Although being married with children is associated with a reduced rate of alcohol use disorder (AUD), is this finding independent of a marital effect, different in mothers and fathers and potentially causal in effect.

Using Cox proportional hazards, we examined, in 1 252 237 married individuals, the association between a resident younger and older child and risk for AUD registration in national medical, criminal, and pharmacy registers. Using logistic regression, we analyzed, in 600 219 parents, within-person models comparing risk for AUD prior to first pregnancy v. with young children. We examined whether risk for AUD in 1302 parents after a first spousal AUD registration was reduced by having a young resident child.

Compared with childless married individuals, resident younger children were associated with a reduced risk for AUD in mothers [hazard ratio (HR) 0.36, 95% confidence interval 0.31–0.41] and fathers (HR 0.66, 0.60–0.73). The reduced risk was attenuated but still significant for older children. Within-person models confirmed the protective effect of young children in mothers [odds ratio (OR) 0.49, 0.30–0.80] but yielded inconclusive results in fathers (OR 0.85, 0.58–1.25). After a first spousal registration for AUD, a resident young child was associated with a substantial reduction in risk for mothers and a weaker marginal effect in fathers.

In married individuals, resident children are associated with a reduction in basal risk for AUD which is stronger in mothers than fathers and with younger v. older children. This effect is also evident during high-risk periods. In mothers, our results are consistent with a largely causal effect.

This study aimed to develop and test the feasibility of a primary care worker-led psychological intervention as the main feature of a collaborative stepped care for depression that is effective, affordable, culturally acceptable, tailored to patients’ clinical condition and easily integrate-able into the primary care schedule in Nigeria.

Using the Medical Research Council framework, in the first stage (modelling/theoretical development), experts reviewed and distilled evidence from literature to form the intervention components. In the second (formative) stage, local stakeholders were consulted on the practical application and feasibility of the proposed intervention. The third (piloting) stage involved testing for the clinical efficacy and acceptability of the components of the draft intervention

The final intervention components included a 2-stage screening (red-flagging and further evaluation), psychoeducation, low-intensity psychological therapy (problem-solving therapy for primary care), antidepressant prescription, proactive mobile telephony adherence support and referral to the mental health specialist if needed. At 3 months, 71.6% of depressed patients on the intervention improved. The intervention was perceived to be acceptable and useful by over 70% of health workers and clients and had high ratings (>70% score) by expert panels on intervention simplicity, facilitation strategies, and quality of delivery.

The development and feasibility testing of our integrated intervention encompassed review of current literature, expert opinions and consultation with local stakeholders and end users. Our intervention package was largely deemed acceptable, relevant, useful, and feasible. Important lessons learnt with this process will help in future intervention developments.

Normative and pathological personality traits have rarely been integrated into a joint large-scale structural analysis with psychiatric disorders, although a recent study suggested they entail a common individual differences continuum.

We explored the joint factor structure of 11 psychiatric disorders, five personality-disorder trait domains (DSM-5 Section III), and five normative personality trait domains (the ‘Big Five’) in a population-based sample of 2796 Norwegian twins, aged 19‒46.

Three factors could be interpreted: (i) a general risk factor for all psychopathology, (ii) a risk factor specific to internalizing disorders and traits, and (iii) a risk factor specific to externalizing disorders and traits. Heritability estimates for the three risk factor scores were 48% (95% CI 41‒54%), 35% (CI 28‒42%), and 37% (CI 31‒44%), respectively. All 11 disorders had uniform loadings on the general factor (congruence coefficient of 0.991 with uniformity). Ignoring sign and excluding the openness trait, this uniformity of factor loadings held for all the personality trait domains and all disorders (congruence 0.983).

Based on our findings, future research should investigate joint etiologic and transdiagnostic models for normative and pathological personality and other psychopathology.

It has been proposed that vascular disease is the mechanism linking depression and cognition, but prospective studies have not supported this hypothesis. This study aims to investigate the inter-relationships between depressive symptoms, cognition and cerebrovascular disease using a well-characterised prospective cohort.

Data came from waves 1 (2005–2007) and 2 (2007–2009) of the Sydney Memory and Ageing Study (n = 462; mean age = 78.3 years).

