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.

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).

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.

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.