Poster #11 - Adverse childhood experiences and mental health: A genetically informed Registered Report

• In Event: Poster Session 04

Abstract

Background: Children who experience adversities have an elevated risk of developing mental health problems. However, the extent to which adverse childhood experiences (ACEs) cause mental health problems remains unclear, as previously observed associations may partly reflect genetic confounding. In this Registered Report, we investigated gene-environment correlations and genetic confounding of the associations between ACEs and mental health.

Methods: Participants included over 11,000 children from the Avon Longitudinal Study of Parents and Children (ALSPAC) in the UK and the Adolescent Brain and Cognitive Development (ABCD) Study in the USA. ACEs (including maltreatment, domestic violence, and parental psychopathology, parental substance abuse, parental criminality, and parental separation) were prospectively measured through parent reports in childhood. Internalizing and externalizing problems at age 9/10 were assessed through parent reports. To index genetic liability to mental health problems, we derived polygenic scores for a range of psychiatric disorders.

Results: Regarding gene-environment correlations, children with higher polygenic scores for mental health problems had a small increase in odds for ACEs (pooled odds ratio=1.07, 95% CI=1.03-1.10). In contrast, negative control polygenic scores (for handedness and cataracts) were not associated with exposure to ACEs (pooled odds ratio=1.00, 95% CI=0.96-1.04). Regarding genetic confounding, polygenic scores for mental health problems explained on average, 3-5% of the associations between ACEs and internalising problems and 5-6% of the associations between ACEs and externalising problems. However, these results likely under-estimate the magnitude of genetic confounding as polygenic scores for mental health problems only capture a very small amount of heritability in internalising and externalising outcomes. To address this, we conducted a genetic sensitivity analysis using latent polygenic scores capturing SNP heritability in internalising and externalising problems (6% and 9%, respectively). This sensitivity analysis suggested that genetic confounding accounted for a large average proportion (>60%) of the associations between ACEs with internalising and externalising problems, in both cohorts. Notably though, some individual ACEs (e.g., childhood maltreatment, parental mental illness) remained associated with mental health problems independent of genetic confounding.

Discussion: Children at higher genetic risk of psychopathology are more vulnerable to experiencing adversities. Future family-based research is needed to understand whether such gene-environment correlations are passive or evocative in nature. Furthermore, our findings suggest that elevated risk of mental health problems in children exposed to ACEs is at least partially due to pre-existing genetic risk. Therefore, in addition to preventing ACEs, interventions should address heritable vulnerabilities in children exposed to adversity to reduce their risk of psychopathology.

Authors

• Jessie R Baldwin, University College London (UCL)
  Presenting Author

• Jean-Baptiste Pingault