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Background and Hypothesis Children exposed to socioenvironmental adversities (eg, urbanicity, pollution, neighborhood deprivation, crime, and family disadvantage) are more likely to subsequently develop subclinical psychotic experiences during adolescence (eg, hearing voices, paranoia). However, the pathways through which this occurs have not been previously investigated. We hypothesized that cognitive ability and inflammation would partly explain this association. Study Design Data were utilized from the Environmental-Risk Longitudinal Twin Study, a cohort of 2232 children born in 1994–1995 in England and Wales and followed to age 18. Socioenvironmental adversities were measured from birth to age 10 and classified into physical risk (defined by high urbanicity and air pollution) and socioeconomic risk (defined by high neighborhood deprivation, neighborhood disorder, and family disadvantage). Cognitive abilities (overall, crystallized, fluid, and working memory) were assessed at age 12; and inflammatory markers (C-reactive protein, interleukin-6, soluble urokinase plasminogen activator receptor) were measured at age 18 from blood samples. Participants were interviewed at age 18 regarding psychotic experiences. Study Results Higher physical risk and socioeconomic risk were associated with increased odds of psychotic experiences in adolescence. The largest mediation pathways were from socioeconomic risk via overall cognitive ability and crystallized ability, which accounted for ~11% and ~19% of the association with psychotic experiences, respectively. No statistically significant pathways were found via inflammatory markers in exploratory (partially cross-sectional) analyses. Conclusions Cognitive ability, especially crystallized ability, may partly explain the association between childhood socioenvironmental adversity and adolescent psychotic experiences. Interventions to support cognitive development among children living in disadvantaged settings could buffer them against developing subclinical psychotic phenomena.

Exposure to childhood victimisation (i.e. abuse, neglect, domestic violence or bullying) can detrimentally impact later psychosocial adjustment. However, this is not the case for all victimised children; some do well despite their experiences and are considered to be resilient. Understanding the factors associated with such resilience is important to inform interventions to support better psychosocial outcomes among victimised children. This review provides an overview of the extant research examining resilience factors for psychosocial outcomes during the transition to adulthood following exposure to childhood victimisation. Studies were identified through a systematic literature search of Embase, PsychINFO and Ovid MEDLINE databases. The 26 included studies spanned a range of psychosocial outcomes between ages 18–25, including education and work, housing and independent living, criminal behaviour, victimisation, and social and psychological adjustment. For each outcome, a variety of putative resilience factors had been investigated including those related to the individual, their family and the wider community within which they lived. However, because few studies had comparable resilience factors and psychosocial outcomes, it is difficult to draw conclusions about which factors are consistently associated with resilience to a particular psychosocial outcome. Additionally, this review revealed that the included studies were of variable methodological quality – many were limited by cross-sectional designs with retrospective self-reports of childhood victimisation, and convenience or unrepresentative samples. In this review, we also highlight gaps in knowledge about the co-occurring impact of multiple resilience factors in combination and the need for studies conducted in non-Western and low- and middle-income countries.

BackgroundGrowing evidence suggests that air pollution exposure may adversely affect the brain and increase risk for psychiatric disorders such as schizophrenia and depression. However, little is known about the potential role of air pollution in severity and relapse following illness onset.AimsTo examine the longitudinal association between residential air pollution exposure and mental health service use (an indicator of illness severity and relapse) among individuals with first presentations of psychotic and mood disorders.MethodWe identified individuals aged ≥15 years who had first contact with the South London and Maudsley NHS Foundation Trust for psychotic and mood disorders in 2008–2012 (n = 13 887). High-resolution (20 × 20 m) estimates of nitrogen dioxide (NO2), nitrogen oxides (NOx) and particulate matter (PM2.5 and PM10) levels in ambient air were linked to residential addresses. In-patient days and community mental health service (CMHS) events were recorded over 1-year and 7-year follow-up periods.ResultsFollowing covariate adjustment, interquartile range increases in NO2, NOx and PM2.5 were associated with 18% (95% CI 5–34%), 18% (95% CI 5–34%) and 11% (95% CI 3–19%) increased risk for in-patient days after 1 year. Similarly, interquartile range increases in NO2, NOx, PM2.5 and PM10 were associated with 32% (95% CI 25–38%), 31% (95% CI 24–37%), 7% (95% CI 4–11%) and 9% (95% CI 5–14%) increased risk for CMHS events after 1 year. Associations persisted after 7 years.ConclusionsResidential air pollution exposure is associated with increased mental health service use among people recently diagnosed with psychotic and mood disorders. Assuming causality, interventions to reduce air pollution exposure could improve mental health prognoses and reduce healthcare costs.