At wave 1, there was an association between depressive symptoms and white matter hyperintensity (WMH) volume [b = 0.016, t(414) = 2.34, p = 0.020]. Both depressive symptoms [b = −0.058, t(413) = −2.64, p = 0.009] and WMH volume [b = −0.011, t(413) = −3.77, p < 0.001], but not stroke/transient ischaemic attack (TIA) [b = −0.328, t(413) = −1.90, p = 0.058], were independently associated with lower cognition. Prospectively, cerebrovascular disease was not found to predict increasing depressive symptoms [stroke/TIA: b = −0.349, t(374.7) = −0.76, p = 0.448; WMH volume: b = 0.007, t(376.3) = 0.875, p = 0.382]. Depressive symptoms predicted increasing WMH severity [b = 0.012, t(265.9) = −3.291, p = 0.001], but not incident stroke/TIA (odds ratio = 0.995; CI 0.949–1.043; p = 0.820). When examined in separate models, depressive symptoms [b = −0.027, t(373.5) = −2.16, p = 0.032] and a history of stroke/TIA [b = −0.460, t(361.2) = −4.45, p < 0.001], but not WMH volume [b = 0.001, t(362.3) = −0.520, p = 0.603], predicted declines in cognition. When investigated in a combined model, a history of stroke/TIA remained a predictor of cognitive decline [b = −0.443, t(360.6) = −4.28, p < 0.001], whilst depressive symptoms did not [b = −0.012, t(359.7) = −0.96, p = 0.336].

This study is contrasted with previous prospective studies which indicate that depressive symptoms predict cognitive decline independently of vascular disease. Future research should focus on further exploring the vascular mechanisms underpinning the relationship between depressive symptoms and cognition.

Given its diverse disease courses and symptom presentations, multiple phenotype dimensions with different biological underpinnings are expected with bipolar disorders (BPs). In this study, we aimed to identify lifetime BP psychopathology dimensions. We also explored the differing associations with bipolar I (BP-I) and bipolar II (BP-II) disorders.

We included a total of 307 subjects with BPs in the analysis. For the factor analysis, we chose six variables related to clinical courses, 29 indicators covering lifetime symptoms of mood episodes, and 6 specific comorbid conditions. To determine the relationships among the identified phenotypic dimensions and their effects on differentiating BP subtypes, we applied structural equation modeling.

We selected a six-factor solution through scree plot, Velicer's minimum average partial test, and face validity evaluations; the six factors were cyclicity, depression, atypical vegetative symptoms, elation, psychotic/irritable mania, and comorbidity. In the path analysis, five factors excluding atypical vegetative symptoms were associated with one another. Cyclicity, depression, and comorbidity had positive associations, and they correlated negatively with psychotic/irritable mania; elation showed positive correlations with cyclicity and psychotic/irritable mania. Depression, cyclicity, and comorbidity were stronger in BP-II than in BP-I, and they contributed significantly to the distinction between the two disorders.

We identified six phenotype dimensions; in addition to symptom features of manic and depressive episodes, various comorbidities and high cyclicity constructed separate dimensions. Except for atypical vegetative symptoms, all factors showed a complex interdependency and played roles in discriminating BP-II from BP-I.

Converging lines of evidence implicate an important role for the immune system in schizophrenia. Microglia are the resident immune cells of the central nervous system and have many functions including neuroinflammation, axonal guidance and neurotrophic support. We aimed to provide a quantitative review of in vivo PET imaging studies of microglia activation in patients with schizophrenia compared with healthy controls.

Demographic, clinical and imaging measures were extracted from each study and meta-analysis was conducted using a random-effects model (Hedge's g). The difference in 18-kDa translocator protein (TSPO) binding between patients with schizophrenia and healthy controls, as quantified by either binding potential (BP) or volume of distribution (VT), was used as the main outcome. Sub-analysis and sensitivity analysis were carried out to investigate the effects of genotype, ligand and illness stage.

In total, 12 studies comprising 190 patients with schizophrenia and 200 healthy controls met inclusion criteria. There was a significant elevation in tracer binding in schizophrenia patients relative to controls when BP was used as an outcome measure, (Hedge's g = 0.31; p = 0.03) but no significant differences when VT was used (Hedge's g = −0.22; p = 0.29).

In conclusion, there is evidence for moderate elevations in TSPO tracer binding in grey matter relative to other brain tissue in schizophrenia when using BP as an outcome measure, but no difference when VT is the outcome measure. We discuss the relevance of these findings as well as the methodological issues that may underlie the contrasting difference between these outcomes.

