Childhood trauma and subclinical hypomania in early adulthood: a genetically informative study

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Abstract

Background: There is preliminary evidence that childhood trauma (e.g., abuse) is associated with subclinical hypomania reported in adolescence. These findings need replicating in early adulthood, as clinical conditions emerge, and the mechanisms underlying this association need elucidating. This study aimed to examine the magnitude of shared genetic and environmental underpinnings of the association between childhood trauma with hypomanic symptoms and high-risk status for bipolar disorder (BD) using a twin design. Gene-environment correlations and interactions between childhood trauma and polygenic scores (PGS) for psychiatric and neurodevelopmental conditions were also investigated.Method: Childhood trauma was reported using the Avon ‘Life at 22+’ questionnaire by 8,464 individuals from a community twin sample. Self-reported hypomanic symptoms were assessed using the Mood Disorder Questionnaire at age 26 by 7,748 participants. PGS for psychiatric and neurodevelopment conditions were derived from independent published discovery samples. Results: Childhood trauma was significantly associated with hypomanic symptoms (β=0.23, 95% CI: 0.20–0.25) and being at high-risk for BD (OR=1.77, 95% CI: 1.59–1.98). These associations were strongly influenced by genetic factors (bivariate heritabilities range: 0.51–0.90). Gene-environment correlations were found between childhood trauma and the PGS for six conditions: Major Depressive Disorder (MDD), schizophrenia, Attention Deficit Hyperactivity Disorder, anxiety disorders, Post-Traumatic Stress Disorder, and BD II (β range=-0.19–0.11). The MDD-PGS was found to significantly interact with childhood trauma in hypomania (β=0.01, p<.05). Conclusion: The associations between childhood trauma and subclinical hypomania and high-risk for BD were partially attributed to shared genetic factors. These associations were also moderated by MDD-PGS. Gene-environment correlations were detected between childhood trauma polygenic vulnerability to psychiatric and neurodevelopmental conditions. The aetiology of hypomania and BD is likely the result of a confluence of genetic and environmental factors, and research in this area should account for potential genetic confounding.

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