Depression and psychosis are often comorbid; they also have overlapping genetic and environmental risk factors, including trauma and area-level exposures. The present study aimed to advance understanding of this comorbidity via a network approach, by (1) identifying bridge nodes that connect clusters of lifetime depression and psychosis symptoms and (2) evaluating the influence of polygenic and environmental risk factors in these symptoms. This study included data from European ancestry participants in UK Biobank, a large population-based sample (N = 77,650). In Step 1, a network model identified bridge nodes between lifetime symptoms of depression and psychosis and functional impairment. In Step 2, genetic and environmental risk factors were incorporated to examine the degree to which symptoms associated with polygenic risk scores for depression and schizophrenia, lifetime exposure to trauma and area-level factors (including deprivation, air pollution and greenspace). Feelings of worthlessness, beliefs in unreal conspiracy against oneself, depression impairment and psychosis impairment emerged as bridges between depression and psychosis symptoms. Polygenic risk scores for depression and schizophrenia were predominantly linked with depression and psychosis impairment, respectively, rather than with specific symptoms. Cumulative trauma emerged as a bridge node associating deprivation with feelings of worthlessness and beliefs in unreal conspiracy, indicating that the experience of trauma is prominently linked with the co-occurrence of depression and psychosis symptoms related to negative views of oneself and others. These key symptoms and risk factors provide insights into the lifetime co-occurrence of depression and psychosis.

BACKGROUND AND AIM: Air pollution exposure has been shown to damage the brain but its associations with the development of psychopathology are not fully characterized. This study tested whether ear...

Key Points Question Is exposure to outdoor air pollution in childhood and adolescence associated with the development of psychopathology at the transition to adulthood? Findings In this cohort study of 2039 UK-born children followed up for 2 decades, early-life exposure to nitrogen oxides was significantly associated with general psychopathology at 18 years of age, representing greater internalizing, externalizing, and thought disorder symptoms. The associations were not attributable to individual or family-level factors or to disadvantageous neighborhood characteristics. Meaning These findings suggest that exposure to nitrogen oxides in early life may be a nonspecific risk factor for the development of psychopathology as young people begin the transition to adulthood., Importance Air pollution exposure damages the brain, but its associations with the development of psychopathology are not fully characterized. Objective To assess whether air pollution exposure in childhood and adolescence is associated with greater psychopathology at 18 years of age. Design, Setting, and Participants The Environmental-Risk Longitudinal Twin Study is a population-based cohort study of 2232 children born from January 1, 1994, to December 4, 1995, across England and Wales and followed up to 18 years of age. Pollution data generation was completed on April 22, 2020; data were analyzed from April 27 to July 31, 2020. Exposures High-resolution annualized estimates of outdoor nitrogen oxides (NOx) and particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5) linked to home addresses at the ages of 10 and 18 years and then averaged. Main Outcomes and Measures Mental health disorder symptoms assessed through structured interview at 18 years of age and transformed through confirmatory factor analysis into continuous measures of general psychopathology (primary outcome) and internalizing, externalizing, and thought disorder symptoms (secondary outcomes) standardized to a mean (SD) of 100 (15). Hypotheses were formulated after data collection, and analyses were preregistered. Results A total of 2039 participants (1070 [52.5%] female) had full data available. After adjustment for family and individual factors, each interquartile range increment increase in NOx exposure was associated with a 1.40-point increase (95% CI, 0.41-2.38; P = .005) in general psychopathology. There was no association between continuously measured PM2.5 and general psychopathology (b = 0.45; 95% CI, −0.26 to 1.11; P = .22); however, those in the highest quartile of PM2.5 exposure scored 2.04 points higher (95% CI, 0.36-3.72; P = .02) than those in the bottom 3 quartiles. Copollutant models, including both NOx and PM2.5, implicated NOx alone in these significant findings. NOx exposure was associated with all secondary outcomes, although associations were weakest for internalizing (adjusted b = 1.07; 95% CI, 0.10-2.04; P = .03), medium for externalizing (adjusted b = 1.42; 95% CI, 0.53-2.31; P = .002), and strongest for thought disorder symptoms (adjusted b = 1.54; 95% CI, 0.50-2.57; P = .004). Despite NOx concentrations being highest in neighborhoods with worse physical, social, and economic conditions, adjusting estimates for neighborhood characteristics did not change the results. Conclusions and Relevance Youths exposed to higher levels of outdoor NOx experienced greater psychopathology at the transition to adulthood. Air pollution may be a nonspecific risk factor for the development of psychopathology., This cohort study examines the association between exposure to outdoor air pollution in childhood and adolescence with the development of psychopathology at the transition to adulthood.

