Neurobehavioral decision profiles have often been neglected in chronic diseases despite their direct impact on major public health issues such as treatment adherence. This remains a major concern in diabetes, despite intensive efforts and public awareness initiatives regarding its complications. We hypothesized that high rates of low adherence are related to risk-taking profiles associated with decision-making phenotypes. If this hypothesis is correct, it should be possible to define these endophenotypes independently based both on dynamic measures of metabolic control (HbA1C) and multidimensional behavioral profiles.

In this study, 91 participants with early-stage type 1 diabetes fulfilled a battery of self-reported real-world risk behaviors and they performed an experimental task, the Balloon Analogue Risk Task (BART).

K-means and two-step cluster analysis suggest a two-cluster solution providing information of distinct decision profiles (concerning multiple domains of risk-taking behavior) which almost perfectly match the biological partition, based on the division between stable or improving metabolic control (MC, N = 49) v. unstably high or deteriorating states (NoMC, N = 42). This surprising dichotomy of behavioral phenotypes predicted by the dynamics of HbA1C was further corroborated by standard statistical testing. Finally, the BART game enabled to identify groups differences in feedback learning and consequent behavioral choices under ambiguity, showing distinct group choice behavioral patterns.

These findings suggest that distinct biobehavioral endophenotypes can be related to the success of metabolic control. These findings also have strong implications for programs to improve patient adherence, directly addressing risk-taking profiles.

Drug classes are grouped based on their chemical and pharmacological properties, but prescription and illicit drugs differ in other important ways. Potential differences in genetic and environmental influences on the (mis)use of prescription and illicit drugs that are subsumed under the same class should be examined. Opioid and stimulant classes contain prescription and illicit forms differentially associated with salient risk factors (common route of administration, legality), making them useful comparators for addressing this etiological issue.

A total of 2410 individual Australian twins [Mage = 31.77 (s.d. = 2.48); 67% women] were interviewed about prescription misuse and illicit use of opioids and stimulants. Univariate and bivariate biometric models partitioned variances and covariances into additive genetic, shared environmental, and unique environmental influences across drug types.

Variation in the propensity to misuse prescription opioids was attributable to genes (41%) and unique environment (59%). Illicit opioid use was attributable to shared (71%) and unique (29%) environment. Prescription stimulant misuse was attributable to genes (79%) and unique environment (21%). Illicit stimulant use was attributable to genes (48%), shared environment (29%), and unique environment (23%). There was evidence for genetic influence common to both stimulant types, but limited evidence for genetic influence common to both opioid types. Bivariate correlations suggested that prescription opioid use may be more genetically similar to prescription stimulant use than to illicit opioid use.

Prescription opioid misuse may share little genetic influence with illicit opioid use. Future research may consider avoiding unitary drug classifications, particularly when examining genetic influences.

Scar models posit that heightened anxiety and depression can increase the risk for subsequent reduced executive function (EF) through increased inflammation across months. However, the majority of past research on this subject used cross-sectional designs. We therefore examined if elevated generalized anxiety disorder (GAD), major depressive disorder (MDD), and panic disorder (PD) symptoms forecasted lower EF after 20 months through heightened inflammation.

Community-dwelling adults partook in this study (n = 614; MAGE = 51.80 years, 50% females). Time 1 (T1) symptom severity (Composite International Diagnostic Interview – Short Form), T2 (2 months after T1) inflammation serum levels (C-reactive protein, fibrinogen, interleukin-6), and T3 (20 months after T1) EF (Brief Test of Adult Cognition by Telephone) were assessed. Structural equation mediation modeling was performed.

Greater T1 MDD and GAD (but not PD) severity predicted increased T2 inflammation (Cohen's d = 0.21–1.92). Moreover, heightened T2 inflammation forecasted lower T3 EF (d = −1.98 to −1.87). T2 inflammation explained 25–32% of the negative relations between T1 MDD or GAD and T3 EF. T1 GAD severity predicting T3 EF via T2 inflammation path was stronger among younger (v. older) adults. Direct effects of T1 MDD, GAD, and PD forecasting decreased T3 EF were found (d = −2.02 to −1.92). Results remained when controlling for socio-demographic, physical health, and lifestyle factors.

Inflammation can function as a mechanism of the T1 MDD or GAD–T3 EF associations. Interventions that successfully treat depression, anxiety, and inflammation-linked disorders may avert EF decrements.

