Sleep Advances

Background Insomnia symptoms are common in older adults. While observational studies suggest physical activity (PA) timing affects health outcomes, its effect on sleep remains unclear. We compared morning versus evening PA effects on insomnia severity and sleep quality in older adults with insomnia symptoms. Methods Eligible participants were aged 60 to 80 years with (sub)clinical insomnia (Insomnia Severity Index [ISI] score [≥]10). In a randomized cross-over trial, participants engaged in coached PA in the morning (10:00 - 11:00) or evening (19:30 - 20:30) for 14 days each. ISI scores were assessed post-intervention. Objective sleep parameters; duration, latency, efficiency, and timing, were assessed with a Withings Sleep Analyzer under the mattress. Subjective sleep quality was reported daily via smartphone app. Salivary dim light melatonin onset (DLMO) was measured on the final day of each intervention. Results Of 37 participants (mean ISI 14.3 {+/-} 3.3), 27 completed the study (mean age 69.8 {+/-} 5; 63% women). ISI scores improved after both morning ({Delta} - 2.5; 95% CI: - 1.14, - 3.83) and evening ({Delta} - 2.0; 95% CI: - 0.63, - 3.38) activity relative to baseline, but were not different between interventions. Compared to evening activity, sleep midpoint occurred earlier with morning activity (03:40 vs 04:00; {Delta} - 20 min; 95% CI: - 31, - 8). No differences in subjective sleep quality or DLMO were found. Exploratory analyses suggested insomnia scores improved specifically in late chronotypes following morning activity. Conclusions While morning vs. evening PA timing did not impact most sleep quality measures, it influenced sleep timing. Larger studies are needed to define optimal and personalized PA timing for improving sleep.

Background: Sleep fragmentation and reduced sleep efficiency are markers of disrupted sleep architecture linked to cognitive and age-related decline. Current assessments rely on subjective reports prone to recall bias, limiting their effectiveness for longitudinal monitoring. Data-driven analysis of sleep using physiological signals such as EEG and EMG remains underutilised, particularly in mid-to-older adults. Objective: We present a deep learning pipeline for automated sleep staging and label-free abnormality scoring, with the primary objective of quantifying deviations in sleep architecture to capture progressive sleep disruption and longitudinal change. Methods: Temporal and attention-based models were benchmarked using datasets from the National Sleep Research Resource and PhysioBank. To improve class-specific performance, we introduce a stacking-based ensemble of sleep stage classifiers, each trained to specialise in a different stage. For longitudinal scoring, we develop a reconstruction loss-based abnormality metric using a temporal convolutional autoencoder trained on hypnograms generated by the sleep staging models. Results: Attention-based models, particularly AttnSleep, achieved the highest performance in both multimodal and single-channel settings (accuracy: 0.85 and 0.83; F1: 0.79 and 0.74, respectively). The encoder-decoder ensemble model improved overall classification accuracy by 3% compared to the best-performing biased base classifier, with a modest gain in N1-stage F1 score (0.444). The proposed abnormality score correlated with Pittsburgh Sleep Quality Index components and showed sensitivity to synthetic hypnogram degradation, highlighting its potential as a label-free indicator of sleep disruption. Conclusion: Automated classification and annotation-free scoring enable an end-to-end multimodal pipeline that supports scalable, objective sleep health monitoring, with relevance for future clinical deployment.

