Sources of covariation among the child-externalizing disorders: informant effects and the shared environment

Abstract

Background: Research has documented high levels of co-morbidity among childhood externalizing disorders, but its etiology remains in dispute. Specifically, although all behavior genetic studies of the etiology of the co-occurrence of attention deficit-hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD) agree that genetic factors are important, differences exist across studies in the relative weight assigned to genetic, shared environmental factors (i.e. factors that increase similarity among family members), and non-shared environmental factors (i.e. factors that decrease similarity among family members). Because heritability estimates can vary across informants, we used a biometric informant-effects model to determine whether these discrepancies were a function of systematic differences in maternal and child informant reports of ADHD, CD, and ODD.

Method: We studied 1782 11-year-old twins from the Minnesota Twin Family Study. Symptom counts for each disorder were obtained from interviews administered to twins and their mothers. We fit a model that allowed us to examine, both across and within informants, the genetic and environmental contributions to the co-occurrence among ADHD, CD, and ODD.

Results: The results revealed that the co-occurrence among the disorders common to maternal and child informant reports was influenced largely by shared environmental forces. Genetic factors also contributed, though their impact was only marginally significant. In contrast, the co-occurrence unique to each informant was influenced exclusively by either genetic or non-shared environmental factors.

Conclusions: Such findings offer additional evidence that shared environmental factors are important to the co-morbidity among ADHD, CD, and ODD, and highlight the necessity of considering informant effects when drawing conclusions about the origins of co-morbidity from analyses of genetically informative data.

Fig. 1

Path diagram of a full ACE informant-effects model for maternal and child informant-reports of attention deficit-hyperactivity disorder (ADHD), conduct disorder (CD), and oppositional defiant disorder (ODD). To promote ease of presentation, this path diagram represents only one twin in a pair (though the results are identical for the co-twin). General Ext represents the primary general factor loading onto both mother and child informant-reports. mother and child represent the secondary relevant informant-specific factors. The variance in each factor is parsed into that which is due to additive genetic effects (A), shared environmental effects (C), and non-shared environmental effects (E). Paths are represented by uppercase letters followed by two subscript numerals (e.g. A₁₁, A₂₂, and A₃₃). Factor loading paths are represented by a lowercase ‘ f ’, followed by two subscript numerals. The first numeral corresponds to variable ‘number’ and the second to the factor that is loading on the variable. The variable-specific residual paths load directly onto each disorder, and are indicated by a lowercase letter followed by a single subscript numeral (e.g. a₁).

Fig. 2

Standardized path diagram of informant-effects model for maternal and child informant-reports of attention defici-thyperactivity disorder (ADHD), conduct disorder (CD), and oppositional defiant disorder (ODD). Standardized path estimates of the genetic and shared environmental contributions to the covariance within each factor and the variance unique to each informant-report of the disorders are illustrated. The paths that are significant at p<0.05 are indicated by an asterisk. ~Indicates path is marginally significant at p<0.10. All paths are squared to estimate the proportion of variance accounted for.