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

In Aotearoa/New Zealand, ethnic inequities in sleep health exist for young children and adults and are largely explained by inequities in socioeconomic deprivation. Poor sleep is related to poor mental health for these age groups but whether sleep inequities and associations with mental health exist for school-aged children is unclear. We aimed to (1) determine the prevalence of poor sleep health including sleep problems by ethnicity, (2) examine social determinants of health associated with poor sleep, and (3) investigate relationships between poor sleep and mental health for 5-14-year-olds using cross-sectional New Zealand Health Survey data (n = 8895). Analyses included weighted prevalence estimates and multivariable logistic regression. Short sleep was more prevalent for Indigenous Māori (17.6%), Pacific (24.5%), and Asian (18.4%) children, and snoring/noisy breathing during sleep was more prevalent for Māori (29.4%) and Pacific (28.0%) children, compared to European/Other (short sleep 10.2%, snoring/noisy breathing 17.6%). Ethnicity and neighborhood socioeconomic deprivation were independently associated with short sleep and snoring/noisy breathing during sleep. Short sleep was associated with increased odds of anxiety, attention deficit hyperactivity disorder, and activity-limiting emotional and psychological conditions after adjusting for ethnicity, deprivation, age, and gender. In addition, long sleep was independently associated with increased odds of depression. These findings demonstrate that for school-aged children ethnic inequities in sleep exist, socioeconomic deprivation is associated with poor sleep, and poor sleep is associated with poor mental health. Sociopolitical action is imperative to tackle social inequities to support sleep equity and mental health across the lifecourse.

Sleep inertia, the temporary period of impairment experienced upon waking, is a safety hazard that has been implicated in serious work-related incidents resulting in injuries as well as the loss of life and assets. As such, sleep inertia warrants formal management in industries where personnel are required to undertake their role soon after waking (e.g. emergency services, engineers, and health care). At present, there is a lack of practical, evidence-based guidance on how sleep inertia could be formally managed at an organizational level. We propose a preliminary framework for managing sleep inertia based on the translation of research findings into specific work procedure modifications/control mechanisms. Within the framework, work procedure modifications/control mechanisms to manage sleep inertia are organized into three levels: (1) modifications/controls that eliminate the chance of sleep inertia, (2) modifications/controls that reduce sleep inertia severity, and (3) modifications/controls that manage the risk of errors during sleep inertia. Practical considerations, limitations, and areas of further research are highlighted for each modification/control to help determine how readily each control measure could be implemented by industries at present. A guide for organizations to use this preliminary framework of sleep inertia management is put forward, as well as the next research priorities to strengthen the utility and evidence base of the framework. This paper is part of the Sleep and Circadian Rhythms: Management of Fatigue in Occupational Settings Collection.

After first recalling the origins of my interest in sleep and dreams at UVa (1969) and my MD thesis at Yale on sleep in mood disorders (1973), I will describe my service to the field of sleep disorders medicine, through various roles in the American Sleep Disorders Association, the Institute of Medicine, the National Institute of Mental Health, and the DSM-5 Task Force of the American Psychiatric Association. I will then present the broad themes of my contributions to psychiatric sleep research, focusing on the neurobiology of sleep as a dimension of the risk and protective architecture for depression in older adults, as a bridge to diagnostic and treatment issues in later-life depression, and to clinical and translational neuroscience addressing the intersections of sleep, aging, and mind/brain health. Throughout this narrative, I highlight many relationships with mentors and mentees. All of my scientific activity has been team-based, providing the social matrix for the physician-scientist I have become. This paper is part of the Living Legends in Sleep Research series, which is sponsored by Idorsia Pharmaceuticals and Jazz Pharmaceuticals.

Herein the major accomplishments, trials and tribulations, and epiphanies experienced by James M. Krueger over the course of his career in sleep research are presented. They include the characterization of a) the supranormal EEG delta waves occurring during NREMS post sleep loss, b) Factor S as a muramyl peptide, c) the physiological roles of cytokines in sleep regulation, d) multiple other sleep regulatory substances, e) the dramatic changes in sleep over the course of infectious diseases, and f) sleep initiation within small neuronal/glial networks. The theory that the preservation of brain plasticity is the primordial sleep function is briefly discussed. These accomplishments resulted from collaborations with many outstanding scientists including James M. Krueger's mentors (John Pappenheimer and Manfred Karnovsky) and collaborators later in life, including Charles Dinarello, Louis Chedid, Mark Opp, Ferenc Obal jr., Dave Rector, Ping Taishi, Linda Toth, Jeannine Majde, Levente Kapas, Eva Szentirmai, Jidong Fang, Chris Davis, Sandip Roy, Tetsuya Kushikata, Fabio Garcia-Garcia, Ilia Karatsoreos, Mark Zielinski, and Alok De, plus many students, e.g. Jeremy Alt, Kathryn Jewett, Erika English, and Victor Leyva-Grado.

Study objective: To investigate whether poor sleep quality is associated with pre-term birth (PTB) risk, overall and independent of sleep apnea and habitual snoring.

Methods: We used longitudinal data from the Washington University Prematurity Research Cohort to investigate the association between poor sleep quality (defined as a Pittsburgh Sleep Quality Index > 5) and PTB, overall and independent of sleep apnea and snoring (defined by the Berlin questionnaire and prior sleep clinic attendance). Associations were investigated for sleep quality early and throughout pregnancy. Stratified analyses were performed by factors previously shown to modify associations between sleep and PTB (race, pre-pregnancy obesity).

