Postpartum Psychosis (PP) is a severe and understudied perinatal mental illness which disproportionately affects women with bipolar disorder (BD). A relationship between sleep disturbance and PP is often assumed, but is poorly understood. From a cohort of 2099 individuals with BD, 343 parous women were identified and screened for perinatal psychiatric complications. We compared 117 women who developed PP with 226 who did not. Polygenic Risk Scores (PRS) for BD, schizophrenia, insomnia, short sleep, long sleep, sleep efficiency and sleep duration were computed using PRS-CS. Logistic regression was used to model the effect of each PRS on PP. Higher PRS for insomnia and short sleep were associated with reduced risk of PP. Individuals in the lowest decile for insomnia PRS (RR 1.96, 95% CI 1.25-3.07, p = 3.50 × 10⁻³) and short sleep PRS (RR 2.23, 95% CI 1.40-3.54, p = 7.94 × 10⁻⁴) had approximately double the risk of PP than individuals in the highest decile. The other PRS were not associated with PP. Mendelian Randomisation analyses did not support a causal relationship between sleep traits and PP. However, we demonstrate that the integration of PRS with bipolar subtype can improve prediction accuracy. Individuals with genetic vulnerability to insomnia or short sleep may develop a heightened tolerance to sleep disruption earlier in life, mitigating the impact of childbirth on mood. These findings suggest that genetic susceptibility to sleep disturbance may be important in the aetiology of PP, offering a new potential avenue for risk stratification and targeted prevention.

Sleep abnormalities are core features of bipolar disorders (BD), but they have not been thoroughly examined across mood phases. This meta-analysis investigated sleep disturbance prevalence and sleep characteristics differences in BD across mood phases. A systematic search through September 2024 identified 44 studies (7614 BD cases, 3164 controls), including 11 prevalence and 34 case-control studies. Poor sleep quality prevalence was 52% during euthymia, and insomnia prevalence was 63% during the depressive phase. Individuals with euthymic BD reported worse sleep quality and objectively measured longer total sleep time and sleep onset latency than controls. Depressive phase BD showed higher rapid eye movement percentages, while manic/mixed phase exhibited shorter total sleep time, lower sleep efficiency, and longer sleep onset latency. During euthymia, BD demonstrated greater variability in sleep duration and continuity, and more prominent sleep differences when assessed with sleep diary versus objective sleep measures, highlighting the importance of integrating objective assessments and patient-reported outcomes. Overall, these findings indicate that poor sleep quality and insomnia are highly prevalent in BD, and that some sleep parameter differences are present during euthymia, while others occur during depressive and manic phases, emphasizing the need for sleep assessments and tailored management throughout the course of BD.

Postpartum Psychosis (PP) is a severe perinatal psychiatric disorder affecting 1–2 in 1000 individuals following childbirth. Most episodes emerge within the first two weeks postpartum and commonly present with mania and decreased need for sleep. The postnatal period is a time of profound sleep disruption and sleep deprivation is a known trigger for mania and psychosis. Despite growing recognition of the role of sleep in the onset and progression of PP, this relationship remains poorly understood. Existing research is largely retrospective, relies on self-reported data and primarily focuses on women with pre-existing bipolar disorder. This prospective study will integrate subjective and objective sleep measures to investigate the relationship between sleep disturbance and postnatal mania. We aim to establish whether sleep patterns in late pregnancy or the early postpartum period can predict mania as a marker of PP. This prospective observational cohort study is recruiting pregnant women and will follow participants from the late third trimester until two weeks postpartum. We aim to recruit 100 participants, including individuals with and without psychiatric illness, to ensure broader applicability of the findings and capture the full spectrum of postnatal mania risk. Participants will wear a wrist accelerometer continuously during this period to monitor rest-activity patterns and infer objective sleep parameters including sleep duration, efficiency and fragmentation. Self-reported sleep quality and mood symptoms will be measured using the Pittsburgh Sleep Quality Index (PSQI), Altman Self-Rating Mania Scale (ASRM) and Edinburgh Postnatal Depression Scale (PSQI) at baseline and at days 3–5 and 12–14 postpartum. Actigraphy data will be analysed using the GGIR package in R. Associations between sleep measures and ASRM scores will be assessed using Pearson and Spearman correlation coefficients. This study is the first to prospectively investigate sleep and postnatal mania risk in a cohort including both high- and low-risk individuals. By integrating actigraphy with validated self-report measures, it aims to identify rest-activity patterns that may serve as early indicators of PP. Early recognition of sleep disturbances associated with postnatal mania could inform targeted interventions, improving clinical outcomes for women and families affected by PP.

