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.

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.

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.

Delayed melatonin circadian timing, lower melatonin output, and sleep disruptions in myopic, or short-sighted, children.

STUDY OBJECTIVES: This study investigated the differences in melatonin circadian timing and output, sleep characteristics, and cognitive function in myopic and non-myopic (or emmetropic) children, aged 8-15 years. METHODS: Twenty-six myopes (refractive error [mean ±â€…standard error mean] -2.06 ±â€…0.23 diopters) and 19 emmetropes (-0.06 ±â€…0.04 diopters), aged 11.74 ±â€…2.31 years were recruited. Circadian timing was assessed using salivary dim-light melatonin onset (DLMO), collected half-hourly for 7 hours, beginning 5 hours before and finishing 2 hours after individual average sleep onset in a sleep laboratory. Nocturnal melatonin output was assessed via aMT6s levels from urine voids collected from 05:30 pm to 8:00 am the following morning. Actigraphy-derived objective sleep timing were acquired for a week prior to the sleep laboratory visit. Cognitive assessments of sustained attention (using psychomotor vigilance task [PVT]) and working memory (using digit spans) were performed on the night of sleep laboratory. RESULTS: Myopic children (9:07 pm ±â€…14 minutes) exhibited a DLMO phase-delay of 1 hour 8 minutes compared to emmetropes (7:59 pm ±â€…13 minutes), p = 0.002. aMT6s melatonin levels were significantly lower among myopes (18.70 ±â€…2.38) than emmetropes (32.35 ±â€…6.93, p = 0.001). Myopes also exhibited significantly delayed sleep onset, delayed wake-up time, poor and reduced sleep, and more evening-type diurnal preference than emmetropes (all p < 0.05). Finally, myopes showed a slower reaction time in the PVT (p < 0.05), but not digit span tasks at night. CONCLUSIONS: These findings suggest a potential association between circadian rhythm dysfunction and myopia in children.

General practitioner assessment and management of insomnia in adults.

BACKGROUND: Sleep disturbance is among the most prevalent presentations in Australian general practice. Insomnia, the most common sleep disorder, is associated with impaired daytime, social and occupational function, reduced quality of life and substantially increased risk of future depression. Guidelines from Australian and international general practice, sleep and medical societies strongly recommend cognitive behavioural therapy for insomnia (CBT-i) as the first-line treatment for chronic insomnia. This is because CBT-i targets the underlying causes of insomnia, results in sustained improvements and commonly improves comorbid conditions such as depression and pain. OBJECTIVE: This article aims to provide an overview of evidence-based assessment, management and referral options for insomnia in Australian general practice. DISCUSSION: Access to brief insomnia assessment and evidenced-based treatments are becoming increasingly available to Australian general practitioners. CBT-i can be delivered through self-guided online programs or by suitably trained general practitioners and psychologists.

General practitioner management of comorbid insomnia and sleep apnoea.

BACKGROUND: Insomnia and obstructive sleep apnoea are the two most common sleep disorders and frequently co-exist. Patients with comorbid insomnia and sleep apnoea experience worse daytime function, mental health and physical health than patients with either disorder alone. General practitioners may face unique challenges in the assessment and management of this prevalent and debilitating condition. OBJECTIVE: This article aims to provide an overview of the prevalence, consequences, assessment and management of patients with comorbid insomnia and sleep apnoea in Australian general practice. DISCUSSION: Patients with either insomnia or sleep apnoea should be assessed for both conditions. Treatments for both disorders should be offered to patients with both conditions. The recommended treatment for insomnia is cognitive behavioural therapy, whereas the recommended first-line treatment for moderate and severe obstructive sleep apnoea is lifestyle/weight management advice (where relevant) and continuous positive airway pressure therapy.

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.

Co-morbid insomnia and sleep apnea (COMISA): recent research and future directions.