Smartphone use among medical students has become pervasive. While existing literature links excessive smartphone use to poor sleep quality, the specific behavioral pattern most strongly associated with sleep disruption remains insufficiently characterized. This study investigated whether the timing of smartphone cessation relative to sleep onset is more strongly associated with poor sleep quality than total daily screen time among medical students in Punjab, Pakistan, and examined the moderating role of exam period status. A cross-sectional anonymous online survey was conducted among medical students across Punjab, Pakistan (May 2026). Sleep quality was assessed using items informed by Pittsburgh Sleep Quality Index (PSQI) response formats. Descriptive statistics, chi-square tests, and binary logistic regression were applied to 369 eligible responses, reported in accordance with STROBE guidelines. Of 369 respondents (49.9% female, 48.2% male), 74.8% reported using smartphones 6 or more hours daily and 61.2% used their smartphone until falling asleep. Overall, 75.7% reported poor sleep quality. Students using smartphones until sleep onset had 95.1% poor sleep quality compared to 44.8% in those who ceased use before sleeping (p<0.001). In logistic regression with both variables entered simultaneously, bedtime use until sleep onset remained independently associated with poor sleep quality (OR 15.3, 95% CI 5.7-41.2, p<0.001), while total daily screen time lost significance (OR 1.8, 95% CI 0.7-4.7, p=0.228). Outside exam periods, 99.0% of students using smartphones until sleep onset reported poor sleep quality versus 24.2% of those who stopped before sleeping, a difference of 74.8 percentage points (p<0.001). During exam periods, no significant association was observed (p=0.075), suggesting exam-related stress may attenuate the bedtime behavior effect. Hostel-dwelling students showed the highest prevalence of bedtime smartphone use, with 79.0% using smartphones until sleep onset compared to 23.2% of family-living students (p<0.001). Bedtime smartphone use until sleep onset is more strongly associated with poor sleep quality than total daily screen time among Pakistani medical students. Medical institutions should consider integrating targeted digital wellness education specifically addressing bedtime cessation timing into student health programs, with particular attention to hostel-dwelling students.

Objectives. To test whether one week of self-administered morning bright light therapy (BLT) improves sleep, daytime sleepiness and alertness, mood, and objective cognition in healthy university students. Methods. Thirty-three healthy students completed a two-week randomized within-subject crossover trial comparing one week of morning BLT (30 min of 10,000 lx; melanopic equivalent daylight illuminance of approximately 8,989 lx) with one week of usual-light control in counterbalanced order, with no washout. Sleep was assessed with wrist-worn Fitbit sleep tracking and daily diaries; daytime sleepiness (Karolinska and Stanford Sleepiness Scales), positive and negative affect (PANAS), mood (POMS), and a cognitive battery (Stroop, Flanker, Corsi, verbal span) were also assessed, alongside post-trial semi-structured interviews. Outcomes were analyzed with linear mixed-effects models, with Holm correction across five primary outcomes. Results. BLT reduced daytime sleepiness in a time-of-day-specific manner (condition x time-of-day interaction; largest reduction at 12:00, dz = -0.58, with a smaller but still significant reduction at 15:00), reduced night-to-night variability in sleep duration (dz = -0.52), increased Fitbit sleep efficiency (dz = 0.81), and increased PANAS positive affect (dz = 0.41). Objective cognition was unchanged across all measures. Interviews indicated that participants experienced BLT primarily as a sleep and alertness intervention, with minor tolerability issues. Conclusions. Brief morning BLT improved alertness, sleep regularity and efficiency, and positive affect, but not objective cognition, in healthy students, supporting morning light as a low-burden strategy for daytime functioning while cautioning against overstating cognitive benefits.

The Empatica E4 wristband provides continuous multi-modal physiological monitoring including blood volume pulse (BVP), electrodermal activity (EDA) and skin temperature (TEMP) but its validity for sleep-stage-specific autonomic and thermoregulatory monitoring has not been systematically evaluated against concurrent polysomnography (PSG). Using the Wearanize+ dataset which provides synchronised PSG, Empatica E4, and Zmax EEG recordings from 100 home-recorded participants; a systematic validation of Empatica E4 physiological signals against PSG ground truth across five sleep stages was conducted. Of 100 participants, 92 had Empatica data; 69 met Zmax EEG signal quality criteria and formed the analysis sample. Heart rate (HR) from the pre-computed Empatica HR channel showed valid stage-specific patterns (Wake: 70.9 bpm, N3: 61.2 bpm) and moderate inter-device MeanNN correspondence with PSG ECG (Spearman r=0.35-0.42 across stages). Skin temperature showed the expected thermoregulatory pattern (Wake: 33.92C, N3: 35.48C) and is recommended for downstream analyses. Tonic EDA showed an inverted stage pattern attributable to wrist sweat accumulation during deep sleep, representing a known confound for wrist-worn EDA during sleep. Phasic EDA showed plausible patterns and may be used with caution. These findings establish a validated feature set for Empatica E4 sleep research and directly inform multimodal psychiatric biomarker studies using the Wearanize+ dataset.

