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Assessing the interplay between multigenic and environmental influences on adolescent to adult pathways of antisocial behaviors

Published online by Cambridge University Press:  22 November 2017

James J. Li*
Affiliation:
University of Wisconsin–Madison
*
Address correspondence and reprint requests to: James J. Li, Department of Psychology, University of Wisconsin–Madison, 1202 West Johnson Street, Madison, WI 53706; E-mail: james.li@wisc.edu.

Abstract

The current investigation utilized a developmental psychopathology approach to test the hypothesis that multigenic (i.e., dopaminergic and serotonergic genes) and multienvironmental factors interactively contribute to developmental pathways of antisocial behavior (ASB). A sample of 8,834 Caucasian individuals from the National Longitudinal Study of Adolescent to Adult Health (Add Health) were used to (a) examine the developmental pathways of ASB from age 13 to 32 using growth mixture modeling, (b) compute weighted multigenic risk scores (Add Health MRS) for ASB from six well-characterized polymorphisms in dopamine and serotonin genes, and (c) test the interaction between the Add Health MRS and a measures of support (incorporating indicators of both positive and negative support from parents and schools). Four pathways of adolescent to adult ASB emerged from the growth mixture models: low, adolescence-peaked, high decline, and persistent. Add Health MRS predicted the persistent ASB pathway, but not other ASB pathways. Males with high Add Health MRS, but not low MRS, had significantly greater odds of being in the adolescence-peaked pathway relative to the low pathway at low levels of school connectedness. Nonfamilial environmental influences during adolescence may have a cumulative impact on the development of ASB, particularly among males with greater underlying genetic risks.

Type
Special Issue Articles
Copyright
Copyright © Cambridge University Press 2017 

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Footnotes

The author was supported in part by a core grant to the Waisman Center from the National Institute of Child Health and Human Development (P30-HD03352). The author also acknowledges contributions from Ben Domingue and Garvesh Raskutti for their assistance in the preparation of this manuscript, including their analytic expertise and critical feedback. This research uses data from the National Longitudinal Study of Adolescent to Adult Health (Add Health), a program project directed by Kathleen Mullan Harris and designed by J. Richard Udry, Peter S. Bearman, and Kathleen Mullan Harris at the University of North Carolina at Chapel Hill, and funded by Grant P01-HD31921 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, with cooperative funding from 23 other federal agencies and foundations. Special acknowledgment is due Ronald R. Rindfuss and Barbara Entwisle for assistance in the original design. Information on how to obtain the Add Health data files is available on the Add Health website (http://www.cpc.unc.edu/addhealth). No direct support was received from Grant P01-HD31921 for this analysis.

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