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We examined whether a polymorphism of the PERIOD3 gene (PER3; rs57875989) modulated the sleep‐promoting effects of melatonin in Delayed Sleep‐Wake Phase Disorder (DSWPD). One hundred and four individuals (53 males; 29.4 ±10.0 years) with DSWPD and a delayed dim light melatonin onset (DLMO) collected buccal swabs for genotyping (PER34/4 n = 43; PER3 5 allele [heterozygous and homozygous] n = 60). Participants were randomised to placebo or 0.5 mg melatonin taken 1 hour before desired bedtime (or ~1.45 hours before DLMO), with sleep attempted at desired bedtime (4 weeks; 5‐7 nights/week). We assessed sleep (diary and actigraphy), Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), Patient‐Reported Outcomes Measurement Information System (PROMIS: Sleep Disturbance, Sleep‐Related Impairment), Sheehan Disability Scale (SDS) and Patient‐ and Clinician‐Global Improvement (PGI‐C, CGI‐C). Melatonin treatment response on actigraphic sleep onset time did not differ between genotypes. For PER34/4 carriers, self‐reported sleep onset time was advanced by a larger amount and sleep onset latency (SOL) was shorter in melatonin‐treated patients compared to those receiving placebo (P =.008), while actigraphic sleep efficiency in the first third of the sleep episode (SE T1) did not differ. For PER3 5 carriers, actigraphic SOL and SE T1 showed a larger improvement with melatonin (P <.001). Melatonin improved ISI (P =.005), PROMIS sleep disturbance (P <.001) and sleep‐related impairment (P =.017), SDS (P =.019), PGI‐C (P =.028) and CGI‐C (P =.016) in PER34/4 individuals only. Melatonin did not advance circadian phase. Overall, PER34/4 DSWPD patients have a greater response to melatonin treatment. PER3 genotyping may therefore improve DSWPD patient outcomes. [ABSTRACT FROM AUTHOR]

A sample of 211 first-year psychology students completed a questionnaire of sleep habits and difficulities. It was discovered that Delayed Sleep Phase Syndrome may be a significant problem in university student populations. (Author/JD)

Background: Delayed Sleep-Wake Phase Disorder (DSWPD) is characterised by sleep initiation insomnia when attempting sleep at conventional times and difficulty waking at the required time for daytime commitments. Although there are published therapeutic guidelines for the administration of melatonin for DSWPD, to our knowledge, randomised controlled trials are lacking. This trial tested the efficacy of 0.5 mg melatonin, combined with behavioural sleep-wake scheduling, for improving sleep initiation in clinically diagnosed DSWPD patients with a delayed endogenous melatonin rhythm relative to patient-desired (or -required) bedtime (DBT). Methods: This randomised, placebo-controlled, double-blind clinical trial was conducted in an Australian outpatient DSWPD population. Following 1-wk baseline, clinically diagnosed DSWPD patients with delayed melatonin rhythm relative to DBT (salivary dim light melatonin onset [DLMO] after or within 30 min before DBT) were randomised to 4-wk treatment with 0.5 mg fast-release melatonin or placebo 1 h before DBT for at least 5 consecutive nights per week. All patients received behavioural sleep-wake scheduling, consisting of bedtime scheduled at DBT. The primary outcome was actigraphic sleep onset time. Secondary outcomes were sleep efficiency in the first third of time in bed (SE T1) on treatment nights, subjective sleep-related daytime impairment (Patient Reported Outcomes Measurement Information System [PROMIS]), PROMIS sleep disturbance, measures of daytime sleepiness, clinician-rated change in illness severity, and DLMO time. Findings: Between September 13, 2012 and September 1, 2014, 307 participants were registered; 116 were randomised to treatment (intention-to-treat n = 116; n = 62 males; mean age, 29.0 y). Relative to baseline and compared to placebo, sleep onset occurred 34 min earlier (95% confidence interval [CI] −60 to −8) in the melatonin group. SE T1 increased; PROMIS sleep-related impairment, PROMIS sleep disturbance, insomnia severity, and functional disability decreased; and a greater proportion of patients showed more than minimal clinician-rated improvement following melatonin treatment (52.8%) compared to placebo (24.0%) (P < 0.05). The groups did not differ in the number of nights treatment was taken per protocol. Post-treatment DLMO assessed in a subset of patients (n = 43) was not significantly different between groups. Adverse events included light-headedness, daytime sleepiness, and decreased libido, although rates were similar between treatment groups. The clinical benefits or safety of melatonin with long-term treatment were not assessed, and it remains unknown whether the same treatment regime would benefit patients experiencing DSWPD sleep symptomology without a delay in the endogenous melatonin rhythm. Conclusions: In this study, melatonin treatment 1 h prior to DBT combined with behavioural sleep-wake scheduling was efficacious for improving objective and subjective measures of sleep disturbances and sleep-related impairments in DSWPD patients with delayed circadian phase relative to DBT. Improvements were achieved largely through the sleep-promoting effects of melatonin, combined with behavioural sleep-wake scheduling. Trial registration This trial was registered with the Australian New Zealand Clinical Trials Registry, ACTRN12612000425897.