Suicide rates are high in borderline personality disorder (BPD) where interpersonal problems trigger intense affective dysregulation and impulses to act on suicidal thoughts. To date, however, no study has examined how interpersonal stressors contribute to momentary within-person links among affect and impulsivity with suicidal ideation (SI), and how those links vary over time in people's daily lives.

A total of 153 individuals diagnosed with BPD and 52 healthy controls completed a 21-day ecological momentary assessment protocol. Of these 153 individuals with BPD, 105 had a history of suicide attempts. Multilevel structural equation modeling was used to examine dynamic links among interpersonal perceptions, affect, state impulsivity, and suicidal intent.

Aggregated across interactions, lower perceived warmth in others was associated with SI. This direct relationship, however, did not extend to momentary within-person associations. Instead, interpersonal conflicts were linked to SI indirectly via greater negative affect and lower positive affect. While a robust within-person link between interpersonal perceptions and impulsivity emerged, impulsivity did not account for the relationship between interpersonal perceptions and SI.

This intensive longitudinal study illustrates momentary interpersonal signatures of an emerging suicidal crisis. Among people with BPD at high risk for suicide, interpersonal triggers initiate a cascade of affective dysregulation, which in turn gives rise to SI.

Genotype-first and within-family studies can elucidate factors that contribute to psychiatric illness. Combining these approaches, we investigated the patterns of influence of parental scores, a high-impact variant, and schizophrenia on dimensional neurobehavioral phenotypes implicated in major psychiatric disorders.

We quantitatively assessed cognitive (FSIQ, VIQ, PIQ), social, and motor functioning in 82 adult individuals with a de novo 22q11.2 deletion (22 with schizophrenia), and 148 of their unaffected parents. We calculated within-family correlations and effect sizes of the 22q11.2 deletion and schizophrenia, and used linear regressions to assess contributions to neurobehavioral measures.

Proband-parent intra-class correlations (ICC) were significant for cognitive measures (e.g. FSIQ ICC = 0.549, p < 0.0001), but not for social or motor measures. Compared to biparental scores, the 22q11.2 deletion conferred significant impairments for all phenotypes assessed (effect sizes −1.39 to −2.07 s.d.), strongest for PIQ. There were further decrements in those with schizophrenia. Regression models explained up to 37.7% of the variance in IQ and indicated that for proband IQ, parental IQ had larger effects than schizophrenia.

This study, for the first time, disentangles the impact of a high-impact variant from the modifying effects of parental scores and schizophrenia on relevant neurobehavioral phenotypes. The robust proband-parent correlations for cognitive measures, independent of the impact of the 22q11.2 deletion and of schizophrenia, suggest that, for certain phenotypes, shared genetic variation plays a significant role in expression. Molecular genetic and predictor studies are needed to elucidate shared factors and their contribution to psychiatric illness in this and other high-risk groups.

Unemployment and being not in the labour force (NILF) are risk factors for suicide, but their association with self-harm is unclear, and there is continuing debate about the role of confounding by prior mental health conditions. We examine associations between employment status and self-harm and suicide in a prospective cohort, taking into account prior mental-health-related factors.

We used linked data from the New Zealand Integrated Data Infrastructure. The outcomes were chosen to be hospital presentation for self-harm and death by suicide. The exposure was employment status, defined as employed, unemployed, or NILF, measured at the 2013 Census. Confounders included demographic factors and mental health history (use of antidepressant medication, use of mental health services, and prior self-harm). Logistic regression was used to model effects. Analyses were stratified by gender.

For males, unemployment was associated with an increased risk of suicide [odds ratio (OR): 1.48, 95% confidence interval (CI): 1.20–1.84] and self-harm (OR: 1.55, 95% CI: 1.45–1.68) after full adjustment for confounders. NILF was associated with an increased risk of self-harm (OR: 1.43, 95% CI: 1.32–1.55), but less of an association was seen with suicide (OR: 1.19, 95% CI: 0.94–1.49). For females, unemployment was associated with an increased risk of suicide (OR: 1.30, 95% CI: 0.93–1.80) and of self-harm (OR: 1.52, 95% CI: 1.43–1.62), and NILF was associated with a similar increase in risk for suicide (OR: 1.31, 95% CI: 0.98–1.75) and self-harm (OR: 1.32, 95% CI: 1.26–1.40).

