Sleep-wake state discrepancy does not impair the efficacy of cognitive behavioural therapy for insomnia: Findings from a large clinic sample.

The current study determined the extent to which sleep-wake state discrepancy impairs the efficacy of cognitive behavioural therapy for insomnia in a real-world clinical sample. Sleep-wake state discrepancy occurs when there is an inconsistency between a person's subjective and objective sleep, and is a common phenomenon amongst patients with insomnia. Limited information is available on the effectiveness of cognitive behavioural therapy for insomnia in treating patients who experience significant sleep-wake state discrepancy in "real-world" samples. In the present study, all patients with insomnia received cognitive behavioural therapy for insomnia through an outpatient insomnia program (N = 386; mean age = 51.96 years, SD = 15.62; 65.97% [N = 254] female). Prior to treatment, participants completed a polysomnography sleep study and sleep diary, which was used to calculate sleep-wake state discrepancy. At pre-treatment, post-treatment and 3-month follow-up, participants completed the Insomnia Severity Index and other questionnaires, and 1 week of sleep diaries from which sleep-onset latency, wake after sleep onset and other sleep variables were calculated. There were no differences in self-reported sleep-onset latency, wake after sleep onset or Insomnia Severity Index scores at post-treatment or 3-month follow-up between quintiles of sleep-wake state discrepancy. These results indicate that sleep-wake state discrepancy at pre-treatment does not predict treatment response to cognitive behavioural therapy for insomnia. Future research could examine multi-night assessments of sleep-wake state discrepancy to determine whether variations in discrepancy may relate to pre-treatment insomnia severity and cognitive behavioural therapy for insomnia outcomes.

Circadian aspects in the aetiology and pathophysiology of insomnia.

Because the endogenous circadian pacemaker is a very strong determinant of alertness/sleep propensity across the 24 h period, its mistiming may contribute to symptoms of insomnia (e.g., difficulties initiating sleep and maintaining sleep) and to the development of insomnia disorder. Despite the separation of insomnia and circadian rhythm disorders in diagnostic nosology implying independent pathophysiology, there is considerable evidence of co-morbidity and interaction between them. Sleep onset insomnia is associated with later timed circadian rhythms and can be treated with morning bright light to shift rhythms to an earlier timing. It is also possible that the causal link may go in both directions and that having a delayed circadian rhythm can result in enough experiences of delayed sleep onset to lead to some conditioned insomnia or insomnia disorder further exacerbating a delayed circadian rhythm. Early morning awakening insomnia is associated with an advanced circadian phase (early timing) and can be treated with evening bright light resulting in a delay of rhythms and an improved ability to sleep later in the morning and to obtain more sleep. There is some evidence suggesting that sleep maintenance insomnia is associated with a blunted amplitude of circadian rhythm that may be treated with increased regularity of sleep and light exposure timing. However, this is an insomnia phenotype that requires considerably more circadian research as well as further insomnia clinical research with the other insomnia phenotypes incorporating circadian timing measures and treatments.

EEG power spectral responses to wind farm compared with road traffic noise during sleep: A laboratory study.

Wind turbine noise is dominated by low frequencies for which effects on sleep relative to more common environmental noise sources such as road traffic noise remain unknown. This study examined the effect of wind turbine noise compared with road traffic noise on sleep using quantitative electroencephalogram power spectral analysis. Twenty-three participants were exposed to 3-min samples of wind turbine noise and road traffic noise at three sound pressure levels (33, 38 and 43 dBA) in randomised order during established sleep. Acute (0-30 s) and more sustained (30-180 s) effects of noise presentations during N2 and N3 sleep were examined using spectral analysis of changes in electroencephalogram power frequency ranges across time in 5-s intervals. Both noise types produced time- and sound pressure level-dependent increases in electroencephalogram power, but with significant noise type by sound pressure level interactions in beta, alpha, theta and delta frequency bands (all p < 0.05). Wind turbine noise showed significantly lower delta, theta and beta activity immediately following noise onset compared with road traffic noise (all p < 0.05). However, alpha activity was higher for wind turbine noise played at lower sound pressure levels (33 dBA [p = 0.001] and 38 dBA [p = 0.003]) compared with traffic noise during N2 sleep. These findings support that spectral analyses show subtle effects of noise on sleep and that electroencephalogram changes following wind turbine noise and road traffic noise onset differ depending on sound pressure levels; however, these effects were mostly transient and had little impact on conventionally scored sleep. Further studies are needed to establish if electroencephalogram changes associated with modest environmental noise exposures have significant impacts on sleep quality and next-day functioning.