Recent years have seen a proliferation of interest in psychological networks, which conceptualise psychopathology as networks of inter-connected, mutually reinforcing symptoms. It has been hypothesised that the topological structure of such networks is associated with clinical presentation. Analysing data from a longitudinal study of participants diagnosed with psychosis, we identify substantial inter-individual variability in network structure, problematising causal inference from cross-sectional networks. Additionally, we do not find strong evidence for an association between network structure and clinical relapse.

The perception of what constitutes mental illness is influenced by various social and medical developments. Prevalence-induced concept change is a phenomenon where decreasing the prevalence of a category leads people to expand their judgment of that concept. In this study, we tested whether changing the prevalence of statements describing mental illness results in a change in the concept of mental illness. Based on a population survey ( n = 1031), we created a validated set of 273 brief statements depicting either clear symptoms of mental illness, clear examples of healthy behaviour, or ambiguous situations. We presented a subset of statements to 138 students, asking them to judge whether each statement represented mental illness, or not. After 96 statements, we reduced the prevalence of clearly mentally ill statements in one group, while the proportion of statements denoting clear mental illness remained the same in the other group. In the group where the proportion of clearly mentally ill statements was reduced during the experiment, a concept change of mental illness evolved: participants were more likely to identify a statement as denoting a mental illness. The results indicate that the perceived prevalence of symptoms of mental illness is important for conceptualizing mental illness and that decreasing prevalence broadens the concept of mental illness. These findings add a novel perspective to current debates around diagnostic thresholds, the treatment-prevalence paradox, the medicalization of emotions, and the focus of anti-stigma campaigns.

Sleep, circadian rhythms, and mental health are reciprocally interlinked. Disruption to the quality, continuity, and timing of sleep can precipitate or exacerbate psychiatric symptoms in susceptible individuals, while treatments that target sleep—circadian disturbances can alleviate psychopathology. Conversely, psychiatric symptoms can reciprocally exacerbate poor sleep and disrupt clock-controlled processes. Despite progress in elucidating underlying mechanisms, a cohesive approach that integrates the dynamic interactions between psychiatric disorder with both sleep and circadian processes is lacking. This review synthesizes recent evidence for sleep—circadian dysfunction as a transdiagnostic contributor to a range of psychiatric disorders, with an emphasis on biological mechanisms. We highlight observations from adolescent and young adults, who are at greatest risk of developing mental disorders, and for whom early detection and intervention promise the greatest benefit. In particular, we aim to a) integrate sleep and circadian factors implicated in the pathophysiology and treatment of mood, anxiety, and psychosis spectrum disorders, with a transdiagnostic perspective; b) highlight the need to reframe existing knowledge and adopt an integrated approach which recognizes the interaction between sleep and circadian factors; and c) identify important gaps and opportunities for further research.

This editorial summarises the clinical relevance of 'chronopsychiatry', defined as the interface between circadian science and mental health science. Chronopsychiatry represents a move towards time-variable perspectives on neurobiology and symptoms, with a greater emphasis on chronotherapeutic interventions.

Postpartum Psychosis (PP) is a severe and understudied perinatal mental illness which disproportionately affects women with bipolar disorder (BD). A relationship between sleep disturbance and PP is often assumed, but is poorly understood. Data from 2099 BD subjects were screened to identify parous women. Individuals who developed PP and those who had not were compared in our analyses. Polygenic Risk Scores (PRS) for BD, schizophrenia, insomnia, short sleep, long sleep and sleep efficiency were computed using PRS-CS. Logistic regression was used to model the effect of each PRS on PP. Higher PRS for insomnia and short sleep were protective against PP. Individuals in the lowest decile for insomnia PRS (RR 1.96, 95% CI 1.25-3.07, p = 3.50 x 10 -3) and short sleep PRS (RR 2.23, 95% CI 1.40-3.54, p = 7.94 x 10 -4) had approximately double the risk of PP than individuals in the highest decile. BD, schizophrenia, long sleep and sleep efficiency PRS were not associated with PP. Mendelian Randomisation analyses did not support a causal relationship between sleep traits and PP. However, we demonstrate that the integration of PRS with clinical variables can improve prediction accuracy. Individuals with genetic vulnerability to insomnia or short sleep may develop a heightened tolerance to sleep disruption earlier in life, mitigating the impact of childbirth on mood. These findings suggest that genetic susceptibility to sleep disturbance may play a crucial role in the aetiology of PP, offering a new potential avenue for risk stratification and targeted prevention.

