Substance use disorder explains much of the excess risk of violent behaviour in psychotic disorders. However, it is unclear to what extent the pharmacological properties and subthreshold use of illicit substances are associated with violence.

Individuals with psychotic disorders were recruited for two nationwide projects: GROUP (N = 871) in the Netherlands and NEDEN (N = 921) in the United Kingdom. Substance use and violent behaviour were assessed with standardized instruments and multiple sources of information. First, we used logistic regression models to estimate the associations of daily and nondaily use with violence for cannabis, stimulants, depressants and hallucinogens in the GROUP and NEDEN samples separately. Adjustments were made for age, sex and educational level. We then combined the results in random-effects meta-analyses.

Daily use, compared with nondaily or no use, and nondaily use, compared with no use, increased the pooled odds of violence in people with psychotic disorders for all substance categories. The increases were significant for daily use of cannabis [pooled odds ratio (pOR) 1.6, 95% confidence interval (CI) 1.2–2.0), stimulants (pOR 2.8, 95% CI 1.7–4.5) and depressants (pOR 2.2, 95% CI 1.1–4.5), and nondaily use of stimulants (pOR 1.6, 95% CI 1.2–2.0) and hallucinogens (pOR 1.5, 95% CI 1.1–2.1). Daily use of hallucinogens, which could only be analysed in the NEDEN sample, significantly increased the risk of violence (adjusted odds ratio 3.3, 95% CI 1.2–9.3).

Strategies to prevent violent behaviour in psychotic disorders should target any substance use.

Among the most disabling and fatal psychiatric illnesses, eating disorders (EDs) often manifest early in life, which encourages investigations into in utero and perinatal environmental risk factors. The objective of this study was to determine whether complications during pregnancy and birth and perinatal conditions are associated with later eating disorder risk in offspring and whether these associations are unique to EDs.

All individuals born in Denmark to Danish-born parents 1989–2010 were included in the study and followed from their 6th birthday until the end of 2016. Exposure to factors related to pregnancy, birth, and perinatal conditions was determined using national registers, as were hospital-based diagnoses of anorexia nervosa (AN), bulimia nervosa, and eating disorder not otherwise specified during follow-up. For comparison, diagnoses of depressive, anxiety, and obsessive-compulsive disorders were also included. Cox regression was used to compare hazards of psychiatric disorders in exposed and unexposed individuals.

1 167 043 individuals were included in the analysis. We found that similar to the comparison disorders, prematurity was associated with increased eating disorder risk. Conversely, patterns of increasing risks of EDs, especially in AN, with increasing parental ages differed from the more U-shaped patterns observed for depressive and anxiety disorders.

Our results suggest that pregnancy and early life are vulnerable developmental periods when exposures may influence offspring mental health, including eating disorder risk, later in life. The results suggest that some events pose more global transdiagnostic risk whereas other patterns, such as increasing parental ages, appear more specific to EDs.

Depression after myocardial infarction (MI) is associated with poor cardiovascular prognosis. There is some evidence that specifically depressive episodes that develop after the acute event are associated with poor cardiovascular prognosis. The aim of the present study was to evaluate whether an increase in the number of depressive symptoms after MI is associated with new cardiac events.

In 442 depressed and 325 non-depressed MI patients the Composite International Diagnostic Interview interview to assess post-MI depression was extended to evaluate the presence of the ICD-10 depressive symptoms just before and after the MI. The effect of an increase in number of depressive symptoms during the year following MI on new cardiac events up to 2.5 years post-MI was assessed with Cox regression analyses.

Each additional increase of one symptom was significantly associated with a 15% increased risk of new cardiac events, and this was stronger for non-depressed than for depressed patients. This association was independent of baseline cardiac disease severity. There was no interaction with the number of depressive symptoms pre-MI.

Our findings suggest that an increase in depressive symptoms after MI irrespective of the state of depression pre-MI explains why post-MI depression is associated with poor cardiovascular prognosis. Also increases in depressive symptoms after MI resulting in subthreshold depression should be evaluated as a prognostic marker. Whether potential mechanisms such as cardiac disease severity or inflammation underlie the association remains to be clarified.

Paternal depressive symptoms are associated with children's emotional and behavioural problems, which may be mediated by negative parenting. But there is no research on the influence of paternal depressive symptoms on children's emotion regulation and limited literature investigating fathers’ parenting as a mediator in the pathway between paternal depressive symptoms and children's externalizing and internalizing problems. We aimed to investigate the mediating role of father–child conflict (at 3 years) in the association between postnatal paternal depressive symptoms (at 9 months) and children's emotional and behavioural problems (at 7 years) (aim 1). We also examined whether mediation pathways were more pronounced for boys or for girls (aim 2).

Secondary data analysis was conducted on the Millennium Cohort Study, when children were 9 months, 3 years and 7 years old (n = 3520). Main study variables were measured by self-report questionnaires. Fathers completed the Rutter Scale (depressive symptoms) and the Parent–Child Relationship Questionnaire (father–child conflict), while mothers completed the Strengths and Difficulties Questionnaire and the Social Behaviour Questionnaire (child emotional and behavioural problems, emotion regulation). We used structural equation modelling to estimate direct, indirect and total effects of paternal depressive symptoms on child outcomes, mediated by father–child conflict whilst adjusting for relevant covariates (maternal depressive symptoms, child temperament, marital conflict, and socio-economic factors such as poverty indicator and fathers’ education level). Multi-group and interaction analysis was then conducted to determine the differential effect by gender of the association between paternal depressive symptoms on child outcomes via father–child conflict.

