Michael C Monuteaux1, Joseph Biederman2, Alysa E Doyle2, Eric Mick2, Stephen V Faraone2. 1. Drs. Monuteaux, Biederman, Doyle, and Mick are with Massachusetts General Hospital; Dr. Faraone is with SUNY Upstate Medical University. Electronic address: mmonuteaux@partners.org. 2. Drs. Monuteaux, Biederman, Doyle, and Mick are with Massachusetts General Hospital; Dr. Faraone is with SUNY Upstate Medical University.
Abstract
OBJECTIVE: Recent studies have suggested an association between candidate genes (i.e., COMT, SLC6A4) and conduct disorder (CD). However, it is not clear if these relations extend to CD within the context of attention-deficit/hyperactivity disorder (ADHD). Also, it is uncertain whether the risk is specific to aggressive symptoms or is a risk for CD generally. The aim of this study was to examine the role of the COMT and SLC6A4 genes in the risk for CD and its symptomatic subtypes in the context of ADHD. METHOD: We examined subjects with ADHD (n = 444, age range 6-55 years) aggregated across four completed studies. Psychiatric diagnoses were determined by structured interviews. We tested the association between genotype and the diagnosis of CD and aggressive and covert symptom counts. RESULTS: There was no significant association between variations in functional polymorphisms of either the COMT gene or the SLC6A4 gene and the risk for CD. The COMT gene was associated with increased aggressive CD symptoms but not covert CD symptoms. The SLC6A4 gene was not associated with either symptom subtype. CONCLUSIONS: These findings contribute to our understanding of the genetic basis of antisocial behavior in the ADHD population and provide additional support for the notion that aggressive and covert CD symptom subtypes are etiologically distinct.
OBJECTIVE: Recent studies have suggested an association between candidate genes (i.e., COMT, SLC6A4) and conduct disorder (CD). However, it is not clear if these relations extend to CD within the context of attention-deficit/hyperactivity disorder (ADHD). Also, it is uncertain whether the risk is specific to aggressive symptoms or is a risk for CD generally. The aim of this study was to examine the role of the COMT and SLC6A4 genes in the risk for CD and its symptomatic subtypes in the context of ADHD. METHOD: We examined subjects with ADHD (n = 444, age range 6-55 years) aggregated across four completed studies. Psychiatric diagnoses were determined by structured interviews. We tested the association between genotype and the diagnosis of CD and aggressive and covert symptom counts. RESULTS: There was no significant association between variations in functional polymorphisms of either the COMT gene or the SLC6A4 gene and the risk for CD. The COMT gene was associated with increased aggressive CD symptoms but not covert CD symptoms. The SLC6A4 gene was not associated with either symptom subtype. CONCLUSIONS: These findings contribute to our understanding of the genetic basis of antisocial behavior in the ADHD population and provide additional support for the notion that aggressive and covert CD symptom subtypes are etiologically distinct.
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