Exclusion from employment is associated with a considerably heightened risk of suicide and self-harm for both men and women, even among those without prior mental health problems.

Cynical hostility (CH), a specific dimension of hostility that consists of a mistrust of others, has been suggested as a high-risk trait for dementia. However, the influence of CH on the incidence of Alzheimer's disease (AD) remains poorly understood. This study investigated whether late-life CH is associated with AD risk and structural neuroimaging markers of AD.

In community-dwelling older adults from the French ESPRIT cohort (n = 1388), incident dementia rate according to CH level was monitored during an 8-year follow-up and analyzed using Cox proportional hazards regression models. Brain magnetic resonance imaging volumes were measured at baseline (n = 508). Using automated segmentation procedures (Freesurfer 6.0), the authors assessed brain grey and white volumes on all magnetic resonance imaging scans. They also measured white matter hyperintensities volumes using semi-automated procedures. Mean volumes according to the level of CH were compared using ANOVA.

Eighty-four participants developed dementia (32 with AD). After controlling for potential confounders, high CH was predictive of AD (HR 2.74; 95% CI 1.10–6.85; p = 0.030) and all dementia types are taken together (HR 2.30; 95% CI 1.10–4.80; p = 0.027). High CH was associated with white matter alterations, particularly smaller anterior corpus callosum volume (p < 0.01) after False Discovery Rate correction, but not with grey matter volumes.

High CH in late life is associated with cerebral white matter alterations, designated as early markers of dementia, and higher AD risk. Identifying lifestyle and biological determinants related to CH could provide clues on AD physiopathology and avenues for prevention strategies.

Many studies have reported an increased risk of autism spectrum disorder (ASD) associated with some maternal diagnoses in pregnancy. However, such associations have not been studied systematically, accounting for comorbidity between maternal disorders. Therefore our aim was to comprehensively test the associations between maternal diagnoses around pregnancy and ASD risk in offspring.

This exploratory case–cohort study included children born in Israel from 1997 to 2008, and followed up until 2015. We used information on all ICD-9 codes received by their mothers during pregnancy and the preceding year. ASD risk associated with each of those conditions was calculated using Cox proportional hazards regression, adjusted for the confounders (birth year, maternal age, socioeconomic status and number of ICD-9 diagnoses during the exposure period).

The analytic sample consisted of 80 187 individuals (1132 cases, 79 055 controls), with 822 unique ICD-9 codes recorded in their mothers. After extensive quality control, 22 maternal diagnoses were nominally significantly associated with offspring ASD, with 16 of those surviving subsequent filtering steps (permutation testing, multiple testing correction, multiple regression). Among those, we recorded an increased risk of ASD associated with metabolic [e.g. hypertension; HR = 2.74 (1.92–3.90), p = 2.43 × 10−8], genitourinary [e.g. non-inflammatory disorders of cervix; HR = 1.88 (1.38–2.57), p = 7.06 × 10−5] and psychiatric [depressive disorder; HR = 2.11 (1.32–3.35), p = 1.70 × 10−3] diagnoses. Meanwhile, mothers of children with ASD were less likely to attend prenatal care appointment [HR = 0.62 (0.54–0.71), p = 1.80 × 10−11].

Sixteen maternal diagnoses were associated with ASD in the offspring, after rigorous filtering of potential false-positive associations. Replication in other cohorts and further research to understand the mechanisms underlying the observed associations with ASD are warranted.

Network approach has been applied to a wide variety of psychiatric disorders. The aim of the present study was to identify network structures of remitters and non-remitters in patients with first-episode psychosis (FEP) at baseline and the 6-month follow-up.

Participants (n = 252) from the Korean Early Psychosis Study (KEPS) were enrolled. They were classified as remitters or non-remitters using Andreasen's criteria. We estimated network structure with 10 symptoms (three symptoms from the Positive and Negative Syndrome Scale, one depressive symptom, and six symptoms related to schema and rumination) as nodes using a Gaussian graphical model. Global and local network metrics were compared within and between the networks over time.

