This study investigated whether the association between parental major depressive disorder (MDD) and elevated risk for disruptive behavior disorders (DBD) in the offspring is accounted for by parental MDD, parental DBD, or both. We found that the offspring of parents with MDD plus DBD had significantly higher rates of DBD in general, and ADHD in particular, than those of parents with MDD alone. Analysis of the unique risk contributed by parental MDD and parental DBD, respectively, revealed that both parental MDD and DBD conferred independent risk for MDD and DBD in the offspring, whereas only parental DBD conferred independent risk for conduct disorder and ADHD, and only parental MDD conferred independent risk for oppositional defiant disorder. These findings support the study hypothesis and suggest that the elevated rates of DBD in the offspring of parents with MDD may be due in part to the presence of DBD in the parents themselves.
Our findings confirm and extend results by other groups suggesting that some of the elevated DBD among offspring of depressed mothers are accounted for by antisocial behaviors in the mothers or fathers (Kim-Cohen et al., 2005
, Marmorstein et al., 2004
). Our study extends these findings by demonstrating that childhood parental history of disruptive behavior disorders (including ADHD and oppositional disorder as well as conduct disorder) contribute to this increased risk.
The specific association between parental DBD and childhood conduct disorder and ADHD in our study is consistent with studies documenting the heritability of conduct disorder (Gelhorn et al., 2006
) and ADHD (Faraone et al., 2005
). The specific association between parental MDD and childhood oppositional defiant disorder is interesting given the frequent comorbidity between oppositional defiant disorder and mood disorders (Kessler et al., 2005
) and the similarities in affective dysregulation between the two disorders (Greene and Doyle, 1999
). Additional work is needed to clarify whether symptoms of oppositional defiant disorder are an early characteristic of or marker of risk for major depression. One hypothesis is that the negative affect reactivity and ease to anger found among children with ODD may represent, in some cases, subthreshhold presentations of irritable depression.
Another possibility is that DBDs in the children and parents may be a reflection of a temperamental factor which may be a precursor to MDD. For example, emotionality or negative affectivity, especially in the absence of positive affectivity, has been associated with risk for MDD (Lonigan et al., 2003
), and high emotionality (in particular expressions of anger) in early childhood has been found also to predict onset of disruptive behavior symptoms (Rydell et al., 2003
). Additionally, our group has found that motivational behavioral disinhibition, defined as the reactive tendency to exhibit boldness, heightened exploration, and talkativeness in unfamiliar settings, measured in the preschool years predicts elevated risk for disruptive behavior disorders and comorbid mood disorders in early and middle childhood (Hirshfeld-Becker et al., 2004, 2007
). Therefore, DBDs may be indexing a temperamental precursor to MDD, which puts the child at risk for a trajectory consisting of behavioral disinhibition in toddlerhood or preschool years, disruptive behavior disorders in childhood, and MDD later in childhood, adolescence or adulthood. Longitudinal studies following disinhibited children over time are needed to further examine this possibility.
The elevated rate of mania among the offspring of parents with MDD+DBD is noteworthy. Although we excluded offspring whose parents had met full criteria for mania, and although we assessed all parents carefully with the SCID, it is possible that some of the parents from the MDD+DBD group might have had undetected bipolar spectrum illness. Family studies have shown that among offspring of parents with bipolar disorder, the rate of ADHD is approximately three times higher than among offspring of normal controls, and that bipolar disorder is twice as common among relatives of ADHD probands compared to relatives of normal control probands (Faraone et al., 1997
). However, since only approximately 20% of the first-degree relatives of patients with bipolar disorder have bipolar disorder themselves, and since it is very common for these relatives to have unipolar depression and disruptive behavior disorders (e.g. Chang et al., 2003
; Joyce et al., 2004
), it is equally plausible that parental unipolar depression and comorbid parental DBDs confer additive risk for bipolar disorder.
The strengths of this study include the complete assessment of both parents in each family with standardized, well-validated diagnostic instruments that evaluated childhood as well as adulthood psychiatric disorders; the blind assessments of children with structured diagnostic interviews; and the large sample size.
However, our results should be considered in light of several limitations. First, parental DBDs were assessed based upon retrospective reports by parents using structured diagnostic interviews and, with the exception of some parents who still met criteria for ADHD, were not observed directly. Second, because parents with MDD+DBD also had more comorbid disorders and had children with higher numbers of comorbid disorders, we cannot be sure whether the associations we observed represent a specific relationship between parental and child DBDs, or a case of greater severity in parents breeding greater severity in children. When we covaried parental comorbidity in our analyses, only the specific associations between parental DBD and child conduct disorder and between parental MDD and child DBD, ODD, and MDD remained. However, the odds ratios for all previously significant associations remained at or close to 2.0, and the significances for most remained at trend level, suggesting that the loss in significance may have been due to reduced power. Moreover, if it was parental comorbid disorders and not parental DBDs that were conferring risk for child DBDs, we would expect that within the group of offspring of MDD and within the group of offspring of MDD+DBD, presence of child DBDs would be associated with higher numbers of parental comorbid disorders. However, this was clearly not the case. In further support of a specific association between parental and child DBDs is the fact that parental MDD+DBD conferred increased risk only for the DBDs (DBDs in general, ADHD, and conduct disorder) and not for all disorders in general (e.g. the anxiety disorders), as would be expected if the effect were simply of severity in parents conferring increased severity in children. Similarly, some disorders (e.g. ADHD) did not show a step-wise increase across groups as would be expected if they were linked to increasing parental comorbidity. This issue needs further study in larger samples.
Third, since our analysis was conducted on a sample of offspring of parents with panic disorder, many affected parents also had comorbid panic disorder. Therefore it is not known how results would generalize to samples of offspring of parents with MDD and DBD alone. Third, the group of offspring of parents with DBD without MDD was very small, and the size of this group may have reduced the study’s power to detect differences, particularly in four-group comparisons. Fourth, assessments of children 12 and under relied on parental report. Future study waves, in which all the children will be old enough to be directly interviewed about their lifetime symptoms, will enable us to further assess the risk conferred by parental MDD and DBD. Finally, whereas our analysis covaried SES, other environmental factors, including exposure to parents’ symptoms of affective or behavioral dysregulation, might also influence the associations noted.
Despite these limitations, this study suggests that elevated rates of disruptive behavior disorders (DBD) in the offspring of parents with major depressive disorder (MDD) may be due in part to increased presence of DBD in the parents themselves. Further studies of samples not selected on the basis of parental panic disorder are needed to confirm these results. Clinically, our findings suggest that offspring of parents with MDD with DBD are at particularly elevated risk for DBD themselves, and that they should be targeted for preventive interventions.