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BACKGROUND AND HYPOTHESIS Previous research in both clinical and non-clinical populations has suggested an association between intelligence quotient (IQ) and psychosis. The social defeat hypothesis posits that low status and repeated humiliation increase the risk of psychosis. The present study investigated the relationship between IQ and subclinical psychosis in the general population, while also examining the potential mediating and confounding roles of psychosocial stressors and core schemata. STUDY DESIGN We analyzed data from 1497 healthy controls in the EU-GEI dataset, a multicenter study conducted across six countries. IQ and the positive dimension of subclinical psychosis (measured by the positive dimension of the Community Assessment of Psychic Experiences questionnaire) were analyzed using linear regression models adjusting for age, sex, childhood trauma, stressful life events, and core schemata (positive and negative schemata). Mediation analysis was conducted to explore indirect effects. STUDY RESULTS IQ was associated with subclinical psychosis. The results remained statistically significant after adjustment for several confounders. In the mediation analysis, IQ had no total or direct effect, but a small negative indirect effect through negative-other schemata (ß = -0.040; 95% Confidence Interval: -0.55, -0.024), childhood trauma (ß = -0.029; 95% CI -0.042, -0.016), negative-self schemata (ß = -0.009; 95% CI -0.017, -0.001), and stressful life events (ß = -0.012; 95% CI -0.021, -0.003). CONCLUSION These findings support the idea that cognitive vulnerability is associated with an increased risk of subclinical psychotic symptoms, with psychosocial stressors and core schemata possibly playing a mediating role, in line with the social defeat hypothesis.
Psychotic disorders are complex, multifactorial conditions influenced by both genetic liability and early environmental adversity. Polygenic risk scores (PRSs) derived from genome-wide association studies have shown utility in capturing genetic predisposition, but their biological interpretability remains limited. In this study, we evaluated whether biologically informed pathway-specific polygenic scores (pPGSs) for psychosis, restricted to neurotransmitter-related pathways, could help clarify gene-environment interplay. Using data from 1 192 individuals in the EU-GEI multi-site case-control study, we constructed pPGSs for dopamine, glutamate, GABA, and serotonin systems. We investigated associations between pPGSs and childhood trauma (rGE), their interactions on psychosis risk (GxE), and the influence of the genome-wide psychosis PRS on these relationships. Serotonin, dopamine, and glutamate pPGSs were positively associated with a composite trauma exposure (i.e., abuse and neglect), suggesting shared genetic factors contributing to both psychosis liability and early adversity. Significant negative GxE effects were observed for both dopamine and serotonin pPGSs, indicating that higher trauma exposure diminished the relative influence of genetic liability on psychosis risk. Adjustment for the genome-wide psychosis PRS attenuated most effects, but serotonergic and dopaminergic associations remained robust, supporting pathway-specific contributions beyond general polygenic risk. These findings provide proof-of-concept for the utility of pPGSs in psychiatric research, suggesting both genetic contributions to trauma exposure and GxE effects on psychosis risk. Further research incorporating epigenetic data and longitudinal designs may enhance mechanistic insight and translational potential.
Prolonged CAL is linked to higher risk of FEP, preferentially affective psychosis in females, poorer functioning, and developmental potentiation of polygenic liability.