Annoyance due to amplitude modulated low-frequency wind farm noise: A laboratory study.

This study tested for differences in perceived annoyance and loudness between road traffic noise (RTN) and wind farm noise (WFN) with amplitude modulation (AM) and tonality. Twenty-two participants, who were primarily university students with no previous exposure to WFN and aged between 19 and 29 (mean, 22 years old; standard deviation, 2) years old with normal hearing, underwent a laboratory-based listening test. Each participant rated perceived annoyance and loudness of WFN and RTN samples played at sound pressure levels (SPLs) ranging from 33 to 48 dBA. Probability modeling revealed that participants were the largest source of variability in ratings of perceived annoyance and loudness while noise type and SPL were relatively minor sources. Overall, no differences were found between WFN and RTN perceived annoyance or loudness ratings. On the other hand, no substantial differences in annoyance were found between low-frequency tonal AM and mid-to-high-frequency AM or "swish" WFN.

A systematic review and meta-analysis of wind turbine noise effects on sleep using validated objective and subjective sleep assessments.

Little is known about the potential impacts of wind turbine noise (WTN) on sleep. Previous research is limited to cross-sectional studies reporting anecdotal impacts on sleep using inconsistent sleep metrics. This meta-analysis sought to comprehensively review studies evaluating the impact of WTN using widely accepted and validated objective and subjective sleep assessments. Search terms included: "wind farm noise", "wind turbine noise", "wind turbine sound", "wind turbine noise exposure" AND "sleep". Only original articles published in English published after the year 2000 and reporting sleep outcomes in the presence of WTN using polysomnography, actigraphy or psychometrically validated sleep questionnaires were included. Uniform outcomes of the retrieved studies were meta-analysed to examine WTN effects on objective and subjective sleep outcomes. Nine studies were eligible for review and five studies were meta-analysed. Meta-analyses (Hedges' g; 95% confidence interval [CI]) revealed no significant differences in objective sleep onset latency (0.03, 95%  CI -0.34 to 0.41), total sleep time (-0.05, 95%  CI -0.77 to 0.67), sleep efficiency (-0.25, 95%  CI -0.71 to 0.22) or wake after sleep onset (1.25, 95%  CI -2.00 to 4.50) in the presence versus absence of WTN (all p > .05). Subjective sleep estimates were not meta-analysed because measurement outcomes were not sufficiently uniform for comparisons between studies. This systematic review and meta-analysis suggests that WTN does not significantly impact key indicators of objective sleep. Cautious interpretation remains warranted given variable measurement methodologies, WTN interventions, limited sample sizes, and cross-sectional study designs, where cause-and-effect relationships are uncertain. Well-controlled experimental studies using ecologically valid WTN, objective and psychometrically validated sleep assessments are needed to provide conclusive evidence regarding WTN impacts on sleep.

Amplitude modulated wind farm noise relationship with annoyance: A year-long field study.

This paper presents results from a one-year study of indoor annoyance and self-reported sleep times for two participants located near different wind farms. Continuous measurements of outdoor and indoor noise and meteorological conditions were taken at each location for the duration of the study. In at least 50% of the annoyance recordings, participants described noise as "swish" or "swoosh." Furthermore, the majority of the annoyance recordings occurred at nighttime and in the early morning. The third quartile of A-weighted indoor sound pressure level [SPL(A)], between 27 and 31 dBA, was associated with an 88% increased probability of annoyance compared to the lowest reference quartile, which was between 12 and 22 dBA [odds ratio and 95% confidence intervals, 7.72 (2.61,22.8), p < 0.001]. The outdoor SPL(A) was also predictive of annoyance but only between 40 and 45 dBA. The outdoor prevalence of amplitude modulation (AM), defined as the percentage of time that AM was detectable by an algorithm for each annoyance period, was also associated with annoyance. Self-reported sleep efficiency (time spent asleep relative to time in bed available for sleep) was significantly associated with nighttime annoyance (ß = -0.66, p = 0.02) but only explained a small fraction of the variance (R2 = 5%).

