Objective-The authors used an adoption study design to investigate environmental influences on risk for psychopathology in adolescents with depressed parents.Method-Participants were 568 adopted adolescents ascertained through large adoption agencies, 416 nonadopted adolescents ascertained through birth records, and their parents. Clinical interviews with parents and adolescents were used to determine lifetime DSM-IV-TR diagnoses of major depressive disorder, oppositional defiant disorder, conduct disorder, attention deficit hyperactivity disorder (ADHD), and substance use disorders in adolescents and major depression in mothers and fathers. Effects of parental depression (either parent with major depression, maternal major depression, and paternal major depression) on adolescent psychopathology were tested in nonadopted and adopted adolescents separately, and interactive effects of parental depression and adoption status were tested.Results-Either parent having major depression and a mother having major depression were associated with a significantly greater risk for major depression and disruptive behavior disorders in both nonadopted and adopted adolescents. Paternal depression did not have a main effect on any psychiatric disorder in adolescents and, with one exception (ADHD in adopted adolescents), did not predict significantly greater likelihoods of disorders in either nonadopted or adopted adolescents.Conclusions-Maternal depression was an environmental liability for lifetime diagnoses of major depression and disruptive disorders in adolescents. Paternal depression was not associated with an increased risk for psychopathology in adolescents.Compared with children of nondepressed parents, children of depressed parents have a higher risk for depression (1) as well as for attention problems, behavior management problems, and conduct disorder (2-5). While there has been considerable research on mechanisms of risk in these families, no study has provided a direct test of the extent to which there is an environmental effect of parental major depressive disorder (that is, separate from genetic influences) on psychopathology in children. In this study, we investigated the influence of environmental factors on risk for psychopathology in adopted and nonadopted adolescents of depressed parents.Most empirically supported models of risk in families of depressed parents include factors that are conceptualized as environmental variables, such as harsh parenting and family conflict (6). Many of these family "environment" variables, however, are genetically influenced (7,8) Address correspondence and reprint requests to Dr. Tully, Department of Psychology, N218 Elliott Hall, University of Minnesota, 75 East River Rd., Minneapolis, MN 55455; and share common genetic influences with psychopathology in adolescents (9,10)). For example, family conflict is characteristic of families with depressed parents (11) and is associated with adolescent depression (12,13). Rice and colleagues (14) found that family conflict ha...

Learning to respond to others’ distress with well-regulated empathy is an important developmental task linked to positive health outcomes and moral achievements. However, this important interpersonal skill set may also, paradoxically, confer risk for depression and anxiety when present at extreme levels and in combination with certain individual characteristics or within particular contexts. The purpose of this review is to describe an empirically-grounded theoretical rationale for the hypothesis that empathic tendencies can be “risky strengths”. We propose a model in which typical development of affective and cognitive empathy can be influenced by complex interplay among intraindividual and interindividual moderators that increase risk for empathic personal distress and excessive interpersonal guilt. These intermediate states, in turn, precipitate internalizing problems that map onto empirically-derived fear/arousal and anhedonia/misery subfactors of internalizing disorders. The intraindividual moderators include a genetically-influenced propensity toward physiological hyperarousal, which is proposed to interact with genetic propensity to empathic sensitivity to contribute to neurobiological processes that underlie personal distress responses others’ pain or unhappiness. This empathic personal distress then increases risk for internalizing problems, particularly fear/arousal symptoms. Similarly, interactions between genetic propensities toward negative thinking processes and empathic sensitivity are hypothesized to contribute to excess interpersonal guilt in response to others’ distress. In turn, this interpersonal guilt increases risk for internalizing problems, especially anhedonia/misery symptoms. Interindividual moderators, such as maladaptive parenting or chronic exposure to parents’ negative affect, further interact with these genetic liabilities to amplify risk for personal distress and interpersonal guilt, as well as for consequent internalizing problems. Age-related increases in the heritability of depression, anxiety, and empathy-related constructs are consistent with developmental shifts toward greater influence of intraindividual moderators throughout childhood and adolescence, with interindividual moderators exerting their greatest influence during early childhood. Efforts to modulate neurobiological and behavioral expressions of genetic dysregulation liabilities and to promote adaptive empathic skills must thus begin early in development.

Empathic tendencies have been associated with interpersonal and psychological benefits, but empathy at extreme levels or in combination with certain personal characteristics may contribute to risk for depression. This study tested the moderating role of cognitive emotion regulation in depression's association with empathy using nonlinear models. Young adults (N = 304; 77% female; M = 19 years) completed measures of cognitive emotion regulation strategies, depression, and affective and cognitive empathy. Individuals with good regulation had low levels of depression overall and their depression symptoms were lowest when levels of affective empathy were average. Individuals with poor regulation had high levels of depression overall, particularly when levels of empathy were moderate to high. Extremely high and low levels of cognitive empathy were associated with elevated depression, and this association was not moderated by regulation. These findings suggest tendencies to respond empathically to others' needs is neither an adaptive nor maladaptive characteristic but rather moderate empathy, particularly in the context of good regulation, may offer the greatest protection against depression.

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OBJECTIVE. The purpose of this study was to examine the relationship between alcohol exposure in pregnancy and offspring conduct disorder symptoms in adolescence and to examine how much this increasingly known association may be mediated by maternal and paternal externalizing diagnoses, including lifetime maternal and paternal alcohol and drug abuse/dependence diagnoses as well as antisocial disorders. Few other studies have examined the contribution of these diagnoses across both parents. METHOD. A population sample of 1252 adolescents (53.8% female; drawn from the Minnesota Twin Family Study) as well as both of their parents completed structured diagnostic interviews to generate lifetime psychiatric diagnoses; mothers were also retrospectively interviewed about alcohol and nicotine use during pregnancy. Linear regression models were used to test the effects of prenatal alcohol exposure on adolescents' conduct-disorder symptoms. RESULTS. Prenatal exposure to alcohol was associated with higher levels of conduct-disorder symptoms in offspring, even after statistically controlling for the effects of parental externalizing disorders (illicit substance use disorders, alcohol dependence, and antisocial/behavioral disorders), prenatal nicotine exposure, monozygosity, gestational age, and birth weight. CONCLUSIONS. Prenatal alcohol exposure contributes to increased risk for conduct disorder in offspring.