It has been suggested that screening interventions may be effective for suicide prevention. Few studies, however, have reported their effects on outcome measures, including death by suicide among middle-aged adults.

We used a quasi-experimental parallel cluster design with matched community-based intervention and control municipalities (total eligible population: 90 000) in Japan. At-risk residents within the intervention area were invited for universal depression screening and subsequent care/support. We compared changes in suicide incidence of adults aged 40–64 years for the 4-year pre- and post-implementation periods in the intervention group with the control group and the whole country. Incidence rate ratios (IRRs) of the outcomes were adjusted for age group, gender and interaction terms, using mixed-effects negative binomial regression models. Suicide rates among intervention and control subgroups were compared.

The screening procedure was offered to 52% of the intervention group, and 61% of those contacted responded over the implementation period. Suicide rates decreased more in the intervention group [IRR 0.57, 95% (CI) 0.41–0.78; F1,36 = 12.52, p = 0.001] than the control group (IRR proportion 1.63, 95% CI 1.06–2.48; F1,82 = 5.20, p = 0.025) or the whole country (IRR proportion 1.64, 95% CI 1.16–2.34; F1,42 = 8.21, p = 0.006). Sensitivity analyses confirmed the results from the primary analysis. There were lower suicide rates among both respondents and non-respondents to the screening than in the control group during the implementation period.

Prevention efforts involved in the depression screening intervention were probably successful in reducing suicide rates.

Studies have shown that there are overlapping traits and symptoms between autism and psychosis but no study to date has addressed this association from an epidemiological approach in the adult general population. Furthermore, it is not clear whether autistic traits are associated with specific symptoms of psychosis or with psychosis in general. We assess these associations for the first time by using the Adult Psychiatric Morbidity Survey (APMS) 2007 and the APMS 2014, predicting an association between autistic traits and probable psychosis, and specific associations between autistic traits and paranoia and strange experiences.

Participants (N = 7353 in 2007 and 7500 in 2014) completed the Psychosis Screening Questionnaire (PSQ) and a 20-item version of the Autism Quotient (AQ-20). Binomial logistic regressions were performed using AQ-20 as the independent variable and probable psychosis and specific symptoms as dependent variables.

In the APMS 2007 dataset, significant associations were found between autism traits and probable psychosis, paranoia, thought insertion, and strange experiences. These results were replicated in APMS 2014 but with the additional significant association between autistic traits and hallucinations. Participants in the highest quartile of the AQ-20, compared with the lowest quartile, had an increased risk of probable psychosis of odds ratio (OR) = 15.5 [95% confidence interval (CI) 4.57–52.6] in APMS 2007 and OR = 22.5 (95% CI 7.64–66.3) in APMS 2014.

Autistic traits are strongly associated with probable psychosis and psychotic experiences with the exception of mania. Limitations such as the cross-sectional nature of the study are discussed.

Since 1999, the rate of fatal prescription opioid overdoses and of suicides has dramatically increased in the USA. These increases, which have occurred among similar demographic groups, have led to the hypothesis that the opioid epidemic contributed to increases in suicidal behavior, though the underlying association remains poorly defined. We examine the association between nonmedical use of prescription opioids/opioid use disorder and suicidal ideation/attempts.

We used longitudinal data from a national representative sample of the US adult population, the National Epidemiologic Survey on Alcohol and Related Conditions. Participants (n = 34 653) were interviewed in 2001–2002 (wave 1) and re-interviewed approximately 3 years later (wave 2). A propensity score analysis estimated the association between exposure to prescription opioids at wave 1 and prevalent/incident suicidal behavior at wave 2.

Heavy/frequent (⩾2–3 times a month) prescription opioid use was associated with prevalent suicide attempts [adjusted risk ratio (ARR) = 2.75, 95% CI 1.35–5.60]. Prescription opioid use disorder was associated with prevalent (ARR = 1.98, 95% CI 1.20–3.28) and incident suicidal ideation (ARR = 2.59, 95% CI 1.25–5.37), and prevalent attempts (ARR = 4.19, 95% CI 1.71–10.27). None of the exposures was associated with incident suicide attempts.

Heavy/frequent opioid use and related disorder were associated with prevalent suicide attempts; opioid use disorder was also associated with the incident and prevalent suicidal ideation. Given population increases in nonmedical use of prescription opioids and disorder, the opioid crisis may have contributed to population increases in suicidal ideation.