Knowledge about early risk factors for major depressive disorder (MDD) is critical to identify those who are at high risk. A multivariable model to predict adolescents' individual risk of future MDD has recently been developed however its performance in a UK sample was far from perfect. Given the potential role of air pollution in the aetiology of depression, we investigate whether including childhood exposure to air pollution as an additional predictor in the risk prediction model improves the identification of UK adolescents who are at greatest risk for developing MDD. We used data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative UK birth cohort of 2232 children followed to age 18 with 93% retention. Annual exposure to four pollutants - nitrogen dioxide (NO2), nitrogen oxides (NOX), particulate matter

Importance: DNA methylation has been proposed as an epigenetic mechanism by which the childhood neighborhood environment may influence the genome to compromise adult health.Objective: To de...

BackgroundAssociations of socioenvironmental features like urbanicity and neighborhood deprivation with psychosis are well-established. An enduring question, however, is whether these associations are causal. Genetic confounding could occur due to downward mobility of individuals at high genetic risk for psychiatric problems into disadvantaged environments.MethodsWe examined correlations of five indices of genetic risk [polygenic risk scores (PRS) for schizophrenia and depression, maternal psychotic symptoms, family psychiatric history, and zygosity-based latent genetic risk] with multiple area-, neighborhood-, and family-level risks during upbringing. Data were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 British twins born in 1994–1995 and followed to age 18 (93% retention). Socioenvironmental risks included urbanicity, air pollution, neighborhood deprivation, neighborhood crime, neighborhood disorder, social cohesion, residential mobility, family poverty, and a cumulative environmental risk scale. At age 18, participants were privately interviewed about psychotic experiences.ResultsHigher genetic risk on all indices was associated with riskier environments during upbringing. For example, participants with higher schizophrenia PRS (OR = 1.19, 95% CI = 1.06–1.33), depression PRS (OR = 1.20, 95% CI = 1.08–1.34), family history (OR = 1.25, 95% CI = 1.11–1.40), and latent genetic risk (OR = 1.21, 95% CI = 1.07–1.38) had accumulated more socioenvironmental risks for schizophrenia by age 18. However, associations between socioenvironmental risks and psychotic experiences mostly remained significant after covariate adjustment for genetic risk.ConclusionGenetic risk is correlated with socioenvironmental risk for schizophrenia during upbringing, but the associations between socioenvironmental risk and adolescent psychotic experiences appear, at present, to exist above and beyond this gene-environment correlation.

PurposeGrowing evidence suggests that prospective informant-reports and retrospective self-reports of childhood maltreatment may be differentially associated with adult psychopathology. However, it remains unknown how associations for these two maltreatment reporting types compare when considering functional outcomes. The present study compared associations between childhood maltreatment and functional outcomes at age 18 years using these two methods.MethodsWe used data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative birth cohort of 2232 children born in England and Wales in 1994–1995. Maltreatment prior to age 12 years was assessed prospectively (during multiple home visits between birth and age of 12 years based on interviews with caregivers, researcher observations, and information from practitioners where child protection referrals were made) and retrospectively (at age 18 via self-report on the Childhood Trauma Questionnaire). Nine functional outcomes were measured at age 18, forming two variables capturing: (i) psychosocial and (ii) vocational disadvantage.ResultsAmong the 2054 participants with available data, childhood maltreatment was associated with poorer functional outcomes regardless of whether this was reported only prospectively, only retrospectively, or both. Stronger associations with psychosocial disadvantage arose in the context of retrospective recall by participants (OR = 8.25, 95% CI 4.93–13.82) than prospective reports by informants (OR = 2.03, 95% CI 1.36–3.04) of maltreatment. Conversely, associations with vocational disadvantage were comparable for both prospective informant-reports (OR = 2.19, 95% CI 1.42–3.38) and retrospective self-reports (OR = 1.93, 95% CI 1.33–2.81) of maltreatment.ConclusionResults highlight the importance of considering the maltreatment report type used when interpreting the functional consequences of childhood maltreatment.

