Recent research (e.g., Rothbaum & Weisz, 1994
; Waschbusch, 2002
) has converged in suggesting a robust association, both concurrent and longitudinal, between conflictive/negative parent–child relationships and child and adolescent externalizing disorders, namely attention-deficit/hyperactivity disorder (ADHD), conduct disorder (CD), and oppositional defiant disorder (ODD). A “parent effects model,” in which a conflictual/negative parenting style causes and
child externalizing behavior, has traditionally been cited as responsible for this association (Collins, Maccoby, Steinberg, Hetherington, & Bornstein, 2000
; Maccoby, 2000
). Supporting this interpretation is the large body of experimental treatment research that has found that improving parents’ discipline strategies leads to a reduction in children’s externalizing problems (Dishion, Andrews, Kavanagh, & Soberman, 1996
; Dishion & Kavanagh, 2000
; Forgatch & DeGarmo, 1999
; Patterson, 1974
; Patterson, Dishion, & Chamberlain, 1993
). Furthermore, numerous correlational studies (Campbell, Pierce, Moore, Marakovitz, & Newby, 1996
; Gardner, Sonuga–Barke, Sayal, 1999
; Loukas, Fitzgerald, Zucker, & von Eye, 2001
; Wasserman, Miller, Pinner, & Jaramillo, 1996
) have also found evidence of significant effects of poor parenting/negative parent–child relationships on later child externalizing, even when controlling for earlier externalizing.
However, some researchers have argued that the association between parent–child conflict and externalizing is not solely parent driven, but may also be instigated by the child, such that the child’s oppositional, irritable behavior elicits
conflictive reactions from his or her parents. Supportive evidence for this “child effects model” comes from a seminal study by Anderson, Lytton, and Romney (1986)
, in which CD and nonproblem boys, and their respective mothers, interacted in unrelated pairs during play and structured tasks. When interacting with nonproblem children, the mothers of CD children did not differ from the mothers of nonproblem children in commands, positive behaviors, or negative behaviors. However, all mothers responded more negatively to and gave more commands to children with CD than to nonproblem children, suggesting that the maladaptive interactions between CD boys and their mothers were driven mainly by the child. Similarly, Kerr and Stattin (2000)
found that low parental knowledge of their child’s daily activities was related to increased delinquency. However, children’s spontaneous disclosures of information explained more of this association than did parents’ surveillance efforts, suggesting that the association between parental monitoring and child adjustment may be partially child driven. Child effects have also been demonstrated in drug treatment experiments. Barkley and Cunningham (1979)
found that when children’s nonattentive and noncompliant behavior is improved by the administration of stimulant drugs, their mothers become less controlling and mother–child interactions are nearly normalized. This improvement in mothers’ directive reactions has been found to be consistent across different doses of Ritalin (Barkley, Karlsson, Pollard, & Murphy, 1984).
Thus, both child-driven and parent-driven mechanisms have been identified. How might we account for these seemingly incompatible results between studies that support child effects and those that support parent effects? This most likely explanation is a bidirectional or reciprocal model, in which parent–child conflict and child externalizing behavior both influence, and are influenced by, each other. For example, it may be that the previously mentioned Kerr and Stattin (2000)
results, which have generally been interpreted as supportive of child effects, are in fact bidirectional in nature. Specifically, adolescents who spontaneously disclose more information to their parents may do so because of parental expectations that were established earlier in life. Thus, both processes may be important but are not revealed because of the restricted age range of the sample (participants were 14 years old).
Recent research has attempted to explicitly test this sort of bidirectional model, with mixed results. Bates, Petit, Dodge, and Ridge (1998)
evaluated child temperament and parental control as interacting predictors of behavioral outcomes independently in two longitudinal samples. In both samples, they found that children’s early unmanageability predicted later externalizing behavior more accurately when the mother had been observed to be low in restrictive control, implicating both child-and parent-driven processes as important for later child externalizing behavior. Similarly, O’Connor, Deater–Deckard, Fulker, Rutter, and Plomin (1998)
used a longitudinal adoption sample to examine possible reciprocity. Analyses revealed that children at genetic risk were more likely to receive negative parenting than those not at genetic risk. However, the results also showed that much of the association between negative parenting and children’s externalizing was not a function of the child’s genetic risk, thereby allowing for the possibility of reciprocal effects. Similar results were obtained in another, although cross-sectional, adoption study, that by Ge, Conger, Cadoret, Neiderhiser, Yates, Troughton, and Stewart (1996)
. In addition, there is research suggesting that children with CD respond more aversively to punishment than do non-CD children (Lytton, 1990
; Patterson, 1976
), results that have generally been interpreted in support of a bidirectional perspective. Other studies, however, have not found evidence of reciprocal effects between poor parenting and child externalizing over time (Campbell et al., 1996
; Vuchinich, Bank, & Patterson, 1992
), although their results have suggested concurrent reciprocal relationships.
Thus, although there is increasing evidence that both parent-driven and child-driven effects may operate in a mutual and reciprocal fashion, the direction of the relationship between conflictual relationships with one’s child and child externalizing behavior has yet to be conclusively resolved. Perhaps as a consequence of this lingering uncertainty, there have been very few studies of the etiology of this relationship (i.e., genetic or environmental). The association may reflect genes that are shared by parents and their children, or it may reflect a direct influence of parents or children on each other (i.e., environmental mediation), or some combination of the two. In the present study, we sought to clarify and unravel both the direction and the etiology of the relationship between conflict and child externalizing over time using a genetically informative twin sample. We specifically sought to answer two questions: Do conflict and externalizing at age 11 independently impact conflict and externalizing at age 14? What is the etiology (i.e., genetic and/or environmental) of these relationships over time?
