Parenting and child impulsivity are consistent predictors of children’s externalizing symptoms; however, the role of the range of parenting (i.e., variation in parenting across contexts), and its interactions with child impulsivity, are poorly understood. We examined whether characteristic parenting practices and parenting range predicted the course of externalizing symptoms in 409 children (M age = 3.43 years at baseline, 208 girls) across ages 3, 5, 8, and 11. We assessed parent positive affectivity (PPA), hostility, and parenting structure at child age 3 using three behavioral tasks that varied in context, examining range by modeling a latent difference score for each parenting dimension. Greater PPA range, mean structure, and parenting structure range all predicted fewer symptoms at age 3 for children with higher impulsivity. Lower mean hostility predicted fewer symptoms at age 3 for children with lower impulsivity. Greater PPA, and smaller PPA range, predicted a decrease in symptoms for children higher in impulsivity. Lower hostility range predicted a decrease in symptoms for children with lower impulsivity but predicted maintaining symptoms for children with higher impulsivity. Results demonstrate the differential roles average parenting practices and parenting range play in the development of child externalizing psychopathology, especially in the context of child impulsivity.

Previous cross-sectional work has consistently found associations between neuroticism and impulsivity and nonsuicidal self-injury (NSSI). However, there are few longitudinal studies of personality risk factors for NSSI. In this study, we examined associations between individual differences in temperament at age 3 and NSSI from ages 9 to 15. At age 3, 559 preschool-aged children (54% male; Mage = 42.2 months [SD = 3.10]) completed laboratory assessments of temperament. Parents also completed questionnaires about their child’s temperament. Children completed a diagnostic interview assessing NSSI engagement at ages 9, 12, and 15. By the age 15 assessment, 12.4% of adolescents reported engaging in NSSI. In univariate models, we found that higher levels of observed sadness and maternal-reported sadness and anger were associated with increased risk for NSSI. In multivariate models, female sex and maternal-reported anger were significantly associated with greater likelihood of NSSI. Laboratory observed sadness and impulsivity were associated with a higher likelihood of NSSI. This work extends the literature on personality risk factors associated with NSSI by finding longitudinal associations between early childhood negative affect and later NSSI engagement during adolescence.

In this article, we consider an often overlooked model that combines mediation and moderation to explain how a third variable can relate to a risk factor–psychopathology relationship. We refer to it as moderation and mediation in a three-variable system. We describe how this model is relevant to studying vulnerability factors and how it may advance developmental psychopathology research. To illustrate the value of this approach, we provide several examples where this model may be applicable, such as the relationships among parental externalizing pathology, harsh parenting, and offspring psychopathology as well as between neuroticism, stressful life events, and depression. We discuss possible reasons why this model has not gained traction and attempt to clarify and dispel those concerns. We provide guidance and recommendations for when to consider this model for a given data set and point toward existing resources for testing this model that have been developed by statisticians and other methodologists. Lastly, we describe important caveats, limitations, and considerations for making this approach most useful for developmental research. Overall, our goal in presenting this information to developmental psychopathology researchers is to encourage testing moderation and mediation in a three-variable system with the aim of advancing analytic strategies for studying vulnerability factors.

Risk for depression is expressed across multiple levels of analysis. For example, parental depression and cognitive vulnerability are known markers of depression risk, but no study has examined their interactive effects on children's cortisol reactivity, a likely mediator of early depression risk. We examined relations across these different levels of vulnerability using cross-sectional and longitudinal methods in two community samples of children. Children were assessed for cognitive vulnerability using self-reports (Study 1; n = 244) and tasks tapping memory and attentional bias (Study 2; n = 205), and their parents were assessed for depression history using structured clinical interviews. In both samples, children participated in standardized stress tasks and cortisol reactivity was assessed. Cross-sectionally and longitudinally, parental depression history and child cognitive vulnerability interacted to predict children's cortisol reactivity; associations between parent depression and elevated child cortisol activity were found when children also showed elevated depressotypic attributions as well as attentional and memory biases. Findings indicate that models of children's emerging depression risk may benefit from the examination of the interactive effects of multiple sources of vulnerability across levels of analysis.

Preliminary work indicates that cognitive vulnerability to depression may be associated with variants of the serotonin transporter promoter polymorphism (5-HTTLPR) and the valine to methionine at position 66 (val66met) polymorphism of the brain-derived neurotrophic factor (BDNF) gene; however, existing reports come from small samples. The present study sought to replicate and extend this research in a sample of 375 community-dwelling children and their parents. Following a negative mood induction, children completed a self-referent encoding task tapping memory for positive and negative self-descriptive traits. Consistent with previous work, we found that children with at least one short variant of the 5-HTTLPR had enhanced memory for negative self-descriptive traits. The BDNF val66met polymorphism had no main effect but was moderated by maternal depression, such that children with a BDNF methionine allele had a heightened memory for negative self-descriptive traits when mothers had experienced depression during children's lifetimes; in contrast, children with a methionine allele had low recall of negative traits when mothers had no depression history. The findings provide further support for the notion that the 5-HTTLPR is associated with cognitive markers of depression vulnerability and that the BDNF methionine allele moderates children's sensitivity to contextual factors.

