and three month follow-up. Contrary to predictions, there were no significant differences in outcomes between treatment groups; and interaction effects between treatment group and time for all outcome variables were not statistically significant. However, adolescents and young adults in morning activity conditions did not meaningfully increase their objective activity (ie movement frequency). Overall, adolescents reported significantly improved sleep timing (d = 0.30-0.46), sleep onset latency (d = 0.32) and daytime functioning (d = 0.45-0.87) post-treatment. Improvements in sleep timing (d = 0.53-0.61), sleep onset latency (d = 0.57), total sleep time (d = 0.51), and daytime functioning (d = 0.52-1.02) were maintained, or improved upon, at the three month follow-up. However, relapse of symptomology was common and 38% of adolescents and young adults requested further treatment in addition to the three weeks of light therapy. Although there is convincing evidence for the short-term efficacy of chronobiological treatments for DSWPD, long-term treatment outcomes can be improved. To address this gap in our current knowledge, avenues for future research are discussed., Clinical Trial: Australian & New Zealand Clinical Trials Registry, https://www.anzctr.org.au, ACTRN12614000308695., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Adolescents are vulnerable to inadequate sleep due to a unique constellation of risk factors. In particular, the puberty-related phase delay in the timing of the circadian system postpones the onset of sleep. Resultantly, disordered sleep is common among teenagers and young adults, with the most common sleep problem being delayed sleep wake-phase disorder (DSWPD). Although current treatments for DSWPD show promise, novel ways to improve our youth's sleep are needed. The purpose of this review is to critically evaluate the evidence for the role of exercise as a method to shift and/or regulate circadian timing, and thus improve sleep, in adolescents and young adults. A growing body of evidence suggests that nocturnal exercise can delay circadian timing. However, exercise administered at different times of the 24-h day may result in phase advances, particularly when the timing of exercise is gradually advanced in small daily increments. The implications of these results for young people's sleep health are discussed and suggestions are provided for ways that exercise could be used clinically, to improve the treatment of DSWPD., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Objective/background: Delayed sleep-wake phase disorder (DSWPD) is associated with a delayed timing of circadian rhythms, and this delay is suggested to be the basis of the disorder. However, this has been questioned due to frequent relapses following treatment based on this aetiology. Recent studies have emerged suggesting personality factors may contribute to sleep patterns in DSWPD. The aim of this study was to further investigate circadian and personality factors in DSWPD patients as well as patients with non-24-h sleep-wake rhythm disorder (N24SWD) relative to control sleepers., Patients/methods: This sample consisted of 16 DSWPD (age = 21.1 ± 2.8, 10 m, 7 f), and three N24SWD patients (age = 24.0 ± 4.4, 2 m, 1 f). Controls were seven males and seven females (age = 23.4 ± 5.9). Before starting an 80-h modified constant routine, eligible participants' sleep patterns were monitored for a week and they completed a personality questionnaire (NEO PI-R). An ultradian routine with alternating 20-min sleep opportunities and 40 min of enforced wakefulness was used to measure the timing of endogenous circadian temperature and melatonin rhythms., Results: As compared with controls, DSWPD patients reported higher neuroticism, significantly lower extraversion, conscientiousness and agreeableness. Similarly, N24SWD patients' patterns of personality traits were similar to that of DSWPD. Conscientiousness, in particular, was associated with phase timings of circadian rhythms as well as sleep measures and lifestyle factors within the DSWPD group., Conclusions: These findings suggest that circadian rhythm sleep-wake disorders (CRSWDs) may not only stem from circadian abnormalities but personality factors may also drive lifestyle choices, including sleep timing., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Our objectives were to investigate the period lengths (i.e., taus) of the endogenous core body temperature rhythm and melatonin rhythm in delayed sleep-wake phase disorder patients (DSWPD) and non-24-h sleep-wake rhythm disorder patients (N24SWD) compared with normally entrained individuals. Circadian rhythms were measured during an 80-h ultradian modified constant routine consisting of 80 ultrashort 1-h "days" in which participants had 20-min sleep opportunities alternating with 40 min of enforced wakefulness. We recruited a community-based sample of 26 DSWPD patients who met diagnostic criteria (17 males, 9 females; age, 21.85 ± 4.97 years) and 18 healthy controls (10 males, 8 females; age, 23.72 ± 5.10 years). Additionally, 4 full-sighted patients (3 males, 1 female; age, 25.75 ± 4.99 years) were diagnosed with N24SWD and included as a discrete study group. Ingestible core temperature capsules were used to record minute temperatures that were averaged to obtain 80 hourly data points. Salivary melatonin concentration was assessed every half-hour to determine time of dim light melatonin onset at the beginning and end of the 80-h protocol. DSWPD patients had significantly longer melatonin rhythm taus (24 h 34 min ± 17 min) than controls (24 h 22 min ± 15 min, p = 0.03, d = 0.70). These results were further supported by longer temperature rhythm taus in DSWPD patients (24 h 34 min ± 26 min) relative to controls (24 h 13 min ± 15 min, p = 0.01, d = 0.80). N24SWD patients had even longer melatonin (25 h ± 19 min) and temperature (24 h 52 min ± 17 min) taus than both DSWPD (p = 0.007, p = 0.06) and control participants (p < 0.001, p = 0.02, respectively). Between 12% and 19% of the variance in DSWPD patients' sleep timing could be explained by longer taus. This indicates that longer taus of circadian rhythms may contribute to the DSWPD patients' persistent tendency to delay, their frequent failure to respond to treatment, and their relapse following treatment. Additionally, other factors can contribute to misalignments in DSWPD and N24SWD disorders., (© 2016 The Author(s).)

