The different origins of stability and change in antisocial personality disorder symptoms.
BACKGROUND
Although adult antisocial personality disorder is generally preceded by a pattern of childhood/adolescent conduct problems, only a subset of those who manifest these developmental precursors go on exhibit significant antisocial behavior in adulthood. To date, however, researchers have yet to resolve the origins of either stability or change in antisocial behavior from childhood/adolescence to adulthood.


METHODS
The present study sought to fill this gap in the literature, making use of a sample of 626 twin pairs from the ongoing Minnesota Twin Family Study (MTFS). Participants were assessed three times between late adolescence and early adulthood. We made use of biometric Cholesky decomposition and latent growth curve modeling techniques, which allow researchers to disambiguate processes of stability and change and evaluate their respective etiologies (i.e. genetic or environmental).


RESULTS
Our results revealed that genetic forces were largely responsible for the stability of adult symptoms of antisocial behavior (AAB) from late adolescence through mid-adulthood, while non-shared environmental influences were primarily responsible for change. Importantly, however, although some of the latter represented systematic and long-lasting influence, much of this non-shared environmental variance appeared transient and idiosyncratic.


CONCLUSIONS
Such findings highlight the enduring impact of genetic influences on AAB, and offer insights into the nature of non-shared environmental influences on development.
Burt
S Alexandra
SA
Department of Psychology, Michigan State University, East Lansing, MI 48824, USA. burts@msu.edu
McGue
Matt
M
Carter
Latanya A
LA
Iacono
William G
WG
D000293:Adolescent; D000328:Adult; D000987:Antisocial Personality Disorder / Q000175:diagnosis / Q000209:etiology* / Q000235:genetics*; D019955:Conduct Disorder / Q000175:diagnosis / Q000209:etiology / Q000235:genetics; D004200:Diseases in Twins / Q000175:diagnosis / Q000209:etiology* / Q000235:genetics*; D005260:Female; D006801:Humans; D008297:Male; D008957:Models, Genetic; D015233:Models, Statistical; D012307:Risk Factors; D012737:Sex Factors; D012931:Social Environment