Sleep-wake regulation arises from the interaction between homeostatic sleep pressure and circadian timing, yet current assessments evaluate these processes independently and fail to capture their dynamic modulation by environmental pressures. This limitation is particularly relevant in adolescents with attention-deficit/hyperactivity disorder (ADHD), who are at increased risk of circadian delay and sleep disruption. Here, we combined month-long wearable-based physiological monitoring with ecological behavioral assessments in adolescents with ADHD to characterize circadian and homeostatic processes dynamically in real-world settings. Using continuous skin temperature recordings, we derived individualized and day-specific estimates of circadian phase through hierarchical modelling, and integrated these measures with actigraphy-based sleep estimates and daily assessments of neurocognitive functioning and functional impairment. Temperature-derived circadian phase correlated with questionnaire-based chronotype but more accurately predicted sleep patterns. Delayed circadian phase was associated with later sleep onset and greater weekday-weekend variability. Importantly, circadian phase exhibited significant day-to-day fluctuations, particularly in individuals with delayed phase, reflecting interactions with environmental constraints. Sleep latency was jointly determined by homeostatic sleep pressure and day-specific circadian phase, with combined models outperforming either process alone. Crucially, both sleep deprivation and day-specific circadian misalignment independently predicted fluctuations in ADHD symptom severity, perceived stress, and neurocognitive impulsivity. In contrast, mean circadian phase alone did not explain behavioral variability. These findings demonstrate that circadian regulation is a dynamic, environmentally sensitive process rather than a fixed trait. Wearable-based estimation of circadian phase provides a scalable approach to capture these dynamics and may enable personalized interventions targeting sleep and circadian dysregulation.

Study Objectives To develop and initially validate the Circadian Disruption Index (CDI), a self-report measure of circadian disruption, and obtain preliminary evidence of its responsiveness to circadian health education. Methods In Study 1, 244 participants completed a 22-item CDI version and external measures. The sample was randomly divided for exploratory and confirmatory factor analyses. Internal consistency, external associations, and discrimination of poor sleep quality were examined. In Study 2, 72 postgraduate students completed the CDI before and 1 week after a 16-hour circadian health education program in an uncontrolled pre-post design. Results Analyses yielded a 15-item, three-factor structure comprising rhythm stability and light exposure, behavioral habits and diet, and sleep quality and subjective complaints. Total-score internal consistency was acceptable (Cronbach's = 0.871). Confirmatory factor analysis showed a comparative fit index of 0.902 and a root mean square error of approximation of 0.072, although the Tucker-Lewis index was 0.882. CDI scores correlated with sleep quality, chronotype, corrected midsleep on free days, depression, and anxiety, but not social jetlag. The area under the curve for poor sleep quality was 0.807 (95% confidence interval, 0.753-0.862), with an exploratory cutoff of [&le;] 23. In Study 2, CDI scores decreased from 22.26 to 19.88 (p = 0.002; Cohen's dz = 0.36). Conclusions The CDI demonstrated satisfactory internal consistency, a meaningful multidimensional structure, and responsiveness to short-term changes following circadian health education, supporting its potential utility for assessing circadian disruption and monitoring circadian-related behavioral changes.

Background: Circadian rest-activity rhythms weaken with age, but whether sleep disorders modify this trajectory is unknown. Methods: We analyzed wrist accelerometry data from 4,386 participants aged 6-80 years in the 2011-2012 National Health and Nutrition Examination Survey (NHANES). Circadian features were extracted using cosinor analysis and nonparametric methods; a Circadian Disruption Index (CDI) was constructed from five standardized components. Survey-weighted regression with natural cubic splines and Wald F-tests tested age-by-sleep-disorder interactions using Taylor series linearization for variance estimation. Results: Doctor-diagnosed sleep disorder (N = 360, 8.2%) was associated with significantly different age-related trajectories of amplitude (F(2,17) = 11.24, p = 0.0008) and MESOR (F(2,17) = 8.22, p = 0.0032), both surviving Bonferroni correction (p < 0.006). CDI was higher in those with a sleep disorder (0.290 vs. 0.131, p < 0.001) and was independently associated with higher BMI (beta = 1.33 kg/m2, p < 0.001), higher HbA1c (beta = 0.089%, p = 0.004), greater diabetes prevalence (beta = 3.8 percentage points, p < 0.001), and worse depressive symptoms (beta = 0.43 PHQ-9 points, p = 0.020). Sensitivity analyses using a broader sleep problem exposure did not replicate these interactions. Conclusions: Doctor-diagnosed sleep disorders are associated with an altered age-related decline in circadian amplitude and mean activity level. CDI was independently linked to cardiometabolic and depressive outcomes, supporting a mechanistic connection between clinically significant sleep pathology and circadian disruption across the lifespan.