Despite the well-documented association between smoking and personality traits such as neuroticism and extraversion, little is known about the potential causal nature of these findings. If it were possible to unpick the association between personality and smoking, it may be possible to develop tailored smoking interventions that could lead to both improved uptake and efficacy.

Recent genome-wide association studies (GWAS) have identified variants robustly associated with both smoking phenotypes and personality traits. Here we use publicly available GWAS summary statistics in addition to individual-level data from UK Biobank to investigate the link between smoking and personality. We first estimate genetic overlap between traits using LD score regression and then use bidirectional Mendelian randomisation methods to unpick the nature of this relationship.

We found clear evidence of a modest genetic correlation between smoking behaviours and both neuroticism and extraversion. We found some evidence that personality traits are causally linked to certain smoking phenotypes: among current smokers each additional neuroticism risk allele was associated with smoking an additional 0.07 cigarettes per day (95% CI 0.02–0.12, p = 0.009), and each additional extraversion effect allele was associated with an elevated odds of smoking initiation (OR 1.015, 95% CI 1.01–1.02, p = 9.6 × 10−7).

We found some evidence for specific causal pathways from personality to smoking phenotypes, and weaker evidence of an association from smoking initiation to personality. These findings could be used to inform future smoking interventions or to tailor existing schemes.

Although relapse in psychosis is common, a small proportion of patients will not relapse in the long term. We examined the proportion and predictors of patients who never relapsed in the 10 years following complete resolution of positive symptoms from their first psychotic episode.

Patients who previously enrolled in a 12-month randomized controlled trial on medication discontinuation and relapse following first-episode psychosis (FEP) were followed up after 10 years. Relapse of positive symptoms was operationalized as a change from a Clinical Global Impression scale positive score of <3 for at least 3 consecutive months to a score of ⩾3 (mild or more severe). Baseline predictors included basic demographics, premorbid functioning, symptoms, functioning, and neurocognitive functioning.

Out of 178 first-episode patients, 37 (21%) never relapsed during the 10-year period. Univariate predictors (p ⩽ 0.1) of patients who never relapsed included a duration of untreated psychosis (DUP) ⩽30 days, diagnosed with non-schizophrenia spectrum disorders, having less severe negative symptoms, and performing better in logical memory immediate recall and verbal fluency tests. A multivariate logistic regression analysis further suggested that the absence of any relapsing episodes was significantly related to better short-term verbal memory, shorter DUP, and non-schizophrenia spectrum disorders.

Treatment delay and neurocognitive function are potentially modifiable predictors of good long-term prognosis in FEP. These predictors are informative as they can be incorporated into an optimum risk prediction model in the future, which would help with clinical decision making regarding maintenance treatment in FEP.

The prevalence of mental disorders among Black, Latino, and Asian adults is lower than among Whites. Factors that explain these differences are largely unknown. We examined whether racial/ethnic differences in exposure to traumatic events (TEs) or vulnerability to trauma-related psychopathology explained the lower rates of psychopathology among racial/ethnic minorities.

We estimated the prevalence of TE exposure and associations with onset of DSM-IV depression, anxiety and substance disorders and with lifetime post-traumatic stress disorder (PTSD) in the Collaborative Psychiatric Epidemiology Surveys, a national sample (N = 13 775) with substantial proportions of Black (35.9%), Latino (18.9%), and Asian Americans (14.9%).

TE exposure varied across racial/ethnic groups. Asians were most likely to experience organized violence – particularly being a refugee – but had the lowest exposure to all other TEs. Blacks had the greatest exposure to participation in organized violence, sexual violence, and other TEs, Latinos had the highest exposure to physical violence, and Whites were most likely to experience accidents/injuries. Racial/ethnic minorities had lower odds ratios of depression, anxiety, and substance disorder onset relative to Whites. Neither variation in TE exposure nor vulnerability to psychopathology following TEs across racial/ethnic groups explained these differences. Vulnerability to PTSD did vary across groups, however, such that Asians were less likely and Blacks more likely to develop PTSD following TEs than Whites.

Lower prevalence of mental disorders among racial/ethnic minorities does not appear to reflect reduced vulnerability to TEs, with the exception of PTSD among Asians. This highlights the importance of investigating other potential mechanisms underlying racial/ethnic differences in psychopathology.

Despite the high prevalence of mental disorders, mental health literacy has been comparatively neglected. People's symptom-management strategies will be influenced by their mental health literacy. This study sought to determine the feasibility of using the World Health Organization mhGAP-Intervention Guide (IG) as an educational tool for one-on-one contact in a clinical setting to increase literacy on the specified mental disorders.

