Parental divorce is a consistent (if modest) predictor of delinquency and other externalizing behaviors during childhood and adolescence (Amato & Keith, 1991
; Fergusson, Horwood, & Lynskey, 1992
; Hetherington, Bridges, & Insabella, 1998
). For example, in his updated meta-analysis on the impact of divorce, Amato (2001)
concluded that the mean Cohen’s d
effect size for conduct problems was .33, suggesting a modest association between youth delinquency and parental divorce. Similarly, Amato & Keith (1991)
reported a Cohen’s d
effect size of .23. Despite the increased social acceptability and prevalence of divorce in recent decades (and thus the sheer number of exposed children) (Thornton & Young-DeMarco, 2001
), the differences in delinquency between youth from intact and divorced families have not decreased (and indeed, appear to have increased) (Amato, 2001
; D’Onofrio et al., 2005
In spite of the robust nature of this association however, relatively little is known regarding its etiology. That is, though generally assumed to be environmental in origin (i.e., causal), such that the experience of parental divorce acts to disrupt the child’s behavior, genetic mediation is also possible (McGue & Lykken, 1992
). Namely, the behavior problems often found in children of divorce could derive from similar pathology in their biological parents, pathology that is both heritable (Rhee & Waldman, 2002
) and increases the risk that the parent will experience, among other things, divorce (Harden et al., 2007
). In other words, parents may provide genes to their biological offspring that increase both the risk of delinquency and the corresponding risk of divorce exposure. The latter possibility represents a core theory within the field of developmental behavioral genetics, and is referred to as a passive gene-environment correlation (i.e., passive rGE) (Plomin, DeFries, & Loehlin, 1977
Though descriptive, identification of the origins of this association as genetic or environmental represents a key public health goal within developmental psychology, as each hypothesized mechanism has distinct ramifications for clinical care and future developmental research. Should the association reflect a passive rGE “in disguise”, future researchers would target the mechanisms through which genetic influences on delinquency influence divorce risk. For example, they could ask whether the association stems from a common genetic association with negative emotionality, which in addition to being genetically influenced itself (Bouchard & Loehlin, 2001
), predicts both antisocial behavior (R. F. Krueger, 1999
) and divorce (McGue & Lykken, 1992
). Alternately, they could ask whether the association is a function of assortative mating for antisocial behavior (R. F. Krueger, Moffitt, Caspi, Bleske, & Silva, 1998
; Taylor, McGue, & Iacono, 2000
), such that those with these predilections select spouses like themselves, and thus indirectly select for probable marital discord and divorce. For their part, clinicians might re-conceptualize parental divorce in the same way that many now consider family history of psychopathology; that is, as an indicator of liability to, rather than as a cause of, antisocial behavior. Put differently, clinicians would not anticipate a decrease in antisocial behavior upon therapeutic resolution of the divorce, as the divorce would simply be an indicator of genetic liability to delinquency. By contrast, should the association reflect a “causal” one, in which divorce increases delinquency via environmental mechanisms, researchers would instead focus on understanding the environmental mechanisms through which divorce increases risk for delinquency, already an important area of research in developmental psychology (Hetherington et al., 1998
)). Such research would likely directly inform intervention efforts, as divorce would be conceptualized as an experience necessitating interventions specifically designed to reduce the subsequent risk of delinquency.
Given these varying trajectories for future research and clinical care, and the clear need to distinguish between them, several genetically-informed studies have already sought to delineate the origins of the association between divorce and delinquency. Most recently, a series of Children-of-Twins studies by D’Onofrio and colleagues (D’Onofrio et al., 2007
; D’Onofrio et al., 2005
) explored whether genetic or environmental factors related to the twin parent accounted for the association between parental divorce and offspring psychopathology. Results consistently supported an environmentally-mediated effect of divorce on offspring externalizing psychopathology/behavior problems. Similarly, O’Connor et al. (2000)
examined 398 adoptive and biological families of 12 year-olds in a prospective longitudinal study, comparing mean externalizing behavior problems across divorced and intact adoptive and biological families (O’Connor, Caspi, DeFries, & Plomin, 2000
). They found that the associations between parental divorce and child behavior problems were not consistently stronger in biological than in adoptive families, results that again suggest environmental mediation.
Although such findings are collectively consistent with an environmental influence of divorce on child behavior problems, additional research is needed to confirm this conclusion. First, only studies of non-biologically related family members can completely exclude passive rGE (Burt, McGue, Krueger, & Iacono, 2007
). Because adoptive parents do not share genes with their adopted children, passive rGE is fully eliminated, thereby providing a direct estimate of family-level or “shared” environmental influences. Additional adoption studies are thus needed to more definitively clarify the origin of the association between divorce and delinquency.
Second, prior studies have relied exclusively on standard behavioral genetic techniques (i.e., comparisons of the association between divorce and delinquency across family members with different degrees of genetic relatedness). Though these designs do allow researchers to generally disambiguate genetic from environmental mediation (though as noted, unless samples include non-biologically related family members, passive rGE cannot be fully resolved), constructive replication using other sorts of “natural experiments” would most certainly serve to strengthen these conclusions. In particular, we could evaluate the association between divorce and delinquency by timing of divorce, comparing parental divorces that preceded the birth/adoption of the adolescents (i.e., those from prior romantic relationships) to parental divorces that occurred during the adolescents’ lifetime (i.e., the divorce of the rearing parents). Should genes common to parent and child mediate the association, we would expect non-adopted youth to manifest higher rates of delinquency in the presence of parental divorce, even if the divorce preceded their birth (i.e., was from a prior parental relationship). Moreover, this pattern would not extend to adopted youth. By contrast, environmental mediation would be indicated if delinquency in non-adopted youth is associated only with divorces during the adolescent’s lifetime, and this association is equivalent to that in adopted youth.
Though the latter design would help to further delineate the roles of passive rGE and the environment in the association between parental divorce and adolescent delinquency, it has never before been used (to our knowledge). The current study sought to do just this, thereby serving to more fully clarify the origin of the association between parental divorce and adolescent delinquency.