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Background Little is known on whether associations between childhood autistic traits and psychotic experiences persist into adulthood and whether genetic confounding and childhood trauma influence them. Here we investigate the associations between childhood autistic traits and psychotic experiences until young adulthood and assess the influence of schizophrenia polygenic risk and childhood traumatic experiences, using the Avon Longitudinal Study of Parents and Children (ALSPAC) population-based birth cohort. Study design We used a measure of broad autistic traits (autism factor mean score), and four dichotomised measures of autistic traits capturing social communication difficulties (age 7), repetitive behaviours (age 5), sociability (age 3), and pragmatic language (age 9). Psychotic experiences were assessed at ages 18 and 24 using the semi-structured Psychosis-Like Symptoms interview (PLIKSi). Traumatic experiences between ages 5 and 11 were assessed with questionnaires and interviews administered to children and parents at multiple ages. Study results Broad autistic traits, as well as social communication difficulties, were associated with psychotic experiences that were distressing and/or frequent until age 24 (autism factor mean score, n = 3707: OR 1.19, 95%CI 1.01–1.39; social communication difficulties, n = 3384: OR 1.54, 95%CI 0.97–2.45). Childhood trauma mediated a substantial proportion of the identified associations (~28% and 36% respectively, maximum n = 3577). Schizophrenia polygenic risk did not appear to confound the associations. Multiple imputation analyses (maximum n = 13 105) yielded comparable results. Conclusions Childhood trauma may be an important, potentially modifiable pathway between autistic features and later onset of psychotic psychopathology. [ABSTRACT FROM AUTHOR]

Background: Traumatic experiences are associated with a higher risk of psychotic illnesses, but little is known about potentially modifiable mechanisms underlying this relationship. This study aims to examine whether post-traumatic stress disorder (PTSD) symptoms mediate the relationship between trauma and psychotic experiences (PEs). Methods: We used data from the Avon Longitudinal Study of Parents and Children to examine whether: PTSD symptoms mediate the relationships between (a) childhood trauma and adolescent PEs (study of adolescent PEs; n = 2952), and (b) childhood/adolescent trauma and PEs in early adulthood (study of adult PEs; n = 2492). We examined associations between variables using logistic regression, and mediation using the parametric g-computation formula. Results: Exposure to trauma was associated with increased odds of PEs (adolescent PEs: ORadjusted 1.48, 95% CI 1.23–1.78; adult PEs: ORadjusted 1.57, 95% CI 1.25–1.98) and PTSD symptoms (adolescent PTSD: ORadjusted 1.59, 95% CI 1.31–1.93; adult PTSD: ORadjusted 1.50, 95% CI 1.36–1.65). The association between PTSD symptoms and PE was stronger in adolescence (ORadjusted 4.63, 95% CI 2.34–9.17) than in adulthood (ORadjusted 1.62, 95% CI 0.80–3.25). There was some evidence that PTSD symptoms mediated the relationship between childhood trauma and adolescent PEs (proportion mediated 14%), though evidence of mediation was weaker for adult PEs (proportion mediated 8%). Conclusions: These findings are consistent with the hypothesis that PTSD symptoms partly mediate the association between trauma exposure and PEs. Targeting PTSD symptoms might help prevent the onset of psychotic outcomes. [ABSTRACT FROM AUTHOR]

Background: There is a wealth of literature on the observed association between childhood trauma and psychotic illness. However, the relationship between childhood trauma and psychosis is complex and could be explained, in part, by gene–environment correlation. Methods: The association between schizophrenia polygenic scores (PGS) and experiencing childhood trauma was investigated using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Norwegian Mother, Father and Child Cohort Study (MoBa). Schizophrenia PGS were derived in each cohort for children, mothers, and fathers where genetic data were available. Measures of trauma exposure were derived based on data collected throughout childhood and adolescence (0–17 years; ALSPAC) and at age 8 years (MoBa). Results: Within ALSPAC, we found a positive association between schizophrenia PGS and exposure to trauma across childhood and adolescence; effect sizes were consistent for both child or maternal PGS. We found evidence of an association between the schizophrenia PGS and the majority of trauma subtypes investigated, with the exception of bullying. These results were comparable with those of MoBa. Within ALSPAC, genetic liability to a range of additional psychiatric traits was also associated with a greater trauma exposure. Conclusions: Results from two international birth cohorts indicate that genetic liability for a range of psychiatric traits is associated with experiencing childhood trauma. Genome-wide association study of psychiatric phenotypes may also reflect risk factors for these phenotypes. Our findings also suggest that youth at higher genetic risk might require greater resources/support to ensure they grow-up in a healthy environment. [ABSTRACT FROM AUTHOR]

