Coaction of stress and serotonin transporter genotype in predicting aggression at the transition to adulthood

• Type of Material: Article
• Authors: Christopher Callahan Conway, University of California, Los Angeles; Danielle Keenan-Miller, Jane & Terry Semel Institute for Neuroscience & Human Behavior; Constance Hammen, University of California, Los Angeles; Penelope A. Lind, QIMR Berghofer Medical Research Institute; Jake M. Najman, University of Queensland; Patricia Brennan, Emory University
• Language: English
• Date: 2012-01-01
• Publisher: Taylor & Francis (Routledge): STM, Behavioural Science and Public Health Titles
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2012 Taylor and Francis Group, LLC.
• Final Published Version (URL): http://dx.doi.org/10.1080/15374416.2012.632351
• Title of Journal or Parent Work: Journal of Clinical Child and Adolescent Psychology
• ISSN: 1537-4416
• Volume: 41
• Issue: 1
• Start Page: 53
• End Page: 63
• Grant/Funding Information: This study was supported by NIMH R01 MH52239 to Brennan, Hammen, and Najman.
• Keywords: Stress, Psychological; Young Adult; Interview, Psychological; Female; Alleles; Male; Genotype; Humans; Aggression; Serotonin Plasma Membrane Transport Proteins; Polymorphism, Genetic; Adolescent
• Research Categories: Biology, Genetics; Psychology, Developmental; Psychology, Clinical

Abstract

Despite consistent evidence that serotonin functioning affects stress reactivity and vulnerability to aggression, research on serotonin gene-stress interactions (G × E) in the development of aggression remains limited. The present study investigated variation in the promoter region of the serotonin transporter gene (5-HTTLPR) as a moderator of the stress-aggression association at the transition to adulthood. Multiple informants and multiple measures were used to assess aggression in a cohort of 381 Australian youth (61% female, 93% Caucasian) interviewed at ages 15 and 20. At age 20, semistructured interviews assessed acute and chronic stressors occurring in the past 12 months. Structural equation modeling analyses revealed a significant main effect of chronic stress, but not 5-HTTLPR or acute stress, on increases in aggression at age 20. Consistent with G × E hypotheses, 5-HTTLPR short allele carriers demonstrated greater increments in aggression following chronic stress relative to long allele homozygotes. The strength of chronic stress G × E did not vary according to sex. Variation at 5-HTTLPR appears to contribute to individual differences in aggressive reactions to chronic stress at the transition to adulthood.