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Study objectivesEstimate the genetic relationship of cannabis use with sleep deficits and an eveningness chronotype.MethodsWe used linkage disequilibrium score regression (LDSC) to analyze genetic correlations between sleep deficits and cannabis use behaviors. Secondly, we generated sleep deficit polygenic risk score (PRS) and estimated their ability to predict cannabis use behaviors using linear and logistic regression. Summary statistics came from existing genome-wide association studies of European ancestry that were focused on sleep duration, insomnia, chronotype, lifetime cannabis use, and cannabis use disorder (CUD). A target sample for PRS prediction consisted of high-risk participants and participants from twin/family community-based studies (European ancestry; n = 760, male = 64%; mean age = 26.78 years). Target data consisted of self-reported sleep (sleep duration, feeling tired, and taking naps) and cannabis use behaviors (lifetime ever use, number of lifetime uses, past 180-day use, age of first use, and lifetime CUD symptoms).ResultsSignificant genetic correlation between lifetime cannabis use and an eveningness chronotype (rG = 0.24, p < 0.001), as well as between CUD and both short sleep duration (

STUDY OBJECTIVES: Sleep problems are common, serving as both a predictor and symptom of posttraumatic stress disorder (PTSD), with these bidirectional relationships well established in the literature. While both sleep phenotypes and PTSD are moderately heritable, there has been a paucity of investigation into potential genetic overlap between sleep and PTSD. Here, we estimate genetic correlations between multiple sleep phenotypes (including insomnia symptoms, sleep duration, daytime sleepiness, and chronotype) and PTSD, using results from the largest genome-wide association study (GWAS) to date of PTSD, as well as publicly available GWAS results for sleep phenotypes within UK Biobank data (23 variations, encompassing four main phenotypes). METHODS: Genetic correlations were estimated utilizing linkage disequilibrium score regression (LDSC), an approach that uses GWAS summary statistics to compute genetic correlations across traits, and Mendelian randomization (MR) analyses were conducted to follow up on significant correlations. RESULTS: Significant, moderate genetic correlations were found between insomnia symptoms (rg range 0.36-0.49), oversleeping (rg range 0.32-0.44), undersleeping (rg range 0.48-0.49), and PTSD. In contrast, there were mixed results for continuous sleep duration and daytime sleepiness phenotypes, and chronotype was not correlated with PTSD. MR analyses did not provide evidence for casual effects of sleep phenotypes on PTSD. CONCLUSION: Sleep phenotypes, particularly insomnia symptoms and extremes of sleep duration, have shared genetic etiology with PTSD, but causal relationships were not identified. This highlights the importance of further investigation into the overlapping influences on these phenotypes as sample sizes increase and new methods to investigate directionality and causality become available.

Study objectivesActivities throughout the day, including sleep, sedentary behavior (SB), light-intensity physical activity (LIPA), and moderate to vigorous physical activity (MVPA) are independently associated with cardiometabolic health. Few studies have examined interrelationships between sleep and 24-hour activity and associations with cardiometabolic risk. The objective of this study is to understand how replacing time in SB, LIPA, or MVPA with sleep impacts cardiometabolic risk.MethodsWomen's Health Initiative OPACH Study participants (N = 3329; mean age = 78.5 ± 6) wore ActiGraph GT3X+ accelerometers 24 hours/7 days. Adjusted linear regression estimated the relationship between sleep duration and cardiometabolic markers. Separately for shorter (

Study Objective: Attempting to recover a sleep debt by extending sleep over the weekend is a common compensatory behavior in the population and is recommended by sleep-focused organizations. However, the purported benefits of catch-up sleep are based on a limited number of cross-sectional studies that relied on self-reported sleep. The objective of this study was to examine the association between accelerometer-derived weekend catch-up sleep and mortality and incident cardiovascular disease (CVD) in adults., Methods: A prospective cohort study of UK adults who wore wrist-attached accelerometers was conducted. Weekend catch-up sleep was defined as a longer average sleep duration on weekends compared to weekdays. Participants were categorized into four groups: no weekend catch-up sleep (reference); > 0 to < 1 hour; ≥ 1 to < 2 hours; and ≥ 2 hours difference. Associations between weekend catch-up sleep and mortality and incident CVD were assessed using Cox proportional hazards regression, adjusted for potential confounders., Results: A total of 73 513 participants (sample for mortality) and 70 518 participants (sample for CVD incidence) were included, with an average (SD) follow-up period of 8.0 (0.9) years. In multivariable-adjusted models, weekend catch-up sleep was not associated with mortality (≥ 2 hours group: hazard ratio [HR], 1.17 [95% CI: 0.97 to 1.41]) or incident CVD (HR, 1.05 [95% CI, 0.94 to 1.18]). Dose-response analyses treating catch-up sleep as a continuous measure or analyses restricted to adults sleeping less than 6 hours on weekdays at baseline were in agreement with these findings., Conclusions: Weekend catch-up sleep was not associated with mortality or CVD incidence. These findings do not align with previous evidence and recommendations by sleep authorities suggesting that extending sleep over the weekend may offer protective health benefits., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Study Objectives: This study aimed to determine the associations between accelerometer-measured sleep durations and the risks of incident cardiovascular disease (CVD) and CVD-related mortality., Methods: A total of 92 261 participants (mean age: 62.4 ± 7.8 years, 56.4% female) were included in UK Biobank between 2013 and 2015. Average daily sleep durations were measured using wrist-worn accelerometers over a 7-day period. Sleep durations were categorized as <7 hours/day, 7-9 hours/day (reference), and >9 hours/day. The incidence of CVD and CVD-related mortality were ascertained by hospital records and death registries., Results: During a median follow-up period of 7.0 years, a total of 13 167 participants developed CVD, and 1079 participants died of CVD. Compared with a sleep duration 7-9 hours/day, an accelerometer-measured sleep duration <7 hours/day but not >9 hours/day was associated with higher risks of incident CVD (HR 1.06, 95% CI: 1.02 to 1.10), CVD-related mortality (HR 1.29, 95% CI: 1.14 to 1.47), coronary heart disease (HR 1.11, 95% CI: 1.03 to 1.19), myocardial infarction (HR 1.14, 95% CI: 1.03 to 1.27), heart failure (HR 1.20, 95% CI: 1.08 to 1.34), and atrial fibrillation (HR 1.15, 95% CI: 1.07 to 1.24). A curvilinear dose‒response pattern was observed between accelerometer-measured sleep durations and incident CVD (poverall < .001), with L-shaped associations found for incident CVD and CVD-related mortality., Conclusions: An accelerometer-measured sleep duration of <7 hours/day but not >9 hours/day was associated with elevated risks of incident CVD and CVD-related mortality. Maintaining adequate sleep may help promote cardiovascular health., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Study Objectives: (1) To describe sleep in infancy and early childhood among children born to mothers with and without clinically significant depressive symptoms, and (2) to explore the relationships between maternal depressive symptoms and sleep patterns and problems during infancy and early childhood., Methods: Secondary analysis of longitudinal data from the Moe Kura: Mother and Child, Sleep and Wellbeing in Aotearoa/New Zealand study. Data was collected in pregnancy (T1), 12 weeks postpartum (T2), and 3 years post-birth (T3). Participants were 262 Māori and 594 non-Māori mother-child dyads. Chi-square and Independent T-tests measured bivariate associations between maternal mood (T1, T2, T3) and child sleep characteristics (T2, T3). Binary logistic regression models examined longitudinal and concurrent associations between maternal depressive symptoms and infant and preschooler sleep. Adjusted models accounted for key socio-demographic variables, as well as infant sleep variables in preschooler models., Results: Bivariate associations were found between prior and concurrent depressive symptomology and many of the infant and preschooler sleep outcomes. In adjusted models, prenatal depressive symptoms remained independently associated with shorter-than-recommended sleep durations in preschoolers. In these models, concurrent depression was also associated with night waking, night LSRSP, and perceived sleep problems at 12 weeks postpartum, and CSHQ-determined and perceived sleep problems at 3 years post birth., Conclusions: Longitudinal and cross-sectional associations were found between maternal depressive symptoms and child sleep. Sleep appears to be one pathway by which maternal depression confers risk for suboptimal child health outcomes. Findings support the need for earlier and better maternal mental health services., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society.)