PURPOSE OF REVIEW: Insomnia and obstructive sleep apnea have previously been viewed as completely independent conditions. However, there is now increasing recognition that insomnia and sleep apnea frequently co-occur. Co-morbid insomnia and sleep apnea (COMISA) is a highly prevalent condition that is associated with impairment of sleep, daytime function, mental health and physical health outcomes, and mortality risk. This review aims to provide an update on COMISA prevalence, consequences, treatment approaches, and future research directions. RECENT FINDINGS: People with COMISA experience worse sleep, mental health, physical health, quality of life and longevity compared to people with neither condition, and often compared to those with insomnia alone and sleep apnea alone. Emerging evidence suggests that cognitive behavioral therapy for insomnia is an effective treatment in the presence of treated and untreated sleep apnea, that may also improve manifestations and subsequent management of sleep apnea. Future research is required to understand the etiology of COMISA, and to develop and implement tailored treatment approaches. SUMMARY: It is important for sleep and respiratory technicians, researchers and clinicians to be aware of the high co-morbidity rates, consequences, and treatment requirements of patients with co-morbid insomnia and sleep apnea.

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.

Development of evening sleep homeostatic pressure in early adolescent boys.

The physiological processes governing sleep regulation show maturational changes during adolescent development. To date, data are available to specify when delays in circadian timing occur; however, no longitudinal data exist to characterize the maturation of the accumulation of sleep pressure across the evening. The aim of this longitudinal study was to test whether this change in evening sleep propensity can be identified during early adolescence. Twenty pre-pubescent boys' (Mage = 10.3, SD = 0.4 years) evening sleep homeostats were assessed using a series of sleep latency tests every hour (7:30 p.m. to 3:30 a.m.) at 6-month intervals across four waves. While results revealed shorter sleep onset latencies with increasing wakefulness (p < .001), this effect was not moderated by study wave (p = .79). Evening sleep propensity thus appears to remain stable in boys during early adolescence. Future studies should expand upon these findings by using larger samples of girls as well as boys across an extended age range during the teenage years.

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.

The efficacy of intensive sleep retraining for insomnia: A systematic review and research agenda.

Intensive sleep retraining (ISR) is a brief behavioural treatment for sleep onset insomnia, administered in just a single overnight treatment session. This systematic review evaluates existing trials about the efficacy of intensive sleep retraining for treating insomnia, to inform whether there is enough evidence to recommend its use for clinical practice. A systematic literature search was conducted across three databases, yielding 108 results. Of these studies, three were deemed suitable for inclusion in this review. The included studies consistently reported significant reductions in insomnia symptoms following intensive sleep retraining, particularly decreases in sleep diary-derived sleep latency and increases in total sleep time. Based on these inconclusive but promising findings, a research agenda is proffered to test intensive sleep retraining as a treatment for insomnia. Large randomised controlled trials are needed to elucidate the potential benefits of intensive sleep retraining for different populations with insomnia, as are mechanistic trials to test which components underlie its seemingly therapeutic effects. Since more practical modalities of intensive sleep retraining administration have been developed, such trials are more feasible to conduct now than ever before.

Wearable Device-Delivered Intensive Sleep Retraining as an Adjunctive Treatment to Kickstart Cognitive-Behavioral Therapy for Insomnia.

Intensive Sleep Retraining is a behavioral treatment for sleep onset insomnia that produces substantial benefits in symptoms after a single treatment session. This technique involves falling asleep and waking up shortly afterward repeatedly: a process that is thought to retrain people to fall asleep quickly when attempting sleep. Although originally confined to the sleep laboratory, recent technological developments mean that this technique is feasible to self-administer at home. With multiple randomised controlled trials required to confirm its efficacy, Intensive Sleep Retraining may serve as an adjunctive treatment to cognitive-behavioral therapy for insomnia, improving short-term efficacy by kick-starting treatment gains.

The Good Sleeper Scale-15 items: a questionnaire for the standardised assessment of good sleepers.

