Association between genetic and socioenvironmental risk for schizophrenia during upbringing in a UK longitudinal cohort

BACKGROUND: Associations 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. METHODS: We 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. RESULTS: Higher 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. CONCLUSION: Genetic 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

Mental health context of food insecurity:a representative cohort of families with young children

International audienceOBJECTIVE: Children from food-insecure families (ie, families that lack access to sufficient, safe, and nutritious food) are at risk for developmental problems. Food insecurity disproportionately occurs among low-socioeconomic status (SES) and low-income families; however, interventions that supplement families' income or diet have not eradicated food insecurity. This may be because food insecurity is also related to nonfinancial factors such as the presence of maternal mental health problems. To clarify whether addressing mothers' mental health problems may be a promising strategy for reducing the burden of food insecurity, we tested the hypothesis that low-SES families are especially vulnerable to food insecurity when the mother experiences depression, alcohol or drug abuse, psychosis spectrum disorder, or domestic violence. METHODS: We used data from a nationally representative cohort of 1116 British families (the Environmental Risk Longitudinal Study). Food insecurity, family SES, maternal mental health and exposure to domestic violence, and children's behavioral outcomes were measured by using validated methods. RESULTS: Overall, 9.7% of study families were food-insecure. Among low-SES families, controlling for income variation, food insecurity co-occurred with maternal depression (odds ratio [OR]: 2.82 [95% confidence interval (CI): 1.62-4.93]), psychosis spectrum disorder (OR: 4.01 [95% CI: 2.03-7.94]), and domestic violence (OR: 2.36 [95% CI: 1.18-4.73]). In addition, food insecurity predicted elevated rates of children's behavior problems. CONCLUSIONS: Among families with young children, food insecurity is frequent, particularly when the mother experiences mental health problems. This suggests that interventions that improve women's mental health may also contribute to decreasing the burden of food insecurity and its impact on the next generation

Mothers and Children as Informants of Bullying Victimization: Results from an Epidemiological Cohort of Children

Stressful events early in life can affect children’s mental health problems. Collecting valid and reliable information about children’s bad experiences is important for research and clinical purposes. This study aimed to (1) investigate whether mothers and children provide valid reports of bullying victimization, (2) examine the inter-rater reliability between the two informants, (3) test the predictive validity of their reports with children’s emotional and behavioral problems and (4) compare the genetic and environmental etiology of bullying victimization as reported by mothers and children. We assessed bullying victimization in the Environmental-Risk (E-Risk) Longitudinal Twin Study, a nationally-representative sample of 1,116 families with twins. We collected reports from mothers and children during private interviews, including detailed narratives. Findings showed that we can rely on mothers and children as informants of bullying victimization: both informants provided information which adhered to the definition of bullying as involving repeated hurtful actions between peers in the presence of a power imbalance. Although mothers and children modestly agreed with each other about who was bullied during primary and secondary school, reports of bullying victimization from both informants were similarly associated with children’s emotional and behavioral problems and provided similar estimates of genetic and environmental influences. Findings from this study suggest that collecting information from multiple informants is ideal to capture all instances of bullying victimization. However, in the absence of child self-reports, mothers can be considered as a viable alternative, and vice versa

Socioenvironmental Adversity and Adolescent Psychotic Experiences: Exploring Potential Mechanisms in a UK Longitudinal Cohort

Background and hypothesisChildren 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 designData 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 resultsHigher 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.ConclusionsCognitive 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

Association between relative age at school and persistence of attention-deficit hyperactivity disorder in prospective studies: an individual participant data meta-analysis

Background The youngest children in a school class are more likely than the oldest to be diagnosed with ADHD, but this relative age effect is less frequent in older than in younger school-grade children. However, no study has explored the association between relative age and the persistence of ADHD diagnosis at older ages. We aimed to quantify the association between relative age and persistence of ADHD at older ages. Methods For this meta-analysis, we searched MEDLINE, Embase, CINAHL, PsycINFO, and PubPsych up to April 1, 2022, with terms related to “cohort” and “ADHD” with no date, publication type, or language restrictions. We gathered individual participant data from prospective cohorts that included at least ten children identified with ADHD before age 10 years. ADHD was defined by either a clinical diagnosis or symptoms exceeding clinical cutoffs. Relative age was recorded as the month of birth in relation to the school-entry cutoff date. Study authors were invited to share raw data or to apply a script to analyse data locally and generate anonymised results. Our outcome was ADHD status at a diagnostic reassessment, conducted at least 4 years after the initial assessment and after age 10 years. No information on sex, gender, or ethnicity was collected. We did a two-stage random-effects individual participant data meta-analysis to assess the association of relative age with persistence of ADHD at follow-up. This study was registered with PROSPERO, CRD42020212650. Findings Of 33 119 studies generated by our search, we identified 130 eligible unique studies and were able to gather individual participant data from 57 prospective studies following up 6504 children with ADHD. After exclusion of 16 studies in regions with a flexible school entry system that did not allow confident linkage of birthdate to relative age, the primary analysis included 41 studies in 15 countries following up 4708 children for a period of 4 to 33 years. We found that younger relative age was not statistically significantly associated with ADHD persistence at follow-up (odds ratio 1·02, 95% CI 0·99–1·06; p=0·19). We observed statistically significant heterogeneity in our model (Q=75·82, p=0·0011, I2=45%). Participant-level sensitivity analyses showed similar results in cohorts with a robust relative age effect at baseline and when restricting to cohorts involving children with a clinical diagnosis of ADHD or with a follow-up duration of more than 10 years. Interpretation The diagnosis of ADHD in younger children in a class is no more likely to be disconfirmed over time than that of older children in the class. One interpretation is that the relative age effect decreases the likelihood of children of older relative age receiving a diagnosis of ADHD, and another is that assigning a diagnostic label of ADHD leads to unexplored carryover effects of the initial diagnosis that persist over time. Future studies should be conducted to explore these interpretations further