James J Li1. 1. Department of Psychology and Waisman Center, University of Wisconsin-Madison, Madison, WI, USA.
Abstract
BACKGROUND: Children with ADHD frequently engage in higher rates of externalizing behaviors in adulthood relative to children without. However, externalizing behaviors vary across development. Little is known about how this risk unfolds across development. Phenotypic and polygenic models of childhood ADHD were used to predict individual differences in adult externalizing trajectories. Supportive parenting, school connectedness, and peer closeness were then examined as causal mechanisms. METHODS: Data were from the National Longitudinal Study of Adolescent to Adult Health (N = 7,674). Externalizing behavior was measured using data from age 18 to 32 and modeled using latent class growth analysis. Child ADHD was measured using retrospective self-report (phenotypic model) and genome-wide polygenic risk scores (polygenic model). Multiple mediation models examined the direct and indirect effects of the phenotypic and polygenic models (separately) on externalizing trajectories through the effects of adolescent supportive parenting, school connectedness, and peer closeness. RESULTS: Phenotypic and polygenic models of ADHD were associated with being in the High Decreasing (3.2% of sample) and Moderate (16.1%) adult externalizing trajectories, but not the severe Low Increasing trajectory (2.6%), relative to the Normal trajectory (78.2%). Associations between both models of ADHD on the High Decreasing and Moderate trajectories were partially mediated through the effects of school connectedness, but not supportive parenting or peer closeness. CONCLUSIONS: Findings shed light on how childhood ADHD affects downstream psychosocial processes that then predict specific externalizing outcomes in adulthood. They also reinforce the importance of fostering a strong school environment for adolescents with (and without) ADHD, as this context plays a critical role in shaping the development of externalizing behaviors in adulthood.
BACKGROUND:Children with ADHD frequently engage in higher rates of externalizing behaviors in adulthood relative to children without. However, externalizing behaviors vary across development. Little is known about how this risk unfolds across development. Phenotypic and polygenic models of childhood ADHD were used to predict individual differences in adult externalizing trajectories. Supportive parenting, school connectedness, and peer closeness were then examined as causal mechanisms. METHODS: Data were from the National Longitudinal Study of Adolescent to Adult Health (N = 7,674). Externalizing behavior was measured using data from age 18 to 32 and modeled using latent class growth analysis. ChildADHD was measured using retrospective self-report (phenotypic model) and genome-wide polygenic risk scores (polygenic model). Multiple mediation models examined the direct and indirect effects of the phenotypic and polygenic models (separately) on externalizing trajectories through the effects of adolescent supportive parenting, school connectedness, and peer closeness. RESULTS: Phenotypic and polygenic models of ADHD were associated with being in the High Decreasing (3.2% of sample) and Moderate (16.1%) adult externalizing trajectories, but not the severe Low Increasing trajectory (2.6%), relative to the Normal trajectory (78.2%). Associations between both models of ADHD on the High Decreasing and Moderate trajectories were partially mediated through the effects of school connectedness, but not supportive parenting or peer closeness. CONCLUSIONS: Findings shed light on how childhood ADHD affects downstream psychosocial processes that then predict specific externalizing outcomes in adulthood. They also reinforce the importance of fostering a strong school environment for adolescents with (and without) ADHD, as this context plays a critical role in shaping the development of externalizing behaviors in adulthood.
Authors: Ditte Demontis; Raymond K Walters; Joanna Martin; Manuel Mattheisen; Thomas D Als; Esben Agerbo; Gísli Baldursson; Rich Belliveau; Jonas Bybjerg-Grauholm; Marie Bækvad-Hansen; Felecia Cerrato; Kimberly Chambert; Claire Churchhouse; Ashley Dumont; Nicholas Eriksson; Michael Gandal; Jacqueline I Goldstein; Katrina L Grasby; Jakob Grove; Olafur O Gudmundsson; Christine S Hansen; Mads Engel Hauberg; Mads V Hollegaard; Daniel P Howrigan; Hailiang Huang; Julian B Maller; Alicia R Martin; Nicholas G Martin; Jennifer Moran; Jonatan Pallesen; Duncan S Palmer; Carsten Bøcker Pedersen; Marianne Giørtz Pedersen; Timothy Poterba; Jesper Buchhave Poulsen; Stephan Ripke; Elise B Robinson; F Kyle Satterstrom; Hreinn Stefansson; Christine Stevens; Patrick Turley; G Bragi Walters; Hyejung Won; Margaret J Wright; Ole A Andreassen; Philip Asherson; Christie L Burton; Dorret I Boomsma; Bru Cormand; Søren Dalsgaard; Barbara Franke; Joel Gelernter; Daniel Geschwind; Hakon Hakonarson; Jan Haavik; Henry R Kranzler; Jonna Kuntsi; Kate Langley; Klaus-Peter Lesch; Christel Middeldorp; Andreas Reif; Luis Augusto Rohde; Panos Roussos; Russell Schachar; Pamela Sklar; Edmund J S Sonuga-Barke; Patrick F Sullivan; Anita Thapar; Joyce Y Tung; Irwin D Waldman; Sarah E Medland; Kari Stefansson; Merete Nordentoft; David M Hougaard; Thomas Werge; Ole Mors; Preben Bo Mortensen; Mark J Daly; Stephen V Faraone; Anders D Børglum; Benjamin M Neale Journal: Nat Genet Date: 2018-11-26 Impact factor: 38.330
Authors: Lucy Riglin; Stephan Collishaw; Ajay K Thapar; Søren Dalsgaard; Kate Langley; George Davey Smith; Evie Stergiakouli; Barbara Maughan; Michael C O'Donovan; Anita Thapar Journal: JAMA Psychiatry Date: 2016-12-01 Impact factor: 21.596