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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: Employment disruptions can impact smoking and alcohol consumption. During the COVID-19 pandemic, many countries implemented furlough schemes to prevent job loss. We examine how furlough was associated with smoking, vaping and alcohol consumption in the UK.Methods: Data from 27,841 participants in eight UK adult longitudinal surveys were analysed. Participants self-reported employment status and current smoking, current vaping and alcohol consumption (>4 days/week or 5+ drinks per typical occasion) both before and during the early stages of the pandemic (April-July 2020). Risk ratios were estimated within each study using modified Poisson regression, adjusting for a range of potential confounders, including pre-pandemic behaviour. Findings were synthesised using random effects meta-analysis.Results: Compared to stable employment and after adjustment for pre-pandemic characteristics, furlough was not associated with smoking (ARR = 1.05; 95% CI: 0.95-1.16; I2: 10%), vaping (ARR = 0.89; 95% CI: 0.74-1.08; I2: 0%) or drinking (ARR = 1.03; 95% CI: 0.94-1.13; I2: 48%). There were similar findings for no longer being employed, and stable unemployment, though this varied by sex: stable unemployment was associated with smoking for women (ARR = 1.35; 95% CI: 1.00-1.82; I2: 47%) but not men (0.84; 95% CI: 0.67-1.05; I2: 0%). No longer being employed was associated with vaping among women (ARR = 2.74; 95% CI: 1.59-4.72; I2: 0%) but not men (ARR = 1.25; 95% CI: 0.83-1.87; I2: 0%).Conclusions: We found no clear evidence of furlough or unemployment having adverse impacts on smoking, vaping or drinking behaviours during the early stages of the COVID-19 pandemic in the UK. Differences in risk compared to those who remained employed were largely explained by pre-pandemic characteristics. [ABSTRACT FROM AUTHOR]

Background: In March 2020, the UK implemented the Coronavirus Job Retention Scheme (furlough) to minimise job losses. Our aim was to investigate associations between furlough and diet, physical activity, and sleep during the early stages of the COVID-19 pandemic. Methods: We analysed data on 25,092 participants aged 16-66 years from eight UK longitudinal studies. Changes in employment, including being furloughed, were based on employment status before and during the first lockdown. Health behaviours included fruit and vegetable consumption, physical activity, and sleep. Study-specific estimates obtained using modified Poisson regression, adjusting for socio-demographic characteristics and pre-pandemic health and health behaviours, were statistically pooled using random effects meta-analysis. Associations were also stratified by sex, age, and education. Results: Across studies, between 8 and 25% of participants were furloughed. Compared to those who remained working, furloughed workers were slightly less likely to be physically inactive (RR = 0.85; [95% CI 0.75-0.97]; I² = 59%) and did not differ overall with respect to low fruit and vegetable consumption or atypical sleep, although findings for sleep were heterogenous (I² = 85%). In stratified analyses, furlough was associated with lower fruit and vegetable consumption among males (RR = 1.11; [1.01-1.22]; I² = 0%) but not females (RR = 0.84; [0.68-1.04]; I² = 65%). Considering changes in quantity, furloughed workers were more likely than those who remained working to report increases in fruit and vegetable consumption, exercise, and hours of sleep. Conclusions: Those furloughed exhibited similar health behaviours to those who remained in employment during the initial stages of the pandemic. There was little evidence to suggest that adoption of such social protection policies in the post-pandemic recovery period and during future economic crises had adverse effects on population health behaviours. [ABSTRACT FROM AUTHOR]

B Correction: BMC Med 20, 147 (2022) b B https://doi.org/10.1186/s12916-022-02343-y b After publication, it came to the authors' attention that 143 individuals from ALSPAC G0 and 24 in ALSPAC G1 were incorrectly coded as "unemployed" pre-pandemic in our manuscript [[1]]. Reference 1 Wielgoszewska B. The UK Coronavirus Job Retention Scheme and diet, physical activity, and sleep during the COVID-19 pandemic: evidence from eight longitudinal population surveys. [Extracted from the article]

Background: Psychotic experiences emerge from abnormalities in perception and belief formation and occur more commonly in those experiencing childhood trauma. However, which precise aspects of belief formation are atypical in psychosis is not well understood. We used a computational modeling approach to characterize belief updating in young adults in the general population, examine their relationship with psychotic outcomes and trauma, and determine the extent to which they mediate the trauma-psychosis relationship., Methods: We used data from 3360 individuals from the Avon Longitudinal Study of Parents and Children birth cohort who completed assessments for psychotic outcomes, depression, anxiety, and two belief updating tasks at age 24 and had data available on traumatic events assessed from birth to late adolescence. Unadjusted and adjusted regression and counterfactual mediation methods were used for the analyses., Results: Basic behavioral measures of belief updating (draws-to-decision and disconfirmatory updating) were not associated with psychotic experiences. However, computational modeling revealed an association between increased decision noise with both psychotic experiences and trauma exposure, although <3% of the trauma-psychotic experience association was mediated by decision noise. Belief updating measures were also associated with intelligence and sociodemographic characteristics, confounding most of the associations with psychotic experiences. There was little evidence that belief updating parameters were differentially associated with delusions compared with hallucinations or that they were differentially associated with psychotic outcomes compared with depression or anxiety., Conclusions: These findings challenge the hypothesis that atypical belief updating mechanisms (as indexed by the computational models and behavioral measures we used) underlie the development of psychotic phenomena., (Copyright © 2022 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

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.

