Research has demonstrated that chronic stress exposure early in development can lead to detrimental alterations in the orbitofrontal cortex (OFC)–amygdala circuit. However, the majority of this research uses functional neuroimaging methods, and thus the extent to which childhood trauma corresponds to morphometric alterations in this limbic-cortical network has not yet been investigated. This study had two primary objectives: (i) to test whether anatomical associations between OFC–amygdala differed between adults as a function of exposure to chronic childhood assaultive trauma and (ii) to test how these environment-by-neurobiological effects relate to pathological personality traits.

Participants were 137 ethnically diverse adults (48.1% female) recruited from the community who completed a clinical diagnostic interview, a self-report measure of pathological personality traits, and anatomical MRI scans.

Findings revealed that childhood trauma moderated bilateral OFC–amygdala volumetric associations. Specifically, adults with childhood trauma exposure showed a positive association between medial OFC volume and amygdalar volume, whereas adults with no childhood exposure showed the negative OFC–amygdala structural association observed in prior research with healthy samples. Examination of the translational relevance of trauma-related alterations in OFC–amygdala volumetric associations for disordered personality traits revealed that trauma exposure moderated the association of OFC volume with antagonistic and disinhibited phenotypes, traits characteristic of Cluster B personality disorders.

The OFC–amygdala circuit is a potential anatomical pathway through which early traumatic experiences perpetuate emotional dysregulation into adulthood and confer risk for personality pathology. Results provide novel evidence of divergent neuroanatomical pathways to similar personality phenotypes depending on early trauma exposure.

Prior work has indicated both theoretical and empirical overlap between social and physical aggression. The extent to which their covariance can be explained by the same underlying genetic or environmental factors, however, remains unclear. It is also uncertain whether or how the origins of their covariance might vary across sex. The current study sought to fill these gaps in the literature.

We examined maternal and teacher reports of youth physical and social aggression in over 1000 6–10 years old (mean age = 8.02 years) twin pairs from the Michigan State University Twin Registry. We made use of the bivariate correlated factors model to clarify the origins of their association. We further tested both sex difference and no-sex difference versions of that model to determine whether there are sex differences in the association between social and physical aggression, as often assumed.

The covariation between social and physical aggression was due to overlapping genetic factors and common environmental conditions. Specifically, 50–57% of the genetic factors, 74–100% of the shared environmental factors, and 28–40% of the unique environmental factors influencing physical aggression also influenced social aggression according to both mother and teacher reports. These shared etiological factors did not differ across sex.

These findings argue against the common assumption that social aggression is the ‘female version’ of male physical aggression, and instead suggest that social aggression may be best conceptualized as a form of antisocial behavior that shares developmental pathways with other manifestations of externalizing pathology.

Studies from high-income countries report moderate-to-strong positive associations between alcohol use disorder (AUD) and other mental disorders, but there is little evidence about the comorbidity of AUD from low-and-middle-income countries.

A sample of 74 752 adults from five provinces that account for >12% of China's adult population was screened using the General Health Questionnaire, and the Structured Clinical Interview for DSM-IV was administered by psychiatrists to a subsample of 9619 males. The associations between AUD and other mental disorders at each site and the characteristics of men with AUD with and without comorbid mental disorders were estimated using logistic regression and summarized across sites using meta-analysis. Generalized estimation equations estimated the associations between the clinical features of alcohol dependence and comorbidity.

Robust inverse associations were found between current AUD and any mood disorder (adjusted OR = 0.6, 95% CI = 0.4–0.8) and any anxiety disorder (OR = 0.5, 95% CI = 0.3–1.0). Compared with men without AUD, men with AUD without comorbid disorders were more likely to be middle-aged, to be currently married, and to have higher family incomes. Men with comorbid AUD and other disorders were more likely to have the clinical features of alcohol dependence than men with AUD without comorbid disorders.

Inverse associations between AUD and other mental disorders and the higher social status of men with AUD than men without AUD found in this large, representative sample of community-dwelling Chinese males highlight the importance of considering the local substance-use culture when designing clinical or preventive interventions for addictive conditions.

