Sleep advances : a journal of the Sleep Research Society最新文献

The first-ever comprehensive report on the sleep health of Aboriginal and Torres Strait Islander peoples (hereafter referred to as First Nations Australians) highlighted an 18% prevalence of poor sleep in First Nations youth. While sleep health is important across the lifespan, adolescence is a critical life stage with increased vulnerability to poor sleep. In adolescents, pubertal changes, social and academic commitments, and peer pressure significantly increase the risk of poor sleep, which often results in social and emotional well-being (SEWB) issues. In First Nations adolescents, high rates of SEWB issues demand effective prevention and management strategies. Evidence from non-First Nations adolescents suggests that timely prevention, identification, diagnosis, and management of poor sleep help reduce the risk and severity of SEWB issues in First Nations adolescents. A research program is proposed to be called "Let's Yarn About Sleep," which will co-design, deliver, and evaluate a tailored sleep improvement program for Australian First Nations adolescents (12-18 years). Co-design workshops will be conducted with First Nations community Elders, parents and carers, youth, and First Nations service providers to develop the sleep health program. The program will also include training Aboriginal Youth Workers (AYWs) to deliver the sleep health program. The program evaluation will be based on a mixed methods design, using self-reported (survey tools and focus group discussions) and technology-based measures (actigraphy data) to measure changes in First Nations adolescents' sleep and SEWB. The evaluation will focus on the impact of training AYWs on program delivery and uptake.

Chronic insomnia is a prevalent sleep disorder where <1% of patients receive the recommended first-line treatment; Cognitive Behavioural Therapy for Insomnia. Digital technologies and self-managed therapies are scalable solutions to address this critical gap in patient care, but it is presently difficult to know which therapies are best. This study will test the comparative efficacy and cost-benefits of Intensive Sleep Retraining administered by the THIM sleep tracker, Sleep Healthy Using the Internet (SHUTi) treatment program, and their combination (THIM then SHUTi) versus a waitlist control group. This study is a 4 (treatment: +/- THIM and +/- SHUTi) × 3 (time: pretreatment, posttreatment, and 2-month follow-up) randomized controlled trial. Participants who meet the diagnostic criteria for Chronic Insomnia Disorder will be randomized to one of four groups. Sleep and daytime functioning symptoms will be assessed via self-report daily and weekly questionnaires, and objective sleep trackers during treatment and for 2 weeks at pre-treatment, post-treatment, and 2-month follow-up. The primary outcome is total wake time, with a reduction of ≥30 minutes considered a clinically meaningful difference. For the primary analysis, the interaction between the treatment group and time on total wake time will be analyzed using repeated measures analyses of variance (ANOVA). This project was approved by the Southern Adelaide Clinical Human Research Ethics Committee (2021/HRE00414) and registered in the Australian and New Zealand Clinical Trials Registry (ACTRN12622000778785). As the first study to investigate the comparative efficacy of two different technology-enabled treatments for insomnia, this study will help inform clinicians and public health policy regarding the use cases for public and private health-funded technology-enabled options for insomnia.

Diminished sleep health is a known warning sign for suicide. However, the contexts and time periods within which diminished sleep elevates suicide risk are unknown. Modeling the complex process by which diminished sleep health impacts daily functioning and establishing proximal suicide risk factors can aid in addressing these important knowledge gaps. This paper describes the methods and research protocol for a study that aims to elucidate the nature of the sleep-suicide relationship and develop an integrated model of proximal suicide risk. Participants will be 200 adults at high risk for suicide recruited from a psychiatric inpatient unit. They will complete a baseline assessment including clinical interviews and self-reports, and laboratory tasks with concurrent electroencephalography to phenotype-relevant risk processes. This baseline assessment will be followed by 4 weeks of ecological momentary assessment and digital phenotyping, coupled with assessments of sleep via a wearable used to generate a minute-by-minute metric of cognitive effectiveness using the Sleep Activity, Fatigue, and Task Effectiveness algorithm index. Follow-up assessments will be conducted 1-, 3-, and 6-months post-hospital discharge to determine how the developed proximal model of risk prospectively predicts suicidal ideation and behavior. The results of this study have the potential to greatly enhance understanding of how and why diminished sleep health is related to real-world fluctuations in suicide risk, knowledge that can inform efforts to better prevent, and intervene to reduce suicides.