Study Objectives: This study evaluated the efficacy of a brief group-based program of cognitive-behavior therapy for insomnia (CBTi) for older adults suffering from chronic insomnia with short objective sleep relative to those with long sleep duration.Method: Ninety-one adults (male = 43, mean age = 63.34, standard deviation (SD) = 6.41) with sleep maintenance insomnia were selected from a community-based sample. The participants were classified as short sleepers (SS; <6 h total sleep time) or long sleepers (LS; ≥6 h total sleep time) based on one night of home-based polysomnography. Participants were randomly allocated to a 4-week, group-based treatment program of CBTi (N = 30 SS; N = 33 LS) or to a wait-list control condition (N = 9 SS, N = 19 LS). One-week sleep diaries, actigraphy, and a comprehensive battery of questionnaires were used to evaluate the efficacy of CBTi for those with short objective sleep relative to those with long sleep duration. Outcome measures were taken at pretreatment, posttreatment, and a 3-month follow-up.Results: CBTi produced robust and durable improvements in quality of sleep, including reduced wake after sleep onset and improved sleep efficiency. Participants reported a reduction of scores on the Insomnia Severity Index, Flinders Fatigue Scale, Epworth Sleepiness Scale, Daytime Feeling and Functioning Scale, Sleep Anticipatory Anxiety Questionnaire, the Dysfunctional Beliefs and Attitudes about Sleep Scale, and gains on the Sleep Self-Efficacy Scale. All improvements were significant relative to their respective SS or LS wait-list group. The benefits of CBTi were comparable with those who had short and long objective sleep before the treatment.Conclusions: Older adults suffering from chronic insomnia with short objective sleep received comparable therapeutic benefits following CBTi relative to those with long objective sleep duration. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Appropriately timed exposure to bright light has been shown to phase shift the circadian rhythm and alleviate associated sleeping difficulties. This study evaluated the effectiveness of a newly developed re-timer portable light device for phase delaying the circadian rhythm. Participants included 12 healthy, good sleepers (M = 32.3 years, SD = 12.5, male = 5). A repeated measures counterbalanced design was used to assess circadian phase delay following the use of either the re-timer or no device on two consecutive evenings. Outcome measures included dim light melatonin onset (DLMO), subjective sleepiness, and adverse effects of the re-timer. Analyses revealed a significant phase delay of DLMO following use of the re-timer (M = 46 min, SD = 76 min) on two consecutive evenings when compared to no light control (M = 3 min, SD = 81 min; p =.016). There was a trend for evening subjective sleepiness to decrease after using the re-timer compared to no light control, however this trend was not statistically significant. Adverse effects of the re-timer were headache, eye irritation, and light bothersome to eyes, however these were not severe and treatment was not requested or required. The re-timer device is an effective method of delaying the circadian rhythm in good sleepers. [ABSTRACT FROM AUTHOR]