Gene-environment interactions explain a substantial portion of variability of common neuropsychiatric disorders.

Cell Rep Med

Committee on Genetics, Genomics and Systems Biology, The University of Chicago, Chicago, IL 60637, USA; Department of Medicine, Institute of Genomics and Systems Biology, The University of Chicago, Chicago, IL 60637, USA; Department of Human Genetics and Committee on Quantitative Methods in Social, Behavioral, and Health Sciences, The University of Chicago, Chicago, IL 60637, USA. Electronic address:

Published: September 2022

In complex diseases, the phenotypic variability can be explained by genetic variation (G), environmental stimuli (E), and interaction of genetic and environmental factors (G-by-E effects), among which the contribution G-by-E remains largely unknown. In this study, we focus on ten major neuropsychiatric disorders using data for 138,383 United States families with 404,475 unique individuals. We show that, while gene-environment interactions account for only a small portion of the total phenotypic variance for a subset of disorders (depression, adjustment disorder, substance abuse), they explain a rather large portion of the phenotypic variation of the remaining disorders: over 20% for migraine and close to or over 30% for anxiety/phobic disorder, attention-deficit/hyperactivity disorder, recurrent headaches, sleep disorders, and post-traumatic stress disorder. In this study, we have incorporated-in the same analysis-clinical data, family pedigrees, the spatial distribution of individuals, their socioeconomic and demographic confounders, and a collection of environmental measurements.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9512674PMC
http://dx.doi.org/10.1016/j.xcrm.2022.100736DOI Listing

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