The determinants of quality of life (QoL) in schizophrenia are largely debated, mainly due to methodological discrepancies and divergence about the concepts concerned. As most studies have investigated bi- or tri-variate models, a multivariate model accounting for simultaneous potential mediations is necessary to have a comprehensive view of the determinants of QOL. We sought to estimate the associations between cognitive reserve, cognition, functioning, insight, depression, schizophrenic symptoms, and QoL in schizophrenia and their potential mediation relationships.

We used structural equation modeling with mediation analyses to test a model based on existing literature in a sample of 776 patients with schizophrenia from the FondaMental Foundation FACE-SZ cohort.

Our model showed a good fit to the data. We found better functioning to be positively associated with a better QoL, whereas better cognition, better insight, higher levels of depression, and schizophrenic symptoms were associated with a lower QoL in our sample. Cognitive reserve is not directly linked to QoL, but indirectly in a negative manner via cognition. We confirm the negative relationship between cognition and subjective QoL which was previously evidenced by other studies; moreover, this relationship seems to be robust as it survived in our multivariate model. It was not explained by insight as some suggested, thus the mechanism at stake remains to be explained.

The pathways to subjective QoL in schizophrenia are complex and the determinants largely influence each other. Longitudinal studies are warranted to confirm these cross-sectional findings.

Current evidence on antipsychotic treatment and risk of psychiatric hospitalization in first-episode schizophrenia (FES) is largely based on the findings from randomized clinical trials (RCTs). However, the generalization of the findings to real-world patients is limited due to inherent caveats of the RCT. We aimed to investigate the treatment discontinuation and risk of psychiatric hospitalization using a nationwide population database.

The Health Insurance Review Agency database in South Korea was obtained, and the observation period started from 1 January 2009 to 31 December 2016. We defined the maintenance period as the period from 6-month after the diagnosis of schizophrenia, which is utilized for the main results. For a total of 44 396 patients with FES, a within-individual Cox regression model was used to compare the risk of the treatment discontinuation and psychiatric hospitalization.

In group comparison, a long-acting injectable (LAI) antipsychotic group was associated with the lowest risk of the treatment discontinuation (0.64, 0.55–0.75) and psychiatric hospitalization (0.29, 0.22–0.38) in comparison with a typical antipsychotic group and no use, respectively. Among individual antipsychotics, the lowest risk of the treatment discontinuation was observed in LAI paliperidone (0.46, 0.37–0.66) compared to olanzapine. Clozapine was found to be the most effective antipsychotic in lowering the risk of psychiatric hospitalization as monotherapy compared to no use (0.23, 0.18–0.31).

In real-world patients with FES, LAI paliperidone and clozapine were associated with low treatment discontinuation and better effectiveness in lowering the risk of psychiatric hospitalization.

Poor cognitive abilities and low intellectual quotient (IQ) are associated with an increased risk of suicide attempts and suicide mortality. However, knowledge of how this association develops across the life-course is limited. Our study aims to establish whether individuals who died by suicide by mid-adulthood are distinguishable by their child-to-adolescence cognitive trajectories.

Participants were from the 1958 British Birth Cohort and were assessed for academic performance at ages 7, 11, and 16 and intelligence at 11 years. Suicides occurring by September 2012 were identified from linked national death certificates. We compared mean mathematics and reading abilities and rate of change across 7–16 years for individuals who died by suicide v. those still alive, with and without adjustment for potential early-life confounding factors. Analyses were based on 14 505 participants.

Fifty-five participants (48 males) had died by suicide by age 54 years. While males who died by suicide did not differ from participants still alive in reading scores at age 7 [effect size (g) = −0.04, p = 0.759], their reading scores had a less steep improvement up to age 16 compared to other participants. Adjustments for early-life confounding factors explained these differences. A similar pattern was observed for mathematics scores. There was no difference between individuals who died by suicide v. participants still alive on intelligence at 11 years.

While no differences in tests of academic performance and IQ were observed, individuals who died by suicide had a less steep improvement in reading abilities over time compared to same-age peers.

This study leveraged machine learning to evaluate the contribution of information from multiple developmental stages to prospective prediction of depression and anxiety in mid-adolescence.