Father–child conflict mediated the association between paternal depressive symptoms and emotion regulation problems [standardized indirect effect (SIE) 95% confidence interval (CI) −0.03 to −0.01, p < 0.001; standardized total effect (STE) 95% CI −0.05 to −0.01, p < 0.05] (aim 1). Father–child conflict mediated a larger proportion of the effect in boys (SIE 95% CI −0.03 to −0.01, p < 0.001; STE 95% CI −0.05 to 0.00, p = 0.063) than it did in girls (SIE 95% CI −0.02 to −0.01, p < 0.001; STE 95% CI −0.04 to 0.01, p = 0.216) (aim 2).

Father–child conflict may mediate the association between postnatal paternal depressive symptoms and children's emotion regulation problems. Paternal depressive symptoms and father–child conflict resolution may be potential targets in preventative interventions.

Major depressive disorder (MDD) is a prevalent mental disorder characterized by impairments in affect, behaviour and cognition. Previous studies have indicated that the anterior cingulate cortex (ACC) may play an essential role in the pathophysiology of depression. In this study, we systematically identified changes in functional connectivity (FC) for ACC subdivisions that manifest in MDD and further investigated the relationship between these changes and the clinical symptoms of depression.

Sub-regional ACC FC was estimated in 41 first-episode medication-naïve MDD patients compared to 43 healthy controls. The relationships between depressive symptom severity and aberrant FC of ACC subdivisions were investigated. In addition, we conducted a meta-analysis to generate the distributions of MDD-related abnormal regions from previously reported results and compared them to FC deficits revealed in this study.

In MDD patients, the subgenual and perigenual ACC demonstrated decreased FC with the posterior regions of the default network (DN), including the posterior inferior parietal lobule and posterior cingulate cortex. FC of these regions was negatively associated with the Automatic Thoughts Questionnaire scores and largely overlapped with previously reported abnormal regions. In addition, reduced FC between the caudal ACC and precuneus was negatively correlated with the Hamilton Anxiety Scale scores. We also found increased FC between the rostral ACC and dorsal medial prefrontal cortex.

Our findings confirmed that functional interaction changes in different ACC sub-regions are specific and associated with distinct symptoms of depression. Our findings provide new insights into the role of ACC sub-regions and DN in the pathophysiology of MDD.

Recent models of major depressive disorder (MDD) have proposed the rostral anterior cingulate (rACC) and dorsomedial prefrontal cortex (dmPFC) as nexus sites in the dysfunctional regulation of cognitive-affective state. Limited evidence from remitted-state MDD supports these theories by suggesting that aberrant neural activity proximal to the rACC and the dmPFC may play a role in vulnerability to recurrence/relapse within this disorder. Here we present a targeted analysis assessing functional activity within these two regions of interest (ROIs) for groups with identified vulnerability to MDD: first, remitted, high predicted recurrence-risk patients; and second, patients suffering observed 1-year recurrence.

Baseline T2* images sensitive to blood oxygen level-dependent (BOLD) contrast were acquired from patients and controls during a Go/No-Go (GNG) task incorporating negative feedback, with 1-year patient follow-up to identify recurrence. BOLD contrast data for error commission (EC) and visual negative feedback (VNF) were used in an ROI analysis based on rACC and dmPFC coordinates from the literature, comparing patients versus controls and recurrence versus non-recurrence versus control groups.

Analysis of patients (n = 20) versus controls (n = 20) showed significant right dmPFC [Brodmann area (BA) 9] hypoactivity within the patient group, co-localized during EC and VNF, with additional significant rACC (BA 32) hypoactivity during EC. The results from the follow-up analysis were undermined by small groups and potential confounders but suggested persistent right dmPFC (BA 9) hypoactivity associated with 1-year recurrence.

Convergent hypoactive right dmPFC (BA 9) processing of VNF and EC, possibly impairing adaptive reappraisal of negative experience, was associated most clearly with clinically predicted vulnerability to MDD.

The overlap between anxiety and major depressive disorder (MDD), the increased risk for depression and anxiety in offspring of depressed parents, the sequence of onset with anxiety preceding MDD, and anxiety as a predictor of depression are well established. The specificity of anxiety disorders in these relationships is unclear. This study, using a longitudinal high-risk design, examined whether anxiety disorders associated with the emotions fear and anxiety mediate the association between parental and offspring depression.

Two hundred and twenty-four second-generation and 155 third-generation descendants at high and low risk for depression because of MDD in the first generation were interviewed over 20 years. Probit and Cox proportional hazard models were fitted with generation 2 (G2) or G3 depression as the outcome and parental MDD as the predictor. In G2 and G3, fear- (phobia or panic) and anxiety-related [overanxious or generalized anxiety disorder (GAD)] disorders were examined as potential mediators of increased risk for offspring depression, due to parental MDD.

In G2, fear-related disorders met criteria for mediating the association between parental MDD and offspring MDD whereas anxiety-related disorders did not. These results were consistent, regardless of the analytic methods used. Further investigation of the mediating effect of fear-related disorders by age of onset of offspring MDD suggests that the mediating effect occurs primarily in adolescent onset MDD. The results for G3 appear to follow similar patterns.

These findings support the separation of anxiety disorders into at least two distinct forms, particularly when examining their role in the etiology of depression.