Study Objectives: Shift work, insufficient sleep, and poor sleep quality at young age have been associated with increased risk of multiple sclerosis (MS). This study aimed to investigate the potential interaction between aspects of inadequate sleep (short sleep, phase shift, and poor sleep quality) during adolescence and HLA-DRB1*15:01 in relation to MS risk., Methods: We used a Swedish population-based case-control study (1253 cases and 1766 controls). Participants with different sleep patterns during adolescence and HLA-DRB1*15:01 status were compared regarding MS risk by calculating odds ratios with 95% confidence intervals (CI) using logistic regression models. Additive interaction between aspects of inadequate sleep and HLA-DRB1*15:01 status was assessed by calculating the attributable proportion due to interaction (AP) with 95% CI., Results: Short sleep duration (<7 hours/night) during adolescence acted synergistically with HLA-DRB1*15:01, increasing the risk of MS (AP 0.38, 95% CI: 0.01 to 0.75, p = .04). Similarly, subjective low sleep quality during adolescence interacted with HLA-DRB1*15:01 regarding risk of MS (AP 0.30, 95% CI: 0.06 to 0.56, p = .03), whereas phase shift did not significantly influence the risk of the disease, irrespective of HLA-DRB1*15:01 status., Conclusions: Our findings underscore the importance of addressing inadequate sleep during adolescence, particularly in the context of the HLA-DRB1*15:01 allele, as it appears to amplify the risk of subsequently developing MS., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society.)

Study Objectives: We examined associations between daily variations in objectively measured sleep and blood glucose in a sample of non-diabetic young adults to complement laboratory studies on how sleep affects blood glucose levels., Methods: 119 university students underwent sleep measurement using an Oura Ring 2 and continuous glucose monitoring (CGM) for up to 14 days. In 69 individuals who consumed a standardised diet across the study, multilevel models examined associations between sleep duration, timing and efficiency and daily CGM profiles. Separately, in 58 individuals, multilevel models were used to evaluate postprandial glycaemic responses to a test meal challenge on 7 days. Participants also underwent oral glucose tolerance testing once after a night of ad libitum sleep, and again following a night of sleep restriction by 1-2 hours relative to that individual's habitual sleep duration. Between-condition glucose and insulin excursions, HOMA-IR and Matsuda index were compared., Results: Nocturnal sleep did not significantly influence following-day CGM profiles, postprandial glucose, or nocturnal mean glucose levels (all Ps>0.05). Longer sleep durations were associated with lower same-night glucose variability (all Ps<0.001). However, the range of variation of sugar levels was small and unlikely to be of functional significance. Considering naps in the analysis did not alter the findings. Sleep restriction by an average of 1.73 hours (SD=0.97) did not significantly impact excursions in glucose or insulin or insulin sensitivity the following morning (all Ps>0.05)., Conclusions: Glucose handling in young, healthy adults may be more resilient to real-life fluctuations in sleep patterns than previously thought., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society.)

To characterize sleep duration, timing and continuity measures in pregnancy and their association with key demographic variables. Multisite prospective cohort study. Women enrolled in the nuMoM2b study (nulliparous women with a singleton gestation) were recruited at the second study visit (16-21 weeks of gestation) to participate in the Sleep Duration and Continuity substudy. Women 9 hours. In multivariable models including age, race/ethnicity, body mass index, insurance status, and recent smoking history, sleep duration was significantly associated with race/ethnicity and insurance status, while time in bed was only associated with insurance status. Sleep continuity measures and sleep midpoint were significantly associated with all covariates in the model, with the exception of age for fragmentation index and smoking for wake after sleep onset. Our results demonstrate the relationship between sleep and important demographic characteristics during pregnancy.

Sleep can be characterized along multiple dimensions. We investigated whether an aggregate measure of sleep health was associated with prevalent and incident clinically significant depression symptoms in a cohort of older women. Participants were older women (mean age 80.1 years) who completed baseline (n = 6485) and follow-up (n = 3806) visits, approximately 6 years apart, in the Study of Osteoporotic Fractures (SOF). Self-reported sleep over the past 12 months was categorized as "good" or "poor" across 5 dimensions: satisfaction with sleep duration, daytime sleepiness, mid-sleep time, sleep onset latency, and sleep duration. An aggregate measure of sleep health was calculated by summing the number of "poor" dimensions. Clinically significant depression symptoms were defined as a score ≥6 on the Geriatric Depression Scale. Relationships between sleep health and depression symptoms were evaluated with multivariate logistic regression, adjusting for health measures and medications. Individual sleep health dimensions of sleep satisfaction, daytime sleepiness, mid-sleep time, and sleep onset latency were significantly associated with prevalent depression symptoms (odds ratios [OR] = 1.26-2.69). Sleep satisfaction, daytime sleepiness, and sleep onset latency were significantly associated with incident depression symptoms (OR = 1.32-1.79). The number of "poor" sleep health dimensions was associated in a gradient fashion with greater odds of prevalent (OR = 1.62-5.41) and incident (OR = 1.47-3.15) depression symptoms. An aggregate, multidimensional measure of sleep health was associated with both prevalent and incident clinically-significant depression symptoms in a gradient fashion. Future studies are warranted to extend these findings in different populations and with different health outcomes.