Global network metrics did not differ between the remitters and non-remitters at baseline or 6 months. However, the network structure and nodal strengths associated with positive-self and positive-others scores changed significantly in the remitters over time. Unique central symptoms for remitters and non-remitters were cognitive brooding and negative-self, respectively. The correlation stability coefficients for nodal strength were within the acceptable range.

Our findings indicate that network structure and some nodal strengths were more flexible in remitters. Negative-self could be an important target for therapeutic intervention.

Previous research in resting-state functional magnetic resonance imaging (rs-fMRI) has shown a mixed pattern of disrupted thalamocortical connectivity in psychosis. The clinical meaning of these findings and their stability over time remains unclear. We aimed to study thalamocortical connectivity longitudinally over a 1-year period in participants with recent-onset psychosis.

To this purpose, 129 individuals with recent-onset psychosis and 87 controls were clinically evaluated and scanned using rs-fMRI. Among them, 43 patients and 40 controls were re-scanned and re-evaluated 12 months later. Functional connectivity between the thalamus and the rest of the brain was calculated using a seed to voxel approach, and then compared between groups and correlated with clinical features cross-sectionally and longitudinally.

At baseline, participants with recent-onset psychosis showed increased connectivity (compared to controls) between the thalamus and somatosensory and temporal regions (k = 653, T = 5.712), as well as decreased connectivity between the thalamus and left cerebellum and right prefrontal cortex (PFC; k = 201, T = −4.700). Longitudinal analyses revealed increased connectivity over time in recent-onset psychosis (relative to controls) in the right middle frontal gyrus.

Our results support the concept of abnormal thalamic connectivity as a core feature in psychosis. In agreement with a non-degenerative model of illness in which functional changes occur early in development and do not deteriorate over time, no evidence of progressive deterioration of connectivity during early psychosis was observed. Indeed, regionally increased connectivity between thalamus and PFC was observed.

Traumatic experiences are associated with a higher risk of psychotic illnesses, but little is known about potentially modifiable mechanisms underlying this relationship. This study aims to examine whether post-traumatic stress disorder (PTSD) symptoms mediate the relationship between trauma and psychotic experiences (PEs).

We used data from the Avon Longitudinal Study of Parents and Children to examine whether: PTSD symptoms mediate the relationships between (a) childhood trauma and adolescent PEs (study of adolescent PEs; n = 2952), and (b) childhood/adolescent trauma and PEs in early adulthood (study of adult PEs; n = 2492). We examined associations between variables using logistic regression, and mediation using the parametric g-computation formula.

Exposure to trauma was associated with increased odds of PEs (adolescent PEs: ORadjusted 1.48, 95% CI 1.23–1.78; adult PEs: ORadjusted 1.57, 95% CI 1.25–1.98) and PTSD symptoms (adolescent PTSD: ORadjusted 1.59, 95% CI 1.31–1.93; adult PTSD: ORadjusted 1.50, 95% CI 1.36–1.65). The association between PTSD symptoms and PE was stronger in adolescence (ORadjusted 4.63, 95% CI 2.34–9.17) than in adulthood (ORadjusted 1.62, 95% CI 0.80–3.25). There was some evidence that PTSD symptoms mediated the relationship between childhood trauma and adolescent PEs (proportion mediated 14%), though evidence of mediation was weaker for adult PEs (proportion mediated 8%).

These findings are consistent with the hypothesis that PTSD symptoms partly mediate the association between trauma exposure and PEs. Targeting PTSD symptoms might help prevent the onset of psychotic outcomes.

Psychiatric comorbidity is common in binge-eating disorder (BED) but effects on treatment outcomes are unknown. The current study aimed to determine whether psychiatric comorbidity predicted or moderated BED treatment outcomes.

In total, 636 adults with BED in randomized-controlled trials (RCTs) were assessed prior, throughout, and posttreatment by doctoral research-clinicians using reliably-administered semi-structured interviews, self-report measures, and measured weight. Data were aggregated from RCTs testing cognitive-behavioral therapy, behavioral weight loss, multi-modal (combined pharmacological plus cognitive-behavioral/behavioral), and/or control conditions. Intent-to-treat analyses (all available data) tested comorbidity (mood, anxiety, ‘any disorder’ separately) as predictors and moderators of outcomes. Mixed-effects models tested comorbidity effects on binge-eating frequency, global eating-disorder psychopathology, and weight. Generalized estimating equation models tested binge-eating remission (zero binge-eating episodes during the past month; missing data imputed as failure).

