Understanding the relative contributions of direct environmental effects and passive genotype–environment correlations in the association between familial risk factors and child disruptive behavior disorders

Current research has established a number of robust predictors of child disruptive behavior disorder (DBD) symptoms. These include maladaptive, inconsistent, harsh, punitive, or abusive parenting; marital conflict among parents; divorce; and parental antisocial behavior. Across both clinical and community samples, maladaptive parental disciplinary practices are linked with offspring attention-deficit hyperactivity disorder (ADHD), oppositional-defiant disorder (ODD) , and conduct disorder (CD) symptoms (Loeber & Stouthamer-Loeber, 1986; Burt et al. 2003; Caspi et al. 2004; Stormshak et al. 2000; Stanger et al. 2004). Similarly, divorce and marital discord are significantly related to DBD symptoms (Gartstein & Fagot, 2003; Burt et al. 2008). Finally, one of the strongest predictors of child conduct problems is parental antisocial behavior (Herndon & Iacono, 2005), as it is consistently associated with offspring DBD symptoms, delinquency, and criminal acts. Arguably, these studies put forth familial factors as environmental risk factors contributing directly to child DBD symptoms. Indeed, a recent meta-analysis of twin studies reported that shared environmental factors (i.e., factors common to both members of a sibling pair that make them similar) accounted for 10%–15% of the variance in child DBD symptoms and diagnoses (Burt, 2009). Other studies indicate familial risk factors are associated with child DBD symptoms in large part through shared environmental mechanisms (McGue et al. 1996; Pike et al. 1996; Burt et al. 2003; Burt et al. 2007;). However, additional research on the link between familial risk factors and child DBD symptoms suggests alternative explanations which implicate genetic influences. One key finding largely supporting this is that parental antisociality is highly heritable. In a review of studies on the etiology of child antisociality, Rhee and Waldman (2002) found genes influenced 32% of the variance in child antisociality, and shared environmental factors influenced 16%. Previous studies (Bornovalova. 2010) indicate parental externalizing psychopathology (including adult antisociality) influences child DBD symptoms through transmitting a common genetic vulnerability. Likewise, multiple studies report genetic influences on marital relationships (Reiss et al. 2000; Spotts et al. 2004; Spotts et al. 2006), divorce (McGue & Lykken, 1992), and maladaptive parenting (Jaffee & Price, 2008; see Kendler & Baker, 2007 for a review). Collectively, this research suggests patterns of influence generally attributed to the familial environment are in part genetically mediated. Putative environmental factors may be indirectly related to offspring DBD symptoms through the mechanism of passive gene-environment correlation (rGE). Passive rGE occurs when parents provide both the genes and environment that lead to a certain child outcome. As applied to the current topic, a heritable propensity toward impulsive and disinhibitory behavior may increase likelihood of exhibiting high antisocial traits, especially while being reared in an environment characterized by marital conflict, divorce, and maladaptive parenting. The combination of genetic and environmental risk in turn increases likely manifestation of child DBD symptoms in the offspring (Bornovalova, 2010; Silberg et al. 2012). Unfortunately, neither studies of biological families nor typical twin designs are able to disentangle environmental sources of influence from passive rGE because parents provide both genes and environment for their biological children. And, in classic twin designs, passive rGE can mimic shared environmental influences when the origins are, in fact, a function of common parent– child genes. An elegant method of disentangling environmental influences from passive rGE involves comparing the effects of putative environmental variables in genetically unrelated families (adoptive families) and genetically related families (biological families). The logic of this design is as follows: In families where the biological parents are rearing their own offspring, parents provide both the child’s environment and his/her genes. Thus, any association between parenting and child DBD symptoms could be due to genetically mediated influences, purely environmental influences, or any combination of the two. In contrast, in an adoptive family, the child’s adoptive parents provide the environment, but the child’s birth parents provide his/her genetic makeup and typically do not provide environmental influences after the child was adopted. As such, the possibility of passive rGE is eliminated (provided children are not selectively placed into adoptive homes). If the magnitude of association between familial factors and child DBD symptoms is significantly greater in biological families than in adoptive families, then some degree of passive rGE is indicated because the association between family environment and biological offspring outcomes depends on both genetic and shared environmental factors. Conversely, if the magnitude of the familial factors-child DBD symptoms association is comparable in biological and adoptive families, then passive rGE effects are ruled out and environmental risk processes are implicated (Plomin, 1994). Six previous studies (Dunn et al. 1985; Dunn & Plomin, 1986; Dunn et al. 1986; Rende et al. 1992; Braungartrieker et al. 1995; O'Connor et al. 2000) used this design to examine contribution of passive rGE in the association between familial risk factors and DBD symptoms. Findings generally indicated, with the exception of divorce (which consistently shows solely a direct environmental effect), a mix of direct environmental effects and passive rGE effects. Using a very different method (the Extended Children of Twins Design, a design incorporating children of twins and their cousins capitalizing on a large range of genetic relatedness in immediate and extended family), at least four other studies (Neiderhiser et al. 2004; Harden et al. 2007; Neiderhiser et al. 2007; Narusyte et al. 2011; Silberg et al. 2012) found similar effects. Collectively, these studies suggest both passive rGE and direct environmental effects account for the relationship between family conflict, parenting behavior, and parental antisociality and child DBD symptoms. Although these studies contribute importantly to understanding the relative influence of environmental effects and rGE, each examined one or two selected contextual risk factors making it difficult to evaluate the relative contribution of each. Moreover, previous work suggests the importance of examining maternal and paternal parenting factors separately (Rothbaum & Weisz, 1994; Denham et al. 2000; Johnson et al. 2001) but only a few studies (Neiderhiser et al. 2004; Neiderhiser et al. 2007) have investigated possible differences between fathering and mothering in the interplay between genetic and environmental factors. This last point is quite important, as the effects of maternal versus paternal parenting effects may differ in (a) strength of effect, and (b) underlying mechanism of transmission (Rothbaum & Weisz, 1994; Denham et al. 2000; Johnson et al. 2001; Neiderhiser et al. 2004; Neiderhiser et al. 2007). Additionally, among these studies there is large variability in offspring age (ranging from toddlers to adolescents). It is important to extend these studies by examining the effects of multiple familial risk factors on child DBD symptoms late enough in development to allow manifestation of such symptoms. Finally, it is especially worthwhile to attempt to replicate and extend findings from multiple studies using widely different methods (e.g., adoptive designs; Extended Children of Twins Designs), since confidence in the veracity of an effect increases if the same results are found using multiple methodological approaches.