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The relationship between executive function and antisocial behavior from age 9-16: a longitudinal twin study
University of Southern California, Los Angeles, California, USA.
University of Southern California, Los Angeles, California, USA.ORCID iD: 0000-0001-8768-6954
University of Southern California, Los Angeles, California, USA.
University of Southern California, Los Angeles, California, USA.
2011 (English)In: Behavior Genetics, ISSN 0001-8244, Vol. 41, no 6, 904-904 p.Article in journal, Meeting abstract (Other academic) Published
Abstract [en]

Behavioral disinhibition and executive dysfunction (EDF) are two key aspects of self-regulation that serve as risk factors for the development of antisocial behavior (ASB). In spite of the well established correlation between EDF and ASB, we do not yet know (1) the direction of the relationship itself, i.e., whether ASB may be result or cause of EF deficits during development, and (2) the extent to which the relationship is mediated by genetic and environmental factors. Cross-lagged regression models were used to investigate these questions in a longitudinal twin study based on data from two occasions when the twins were age 9–10 (Time 1) and age14–16 (Time 2). Preliminary phenotypic results demonstrated a strong association between EF and ASB at Time 1 (r=.27,p\.01), Time 2 (r=.29,p\.01), and longitudinally (r=.25,p\.01). In addition, ASB at Time 1 also correlated with future EF at Time 2 (r=.24,p\.01), which is, at the very least, suggestive of bi-directional effects. A fully cross-lagged model was found to best fit the data, such that deficits in early EF led to higher rates of later ASB (b12=0.12, Est./S.E.=2.318), and early ASB affected later EF (b21=0.10, Est./S.E.=2.58) while controlling for their pre-existing relationships and stabilities over time. Genetic factors contributed to the variation in EF from ages 9–16 (Time 1: 26%; Time 2: 29%), with no effect of shared environment. For ASB, genetic factors accounted for 43% of the variance during Time 1 and 55% of the variance during Time 2, with the remaining variance being comprised of shared environmental (Time 1: 20%; Time 2: 16%) and non-shared environmental factors (Time 1: 37%; Time 2: 29%). Biometric cross-lagged analyses will be used to examine the genetic and environmental contributions to the direction of effects between EF and ASB; these analyses are currently underway.

Place, publisher, year, edition, pages
2011. Vol. 41, no 6, 904-904 p.
National Category
Psychology
Research subject
Psychology
Identifiers
URN: urn:nbn:se:oru:diva-43822DOI: 10.1007/s10519-011-9495-9ISI: 000295326600058OAI: oai:DiVA.org:oru-43822DiVA: diva2:797555
Conference
41st Annual Meeting of the Behaviour-Genetics-Association, Newport, RI, June 6-9, 2011
Available from: 2015-03-24 Created: 2015-03-24 Last updated: 2015-04-13Bibliographically approved

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Tuvblad, Catherine
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