Overall, 41% of patients had current psychiatric comorbidity; 22% had mood and 23% had anxiety disorders. Psychiatric comorbidity did not significantly moderate the outcomes of specific treatments. Psychiatric comorbidity predicted worse eating-disorder psychopathology and higher binge-eating frequency across all treatments and timepoints. Patients with mood comorbidity were significantly less likely to remit than those without mood disorders (30% v. 41%). Psychiatric comorbidity neither predicted nor moderated weight loss.

Psychiatric comorbidity was associated with more severe BED psychopathology throughout treatment but did not moderate outcomes. Findings highlight the need to improve treatments for BED with psychiatric comorbidities but challenge perspectives that combining existing psychological and pharmacological interventions is warranted. Treatment research must identify more effective interventions for BED overall and for patients with comorbidities.

Definition of disorder subtypes may facilitate precision treatment for posttraumatic stress disorder (PTSD). We aimed to identify PTSD subtypes and evaluate their associations with genetic risk factors, types of stress exposures, comorbidity, and course of PTSD.

Data came from a prospective study of three U.S. Army Brigade Combat Teams that deployed to Afghanistan in 2012. Soldiers with probable PTSD (PTSD Checklist for Diagnostic and Statistical Manual of Mental Disorders-Fifth Edition ≥31) at three months postdeployment comprised the sample (N = 423) for latent profile analysis using Gaussian mixture modeling and PTSD symptom ratings as indicators. PTSD profiles were compared on polygenic risk scores (derived from external genomewide association study summary statistics), experiences during deployment, comorbidity at three months postdeployment, and persistence of PTSD at nine months postdeployment.

Latent profile analysis revealed profiles characterized by prominent intrusions, avoidance, and hyperarousal (threat-reactivity profile; n = 129), anhedonia and negative affect (dysphoric profile; n = 195), and high levels of all PTSD symptoms (high-symptom profile; n = 99). The threat-reactivity profile had the most combat exposure and the least comorbidity. The dysphoric profile had the highest polygenic risk for major depression, and more personal life stress and co-occurring major depression than the threat-reactivity profile. The high-symptom profile had the highest rates of concurrent mental disorders and persistence of PTSD.

Genetic and trauma-related factors likely contribute to PTSD heterogeneity, which can be parsed into subtypes that differ in symptom expression, comorbidity, and course. Future studies should evaluate whether PTSD typology modifies treatment response and should clarify distinctions between the dysphoric profile and depressive disorders.

The association between suicide attempts (SAs) in parents and children is unclear, and risk indicators for intergenerational transmission remain undocumented. We aimed to assess this association, considering the child's developmental period at the time of parents' attempted suicide, and the parental relation.

Using a prospective cohort design, nationwide population data were linked to the Psychiatric Central Register and National Patient Register for all individuals aged 10 years or older living in Denmark between 1980 and 2016. We assessed incidence rate ratios (IRRs) and cumulative hazards for children's first SA.

In a cohort of 4 419 651 children, 163 056 (3.7%) had experienced a parental SA. An SA was recorded among 6996 (4.3%) of the exposed children as opposed to 70112 (1.6%) in unexposed individuals. Higher rates were noted when a parental SA occurred during early childhood (0 ⩽ age < 2) [IRR, 4.7; 95% confidence interval (CI) 4.2–5.4] v. late childhood (6 ⩽ age < 13) (IRR, 3.6; 95% CI 3.4–3.8) when compared to those unexposed. Children exposed prior to age 2 had the highest rates of all sub-groups when reaching age 13–17 (IRR, 6.5; 95% CI 6.0–7.1) and 18–25 years (IRR, 6.8; 95% CI 6.2–7.4). Maternal SA (IRR, 3.4; 95% CI 3.2–3.5) was associated with higher rates than paternal (IRR, 2.8; 95% CI 2.7–2.9).

Parental SA was associated with children's own SA. Exposure during early developmental stages was associated with the highest rates. Early preventive efforts are warranted as is monitoring of suicide risk in the children from age 13.

Bipolar disorder (BD) represents one of the most therapeutically complex psychiatric disorders. The development of a feasible comprehensive psychological approach to complement pharmacotherapy to improve its clinical management is required. The main objective of the present randomized controlled trial (RCT) was to test the efficacy of a novel adjunctive treatment entitled integrative approach in patients with BD, including: psychoeducation, mindfulness training, and functional remediation.