According to classification manuals for sleep disorders, nine disorders are directly related to biological clock timing misalignments. Of all, delayed sleep phase disorder (DSPD) is the most commonly diagnosed, predominantly affecting adolescents, young adults, and insomnia patients. It is a persistent inability to fall asleep at earlier, more desirable and socially conventional times, coupled with extreme difficulty awakening in the morning. Considerable evidence shows a delay in the circadian clock to be associated with DSPD. Therefore, treatments have mainly focused on advancing the biological clock and sleep timing through pharmacotherapy, phototherapy and behavioral therapies. The clinical evidence indicates that these treatments are efficacious, at least in the short term. However, follow up studies show frequent patient relapse, leading researchers to speculate that alternative etiologies may be contributing to sleep and circadian clock delays in DSPD. The aim of the present paper is to review and collate current literature related to DSPD etiology in order to outline gaps in current knowledge and suggest future research., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

A significant delay in the timing of endogenous circadian rhythms has been associated with delayed sleep phase disorder (DSPD). More recently, other mechanisms have also been proposed to account for this disorder. To further explore the etiology of DSPD, the present study compared nocturnal melatonin profiles of 26 DSPD patients (18 males, 8 females; age, 21.73 ± 4.98 years) and 17 normally timed good sleepers (10 males, 7 females; age, 23.82 ± 5.23 years) in a time-free, dim-light (<10 lux) laboratory environment. A 30-h modified constant routine with alternating 20-min sleep opportunities and 40 min of enforced wakefulness was used to measure the endogenous melatonin circadian rhythm. Salivary melatonin was sampled half-hourly from 1820 h to 0020 h and then hourly from 0120 h to 1620 h. DSPD patients had significantly later timed melatonin profiles that were delayed by approximately 3 h compared to normal sleepers, and there were no notable differences in the relative duration of secretion between groups. However, melatonin secretion between dim-light melatonin onset (DLMO) and acrophase was less prominent in DSPD patients compared to good sleepers, who showed a more acute initial surge of melatonin following the DLMO. Although the regulatory role of melatonin is unknown, abnormal melatonin profiles have been linked to psychiatric and neurological disorders (e.g., major depression, obsessive compulsive disorder, Parkinson disease). These results therefore suggest that in addition to a delayed endogenous circadian rhythm, a diminished initial surge of melatonin secretion following DLMO may contribute to the etiology of DSPD., (© 2015 The Author(s).)