To answer these questions, however, we did not simply examine the similarity of genetic influences over time. Instead, we employed a biometric cross-lagged design that, that, to our knowledge, has not been fit in any previous study (although it is similar to that employed by Neiderhiser, Reiss, Hetherington, & Plomin, 1999
). This design is advantageous because it constrains all cross-age associations to take the form of phenotypic partial regression coefficients, thereby controlling for the association between conflict and externalizing at age 11 when examining their effects on each other at age 14. In other words, the use of partial regression coefficients ensures that the relationship between, for example, conflict at 11 and externalizing at 14 is not actually being driven by conflict’s “preexisting” relationship with externalizing at age 11. In addition, because the study is genetically informative, we were able to decompose the cross-lagged coefficients into their genetic and environmental components.
However, the most salient feature of this design is that it enables us to examine not only the proportions of genetic and environmental influences on the cross-lags, but also the processes by which parent–child relations and child misbehavior impact each other over time. As put forth by Turkheimer and Waldron (2000)
, parents do not respond directly to their children’s genes, but instead do so indirectly, via their children’s phenotypes. (The children’s phenotypes, or observed characteristics, are thought to result from their genetic predispositions, prenatal, and postnatal environmental experiences.) They challenged the behavioral genetics field to incorporate these psychological processes, happening at the level of the phenotype, into their studies. Along these lines, we attempted to answer questions about the etiology of the longitudinal relationship between parenting and externalizing by modeling the impact of the phenotypic cross-lags on the genetic and environmental expression of conflict and externalizing (EXT) symptoms at age 14. Such modeling would enable us to address the challenge laid out by Turkheimer and Waldron (2000)
, and determine how (i.e., via genetic and environmental influences) conflict and EXT at age 14 were influenced by the observed characteristics
of conflict and EXT present at age 11 (via the cross-lags). In this way, it was possible to address previously unanswered questions. Is conflict at 14 heritable because it is a response to the child’s observed EXT symptoms at age 11? Does conflict at age 11 account for environmental variance in EXT at 14? If so, we could then conclude that the observed conflict between parents and children exerts an environmentally mediated impact on child EXT behavior.
As indicated, Neiderhiser et al. (1999)
conducted a similar study, in which they examined 395 families with adolescent siblings who participated in the Nonshared Environment and Adolescent Development study at two points of assessment, 3 years apart (also presented in Reiss, Neiderhiser, Hetherington, & Plomin, 2000
). The adolescents ranged in age from 10 to 18 during their intake assessment. Similarly to the present analyses, they examined the cross-lagged associations between parental conflict–negativity and adolescent antisocial behavior, although they did so in two independent models rather than in a single, nested model. They found that much of the etiology of the cross-lagged coefficients was genetic in nature. However, the Neiderhiser et al. (1999)
study centered on the decomposition of the phenotypic cross-lagged correlations into their genetic and environmental components, and did not examine the phenotypic-driven processes by which parent–child relations and child misbehavior impact each other over time (i.e., what is the impact of the phenotypic cross-lags on the genetic and environmental expression of the age 14 phenotypes?). This is an important distinction, because although useful, decomposing the cross-lagged coefficients does not reveal how the cross-lags impacted conflict and EXT at age 14. Thus, the present study seeks to expand upon the pioneering work of Neiderhiser et al. (1999)
by examining the phenotypic-driven contributions of the cross-lagged coefficients to the genetic and environmental components composing conflict and EXT at age 14.
Consistent with both the child effects and parent effects models, we hypothesized that we would find evidence of a bidirectional relationship between conflict and child EXT. Furthermore, we hypothesized that the phenotypic cross-lags will impact both the genetic and environmental components of conflict and EXT at age 14. Specifically, the results of Anderson et al. (1986)
indicated that parents may be responding to their child’s oppositional/delinquent behavior. Consistent with this notion is the finding that parenting variables have been found to be moderately heritable (Burt, Krueger, McGue, & Iacono, 2003
; Neiderhiser et al., 1999
). Thus, we suspected that parenting variables were heritable because parents were, to some extent, responding to their child’s externalizing behaviors, which were themselves genetically influenced (see Burt, Krueger, McGue, & Iacono, 2001
). Given this, we proposed that the heritability of conflict at 14 owed in part to the observed effects of externalizing at age 11 (i.e., the child effects path).
However, there is a large body of treatment literature that finds that improving parenting styles results in a decrease in child externalizing (Dishion et al., 1996
; Dishion & Kavanagh, 2000
; Patterson, 1974
; Patterson et al., 1993
). Thus, we further suspected that a conflictive relationship with one’s child independently exacerbated and/or maintained the child’s oppositional/delinquent behavior, even when controlling for genetic influences on that behavior. Given this, we proposed that the environmental variance in EXT at 14 owes in part to contributions from observed conflict between parents and children at age 11 (i.e., the parent effects path). We did not have any specific hypotheses regarding whether the environmental variance accounted for in EXT would be shared environmental (i.e., family-wide and similarly impacting all children in the family) or nonshared environmental (i.e., child-specific and unique to each child; also includes measurement error).