This cohort study traces the biological responses and associated phenotypes of an upbringing in a socially and economically disadvantaged environment., Key Points Question Is childhood neighborhood disadvantage associated with differential DNA methylation? Findings In this cohort study of 1619 children in Great Britain, exposure to neighborhood socioeconomic disadvantage during childhood was associated with differential DNA methylation at age 18 years in genes involved in inflammation, exposure to tobacco smoke, and metabolism of toxic air pollutants. Meaning The study found that children who were raised in socioeconomically disadvantaged neighborhoods appeared to enter young adulthood epigenetically distinct from their more advantaged peers., Importance DNA methylation has been proposed as an epigenetic mechanism by which the childhood neighborhood environment may have implications for the genome that compromise adult health. Objective To ascertain whether childhood neighborhood socioeconomic disadvantage is associated with differences in DNA methylation by age 18 years. Design, Setting, and Participants This longitudinal cohort study analyzed data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative birth cohort of children born between 1994 and 1995 in England and Wales and followed up from age 5 to 18 years. Data analysis was performed from March 15, 2019, to June 30, 2019. Exposures High-resolution neighborhood data (indexing deprivation, dilapidation, disconnection, and dangerousness) collected across childhood. Main Outcomes and Measures DNA methylation in whole blood was drawn at age 18 years. Associations between neighborhood socioeconomic disadvantage and methylation were tested using 3 prespecified approaches: (1) testing probes annotated to candidate genes involved in biological responses to growing up in socioeconomically disadvantaged neighborhoods and investigated in previous epigenetic research (stress reactivity–related and inflammation-related genes), (2) polyepigenetic scores indexing differential methylation in phenotypes associated with growing up in disadvantaged neighborhoods (obesity, inflammation, and smoking), and (3) a theory-free epigenome-wide association study. Results A total of 1619 participants (806 female individuals [50%]) had complete neighborhood and DNA methylation data. Children raised in socioeconomically disadvantaged neighborhoods exhibited differential DNA methylation in genes involved in inflammation (β = 0.12; 95% CI, 0.06-0.19; P

Background Associations of environmental exposures such as urban upbringing, deprivation and crime victimization with psychosis are well-established. An enduring question, however, is whether associations reflect a causal process. Emerging evidence using polygenic risk scores (PRS) suggests reverse causation, with adults at higher genetic risk for schizophrenia being more likely to live in crowded and deprived areas. This process could occur due to the downward mobility of individuals at higher genetic risk for schizophrenia into more disadvantaged environments. However, the handful of studies on this topic to date have typically focused on environmental conditions during adulthood and have typically examined only macro-level environmental features (e.g., urbanicity). Methods We examined associations between two measures of genetic risk (PRS for schizophrenia and family psychiatric history) with multiple features of children’s family-, neighborhood-, and wider- environments during upbringing. Data were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2,232 British twins born in 1994–1995 and followed to age 18 (with 93% retention). Environmental risk factors were measured from early childhood to late adolescence, and included urbanicity, air pollution, neighborhood deprivation, neighborhood crime, neighborhood disorder, social cohesion, family poverty, residential mobility, and crime victimization. At age 18, participants were privately interviewed about psychotic experiences (e.g., hallucinations and delusions) occurring since age 12. Results Children with higher schizophrenia PRS and a greater family psychiatric history were exposed to a wide range of riskier environments during upbringing. For schizophrenia PRS, associations were significant at p Discussion Consistent with a degree of reverse causation, we found that children with higher genetic risk for schizophrenia also experienced riskier environments during upbringing. In particular, children at higher genetic risk were more likely to grow up in dangerous neighborhoods, poorer families, and move houses more frequently across childhood. However, genetic risk for schizophrenia (using polygenic risk scores and family psychiatric history) does not appear to confound associations of environmental risks with early expressions of psychosis. Nevertheless, future research into environmental conditions and psychosis should acknowledge and ideally examine the possibility of reverse-causation due to the downward mobility of individuals at higher genetic risk for schizophrenia into riskier environments.