A community sample (N = 374; 53.5% male) of children and their families completed tri-annual assessments across ages 3–15. The feature set included several important risk factors spanning psychopathology, temperament/personality, family environment, life stress, interpersonal relationships, neurocognitive, hormonal, and neural functioning, and parental psychopathology and personality. We used canonical correlation analysis (CCA) to reduce the large feature set to a lower dimensional space while preserving the longitudinal structure of the data. Ablation analysis was conducted to evaluate the relative contributions to prediction of information gathered at different developmental periods and relative to previous disorder status (i.e. age 12 depression or anxiety) and demographics (sex, race, ethnicity).

CCA components from individual waves predicted age 15 disorder status better than chance across ages 3, 6, 9, and 12 for anxiety and 9 and 12 for depression. Only the components from age 12 for depression, and ages 9 and 12 for anxiety, improved prediction over prior disorder status and demographics.

These findings suggest that screening for risk of adolescent depression can be successful as early as age 9, while screening for risk of adolescent anxiety can be successful as early as age 3. Assessing additional risk factors at age 12 for depression, and going back to age 9 for anxiety, can improve screening for risk at age 15 beyond knowing standard demographics and disorder history.

Depression, the most frequent and harmful mental disorder, has been associated with specific somatic diseases as the leading cause of death. The purposes of this prospective study were to predict incident chronic diseases based on baseline depressive symptoms and to test sex-dependent effects.

In a representative German community sample of over 12 000 participants, baseline depressive symptoms (assessed using the Patient Health Questionnaire-9) were tested as a predictor of new onset of cardiovascular disease (CVD), chronic obstructive lung disease, diabetes, cancer, and migraine at 5-year follow-up. To study disease incidence, we created subsamples for each chronic disease by excluding participants who already had the respective disease at baseline. Potential confounders were included in logistic regression models and sex-specific analyses were performed.

Controlling for demographic characteristics and loneliness, in men and women, baseline depressive symptoms were predictive of CVD, chronic obstructive lung disease, diabetes, and migraine, but not of cancer. When we additionally adjusted for metabolic and lifestyle risk factors, there was an 8% increase of chronic obstructive lung disease and migraine per point of depressive symptoms. There was a trend for CVD (4%; p = 0.053). Sex-sensitive analyses revealed trends for the relevance of depressive symptoms for CVD in men (p = 0.065), and for diabetes in women (p = 0.077).

These findings underscore the need to implement screening for depression in the treatment of major somatic illnesses. At the same time, depressed patients should be screened for metabolic and lifestyle risk factors and for somatic diseases and offered lifestyle interventions.

Impairments in social cognition contribute significantly to disability in schizophrenia patients (SzP). Perception of facial expressions is critical for social cognition. Intact perception requires an individual to visually scan a complex dynamic social scene for transiently moving facial expressions that may be relevant for understanding the scene. The relationship of visual scanning for these facial expressions and social cognition remains unknown.

In 39 SzP and 27 healthy controls (HC), we used eye-tracking to examine the relationship between performance on The Awareness of Social Inference Test (TASIT), which tests social cognition using naturalistic video clips of social situations, and visual scanning, measuring each individual's relative to the mean of HC. We then examined the relationship of visual scanning to the specific visual features (motion, contrast, luminance, faces) within the video clips.

TASIT performance was significantly impaired in SzP for trials involving sarcasm (p < 10−5). Visual scanning was significantly more variable in SzP than HC (p < 10−6), and predicted TASIT performance in HC (p = 0.02) but not SzP (p = 0.91), differing significantly between groups (p = 0.04). During the visual scanning, SzP were less likely to be viewing faces (p = 0.0001) and less likely to saccade to facial motion in peripheral vision (p = 0.008).

SzP show highly significant deficits in the use of visual scanning of naturalistic social scenes to inform social cognition. Alterations in visual scanning patterns may originate from impaired processing of facial motion within peripheral vision. Overall, these results highlight the utility of naturalistic stimuli in the study of social cognition deficits in schizophrenia.

Psychopathic traits involve interpersonal manipulation, callous affect, erratic lifestyle, and antisocial behavior. Though adult psychopathic traits emerge from both genetic and environmental risk, no studies have examined etiologic associations between adult psychopathic traits and experiences of parenting in childhood, or the extent to which parenting practices may impact the heritability of adult psychopathic traits using a genetically-informed design.