The currently assumed aetiology for delayed sleep phase disorder (DSPD) is a delay of the circadian system. Clinicians have sought to use bright light therapy, exogenous melatonin or chronotherapy to correct the disorder. However, these treatments have achieved unreliable outcomes for DSPD patients and, as such, one suggestion has been that the disorder may be caused by a longer than normal circadian rhythm period length (i.e. tau). The present study investigated this premise using a 78-h ultradian, ultra-short sleep-wake cycle. This constant bedrest routine was used to simulate a series of 1-h long 'days' by alternating 20-min sleep opportunities and 40 min of enforced wakefulness. Thirteen participants were recruited for the study including, six people diagnosed with DSPD according to the International Classification of Sleep Disorders-2 [mean age = 22.0, standard deviation (SD) = 3.3] and seven good sleepers (mean age = 23.1, SD = 3.9) with normal sleep timing. The DSPD participants' core temperature rhythm tau (mean = 24 h 54 min, SD = 23 min) was significantly longer (t = -2.33, P = 0.04, Cohen's d = 1.91) than the good sleepers' (mean 24 h 29 min, SD = 16 min). The temperature rhythm of the DSPD participants delayed more rapidly (i.e. >25 min day(-1) ) than the good sleepers'. These findings provide an explanation for the difficulty that DSPD patients have in phase advancing to a more conventional sleep time and their frequent relapse following treatment. The outcomes of this study support a vigorous and continued application of chronobiological and behavioural therapies to entrain DSPD patients to their desired earlier sleep times., (© 2013 European Sleep Research Society.)

Purpose of Review: For over 30 years, delayed sleep phase disorder (DSPD) has been defined as a debilitating sleep condition. Recently, there is more awareness of DSPD in young people, yet considerable information is needed to understand its cause and treatment. This review describes the latest research findings describing the clinical features, cause, and treatment of DSPD., Recent Findings: The prevalence of DSPD in adolescents and young adults ranges from 1 to 16%. The impact on the individuals is significant, particularly in the domains of school/work performance and mental health. We describe various contributing factors including reduced homeostatic sleep pressure, a lengthened and delayed circadian rhythm, insensitivity to clock-resetting morning light, and heightened cognitive activity. Evening melatonin administration as a sole treatment appears promising, as is a combination of cognitive-behavior therapy and morning bright light., Summary: Recent findings suggest clinicians to be aware of the clinical features (i.e., significant daytime sleepiness, anxiety and depression symptoms, potential for school dropout) of DSPD, as several biological features underpinning this disorder are unseen in clinical settings. We advise clinicians to become familiar with exogenous evening melatonin administration, and cognitive and behavioral techniques to simultaneously treat the delayed circadian rhythm and associated sleep-onset insomnia.

Study Objectives: To establish the extent to which the developmental changes in sleep timing experienced by Australian adolescents meet the International Classification of Sleep Disorders (ICSD-2) diagnostic criteria for delayed sleep phase disorder (DSPD), and whether adolescents with DSPD engage in poorer lifestyle choices, and are more impaired compared to good sleeping adolescents., Methods: Three-hundred seventy-four Australian adolescents (mean age 15.6 years, SD 1.0) participants completed a 7-day sleep diary, wore wrist actigraphy, and completed a battery of questionnaires to assess DSPD criteria., Results: The ICSD-2 criteria for DSPD were met by 1.1% (N = 4) of the adolescents sampled. The majority of adolescents (51.9%, N = 194) met one criterion, 14% (N = 52) of the adolescents met 2 criteria, while 33.2% (N = 124) did not fulfill any DSPD criteria. Despite having significantly delayed sleep timing, adolescents who met all criteria for DSPD reported similar lifestyle habits and daytime functioning. However, there were trends for greater alcohol and caffeine consumption, less sport participation, yet more time spent on extracurricular activities (i.e., learning to play a musical instruments for adolescents with DSPD., Conclusions: Despite the majority of adolescents reporting DSPD symptoms, only a small minority met full diagnostic criteria. Adolescents with DSPD reported similar lifestyle habits and daytime functioning to those with some or no symptoms. Future investigations of non-school-attending DSPD adolescents are needed to confirm the trends for lifestyle behaviors found in the present study.