This is a parallel two-armed, rater-blind RCT of an integrative approach plus treatment as usual (TAU), v. TAU alone. Participants were recruited at the Hospital Clinic of Barcelona and randomized to one of the two conditions. They were assessed at baseline and after finishing the intervention. The main outcome variable included changes in psychosocial functioning assessed through the Functioning Assessment Short Test (FAST).

After finishing the treatment, the repeated-measures analyses revealed a significant group × time interaction in favor of the patients who received the integrative approach (n = 28) compared to the TAU group (n = 37) (Pillai's trace = 0.10; F(1,57) = 6.9; p = 0.01), improving the functional outcome. Significant effects were also found in two out of the six domains of the FAST, including the cognitive domain (Pillai's trace = 0.25; F(1,57) = 19.1; p < 0.001) and leisure time (Pillai's trace = 0.11; F(1,57) = 7.15; p = 0.01). Regarding the secondary outcomes, a significant group × time interaction in Hamilton Depression Rating Scale changes was detected (Pillai's trace = 0.08; F(1,62) = 5.6; p = 0.02).

This preliminary study suggests that the integrative approach represents a promising cost-effective therapy to improve psychosocial functioning and residual depressive symptoms in patients suffering from BD.

Depression treatment might be enhanced by ecological momentary interventions (EMI) based on self-monitoring and person-specific feedback. This study is the first to examine the efficacy of two different EMI modules for depression in routine clinical practice.

Outpatients starting depression treatment at secondary mental health services (N = 161; MIDS−DEPRESSION = 35.9, s.d. = 10.7; MAGE = 32.8, s.d. = 12.1; 46% male) participated in a pragmatic randomized controlled trial with three arms. Two experimental groups engaged in 28 days of systematic self-monitoring (5 times per day), and received weekly feedback on either positive affect and activities (Do-module) or negative affect and thinking patterns (Think-module). The control group received no additional intervention. Participants completed questionnaires on depressive symptoms (primary outcome), social functioning, and empowerment before and after the intervention period, and at four measurements during a 6-month follow-up period.

Of the 90 (out of 110) participants who completed the intervention, 86% would recommend it. However, the experimental groups did not show significantly more or faster changes over time than the control group in terms of depressive symptoms, social functioning, and empowerment. Furthermore, the trajectories of the two EMI modules were very similar.

We did not find statistical evidence that this type of EMI augments the efficacy of regular depression treatment, regardless of module content. We cannot rule out that EMIs have a positive impact on other domains or provide a more efficient way of delivering care. Nonetheless, EMI's promise of effectiveness has not materialized yet.

Social cognition has not previously been assessed in treatment-naive patients with chronic schizophrenia, in patients over 60 years of age, or in patients with less than 5 years of schooling.

We revised a commonly used measure of social cognition, the Reading the Mind in the Eyes Test (RMET), by expanding the instructions, using both self-completion and interviewer-completion versions (for illiterate respondents), and classifying each test administration as ‘successfully completed’ or ‘incomplete’. The revised instrument (RMET-CV-R) was administered to 233 treatment-naive patients with chronic schizophrenia (UT), 154 treated controls with chronic schizophrenia (TC), and 259 healthy controls (HC) from rural communities in China.

In bivariate and multivariate analyses, successful completion rates and RMET-CV-R scores (percent correct judgments about emotion exhibited in 70 presented slides) were highest in HC, intermediate in TC, and lowest in UT (adjusted completion rates, 97.0, 72.4, and 49.9%, respectively; adjusted RMET-CV-R scores, 45.4, 38.5, and 34.6%, respectively; all p < 0.02). Stratified analyses by the method of administration (self-completed v. interviewer-completed) and by education and age (‘educated-younger’ v. ‘undereducated-older’) show the same relationship between groups (i.e. NC>TC>UT), though not all differences remain statistically significant.

We find poorer social cognition in treatment-naive than in treated patients with chronic schizophrenia. The discriminant validity of RMET-CV-R in undereducated, older patients demonstrates the feasibility of administering revised versions of RMET to patients who may otherwise be considered ineligible due to education or age by changing the method of test administration and carefully assessing respondents' ability to complete the task successfully.