Importance:Abnormal sleep is frequent in psychosis; however, sleep abnormalities in different stages (ie, clinical high risk for psychosis [CHR-P], early psychosis [EP], and chronic psychosis [CP]) have not been characterized. Objective:To identify sleep abnormalities across psychosis stages. Data Sources:Web of Science and PubMed were searched between inception and June 15, 2022. Studies written in English were included. Study Selection:Sleep disturbance prevalence studies and case-control studies reporting sleep quality, sleep architecture, or sleep electroencephalography oscillations in CHR-P, EP, or CP. Data Extraction and Synthesis:This systematic review and meta-analysis followed Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) reporting guideline. Stage-specific and pooled random-effects meta-analyses were conducted, along with the assessment of heterogeneity, study quality, and meta-regressions (clinical stage, sex, age, medication status, and psychotic symptoms). Main Outcomes and Measures:Sleep disturbance prevalence, self-reported sleep quality, sleep architecture (total sleep time, sleep latency, sleep efficiency, nonrapid eye movement, rapid eye movement stages, and number of arousals), and sleep electroencephalography oscillations (spindle density, amplitude, and duration, and slow wave density). Results:Fifty-nine studies with up to 6710 patients (n = 5135 for prevalence) and 977 controls were included. Sleep disturbance prevalence in pooled cases was 50% (95% CI, 40%-61%) and it was similar in each psychosis stage. Sleep quality was worse in pooled cases vs controls (standardized mean difference [SMD], 1.00 [95% CI, 0.70-1.30]). Sleep architecture alterations included higher sleep onset latency (SMD [95% CI]: pooled cases, 0.96 [0.62-1.30]; EP, 0.72 [0.52-0.92]; CP, 1.36 [0.66-2.05]), higher wake after sleep onset (SMD [95% CI]: pooled cases, 0.5 [0.29-0.71]; EP, 0.62 [0.34-0.89]; CP, 0.51 [0.09-0.93]), higher number of arousals (SMD [95% CI]: pooled cases, 0.45 [0.07-0.83]; CP, 0.81 [0.30-1.32]), higher stage 1 sleep (SMD [95% CI]: pooled cases, 0.23 [0.06-0.40]; EP, 0.34 [0.15-0.53]), lower sleep efficiency (SMD [95% CI]: pooled cases, -0.75 [-0.98 to -0.52]; EP, -0.90 [-1.20 to -0.60]; CP, -0.73 [-1.14 to -0.33]), and lower rapid eye movement density (SMD [95% CI]: pooled cases, 0.37 [0.14-0.60]; CP, 0.4 [0.19-0.77]). Spindle parameter deficits included density (SMD [95% CI]: pooled cases, -1.06 [-1.50 to -0.63]; EP, -0.80 [-1.22 to -0.39]; CP, -1.39 [-2.05 to -0.74]; amplitude: pooled cases, -1.08 [-1.33 to -0.82]; EP, -0.86 [-1.24 to -0.47]; CP, -1.25 [-1.58 to -0.91]; and duration: pooled cases: -1.2 [-1.69 to -0.73]; EP, -0.71 [-1.08 to -0.34]; CP, -1.74 [-2.10 to -1.38]). Individuals with CP had more frequent arousals vs CHR-P (z = 2.24, P = .02) and reduced spindle duration vs EP (z = -3.91, P < .001). Conclusions and Relevance:In this systematic review and meta-analysis, sleep disturbances were found to be prevalent throughout the course of psychosis, and different psychosis stages showed both shared and distinct abnormalities in sleep quality, architecture, and spindles. These findings suggest that sleep should become a core clinical target and research domain from at-risk to early and chronic stages of psychosis.