Short sleep duration is a risk factor for childhood obesity. Mechanisms are unclear, but may involve selection of high carbohydrate foods. This study examined the association between estimated sleep duration and macronutrient intake as percentages of total energy among Mexican American (MA) 9-11 year olds.This cross-sectional study measured diet using two 24-hour recalls and estimated sleep duration using hip-worn accelerometry in MA children (n=247) who were part of a cohort study. Child and maternal anthropometry were obtained; mothers reported on demographic information. Using linear regression, we examined the relationship of sleep duration with energy intake, sugar intake, and the percentage of energy intake from carbohydrates, fat and protein.Children were 47% male; mean age was 10 (SD=0.9) years. Mean sleep duration was 9.6 (SD=0.8) hours; 53% were overweight/obese, with a mean energy intake of 1759 (SD=514) calories. Longer sleep duration was independently associated with a lower percentage of energy intake from carbohydrates (B= -0.22, P< 0.01) and a higher percentage of energy from fat (B=0.19, P< 0.01), driven by the percentage of energy from polyunsaturated fatty acids (PUFA; B=0.17, P< 0.05). No association was found with the intake of energy or total sugars, or the percent of calories from protein.MA children who slept longer consumed diets with a lower percentage of calories from carbohydrates and a higher percentage from fat, especially from PUFA. Short sleep duration may be a risk factor for food cravings that are high in carbohydrate content, and may displace heart-healthy dietary fat, and thereby increase obesity risk among children.

OBJECTIVES: To determine the interaction of age and habitual sleep duration in predicting cognitive performance in a large sample of participants aged 15 to 89 years. METHODS: This study is a cross-sectional analysis of performance data gathered between January 2012 and September 2013. First-time players (N = 512823) of three internet cognitive training games measuring processing speed, working memory, visuospatial memory, and arithmetic participated in the study. RESULTS: Performance was based on a measure of speed and accuracy for each game. The relationship between performance and self-reported habitual sleep duration was examined in the sample as a whole and across 10-year age groups starting at age 15 and ending at 75 and older. Performance peaked at 7 h of sleep duration for all three games in the sample as a whole, and the decrements in performance for sleep durations greater than 7 h were either comparable or greater in the youngest as compared to the oldest age groups. CONCLUSIONS: These findings challenge the hypothesis that deteriorating cognitive performance with long sleep duration is driven by medical comorbidities associated with aging. Further, these data are consistent with an optimal dose model of sleep and suggest that the model for the homeostatic recovery of cognitive function as a function of sleep duration should incorporate a curvilinear decline with longer duration sleep, indicating that there may be a cost to increased sleep. Replication and further research is essential for clarifying the sleep duration-cognition relationship in youth and adults of all ages.

STUDY OBJECTIVES: The mechanisms linking short sleep duration to cardiovascular disease (CVD) are poorly understood. Emerging evidence suggests that endothelial dysregulation may lie along the causal pathway linking sleep duration to cardiovascular risk, although current evidence in humans is based on cross-sectional studies. Our objective was to evaluate the prospective association between objectively assessed sleep duration and clinical indices of endothelial health. METHODS: A total of 141 medically healthy adults underwent an overnight laboratory sleep study when they were between the ages of 21 and 60 years. Total sleep time was objectively assessed by polysomnography at study entry. Endothelial health, including brachial artery diameter (BAD) and flow-mediated dilation (FMD), was measured 18.9 ± 4.6 years later. Medical health and psychiatric status were assessed at both time points. Approximately half of the sample had a lifetime history of major depressive disorder. RESULTS: In univariate analyses, shorter sleep duration was associated with increased BAD (β = -0.24, p = .004) and decreased FMD (β = 0.17, p = .042). BAD, but not FMD, remained significantly associated with sleep duration after adjusting for sex, age, body mass index (BMI), smoking, diabetes, hypertension, and lifetime history of major depressive disorder (MDD) at T2. The association between sleep duration and BAD was stronger than the association between BAD and an aggregate measure of CVD risk including three or more of the following risk factors: male sex, age ≥ 65 years, smoker, BMI ≥ 30, diabetes, hypertension, and MDD. CONCLUSIONS: Objectively assessed short sleep duration was prospectively associated with increased BAD over a 12- to 30-year period.

To investigate cross-sectional associations of neighborhood social environment (social cohesion, safety) with objective measures of sleep duration, timing and disturbances.A racially/ethnically diverse population of men and women (N=1949) aged 54-93 participating in the Multi-Ethnic Study of Atherosclerosis Sleep and Neighborhood Ancillary studies. Participants underwent 1-week actigraphy between 2010 and 2013. Measures of sleep duration, timing and disruption were averaged over all days. Neighborhood characteristics were assessed via questionnaires administered to participants and an independent sample within the same neighborhood and aggregated at the neighborhood (census tract, N=783) level using empirical Bayes estimation. Multilevel linear regression models were used to assess the association between the neighborhood social environment and each sleep outcome.Neighborhood social environment characterized by higher levels of social cohesion and safety were associated with longer sleep duration and earlier sleep midpoint. Each 1 standard deviation higher neighborhood social environment score was associated with 6.1 minutes longer (95% Confidence Interval (CI): 2.0, 10.2) sleep duration and 6.4 minutes earlier (CI: 2.2, 10.6) sleep midpoint after adjustment for age, sex, race, socioeconomic status and marital status. These associations persisted after adjustment for other risk factors. Neighborhood social factors were not associated with sleep efficiency or sleep fragmentation index.A more favorable neighborhood social environment is associated with longer objectively measured sleep duration and earlier sleep timing. Intervening on the neighborhood environment may improve sleep and subsequent health outcomes.

Study objectivesSleep duration has been associated with risk of dementia and stroke, but few studies have investigated the relationship between sleep duration and brain MRI measures, particularly in middle age.MethodsIn a prospective cohort of 613 black and white adults (mean age = 45.4 years) enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) study, participants reported typical sleep duration, dichotomized into moderate sleep duration (> 6 to ≤ 8 h) and short sleep duration (≤ 6 h) at baseline (2005-2006). Five years later, we obtained brain MRI markers of white matter including fractional anisotropy, mean diffusivity, and white matter hyperintensities.ResultsCompared to moderate sleepers, short sleepers had an elevated ratio of white matter hyperintensities to normal tissue in the parietal region (OR = 2.31, 95% CI: 1.47, 3.61) adjusted for age, race/sex, education, hypertension, stroke/TIA, depression, smoking status, and physical activity. White matter diffusivity was also higher, approximately a 0.2 standard deviation difference, in frontal, parietal, and temporal white matter regions, among those reporting shorter sleep duration in (P < 0.05 for all).ConclusionsShort sleep duration was associated with worse markers of white matter integrity in midlife. These mid-life differences in white matter may underlie the link between poor sleep and risk of dementia and stroke.