Objective: To investigate associations between the characteristics of the neighbourhoods young adults live in and their feelings of loneliness, using data from different sources.Method: Data were drawn from the Environmental Risk Longitudinal Twin Study. Loneliness was measured via self-reports at ages 12 and 18, and also by interviewer ratings at age 18. Neighbourhood characteristics were assessed between ages 12 and 18 via government data, systematic social observations, a resident survey, and participants’ self-reports.Results: Greater loneliness was associated with perceptions of lower collective efficacy and greater neighbourhood disorder, but not with more objective measures of neighbourhood characteristics. Lonelier individuals perceived the collective efficacy of their neighbourhoods to be lower than did their less lonely siblings who lived at the same address.Conclusion: These findings suggest that feelings of loneliness are associated with negatively-biased perceptions of neighbourhood characteristics, which may have implications for lonely individuals’ likelihood of escaping loneliness.Keywords: loneliness, social isolation, neighbourhood, collective efficacy, social cohesion

Importance Childhood maltreatment is associated with mental illness. Researchers, clinicians, and public health professionals use prospective or retrospective measures interchangeably to assess childhood maltreatment, assuming that the 2 measures identify the same individuals. However, this assumption has not been comprehensively tested. Objective To meta-analyze the agreement between prospective and retrospective measures of childhood maltreatment. Data Sources MEDLINE, PsycINFO, Embase, and Sociological Abstracts were searched for peer-reviewed, English-language articles from inception through January 1, 2018. Search terms included child* maltreatment, child* abuse, child* neglect, child bull*, child* trauma, child* advers*, and early life stress combined with prospective* and cohort. Study Selection Studies with prospective measures of childhood maltreatment were first selected. Among the selected studies, those with corresponding retrospective measures of maltreatment were identified. Of 450 studies with prospective measures of childhood maltreatment, 16 had paired retrospective data to compute the Cohen κ coefficient. Data Extraction and Synthesis Multiple investigators independently extracted data according to PRISMA and MOOSE guidelines. Random-effects meta-analyses were used to pool the results and test predictors of heterogeneity. Main Outcomes and Measures The primary outcome was the agreement between prospective and retrospective measures of childhood maltreatment, expressed as a κ coefficient. Moderators of agreement were selected a priori and included the measure used for prospective or retrospective assessment of childhood maltreatment, age at retrospective report, sample size, sex distribution, and study quality. Results Sixteen unique studies including 25 471 unique participants (52.4% female [SD, 10.6%]; mean [SD] age, 30.6 [11.6] years) contained data on the agreement between prospective and retrospective measures of childhood maltreatment. The agreement between prospective and retrospective measures of childhood maltreatment was poor, with κ = 0.19 (95% CI, 0.14-0.24; P

Adolescent psychotic experiences increase risk for schizophrenia and other severe psychopathology in adulthood. Converging evidence implicates urban and adverse neighborhood conditions in the etiology of adolescent psychotic experiences, but the role of young people's personal perceptions of disorder (i.e., physical and social signs of threat) in their neighborhood is unknown. This was examined using data from the Environmental Risk Longitudinal Twin Study, a nationally representative birth cohort of 2,232 British twins. Participants were interviewed at age 18 about psychotic phenomena and perceptions of disorder in the neighborhood. Multilevel, longitudinal, and genetically sensitive analyses investigated the association between perceptions of neighborhood disorder and adolescent psychotic experiences. Adolescents who perceived higher levels of neighborhood disorder were significantly more likely to have psychotic experiences, even after accounting for objectively/independently measured levels of crime and disorder, neighborhood- and family-level socioeconomic status, family psychiatric history, adolescent substance and mood problems, and childhood psychotic symptoms: odds ratio = 1.62, 95% confidence interval [1.27, 2.05], p < .001. The phenotypic overlap between adolescent psychotic experiences and perceptions of neighborhood disorder was explained by overlapping common environmental influences, rC = .88, 95% confidence interval [0.26, 1.00]. Findings suggest that early psychological interventions to prevent adolescent psychotic experiences should explore the role of young people's (potentially modifiable) perceptions of threatening neighborhood conditions.