Introduction A variety of dimensions of psychopathology are observed in psychosis. However, the validation of clinical assessment scales, and their latent variable structure, is often derived from cross-sectional rather than longitudinal data, limiting our understanding of how variables interact and reinforce one another. Objectives Using experience sampling methodology (ESM) and analytic approaches optimised for longitudinal data, we assess potential latent variables of commonly-reported symptoms in psychosis, and explore the temporal relationship between them. Methods N=36 participants with a diagnosis of schizophrenia or schizoaffective disorder provided data for up to one year, as part of the Sleepsight study. Using a smartphone app, participants self-reported clinical symptoms once daily for a mean duration of 323 days (SD: 88), with a response rate of 69%. Symptoms were rated using seven-point Likert scale items. Items included symptoms traditionally implicated in psychosis (feeling “cheerful”, “anxious”, “relaxed”, “irritable”, “sad”, “in control”, “stressed”, “suspicious”, “trouble concentrating”, “preoccupied by thoughts”, “others dislike me”, “confused”, “others influence my thoughts” and “unusual sights and sounds”). We used a sparse PCA (SPCA) model to identify latent variables in the longitudinal data. SPCA has previously been applied to longitudinal ESM data, and was developed to achieve a compromise between the explained variance and the interpretability of the principal components. We then used a multistage exploratory and confirmatory differential time-varying effect model (DTVEM) to explore the temporal relationship between the latent variables. DTVEM generates a standardised β coefficient reflecting the strength of relationship between variables across multiple time lags. Only significant lags (p<0.05) are reported here. Results The SPCA analysis identified five latent variables, explaining 61.4% of the total variance. Tentative interpretation of the SPCA loadings suggested these latent variables corresponded to i) cognitive symptoms, ii) feeling in-control, iii) thought interference and perceptual disturbance, iv) irritability and stress and v) paranoia. Time lag analysis revealed an effect of feeling in-control on subsequent cognitive symptoms (β=-0.19), and of cognitive symptoms on subsequent thought interference and perceptual disturbance (β=0.14). Irritability and stress was also associated with subsequent cognitive symptoms (β=0.09). Conclusions Using longitudinal data, we employ novel methodology to identify potential latent symptoms among commonly reported symptoms in psychosis. We identify five latent symptoms, and elucidate important temporal relationships between them. These findings may inform our understanding of the psychopathology of psychosis, potentially offering data-driven simplification of clinical assessment and novel insights for future research. Disclosure of Interest None Declared

and circadian function are leading candidate markers for early relapse identification in MDD. Consumer-grade wearable devices may offer opportunity for remote and real-time examination of dynamic changes in sleep. Objective: We used FitBit data from individuals with recurrent MDD to describe longitudinal associations of sleep duration, quality, and regularity with subsequent depressive relapse and depression severity.Design: Data were collected as part of a longitudinal remote measurement technologies (RMT) cohort study in people with recurrent MDD. Participants: A total of 623 people with MDD wore a FitBit and completed regular outcome assessments via email for a median follow-up of 541 days. Multivariable regression models tested for associations between sleep features and depression outcomes. We considered two samples of people with at least one assessment of relapse (n=213) or at least one assessment of depression severity (n=390). Results: Increased intra-individual variability in total sleep time, greater sleep fragmentation, and later sleep mid-points were associated with worse depression outcomes. Adjusted Population Attributable Fractions (PAFs) suggested that an intervention to increase sleep consistency in adults with MDD could reduce the population risk for depression by up to 18-37%. Conclusion: We found consistent associations between wearable-derived sleep features and the probability of depressive relapse and increased depressive symptom severity. Disordered sleep is prevalent and disruptive, and challenging to capture longitudinally via conventional laboratory sleep assessments. Our study demonstrates a role for consumer-grade activity trackers to predict relapse risk and depression severity in people with recurrent MDD.

