It has been argued that disruptions to epistemic trust are implicated in psychopathology; however, this requires empirical testing, and an existing scale evaluating epistemic trust, the Epistemic Trust, Mistrust and Credulity Questionnaire (ETMCQ), requires improvement.

This study tested a revised version of the Epistemic Trust, Mistrust and Credulity Questionnaire (the ETMCQ-R), examining the strength of associations between the updated scale and mental health symptoms, epistemic vice, psychological resilience, perceived social support, attachment style, history of childhood adversity and an experimental measure of trust, and epistemic stance as a mediator between adversity and psychopathology.

Using an online survey design, 525 participants completed the ETMCQ-R alongside other measures. Exploratory and confirmatory factor analyses were conducted to assess the structure of the ETMCQ-R and correlational and mediational analyses were used to further assess validity of the measure.

The ETMCQ-R possesses greater model fit and a stronger three-factor structure (Trust, Mistrust and Credulity) compared with the ETMCQ. Significant negative correlations were identified between Trust (r = −0.12) and higher scores on global psychopathology severity, while Mistrust (r = 0.41) and Credulity (r = 0.36) showed positive correlations. Trust negatively correlated with borderline features (r = −0.10), whereas Mistrust and Credulity positively correlated (r = 0.54 and r = 0.48, respectively). Mistrust and credulity partially mediated the relationship between childhood adversity and psychopathology, with stronger mediation effects for borderline features than general psychopathology.

The study demonstrated strong psychometric properties of the ETMCQ-R, and further analyses indicate the three factors are differentially related to wider domains of socio-emotional functioning.

Cannabis use in young adulthood is common, yet few studies have explored how it predicts changes in psychopathology and functional well-being in community samples. We assessed these links using both self-reported frequency of cannabis use and hair THC concentrations.

Data came from a community sample of young adults (N = 863) who reported cannabis use (weekly-to-daily use: n = 150) and provided hair samples at age 20 (cannabis detected: n = 110). Liquid chromatography–tandem mass spectrometry quantified delta-9-tetrahydrocannabinol (THC) and cannabinol (CBN) concentrations in hair. At ages 20 and 24, participants reported psychopathology (psychotic-like experiences, problematic substance use, internalizing symptoms, and aggression) and functional wellbeing (general well-being, delinquency, and not being in employment, education, or training). Multiple linear and logit regression models tested associations between six different continuous and dichotomous operationalizations of self-reported and objective cannabis exposure at age 20 and psychological and functional well-being at age 24, adjusting for sex, sociodemographic characteristics, and the outcomes measured at age 20.

Both self-reported frequency of cannabis use and hair THC concentrations predicted increases in psychotic-like experiences and internalizing symptoms, increased aggression, decreased general well-being, higher odds of not being in employment, training, or education, and more problematic substance use from age 20 to 24, with small effect sizes. Composite exposure scores derived from self-reports and hair data were not more informative than either source alone.

Frequent cannabis use predicted adverse changes in psychopathological outcomes from ages 20 to 24, regardless of how it was assessed.

Longitudinal studies have revealed that raised levels of inflammatory markers and trauma in childhood are associated with psychopathology in adulthood.

To examine whether inflammation in childhood mediates the effects of genetic risk and trauma on psychopathology in early adulthood.

Measures of trauma exposure, inflammation and psychopathology were collected from the Avon Longitudinal Study of Parents and Children. Exposure to trauma was measured from 5 to 11 years of age; C-reactive protein and interleukin-6 levels were measured at 9 years; and depression, anxiety disorders, negative symptoms and psychotic experiences were assessed at 24 years. Polygenic risk scores (PRSs) were created for schizophrenia, depression, anxiety and psychotic experiences. Mediation analyses were conducted using imputed data (N: 7859 to 8700) to investigate whether inflammation mediated the associations of genetic risk and childhood trauma with psychopathology.