Study Objectives: We examined growth trajectories of four actigraphy-derived sleep parameters (sleep minutes, sleep efficiency, and variability in sleep minutes and efficiency across a week of assessments) across childhood and adolescence and examined individual differences in trajectories according to participants' race/ethnicity and sex. We also assessed the predictive effect of growth trajectories of sleep parameters on growth trajectories of mental health outcomes and moderation by race and sex., Method: Youth (N = 199, 49% female, 65% white, 32% black, 3% biracial) and their parents participated in five waves of data (M ages were 9, 10, 11, 17, and 18 across waves). Participants were from a diverse range of socioeconomic backgrounds., Results: Across participants, sleep minutes, sleep efficiency, and variability in sleep minutes and efficiency demonstrated significant linear change across childhood and adolescence. Whereas sleep duration shortened over time, sleep efficiency improved. Youth exhibited increases in night-to-night variability in sleep minutes and reductions in night-to-night variability in sleep efficiency. Highlighting the importance of individual differences, some race- and sex-related effects emerged. Black youth and male youth experienced steeper declines in their sleep duration across development relative to their respective counterparts. Black youth also demonstrated smaller improvements in sleep efficiency and greater variability in sleep efficiency compared to white youth. Finally, trajectories of sleep efficiency and variability in sleep minutes predicted trajectories of internalizing symptoms and externalizing behaviors., Conclusions: Findings showed significant changes in developmental trajectories of four sleep parameters across childhood and adolescence. We discuss the empirical and translational implications of the findings., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society.)

Study Objectives: There is mixed evidence regarding associations of sleep duration with academic functioning in adolescents and a lack of research on other sleep dimensions, particularly using objective sleep measures. We examined associations of multiple actigraphic sleep dimensions with academic functioning among adolescents., Methods: Data were from the sleep sub-study of the age 15 wave of the Future of Families and Child Wellbeing Study (n = 774-782; 52% female), a national, diverse sample of teens. Adolescents wore wrist-actigraphs for ~1 week and completed a survey reporting academic performance and school-related behavioral problems. Regression models assessed whether average sleep duration, timing, maintenance efficiency, and SD-variability were associated with self-reported academic functioning in cross-sectional analyses adjusted for demographic characteristics, depressive symptoms, and anxious symptoms., Results: Later sleep timing (hours) and greater sleep variability (SD-hours) were associated with poorer academic outcomes, including sleep onset variability with higher odds of receiving a D or lower (OR = 1.29), sleep onset (β = -.07), sleep offset (β = -.08), and sleep duration variability (β = -.08) with fewer A grades, sleep offset with lower GPA (β = -.07), sleep offset (OR = 1.11), sleep duration variability (OR = 1.31), and sleep onset variability (OR = 1.42) with higher odds of being suspended or expelled in the past 2 years, and sleep duration variability with greater trouble at school (β = .13). Sleep duration, sleep maintenance efficiency, and sleep regularity index were not associated with academic functioning., Conclusions: Later sleep timing and greater sleep variability are risk factors for certain academic problems among adolescents. Promoting sufficient, regular sleep timing across the week may improve adolescent academic functioning., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Study Objectives: Although short sleep could promote neurodegeneration, long sleep may be a marker of ongoing neurodegeneration, potentially as a result of neuroinflammation. The objective was to evaluate sleep patterns with age of expected Alzheimer's disease (AD) onset and neuroinflammation., Methods: We tested 203 dementia-free participants (68.5 ± 5.4 years old, 78M). The PREVENT-AD cohort includes older persons with a parental history of AD whose age was nearing their expected AD onset. We estimated expected years to AD onset by subtracting the participants' age from their parent's at AD dementia onset. We extracted actigraphy sleep variables of interest (times of sleep onset and morning awakening, time in bed, sleep efficiency, and sleep duration) and general profiles (sleep fragmentation, phase delay, and hypersomnia). Cerebrospinal fluid (CSF) inflammatory biomarkers were assessed with OLINK multiplex technology., Results: Proximity to, or exceeding, expected age of onset was associated with a sleep profile suggestive of hypersomnia (longer sleep and later morning awakening time). This hypersomnia sleep profile was associated with higher CSF neuroinflammatory biomarkers (IL-6, MCP-1, and global score). Interaction analyses revealed that some of these sleep-neuroinflammation associations were present mostly in those closer/exceeding the age of expected AD onset, APOE4 carriers, and those with better memory performance., Conclusions: Proximity to, or exceeding, parental AD dementia onset was associated with a longer sleep pattern, which was related to elevated proinflammatory CSF biomarkers. We speculate that longer sleep may serve a compensatory purpose potentially triggered by neuroinflammation as individuals are approaching AD onset. Further studies should investigate whether neuroinflammatory-triggered long sleep duration could mitigate cognitive deficits., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society.)

Study objectivesShort sleep duration and poor sleep continuity have been implicated in the susceptibility to infectious illness. However, prior research has relied on subjective measures of sleep, which are subject to recall bias. The aim of this study was to determine whether sleep, measured behaviorally using wrist actigraphy, predicted cold incidence following experimental viral exposure.Design, measurements, and resultsA total of 164 healthy men and women (age range, 18 to 55 y) volunteered for this study. Wrist actigraphy and sleep diaries assessed sleep duration and sleep continuity over 7 consecutive days. Participants were then quarantined and administered nasal drops containing the rhinovirus, and monitored over 5 days for the development of a clinical cold (defined by infection in the presence of objective signs of illness). Logistic regression analysis revealed that actigraphy- assessed shorter sleep duration was associated with an increased likelihood of development of a clinical cold. Specifically, those sleeping < 5 h (odds ratio [OR] = 4.50, 95% confidence interval [CI], 1.08-18.69) or sleeping between 5 to 6 h (OR = 4.24, 95% CI, 1.08-16.71) were at greater risk of developing the cold compared to those sleeping > 7 h per night; those sleeping 6.01 to 7 h were at no greater risk (OR = 1.66; 95% CI 0.40-6.95). This association was independent of prechallenge antibody levels, demographics, season of the year, body mass index, psychological variables, and health practices. Sleep fragmentation was unrelated to cold susceptibility. Other sleep variables obtained using diary and actigraphy were not strong predictors of cold susceptibility.ConclusionsShorter sleep duration, measured behaviorally using actigraphy prior to viral exposure, was associated with increased susceptibility to the common cold.

The American Academy of Sleep Medicine and Sleep Research Society recently released a Consensus Statement regarding the recommended amount of sleep to promote optimal health in adults. This paper describes the methodology, background literature, voting process, and voting results for the consensus statement. In addition, we address important assumptions and challenges encountered during the consensus process. Finally, we outline future directions that will advance our understanding of sleep need and place sleep duration in the broader context of sleep health.

Study objectivesTo investigate the associations of specific neighborhood features (disorder, safety, social cohesion, physical environment, and socioeconomic status) with sleep duration and quality.DesignCross-sectional. One wave of a population-based study (Multi-Ethnic Study of Atherosclerosis).SettingCommunity-dwelling participants in New York, NY and Los Angeles, CA.ParticipantsThere were 1,406 participants (636 males, 770 females).InterventionsNA.Measurements and resultsSleep was assessed using reported hours of sleep, the Epworth Sleepiness Scale, and insomnia symptoms. Neighborhood characteristics were assessed via questionnaires administered to neighbors of study participants and were aggregated to the neighborhood (census tract) level using empirical Bayes estimation. An adverse social environment (characterized by high disorder, and low safety and social cohesion) was associated with shorter sleep duration after adjustment for the physical environment, neighborhood and individual-level socioeconomic status (SES), and other short sleep risk factors (mean difference per standard deviation increase in summary social environment scale 0.24 h 95% confidence interval 0.08, 0.43). Adverse neighborhood social and physical environments, and neighborhood SES were associated with greater sleepiness, but associations with physical environments were no longer statistically significant after adjustment for sociodemographic characteristics. Neighborhood SES was a weaker and less consistent predictor of specific measures of neighborhood social and physical environments. Neighborhood characteristics were not associated with insomnia.ConclusionsShortened sleep related to adverse social environments represents one potential pathway through which neighborhoods may influence health.