Sex differences in response to cognitive behavioural therapy for insomnia: A chart review of 455 patients with chronic insomnia.

BACKGROUND: Insomnia is more prevalent in females, however studies examining sex differences in response to insomnia treatment are scarce. This study assessed sex-specific differences in cognitive behavioural therapy for insomnia (CBT-I)-related changes in insomnia symptoms in a large clinical cohort. METHODS: A chart review was conducted of a clinical cohort (females n = 305, males n = 150) referred to a sleep clinic. Participants had a registered psychologist confirm diagnosis of chronic insomnia according to DSM-IV/V criteria and a Level 1 or 2 sleep study. Daily sleep diaries and questionnaires including the Insomnia Severity Index (ISI), Flinders Fatigue Scale (FFS), the Daytime Feelings and Functioning Scale (DFFS), and the Depression, Anxiety and Stress Scale-21 items (DASS), were administered at baseline, post-treatment, and three-month follow-up. Linear mixed models determined interactions between sex and timepoint on symptoms. RESULTS: Mean (SD) age was 51.7 yrs (15.7, range = 18-90 yrs), and mean BMI was 26.3 kg/m2 (4.9), neither of which differed by sex. At pre-treatment, females demonstrated higher objective total sleep time (min) [343.5 (97.6) vs 323.8 min (92.1), p = 0.044], ISI [19.7 (4.2) vs 18.6 (4.4), p = 0.033], and FFS scores [19.2 (6.0) vs 16.9 (7.2), p = 0.003]. Compared to males, females experienced a greater reduction in FFS and DFFS scores and DASS depressive symptoms (p for interaction: 0.017, 0.043, 0.016 respectively) from baseline to follow-up. The greater reduction in depressive symptoms did not persist after controlling for age, BMI, and sleep apnea severity. Subjective total sleep time similarly increased across treatment for both males [baseline: 335.7 (15.1), post: 357.9 (15.5)] and females [baseline: 318.3 (10.4), post: 354.4 (10.7)], p for interaction: 0.22. CONCLUSION: Females and males experience similar, substantial benefits from CBT-I after accounting for comorbidities, suggesting the same treatment can resolve insomnia in both sexes.

A circadian-informed lighting intervention accelerates circadian adjustment to a night work schedule in a submarine lighting environment.

STUDY OBJECTIVE: Night work has detrimental impacts on sleep and performance, primarily due to misalignment between sleep-wake schedules and underlying circadian rhythms. This study tested whether circadian-informed lighting accelerated circadian phase delay, and thus adjustment to night work, compared to blue-depleted standard lighting under simulated submariner work conditions. METHODS: Nineteen healthy sleepers (12 males; mean±SD aged 29 ±10 y) participated in two separate 8-day visits approximately one month apart to receive, in random order, circadian-informed lighting (blue-enriched and dim, blue-depleted lighting at specific times) and standard lighting (dim, blue-depleted lighting). After an adaptation night (day 1), salivary dim light melatonin onset (DLMO) assessment was undertaken from 18:00-02:00 on days 2-3. During days 3-7, participants completed simulated night work from 00:00-08:00 and a sleep period from 10:00-19:00. Post-condition DLMO assessment occurred from 21:00-13:00 on days 7-8. Ingestible capsules continuously sampled temperature to estimate daily core body temperature minimum (Tmin) time. Tmin and DLMO circadian delays were compared between conditions using mixed effects models. RESULTS: There were significant condition-by-day interactions in Tmin and DLMO delays (both p<0.001). After four simulated night shifts, circadian-informed lighting produced a mean [95%CI] 4.3 [3.3 to 5.4] h greater delay in Tmin timing and a 4.2 [3 to 5.6] h greater delay in DLMO timing compared to standard lighting. CONCLUSIONS: Circadian-informed lighting accelerates adjustment to shiftwork in a simulated submariner work environment. Circadian lighting interventions warrant consideration in any dimly lit and blue-depleted work environments where circadian adjustment is relevant to help enhance human performance, safety, and health.

