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, 118 (1), 117-30

Behavioral Disinhibition: Liability for Externalizing Spectrum Disorders and Its Genetic and Environmental Relation to Response Inhibition Across Adolescence

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Behavioral Disinhibition: Liability for Externalizing Spectrum Disorders and Its Genetic and Environmental Relation to Response Inhibition Across Adolescence

Susan E Young et al. J Abnorm Psychol.

Abstract

Behavioral disinhibition has been characterized as a generalized vulnerability to externalizing disorders. Despite increasing evidence for its validity and heritability, the structural stability of behavioral disinhibition across adolescence and the strength and etiology of its relation to executive functions have not been studied. In this multivariate twin study, the authors assessed behavioral disinhibition using measures tapping substance use, conduct disorder, attention-deficit/hyperactivity disorder (ADHD), and novelty seeking at ages 12 and 17. Executive functions were assessed with laboratory-based cognitive tasks at age 17. Results indicated that, at age 12, behavioral disinhibition was dominated by ADHD and conduct problems and was highly heritable. At age 17, the contributions of the 4 components were more balanced, and the proportion of variance attributable to genetic factors was somewhat smaller, with additional variance due to shared environmental influences. At both ages, behavioral disinhibition was more closely related to response inhibition than other executive functions (working memory updating and task-set shifting), and this relationship was primarily genetic in origin. These results highlight the dynamic nature of behavioral disinhibition across adolescence and suggest that response inhibition may be an important mechanism underlying vulnerability to disinhibitory psychopathology.

Figures

Figure 1
Figure 1
Hierarchical model fitting results from Wave 1 (age 12). Observed variables, represented by boxes, are as follows: SU = substance use; CD = conduct disorder; AD = attention-deficit/hyperactivity disorder composite; NS = novelty seeking; Anti = antisaccade task; Stop = stop-signal task; Stroop = Stroop task. The latent variables, represented by ovals, are as follows: BD = behavioral disinhibition; INH = inhibiting of prepotent responses; A = additive genetic influences; C = environmental influences shared by twins; E = nonshared environmental influence. The double-headed arrows between the latent variables represent factor correlations. Factor loadings on each latent constructs are standardized. Proportions of variance are expressed as percentages. Solid lines indicate significant loadings/proportions of variance (p < .05); dashed lines indicate nonsignificant loadings/proportions of variance (p > .05).
Figure 2
Figure 2
Hierarchical model fitting results from Wave 2 (age 17). Observed variables, represented by boxes, are as follows: SU = substance use; CD = conduct disorder; AD = attention-deficit/hyperactivity disorder composite; NS = novelty seeking; Anti = antisaccade task; Stop = stop-signal task; Stroop = Stroop task. The latent variables, represented by ovals, are as follows: BD = behavioral disinhibition; INH = inhibiting of prepotent responses; A = additive genetic influences; C = environmental influences shared by twins; E = nonshared environmental influence. The double-headed arrows between the latent variables represent factor correlations. Factor loadings on each latent constructs are standardized. Proportions of variance are expressed as percentages. Solid lines indicate significant loadings/proportions of variance (p < .05); dashed lines indicate nonsignificant loadings/proportions of variance (p > .05).

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