Study Objectives: To investigate the effect of increasing sleep duration for 1 week, compared to a week of habitual and decreased sleep, on insulin sensitivity (IS) in adolescents at risk for type 2 diabetes (T2D)., Methods: Adolescents, 13-18 years old, at risk for T2D, with obesity and other risk factors, were recruited for a randomized (1:1), open-label, sex-stratified crossover study, that manipulated time-in-bed to modify sleep duration (measured by actigraphy). Following a week of habitual (HB) sleep, time-in-bed was increased (IN) and decreased (DE) by 1 hour 30 min/night for 1 week, counterbalanced across participants (HBINDE or HBDEIN), and separated by a week of washout sleep. The main outcome measure was IS, obtained via 2-hour oral-glucose-tolerance-test conducted after each sleep week., Results: Of the 43 participants recruited, 36 (84%) completed all sleep interventions (52.8% female, age = 15.1 years, body mass index = 99.9th percentile, order: HBINDE = 18 and HBDEIN = 18). On average, during the HB week, participants slept 7 hours 31 min/night; sleep duration was 1 hour 02 min/night higher during the IN week and 1 hour 19 min/night lower during the DE week. We found a significant effect of sleep week on IS with a large effect size. Following the IN sleep week, IS was 20% higher compared to after the HB and DE sleep weeks, but there was no significant difference in IS following HB versus DE sleep weeks., Conclusions: Whenever possible, clinicians should empower youth at risk of T2D to improve their sleep duration, since even a modest increase in sleep duration of 1 h/night for 1 week can have a positive impact on IS in this population., Clinical Trials: Sleep Extension and IS in Adolescents, https://clinicaltrials.gov/study/NCT03754036, November 23rd, 2018., Trial Registration: ClinicalTrials.gov (ID:NCT03754036)., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Study Objectives: To investigate whether neurobehavioral impairments are exacerbated during successive cycles of sleep restriction and recovery in young adults, and whether a variable short sleep schedule can mitigate these impairments relative to a stable one., Methods: Fifty-two healthy young adults (25 males, aged: 21-28) were randomly assigned to the stable short sleep group, the variable short sleep group, or the control group in this laboratory-based study. They underwent two baseline nights of 8-hour time-in-bed (TIB), followed by two cycles of "weekday" sleep opportunity manipulation and "weekend" recovery (8-hour TIB). During each manipulation period, the stable short sleep and the control groups received 6- and 8-hour TIBs each night respectively, while the variable short sleep group received 8-hour, 4-hour, 8-hour, 4-hour, and 6-hour TIBs from the first to the fifth night. Neurobehavioral functions were assessed five times each day., Results: The stable short sleep group showed faster vigilance deterioration in the second week of sleep restriction as compared to the first. This effect was not observed in the variable short sleep group. Subjective alertness and practice-based improvement in processing speed were attenuated in both short sleep groups., Conclusions: In young adults, more variable short sleep schedules incorporating days of prophylactic or recovery sleep might mitigate compounding vigilance deficits resulting from recurrent cycles of sleep restriction. However, processing speed and subjective sleepiness were still impaired in both short sleep schedules. Getting sufficient sleep consistently is the only way to ensure optimal neurobehavioral functioning., Clinical Trial: Performance, Mood, and Brain and Metabolic Functions During Different Sleep Schedules (STAVAR), https://www.clinicaltrials.gov/study/NCT04731662, NCT04731662., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Study Objectives: Sleep disturbance may cause suicidal ideation (SI). This study aimed to examine their co-occurrence rate among adolescents and investigate whether psychotic-like experiences (PLEs) mediate this association., Methods: A total of 17 722 Chinese adolescents were included in this two-wave longitudinal study. The baseline survey (time 1, T1) was conducted between April 21 and May 12, 2021, and the follow-up survey (time 2, T2) was implemented between December 17 and 26, 2021. At T1, participants completed questionnaires to assess their sleep disturbance, sleep duration, PLEs, SI, depressive symptoms, and sociodemographic characteristics. At T2, participants reported their PLEs, SI, and negative life events., Results: The SI prevalence decreased from 20.2% (T1) to 18.4% (T2). Participants with SI showed significantly higher prevalence of sleep disturbance and short sleep duration compared to those without SI. Baseline sleep disturbance and short sleep duration were both associated with the increased risk of SI 6 months later. These longitudinal links were mediated by PLEs, independent of baseline covariates and negative life events., Conclusions: These findings provide a novel insight into the mechanism linking sleep problems and suicidality, and stress the significance of assessing and addressing sleep problems and PLEs for adolescent suicide prevention and intervention., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Study Objectives: Alterations in gut microbiota composition have been associated with several conditions, and there is emerging evidence that sleep quantity and quality are associated with the composition of the gut microbiome. Therefore, this study aimed to assess the associations between several measures of sleep and the gut microbiome in a large, population-based sample., Methods: Data were collected from participants in the Survey of the Health of Wisconsin from 2016 to 2017 (N = 720). Alpha diversity was estimated using Chao1 richness, Shannon's diversity, and Inverse Simpson's diversity. Beta diversity was estimated using Bray-Curtis dissimilarity. Models for each of the alpha-diversity outcomes were calculated using linear mixed effects models. Permutational multivariate analysis of variance tests were performed to test whether gut microbiome composition differed by sleep measures. Negative binomial models were used to assess whether sleep measures were associated with individual taxa relative abundance., Results: Participants were a mean (SD) age of 55 (16) years and 58% were female. The sample was 83% non-Hispanic white, 10.6% non-Hispanic black, and 3.5% Hispanic. Greater actigraphy-measured night-to-night sleep duration variability, wake-after-sleep onset, lower sleep efficiency, and worse self-reported sleep quality were associated with lower microbiome richness and diversity. Sleep variables were associated with beta-diversity, including actigraphy-measured night-to-night sleep duration variability, sleep latency and efficiency, and self-reported sleep quality, sleep apnea, and napping. Relative abundance of several taxa was associated with night-to-night sleep duration variability, average sleep latency and sleep efficiency, and sleep quality., Conclusions: This study suggests that sleep may be associated with the composition of the gut microbiome. These results contribute to the body of evidence that modifiable health habits can influence the human gut microbiome., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Study Objectives: To examine the associations between sleep duration, continuity, timing, and mortality using actigraphy among adults., Methods: Data were from a cohort of 88 282 adults (40-69 years) in UK Biobank that wore a wrist-worn triaxial accelerometer for 7 days. Actigraphy data were processed to generate estimates of sleep duration and other sleep characteristics including wake after sleep onset (WASO), number of 5-minute awakenings, and midpoint for sleep onset/wake-up and the least active 5 hours (L5). Data were linked to mortality outcomes with follow-up to October 31, 2021. We implemented Cox models (hazard ratio, confidence intervals [HR, 95% CI]) to quantify sleep associations with mortality. Models were adjusted for demographics, lifestyle factors, and medical conditions., Results: Over an average of 6.8 years 2973 deaths occurred (1700 cancer, 586 CVD deaths). Overall sleep duration was significantly associated with risk for all-cause (p < 0.01), cancer (p < 0.01), and CVD (p = 0.03) mortality. For example, when compared to sleep durations of 7.0 hrs/d, durations of 5 hrs/d were associated with a 29% higher risk for all-cause mortality (HR: 1.29 [1.09, 1.52]). WASO and number of awakenings were not associated with mortality. Individuals with L5 early or late midpoints (<2:30 or ≥ 3:30) had a ~20% higher risk for all-cause mortality, compared to those with intermediate L5 midpoints (3:00-3:29; p ≤ 0.01; e.g. HR ≥ 3:30: 1.19 [1.07, 1.32])., Conclusions: Shorter sleep duration and both early and late sleep timing were associated with a higher mortality risk. These findings reinforce the importance of public health efforts to promote healthy sleep patterns in adults., (Published by Oxford University Press on behalf of Sleep Research Society (SRS) 2023.)

