Effects of cognitive behavioural therapy and bright light therapy for insomnia in youths with eveningness: study protocol for a randomised controlled trial.

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.

Sleep's role in the development and resolution of adolescent depression.

Two adolescent mental health fields - sleep and depression - have advanced largely in parallel until about four years ago. Although sleep problems have been thought to be a symptom of adolescent depression, emerging evidence suggests that sleep difficulties arise before depression does. In this Review, we describe how the combination of adolescent sleep biology and psychology uniquely predispose adolescents to develop depression. We describe multiple pathways and contributors, including a delayed circadian rhythm, restricted sleep duration and greater opportunity for repetitive negative thinking while waiting for sleep. We match each contributor with evidence-based sleep interventions, including bright light therapy, exogenous melatonin and cognitive-behaviour therapy techniques. Such treatments improve sleep and alleviate depression symptoms, highlighting the utility of sleep treatment for comorbid disorders experienced by adolescents.

Depressed mood and repetitive negative thinking in Delayed Sleep-Wake Phase Disorder: Treatment effects and a comparison with good sleepers.

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.

Low-intensity scheduled morning exercise for adolescents with a late chronotype: a novel treatment to advance circadian phase?

Study Objectives: During adolescence, an interplay between biological and environmental factors leads to constrained sleep duration and timing. The high prevalence of sleep deprivation during this developmental period is a public health concern, given the value of restorative sleep for mental, emotional, and physical health. One of the primary contributing factors is the normative delay of the circadian rhythm. Therefore, the present study aimed to evaluate the effect of a gradually advanced morning exercise schedule (30 min shift each day) completed for 45 min on 5 consecutive mornings, on the circadian phase and daytime functioning of adolescents with a late chronotype, compared with a sedentary control group. Methods: A total of 18 physically inactive male adolescents aged 15-18 years spent 6 nights at the sleep laboratory. The morning procedure included either 45 min walking on a treadmill or sedentary activities in dim light. Saliva dim light melatonin onset, evening sleepiness, and daytime functioning were assessed during the first and last night of laboratory attendance. Results: The morning exercise group had a significantly advanced (earlier) circadian phase (27.5 min ± 32.0), while sedentary activity resulted in a phase delay (-34.3 min ± 53.2). Morning exercise also led to higher evening sleepiness in the earlier hours of the night, but not at bedtime. Mood measures improved slightly in both study conditions. Conclusions: These findings highlight the phase-advancing effect of low-intensity morning exercise among this population. Future studies are needed to test the transference of these laboratory findings to adolescents' real life.

Readiness to change and commitment as predictors of therapy compliance in adolescents with Delayed Sleep-Wake Phase Disorder.

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.

Cognitive "insomnia" processes in delayed sleep-wake phase disorder: Do they exist and are they responsive to chronobiological treatment?

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).

Brief school-based interventions to assist adolescents' sleep-onset latency: Comparing mindfulness and constructive worry versus controls.

Difficulties falling asleep are common among adolescents, especially during times of stress. Adolescents may thus benefit from brief techniques (15 min) that decrease pre-sleep cognitive-emotional arousal and sleep-onset latency. The present study used a 3 (intervention: mindfulness bodyscan mp3, constructive worry, control) by 3 (time: baseline, week 1, week 2) mixed-model design on a school-based sample of adolescents (N = 232; Mage  = 15.9 ± 0.8 years, range = 14-18 years; 19% male), and a sub-sample of adolescents with prolonged sleep-onset latency (i.e. ≥30 min; N = 119; Mage  = 16.9 ± 0.9 years; 21% male). It was expected that the 15-min pre-recorded breath-based mindfulness bodyscan, and constructive worry, would decrease sleep-onset latency and pre-sleep arousal similarly over time, relative to the control condition. A significant interaction was observed among adolescents with prolonged sleep-onset latency, who completed ≥3 days for at least 1 week (p = .001), where mindfulness decreased sleep-onset latency relative to constructive worry and the control. Neither technique changed pre-sleep worry or cognitive-emotional arousal, or associated daytime functioning (both the whole sample and sub-sample). A pre-recorded mp3 breath-based mindfulness bodyscan technique is a promising means by which adolescents with prolonged sleep-onset latency can decrease sleep-onset latency. This simple tool has potential for scalable dissemination by stakeholders (e.g. teachers), unqualified to treat adolescent sleep difficulties. Future studies are needed to determine whether benefits may extend to academic performance and mental health, if performed for a longer time period with increased compliance.

The etiology of delayed sleep phase disorder.

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.

Nocturnal Melatonin Profiles in Patients with Delayed Sleep-Wake Phase Disorder and Control Sleepers.

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.

Evaluation of novel school-based interventions for adolescent sleep problems: does parental involvement and bright light improve outcomes?