Most psychiatric PRSs were associated with multiple psychopathological outcomes in adulthood, with the exception of the PRS for psychotic experiences. Childhood trauma was associated with all psychopathology. However, there was no strong evidence that inflammatory markers in childhood mediated associations among PRSs, trauma and psychopathology. Sensitivity analyses using outcomes from age 18 and PRSs based on single-nucleotide polymorphisms that met more stringent standards of evidence of association gave results consistent with those of our primary analyses.

We found little evidence that interleukin-6 or C-reactive protein mediated the pathway between genetic liability for psychiatric phenotypes or trauma and subsequent psychopathology. Longitudinal investigation of other inflammatory and non-inflammatory pathways is required to identify modifiable targets and inform novel treatment strategies for individuals at genetic or trauma-related risk of psychiatric illness.

Measurement-based care (MBC) is widely recommended in psychiatry but remains underutilized in routine clinical settings. The Transdiagnostic Global Impression – Psychopathology (TGI-P) scale was developed to provide a brief yet comprehensive assessment of 10 core transdiagnostic symptom domains. To support more inclusive care and promote patient and caregiver engagement in treatment planning, two new versions of the TGI-P, that is, a patient-rated and a separate informant-rated, were developed, complementing the previously published clinician-rated version.

The patient and informant versions mirror the original clinician-rated TGI-P, assessing the identical 10 domains using a seven-point Likert severity scale, with results displayed via a personalized symptom map. A user satisfaction/feasibility study was conducted with 50 participants (25 patients and 25 caregivers) from the UK and US. After completing the scale, participants provided feedback on its clarity, usability, emotional impact, and comparative utility.

Most participants completed the scale in less than 5 min. Instructions were considered clear, and the format was rated easy to follow. Response options were deemed appropriate by 86% of participants, and the visual output was widely appreciated. While one-third reported mild emotional triggering, overall burden was described as manageable. Approximately, three-quarters of participants rated the TGI-P as equal to or better than other tools they had used.

TGI-P patient and informant versions were developed and, informed by the feasibility study, refined to offer brief, user-friendly tools that support multi-informant assessment as input to MBC. Both versions of the TGI-P, with their graphical output, may support shared understanding and collaborative decision making among clinicians, patients, and caregivers. A validation study of the TGI-P is underway.

Executive functioning (EF) impairments are widely known to represent transdiagnostic risk factors of psychopathology. However, a recent alternative account has been proposed, according to which EF impairments emerge as consequences of psychopathology.

Using a longitudinal cross-lagged panel network analysis approach, we tested these competing theoretical accounts at different stages during adolescence. We used data from the Brazilian High-Risk Cohort Study for the Development of Childhood Psychiatric Disorders, in which 61% of individuals at wave 1 were selected due to their high risk for psychopathology. Participants were assessed across three assessment waves during early (wave 1: n = 1,992, mean age = 10.20 years) and middle adolescence (wave 2: n = 1,633, mean age = 13.48 years; wave 3: n = 1,439, mean age = 18.20 years). We examined associations between working memory, inhibitory control, and broad-band measures of psychopathology.

During early adolescence, lower inhibitory control was a risk factor for externalizing problems that, in turn, predicted lower working memory capacity. During middle adolescence, bidirectional associations became more prominent: inhibitory control and working memory functioned as both risk factors and consequences. Externalizing problems both predicted and were predicted by poor inhibitory control. Internalizing and externalizing symptoms showed bidirectional associations over time. Externalizing problems predicted more internalizing symptoms, whereas internalizing symptoms predicted fewer externalizing problems during middle adolescence.

Our results corroborate dynamic theories that describe executive dysfunctions as precursors and consequences of psychopathology in middle adolescence.

Mental health problems commonly persist from childhood to adulthood. This study tested whether young adult life transitions can improve adult mental health symptoms after adjusting for childhood mental health symptoms.

The analysis uses data from the prospective, representative Great Smoky Mountains Study. Life transitions (e.g., high school completion, partnering, parenthood, and living independently) were assessed up to three times in young adulthood (ages 18 to 26; 3,241 observations). A cumulative variable counted the number of young adult transitions. Emotional, substance use, and antisocial personality symptoms were assessed at age 30 (1,154 participants or 81.2% of the original sample). Propensity models adjusted for early life adversities and psychiatric symptoms.