The effects of diet quality and timing on sleep quality remain poorly understood, particularly at the level of sleep microarchitecture. Traditional visual scoring captures only coarse sleep stages, overlooking the marked heterogeneity of electroencephalographic (EEG) patterns in non-rapid eye movement (NREM) sleep of mice. Here, we apply a pipeline that combines EEG feature extraction with unsupervised machine-learning-based clustering to resolve discrete NREM substates and ask how a high-fat diet (HFD) and time- restricted feeding (TRF) affect sleep microarchitectures. HFD increases sleep latency and sleep fragmentation; both abnormalities were ameliorated by active phase TRF. Clustering of 10s epochs identified two high-amplitude NREM substates sensitive to TRF: Cluster 1, enriched in low-delta power and peaking early in the light phase (ZT 0-6), consistent with canonical slow-wave sleep, and Cluster 6, characterized by elevated alpha, sigma, and beta power and peaking in the latter half of the light phase (ZT6-12). TRF increases the frequency of both NREM substates, particularly within longer uninterrupted sleep episodes during the light phases. These findings introduce an objective framework for quantifying murine sleep microarchitecture and show that aligning caloric intake with the circadian active window mitigates HFD-induced macro-level sleep disruption while selectively enhancing two physiologically distinct NREM substates. Significance StatementTime-restricted eating - targeting food intake to a defined window during the circadian active phase - confers well-established metabolic benefits, but its impact on sleep is largely underexplored. Using continuous EEG/EMG recordings, we show that an active- phase eating window mitigates high-fat-diet-induced sleep disruption in mice. We employed a novel machine-learning pipeline, further revealing that timed eating selectively increases distinct NREM substates, demonstrating that "when we eat" fine-tunes the macro- and microarchitecture of sleep. These insights lay the foundation for future translational studies and clinical trials aimed at harnessing timed eating to enhance both metabolic and sleep health.

Background: Regularity of sleep patterns over time has increasingly gained traction as an important axis of sleep health. Since sleep habits are under some degree of behavioral control, understanding such patterns in naturalistic settings is particularly important. We quantified sleep variability and tested the hypothesis that regularity correlates with physical activity, resting heart rate (rHR), and heart rate variability (HRV). Methods: We analyzed real-world digital health data from over 81,000 participants (over 18 million nights) who provided informed consent to participate in the Apple Heart and Movement Study and elected to contribute sleep, activity, and heart rate data to the study. Variability was quantified using the standard deviation (SD) computed from total sleep time (TST), sleep start time (S-start), end time (S-end), and midpoint time (MP), as well as the Sleep Regularity Index (SRI). Results: The SD-based variability metrics correlated with one another (R values 0.74-0.92), and with the SRI metric (R values 0.62-0.64). More consistent sleep, by any metric, was associated with more activity and better rHR and HRV. The most consistent tertile for TST variability had higher median TST (6.9 vs 5.9 hours), more daily exercise (32.8 vs 20.4 minutes), lower rHR (62.4 vs 65.6 beats per minute), and higher HRV (40.6 vs 37.3), all p<1e-100. The findings were similar when variability was defined by S-start SD, S-end SD, MP SD, or SRI. Conclusion: Sleep consistency metrics are highly correlated with each other, and consistency by any metric was associated with more activity, lower rHR, and higher HRV. While causality cannot be established, the results of this large, naturalistic observational cohort are consistent with the growing literature on the potential positive health associations of sleep consistency.

