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OBJECTIVE: To test whether polygenic risk score for schizophrenia (PRS-S) interacts with childhood adversity and daily-life stressors to influence momentary mental state domains (negative affect, positive affect, and subtle psychosis expression) and stress-sensitivity measures. METHODS: The data were retrieved from a general population twin cohort including 593 adolescents and young adults. Childhood adversity was assessed using the Childhood Trauma Questionnaire. Daily-life stressors and momentary mental state domains were measured using ecological momentary assessment. PRS-S was trained on the latest Psychiatric Genetics Consortium schizophrenia meta-analysis. The analyses were conducted using multilevel mixed-effects tobit regression models. RESULTS: Both childhood adversity and daily-life stressors were associated with increased negative affect, decreased positive affect, and increased subtle psychosis expression, while PRS-S was only associated with increased positive affect. No gene-environment correlation was detected. There is novel evidence for interaction effects between PRS-S and childhood adversity to influence momentary mental states [negative affect (b = 0.07, P = 0.013), positive affect (b = -0.05, P = 0.043), and subtle psychosis expression (b = 0.11, P = 0.007)] and stress-sensitivity measures. CONCLUSION: Exposure to childhood adversities, particularly in individuals with high PRS-S, is pleiotropically associated with emotion dysregulation and psychosis proneness. ispartof: ACTA PSYCHIATRICA SCANDINAVICA vol:141 issue:5 pages:465-475 ispartof: location:United States status: published

Objective: The daily life, affective phenotypes of momentary negative affect (NA), positive affect (PA) variability and NA variability are associated with future depressive symptomatology. This study investigates the extent to which genetic and environmental factors contribute to the inter-individual differences in these daily life, affective phenotypes. Method: Two hundred and seventy-nine female twins from the Flemish (Belgium) general population participated in an experience sampling study measuring affect in daily life. Structural equation modelling was used to fit univariate and bivariate models. Results: Genetic factors explained, respectively, 18%, 18% and 35% of the inter-individual differences in momentary NA, PA variability and NA variability. Non-shared environmental factors were found to explain the remaining inter-individual variation. In addition, 41% of the association between positive and NA variability was attributed to shared genetic factors. Conclusion: Results of this study show that daily life patterns of affective expression are subject to substantial environmental influence. Prospective assessments of the effect of interventions on these expressions may therefore represent a powerful tool to prevent transition from subclinical depressive symptomatology to a clinical outcome or to reduce symptomatology in those with clinical depression.

Objective: To examine prospectively whether high reward experience (the ability to generate positive affect boosts from pleasurable daily events) protects against affective symptoms and whether environmental or genetic risk factors moderate protective effects. Method: At baseline, 498 female twins participated in an experience sampling study measuring reward experience in daily life. They also completed questionnaires on childhood adversity and recent stressful life events (SLE). Affective symptoms were measured at baseline and at four follow-ups using SCL-90 anxiety and depression subscales. Co-twin affective symptoms were used as indicators of genetic risk. Results: Baseline reward experience did not predict follow-up affective symptoms, regardless of level of genetic risk. However, high reward experience was associated with reduced future affective symptoms after previous exposure to childhood adversity or recent SLE. Conclusion: High daily life reward experience increases resilience after environmental adversity; modification of reward experience may constitute a novel area of therapeutic intervention.

Objective: This study assessed the relationship between stress reactivity (trait 1) and psychosis (trait 2) across genetically related persons (cross-twin, cross-trait design) to examine whether stress reactivity is an uncontaminated and unconfounded familial marker of psychosis risk. Method: Reactivity to stress and subclinical psychotic experiences were assessed in 289 female, general population twin-pairs. Cross-trait, within-twin associations investigating the association between stress reactivity and subclinical psychotic experiences in each person, were calculated. In addition, cross-trait, cross-twin associations were calculated to assess whether stress reactivity in one twin was moderated by subclinical psychotic experiences in the co-twin. Results: Cross-trait, within-twin analyses showed significant associations between stress reactivity and subclinical psychotic experiences in each person. In addition, the cross-trait cross-twin analyses showed that stress reactivity in twin 1 was significantly moderated by subclinical experiences in the co-twin. Conclusion: The results suggest that the psychosis phenotype cosegregates with increased emotional reactivity to stress in daily life.

Objective: Genetic and environmental influences on variation in distress associated with subclinical psychotic experiences were examined. Method: A total of 289 twin pairs filled in the Community Assessment of Psychic Experiences, a self-report instrument assessing subclinical positive and negative psychotic experiences and associated distress (distresspos and distressneg). Using structural equation modelling, univariate and bivariate models were fitted. Results: Univariate model fitting showed genetic and non-shared environmental influences on both distresspos and distressneg. Bivariate model fitting showed that 52% of the correlation between the two phenotypes (r = 0.46) was because of shared genes and that non-shared environmental factors accounted for 48% of the correlation. Conclusion: Liability to psychosis not only refers to the development of psychosis per se, but also to the liability to develop dysfunctional emotional appraisals. The emotive component of psychosis liability involves genetic transmission of a general, non-symptom-specific distress factor that may be a target for molecular genetic research.