ImportanceAbnormal sleep is frequent in psychosis; however, sleep abnormalities in different stages (ie, clinical high risk for psychosis [CHR-P], early psychosis [EP], and chronic psychosis [CP]) have not been characterized.ObjectiveTo identify sleep abnormalities across psychosis stages.Data SourcesWeb of Science and PubMed were searched between inception and June 15, 2022. Studies written in English were included.Study SelectionSleep disturbance prevalence studies and case-control studies reporting sleep quality, sleep architecture, or sleep electroencephalography oscillations in CHR-P, EP, or CP.Data Extraction and SynthesisThis systematic review and meta-analysis followed Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) reporting guideline. Stage-specific and pooled random-effects meta-analyses were conducted, along with the assessment of heterogeneity, study quality, and meta-regressions (clinical stage, sex, age, medication status, and psychotic symptoms).Main Outcomes and MeasuresSleep disturbance prevalence, self-reported sleep quality, sleep architecture (total sleep time, sleep latency, sleep efficiency, nonrapid eye movement, rapid eye movement stages, and number of arousals), and sleep electroencephalography oscillations (spindle density, amplitude, and duration, and slow wave density).ResultsFifty-nine studies with up to 6710 patients (n = 5135 for prevalence) and 977 controls were included. Sleep disturbance prevalence in pooled cases was 50% (95% CI, 40%-61%) and it was similar in each psychosis stage. Sleep quality was worse in pooled cases vs controls (standardized mean difference [SMD], 1.00 [95% CI, 0.70-1.30]). Sleep architecture alterations included higher sleep onset latency (SMD [95% CI]: pooled cases, 0.96 [0.62-1.30]; EP, 0.72 [0.52-0.92]; CP, 1.36 [0.66-2.05]), higher wake after sleep onset (SMD [95% CI]: pooled cases, 0.5 [0.29-0.71]; EP, 0.62 [0.34-0.89]; CP, 0.51 [0.09-0.93]), higher number of arousals (SMD [95% CI]: pooled cases, 0.45 [0.07-0.83]; CP, 0.81 [0.30-1.32]), higher stage 1 sleep (SMD [95% CI]: pooled cases, 0.23 [0.06-0.40]; EP, 0.34 [0.15-0.53]), lower sleep efficiency (SMD [95% CI]: pooled cases, −0.75 [−0.98 to −0.52]; EP, −0.90 [−1.20 to −0.60]; CP, −0.73 [−1.14 to −0.33]), and lower rapid eye movement density (SMD [95% CI]: pooled cases, 0.37 [0.14-0.60]; CP, 0.4 [0.19-0.77]). Spindle parameter deficits included density (SMD [95% CI]: pooled cases, −1.06 [−1.50 to −0.63]; EP, −0.80 [−1.22 to −0.39]; CP, −1.39 [−2.05 to −0.74]; amplitude: pooled cases, −1.08 [−1.33 to −0.82]; EP, −0.86 [−1.24 to −0.47]; CP, −1.25 [−1.58 to −0.91]; and duration: pooled cases: −1.2 [−1.69 to −0.73]; EP, −0.71 [−1.08 to −0.34]; CP, −1.74 [−2.10 to −1.38]). Individuals with CP had more frequent arousals vs CHR-P (z = 2.24, P = .02) and reduced spindle duration vs EP (z = −3.91, P < .001).Conclusions and RelevanceIn this systematic review and meta-analysis, sleep disturbances were found to be prevalent throughout the course of psychosis, and different psychosis stages showed both shared and distinct abnormalities in sleep quality, architecture, and spindles. These findings suggest that sleep should become a core clinical target and research domain from at-risk to early and chronic stages of psychosis.

We read with interest the recent International Society on Thrombosis and Haemostasis Scientific and Standardization Committee communication regarding the challenges in the management of women with type 2b von Willebrand disease during pregnancy [ [1] Miljic P. Noureldin A. Lavin M. Kazi S. Sanchez-Luceros A. James P.D. Othman M. Challenges in the management of women with type 2B von Willebrand disease durig pregnancy and the postpartum period:evidence from literature, and data from an international registry and physicians’ survey –communication from the Scientific and Standardization Committees of the International Society on Thrombosis and Haemostasis. J Throb Haemost. 2023; 21: 154-163 Abstract Full Text Full Text PDF PubMed Scopus (1) Google Scholar ]. This is a difficult situation to manage given the dynamic nature of hemostatic parameters during pregnancy and the paucity of cases.

The daily alternation between sleep and wakefulness is one of the most dominant features of our lives and is a manifestation of the intrinsic 24 h rhythmicity underlying almost every aspect of our physiology. Circadian rhythms are generated by networks of molecular oscillators in the brain and peripheral tissues that interact with environmental and behavioural cycles to promote the occurrence of sleep during the environmental night. This alignment is often disturbed, however, by contemporary changes to our living environments, work or social schedules, patterns of light exposure, and biological factors, with consequences not only for sleep timing but also for our physical and mental health. Characterised by undesirable or irregular timing of sleep and wakefulness, in this Series paper we critically examine the existing categories of circadian rhythm sleep-wake disorders and the role of the circadian system in their development. We emphasise how not all disruption to daily rhythms is driven solely by an underlying circadian disturbance, and take a broader, dimensional approach to explore how circadian rhythms and sleep homoeostasis interact with behavioural and environmental factors. Very few high-quality epidemiological and intervention studies exist, and wider recognition and treatment of sleep timing disorders are currently hindered by a scarcity of accessible and objective tools for quantifying sleep and circadian physiology and environmental variables. We therefore assess emerging wearable technology, transcriptomics, and mathematical modelling approaches that promise to accelerate the integration of our knowledge in sleep and circadian science into improved human health.