Emerging evidence links the gut microbiome to sleep quality, yet measuring sleep at scale remains challenging. Commercial wearables, such as Fitbit, capture objective sleep and activity data in naturalistic settings. We integrated Fitbit data from a large, deeply-phenotyped cohort with paired lifestyle and health questionnaires. Wearable-derived measures aligned well with self-reported sleep, activity, and happiness. We identified dozens of covariate-adjusted associations between Fitbit-derived sleep features, lifestyle factors, and multi-omic data. Among molecular feature sets, the gut microbiome showed the greatest number of associations with sleep quality: butyrate-producing genera were positively associated with sleep and amplified the benefits of physical activity. Oscillospira, in particular, was consistently associated with better sleep. In blood, insulin, omega-3, and cortisol correlated with poorer sleep, whereas lower alcohol intake and mineral supplements correlated with better sleep. These robust, covariate-adjusted findings advance mechanistic understanding of the gut-sleep axis and broader molecular and lifestyle determinants of sleep quality.

Objectives: Self-applied, low-density EEG offers opportunities to examine sleep in the home environment, yet its feasibility during behavioural sleep interventions remains unexplored. This pilot study aimed to evaluate the feasibility and acceptability of a self-applied, low-density EEG device during sleep restriction therapy (SRT) and explore effects on sleep and affect. Methods: Seventeen adults with insomnia and depressive symptoms completed a 2-week baseline and 4 weeks of SRT. The primary outcome was the proportion of expected EEG recordings completed and scoreable. Secondary outcomes included clinical measures, sleep continuity (sleep diary, actigraphy), sleep architecture (low-density EEG for 9 nights), power spectral density, and affect. Data were analysed with linear mixed models. Cohen's d and 95% confidence intervals were reported. Results: Feasibility was demonstrated (92% of expected EEG nights completed). SRT was associated with reductions in insomnia severity, depressive symptoms, negative affect, and increases in positive affect. Robust improvements were observed across treatment in sleep continuity (SOL, WASO, SE) from diary, which were paralleled by actigraphy. EEG revealed reduced TIB, TST, N1, N2, REM sleep, and REM latency during week one. Reductions in EEG-derived TIB and N1 sleep were maintained at night 28. There were no reliable differences for spectral or spindle measures. Conclusions: These findings suggest that self-applied, low-density EEG during SRT is feasible, acceptable, and may capture sleep changes during treatment. They highlight the potential for multi-night monitoring of sleep interventions at home and elucidating mechanisms underlying therapeutic change.

Background: Accurate REM identification is critical for diagnosing REM sleep behaviour disorder (RBD), yet many automated sleep staging systems, especially single-channel EEG models trained on healthy cohorts, do not generalise well to real-life polysomnography (PSG) performed in patients. Objective: To compare a feature-based Random Forest (RF) model tuned for RBD with a state-of-the-art single-EEG deep architecture (AttnSleep), and to assess the impact of cohort adaptation and multimodal inputs (EEG, EOG, EMG, ECG). Methods: Experiments used 89 multi-site in-clinic PSGs (SleepWearables Phase-1) plus 53 MASS healthy controls (mean age 63, std 5 years), with 10-fold cross-validation and out-of-fold evaluation. Model performance was assessed using Cohen's kappa, and attention-based modality analysis was performed to quantify signal contributions. Results: When applied out-of-the-box after training on open-source healthy datasets, both models achieved moderate agreement overall (Cohen's kappa = 0.46), but performance declined in RBD, particularly for REM sleep (AttnSleep Cohen's kappa = 0.19 vs RF Cohen's kappa = 0.44), highlighting limited cross-cohort generalisation. The multimodal model improved overall agreement (Cohen's kappa 0.59 - 0.60) and performance in RBD (Cohen's kappa 0.45 - 0.46), with gains most pronounced in REM (Cohen's kappa 0.45 - 0.49). Attention-based modality analysis identified EEG as the dominant signal, increased EOG contribution during REM, and elevated ECG importance during N3. In RBD subjects, EOG weighting increased relative to non-RBD controls (Delta = +0.081). Guided by these weights, a reduced four-channel EEG model matched full multimodal performance in non-RBD subjects, and adding EOG achieved the best overall configuration (Cohen's kappa = 0.61 overall; Cohen's kappa = 0.48 in RBD) with improved REM classification (53% vs 45% recall). Inclusion of EOG also reduced inter-dataset variability in REM staging. Nonetheless, staging performance in RBD remained lower than in controls, particularly for REM. Conclusions: These results highlight the limited generalisability of minimal-sensor models trained on healthy cohorts, the value of mixed cohort-specific training, and the benefit of multimodal integration and attention-guided channel selection, rather than minimal-sensor approaches alone, for robust clinical sleep staging in pathological populations such as RBD.

