DSM-IV defined conduct disorder and oppositional defiant disorder: an investigation of shared liability in female twins

Abstract

Background DSM-IV specifies a hierarchal diagnostic structure such that an ODD diagnosis is applied only if criteria are not met for CD. Genetic studies of ODD and CD support a combination of shared genetic and environmental influences, but largely ignore the imposed diagnostic structure. Methods We examined whether ODD and CD share an underlying etiology while accounting for DSM-IV diagnostic specifications. Data from 1446 female twin pairs, aged 11–19, were fitted to two-stage models adhering to the DSM-IV diagnostic hierarchy. Results Models suggested that DSM-IV ODD-CD covariation is attributed largely to shared genetic influences. Conclusions This is the first study, to our knowledge, to examine genetic and environmental overlap among these disorders while maintaining DSM-IV hierarchical structure. Findings reflect primarily shared genetic influences and specific (i.e., uncorrelated) shared/familial environmental effects on these DSM-IV defined behaviors. These results have implications for how best to define CD and ODD for future genetically-informed analyses.

Codevelopment of ADHD and externalizing behavior from childhood to adulthood

“…In line with previous research, we found that the overlap between ADHD-like and externalizing traits was largely explained by shared genetic factors (Dick et al, 2005; Knopik et al, 2013; Nadder et al, 2002; Tuvblad et al, 2009). Particularly, one study has shown that the covariation between the two traits across time is governed by genetics (Nadder et al, 2002).…”

“…There is also evidence that the overlap between ADHD-like and externalizing traits, such as ODD and CD symptoms, are mainly of genetic origin (Dick, Viken, Kaprio, Pulkkinen, & Rose, 2005; Knopik et al, 2013; Nadder, Rutter, Silberg, Maes, & Eaves, 2002; Tuvblad, Zheng, Raine, & Baker, 2009); however, not all studies have reached that conclusion (Burt, Krueger, McGue, & Iacono, 2001). …”

“…Twin studies of ADHD‐like traits among children and adolescents have consistently showed strong genetic influences, with heritability estimates around 60–90% (Burt, ; Faraone et al., ), whereas both genetic and shared environmental influences seem to be important for externalizing traits, especially during childhood (Burt, ; Rhee & Waldman, ). There is also evidence that the overlap between ADHD‐like and externalizing traits, such as ODD and CD symptoms, are mainly of genetic origin (Dick, Viken, Kaprio, Pulkkinen, & Rose, ; Knopik et al., ; Nadder, Rutter, Silberg, Maes, & Eaves, ; Tuvblad, Zheng, Raine, & Baker, ); however, not all studies have reached that conclusion (Burt, Krueger, McGue, & Iacono, ).…”

Association of norepinephrine transporter (NET, SLC6A2) genotype with ADHD-related phenotypes: Findings of a longitudinal study from birth to adolescence

“…High scores on the CBCL externalizing behavior scale may, however, point to comorbid disorders and phenotypic dimensions, such as oppositional defiant disorder (ODD), conduct disorder (CD) or irritability, the overlap of which being largely explained by shared genetic factors (Dick et al, 2005;Knopik et al, 2014;Kuja-Halkola et al, 2014;Tuvblad et al, 2009). Also, recent studies have emphasized the importance of pleiotropic effects of genetic risk variants of psychiatric disorders (CrossDisorder Group of the Psychiatric Genomics Consortium, 2013).…”

Identification of risk variants and characterization of the polygenic architecture of disruptive behavior disorders in the context of ADHD

“…Family studies have found that ADHD and DBDs have distinct genetic architectures with moderate to high genetic overlap in the range of 0.34 -0.74 23,24,25 . The existence of genetic risk factors specific to the aggressive and disruptive component of ADHD+DBDs finds support from a twin study where DBDs had an estimated heritability of 0.33-0.64 after controlling for ADHD, with a significant genetic component also observed for DBDs in individuals without ADHD 26 .…”