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Childhood quality influences genetic sensitivity to environmental influences across adulthood: A life-course Gene × Environment interaction study

  • Robert Keers (a1) and Michael Pluess (a1)

While environmental adversity has been shown to increase risk for psychopathology, individuals differ in their sensitivity to these effects. Both genes and childhood experiences are thought to influence sensitivity to the environment, and these factors may operate synergistically such that the effects of childhood experiences on later sensitivity are greater in individuals who are more genetically sensitive. In line with this hypothesis, several recent studies have reported a significant three-way interaction (Gene × Environment × Environment) between two candidate genes and childhood and adult environment on adult psychopathology. We aimed to replicate and extend these findings in a large, prospective multiwave longitudinal study using a polygenic score of environmental sensitivity and objectively measured childhood and adult material environmental quality. We found evidence for both Environment × Environment and Gene × Environment × Environment effects on psychological distress. Children with a poor-quality material environment were more sensitive to the negative effects of a poor environment as adults, reporting significantly higher psychological distress scores. These effects were further moderated by a polygenic score of environmental sensitivity. Genetically sensitive children were more vulnerable to adversity as adults, if they had experienced a poor childhood environment but were significantly less vulnerable if their childhood environment was positive. These findings are in line with the differential susceptibility hypothesis and suggest that a life course approach is necessary to elucidate the role of Gene × Environment in the development of mental illnesses.

Corresponding author
Address correspondence and reprint requests to: Michael Pluess, Department of Biological and Experimental Psychology, School of Biological and Chemical Sciences, Queen Mary University of London, Mile End Road, London E1 4NS, UK; E-mail:
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This work made use of data and samples generated by the 1958 Birth Cohort (National Child Development Study), which is managed by the Centre for Longitudinal Studies at the University College London Institute of Education, funded by Economic and Social Research Council Grant ES/M001660/1. Access to these resources was enabled via the 58READIE Project funded by Wellcome Trust and Medical Research Council Grant WT095219MA and G1001799. A full list of the financial, institutional, and personal contributions to the development of the 1958 Birth Cohort Biomedical resource is available at Genotyping was undertaken as part of the Wellcome Trust Case-Control Consortium under Wellcome Trust Award 076113, and a full list of the investigators who contributed to the generation of the data is available at Dr. Keers was supported by MRC Population Health Scientist Award MR/K021281/1. We are grateful to the Centre for Longitudinal Studies, Institute of Education, for the use of these data and to the UK Data Service for making them available. However, neither Centre for Longitudinal Studies nor the UK Data Service bears any responsibility for the analysis or interpretation of these data.

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