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.

The impact of prolonged violent video-gaming on adolescent sleep: an experimental study.

Video-gaming is an increasingly prevalent activity among children and adolescents that is known to influence several areas of emotional, cognitive and behavioural functioning. Currently there is insufficient experimental evidence about how extended video-game play may affect adolescents' sleep. The aim of this study was to investigate the short-term impact of adolescents' prolonged exposure to violent video-gaming on sleep. Seventeen male adolescents (mean age = 16 ± 1 years) with no current sleep difficulties played a novel, fast-paced, violent video-game (50 or 150 min) before their usual bedtime on two different testing nights in a sleep laboratory. Objective (polysomnography-measured sleep and heart rate) and subjective (single-night sleep diary) measures were obtained to assess the arousing effects of prolonged gaming. Compared with regular gaming, prolonged gaming produced decreases in objective sleep efficiency (by 7 ± 2%, falling below 85%) and total sleep time (by 27 ± 12 min) that was contributed by a near-moderate reduction in rapid eye movement sleep (Cohen's d = 0.48). Subjective sleep-onset latency significantly increased by 17 ± 8 min, and there was a moderate reduction in self-reported sleep quality after prolonged gaming (Cohen's d = 0.53). Heart rate did not differ significantly between video-gaming conditions during pre-sleep game-play or the sleep-onset phase. Results provide evidence that prolonged video-gaming may cause clinically significant disruption to adolescent sleep, even when sleep after video-gaming is initiated at normal bedtime. However, physiological arousal may not necessarily be the mechanism by which technology use affects sleep.

Pharmacological management of co-morbid obstructive sleep apnoea and insomnia.

INTRODUCTION: Clinical presentation of both insomnia and obstructive sleep apnea (COMISA) is common. Approximately 30% of clinical cohorts with OSA have insomnia symptoms and vice versa. The underlying pathophysiology of COMISA is multifactorial. This poses a complex clinical challenge. Currently, there are no clinical guidelines or recommendations outside of continuous positive airway pressure (CPAP) therapy and cognitive behavioral therapy for insomnia (CBTi). Clinically translatable precision medicine approaches to characterize individual causes or endotypes may help optimize future pharmacological management of COMISA. AREAS COVERED: This review article provides an up-to-date account of COMISA and its consequences, the underlying pathophysiology of sleep apnea, insomnia and COMISA, current treatment approaches and limitations, pharmacotherapy targets and future priorities. EXPERT OPINION: There are multiple promising emerging therapies, but clinical trial data specifically in COMISA populations are lacking. This is a priority for future investigation to inform development of evidence-based guidelines. Pharmacotherapies, particularly for insomnia, do not target the underlying causes of the disorder thus, are indicated for short-term use only and should remain second line. Future multidisciplinary research should be directed toward the multifactorial nature of COMISA and the challenges of adapting COMISA treatment in clinical practice and overcoming the practical barriers that health-care providers and consumers encounter.

The mortality risk of night-time and daytime insomnia symptoms in an older population.

The current study examined the association between insomnia symptoms and all-cause mortality in older adults (≥ 65 years). Data was used from 1969 older adults [M = 78 years, SD = 6.7 years] who participated in the Australian Longitudinal Study of Ageing. Insomnia symptoms were defined by nocturnal symptoms (difficulty falling asleep, difficulty maintaining sleep, early morning awakenings) and daytime symptoms (concentration difficulties, effort, inability to get going). Frequency of symptoms were combined to calculate an insomnia symptom score ranging from 0 (no symptoms) to 24 (sever symptoms) and quintiles of the score were constructed to provide a range of symptom severity. Multivariable Cox models were conducted to assess associations between insomnia symptom severity and mortality risk. In the median follow up of 9.2 years, there were 17,403 person-years at risk and the mortality rate was 8-per 100 person-years. Insomnia symptom severity was associated with increased mortality in the most severe quintile (adjusted HRQ1vsQ5 = 1.26, 95%CI [1.03-1.53], p = .02). Subsequent analyses showed this association was driven by daytime symptoms (adjusted HRQ1vsQ5 = 1.66, [1.39-2.00], p < .0001), since nocturnal symptoms alone were not associated with increased mortality (adjusted HR Q1vsQ5 = 0.89, [0.72-1.10], p = .28). Findings suggest daytime symptoms drive increased mortality risk associated with insomnia symptoms. Findings may be therapeutically helpful by reassuring individuals with nocturnal insomnia symptoms alone that their longevity is unlikely to be impacted.