In total, 1842 adult twins from the community reported their current psychopathic traits and experiences of negative parenting during childhood. We fit bivariate genetic models to the data, decomposing the variance within, and the covariance between, psychopathic traits and perceived negative parenting into their genetic and environmental components. We then fit a genotype × environment interaction model to evaluate whether negative parenting moderated the etiology of psychopathic traits.

Psychopathic traits were moderately heritable with substantial non-shared environmental influences. There were significant associations between perceived negative parenting and three of four psychopathy facets (interpersonal manipulation, erratic lifestyle, antisocial tendencies, but not callous affect). These associations were attributable to a common non-shared environmental pathway and not to overlapping genetic effects. Additionally, we found that primarily shared environmental influences were stronger on psychopathic traits for individuals with a history of greater negative parenting.

Utilizing a genetically-informed design, we found that both genetic and non-shared environmental factors contribute to the emergence of psychopathic traits. Moreover, perceptions of negative parenting emerged as a clear environmental influence on the development of interpersonal, lifestyle, and antisocial features of psychopathy.

Subclinical psychotic-like experiences (PLE), resembling key symptoms of psychotic disorders, are common throughout the general population and possibly associated with psychosis risk. There is evidence that such symptoms are also associated with structural brain changes.

In 672 healthy individuals, we assessed PLE and associated distress with the symptom-checklist-90R (SCL-90R) scales ‘schizotypal signs’ (STS) and ‘schizophrenia nuclear symptoms’ (SNS) and analysed associations with voxel- and surfaced-based brain structural parameters derived from structural magnetic resonance imaging at 3 T with CAT12.

For SNS, we found a positive correlation with the volume in the left superior parietal lobule and the precuneus, and a negative correlation with the volume in the right inferior temporal gyrus [p < 0.05 cluster-level Family Wise Error (FWE-corrected]. For STS, we found a negative correlation with the volume of the left and right precentral gyrus (p < 0.05 cluster-level FWE-corrected). Surface-based analyses did not detect any significant clusters with the chosen statistical threshold of p < 0.05. However, in exploratory analyses (p < 0.001, uncorrected), we found a positive correlation of SNS with gyrification in the left insula and rostral middle frontal gyrus and of STS with the left precuneus and insula, as well as a negative correlation of STS with gyrification in the left temporal pole.

Our results show that brain structures in areas implicated in schizophrenia are also related to PLE and its associated distress in healthy individuals. This pattern supports a dimensional model of the neural correlates of symptoms of the psychotic spectrum.

Neurodevelopmental disorders (NDs) are associated with experiences of victimization, but mechanisms remain unclear. We explored sex differences and the role of familial factors and externalizing problems in the association between several NDs and violent victimization in adolescence and young adulthood.

Individuals born in Sweden 1985–1997, residing in Sweden at their 15th birthday, were followed until date of violent victimization causing a hospital visit or death, death due to other causes, emigration, or December 31, 2013, whichever came first. The exposures were diagnoses of attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), intellectual disability (ID) and other NDs. We used three different Cox regression models: a crude model, a model adjusted for familial confounding using sibling-comparisons, and a model additionally adjusted for externalizing problems.

Among 1 344 944 individuals followed, on average, for 5 years, 74 487 were diagnosed with NDs and 37 765 had a hospital visit or died due to violence. ADHD was associated with an increased risk of violent victimization in males [hazard ratio (HR) 2.56; 95% confidence interval (CI) 2.43–2.70) and females (HR 5.39; 95% CI 4.97–5.85). ASD and ID were associated with an increased risk of violent victimization in females only. After adjusting for familial factors and externalizing problems, only ADHD was associated with violent victimization among males (HR 1.27; 95% CI 1.06–1.51) and females (HR 1.69; 95% CI 1.21–2.36).

Females with NDs and males with ADHD are at greater risk of being victim of severe violence during adolescence and young adulthood. Relevant mechanisms include shared familial liability and externalizing problems. ADHD may be independently associated with violent victimization.

Contemporary views of emotion dysregulation in post-traumatic stress disorder (PTSD) highlight reduced ability to flexibly select regulatory strategies according to differing situational demands. However, empirical evidence of reduced regulatory selection flexibility in PTSD is lacking. Multiple studies show that healthy individuals demonstrate regulatory selection flexibility manifested in selecting attentional disengagement regulatory strategies (e.g. distraction) in high-intensity emotional contexts and selecting engagement meaning change strategies (e.g. reappraisal) in low-intensity contexts. Accordingly, we hypothesized that PTSD populations will show reduced regulatory selection flexibility manifested in diminished increase in distraction (over reappraisal) preference as intensity increases from low to high intensity.