Study Objectives: To assess for associations between sleeping more than or less than recommended by the National Sleep Foundation (NSF), and self-reported insomnia, with brain structure., Methods: Data from the UK Biobank cohort were analyzed (N between 9K and 32K, dependent on availability, aged 44 to 82 years). Sleep measures included self-reported adherence to NSF guidelines on sleep duration (sleeping between 7 and 9 hours per night), and self-reported difficulty falling or staying asleep (insomnia). Brain structural measures included global and regional cortical or subcortical morphometry (thickness, surface area, volume), global and tract-related white matter microstructure, brain age gap (difference between chronological age and age estimated from brain scan), and total volume of white matter lesions., Results: Longer-than-recommended sleep duration was associated with lower overall grey and white matter volumes, lower global and regional cortical thickness and volume measures, higher brain age gap, higher volume of white matter lesions, higher mean diffusivity globally and in thalamic and association fibers, and lower volume of the hippocampus. Shorter-than-recommended sleep duration was related to higher global and cerebellar white matter volumes, lower global and regional cortical surface areas, and lower fractional anisotropy in projection fibers. Self-reported insomnia was associated with higher global gray and white matter volumes, and with higher volumes of the amygdala, hippocampus, and putamen., Conclusions: Sleeping longer than recommended by the NSF is associated with a wide range of differences in brain structure, potentially indicative of poorer brain health. Sleeping less than recommended is distinctly associated with lower cortical surface areas. Future studies should assess the potential mechanisms of these differences and investigate long sleep duration as a putative marker of brain health., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society.)

Study Objectives: Given the established racial disparities in both sleep health and dementia risk for African American populations, we assess cross-sectional and longitudinal associations of self-report sleep duration (SRSD) and daytime sleepiness with plasma amyloid beta (Aβ) and cognition in an African American (AA) cohort., Methods: In a cognitively unimpaired sample drawn from the African Americans Fighting Alzheimer's in Midlife (AA-FAiM) study, data on SRSD, Epworth Sleepiness Scale, demographics, and cognitive performance were analyzed. Aβ40, Aβ42, and the Aβ42/40 ratio were quantified from plasma samples. Cross-sectional analyses explored associations between baseline predictors and outcome measures. Linear mixed-effect regression models estimated associations of SRSD and daytime sleepiness with plasma Aβ and cognitive performance levels and change over time., Results: One hundred and forty-seven participants comprised the cross-sectional sample. Baseline age was 63.2 ± 8.51 years. 69.6% self-identified as female. SRSD was 6.4 ± 1.1 hours and 22.4% reported excessive daytime sleepiness. The longitudinal dataset included 57 participants. In fully adjusted models, neither SRSD nor daytime sleepiness is associated with cross-sectional or longitudinal Aβ. Associations with level and trajectory of cognitive test performance varied by measure of sleep health., Conclusions: SRSD was below National Sleep Foundation recommendations and daytime sleepiness was prevalent in this cohort. In the absence of observed associations with plasma Aβ, poorer self-reported sleep health broadly predicted poorer cognitive function but not accelerated decline. Future research is necessary to understand and address modifiable sleep mechanisms as they relate to cognitive aging in AA at disproportionate risk for dementia., Clinical Trial Information: Not applicable., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Study Objectives: To evaluate at-home use of eye-mask and earplugs (EMEP) versus sleep hygiene advice leaflet (AL) on actigraphy-derived night sleep duration in sleep-deprived pregnant women., Methods: A randomized controlled trial was conducted in the antenatal clinic of University Malaya Medical Centre from June 2021 to June 2022. Women at 34-36 weeks gestation with self-reported night sleep duration ≤6 hours were recruited. Participants wore an actigraphy device at night for seven consecutive nights (Observation/Baseline week). Only women whose actigraphy-derived night sleep duration was confirmed to be ≤360 minutes were randomized to use EMEP or AL. Actigraphy was continued for another week (Intervention week). Primary outcome was change in actigraphy-derived night sleep duration from observation to intervention week across trial arms. Secondary outcomes include participants' sleep quality, labor, and neonatal outcome. Comparisons were by Student t-test, Mann-Whitney U test, and chi-square test., Results: A total of 210 women were randomized: 105 each to EMEP and AL. The increase in night sleep duration over baseline was significantly longer with both EMEP (mean ± SD) 23 ± 41 minutes, p < .001, and AL 10 ± 35 minutes, p = .007. Night sleep duration was longer by 12.9 (95% CI = 2.2 to 23.7) minutes, p = .019 with EMEP over AL. Sleep quality (Global Pittsburgh Sleep Quality Index score) was significantly improved with EMEP (mean ± SD) -2.0 ± 2.5, p < .001, but not with AL -0.3 ± 2.2, p = .246. Labor and neonatal outcomes were not significantly different., Conclusion: EMEP significantly lengthened night sleep duration in sleep-deprived women in late pregnancy and is superior to AL., Clinical Trial Information: "Use of eye masks and earplugs compared with standard advice to improve sleep in pregnancy". https://doi.org/10.1186/ISRCTN19061849. Registered with ISRCTN on 07 May 2021, trial identification number: ISRCTN19061849., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Worldwide, approximately one in three people are myopic or short-sighted. Myopia in children is of particular concern as younger onset age implies a higher risk of progression, and consequently greater risk of developing vision-threatening complications. The importance of sleep in children's health has long been acknowledged, but evidence for its role in childhood myopia is fairly new and mixed results were presented across studies. To facilitate better understanding of this relationship, a broad literature search, up to and including October 31, 2022, was performed using three databases (PubMed, Embase, and Scopus). Seventeen studies were included in the review, covering four main aspects of sleep, namely duration, quality, timing, and efficiency, and their associations with myopia in children. The present literature review discussed these studies, revealed potential limitations in their methodologies, and identified gaps that need to be addressed in the future. The review also acknowledges that current evidence is insufficient, and the role of sleep in childhood myopia is far from being fully understood. Future studies that primarily, objectively, and accurately assess sleep and myopia, taking other characteristics of sleep beyond duration into consideration, with a more diverse sample in terms of age, ethnicity, and cultural/environmental background, and control for confounders such as light exposure and education load are much needed. Although more research is required, myopia management should be a holistic approach and the inclusion of sleep hygiene in myopia education targeting children and parents ought to be encouraged., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society.)