Researchers have long been interested in whether particular temperamental traits in childhood connote risk for depressive disorders. For example, children characterized as having high negative emotionality (NE; sadness, fear, anger) and low positive emotionality (PE; anhedonia, listlessness, and lack of enthusiasm) are hypothesized to be at risk for depression. Few studies, however, have examined whether (and how) these two temperamental dimensions interact to confer risk. In a sample of 329 preschoolers, the present study addressed this question by examining the relation between PE and NE and asymmetry in resting EEG activity in frontal and posterior regions, which are putative biomarkers for depression. Using a laboratory battery to define temperament, we found an interaction of PE and NE on posterior asymmetry. Specifically, when PE was high, NE was associated with greater relative right activity. When PE was low, NE was not related to posterior asymmetry. These results were driven by differences in EEG activity in right posterior regions, an area associated with emotional processing and arousal, and were specific to girls. We found no relation between temperament and frontal asymmetry. These findings suggest that, at least for girls, PE and NE may have an interactive effect on risk for depression.

This study examined associations between temperament at age 3 and depressotypic cognitive styles at age 7 in a community sample of children. Sixty-four preschool aged children were assessed for positive emotionality (PE) and negative emotionality (NE) using a standardized battery of laboratory tasks and naturalistic home observations. At follow-up 4 years later, the children completed laboratory tasks designed to tap helplessness in social and problem-solving situations, positive and negative information-processing biases, and self-reports of attributional style. Lower PE at age 3 predicted greater helplessness in the interpersonal task and decreased positive schematic processing. There was little evidence for a relationship between NE and depressotypic cognitive styles. Our findings are consistent with the hypothesis that some portion of cognitive vulnerability to depression may stem from early-emerging differences in the expression of positive emotions.This work is based upon a dissertation submitted to the Graduate School of SUNY at Stony Brook by the first author. Portions of this work were supported by NIMH Research Grants RO1 MH45757 and RO1 MH069942. The authors acknowledge the consultation and support of Hill Goldsmith and Everett Waters, and the assistance of Cindy Huang, Grace Lee, Magda Kulesza, Suzanne Rose, and Jayanta Hegde for their help in data collection. Thanks also to the families who participated in this study.

Background. Offspring of depressed parents experience impairment in a number of domains of functioning. Few studies have examined the impact of both maternal and paternal depression and co-morbid psychopathology on offspring functioning.

Method. Oregon Adolescent Depression Project participants were administered diagnostic interviews and completed measures of psychosocial functioning during adolescence (mean=16·6, S.D.=1·19) and again during young adulthood (mean=24·5, S.D.=0·51). Diagnostic interviews were also conducted with the mothers and fathers of the target individual.

Results. After controlling for relevant demographic characteristics, parental co-morbid psychopathology, and offspring psychopathology, maternal depression was associated with higher levels of physical symptoms (β=0·14, S.E.=0·07) during adolescence, and higher levels of minor stressors (β=2·52, S.E.=1·07) and a greater risk for using mental health services (OR 1·86, 95% CI 1·14–3·03) in young adulthood. Paternal depression was associated with offspring experiencing more major stressors (β=0·27, S.E.=0·07), having lower perceived social competence (β=−0·17, S.E.=0·08), and being more likely to attempt suicide (OR 2·65, 95% CI 1·19–5·92) during adolescence, as well as lower perceived social competence (β=−1·21, S.E.=0·49) in young adulthood.

Conclusions. Offspring of depressed parents demonstrate impairment in a variety of domains, even after controlling for the effects of their own psychopathology. Further research on the mechanisms that lead to these impairments, as well as the role of these impairments in the subsequent development of psychopathology, is warranted.

Background. There is a large literature indicating that the offspring of mothers with Major Depressive Disorder (MDD) are at increased risk for depression. However, much less is known about the effects of paternal MDD on offspring psychopathology.

Method. We addressed this issue using a large community sample of parents and their adolescent and young adult offspring (n=775). Parents and offspring were independently assessed with semi-structured diagnostic interviews. Offspring were interviewed three times from mid-adolescence to age 24 years.

Results. Maternal MDD was significantly associated with offspring MDD. Paternal MDD was also significantly associated with MDD in offspring, but only among offspring with depressive episodes of moderate or greater severity. These effects persisted after controlling for socio-economic status, family intactness, and non-mood disorders in both parents. Rates of MDD were particularly elevated in offspring of mothers and fathers with early-onset MDD, and offspring of fathers with recurrent MDD. The magnitude of the associations between MDD in parents and offspring was generally in the small-to-medium range.

Conclusions. These results confirm previous findings of elevated risk of MDD in the offspring of depressed mothers. In addition, the results suggest that MDD in fathers is associated with increased risk of depression in offspring, but that it is limited to MDD episodes in offspring of moderate or greater severity.