Establishing the acute physiological and sleep disruption characteristics of wind farm versus road traffic noise disturbances in sleep: a randomized controlled trial protocol.

Study Objectives: Despite the global expansion of wind farms, effects of wind farm noise (WFN) on sleep remain poorly understood. This protocol details a randomized controlled trial designed to compare the sleep disruption characteristics of WFN versus road traffic noise (RTN). Methods: This study was a prospective, seven night within-subjects randomized controlled in-laboratory polysomnography-based trial. Four groups of adults were recruited from; <10 km away from a wind farm, including those with, and another group without, noise-related complaints; an urban RTN exposed group; and a group from a quiet rural area. Following an acclimation night, participants were exposed, in random order, to two separate nights with 20-s or 3-min duration WFN and RTN noise samples reproduced at multiple sound pressure levels during established sleep. Four other nights tested for continuous WFN exposure during wake and/or sleep on sleep outcomes. Results: The primary analyses will assess changes in electroencephalography (EEG) assessed as micro-arousals (EEG shifts to faster frequencies lasting 3-15 s) and awakenings (>15 s events) from sleep by each noise type with acute (20-s) and more sustained (3-min) noise exposures. Secondary analyses will compare dose-response effects of sound pressure level and noise type on EEG K-complex probabilities and quantitative EEG measures, and cardiovascular activation responses. Group effects, self-reported noise sensitivity, and wake versus sleep noise exposure effects will also be examined. Conclusions: This study will help to clarify if wind farm noise has different sleep disruption characteristics compared to road traffic noise.

Understanding Sleep-Wake Behavior in Late Chronotype Adolescents: The Role of Circadian Phase, Sleep Timing, and Sleep Propensity.

Background: Adolescents with a late chronotype are at greater risk for mood disorders, risk-taking behaviors, school absenteeism, and lower academic achievement. As there are multiple causes for late chronotype, the field lacks studies on the relationship between mood, circadian phase, and phase angle of entrainment in late chronotype adolescents. Three objectives guide this explorative study: (1) to describe sleep, circadian phase, and phase angle of entrainment in late chronotype adolescents, (2) to explore how different levels of lateness are associated with sleep quality, sleep propensity, and mood, and (3) to investigate the influence of circadian phase on bedtime choice and sleep duration. Methods: Baseline data from 19 male adolescents (M = 16.4 ± 1.0 yrs), who were part of a larger intervention trial, were analyzed. Chronotype was measured with the Munich Chronotype Questionnaire, circadian timing via dim light melatonin onset (DLMO), and sleep habits with a 7-day sleep log. Further questionnaires assessed daytime sleepiness, sleep quality, and mood. Evening sleepiness and sustained attention were used as a proxy for evening sleep propensity. Results: On school nights, sleep duration averaged 7.78 h (±1.65), and 9.00 h (±1.42) on weekend nights. Mean DLMO was observed at 23.13 h (± 1.65), with a weekend phase angle of entrainment of 2.48 h. Regression fittings revealed a tendency for shorter phase angles with delayed DLMOs. Further analysis with chronotype subgroups revealed that this was only true for light and moderate late types, whereas extreme late types showed wide phase angles. Even though daytime sleepiness and sleep duration did not differ between subgroups, mood and sleep quality declined as lateness increased. Extreme late chronotypes experienced higher evening sleepiness, while slight late chronotypes showed higher evening attention. Chronotype but not DLMO predicted bedtime on school- and particularly weekend-nights. Conclusions: Our findings suggest that with increasing lateness, the likelihood of experiencing poor sleep quality and mood disorders increases. As DLMO did not predict bedtime, our data indicate that the factors contributing to a late chronotype are versatile and complex, particularly for extreme late types. Further studies involving a larger and gender-balanced sample are needed to confirm findings.

