Given the importance of early childhood in psychopathology, identification of social and biological mechanisms of cognitive and psychological development in preadolescence is essential for better diagnostics and therapeutics.
To examine causal relationships among genotypes, negative and positive environments, cognitive outcomes, and psychotic-like experiences in preadolescents.
This cross-sectional study evaluated baseline samples of the ongoing Adolescent Brain Cognitive Development (ABCD) Study. Data were collected from September 2016 to February 2020.
A multicenter (21 research sites) epidemiological study in the US.
In total, 7,632 multiethnic children (9-10 years old) in the US (European 77.37%, African 14.77%, Native American 3.52%, East Asian 1.32%, not specified 3.01%).
Main Outcome(s) and Measure(s)
Genome-wide polygenic scores of cognitive performance (CP GPS) and education attainment (EA GPS), Area Deprivation Index, years of residence, neighborhood poverty level, parenting behavior, school environment, NIH Toolbox Intelligence, and PQ-BC psychotic-like experiences.
Our main analyses were based on 5,902 European ancestry samples (females 46.76%, mean age 118.99 [SD 7.46]). Higher intelligence and less psychotic-like experiences were significantly associated with higher CP and EA GPS (Intelligence: all β> 0.0747, p<0.0001; Psychotic-like experiences: all β< -0.0326, p=0.0169), lower Area Deprivation Index (Intelligence: all β< -0.0489, p=0.0187; Psychotic-like experiences: all β> 0.0496, p=0.0258), higher supportive parenting behavior of the first caregiver (Psychotic-like experiences: all β< -0.0588, p<0.0001), and positive school environment (Intelligence: all β> 0.0348, p=0.0111; Psychotic-like experiences: all β< -0.0540, p=0.0008). In path modeling, intelligence significantly mediated the effects of cognitive capacity GPS (β=-0.0493, 95% CI=-0.0708∼-0.0386), residential disadvantage (β=0.0170, 95% CI=0.0105∼0.0279), and positive family and school environment (β=-0.0088, 95% CI=-0.0170∼-0.0044) on the risk of psychosis.
Conclusions and Relevance
Our results support that impoverished cognition during development significantly mediates the impact of genetic and environmental variables on greater psychotic-like experiences. These findings underscore the utility of data-driven precision intervention and policies targeting family, school, and neighborhood environments for young children to promote cognitive development and lower the risk for psychopathology.
What are the causal relationships among genes, the environment, intelligence, and psychotic-like experiences in neurocognitive development?
In this study of 7,632 multiethnic children (5,905 of European ancestry) aged 9-10 years, greater psychotic-like experiences were causally linked to lower genetic loadings of cognitive capacity, higher residential disadvantage, a lack of supportive parenting behavior, and a hostile school environment through impoverished cognitive development.
Improving family, school, and neighborhood environments can promote the cognitive and psychological development of preadolescents.
Identifying the social and biological mechanisms of cognitive and psychological development of children is essential for optimizing preventive and educational efforts. However, the causal pathways by which genetic and environmental factors affect cognitive and psychiatric outcomes remain unknown, especially in early childhood. We examined the causal relationships among genes, the environment, intelligence, and psychotic-like experiences in 7,632 multiethnic (5,905 with European ancestry) children aged 9-10 years old from the Adolescent Brain Cognitive Development (ABCD) Study. Using up-to-date computational causal analysis and rigorous path modeling, we found a significant causal influence of residential, family, and school environments and genome-wide polygenic scores of cognitive capacities on preadolescents’ psychotic-like experiences mediated by intelligence. Mitigation of good parenting behavior and positive school environments on psychotic-like experiences dominated the pernicious effects of genetic and residential adversities. Our findings support that intelligence may be a biological resilience factor for psychosis. To the best of our knowledge, this is the first study to identify casual trajectories of neurocognitive development in early childhood and the first to provide empirical evidence that positive parenting behavior and school environment can impose a considerable degree of causal impact on children’s cognitive and psychiatric outcomes. We suggest the implementation of socioeconomic policies to improve family and school environments and promote local economic development to enhance children’s cognitive ability and mental health.