Results: Of the 976 eligible participants, 50.1% experienced poor sleep quality early in pregnancy (<20 completed weeks) and 14.2% delivered pre-term (n = 50 without and 89 with poor sleep quality). In multivariable-adjusted analyses, poor sleep quality early in pregnancy was associated with increased PTB risk (hazard ratio [HR] = 1.48, 95% confidence interval [CI] = 1.02-2.14). This association persisted after further adjustment for sleep apnea and snoring (HR = 1.50, 95% CI = 1.02-2.20) and in analyses stratified by race. It varied, however, by pre-pregnancy obesity. Among individuals without obesity, no association was observed between poor sleep and PTB (HR = 1.08, 95% CI = 0.65-1.79), whereas among those with obesity, a positive association was observed (HR = 2.94, 95% CI = 1.52-5.69, p-interaction = .05). This association was limited to individuals with obesity who experienced poor sleep both earlier and later in pregnancy (HR = 3.94, 95% CI = 1.56-9.99).

Conclusion: Our findings suggest that improving sleep quality early in pregnancy may be important for PTB prevention, particularly among individuals with obesity.

Objectives: The aims were to explore multidimensional sleep health and the different dimensions of sleep health in the adult Norwegian population in relation to sex, age, education, circadian preference, and chronic insomnia.

Methods: A representative sample of 1028 Norwegians, aged 18 + years completed a cross-sectional web-based survey. Sleep health was measured with the multidimensional RU_SATED scale, which assesses the dimensions of regularity, satisfaction, alertness, timing, efficiency, and duration. Insomnia was assessed with the Bergen Insomnia Scale. Data were analyzed with chi-square tests, t-tests, one-way ANOVAs, and regression analyses, as appropriate. Response rate was 33.5%.

Results: Sleep health was better in males, with increasing age, and with higher educational level, and was poorer in participants with evening preference and chronic insomnia, compared to their respective counterparts. When investigating the different sleep health dimensions, males scored better than females on satisfaction (adjusted odds ratio [aOR] = 0.69, 95% CI = 0.51 to 0.93), timing (aOR = 0.66, 95% CI = 0.49 to 0.88), and efficiency (aOR = 0.68, 95% CI = 0.52 to 0.89). Older age was associated with better scores on regularity and satisfaction, whereas young age was associated with better scores on alertness and duration. High educational level was associated with better scores on alertness, timing, and duration. Evening types scored worse than morning types on regularity (aOR = 0.27, 95% CI = 0.18 to 0.41), satisfaction (aOR = 0.37, 95% CI = 0.26 to 0.53), and timing (aOR = 0.36, 95% CI = 0.26 to 0.51). Participants with chronic insomnia scored worse than participants without insomnia on all six sleep health dimensions.

Conclusions: Sleep health differed significantly in relation to sex, age, education, circadian preference, and chronic insomnia. However, specific group differences were not equally evident in all sleep health dimensions.

We have recently demonstrated that the alkaloid rhynchophylline (RHY; purified from Uncaria plants) induces sleep and modifies electrocorticographic (ECoG) activity throughout the 24-h day in a vigilance state-dependent manner in wild-type mice. We here asked whether this alkaloid impacts wake/sleep variables in the absence of the cell adhesion protein EPHA4, via ECoG recording in EphA4 knockout (KO) mice submitted to the same RHY treatment contemporaneously to the wild-type mice (littermates). We uncover that RHY decreases time spent awake and increases time spent in slow wave sleep in EphA4 KO mice and alters the 24-h time course of ECoG activity during wakefulness and sleep states. These observations are similar to the reported effects of RHY in wild-type littermate animals, which strongly supports that RHY-driven sleep alterations are not dependent on the presence of EPHA4.

Study objectives: To determine the trajectory of: (i) objective sleep parameters and (ii) caregiver-reported sleep questionnaire scores over 3 years in children with Smith-Magenis syndrome (SMS) compared to age-matched typically developing (TD) controls. We also aimed to (iii) describe individual profiles of change in sleep parameters over time.

Methods: Week-long, overnight actigraphy and questionnaire data from 13 children with SMS and 13 age-matched TD children were collected at Time 1 and Time 2 (3 years later). Independent samples t-tests, paired samples t-tests, and Bayesian analyses were used to compare sleep parameters and sleep questionnaire scores between groups at each time point and compare data within groups to assess change over time.

Results: Sleep parameters were consistently more disrupted in the SMS group than the TD group, with significantly reduced sleep efficiency, increased wake after sleep onset and earlier get up times at both time points. This was mirrored in the questionnaire data, with children with SMS evidencing higher scores for overall sleep disturbance, night waking, and daytime sleepiness. While TD sleep parameters demonstrated expected developmental changes over 3 years, in the SMS group sleep parameters and variability between and within children remained largely stable. However, some children with SMS showed substantial variation in sleep parameters over time. Questionnaire scores remained stable over 3 years in both groups.

Conclusions: Overall, sleep disturbance appears to be a stable feature of SMS, indicative of a divergent sleep trajectory compared to TD peers. Proactive intervention approaches should be considered for poor sleep in SMS.

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.