Does Childhood Adversity Cause Mental Health Problems?
It’s well known that experiencing adverse events in childhood (such as maltreatment, domestic violence, or…

It’s well known that experiencing adverse events in childhood (such as maltreatment, domestic violence, or parental substance abuse) is associated with mental health problems. But, despite decades of research, we still don’t know the extent to which these adverse childhood experiences (ACEs) cause mental health problems.
This confusion arises from the fact that children exposed to ACEs are likely to experience other risk factors for mental health problems, including social factors like poverty, as well as genetic factors. So it’s not clear whether higher rates of mental health problems in individuals who experienced ACEs are due to the adversity per se or to other risks.
It’s understandable that children exposed to ACEs are likely to experience other social risk factors, like poverty. But why might children exposed to adversities have a greater genetic predisposition to mental health problems?

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First, we know that ACEs are more common in families in which parents have mental health problems, and experiencing severe parental mental health problems is also considered to be an ACE. This means that children living in these families may be more likely to inherit a genetic predisposition to mental health problems from their parents and also experience adverse environments.
Second, it’s also possible that children who inherit mental health problems might be responded to in a negative way by their parents. For example, parents may lose their tempers more often with hyperactive children, increasing the likelihood that these children experience shouting or physical discipline.
These are examples of gene-environment correlation, whereby exposure to environmental experiences depends on a person’s genotype. Such gene-environment correlations can mean that the association between ACEs and mental health may be at least partly explained by genetic factors.
In a recent study, we aimed to account for genetics to better understand the environmental impact of ACEs on mental health. To do so, we studied over 11,000 genotyped children taking part in the UK-based Avon Longitudinal Study of Parents and Children or the US-based Adolescent Brain and Cognitive Development Study. To assess ACEs (maltreatment, domestic violence, parental mental health problems, parental substance abuse, parental criminality, and parental separation), we used information from parent and child interviews. We assessed children’s internalising problems (e.g., anxiety and depression), and externalising problems (e.g., ADHD and disruptive behaviours) through parent reports when children were aged 9 or 10 years.
To assess a child’s genetic predisposition to mental health problems, we calculated polygenic risk scores. Polygenic risk scores index a person’s genetic liability for a disorder (e.g., depression) based on the number of genetic risk variants they have for that disorder. We calculated children’s polygenic risk scores for a range of mental health problems, including depression, anxiety, schizophrenia, bipolar disorder, ADHD, autism, antisocial behaviour, and alcohol abuse.
We first examined whether children with a greater genetic predisposition to mental health problems were more likely to experience ACEs. We found that this was the case: children with higher polygenic risk scores for mental health problems (such as depression, ADHD, and schizophrenia) were, on average, slightly more likely to experience ACEs.
Importantly, this doesn’t mean that exposure to ACEs is determined by genes, is the fault of the child, or is not preventable. Rather, the findings suggest that children with a greater genetic predisposition to mental health problems are, on average, slightly more likely to experience ACEs.
This finding is likely to at least partly reflect passive gene-environment correlation, whereby parents with mental health problems pass on this genetic predisposition to their children and provide adverse environments. For example, a parent with depression might transmit genetic risk variants linked to depression to their child and also find it harder to interact with the child.
But despite these genetic influences, it’s important to emphasise that ACEs are also influenced by modifiable social and environmental risk factors and can be effectively prevented through environmental interventions, like parenting support programmes.
We next examined the extent to which any associations between ACEs and mental health might be explained by children’s genetic predisposition to mental health problems. After controlling for polygenic risk scores for mental health problems, we found that ACEs remained associated with mental health problems.
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However, polygenic risk scores aren’t the best way to account for genetic factors because they only partially capture a person’s genetic liability to mental health problems. To address this limitation, we used a new statistical method which estimates associations between environmental factors and outcomes under a scenario in which polygenic risk scores could explain greater genetic liability to mental health problems.
Using this method, we found that genetic factors accounted for at least part of the associations between ACEs and mental health. Notably, though, child maltreatment and parental mental health problems were still associated with child mental health problems, independent of genetic factors. This suggests that the environmental experience of maltreatment and living with a parent with mental health problems could influence children’s mental health.
Our study is not without limitations. First, we examined a narrow set of ACEs, but many other adversities affect children, such as bullying or death of a family member. Second, our study was based on participants with European ancestry, so it’s important to investigate whether the findings generalise to populations with different ancestral backgrounds. Finally, although we examined the role of individual risk factors (e.g., genetic predisposition and ACEs), wider structural inequalities (e.g., poverty) can play an important role in influencing both ACEs and mental health.
Overall, though, our findings can help to inform interventions to help prevent children from developing mental health problems. Because maltreatment and parental mental health problems were associated with children’s mental health problems through environmental pathways, preventing those experiences might help to prevent mental health problems in the population. Therefore, investing in parenting support programmes and effective parental mental health care could not only improve family functioning but also prevent later costly mental health problems.
To prevent children exposed to ACEs from developing mental health problems, accessible mental health support is essential. Because children exposed to ACEs were more likely to have genetic predispositions to mental health problems, therapeutic techniques that address heritable psychiatric vulnerabilities (e.g., through skills-building) could reduce their risk of developing mental health problems.
This post was written by Jessie Baldwin, PhD, Megan Briggs, and Jean-Baptiste Pingault, PhD.