Research with 'good sleepers' is ubiquitous, yet there are no standardised criteria to identify a 'good sleeper'. The present study aimed to create and validate a questionnaire for identifying good sleepers for use in research studies known as the Good Sleeper Scale-15 items (GSS-15). Data were derived from a population-based survey of Australian adults (n = 2,044). A total of 23 items were chosen for possible inclusion. An exploratory factor analysis (EFA) was conducted on ~10% of the survey dataset (n = 191) for factor identification and item reduction. A confirmatory factor analysis (CFA) was conducted on the remaining data (n = 1,853) to test model fit. Receiver operating characteristic curves and correlations were conducted to derive cut-off scores and test associations with sleep, daytime functioning, health, and quality-of-life. The EFA identified six factors: 'Sleep Difficulties', 'Timing', 'Duration', 'Regularity', 'Adequacy', and 'Perceived Sleep Problem'. The CFA showed that model fit was high and comparable to other sleep instruments, χ2 (63) = 378.22, p < 0.001, root mean square error of approximation = 0.05, with acceptable internal consistency (α = 0.76). Strong correlations were consistently found between GSS-15 global scores and outcomes, including 'a good night's sleep' (r = 0.7), 'feeling un-refreshed' (r = -0.59), and 'experienced sleepiness' (r = -0.51), p < 0.001. Cut-off scores were derived to categorise individuals likely to be a good sleeper (GSS-15 score ≥40) and those very likely to be a good sleeper (GSS-15 score ≥45). The GSS-15 is a freely available, robust questionnaire that will assist in identifying good sleepers for the purpose of sleep research. Future work will test relationships with other sleep measures in community and clinical samples.

Comorbid Insomnia and Sleep Apnea: Assessment and Management Approaches.

Comorbid insomnia and sleep apnea (COMISA) is a highly prevalent and debilitating condition that is more difficult to treat compared with insomnia alone or sleep apnea alone. Approximately 30% to 50% of sleep clinic patients with sleep apnea report comorbid insomnia symptoms. Comorbid insomnia is associated with lower adherence to positive airway pressure therapy for obstructive sleep apnea. Management approaches that include targeted treatments for both insomnia and sleep apnea lead to the best treatment outcomes for patients with COMISA. Therefore, sleep clinics should incorporate insomnia and COMISA management pathways including access to cognitive behavioral therapy for insomnia.

Electric lighting, adolescent sleep and circadian outcomes, and recommendations for improving light health.

Light is a potent circadian entraining agent. For many people, daily light exposure is fundamentally dysregulated with reduced light during the day and increased light into the late evening. This lighting schedule promotes chronic disruption to circadian physiology resulting in a myriad of impairments. Developmental changes in sleep-wake physiology suggest that such light exposure patterns may be particularly disruptive for adolescents and further compounded by lifestyle factors such as early school start times. This narrative review describes evidence that reduced light exposure during the school day delays the circadian clock, and longer exposure durations to light-emitting electronic devices in the evening suppress melatonin. While home lighting in the evening can suppress melatonin secretion and delay circadian phase, the patterning of light exposure across the day and evening can have moderating effects. Photic countermeasures may be flexibly and scalably implemented to support sleep-wake health; including manipulations of light intensity, spectra, duration and delivery modality across multiple contexts. An integrative approach addressing physiology, attitudes, and behaviors will support optimization of light-driven sleep-wake outcomes in adolescents.

Intensive sleep retraining treatment for insomnia administered by smartphone in the home: an uncontrolled pilot study.

STUDY OBJECTIVES: Intensive sleep retraining (ISR) is a behavioral treatment that involves a patient falling asleep repeatedly over 1 treatment session (< 24 hours in duration) to treat sleep-onset insomnia. ISR relies on high homeostatic sleep and circadian rhythm drives to facilitate rapid sleep onsets overnight. The high cost and inaccessibility of laboratory-based ISR is a significant practical barrier to treatment uptake. Smartphone-delivered ISR offers a significantly more affordable, flexible, and efficient method to treat chronic insomnia. The present study is the first trial of ISR administered via smartphone in the home environment. METHODS: Smartphone-delivered ISR was investigated with 12 individuals with chronic insomnia (9 women, 3 men, aged 49.75 ± 7.71 years) using a single-group, repeated-measures, case-replication series design. Participants received a single overnight session of home-based ISR treatment administered by smartphone. Sleep onset trials started at 23:00 and concluded after 40 trials or at 11:00 the following morning, whichever occurred first. Sleep diary and psychological variables associated with insomnia were measured at pretreatment, post-treatment, and 4- and 7-week follow-up. RESULTS: Significant improvements with moderate to strong effects (d = 0.59-1.94) were indicated for sleep-onset latency, sleep efficiency, insomnia symptom severity, sleep self-efficacy, anticipatory sleep anxiety, dysfunctional beliefs about sleep, and daytime fatigue and functioning compared to baseline. Therapeutic benefits were largely maintained at the 7-week follow up. CONCLUSIONS: This pilot study suggests that ISR may be feasibly administered via smartphone in the home. With fewer trials and a shorter treatment session, smartphone-delivered ISR seemed to achieve similar outcomes to the earlier laboratory-based ISR procedure. Randomized controlled trials are warranted to investigate the efficacy of smartphone-administered ISR. CITATION: Mair A, Scott H, Lack L. Intensive sleep retraining treatment for insomnia administered by smartphone in the home: an uncontrolled pilot study. J Clin Sleep Med. 2022;18(6):1515-1522.