Environmental noise-induced cardiovascular responses during sleep.

STUDY OBJECTIVES: This study was designed to test the utility of cardiovascular responses as markers of potentially different environmental noise disruption effects of wind farm compared to traffic noise exposure during sleep. METHODS: Twenty participants underwent polysomnography. In random order, and at six sound pressure levels from 33 dBA to 48 dBA in 3 dB increments, three types of wind farm and two types of road traffic noise recordings of 20-s duration were played during established N2 or deeper sleep, each separated by 20 s without noise. Each noise sequence also included a no-noise control. Electrocardiogram and finger pulse oximeter recorded pulse wave amplitude changes from the pre-noise onset baseline following each noise exposure and were assessed algorithmically to quantify the magnitude of heart rate and finger vasoconstriction responses to noise exposure. RESULTS: Higher sound pressure levels were more likely to induce drops in pulse wave amplitude. Sound pressure levels as low as 39 dBA evoked a pulse wave amplitude response (Odds ratio [95% confidence interval]; 1.52 [1.15, 2.02]). Wind farm noise with amplitude modulation was less likely to evoke a pulse wave amplitude response than the other noise types, but warrants cautious interpretation given low numbers of replications within each noise type. CONCLUSIONS: These preliminary data support that drops in pulse wave amplitude are a particularly sensitive marker of noise-induced cardiovascular responses during. Larger trials are clearly warranted to further assess relationships between recurrent cardiovascular activation responses to environmental noise and potential long-term health effects.

An experimental investigation on the impact of wind turbine noise on polysomnography-measured and sleep diary-determined sleep outcomes.

STUDY OBJECTIVES: Carefully controlled studies of wind turbine noise (WTN) and sleep are lacking, despite anecdotal complaints from some residents in wind farm areas and known detrimental effects of other noises on sleep. This laboratory-based study investigated the impact of overnight WTN exposure on objective and self-reported sleep outcomes. METHODS: Sixty-eight participants (38 females) aged (mean ± SD) 49.2 ± 19.5 were recruited from four groups; N = 14, living <10 km from a wind farm and reporting WTN related sleep disruption; N = 18, living <10 km from a wind farm and reporting no WTN sleep disruption; N = 18, reporting road traffic noise-related sleep disruption; and N = 18 control participants living in a quiet rural area. All participants underwent in-laboratory polysomnography during four full-night noise exposure conditions in random order: a quiet control night (19 dB(A) background laboratory noise), continuous WTN (25 dB(A)) throughout the night; WTN (25 dB(A)) only during periods of established sleep; and WTN (25 dB(A)) only during periods of wake or light N1 sleep. Group, noise condition, and interaction effects on measures of sleep quantity and quality were examined via linear mixed model analyses. RESULTS: There were no significant noise condition or group-by-noise condition interaction effects on polysomnographic or sleep diary determined sleep outcomes (all ps > .05). CONCLUSIONS: These results do not support that WTN at 25 dB(A) impacts sleep outcomes in participants with or without prior WTN exposure or self-reported habitual noise-related sleep disruption. These findings do not rule out effects at higher noise exposure levels or potential effects of WTN on more sensitive markers of sleep disruption. CLINICAL TRIAL REGISTRATION: ACTRN12619000501145, UTN U1111-1229-6126. Establishing the physiological and sleep disruption characteristics of noise disturbances in sleep. https://www.anzctr.org.au/. This study was prospectively registered on the Australian and New Zealand Clinical Trial Registry.

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.

The effect of wind turbine noise on polysomnographically measured and self-reported sleep latency in wind turbine noise naïve participants.