This study was conducted in 20 health facilities in Makueni County, southeast Kenya which has one of the poorest economies in Kenya. It has no psychiatrist or clinical psychologist. We recruited 3267 participants from a community that had already been exposed to community mental health services. We used Mental Health Knowledge Schedule to measure the changing patterns of mental health knowledge after a period of 3 months, following a training intervention using the WHO mhGAP-IG.

Overall, there was a significant increase in mental health related knowledge [mean range 22.4–23.5 for both post-test and pre-test scores (p < 0.001)]. This increase varied with various socio-demographic characteristics such as sex, marital status, level of education, employment status and wealth index.

mhGAP-IG is a feasible tool to increase mental health literacy in low-resource settings where there are no mental health specialists. Our study lends evidence that the WHO Mental Health Action Plan 2013–2020 and reduction of the treatment gap may be accelerated by the use of mhGAP-IG through improving knowledge about mental illness and potentially subsequent help seeking for early diagnosis and treatment.

Research is needed to identify the factors that explain the link between prior and future suicidality. This study evaluated possible mediators of the relationship between: (1) the severity of prior suicidality and (2) suicidal ideation severity at 3-month follow-up among a sample of high-risk military personnel.

US military service members referred to or seeking care for suicide risk (N = 624) completed self-report psychiatric domain measures and a clinician interview assessing prior suicidality severity at baseline. Three months later, participants completed a self-report measure of suicidal ideation severity. Three separate percentile bootstrap mediation models were used to examine psychiatric factors (i.e. alcohol abuse, anxiety sensitivity, hopelessness, insomnia, posttraumatic stress symptoms, suicidal ideation, and thwarted belongingness) as parallel mediators of the relationship between prior suicidality severity (specifically, suicidal ideation, suicide attempt, and overall suicidality – i.e. ideation/attempt severity combined) at baseline and suicidal ideation severity at follow-up.

Hopelessness, specifically, and the total effect of all mediators, each significantly accounted for the relationship between prior suicidality severity and subsequent ideation severity across models. In the models with attempt severity and overall suicidality severity as predictors, thwarted belongingness was also a significant mediator.

Hopelessness, thwarted belongingness, and overall severity of psychiatric indices may explain the relationship between prior suicidality severity and future suicidal ideation severity among service members at elevated suicide risk. Research is needed to replicate these findings and examine other possible mediators.

Autism spectrum disorder (ASD) and obsessive–compulsive disorder (OCD) are neurodevelopmental disorders with considerable overlap in terms of their defining symptoms of compulsivity/repetitive behaviour. Little is known about the extent to which ASD and OCD have common versus distinct neural correlates of compulsivity. Previous research points to potentially common dysfunction in frontostriatal connectivity, but direct comparisons in one study are lacking. Here, we assessed frontostriatal resting-state functional connectivity in youth with ASD or OCD, and healthy controls. In addition, we applied a cross-disorder approach to examine whether repetitive behaviour across ASD and OCD has common neural substrates.

A sample of 78 children and adolescents aged 8–16 years was used (ASD n = 24; OCD n = 25; healthy controls n = 29), originating from the multicentre study COMPULS. We tested whether diagnostic group, repetitive behaviour (measured with the Repetitive Behavior Scale-Revised) or their interaction was associated with resting-state functional connectivity of striatal seed regions.

No diagnosis-specific differences were detected. The cross-disorder analysis, on the other hand, showed that increased functional connectivity between the left nucleus accumbens (NAcc) and a cluster in the right premotor cortex/middle frontal gyrus was related to more severe symptoms of repetitive behaviour.

We demonstrate the fruitfulness of applying a cross-disorder approach to investigate the neural underpinnings of compulsivity/repetitive behaviour, by revealing a shared alteration in functional connectivity in ASD and OCD. We argue that this alteration might reflect aberrant reward or motivational processing of the NAcc with excessive connectivity to the premotor cortex implementing learned action patterns.

Jumping to conclusions (JTC), which is the proneness to require less information before forming beliefs or making a decision, has been related to formation and maintenance of delusions. Using data from the National Institute of Health Research Biomedical Research Centre Genetics and Psychosis (GAP) case–control study of first-episode psychosis (FEP), we set out to test whether the presence of JTC would predict poor clinical outcome at 4 years.