Objective: Sleep health and depression are interconnected multidimensional constructs, yet their shared determinants remain obscure. Understanding the role of socioeconomic/lifestyle factors in predicting sleep-related depression (SRD) is critical for preventive strategies. This study aimed to identify the key socioeconomic/lifestyle predictors of SRD in the general population and patients with clinical depression. Methods: To characterize SRD, we performed regularized canonical correlation analysis between sleep and depression to identify latent phenotypes of SRD in a general population subsample (GP1; n=87,405) from the UK Biobank. Subsequently, machine-learning predictive models were developed in GP1 to predict SRD using socioeconomic/lifestyle factors. The best-performing predictive model was subsequently validated in GP2 at both baseline and follow-up (GP2; n=5,187), and in clinical depression (n=7,454) to assess its generalizability. Complementary analyses were conducted to assess other latent phenotypes (i.e., depression-related sleep, non-SRD, non-depression-related sleep, overall sleep health, and overall depression). Results: A robust multivariate association was identified between sleep and depression in GP1 (canonical r = 0.42, PFDR < 0.001). Socioeconomic/lifestyle factors moderately predicted SRD (r = 0.25; 95% CI: [0.24, 0.25]; R2 = 0.06; 95% CI: [0.06, 0.06]; rMSE = 1.08; 95% CI: [1.08, 1.09]). The top predictors were less frequency of confiding in others, more sedentary television viewing, less vigorous physical activity, and passive smoking exposure. Out-of-sample validation of the predictive model showed similar patterns in GP2 at baseline, at follow-up, and in clinical depression subsamples. Similarly, less frequency of confiding in others and greater sedentary television viewing were the main predictors of other depression-related profiles, whereas more alcohol consumption frequency, less walking frequency, and less time spent outdoors in winter predicted poor sleep-related profiles. Conclusions: Our generalizable predictive model identifies critical modifiable predictors of the association between sleep health and depression that could serve as potential targets for personalized interventions.

Introduction: Actigraphy sleep-wake classification methods increasingly seek to leverage raw acceleration data and machine-learning-based classification, but performance evaluation in pediatrics is limited. We trained machine-learning models using pediatric data and compared their sleep-wake classification performance with existing algorithms for children. Methods: Sixty-five children (46% female, ages 5.3 to 17.7 years) completed in-lab overnight polysomnography and wore a GENEActiv device on their non-dominant wrist. The acceleration data were converted into 30-second epochs and aligned with physician-scored sleep-wake data from electroencephalography. Seven machine-learning models were trained using leave-one-subject-out cross-validation. Epoch-by-epoch analyses generated performance metrics (e.g., balanced accuracy [BA]) and discrepancy analyses provided overall sleep duration bias estimates. The combination of highest performance and least bias was used to rank using Euclidean distance scores - where a lower score represents closer to perfect performance and zero bias. For benchmarking, we included GGIR sleep scoring algorithms and an adult trained random forest classifier. Results: Overall, 560.1 hours of polysomnography and actigraphy data were collected (74.4% of epochs were scored as sleep). The pediatric-trained local-global long-short term memory (LSTM) classifier had the most optimal epoch-by-epoch performance (e.g., BA=0.85, sensitivity=0.88, specificity=0.83, ROC-AUC=0.95, and Cohen kappa=0.67). These metrics exceeded that of an adult-trained random forest classifier and GGIR-based algorithms. Discrepancy analyses revealed that overall sleep duration was underestimated by an average of 25 minutes using the LSTM classifier with no proportional bias. Conclusion: We trained seven pediatric sleep-wake classifiers that had strong ability to detect sleep and wake, with the LSTM classifier being most optimal.

