Format

Send to

Choose Destination
See comment in PubMed Commons below
Eur Child Adolesc Psychiatry. 2005 Jul;14(4):216-25.

The development of antisocial behaviour from childhood to adolescence. A longitudinal twin study.

Author information

1
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, P.O. Box 281, 17177 Stockholm, Sweden. Catherine.Tuvblad@meb.ki.se

Abstract

Recent theory proposes that aggressive and nonaggressive antisocial behaviour (ASB) represent different pathways toward delinquency. It has also been suggested that Aggressive ASB is heritable, whereas nonaggressive ASB is more influenced by shared environment. The twin study of child and adolescent development is a Swedish population-based study of 1,480 twin pairs. The present study included 1,226 twin pairs. We used the parental-reported Aggression and Delinquency scales from the CBCL measured at age 8-9. Delinquent behaviour was measured through self-report at age 16-17. We explored how genetic and environmental effects influence the relationships between aspects of ASB in childhood and adolescent delinquency using structural equations modelling. For girls we found that the relationship between Aggressive Behaviour and Self-Reported Delinquency was explained by genetic influences. The correlation between Delinquent Behaviour and Self-Reported Delinquency was due to continuity of genetic influences. For boys, there was no significant mediation between Aggressive Behaviour and Self-Reported Delinquency, but there were significant shared environmental effects on the relationship between Delinquent Behaviour and Self-Reported Delinquency. Our results suggest that there are sex differences in the development of ASB. The hypothesis that the aggressive pathway is genetically mediated was supported in girls, whereas the hypothesis that the nonaggressive pathway is environmentally dependent was supported in boys.

PMID:
15981133
DOI:
10.1007/s00787-005-0458-7
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center