Background: Childhood maltreatment is associated with poor mental and physical health. However, the mechanisms of gene-environment correlations and the potential causal effects of childhood maltreatment on health are unknown. Using genetics, we aimed to delineate the sources of gene-environment correlation for childhood maltreatment and the causal relationship between childhood maltreatment and health., Methods: We did a genome-wide association study meta-analysis of childhood maltreatment using data from the UK Biobank (n=143 473), Psychiatric Genomics Consortium (n=26 290), Avon Longitudinal Study of Parents and Children (n=8346), Adolescent Brain Cognitive Development Study (n=5400), and Generation R (n=1905). We included individuals who had phenotypic and genetic data available. We investigated single nucleotide polymorphism heritability and genetic correlations among different subtypes, operationalisations, and reports of childhood maltreatment. Family-based and population-based polygenic score analyses were done to elucidate gene-environment correlation mechanisms. We used genetic correlation and Mendelian randomisation analyses to identify shared genetics and test causal relationships between childhood maltreatment and mental and physical health conditions., Findings: Our meta-analysis of genome-wide association studies (N=185 414) identified 14 independent loci associated with childhood maltreatment (13 novel). We identified high genetic overlap (genetic correlations 0·24-1·00) among different maltreatment operationalisations, subtypes, and reporting methods. Within-family analyses provided some support for active and reactive gene-environment correlation but did not show the absence of passive gene-environment correlation. Robust Mendelian randomisation suggested a potential causal role of childhood maltreatment in depression (unidirectional), as well as both schizophrenia and ADHD (bidirectional), but not in physical health conditions (coronary artery disease, type 2 diabetes) or inflammation (C-reactive protein concentration)., Interpretation: Childhood maltreatment has a heritable component, with substantial genetic correlations among different operationalisations, subtypes, and retrospective and prospective reports of childhood maltreatment. Family-based analyses point to a role of active and reactive gene-environment correlation, with equivocal support for passive correlation. Mendelian randomisation supports a (primarily bidirectional) causal role of childhood maltreatment on mental health, but not on physical health conditions. Our study identifies research avenues to inform the prevention of childhood maltreatment and its long-term effects., Funding: Wellcome Trust, UK Medical Research Council, Horizon 2020, National Institute of Mental Health, and National Institute for Health Research Biomedical Research Centre., (Copyright © 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Importance: Cross-sectional and longitudinal studies have consistently reported associations between childhood trauma and psychotic experiences and disorders. However, few studies have examined whether the age of exposure or specific trauma types are differently associated with the risk of developing psychotic experiences., Objective: To examine whether exposure to trauma, assessed at multiple age periods between 0 and 17 years of age, is associated with an increased risk of psychotic experiences by age 18 years and whether this association varies according to trauma type as well as age and frequency of exposure., Design, Setting, and Participants: This study used data from the Avon Longitudinal Study of Parents and Children, a large population-based birth cohort in the United Kingdom that recruited women who resided in the Avon Health Authority area and had an expected delivery date between April 1, 1991, and December 31, 1992. Data on psychotic experiences were included in the study, along with trauma variables derived from assessments completed by the parents or self-reported by the participants. The variables represent exposure to any trauma type between ages 0 and 17 years; any trauma type within a distinct age period: early childhood (0-4.9 years), middle childhood (5-10.9 years), or adolescence (11-17 years); specific trauma types between ages 0 and 17 years; and specific trauma types within early childhood, middle childhood, or adolescence. Data were analyzed from January 9, 2017, to November 30, 2017., Main Outcomes and Measures: Suspected or definite psychotic experiences were assessed using the psychosis-like symptoms semistructured interview at age 12 years and then at age 18 years., Results: The sample of 4433 participants included 2504 (56.5%) females, with a mean (SD) age of 17.8 (0.38) years. Exposure to any trauma up to age 17 years was associated with increased odds of psychotic experiences at age 18 years (adjusted odds ratio, 2.91; 95% CI, 2.15-3.93). All trauma types from age 0 to 17 years were associated with an increased odds of psychotic experiences. The population-attributable fraction for childhood and adolescent trauma on psychotic experiences at age 18 years was 45% (95% CI, 25%-60%). Effect sizes for most trauma types were greater for exposure that was more proximal to the outcome, although CIs overlapped with those for more distal trauma. Evidence supported dose-response associations for exposure to multiple trauma types and at multiple age periods. In an analysis aimed at minimizing reverse causality, adolescent trauma was also associated with past-year incident psychotic experiences at age 18 years., Conclusions and Relevance: These findings are consistent with the thesis that trauma could have a causal association with psychotic experiences; if so, identification of modifiable mediators is required to inform prevention strategies.