Objective: To evaluate cognitive-behavior therapy plus bright light therapy (CBT plus BLT) for adolescents diagnosed with delayed sleep phase disorder (DSPD)., Design: Randomized controlled trial of CBT plus BLT vs. waitlist (WL) control with comparisons at pre- and post-treatment. There was 6-month follow-up for the CBT plus BLT group only., Setting: Flinders University Child & Adolescent Sleep Clinic, Adelaide, South Australia., Patients: 49 adolescents (mean age 14.6 ± 1.0 y, 53% males) diagnosed with DSPD; mean chronicity 4 y 8 months; 16% not attending school. Eighteen percent of adolescents dropped out of the study (CBT plus BLT: N = 23 vs. WL: N = 17)., Interventions: CBT plus BLT consisted of 6 individual sessions, including morning bright light therapy to advance adolescents' circadian rhythms, and cognitive restructuring and sleep education to target associated insomnia and sleep hygiene., Measurements and Results: DSPD diagnosis was performed via a clinical interview and 7-day sleep diary. Measurements at each time-point included online sleep diaries and scales measuring sleepiness, fatigue, and depression symptoms. Compared to WL, moderate-to-large improvements (d = 0.65-1.24) were found at post-treatment for CBT plus BLT adolescents, including reduced sleep latency, earlier sleep onset and rise times, total sleep time (school nights), wake after sleep onset, sleepiness, and fatigue. At 6-month follow-up (N = 15), small-to-large improvements (d = 0.24-1.53) continued for CBT plus BLT adolescents, with effects found for all measures. Significantly fewer adolescents receiving CBT plus BLT met DPSD criteria at post-treatment (WL = 82% vs. CBT plus BLT = 13%, P < 0.0001), yet 13% still met DSPD criteria at the 6-month follow-up., Conclusions: CBT plus BLT for adolescent DSPD is effective for improving multiple sleep and daytime impairments in the immediate and long-term. Studies evaluating the treatment effectiveness of each treatment component are needed., Clinical Trial Information: Australia-New Zealand Trials Registry Number: ACTRN12610001041044.

Study Objectives: The present study investigated the effectiveness of a school-based intervention in increasing sleep knowledge and improving adolescent sleep problems., Design: A randomized, controlled trial using 2 groups (program class, classes-as-usual: [CAU]) assessed over 3 time points (pre-program, post-program, 6-week follow-up)., Participants/setting: Eighty-one students (mean age = 15.6 +/- 0.6 y; 33% male) from 2 schools in South Australia. Schools provided one class to participate in the sleep intervention program (N = 41) and a second class to act as a control class (N = 40)., Intervention: Four 50-minute classes across a 4-week period. Classes consisted of educating adolescents on promoting and maintaining a healthy lifestyle based on a cognitive-behavior therapy framework., Measurements and Results: Data were collected pre-program, post-program, and at 6-week follow-up using an online questionnaire. Qualitative student and teacher data were collected at post-program. Baseline data indicated sleep problems were prevalent (53.1% insufficient sleep on school nights [< 8 h] and 77.8% discrepant school/weekend rise times [> 2 h]). These 2 criteria identified 36 adolescents with a delayed sleep timing (DST; Program, N = 21; CAU, N = 15). The program increased sleep knowledge (P = 0.001); however, analyses revealed no significant effects on target sleep variables as compared with the CAU class for the entire group (all P > 0.05). For DST adolescents, there was a significant interaction for reducing the discrepancy between school and weekend out of bed times (P = 0.002). There was no impact on other sleep parameters or depressed mood., Conclusions: School-based sleep interventions for adolescents are a novel method for addressing a prevalent problem. Future programs should develop ways to motivate adolescents to change sleep practices.