Sleep regularity, the consistency of sleep-wake timing from one day to the next, is more strongly associated with longevity than adequate sleep duration. Whether this relationship persists across common diseases is unknown. We compared sleep regularity vs. sleep duration as risk factors for 199 diseases and disorders, using ten million hours of objective sleep-wake data (N=60,998, age[mean{+/-}SD]=62.8{+/-}7.8, 55% female). Multivariable-adjusted risks of incident diseases/disorders for regular/irregular and short/adequate sleepers were compared across 9.5 years of follow-up. Irregular sleep predicted risks for 131 diseases/disorders, more than double the number predicted by short sleep duration (63). Irregular sleep was a superior predictor than short sleep duration for 90 diseases/disorders, including circulatory, metabolic, digestive, renal, infectious, neurological, and musculoskeletal conditions, and mental disorders, whereas short sleep duration was the superior predictor for only 9 diseases/disorders. For models where short sleep duration explained disease risks, 83% were improved by adding sleep regularity. Sleep regularity was a stronger predictor of diseases/disorders than sleep duration in this cohort and should be considered an essential dimension of sleep health.

Background: Sleep debt and irregular sleep patterns are highly prevalent amongst adolescents. However, whether the absence of these sleep behaviours protects against subsequent depression remains unclear. Here, we examined the association of sleep debt, weekend catch-up sleep (WCS), and social jetlag (SJL) in adolescence with depression in young adulthood and identified underlying biopsychosocial mechanisms. Methods: Secondary data analyses were conducted using the Avon Longitudinal Study of Parents and Children. Bedtimes and wake-up times on school days and weekends (i.e., sleep duration) and sleep need were self-reported at 15 years. This was used to generate sleep debt (sleep need minus school day sleep duration), WCS (weekend sleep duration minus school day sleep duration), and SJL (absolute difference in the midpoint of sleep times between school days and weekends). Depression was assessed at 24 years with the Clinical Interview Schedule-Revised. Common mental health symptoms, biological, and school-related factors at 17 years were the mediators. Results: Logistic regression analyses revealed that greater WCS (adjusted odds ratio [AOR]=0.90; 95% CI=0.84-0.97; p=0.004) and lower sleep debt (AOR=1.10; 95% confidence interval [CI]=1.03-1.18; p=0.005) at age 15 reduced the likelihood of depression at 24 years. Irritability at 17 years partially mediated the relationship between sleep debt and depression (bias-corrected estimate=0.003; 95% CI=0.002-0.004; p<0.001). Conclusions: Adolescents who experience less sleep debt (i.e., less discrepancies between their actual sleep and their perceived sleep need) and those who extend their sleep duration on weekends are at reduced risk for depression in young adulthood. These findings underscore the need for greater opportunities for adolescents to obtain more hours of sleep to protect them against later poor mental health outcomes, such as depression. Keywords: Sleep; longitudinal studies; depression; ALSPAC

Young adults frequently report cognitive complaints often attributed to sleep loss alone. However, subjective cognitive functioning is shaped by broader lifestyle and affective factors. Cross-sectional data were analyzed from 530 young adults (mean age 22.1 +/- 2.3 years) to examine the independent, interactive, and cumulative associations of short sleep duration, low physical activity, and psychological distress with everyday cognitive failures. Cognitive failures were strongly associated with sleep duration, physical activity, sleep quality, and distress in univariate analyses. However, hierarchical regression revealed that psychological distress, poor sleep quality, and short sleep duration were the dominant independent correlates of cognitive failures, collectively explaining a substantial proportion of variance in Cognitive Failures Questionnaire scores (R-squared = 0.585, p < 0.001). In contrast, the apparent protective effect of physical activity was not observed after adjustment for sleep and distress (p = 0.976), and no significant sleep-by-physical activity interaction was observed. Further, cumulative risk modeling demonstrated a robust dose-dependent relationship, with cognitive failures increasing progressively as behavioral and psychological risk factors accumulated (p < 0.001). Individuals exposed to all three risk factors exhibited more than double the cognitive failure burden observed in individuals with no risk factors. These results indicate that the cognitive burden in young adults can best be described by an additive increase of behavioral and psychological risk factors as a function of the co-occurrence, rather than by the presence of compensatory effects of lifestyle risk factors. Interventions aimed at preserving cognitive function may therefore benefit from simultaneously targeting sleep health and psychological well-being rather than relying on physical activity alone to offset cognitive burden.