Topic: 33. Bleeding disorders (congenital and acquired) Background: Direct Oral Anticoagulant (DOAC) use is increasing with their favourable safety profile and ease of administration. Haemarthrosis is a potentially devastating complication of anticoagulation and the natural history of DOAC associated haemarthrosis is poorly described. Aims: We aimed to better define the epidemiology, diagnosis and natural history of DOAC associated haemarthrosis in an urban Irish population Methods: Retrospective chart review review of all presentations of monoarticular arthritis to a tertiary referral hospital in Ireland over a two-year period. Results: 38 patients were identified with an isolated monoarticular arthritis. 11 (29%) of patients were found to have a haemarthrosis with the remaining 27 patients diagnosed with either crystal arthropathies (gout, pseudogout) or septic arthritis. Of the haemarthroses, 7 patients were diagnosed via joint aspirate and 4 by imaging studies alone. All patients with haemarthroses were on antithrombotic therapy at presentation. 7 patients were taking a DOAC, 3 patients on warfarin and 1 patient on aspirin alone. 10 patients were anticoagulated for atrial fibrillation and one for a history of ischaemic heart disease. Patients were predominantly older (mean age 85, Range 76-94) and male (8 male vs 3 female). Most (8/11) haemarthroses were spontaneous with only 2 associated with minor trauma and one with major trauma. Renal function was normal in 9/11 patients with one mild and one moderate AKI. No patients had underlying CKD. All patients were managed conservatively with physiotherapy and cessation of anticoagulation. Two patients required bracing. One patient died of hospital acquired pneumonia during admission and a second patient was found to have no current indication for ongoing anticoagulation. In all other patients antithrombotic therapy was reinstituted no patient was readmitted with further joint bleeding Summary/Conclusion: Haemarthrosis represents a significant percentage of acute presentations of isolated monoarthritis. Most are spontaneous and all occurred in patients on antithrombotic therapy. Fewer patients than expected had risk factors that would be associated with DOAC induced bleeding (dual antithrombotic therapy, significant renal dysfunction). All bleeds were managed conservatively and antithrombotics recommenced without readmission for further bleeds. Our findings are similar to a recently published study from the United Kingdom (Dalrymple et. al.) suggesting that anithrombotic therapy can be safely reinstituted in these patients and the general outcome is favourable. Keywords: Antithrombotic therapy, Anticoagulation, Bleeding

Sleep and circadian rhythm dysfunction is prevalent in schizophrenia, is associated with distress and poorer clinical status, yet remains an under-recognized therapeutic target. The development of new therapies requires the identification of the primary drivers of these abnormalities. Understanding of the regulation of sleep-wake timing is now sufficiently advanced for mathematical model-based analyses to identify the relative contribution of endogenous circadian processes, behavioral or environmental influences on sleep-wake disturbance and guide the development of personalized treatments. Here, we have elucidated factors underlying disturbed sleep-wake timing by applying a predictive mathematical model for the interaction of light and the circadian and homeostatic regulation of sleep to actigraphy, light, and melatonin profiles from 20 schizophrenia patients and 21 age-matched healthy unemployed controls, and designed interventions which restored sleep-circadian function. Compared to controls, those with schizophrenia slept longer, had more variable sleep timing, and received significantly fewer hours of bright light (light > 500 lux), which was associated with greater variance in sleep timing. Combining the model with the objective data revealed that non 24-h sleep could be best explained by reduced light exposure rather than differences in intrinsic circadian period. Modeling implied that late sleep offset and non 24-h sleep timing in schizophrenia can be normalized by changes in environmental light-dark profiles, without imposing major lifestyle changes. Aberrant timing and intensity of light exposure patterns are likely causal factors in sleep timing disturbances in schizophrenia. Implementing our new model-data framework in clinical practice could deliver personalized and acceptable light-dark interventions that normalize sleep-wake timing.