Depression frequently co-occurs with somatization, and somatic complaints have been reported as a vulnerability marker for affective disorders observable before disease onset. Somatization is thought to result from an increased attention to somatic sensations, which should be reflected in long-latency somatosensory evoked electroencephalogram (EEG) potentials (SSEPs) at the physiological level. Previous studies revealed that SSEPs are altered in depressed patients and suggested late SSEP components as vulnerability markers for affective disorders. Neurotransmitters such as serotonin, γ-aminobutyric acid (GABA) and the neuropeptide substance P may play an important role for both affective disorders and somatosensory processing.

We investigated the associations between SSEPs and polymorphisms within candidate genes of the serotonergic, GABAergic as well as the substance P system in subjects at high risk for affective disorders. The sample was composed of high-risk families participating in the Munich Vulnerability Study and genetic association analyses were calculated using qfam (family-based association tests for quantitative traits) implemented in PLINK 1.05.

We observed significant associations (false discovery rate <0.05) withstanding correction for multiple testing between late SSEP components (response strength 170–370 ms after stimulation) and four single nucleotide polymorphisms within the GABA transaminase (ABAT) gene region coding for a protein responsible for GABA degradation. No effects were found with the classical disease trait approach, suggesting SSEP marker specificity of the observed associations.

Our findings point to a possible role of ABAT gene-regulated GABA catabolism for an altered processing of somatosensory stimuli as a potential vulnerability marker for affective disorders.

Despite increasing knowledge on the neuroimaging patterns of eating disorder (ED) symptoms in non-clinical populations, studies using whole-brain machine learning to identify connectome-based neuromarkers of ED symptomatology are absent. This study examined the association of connectivity within and between large-scale functional networks with specific symptomatic behaviors and cognitions using connectome-based predictive modeling (CPM).

CPM with ten-fold cross-validation was carried out to probe functional networks that were predictive of ED-associated symptomatology, including body image concerns, binge eating, and compensatory behaviors, within the discovery sample of 660 participants. The predictive ability of the identified networks was validated using an independent sample of 821 participants.

The connectivity predictive of body image concerns was identified within and between networks implicated in cognitive control (frontoparietal and medial frontal), reward sensitivity (subcortical), and visual perception (visual). Crucially, the set of connections in the positive network related to body image concerns identified in one sample was generalized to predict body image concerns in an independent sample, suggesting the replicability of this effect.

These findings point to the feasibility of using the functional connectome to predict ED symptomatology in the general population and provide the first evidence that functional interplay among distributed networks predicts body shape/weight concerns.

The aggregation of neurocognitive deficits among the non-psychotic first-degree relatives of adult- and childhood-onset schizophrenia patients suggests that there may be a common etiology for these deficits in childhood- and adult-onset illness. However, there is considerable heterogeneity in the presentation of neurobiological abnormalities, and whether there are differences in the extent of familial transmission for specific domains of cognitive function has not been systematically addressed.

We employed variance components analysis, as implemented in SOLAR-Eclipse, to evaluate the evidence of familial transmission for empirically derived composite scores representing attention, working memory, verbal learning, verbal retention, and memory for faces. We contrast estimates for adult- and childhood-onset schizophrenia families and matched community control pedigrees, and compare our findings to previous reports based on analogous neurocognitive assessments.

We observed varying degrees of familial transmission; attention and working memory yielded comparable, significant estimates for adult-onset and community control pedigrees; verbal learning was significant for childhood-onset and community control pedigrees; and facial memory demonstrated significant familial transmission only for childhood-onset schizophrenia. Model-fitting analyses indicated significant differences in familiality between adult- and childhood-onset schizophrenia for attention, working memory, and verbal learning.

By comprehensively assessing a wide range of neurocognitive domains in adult- and childhood-onset schizophrenia families, we provide additional support for specific neurocognitive domains as schizophrenia endophenotypes. Whereas comparable estimates of familial transmission for certain dimensions of cognitive functioning support a shared etiology of adult- and childhood-onset neurocognitive function, observed differences may be taken as preliminary evidence of partially divergent multifactorial architectures.

Recommendations for promoting mental health during the COVID-19 pandemic include maintaining social contact, through virtual rather than physical contact, moderating substance/alcohol use, and limiting news and media exposure. We seek to understand if these pandemic-related behaviors impact subsequent mental health.