Background: Trauma exposure is linked to the development of psychotic illnesses, but little is known about potentially modifiable mechanisms underlying this relationship. Despite the high prevalence of PTSD symptoms in psychotic illnesses, only a few studies have examined the role of PTSD as a mediator, and these were all cross-sectional. This study aims to examine whether PTSD symptoms mediate the relationship between trauma and psychotic experiences (PE), using data from a large birth cohort study. Methods: We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC) to test whether: a) PTSD symptoms (at age 15) mediate the relationship between childhood trauma (age 0–14 years) and adolescent frequent or distressing psychotic experiences (age 12–18 years) (study of adolescent PE; n = 2,952), and b) PTSD symptoms (reported at age 24 for traumatic event occurring before age 19) mediate the relationship between childhood/adolescent trauma (age 0–17 years) and incident frequent or distressing psychotic experiences in early adulthood (age 19–24 years) (study of adult PE; n = 2,492). Associations between the variables of interest were examined with logistic regression, and mediation with the parametric g-computation formula. As sensitivity analyses, we i) examined broader and narrower psychotic outcomes, ii) included a measure of psychotic-like experiences at age 14 years as an intermediate confounder in the mediation model for adolescent psychotic experiences, and iii) repeated analyses using imputed data. Results: Exposure to trauma was associated with increased odds of psychotic experiences and PTSD symptoms both in adolescence and early adulthood (p<0.001). The association between PTSD and psychotic experiences was stronger in adolescence (p<0.001) than in adulthood (p=0.03). There was moderate evidence that PTSD symptoms mediated the relationship between childhood trauma and adolescent psychotic experiences (proportion mediated 14%), though evidence of mediation was much weaker for adult PE (proportion mediated 8%). In sensitivity analyses we observed similar results when using imputed data, and when modelling psychotic experiences at age 14 as an intermediate confounding for the adolescent PE outcome. The proportion mediated increased when examining more narrowly defined outcomes (19% for adolescent psychotic disorder). Discussion: These findings provide some evidence consistent with the thesis that psychotic experiences and disorder can occur consequent to PTSD symptoms after trauma exposure. Targeting PTSD symptoms might help prevent the occurrence of psychotic experiences and disorder in people with a trauma history. [ABSTRACT FROM AUTHOR]

Background: A number of studies show that people with psychotic disorders have abnormal belief-updating processes. In a commonly-used decision-making task, the beads task, participants infer which of two jars, each with a different ratio of coloured beads, a presented bead is drawn from, with an option to request further beads before reaching a decision. Previous studies suggest that people with psychotic symptoms request fewer beads (draws to decision; DTD) indicative of a ‘Jumping to conclusion’ (JTC) bias. In a modified version of this task, participants estimate the probability that beads have been drawn from one of the two jars on a sliding scale over a sequence of beads and are also told that the jar the beads are drawn from may switch. In this task, people with psychotic symptoms revise their estimations disproportionately in response to a change in colour of beads in a sequence (overadjustment bias). It is not clear what specific belief-updating processes drive these biases, how they arise, or if their association with psychotic symptoms is independent of confounding. We examined whether abnormal belief-updating processes are associated with psychotic experiences in a large, populationbased sample, and whether they mediate the association between trauma and psychotic symptoms. Methods: We used data from the Avon Longitudinal Study of Parents and Children birth cohort (n=2,879). Past-year frequent or distressing psychotic experiences (PEs) were assessed using the semi-structured PLIKS interview at age 24. Performance on the DTD and probability estimation tasks at age 24 were assessed using behavioural indices and computational modelling parameters (using ‘costed Bayesian’ and Hidden Markov Models respectively). Logistic regression was used to examine the association between belief-updating parameters (DTD task: cost of sampling, decision noise; Probability estimation task: adjustment rate, inference length, decision confidence, prior expectation of reversal, decision noise) and PEs. Estimates were adjusted for confounders (genetic risk for schizophrenia, socio-economic status, cognitive function). Mediation analysis tested abnormal belief-updating processes as a mediator between exposure to trauma (assessed ages 0–17 years) and age-24 PEs. Results: In the DTD task, increased decision noise was associated with PEs (adjusted OR=1.89, 95% CI: 1.14, 3.13, p=0.014). There was little evidence of an association between the JTC bias and PEs (OR= 1.13; 95% CI: 0.45, 2.82). For the probability estimation task, there was an association between a higher prior expectation that the jars that will switch during the sequence (expectation of reversal) and PEs (adjusted OR = 2.28; 95% CI 1.39, 3.74, p=0.001). Our findings were minimally attenuated by confounding (<10%). Exposure to trauma was also associated with greater decision noise in the DTD task, but there was little evidence that this abnormal belief-updating parameter mediated the relationship between trauma and PEs (<1% mediated). Discussion: Our results suggest that abnormal belief-updating processes (increased decision noise; greater prior expectation of reversal) are associated with PEs, and that this is not explained by general cognitive ability, shared genetic risk, or social background. Previous observations of association between the JTC bias and psychosis may be due to sub-optimal performance rather than a bias for making a decision on less evidence. The results also suggest that an increased expectation of change is associated with the early stages of psychosis symptom development. Our mediation result does not support the hypothesis that the belief-updating processes examined here lie on the causal pathway between trauma exposure and PEs. [ABSTRACT FROM AUTHOR]