No studies have investigated the effects of virtual reality (VR) on the persecutory idea of reference (IOR) or delusions of reference (DOR) in patients with psychosis. This study examined the efficacy and safety of VR therapy in stable outpatients with psychosis and explored relationships between primary outcomes and psychological factors using path analysis.

Seventy-eight patients were randomly assigned to either the VR-treatment (VR-T) or VR-control (VR-C) group. The VR-T group viewed three 360° 3D videos or four animated videos; the VR-C group viewed the same seven videos with muted voices or 11 360° 3D videos of natural scenes. Pre- and post-assessments were performed using the Psychotic Symptom Rating Scale-Delusions (PSYRATS-D) and Revised Green et al. Paranoid Thought Scale (R-GPTS) as a primary outcome measure. Several self-rating scales measuring schema, depression, brooding, negative evaluation, attribution bias, and self-esteem were administered. Safety was assessed after sessions 1 and 10, and path models were constructed.

Between-group analysis showed a significant improvement in PSYRATS-D scores in the VR-T group compared with the VR-C group. Regarding self-rating scales, the between-group analysis revealed a significant group × time interaction only for the Social and Occupational Functioning Assessment Scale (SOFAS) score. The frequency of VR sickness was high, but its severity was mild. Fear of Negative Evaluation Scale and Beck Depression Inventory scores were found to have mediating roles.

VR therapy effectively reduced delusions in young, stable psychosis patients with mild and tolerable side effects. Future studies should develop diverse VR content for older populations.

Individuals with long-term physical health conditions (LTCs) experience higher rates of depression and anxiety. Conventional self-report measures do not distinguish distress related to LTCs from primary mental health disorders. This difference is important as treatment protocols differ. We developed a transdiagnostic self-report measure of illness-related distress, applicable across LTCs.

The new Illness-Related Distress (IRD) scale was developed through thematic coding of interviews, systematic literature search, think-aloud interviews with patients and healthcare providers, and expert-consensus meetings. An internet sample (n = 1,398) of UK-based individuals with LTCs completed the IRD scale for psychometric analysis. We randomly split the sample (1:1) to conduct: (1) an exploratory factor analysis (EFA; n = 698) for item reduction, and (2) iterative confirmatory factor analysis (CFA; n = 700) and exploratory structural equation modeling (ESEM). Here, further item reduction took place to generate a final version. Measurement invariance, internal consistency, convergent, test–retest reliability, and clinical cut-points were assessed.

EFA suggested a 2-factor structure for the IRD scale, subsequently confirmed by iteratively comparing unidimensional, lower order, and bifactor CFAs and ESEMs. A lower-order correlated 2-factor CFA model (two 7-item subscales: intrapersonal distress and interpersonal distress) was favored and was structurally invariant for gender. Subscales demonstrated excellent internal consistency, very good test–retest reliability, and good convergent validity. Clinical cut points were identified (intrapersonal = 15, interpersonal = 12).

The IRD scale is the first measure that captures transdiagnostic distress. It may aid assessment within clinical practice and research related to psychological adjustment and distress in LTCs.

Second-generation antipsychotics (SGAs) cause metabolic side effects. However, patients’ metabolic profiles were influenced by time-invariant and time-varying confounders. Real-world evidence on the long-term, dynamic effects of SGAs (e.g. different treatment sequences) are limited. We employed advanced causal inference methods to evaluate the metabolic impact of SGAs in a naturalistic cohort.

We followed 696 Chinese patients with schizophrenia-spectrum disorders receiving SGAs. Longitudinal targeted maximum likelihood estimation (LTMLE) was used to estimate the average treatment effects (ATEs) of continuous SGA treatment versus ‘no treatment’ on metabolic outcomes, including total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglyceride (TG), fasting glucose (FG), and body mass index (BMI), over 6–18 months at 3-month intervals. LTMLE accounted for time-invariant and time-varying confounders. Post-SGA discontinuation side effects were also assessed.

The ATEs of continuous SGA treatment on BMI and TG showed an inverted U-shaped pattern, peaking at 12 months and declining afterwards. Similar patterns were observed for TC and LDL, albeit the ATEs peaked at 15 months. For FG and HDL, the ATEs peaked at ~6 months. The adverse impact of SGAs on BMI persisted even after medication discontinuation, yet other metabolic parameters did not show such lingering side effects. Clozapine and olanzapine exhibited greater metabolic side effects compared to other SGAs.

Our real-world study suggests that metabolic side effects may stabilize with prolonged continuous treatment. Clozapine and olanzapine confer higher cardiometabolic risks than other SGAs. The side effects of SGAs on BMI may persist after drug discontinuation. These insights may guide antipsychotic choice and improve management of metabolic side effects.

Antisocial behavior (ASB) is relatively common in childhood and adolescence. While it harms victims, perpetrators are at increased risk of disadvantageous adult outcomes. Developmental heterogeneity is well documented; distinctions have been drawn between early-onset persistent, adolescent-onset, and childhood-limited pathways. We examine whether individuals in some pathways face worse mid-life outcomes than others and whether the pattern differs across sexes.

The 1970 British Cohort Study assessed parent-reported ASB measures at ages 5, 10, and 16. We classified developmental pathways using the Rutter A scale conduct questions. We categorized children scoring in the top 10% of the distribution as showing high ASB, separately at each assessment. Approximately 6000 individuals were classified into low (73%), childhood-limited (11%), adolescent-onset (9%), and early-onset persistent (7%) groups. We tested associations of ASB grouping with age 46 social, economic, and health outcomes, controlling for a range of covariates.

The childhood-limited group showed little mid-life difficulty. The early-onset persistent and adolescent-onset groups both showed a pattern of worse midlife outcomes for boys and girls.

The results highlight that ASB in young people is not transient and that prevention and treatment during early childhood and adolescence are warranted.

Functional Somatic Disorders (FSD) and Internalizing Psychiatric Disorders (IPD) are frequently comorbid and likely share familial/genetic risk factors.

We performed a Common Factor Multivariate Analysis of 2 FSDs, Fibromyalgia (FM) and Irritable Bowel Syndrome (IBS), and two IPDs, Major Depression (MD) and Anxiety Disorders (AD), in five kinds of Swedish female–female relative pairs: monozygotic (n = 8,052) dizygotic (n = 7216), full siblings (n = 712,762), half-siblings reared together (n = 23,623), and half-siblings reared apart (n = 53,873). Model fitting was by full information maximum likelihood using OpenMx.

The best-fit model included genetic, shared environmental, and unique environmental factors. The common factor, ~50% heritable with a small shared environmental effect, loaded more strongly on the two IPDs (~0.80) than the 2 FSDs (0.40). Disorder-specific genetic effects were larger for the 2 FSDs (~0.30) than the 2 IPDs (~0.03). Estimated genetic correlations were high for MD and AD (+0.91), moderate between IBS and IPDs (+0.62), and intermediate between FM and MD (+0.54), FM and AD (+0.28), and FM and IBS (+0.38). Shared environmental influences on all disorders were present but small.

In women, FSDs and IPDs shared a moderate proportion of their genetic risk factors, greater for IBS than for FM. However, the genetic sharing between IBS and FM was less than between MD and AD, suggesting that FSDs do not form a highly genetically coherent group of disorders. The shared environment made a modest contribution to the familial aggregation of FSDs and IPDs.