Daily online survey data were collected on adults during May/June 2020. Measures were of daily physical and virtual (online) contact with others; substance and media use; and indices of psychological striving, struggling and COVID-related worry. Using random-intercept cross-lagged panel analysis, dynamic within-person cross-lagged effects were separated from more static individual differences.

In total, 1148 participants completed daily surveys [657 (57.2%) females, 484 (42.1%) males; mean age 40.6 (s.d. 12.4) years]. Daily increases in news consumed increased COVID-related worrying the next day [cross-lagged estimate = 0.034 (95% CI 0.018–0.049), FDR-adjusted p = 0.00005] and vice versa [0.03 (0.012–0.048), FDR-adjusted p = 0.0017]. Increased media consumption also exacerbated subsequent psychological struggling [0.064 (0.03–0.098), FDR-adjusted p = 0.0005]. There were no significant cross-lagged effects of daily changes in social distancing or virtual contact on later mental health.

We delineate a cycle wherein a daily increase in media consumption results in a subsequent increase in COVID-related worries, which in turn increases daily media consumption. Moreover, the adverse impact of news extended to broader measures of psychological struggling. A similar dynamic did not unfold between the daily amount of physical or virtual contact and subsequent mental health. Findings are consistent with current recommendations to moderate news and media consumption in order to promote mental health.

Cannabis use has been linked to psychotic disorders but this association has been primarily observed in the Global North. This study investigates patterns of cannabis use and associations with psychoses in three Global South (regions within Latin America, Asia, Africa and Oceania) settings.

Case–control study within the International Programme of Research on Psychotic Disorders (INTREPID) II conducted between May 2018 and September 2020. In each setting, we recruited over 200 individuals with an untreated psychosis and individually-matched controls (Kancheepuram India; Ibadan, Nigeria; northern Trinidad). Controls, with no past or current psychotic disorder, were individually-matched to cases by 5-year age group, sex and neighbourhood. Presence of psychotic disorder assessed using the Schedules for Clinical Assessment in Neuropsychiatry and cannabis exposure measured by the World Health Organisation Alcohol, Smoking and Substance Involvement Screening Test (ASSIST).

Cases reported higher lifetime and frequent cannabis use than controls in each setting. In Trinidad, cannabis use was associated with increased odds of psychotic disorder: lifetime cannabis use (adj. OR 1.58, 95% CI 0.99–2.53); frequent cannabis use (adj. OR 1.99, 95% CI 1.10–3.60); cannabis dependency (as measured by high ASSIST score) (adj. OR 4.70, 95% CI 1.77–12.47), early age of first use (adj. OR 1.83, 95% CI 1.03–3.27). Cannabis use in the other two settings was too rare to examine associations.

In line with previous studies, we found associations between cannabis use and the occurrence and age of onset of psychoses in Trinidad. These findings have implications for strategies for prevention of psychosis.

According to the cognitive neuropsychological model, antidepressants reduce symptoms of depression and anxiety by increasing positive relative to negative information processing. Most studies of whether antidepressants alter emotional processing use small samples of healthy individuals, which lead to low statistical power and selection bias and are difficult to generalise to clinical practice. We tested whether the selective serotonin reuptake inhibitor (SSRI) sertraline altered recall of positive and negative information in a large randomised controlled trial (RCT) of patients with depressive symptoms recruited from primary care.

The PANDA trial was a pragmatic multicentre double-blind RCT comparing sertraline with placebo. Memory for personality descriptors was tested at baseline and 2 and 6 weeks after randomisation using a computerised emotional categorisation task followed by a free recall. We measured the number of positive and negative words correctly recalled (hits). Poisson mixed models were used to analyse longitudinal associations between treatment allocation and hits.

A total of 576 participants (88% of those randomised) completed the recall task at 2 and 6 weeks. We found no evidence that positive or negative hits differed according to treatment allocation at 2 or 6 weeks (adjusted positive hits ratio = 0.97, 95% CI 0.90–1.05, p = 0.52; adjusted negative hits ratio = 0.99, 95% CI 0.90–1.08, p = 0.76).

In the largest individual placebo-controlled trial of an antidepressant not funded by the pharmaceutical industry, we found no evidence that sertraline altered positive or negative recall early in treatment. These findings challenge some assumptions of the cognitive neuropsychological model of antidepressant action.