Does total sleep time substantially increase after cognitive behavioral therapy for insomnia?

STUDY OBJECTIVES: In most standardized approaches to cognitive behavioral therapy for insomnia, it is commonly the case that total wake time is reduced substantially during sleep restriction, but self-reported total sleep time (TST) is minimally affected. By follow-up, however, TST increases by almost 1 hour on average. A secondary analysis was undertaken to assess what percentage of participants meet or appreciably exceed baseline TST after cognitive behavioral therapy for insomnia. METHODS: Data were drawn from a randomized controlled trial assessing acute and maintenance therapies for chronic insomnia (n = 80). The present analyses assessed the percentage of participants that 1) reached (≥ 0 minute increase) and 2) appreciably exceeded (≥ 30 minutes increase) baseline TST as assessed via daily sleep diaries at posttreatment and 3, 6, 12, and 24 months following treatment. RESULTS: By the end of acute treatment, 45% of participants reached or exceeded baseline TST. By 24 months follow-up, this percentage had increased to 86%. Only 17% of participants achieved a 30-minute increase in TST by the end of acute treatment, and this proportion only increased to 58% over time. CONCLUSIONS: These findings suggest that cognitive behavioral therapy for insomnia in its current form does not appreciably increase self-reported TST in a significant proportion of patients with insomnia. Whether participants would benefit from further increases in TST warrants investigation. The further titration of sleep opportunity may be useful to accelerate increases in TST, to extend the effect to a larger subset of patients, and/or to increase the magnitude of the TST gain. CITATION: Scott H, Cheung JMY, Muench A, et al. Does total sleep time substantially increase after cognitive behavioral therapy for insomnia? J Clin Sleep Med. 2022;18(7):1823-1829.

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.

The association of co-morbid insomnia and sleep apnea with prevalent cardiovascular disease and incident cardiovascular events.

Insomnia and obstructive sleep apnea commonly co-occur (co-morbid insomnia and sleep apnea), and their co-occurrence has been associated with worse cardiometabolic and mental health. However, it remains unknown if people with co-morbid insomnia and sleep apnea are at a heightened risk of incident cardiovascular events. This study used longitudinal data from the Sleep Heart Health Study (N = 5803) to investigate potential associations between co-morbid insomnia and sleep apnea and cardiovascular disease prevalence at baseline and cardiovascular event incidence over ~11 years follow-up. Insomnia was defined as self-reported difficulties initiating and/or maintaining sleep AND daytime impairment. Obstructive sleep apnea was defined as an apnea-hypopnea index ≥ 15 events per hr sleep. Co-morbid insomnia and sleep apnea was defined if both conditions were present. Data from 4160 participants were used for this analysis. The prevalence of no insomnia/obstructive sleep apnea, insomnia only, obstructive sleep apnea only and co-morbid insomnia and sleep apnea was 53.2%, 3.1%, 39.9% and 1.9%, respectively. Co-morbid insomnia and sleep apnea was associated with a 75% (odd ratios [95% confidence interval]; 1.75 [1.14, 2.67]) increase in likelihood of having cardiovascular disease at baseline after adjusting for pre-specified confounders. In the unadjusted model, co-morbid insomnia and sleep apnea was associated with a twofold increase (hazard ratio, 95% confidence interval: 2.00 [1.33, 2.99]) in risk of cardiovascular event incidence. However, after adjusting for pre-specified covariates, co-morbid insomnia and sleep apnea was not significantly associated with incident cardiovascular events (hazard ratio 1.38 [0.92, 2.07]). Comparable findings were obtained when an alternative definition of insomnia (difficulties initiating and/or maintaining sleep without daytime impairment) was used.