A hierarchical biometric model is presented of the origins of comorbidity among substance dependence, antisocial behavior, and a disinhibited personality style. The model posits a spectrum of personality and psychopathology, united by an externalizing factor linked to each phenotype within the spectrum, as well as specific factors that account for distinctions among phenotypes within the spectrum. This model fit self-report and mother-report data from 1,048 male and female 17-year-old twins. The variance of the externalizing factor was mostly genetic, but both genetic and environmental factors accounted for distinctions among phenotypes within the spectrum. These results reconcile evidence for general and specific causal factors within the externalizing spectrum and offer the externalizing factor as a novel target for future research.

One variant of substance-use disorder is characterized by behavioral disinhibition. In this report, we martial evidence for a model for the development of this variant. We hypothesize that genetic liability for this variant is reflected in a spectrum of risk indicators linked to the inability or unwillingness to inhibit behavioral impulses. Included in this spectrum are personality traits suggesting low constraint, and externalizing psychopathology, including conduct, oppositional defiant, and attention-deficit disorder in children and antisocial personality disorder and behavior in adults. We further hypothesize that these individual differences in behavioral disinhibition are manifestations of underlying central nervous system processes associated with various psychophysiological anomalies, some of which may index genetic risk for substance abuse. Support for the model is derived from the analysis of findings from the Minnesota Twin Family Study, an epidemiological investigation of approximately 2,700 adolescent twins and their parents.

Small amplitude P3 may indicate genetic risk for a dimension of disinhibiting psychiatric disorders, including childhood externalizing, adult antisocial personality disorder, and substance use disorders.

Common mental disorders are often correlated with each other, cooccurring at greater than chance rates in both clinical and epidemiological samples (

The present study examined the heritability of the P3 waveform and the N1, P2, and N2 components by assessing the visual event-related potential (ERP) of 30 monozygotic (MZ) and 34 dizygotic (DZ) twin pairs. Electroencephalogram activity was recorded from Pz, P3, and P4 scalp sites while individuals performed a reaction time task involving two conditions differing in difficulty. Genetic modeling indicated substantial genetic influence on P3 amplitude, P3 latency, and manual reaction time for the difficult condition. No significant heritability was found for the latency of P3 or manual reaction time for the easy condition, but P3 amplitude was heritable for this condition. The amplitude of the early components (N1, P2, and N2) was heritable, but no significant genetic influences were found for the latency of these components. Compared with the DZ twins, the greater similarity of the MZ pairs on the event-related potential measures was not due to their greater similarity in either head dimensions or mental ability, despite the facts that IQ scores were weakly correlated with P3 and N2 amplitude and that amplitude and latency were related to some measures of head size. These findings suggest that P3 amplitude and the amplitude of earlier ERP components are under partial genetic control, supporting the notion that these ERP components could perhaps be used to identify genetic risk for psychopathology.