Higher-order genetic and environmental structure of prevalent forms of child and adolescent psychopathology

• Authors: Benjamin B. Lahey, University of Chicago; Carol A. Van Hulle, University of Wisconsin; Amber L. Singh, Indiana University; Irwin Waldman, Emory University; Paul J. Rathouz, University of Chicago
• Journal Title: Archives of General Psychiatry
• Volume: Volume 68, Number 2
• Publisher: American Medical Association (AMA) | 2011-02-01, Pages 181-189
• Type of Work: Article | Final Publisher PDF
• Publisher DOI: http://doi.org/10.1001/archgenpsychiatry.2010.192
• Subjects: Psychology, Developmental; Biology, Genetics
• Keywords: Adolescent; Agoraphobia; Anxiety Disorders; Attention Deficit Disorder with Hyperactivity; Attention Deficit and Disruptive Behavior Disorders; Child; Conduct Disorder; Cross-Sectional Studies; Depressive Disorder, Major; Diseases in Twins; Factor Analysis, Statistical; Female; Genetic Pleiotropy; Genetic Predisposition to Disease; Genetic Variation; Humans; Incidence; Internal-External Control; Male; Mental Disorders; Models, Psychological; Obsessive-Compulsive Disorder; Phenotype; Phobic Disorders; Risk Factors; Social Environment

Abstract

Context: It is necessary to understand the etiologic structure of child and adolescent psychopathology to advance theory and guide future research. Objective: To test alternative models of the higher-order structure of etiologic effects on 11 dimensions of child and adolescent psychopathology using confirmatory factor analyses of genetic and environmental covariances. Design: Representative sample of twins. Setting: Home interviews. Participants: A total of 1571 pairs of 9- to 17-year-old twins. Main Outcome Measures: Structured assessments of psychopathology using adult caregivers and youth as informants. Results: The best-fitting genetic model revealed that most genetic factors nonspecifically influence risk for either all 11 symptom dimensions or for dimensions of psychopathology within 1 of 2 broad domains. With some notable exceptions, dimension-specific genetic influences accounted for modest amounts of variance. Conclusions: To inform theory and guide molecular genetic studies, an etiologic model is offered in which 3 patterns of pleiotropy are hypothesized to be the principal modes of genetic risk transmission for common forms of child and adolescent psychopathology. Some common environmental influences were found, but consistent with a "generalist genes, specialist environments" model, there was little sharing of environmental influences. This implies that prevalent dimensions of child and adolescent psychopathology mostly share their genetic liabilities but are differentiated by nonshared experiences.