Study Objectives: This study aimed to quantify the temporal associations between nightly sleep quantity and timing with daytime eating behavior and activity levels in free-living (i.e. non-experimental) settings., Methods: Generally healthy young adults (N = 63; 28.9 ± 7.1 years) completed concurrent sleep (wrist actigraphy), eating (photo-assisted diet records), and activity (waist actigraphy) assessments over 14 days. Multilevel models quantified the associations between nightly sleep (total sleep time, timing of sleep and wake onset) with next-day eating behavior (diet quality, caloric intake, timing of eating onset/offset, eating window duration) and activity levels (total physical activity, sedentary time). Associations in the reverse direction (i.e. eating and activity predicting sleep) were explored. Models adjusted for demographic and behavioral confounders and accounted for multiple testing., Results: At within- and between-subject levels, nights with greater-than-average total sleep time predicted a shorter eating window the next day (all p ≤ 0.002). Later-than-average sleep and wake timing predicted within- and between-subject delays in next-day eating onset and offset, and between-subject reductions in diet quality and caloric intake (all p ≤ 0.008). At within- and between-subject levels, total sleep time was bidirectionally, inversely associated with sedentary time (all p < 0.001), while later-than-average sleep and wake timing predicted lower next-day physical activity (all p ≤ 0.008)., Conclusions: These data underscore the complex interrelatedness between sleep, eating behavior, and activity levels in free-living settings. Findings also suggest that sleep exerts a greater influence on next-day behavior, rather than vice versa. While testing in more diverse samples is needed, these data have potential to enhance health behavior interventions and maximize health outcomes., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Study Objectives: Growing evidence linked inflammation with sleep. This study aimed to evaluate the associations and causal effects of sleep traits including insomnia, excessive daytime sleepiness (EDS), and sleep duration (short: <7 h; normal: 7-9 h; long: ≥9 h), with levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), and interleukins., Methods: Standard procedures of quantitative analysis were applied to estimate the expression differences for each protein in compared groups. Then, a two-sample Mendelian randomization (MR) analysis was performed to explore their causal relationships with published genome-wide association study summary statistics. The inverse-variance weighted was used as the primary method, followed by several complementary approaches as sensitivity analyses., Results: A total of 44 publications with 51 879 participants were included in the quantitative analysis. Our results showed that the levels of CRP, interleukin-1β (IL-1β), IL-6, and TNF-α were higher from 0.36 to 0.58 (after standardization) in insomnia compared with controls, while there was no significant difference between participants with EDS and controls. Besides, there was a U/J-shaped expression of CRP and IL-6 with sleep durations. In MR analysis, the primary results demonstrated the causal effects of CRP on sleep duration (estimate: 0.017; 95% confidence intervals [CI], [0.003, 0.031]) and short sleep duration (estimate: -0.006; 95% CI, [-0.011, -0.001]). Also, IL-6 was found to be associated with long sleep duration (estimate: 0.006; 95% CI, [0.000, 0.013]). These results were consistent in sensitivity analyses., Conclusions: There are high inflammatory profiles in insomnia and extremes of sleep duration. Meanwhile, elevated CRP and IL-6 have causal effects on longer sleep duration. Further studies can focus on related upstream and downstream mechanisms., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Study Objectives: Parental warmth in adolescence protects sleep in early adulthood, yet the nature, directions, and mechanisms of this association across adolescence are unknown. This study examined parental warmth, adolescent sleep hygiene and sleep outcomes (morning/eveningness, school night sleep duration, and daytime sleepiness) across five annual waves, spanning four years, using a cross-lagged panel design., Methods: Adolescents and one primary caregiver (96% mothers) completed questionnaires assessing parental warmth (child- and parent-report) and adolescent sleep hygiene and sleep (child-report), across five annual waves: Wave 1 (N = 531, Mage = 11.18, SD = 0.56, 51% male), Wave 2 (N = 504, Mage = 12.19, SD = 0.53, 52% male), Wave 3 (N = 478, Mage = 13.19, SD = 0.53, 52% male), Wave 4 (N = 440, Mage = 14.76, SD = 0.47, 51% male), and Wave 5 (N = 422, Mage = 15.75, SD = 0.49, 51% male)., Results: Greater child-reported parental warmth was indirectly associated with better adolescent sleep (greater morningness, longer school night sleep duration, less sleepiness) through healthier sleep hygiene. The inverse was also often observed. Warmth had a direct relationship with sleep duration and sleepiness, independent of sleep hygiene. Parent-reported parental warmth did not predict, nor was predicted by child-reported adolescent sleep., Conclusions: Parental warmth may protect against developmental changes in adolescent sleep, partially by improving sleep hygiene practices. Similarly, inadequate adolescent sleep may negatively impact parental warmth via deteriorating sleep hygiene. Sleep hygiene emerged as a key mechanism for protecting adolescent sleep and parent-child relationships., (© Sleep Research Society 2022. Published by Oxford University Press on behalf of the Sleep Research Society.)