One-hundred and twenty-three FEP patients were assessed with the Positive and Negative Syndrome Scale (PANSS), Global Assessment of Functioning (GAF) and the probabilistic reasoning ‘Beads’ Task at the time of recruitment. The sample was split into two groups based on the presence of JTC bias. Follow-up data over an average of 4 years were obtained concerning clinical course and outcomes (remission, intervention of police, use of involuntary treatment – the Mental Health Act (MHA) – and inpatient days).

FEP who presented JTC at baseline were more likely during the follow-up period to be detained under the MHA [adjusted OR 15.62, 95% confidence interval (CI) 2.92–83.54, p = 0.001], require intervention by the police (adjusted OR 14.95, 95% CI 2.68–83.34, p = 0.002) and have longer admissions (adjusted IRR = 5.03, 95% CI 1.91–13.24, p = 0.001). These associations were not accounted for by socio-demographic variables, IQ and symptom dimensions.

JTC in FEP is associated with poorer outcome as indicated and defined by more compulsion police intervention and longer periods of admission. Our findings raise the question of whether the implementation of specific interventions to reduce JTC, such as Metacognition Training, may be a useful addition in early psychosis intervention programmes.

Early-life adversity (ELA) is a risk factor for internalizing psychopathology (IP). ELA is also linked to alterations in neural phenotypes of emotion processing and maladaptive emotion regulatory strategies, such as ruminative brooding, in adulthood. We therefore expected that ELA would predict cortical brain activation to emotional faces in transdiagnostic IP and in turn, mediate the extent of rumination amongst patients with IPs and ELA (IP + ELA).

One hundred and thirty-two individuals, including 102 treatment-seeking adults with heterogeneous IPs and 30 healthy controls (HCs) performed an Emotional Face-Matching Task during functional magnetic resonance imaging. Whole-brain analyses compared HC (n = 30), IP (n = 52), and IP + ELA (n = 50) neural responses to emotional (angry, fearful, happy, and sad) faces v. shapes, controlling for depression and anxiety symptoms. Parameter estimates of activation were extracted for significant between-group differences and tested as a mediator of ruminative brooding in IP + ELA.

IP + ELA demonstrated increased activation in the superior frontal gyrus and anterior cingulate cortex (fear), superior parietal lobule, precuneus, posterior cingulate, and inferior temporal gyrus (fear only), and cuneus (fear and angry). These regions were preferentially correlated with ruminative brooding in IP + ELA, many of which mediated the link between IP + ELA and ruminative brooding.

Results provide evidence that ELA history amongst IP patients augments engagement of brain regions involved in emotion processing, above and beyond what is accounted for by current symptoms. Though longitudinal designs are needed, alterations in the neural correlates of maladaptive processing of socio-emotional information may be a common pathway by which ELA poses risk for psychopathology.

High body mass index (BMI) has been associated with lower risks of suicidal behaviour and being underweight with increased risks. However, evidence is inconsistent and sparse, particularly for women. We aim to study this relationship in a large cohort of UK women.

In total 1.2 million women, mean age 56 (s.d. 5) years, without prior suicide attempts or other major illness, recruited in 1996–2001 were followed by record linkage to national hospital admission and death databases. Cox regression yielded relative risks (RRs) and 95% confidence intervals (CIs) for attempted suicide and suicide by BMI, adjusted for baseline lifestyle factors and self-reported treatment for depression or anxiety.

After 16 (s.d. 3) years of follow-up, 4930 women attempted suicide and 642 died by suicide. The small proportion (4%) with BMI <20 kg/m2 were at clearly greater risk of attempted suicide (RR = 1.38, 95% CI 1.23–1.56) and suicide (RR = 2.10, 1.59–2.78) than women of BMI 20–24.9 kg/m2; p < 0.0001 for both comparisons. Small body size at 10 and 20 years old was also associated with increased risks. Half the cohort had BMIs >25 kg/m2 and, while risks were somewhat lower than for BMI 20–24.9 kg/m2 (attempted suicide RR = 0.91, 0.86–0.96; p = 0.001; suicide RR = 0.79, 0.67–0.93; p = 0.006), the reductions in risk were not strongly related to level of BMI.

Being underweight is associated with a definite increase in the risk of suicidal behaviour, particularly death by suicide. Residual confounding cannot be excluded for the small and inconsistent decreased risk of suicidal behaviour associated with being overweight or obese.