Multiple young adult transitions were common (m = 4.62; SD = 1.57). After adjusting for childhood mental health problems and adversities, each additional transition was significantly associated with a reduction in subsequent adult emotional symptoms (β = −0.34, 95% CI: −0.59, −0.08, p = 0.01) and adult antisocial personality disorder symptoms (β = −0.08, 95% CI: −0.14, −0.02, p < 0.001. These associations were stronger in males than in females. Young adult transitions were not associated with reductions in subsequent substance use symptoms (β = −0.04; 95% CI: −0.11, 0.03, p = 0.30). Young adult transitions related to educational milestones and consistent employment were associated with the largest reductions in symptoms.

In this cohort study, life transitions during young adulthood were associated with reduced emotional and behavioral symptoms in adulthood. These transitions may constitute a potential mental health turning point and a specific, modifiable target for social policies.

The Hierarchical Taxonomy of Psychopathology (HiTOP) and Research Domain Criteria (RDoC) frameworks emphasize transdiagnostic and mechanistic aspects of psychopathology. We used a multi-omics approach to examine how HiTOP’s psychopathology spectra (externalizing [EXT], internalizing [INT], and shared EXT + INT) map onto RDoC’s units of analysis.

We conducted analyses across five RDoC units of analysis: genes, molecules, cells, circuits, and physiology. Using genome-wide association studies from the companion Part I article, we identified genes and tissue-specific expression patterns. We used drug repurposing analyses that integrate gene annotations to identify potential therapeutic targets and single-cell RNA sequencing data to implicate brain cell types. We then used magnetic resonance imaging data to examine brain regions and circuits associated with psychopathology. Finally, we tested causal relationships between each spectrum and physical health conditions.

Using five gene identification methods, EXT was associated with 1,759 genes, INT with 454 genes, and EXT + INT with 1,138 genes. Drug repurposing analyses identified potential therapeutic targets, including those that affect dopamine and serotonin pathways. Expression of EXT genes was enriched in GABAergic, cortical, and hippocampal neurons, while INT genes were more narrowly linked to GABAergic neurons. EXT + INT liability was associated with reduced gray matter volume in the amygdala and subcallosal cortex. INT genetic liability showed stronger causal effects on physical health – including chronic pain and cardiovascular diseases – than EXT.

Our findings revealed shared and distinct pathways underlying psychopathology. Integrating genomic insights with the RDoC and HiTOP frameworks advanced our understanding of mechanisms that underlie EXT and INT psychopathology.

This systematic review aims to update the current evidence on the effects of institutionalisation in minors living in residential care homes, specifically focusing on alterations in neuronal systems and their association with psychopathological and neuropsychological outcomes.

Searches were conducted in the Web of Science, Scopus, PubMed, and Google Scholar databases, following PRISMA methodology for peer-reviewed empirical articles. The final selection comprised 10 studies that met the inclusion criteria: (1) published articles with quantitative data, (2) aimed at observing the relationship between psychological and neuropsychological symptoms and the electroencephalogram (EEG) activity in institutionalised children, (3) published between 2016 and 2023, and (4) examining institutionalised minors in residential care homes.

The articles show that these children exhibit general immaturity in EEG patterns, with a predominance of slow waves (primarily in the theta band). They also demonstrate poorer performance in executive functions (e.g. working memory, inhibition, and processing speed) and cognitive processes, along with a higher risk of externalising problems. However, current evidence does not allow definitive conclusions on whether early EEG abnormalities predict long-term neuropsychological deficits, despite data showing associations between EEG changes and certain cognitive dysfunctions at the time of evaluation.

The reviewed evidence suggests that EEG alterations in institutionalised minors are linked to executive dysfunction and increased psychopathological risk. These findings highlight the value of EEG in identifying at-risk children and inform the design of preventive interventions. Longitudinal studies are needed to clarify causal relationships.

