Discerning the differential contribution of sleep behavior and sleep physiology to the subsequent development of posttraumatic-stress-disorder (PTSD) symptoms following military operational service among combat soldiers. Longitudinal design with three measurement time points: during basic training week (T1), during intensive stressed training week (T2), and following military operational service (T3). Participating soldiers were all from the same unit, ensuring equivalent training schedules and stress exposures. During measurement weeks soldiers completed the Depression Anxiety and Stress Scale (DASS) and the PTSD Checklist for DSM-5 (PCL-5). Sleep physiology (sleep heart-rate) and sleep behavior (duration, efficiency) were monitored continuously in natural settings during T1 and T2 weeks using wearable sensors. Repeated measures ANOVA revealed a progressive increase in PCL-5 scores from T1 and T2 to T3, suggesting an escalation in PTSD symptom severity following operational service. Hierarchical linear regression analysis uncovered a significant relation between the change in DASS stress scores from T1 to T2 and subsequent PCL-5 scores at T3. Incorporating participants' sleep heart-rate markedly enhanced the predictive accuracy of the model, with increased sleep heart-rate from T1 to T2 emerging as a significant predictor of elevated PTSD symptoms at T3, above and beyond the contribution of DASS stress scores. Sleep behavior did not add to the accuracy of the model. Findings underscore the critical role of sleep physiology, specifically elevated sleep heart-rate following stressful military training, in indicating subsequent PTSD risk following operational service among combat soldiers. These findings may contribute to PTSD prediction and prevention efforts.

Numerous observational studies link obstructive sleep apnea (OSA) to inflammatory proteins, yet the directionality of these associations remains ambiguous. Therefore, we aimed to clarify the potential associations of gene-predicted inflammatory proteins with OSA. Based on genome-wide association study data, we applied Mendelian randomization (MR) to explore potential connections between circulating inflammatory proteins and OSA, primarily using the inverse variance weighting method for robustness. Cochran's Q test, MR‒Egger intercept test, MR-PRESSO, and leave-one-out method were used to perform sensitivity tests for pleiotropy and heterogeneity. Replication analyses and meta-analyses were performed using other independent data. Steiger tests and multivariate MR assessed the independent effects of exposure factors, and the functional mapping and annotation (FUMA) platform was used to identify key genes to enhance the understanding of genetics. Our investigation revealed 21 circulating inflammatory proteins significantly associated with OSA-related phenotypes. Notably, IL-10RA, IL-18R1, TNFSF14, CCL23, ADA, and SLAMF1 had significant effects on multiple phenotypes. After FDR correction, IL-18R1, SLAMF1, IL-10RA, and IL-17C were identified as important candidates for OSA, and multivariate MR analysis strengthened the independent heritability of 20 inflammatory factors. The FUMA platform revealed seven overlapping genes: ROBO1, PRIM1, NACA, SHBG, HSD17B6, RBMS2, and WWOX. All reverse MR analyses and sensitivity analyses confirmed the robustness of these associations. Our results underscore crucial associations between inflammatory proteins and OSA pathogenesis, revealing new correlates and susceptibility genes. These findings advance biomarker identification for OSA risk and highlight the importance of genetic and inflammatory profiles in OSA management.

This study examined the longer-term individual- and school-level changes in students seven months after a one-hour delay in school start time (SST). Two cohorts of Grade 11 students (N = 227; 60.8% female, age = 17.0 [0.85]) at a residential high school in Hong Kong completed a questionnaire assessing sleep duration, insomnia symptoms, depression, anxiety, stress, and subjective well-being in 2017 and 2018, respectively. One of the cohorts was reassessed seven months after the implementation of a delay in SST, from 7:30am to 8:30am (n = 83, 65.1% female). School-level data on breakfast consumption, attendance, tardiness, and health clinic visits were collected. Between-group and within-group prospective comparisons suggest that the delay in SST was associated with improved sleep duration, mental health, and life satisfaction. School-level data revealed increased breakfast consumption and decreased unexcused absences, tardiness, and clinic visits.

Shiftwork is associated with cognitive impairment and reduced sleep time and quality, largely due to circadian misalignment. This study tested if circadian-informed lighting could improve cognitive performance and sleep during simulated night shifts versus dim control lighting. Nineteen healthy participants (Mean±SD 29±10 years, 12 males, 7 females) were recruited to a laboratory study consisting of two counterbalanced 8-day lighting conditions (order randomized) 1-month apart: 1) control lighting condition- dim, blue-depleted and 2) circadian-informed lighting condition- blue-enriched and blue-depleted where appropriate. Participants underwent an adaptation night (22:00h - 07:00h), then four nights of simulated nightwork (cognitive testing battery of nine tasks, 00:00h - 08:00h) and sleep during the day (10:00h - 19:00h). Psychomotor vigilance task (PVT) lapses, Karolinska Sleepiness Scale (KSS) scores, and polysomnography-derived sleep outcomes were compared between conditions and across days using mixed models. Significant condition-by-day-by-time of task interaction effects were found for PVT lapses, median reaction time, and reaction speed, with ~50% fewer lapses by the end of simulated shiftwork with circadian-informed lighting versus control (mean±SD 7.4±5.0 vs. 15.6±6.1). KSS was lower around the nightshift midpoints on days 6 and 7 with circadian versus control lighting. Participants slept 52 minutes longer [95% CIs: 27.5, 76.5 mins] by Day 7 with circadian-informed versus control lighting, p<0.001. Effects were inconsistent on other performance tasks. Circadian-informed lighting improved sleep, sleepiness, and vigilance compared to control lighting. These findings support the potential for lighting interventions to improve sleep and vigilance in night shift workers chronically exposed to dim lighting.