Study Objectives: We studied the associations between polygenic risk score (PRS) for attention deficit and hyperactivity disorder (ADHD) and (1) ADHD symptoms in 5-year-old children, (2) sleep duration throughout childhood, and (3) the interaction between PRS for ADHD and short sleep duration relative to ADHD symptoms at 5 years., Methods: This study is based on the population-based CHILD-SLEEP birth cohort (N = 1420 children). PRS was used to quantitate the genetic risk for ADHD. Parent-reported ADHD symptoms at 5 years were obtained from 714 children, using the Strengths and Difficulties Questionnaire (SDQ) and the Five-to-Fifteen (FTF). Our primary outcomes were SDQ-hyperactivity and FTF-ADHD total scores. Parent-reported sleep duration was measured at 3, 8, 18, 24 months, and 5 years in the whole sample and actigraphy-based sleep duration at 2 and 24 months in a subsample., Results: PRS for ADHD associated with SDQ-hyperactivity (β = 0.214, p = .012) and FTF-ADHD total (β = 0.639, p = .011), and FTF-inattention and hyperactivity subscale scores (β = 0.315, p = .017 and β = 0.324, p = .030), but not with sleep duration at any time point. Significant interactions were found between high PRS for ADHD and parent-reported short sleep throughout childhood in FTF-ADHD total score (F = 4.28, p = .039) and FTF-inattention subscale (F = 4.66, p = .031). We did not find any significant interaction between high PRS for ADHD and actigraphy-based short sleep., Conclusions: Parent-reported short sleep moderates the association between genetic risk of ADHD and ADHD symptoms in early childhood in the general population, so that children with short sleep, in combination with high genetic risk for ADHD, could be at highest risk for ADHD symptoms., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Study Objectives: The long-term effects of sleep health and shift work on cognitive performance are unclear. In addition, research has been limited by small sample sizes and short follow-up periods. We conducted one of the largest examinations of the longitudinal influence of sleep health dimensions and shift work on cognitive performance in people of middle and old age using data from the UK Biobank. The hypothesis was that poor sleep health and shift work would predict lower cognitive performance., Methods: Self-reported sleep duration, daytime sleepiness, insomnia symptoms, chronotype, and shift work status were assessed as predictors at baseline. Cognitive performance was operationalized by a touchscreen test battery at follow-up between 7.4 ± 2.2 and 9.0 ± 0.9 years after baseline assessment, depending on the specific task. Models were performed for each cognitive domain including relevant confounders (e.g. depression). The alpha level was set at p < 0.01 for all analyzes., Results: The study sample comprised 9394 participants for the reasoning task, 30 072 for the reaction time task, 30 236 for the visual memory task, 2019 for the numeric memory task, and 9476 for the prospective memory task. Shift work without night shifts (β = -2.0 × 10-1 ± 6.5 × 10-2, p = 0.002) and with night shifts (β = -1.9 × 10-1 ± 7.2 × 10-2, p = 0.010) predicted a significantly reduced performance in the reasoning task. Short sleep duration (β = -2.4 × 10-1 ± 7.9 × 10-2, p = 0.003) and shift work without night shifts (β = -3.9 × 10-1 ± 1.2 × 10-1, p = 0.002) predicted a significantly lower performance in the task probing prospective memory., Conclusions: Our results suggest that, after controlling for confounding variables, shift work, and short sleep duration are important predictors for cognitive performance in people of middle and old age. Further work is required to examine causal mechanisms of the observed associations., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Previous research has linked having an eveningness chronotype with a higher tolerance for night shift work, suggesting the ability to work nights without health consequences may partially depend upon having a circadian clock optimized for these times. As chronotypes entrain over time to environmental cues, it remains unclear whether higher relative eveningness among healthy night workers reflects a moderating or mediating effect of chronotype on health. We address these concerns conducting a genome-wide association study and utilizing a polygenic score (PGS) for eveningness as a time-invariant measure of chronotype. On a sample of 53 211 workers in the UK Biobank (2006-2018), we focus on the effects of night shift work on sleep duration, a channel through which night shift work adversely affects health. We ask whether a higher predisposition toward eveningness promotes night shift work tolerance. Results indicate that regular night shift work is associated with a 13-minute (3.5%) reduction in self-reported sleep per night relative to those who never work these hours (95% confidence interval [CI] = -17:01, -8:36). We find that eveningness has a strong protective effect on night workers: a one-SD increase in the PGS is associated with a 4-minute (28%) reduction in the night shift work sleep penalty per night (CI = 0:10, 7:04). This protective effect is pronounced for those working the longest hours. Consistent patterns are observed with an actigraphy-derived measure of sleep duration. These findings indicate that solutions to health consequences of night shift work should take individual differences in chronotype into account., (© Sleep Research Society 2023. Published by Oxford University Press on behalf of the Sleep Research Society.)

Study Objectives: Insufficient sleep may attenuate weight loss, but the role of sleep in weight loss maintenance is unknown. Since weight regain after weight loss remains a major obstacle in obesity treatment, we investigated whether insufficient sleep predicts weight regain during weight loss maintenance., Methods: In a randomized, controlled, two-by-two factorial study, 195 adults with obesity completed an 8-week low-calorie diet and were randomly assigned to 1-year weight loss maintenance with or without exercise and liraglutide 3.0 mg/day or placebo. Sleep duration and quality were measured before and after the low-calorie diet and during weight maintenance using wrist-worn accelerometers (GENEActiv) and Pittsburgh Sleep Quality Index (PSQI). To test associations between insufficient sleep and weight regain, participants were stratified at randomization into subgroups according to sleep duration (5)., Results: After a diet-induced 13.1 kg weight loss, participants with short sleep duration at randomization regained 5.3 kg body weight (p = .0008) and had less reduction in body fat percentage compared with participants with normal sleep duration (p = .007) during the 1-year weight maintenance phase. Participants with poor sleep quality before the weight loss regained 3.5 kg body weight compared with good quality sleepers (p = .010). During the weight maintenance phase, participants undergoing liraglutide treatment displayed increased sleep duration compared with placebo after 26 weeks (5 vs. -15 min/night) but not after 1 year. Participants undergoing exercise treatment preserved the sleep quality improvements attained from the initial weight loss., Conclusions: Short sleep duration or poor sleep quality was associated with weight regain after weight loss in adults with obesity., (© Sleep Research Society 2022. Published by Oxford University Press on behalf of the Sleep Research Society.)

Study Objectives: Examine how different trajectories of reported sleep duration associate with early childhood cognition., Methods: Caregiver-reported sleep duration data (n = 330) were collected using the Brief Infant Sleep Questionnaire at 3, 6, 9, 12, 18, and 24 months and Children's Sleep Habits Questionnaire at 54 months. Multiple group-based day-, night-, and/or total sleep trajectories were derived-each differing in duration and variability. Bayley Scales of Infant and Toddler Development-III (Bayley-III) and the Kaufman Brief Intelligence Test- 2 (KBIT-2) were used to assess cognition at 24 and 54 months, respectively., Results: Compared to short variable night sleep trajectory, long consistent night sleep trajectory was associated with higher scores on Bayley-III (cognition and language), while moderate/long consistent night sleep trajectories were associated with higher KBIT-2 (verbal and composite) scores. Children with a long consistent total sleep trajectory had higher Bayley-III (cognition and expressive language) and KBIT-2 (verbal and composite) scores compared to children with a short variable total sleep trajectory. Moderate consistent total sleep trajectory was associated with higher Bayley-III language and KBIT-2 verbal scores relative to the short variable total trajectory. Children with a long variable day sleep had lower Bayley-III (cognition and fine motor) and KBIT-2 (verbal and composite) scores compared to children with a short consistent day sleep trajectory., Conclusions: Longer and more consistent night- and total sleep trajectories, and a short day sleep trajectory in early childhood were associated with better cognition at 2 and 4.5 years., (© Sleep Research Society 2022. Published by Oxford University Press on behalf of the Sleep Research Society.)