STUDY OBJECTIVES: Wind turbine noise (WTN) exposure could potentially interfere with the initiation of sleep. However, effects on objectively assessed sleep latency are largely unknown. This study sought to assess the impact of WTN on polysomnographically measured and sleep diary-determined sleep latency compared to control background noise alone in healthy good sleepers without habitual prior WTN exposure. METHODS: Twenty-three WTN naïve urban residents (mean ± SD age: 21.7 ± 2.1 years, range 18-29, 13 females) attended the sleep laboratory for two polysomnography studies, one week apart. Participants were blind to noise conditions and only informed that they may or may not hear noise during each night. During the sleep onset period, participants were exposed to counterbalanced nights of WTN at 33 dB(A), the upper end of expected indoor values; or background noise alone as the control condition (23 dB(A)). RESULTS: Linear mixed model analysis revealed no differences in log10 normalized objective or subjective sleep latency between the WTN versus control nights (median [interquartile range] objective 16.5 [11.0 to 18.5] vs. 16.5 [10.5 to 29.0] min, p = .401; subjective 20.0 [15.0 to 25.0] vs. 15.0 [10.0 to 30.0] min, p = .907). CONCLUSIONS: Although undetected small effects cannot be ruled out, these results do not support that WTN extends sleep latency in young urban-dwelling individuals without prior WTN exposure.

A Novel Electroencephalogram-derived Measure of Disrupted Delta Wave Activity during Sleep Predicts All-Cause Mortality Risk.

Rationale: Conventional markers of sleep disturbance, based on manual electroencephalography scoring, may not adequately capture important features of more fundamental electroencephalography-related sleep disturbance. Objectives: This study aimed to determine if more comprehensive power-spectral measures of delta wave activity during sleep are stronger independent predictors of mortality than conventional sleep quality and disturbance metrics. Methods: Power spectral analysis of the delta frequency band and spectral entropy-based markers to quantify disruption of electroencephalography delta power during sleep were performed to examine potential associations with mortality risk in the Sleep Heart Health Study cohort (N = 5,804). Adjusted Cox proportional hazard models were used to determine the association between disrupted delta wave activity at baseline and all-cause mortality over an approximately 11-year follow-up period. Results: Disrupted delta electroencephalography power during sleep was associated with a 32% increased risk of all-cause mortality compared with no fragmentation (hazard ratio, 1.32 [95% confidence interval, 1.14-1.50]), after adjusting for total sleep time and other clinical and lifestyle-related covariates, including sleep apnea. The association was of similar magnitude to a reduction in total sleep time from 6.5 hours to 4.25 hours. Conventional measures of sleep quality, including wake after sleep onset and arousal index, were not predictive of all-cause mortality. Conclusions: Delta wave activity disruption during sleep is strongly associated with all-cause mortality risk, independent of traditional potential confounders. Future investigation into the potential role of delta sleep disruption on other specific adverse health consequences such as cardiometabolic, mental health, and safety outcomes has considerable potential to provide unique neurophysiological insight.

Sleep misestimation among older adults suffering from insomnia with short and normal objective sleep duration and the effects of cognitive behavior therapy.

STUDY OBJECTIVES: Compare the degree of sleep misestimation in older adults with insomnia presenting with objectively short relative to normal sleep duration, and investigate the differential therapeutic response on sleep misestimation between the proposed sleep duration phenotypes to cognitive-behavior therapy for insomnia (CBTi). METHODS: Ninety-one adults (male = 43, mean age = 63.34, SD = 6.41) with sleep maintenance insomnia were classified as short sleepers (SS; <6 h total sleep time [TST]) or normal sleepers (NS; ≥6 h TST) based on one night of home-based polysomnography. Participants were randomly allocated to CBTi (N = 30 SS, N = 33 NS) or to a wait-list control condition (N = 9 SS, N = 19 NS). Sleep misestimation was calculated as the difference scores of subjective (sleep diary reported) and objective (derived from actigraphy) sleep onset latency (SOL), wake after sleep onset (WASO), and TST at pre- and post-treatment, and 3-month follow-up. RESULTS: Prior to treatment, perception of SOL, WASO, and TST did not differ between patients with objectively short sleep duration relative to those with objectively normal sleep duration. Patients' perception of WASO and TST, improved immediately following treatment and at 3-month follow-up relative to the waitlist group. These improvements did not differ significantly between those with short or normal objective sleep duration prior to treatment. CONCLUSIONS: The degree of sleep misestimation is similar for older adults suffering from chronic insomnia with short or normal objective sleep duration. Irrespective of objective sleep duration prior to treatment, CBTi produces significant improvements in sleep perception. CLINICAL TRIAL REGISTRATION NUMBER: ACTRN12620000883910.