We completed a video-based, four-night, in-home, level 3 sleep apnea study of healthy, low-risk pregnant participants and their bed partners in order to characterize sleep physiology in the third trimester of pregnancy. Demographic, anthropometric, and baseline sleep health characteristics were recorded, and the NightOwl home sleep apnea test device was used to measure sleep breathing, posture, and architecture parameters. Symptoms of restless legs syndrome were elicited in the exit interview. Forty-one pregnant participants and 36 bed partners completed the study. Bed partners had a significantly higher prevalence of sleep apnea than their pregnant co-sleepers (31% vs. 5.9%). Bed partners also had more severe sleep apnea than their pregnant co-sleepers, and this persisted on an adjusted analysis for baseline differences in factors known to increase risk of sleep apnea. In pregnant participants, increasing gestational age was found to be protective against mild respiratory events but not more severe events. While the correlation between STOP-Bang score and measures of sleep apnea severity was weak, an affirmative response to the "witnessed apneas" item on the STOP-Bang questionnaire was a strong predictor of more severe sleep apnea for all participants. Smoking history also increased sleep apnea risk. Pregnant participants had lower sleep efficiency and longer self-reported sleep onset latency. Restless legs syndrome was experienced by 39.5% of the pregnant participants but no bed partners. From a sleep breathing perspective, people with healthy, low-risk pregnancies have better sleep than their bed partners despite lower sleep efficiency and higher rates of restless legs syndrome. Clinical Study RegistrationSleep in Late Pregnancy - Artificial Intelligence Development for the Detection of Disturbances and Disorders (SLeeP AID4), https://clinicaltrials.gov/study/NCT05376475, registration ID NCT05376475. Statement of SignificancePregnancy negatively impacts sleep, and poor sleep in pregnancy negatively impacts maternal and fetal health. Pregnancy represents a unique challenge to sleep breathing physiology and, thus, an opportunity to test for sleep apnea. Sleep apnea however, while increased in pregnancy, is more common in males. This novel study tested healthy people with low-risk pregnancies and their bed partners for sleep apnea in the comfort of their home over four nights in late pregnancy. Sleep apnea was more common and worse in the bed partners. Advancing gestational age was protective against mild but not severe sleep apnea, and a critical remaining knowledge gap is this interplay in high-risk pregnancies. Future sleep in pregnancy research should make efforts to include high-risk pregnancies.

Background: Automatic sleep staging algorithms are increasingly applied in clinical and home-based recordings. However, their performance may degrade when transferred to new montages and clinical populations. This is particularly relevant in reduced-channel portable PSG and in disorders such as REM sleep behaviour disorder (RBD), where altered sleep architecture may challenge pretrained models. Objective: To evaluate and compare multiple open-source sleep staging algorithms on a minimal portable PSG setup in controls and patients with and without RBD, and to assess the impact of fine-tuning on clinic-ascertained data. Methods: Six open-source models were applied to 76 subjects recruited from three clinical sleep medicine sites. Performance was assessed using accuracy, F1 scores, and Cohen's kappa, both overall and per sleep stage. Each model was evaluated out-of-the-box and after fine-tuning on clinical data. Results: Out-of-the-box performance varied substantially across models (Cohen's kappa 0.21-0.54). Fine-tuning consistently improved agreement, with the best-performing model (GSSC) reaching Cohen's kappa = 0.58 indicating moderate to good agreement. Performance was highest in controls and lower in patient groups. N3 was the most reliably classified stage across models, whereas N1 remained consistently challenging. REM classification improved after fine-tuning in several architectures but remained model, and subgroup-dependent, particularly in RBD subjects. Conclusion: Fine-tuning substantially mitigates domain shift, updating model parameters to align with new data distributions, when applying automatic sleep staging algorithms to portable clinical recordings. Model architecture influences robustness, with feature-learning approaches demonstrating greater adaptability than fixed-feature models. Despite moderate agreement after adaptation, performance, especially for REM and N1 remains insufficient for fully automated diagnostic use in clinical populations.