There is considerable comorbidity between externalizing (EXT) and internalizing (INT) psychopathology. Understanding the shared genetic underpinnings of these spectra is crucial for advancing knowledge of their biological bases and informing empirical models like the Research Domain Criteria (RDoC) and Hierarchical Taxonomy of Psychopathology (HiTOP).

We applied genomic structural equation modeling to summary statistics from 16 EXT and INT traits in individuals genetically similar to European reference panels (EUR-like; n = 16,400 to 1,074,629). Traits included clinical (e.g. major depressive disorder, alcohol use disorder) and subclinical measures (e.g. risk tolerance, irritability). We tested five confirmatory factor models to identify the best fitting and most parsimonious genetic architecture and then conducted multivariate genome-wide association studies (GWAS) of the resulting latent factors.

A two-factor correlated model, representing EXT and INT spectra, provided the best fit to the data. There was a moderate genetic correlation between EXT and INT (r = 0.37, SE = 0.02), with bivariate causal mixture models showing extensive overlap in causal variants across the two spectra (94.64%, SE = 3.27). Multivariate GWAS identified 409 lead genetic variants for EXT, 85 for INT, and 256 for the shared traits.

The shared genetic liabilities for EXT and INT identified here help to characterize the genetic architecture underlying these frequently comorbid forms of psychopathology. The findings provide a framework for future research aimed at understanding the shared and distinct biological mechanisms underlying psychopathology, which will help to refine psychiatric classification systems and potentially inform treatment approaches.

Current empirical understanding of the relationship between psychopathology and terrorist behaviours in women is limited, because most research focuses on male perpetrators and relies on secondary sources. Addressing this gap is crucial, particularly given previous research that highlights significant differences in mental health problems between women and men involved in non-terrorist violent activities.

To empirically examine the presence of psychopathology in women exhibiting terrorist behaviours, as well as its potential role in these behaviours.

A case series study of 14 Dutch female convicts associated with the (so-called) Islamic State of Iraq and Syria (ISIS), examining the occurrence and types of mental disorders, psychopathological problems and pathological personality traits, and exploring their potential role in terrorist behaviours based on forensic mental health reports from psychiatrists and psychologists.

Half of the women (n = 7) exhibited mental disorders during terrorist activities, primarily personality disorders. Psychopathological problems included susceptibility to influence (71%, n = 10), identity problems (64%, n = 9), feelings of inferiority (57%, n = 8) and naivety (50%, n = 7). A significant link between terrorism and mental disorders, psychopathological problems or pathological personality traits was identified in almost half of the women (43%, n = 6).

Psychopathology is present in some women involved in terrorist behaviours, influencing their involvement, but is absent or irrelevant in others. Identifying psychopathology in women with terrorist tendencies is essential for early prevention and should be a core competency for psychiatrists.

The diagnosis of ADHD in adults is on the rise. Applying the ADHD diagnosis, which originally was described in children, to adults has involved a “subjectivization” of some of the diagnostic criteria, i.e., some behavioral features (signs) in children have become experiences (symptoms) in adults. These issues raise the question of how ADHD is best diagnosed in adults? Thus, we examined how ADHD is diagnosed in adults in research.

A review of how ADHD is diagnosed in adults in randomized controlled studies (RCTs).

We include 292 RCTs. We found substantial variation and no consensus about the diagnostic method. More than half of the studies did not seem to include an assessment of general psychopathology, and only in 35% of studies was the ADHD diagnosis allocated by psychiatrists or psychologist. More than half of the studies included patients with psychiatric comorbidity.

These findings raise concerns about the validity of the ADHD diagnosis in many of the included RCTs. It is worrying that securing a reasonably accurate diagnosis is not prioritized in more than half of the studies. If neither clinicians nor researchers can rely on the basic fact the patients in scientific studies diagnostically resemble the patients they are facing, scientific studies risk losing their clinical relevance. Since RCTs can lead to changes in clinical practice, they must be conducted carefully. To advance research on adult ADHD, the quality of the diagnostic assessment must be prioritized, requiring comprehensive differential diagnosis by a skilled psychiatrist or psychologist.