Demonstrating that what connects the components of behavioral disinhibition is genetic in nature is only the first step toward understanding underlying mechanisms that lead to this confluence of problems. In this study, we also examined whether deficits in executive functions represent one key set of such explanatory mechanisms. We focused particularly on response inhibition because it has been previously suggested as the component of executive function that is most conceptually linked to disinhibitory psychopathology (e.g., Barkley, 1997
The relationship between behavioral disinhibition and executive functions has never been explicitly tested at the level of latent variables. However, a number of studies have reported correlations between particular disinhibitory disorders and a variety of neuropsychological measures of executive function, most notably in children with ADHD. In a recent meta-analytic review of results from 83 studies evaluating the evidence for deficits in executive functions as primary etiological factors in the development of ADHD, Willcutt, Doyle, Nigg, Faraone, and Pennington (2005)
concluded that although the effect sizes are modest and inconsistent, executive function deficits are one important component in ADHD.
Executive functions have also been hypothesized as a core component of risk for the development of substance use disorders (Giancola, Mezzich, & Tarter, 1998
). A recent study of adolescent substance use disorders found that response inhibition ability predicted the onset of alcohol use–related problems and illicit drug use in adolescents independently of their ADHD and conduct disorder status (Nigg et al., 2006
Although these studies provide some evidence for a link between particular externalizing disorders and executive functions, they did not examine how the more general concept of behavioral disinhibition relates to executive functions, especially deficits in the ability to inhibit prepotent (i.e., dominant or automatic) responses. Thus, the second question we addressed in this study was as follows: Can we empirically demonstrate that the covariance among adolescent externalizing disorders and novelty seeking is explained, in part, by deficits in an underlying cognitive process, namely, response inhibition? In other words, is behavioral disinhibition really a problem with inhibition?
The response inhibition construct under study here was previously validated through factor analytic work by Miyake, Friedman, et al. (2000)
, who demonstrated that three common executive functions (response inhibition, working memory updating, and task-set switching) were correlated but separable at the level of latent variables (see also Friedman et al., 2006
). A replication and extension of this work demonstrated that these three executive functions share a highly heritable common factor that can be distinguished from that of IQ or speed (Friedman et al., 2008
). In light of the finding that behavioral disinhibition itself is also highly heritable, the third question we asked in this study is as follows: Can the relationship between behavioral disinhibition and response inhibition be explained by shared genetic factors and, if so, to what extent?
Ours is the first study to empirically test this hypothesis. To do so, we applied a hierarchical genetic and environmental model in our adolescent twin sample to the two latent constructs of behavioral disinhibition and response inhibition. This model simultaneously estimates the contributions of genetic influences, shared (family) environmental influences, and nonshared (individual) environmental influences, as well as the correlations between the etiological factors of the two constructs. Our design was strengthened by the fact that we assessed psychiatric and personality characteristics longitudinally. Specifically, we compared the relationship between behavioral disinhibition and response inhibition in early and late adolescence.