Circadian rhythm disruption and multiple sclerosis: The role of affective symptoms and temperamental traits.

Individual Differences in Sleep Quality: Exploring the Impact of Temperament on Sleep Through Anxiety and Depression

ABSTRACT According to the functional ensemble of temperament (FET) model, individual differences in temperament arise from the balance of neurotransmitter systems also crucial for regulating circadian rhythms and sleep, suggesting a strong neurobiological link between temperament and sleep behavior. The present cross‐sectional study examined whether FET‐defined temperamental traits predict interindividual variation in sleep measures. A total of 394 healthy adults completed the Structure of Temperament Questionnaire (STQ‐77) and validated measures of sleep quality, insomnia severity, daytime sleepiness, and presleep arousal, together with indices of anxiety and depression. Several temperamental traits showed robust associations with sleep outcomes. Neuroticism and impulsivity were associated with poorer sleep quality, greater insomnia severity, and heightened presleep cognitive arousal; these effects were largely mediated by anxiety and depression. Higher social tempo was associated with better sleep and reduced daytime sleepiness. Additional associations emerged for empathy, probabilistic thinking, plasticity, and physical endurance, indicating that orientation, integration, and maintenance FET systems contribute to shaping sleep behavior. These findings indicate that stable, neurochemically grounded temperamental traits may shape interindividual sleep differences, with affective distress as a central mediator. Integrating temperament models into sleep research provides a biologically coherent framework for identifying both risk and resilience factors and informs personalized sleep interventions.

Night eating in Cushing's disease: Disentangling psychological, sleep, and endocrine contributions.

OBJECTIVE Cushing's disease (CD) is characterized by chronic exposure to excess cortisol and disruption of circadian cortisol rhythms. Given cortisol's role in affective regulation and circadian synchronization, eating disturbances-particularly those linked to mood and sleep-may represent an underexplored aspect of CD. We investigated night eating symptoms and chronotype in CD and examined their clinical, psychological, sleep-related, and endocrine correlates. METHODS Ninety-eight participants were included (22 active CD, 33 remission, 43 healthy controls). Night eating symptoms were assessed using the Night Eating Questionnaire (NEQ) and chronotype with the Morningness-Eveningness Questionnaire. Psychological distress and sleep were measured using Hospital Anxiety and Depression Scale, Pittsburgh Sleep Quality Index, and Insomnia Severity Index. Endocrine measures included 24-hour urinary free cortisol, late-night salivary cortisol, and 1-mg dexamethasone suppression test. Hierarchical regression models identified independent predictors of NEQ scores. RESULTS Patients with active CD exhibited greater night eating severity than controls (p = .005), with 16.4% meeting criteria for night eating syndrome. Chronotype did not differ across groups (p = .917). Night eating severity was not associated with cortisol biomarkers. The active disease-night eating association diminished after adjusting for psychological distress. Psychological distress and sleep disturbance independently predicted night eating, accounting for ∼59% of variance. CONCLUSION Night eating symptoms are elevated in active CD but appear more closely linked to psychological distress and sleep disruption than to concurrent cortisol levels. Similar chronotype across groups suggests sleep problems may occur without a shift in circadian preference. Screening for night eating may inform multidisciplinary care in CD.

Sleep and circadian disruption as transdiagnostic drivers of psychosis: a unified mechanistic framework.

INTRODUCTION Psychosis is increasingly understood as a disorder of brain systems that are also central to sleep regulation. Indeed, sleep disturbances are both highly prevalent in psychotic disorders and are likely to contribute to the emergence and maintenance of psychotic experiences. AREAS COVERED This narrative review, based on a comprehensive search of MEDLINE/PubMed, Embase, PsycINFO, and Web of Science (March 2026), examines the bidirectional relationship between sleep dysfunction and psychosis, the shared biological mechanisms underlying both, the utility of sleep assessment as an early warning marker for relapse, and the current gaps in sleep-targeted intervention evidence. EXPERT OPINION Sleep dysfunction constitutes a transdiagnostic pathway to psychosis, with varying temporal profiles across diagnoses: organic and substance-induced psychoses emerge acutely over hours to days with rapid reversibility; mood- and trauma-related psychoses develop subacutely over days to weeks; schizophrenia spectrum disorders show insidious onset over years with chronic persistence. Across these presentations, disturbances in sleep continuity, architecture, and circadian regulation may act as mechanistic drivers rather than epiphenomena, interacting with disorder-specific vulnerabilities to shape the timing, severity, and course of psychosis. Translating this understanding into practice requires routine sleep-circadian assessment from the earliest clinical stages, integration of scalable interventions into transdiagnostic care pathways, and recognition of sleep as both a clinically relevant outcome and a stratification variable in future psychosis trials. This framework positions sleep-circadian dysfunction not only as a marker of risk and progression, but also as a promising modifiable target for prevention, early intervention, and relapse reduction across psychotic disorders.

The Circadian Disruption Index: development, validation, and responsiveness to circadian health education

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 [≤] 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.

Revisiting infradian rhythms in depressive symptoms: wearable signals identify individualised mood cycles in healthy adults

Quality beats quantity: Predicting affective states by different sleep indices in psychiatric patients with suicidal thoughts and behavior.

Sleep disturbances are a transdiagnostic risk factor for affective dysregulation, which is assumed to mediate the association with suicide-related thoughts and behaviors (STBs). Yet most ecological momentary assessment (EMA) studies rely on single-night sleep metrics. With the aim of examining the link between sleep and affect, this study compared the predictive utility of multiple EMA-derived sleep indices with raw sleep measures in a sample at high risk of STBs. Following discharge, psychiatric inpatients with recent suicidal crises (N = 136) completed EMAs of sleep quality (SQ), total sleep time (TST), and affect. Multilevel models examined whether cumulative or variability-sensitive sleep indices better predicted next-day positive and negative affect (PA, NA) and affective instability compared to raw scores. Cumulative SQ, indexed by a three-night pile-up measure, consistently outperformed raw SQ and alternative indices in predicting higher PA and lower NA at both within- and between-person levels. In contrast, TST indices showed no robust associations with affect. These findings highlight cumulative sleep quality as a clinically relevant marker of short-term affective vulnerability. Future studies should explore whether this translates into increased STB risk to explore potential implications for risk monitoring and just-in-time interventions.