Childhood attention-deficit/hyperactivity disorder symptoms and the development of adolescent alcohol problems: A prospective, population-based study of Swedish twins

Abstract

Children with attention-deficit/hyperactivity disorder (ADHD) are at increased risk of problematic alcohol and other substance use in adolescence. This study used data from an ongoing, prospective, population-based twin study of Swedish children and adolescents to evaluate the extent to which the association between ADHD symptoms and alcohol problems reflects a unique source of genetic or environmental risk related to ADHD versus a broader predisposition to youth externalizing behavior. We used all available data from same-sex monozygotic (MZ) and dizygotic (DZ) twins on ADHD symptoms in childhood (age 9/12; N = 15,549) and alcohol problems in late adolescence (age 18; N = 2,564). Consistent with prior longitudinal studies, the phenotypic association between hyperactive/impulsive ADHD symptoms and alcohol problems was small in magnitude, whereas the association for inattentive symptoms was even weaker. Additive genetic influences explained 99.8% of the association between hyperactive/impulsive symptoms and alcohol problems. Furthermore, we found that the genetic risk specifically associated with hyperactive/impulsive symptoms was attenuated when estimated in the context of externalizing behavior liability during childhood, of which ADHD symptoms were specific expressions. In sensitivity analyses exploring hyperactivity in mid-adolescence, we found a similar pattern of genetic associations. These results are consistent with previous findings of genetically driven overlap in the etiology of ADHD and problematic alcohol use. At least some of this co-occurrence may result from a general predisposition to externalizing behaviors in youth. © 2015 Wiley Periodicals, Inc.

Keywords: ADHD; behavioral genetics; externalizing; neurodevelopmental problems; substance misuse.

Figure 1

Illustration of Cholesky decompositions (one twin per pair shown only). Dashed objects indicate components added in trivariate decompositions. A = additive genetic, D = dominant genetic, and E = non-shared environmental. Sibling contrast paths and pair-sex covariate not shown.

Figure 2

Illustrations of Independent Pathway (Panel A) and Common Pathway (Panel B) models (one twin per pair shown only). Sibling contrast paths and pair-sex covariate not shown. In the Common Pathway model, factors A_e and E_e are the common additive genetic and non-shared environmental factors, respectively, whereas factors A_o, E_o, A_c, E_c, A_h, E_h, A_i, and E_i are the specific factors. Paths are estimated but, for ease of reading, are not labeled. Common factor loading for ODP constrained to 1 to identify the externalizing (EXT) factor. CP = conduct problems, H/I = hyperactive/impulsive ADHD symptoms, In = Inattentive ADHD symptoms, ODP = oppositional/defiant problems.

Figure 3

Additive genetic (Panel A) and non-shared environmental (Panel B) correlations between hyperactive/impulsive symptoms or hyperactivity and alcohol problems. In trivariate and common pathway models, correlations represent the variance shared between alcohol problems and the unique variance in hyperactive/impulsive symptoms (or hyperactivity), net of variance in common with other disruptive or conduct problems. Error bars are 95% CIs.