The reciprocal relationship between sleep and epilepsy has been reported by numerous clinical studies. However, the underlying neural mechanisms are poorly understood. Animal models of epilepsy are powerful tools to tackle this question. A lagging research area is the understudied sleep in epilepsy models. Here, we characterize sleep architecture and its relationship with seizures in a mouse model of sleep-related hypermotor epilepsy, caused by mutation of KCNT1. We demonstrated that nocturnal tonic-clonic seizures induce more non-rapid eye movement (NREM) sleep but suppress rapid eye movement (REM) sleep, resulting in altered sleep architecture in this mouse model. Importantly, the seizure number is quantitatively anticorrelated with the amount of REM sleep. Strikingly, this modulation of NREM and REM sleep states can be repeated in another mouse model of epilepsy with diurnal tonic-clonic seizures. Together, our findings provide evidence from rodent models to substantiate the close interplay between sleep and epilepsy, which lays the ground for mechanistic studies.

Study objectives: Airline transport pilot sleep during layover is an important factor for alertness on subsequent flights. Assessing pilots' sleep on layover is an important first step in helping them obtain the most recuperative sleep possible on layover. Here, we investigate the quantity and timing of sleep during layovers and determine predictors for layover sleep.

Methods: Sleep was assessed in 256 pilots flying a total of 473 long-range (LR; flight time 12-16 hours) or ultra-long-range (ULR; flight time > 16 hours) trips. Sleep was assessed using actigraphy. We employed linear mixed-effects models with layover sleep characteristics as the outcomes. The predictor variables included operational factors and sleep history.

Results: Overall, pilots averaged 7.2 hours of sleep per 24 hours of layover, which was significantly less than their daily sleep before or after the trip. Layover start time (relative to home base time) was the most salient predictor of sleep timing and quantity during both shorter (∼24-hour) and the first 24 hours of longer (∼48-hour) layovers. During the last 24 hours of longer layovers, crew type predicted sleep quantity.

Conclusions: Although average sleep quantity during layovers was within the margins of recommended sleep duration, it was still less than pre- and post-trip sleep duration, suggesting modest sleep loss on layovers. Layover start timing was the strongest predictor of layover sleep quantity and timing and, thus, may be a modifiable factor to protect circadian-aligned sleep opportunities during layover.

Study objectives: We investigated how a dimension of early life adversity (ELA), capturing threat in the home, relates to later epigenetic age acceleration in adolescence through sleep (duration, efficiency, and timing) to empirically test theoretical models suggesting the importance of sleep as a key mechanism linking ELA with poor health outcomes and to expand the limited literature on sleep and epigenetic aging among youth.

Methods: We utilized data from 861 participants in the Future of Families and Child Wellbeing Study who participated in the actigraphy substudy at age 15. Sleep variables used were average total sleep time (TST), sleep efficiency (SE), and sleep onset timing. Home threat was determined at ages 3, 5, and 9 from parent reports on the Child Conflict Tactics Scale, and epigenetic aging was measured through DNA methylation analyses of saliva samples collected at age 15.

Results: Higher levels of childhood home threat exposure were associated with less adolescent TST, lower SE, and later sleep onset timing. Adolescent SE and timing were associated with a faster pace of aging and epigenetic age acceleration. SE and timing mediated the link between childhood home threat exposure and adolescent epigenetic aging.

Conclusions: Epigenetic embedding of childhood threat exposure in the home may occur through adversity-related sleep disturbances in adolescence. Findings warrant greater attention to pediatric sleep health in theoretical models of biological embedding of adversity and point to sleep health improvement as a potential way to prevent adversity-related epigenetic age acceleration. This paper is part of the Genetic and other Molecular Underpinnings of Sleep, Sleep Disorders, and Circadian Rhythms Including Translational Approaches collection.

Despite extensive evidence on the roles of nonrapid eye movement (NREM) and REM sleep in memory processing, a comprehensive model that integrates their complementary functions remains elusive due to a lack of mechanistic understanding of REM's role in offline memory processing. We present the REM Refining and Rescuing (RnR) Hypothesis, which posits that the principal function of REM sleep is to increase the signal-to-noise ratio within and across memory representations. As such, REM sleep selectively enhances essential nodes within a memory representation while inhibiting the majority (Refine). Additionally, REM sleep modulates weak and strong memory representations so they fall within a similar range of recallability (Rescue). Across multiple NREM-REM cycles, tuning functions of individual memory traces get sharpened, allowing for integration of shared features across representations. We hypothesize that REM sleep's unique cellular, neuromodulatory, and electrophysiological milieu, marked by greater inhibition and a mixed autonomic state of both sympathetic and parasympathetic activity, underpins these processes. The RnR Hypothesis offers a unified framework that explains diverse behavioral and neural outcomes associated with REM sleep, paving the way for future research and a more comprehensive model of sleep-dependent cognitive functions.

[This corrects the article DOI: 10.1093/sleepadvances/zpae070.153.].