Study 1 compared student participants with high (N = 22) post-traumatic symptoms (PTS, meeting the clinical cutoff for PTSD) and participants with low (N = 22) post-traumatic symptoms. Study 2 compared PTSD diagnosed women (N = 31) due to childhood sexual abuse and matched non-clinical women (N = 31). In both studies, participants completed a well-established regulatory selection flexibility performance-based paradigm that involves selecting between distraction and reappraisal to regulate negative emotional words of low and high intensity.

Beyond demonstrating adequate psychometric properties, Study 1 confirmed that relative to the low PTS group, the high PTS group presented reduced regulatory selection flexibility (p = 0.01, $\eta _{\rm p}^2$ = 0.14). Study 2 critically extended findings of Study 1, in showing similar reduced regulatory selection flexibility in a diagnosed PTSD population, relative to a non-clinical population (p = 0.002, $\eta _{\rm p}^2$ = 0.114).

Two studies provide converging evidence for reduced emotion regulatory selection flexibility in two PTSD populations.

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.

It remains unknown whether coronavirus disease 2019 (COVID-19) patients with bipolar disorders (BDs) are at an increased risk of mortality. We aimed to establish whether health outcomes and care differed between patients infected with COVID-19 with BD and patients without a diagnosis of severe mental illness.

We conducted a population-based cohort study of all patients with identified COVID-19 and respiratory symptoms who were hospitalized in France between February and June 2020. The outcomes were in-hospital mortality and intensive care unit (ICU) admission. We used propensity score matching to control for confounding factors.

In total, 50 407 patients were included, of whom 480 were patients with BD. Patients with BD were 2 years older, more frequently women and had more comorbidities than controls without a diagnosis of severe mental illness. Patients with BD had an increased in-hospital mortality rate (26.6% v. 21.9%; p = 0.034) and similar ICU admission rate (27.9% v. 28.4%, p = 0.799), as confirmed by propensity analysis [odds ratio, 95% confidence interval (OR, 95% CI) for mortality: 1.30 (1.16–1.45), p < 0.0001]. Significant interactions between BD and age and between BD and social deprivation were found, highlighting that the most important inequalities in mortality were observed in the youngest [OR, 95% CI 2.28 (1.18–4.41), p = 0.0015] and most deprived patients with BD [OR, 95% CI 1.60 (1.33–1.92), p < 0.001].

COVID-19 patients with BD were at an increased risk of mortality, which was exacerbated in the youngest and most deprived patients with BD. Patients with BD should thus be targeted as a high-risk population for severe forms of COVID-19, requiring enhanced preventive and disease management strategies.

Examining neurobiological mechanisms that may transmit the effects of childhood maltreatment on mental health in youth is crucial for understanding vulnerability to psychopathology. This study investigated associations between childhood maltreatment, adolescent structural brain development, and mental health trajectories into young-adulthood.

Structural magnetic resonance imaging data was acquired from 144 youth at three time points (age 12, 16, and 18 years). Childhood maltreatment was reported to occur prior to the first scan. Linear mixed models were utilized to examine the association between total childhood maltreatment, neglect, abuse and (i) amygdala and hippocampal volume development, and (ii) maturational coupling between amygdala/hippocampus volume and the thickness of prefrontal regions. We also examined whether brain development mediated the association between maltreatment and depressive and anxiety symptoms trajectories from age 12 to 28.

Total maltreatment, and neglect, were associated with positive maturational coupling between the amygdala and caudal anterior cingulate cortex (cACC), whereby at higher and lower levels of amygdala growth, maltreatment was associated with lower and higher PFC thinning, respectively. Neglect was also associated with maturational coupling of the hippocampus with prefrontal regions. While positive amygdala-cACC maturational coupling was associated with greater increases in anxiety symptoms, it did not significantly mediate the association between maltreatment and anxiety symptom trajectories.

We found maltreatment to be associated with altered patterns of coupling between subcortical and prefrontal regions during adolescence, suggesting that maltreatment is associated with the development of socio-emotional neural circuitry. The implications of these findings for mental health require further investigation.