A Replicated Molecular Genetic Basis for Subtyping Antisocial Behavior in Children With Attention-Deficit/Hyperactivity Disorder

2008/02/01 by Avshalom Caspi, K. Langley, Kate Langley +12 · 222 citations
Medicine · Neuroscience · Psychology · #Attention Deficit Hyperactivity Disorder #Attention deficit hyperactivity disorder #Biology #Catechol-O-methyl transferase #Clinical psychology #Cohort #Conduct disorder #Gene #Genetics #Genotype #Internal medicine #Medicine #Neurodevelopmental disorder #Neurotransmitter Receptor Influence on Behavior #Psychiatry #Psychology #Psychopathy, Forensic Psychiatry, Sexual Offending #Subtyping

paper · doi:10.1001/archgenpsychiatry.2007.24

published in Archives of General Psychiatry 65(2), 203 (American Medical Association)

openalex publication_date 2008/02/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01

Abstract

CONTEXT: Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous neurodevelopmental disorder that in some cases is accompanied by antisocial behavior. OBJECTIVE: To test if variations in the catechol O-methyltransferase gene (COMT) would prove useful in identifying the subset of children with ADHD who exhibit antisocial behavior. DESIGN: Three independent samples composed of 1 clinical sample of ADHD cases and 2 birth cohort studies. PARTICIPANTS: Participants in the clinical sample were drawn from child psychiatry and child health clinics in England and Wales. The 2 birth cohort studies included 1 sample of 2232 British children born in 1994-1995 and a second sample of 1037 New Zealander children born in 1972-1973. MAIN OUTCOME MEASURES: Diagnosis of ADHD and measures of antisocial behavior. RESULTS: We present replicated evidence that the COMT valine/methionine polymorphism at codon 158 (COMT Val158Met) was associated with phenotypic variation among children with ADHD. Across the 3 samples, valine/valine homozygotes had more symptoms of conduct disorder, were more aggressive, and were more likely to be convicted of criminal offenses compared with methionine carriers. CONCLUSIONS: The findings confirm the presence of genetic heterogeneity in ADHD and illustrate how genetic information may provide biological evidence pointing to clinical subtypes.

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