OBJECTIVES: The current study aimed to evaluate school-based motivational sleep education programs (SEPs) with adjunct bright light therapy (BLT) and/or parental involvement (PI). DESIGN: Randomized controlled trial. SETTING: Six high schools, matched on socio-economic status (SES). PARTICIPANTS: A total of 193 adolescents (mean age, 16.3 ± 0.4 years, 79%f). INTERVENTION: Classes were randomly assigned to (i) SEP + BLT, (ii) SEP + PI, (iii) SEP + BLT + PI, or (iv) classes-as-usual (CAU). Sleep education programs involved 4×50 minute classes (over 4 weeks) based on a Motivational Interviewing framework (Sleep Med 2011;12:246-251). Students in BLT groups attempted a weekend phase advance using portable green light LED glasses (500 nm; 506 lux). Parents of PI groups watched a series of 4 YouTube clips (2-3 minutes in length) outlining their adolescent's learning in class and how they could assist. Students in the CAU groups continued their regular classes. MEASUREMENTS: Online questionnaires measuring sleep knowledge, sleep patterns (bedtime, sleep latency, total sleep time [TST], etc) and mood at preintervention and postintervention and 6-week follow-up. Intervention groups also completed a motivation-to-change questionnaire and provided qualitative feedback. RESULTS: Improvements in sleep knowledge (d = 0.59-0.88), sleep onset latency (d = 0.45-0.50), TST (d = 0.32-0.57), and mood (d = 0.24-0.46) were observed in all intervention groups relative to the CAU group. Similar improvements were observed in a subgroup of students identified as having delayed sleep timing (ie, sleep knowledge: d = 0.45-0.92; sleep onset latency: d = 0.59-0.82; TST: d = 0.82-1.18). Increases in motivation to regularize out of bedtimes, obtain morning bright light (BLT groups), and avoid sleeping-in on weekends occurred (all P < .005). CONCLUSIONS: This motivational SEP produced meaningful and similar benefits for adolescents in all intervention groups. Longer BLT (ie, over school holidays) and more intensive parental inclusion should be investigated in future studies.

Delayed sleep phase disorder in youth.

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.

The endogenous circadian temperature period length (tau) in delayed sleep phase disorder compared to good sleepers.

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.

A randomized controlled trial of cognitive-behavior therapy plus bright light therapy for adolescent delayed sleep phase disorder.

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.

The relationship between insomnia and body temperatures.

Sleepiness and sleep propensity are strongly influenced by our circadian clock as indicated by many circadian rhythms, most commonly by that of core body temperature. Sleep is most conducive in the temperature minimum phase, but is inhibited in a "wake maintenance zone" before the minimum phase, and is disrupted in a zone following that phase. Different types of insomnia symptoms have been associated with abnormalities of the body temperature rhythm. Sleep onset insomnia is associated with a delayed temperature rhythm presumably, at least partly, because sleep is attempted during a delayed evening wake maintenance zone. Morning bright light has been used to phase advance circadian rhythms and successfully treat sleep onset insomnia. Conversely, early morning awakening insomnia has been associated with a phase advanced temperature rhythm and has been successfully treated with the phase delaying effects of evening bright light. Sleep maintenance insomnia has been associated not with a circadian rhythm timing abnormality, but with nocturnally elevated core body temperature. Combination of sleep onset and maintenance insomnia has been associated with a 24-h elevation of core body temperature supporting the chronic hyper-arousal model of insomnia. The possibility that these last two types of insomnia may be related to impaired thermoregulation, particularly a reduced ability to dissipate body heat from distal skin areas, has not been consistently supported in laboratory studies. Further studies of thermoregulation are needed in the typical home environment in which the insomnia is most evident.

Intensive Sleep Retraining treatment for chronic primary insomnia: a preliminary investigation.

The aim of this study was to assess the effectiveness of Intensive Sleep Retraining, a novel, short duration behavioural therapy in treating chronic primary insomnia. Seventeen consecutive volunteers from the general public (mean age = 39.1 years), meeting selection criteria for chronic primary insomnia participated in the treatment study. The study was performed as a case replication series. Assessment involved sleep diary, actigraph and questionnaire measures of sleep and daytime functioning for a period of 2 weeks prior to, immediately after, and 6 weeks following the treatment. Treatment involved a single night of sleep deprivation, facilitating short sleep latencies (mean: 6.9 min) to a series of 50 brief nap opportunities. Following treatment, Sleep Onset Latency significantly decreased by a mean of 30.5 min (SD = 28.3), Wake Time after Sleep Onset significantly decreased by a mean of 28 min (SD = 34.0), and Total Sleep Time significantly increased by 64.6 min (SD = 45.5). Significant improvements were also seen in the daytime functioning and psychological measures of fatigue and vigour, cognitive sleep anticipatory anxiety and self-efficacy for sleep. This brief therapy was effective in improving sleep and some daytime functioning and psychological questionnaire measures. These improvements were maintained up to 2 months following the treatment weekend. Further exploration of this brief therapy is needed, with larger, randomized, placebo-controlled trials over longer follow-up periods, and in comparison to other traditional therapies for insomnia.