Policy in many high-income settings supports giving pregnant women with previous caesarean section a choice between an elective repeat caesarean section (ERCS) or planning a vaginal birth after previous caesarean (VBAC), provided they have no contraindications to VBAC. Despite the potential for this choice to influence women's mental health, evidence about the associated effect to counsel women and identify potential targets for intervention is limited. This study investigated the association between planned mode of birth after previous caesarean and women's subsequent use of psychotropic medications.

A population-based cohort study of 31 131 women with one or more previous caesarean sections who gave birth to a term singleton in Scotland between 2010 and 2015 with no prior psychotropic medications in the year before birth was conducted using linked Scottish national datasets. Cox regression was used to investigate the association between planned mode of birth and being dispensed psychotropic medications in the first year postpartum adjusted for socio-demographic, medical, pregnancy-related factors and breastfeeding.

Planned VBAC (n = 10 220) compared to ERCS (n = 20 911) was associated with a reduced risk of the mother being dispensed any psychotropic medication [adjusted hazard ratio (aHR) 0.85, 95% confidence interval (CI) 0.78–0.92], an antidepressant (aHR 0.83, 95% CI 0.76–0.90), and at least two consecutive antidepressants (aHR 0.83, 95% CI 0.75–0.91) in the first year postpartum.

Women giving birth by ERCS were more likely than those having a planned VBAC to be dispensed psychotropic medication including antidepressants in the first year postpartum. Further research is needed to establish the reasons behind this new finding.

Sleep disruption is a common precursor to deterioration and relapse in people living with psychotic disorders. Understanding the temporal relationship between sleep and psychopathology is important for identifying and developing interventions which target key variables that contribute to relapse.

We used a purpose-built digital platform to sample self-reported sleep and psychopathology variables over 1 year, in 36 individuals with schizophrenia. Once-daily measures of sleep duration and sleep quality, and fluctuations in psychopathology (positive and negative affect, cognition and psychotic symptoms) were captured. We examined the temporal relationship between these variables using the Differential Time-Varying Effect (DTVEM) hybrid exploratory-confirmatory model.

Poorer sleep quality and shorter sleep duration maximally predicted deterioration in psychosis symptoms over the subsequent 1–8 and 1–12 days, respectively. These relationships were also mediated by negative affect and cognitive symptoms. Psychopathology variables also predicted sleep quality, but not sleep duration, and the effect sizes were smaller and of shorter lag duration.

Reduced sleep duration and poorer sleep quality anticipate the exacerbation of psychotic symptoms by approximately 1–2 weeks, and negative affect and cognitive symptoms mediate this relationship. We also observed a reciprocal relationship that was of shorter duration and smaller magnitude. Sleep disturbance may play a causal role in symptom exacerbation and relapse, and represents an important and tractable target for intervention. It warrants greater attention as an early warning sign of deterioration, and low-burden, user-friendly digital tools may play a role in its early detection.

Vitamin D insufficiency and child antisocial behavior are public health concerns. It is unknown whether vitamin D plays a role in antisocial outcomes. This study examines whether higher levels of vitamin D can act as a protective factor against antisocial behavior for children who are exposed to early social adversity.

In a community sample of 300 children aged 11–12 years (151 females, 149 males), serum concentrations of 25-hydroxyvitamin D [25(OH)D] were assessed alongside early social adversity, and both parent and child-reported antisocial behavior.

Vitamin D moderated the association between early social adversity and multiple antisocial outcomes. Higher social adversity was associated with greater antisocial behavior among vitamin D-insufficient [25(OH)D < 30 ng/mL], but not vitamin D-sufficient children [25(OH)D ⩾ 30 ng/mL], after adjusting for other variables. Results from child reports of antisocial behavior were replicated with parent reports, providing support for the robustness of the findings. At serum 25(OH)D concentrations above 27.16–30.69 ng/mL (close to 30 ng/mL, the recommended optimal vitamin D level for pediatric populations), the effect of social adversity on antisocial behavior outcomes was nullified.

To our knowledge, this study is the first to document that a nutritional factor, vitamin D, can potentially confer resilience to antisocial behavior. Our findings in a pediatric population suggest a possible role of vitamin D supplementation in interventions to reduce antisocial behavior, which may be further investigated in future randomized controlled trials.