Child self-regulation (SR), a key indicator for later optimal developmental outcomes, may be compromised in the presence of parental mental disorders, especially those characterized by affective dysregulation. However, positive parental behaviors have been shown to buffer against such negative effects, especially during infancy when SR shows great plasticity to environmental inputs. The current study investigated the effect of maternal and paternal lifetime and current internalizing disorders on the developmental trajectory of infant SR from 3 to 24 months, and the potential moderating role of positive parental behaviors. A latent growth model revealed that SR increased overall from 3 to 24 months. Mothers’ positive parental behaviors demonstrated significant moderation effects, such that maternal lifetime internalizing disorder was associated with higher SR intercept only among those with low levels of positive parental behavior. Mothers’ lifetime internalizing disorder was also associated with a lower linear slope in SR development with a moderate effect size. Fathers’ current internalizing disorder was significantly associated with a higher intercept and lower linear slope of the SR trajectory. The current study expands the infant SR literature by describing its early developmental trajectory as well as early risk and protective factors within the parent–infant environment, taking into consideration developmental inputs from both parents.

It is unclear how individual differences in parenting and brain development interact to influence adolescent mental health outcomes. This study examined interactions between structural brain development and observed maternal parenting behavior in the prediction of adolescent depressive symptoms and psychological well-being. Whether findings supported diathesis-stress or differential susceptibility frameworks was tested. Participants completed observed interactions with their mothers during early adolescence (age 13), and the frequency of positive and aggressive maternal behavior were coded. Adolescents also completed structural magnetic resonance imaging scans at three time points: mean ages 13, 17, and 19. Regression models analyzed interactions between maternal behavior and longitudinal brain development in the prediction of late adolescent (age 19) outcomes. Indices designed to distinguish between diathesis-stress and differential susceptibility effects were employed. Results supported differential susceptibility: less thinning of frontal regions was associated with higher well-being in the context of low levels of aggressive maternal behavior, and lower well-being in the context of high levels of aggressive maternal behavior. Findings suggest that reduced frontal cortical thinning during adolescence may underlie increased sensitivity to maternal aggressive behavior for better and worse and highlight the importance of investigating biological vulnerability versus susceptibility.

The prevalence of depression rises steeply during adolescence. Family processes have been identified as one of the important factors that contribute to affect (dys)regulation during adolescence. In this study, we explored the affect expressed by mothers, fathers, and adolescents during a problem-solving interaction and investigated whether the patterns of the affective interactions differed between families with depressed adolescents and families with nondepressed adolescents. A network approach was used to depict the frequencies of different affects, concurrent expressions of affect, and the temporal sequencing of affective behaviors among family members. The findings show that families of depressed adolescents express more anger than families of nondepressed adolescents during the interaction. These expressions of anger co-occur and interact across time more often in families with a depressed adolescent than in other families, creating a more self-sustaining network of angry negative affect in depressed families. Moreover, parents’ angry and adolescents’ dysphoric affect follow each other more often in depressed families. Taken together, these patterns reveal a particular family dynamic that may contribute to vulnerability to, or maintenance of, adolescent depressive disorders. Our findings underline the importance of studying affective family interactions to understand adolescent depression.

Affective family processes are associated with the development of depression during adolescence. However, empirical description of these processes is generally based on examining affect at the individual or dyadic level. The purpose of this study was to examine triadic patterns of affect during parent–adolescent interactions in families with or without a depressed adolescent. We used state space grid analysis to characterize the state of all three actors simultaneously. Compared to healthy controls, triads with depressed adolescents displayed a wider range of affect, demonstrated less predictability of triadic affective sequences, spent more time in and returned more quickly to discrepant affective states, and spent less time in and returned more slowly to matched affective states, particularly while engaged in a problem-solving interaction. Furthermore, we identified seven unique triadic states in which triads with depressed adolescents spent significantly more time than triads with healthy controls. The present study enhances understanding of family affective processes related to depression by taking a more systemic approach and revealing triadic patterns that go beyond individual and dyadic analyses.

Investigating etiological processes early in the life span represents an important step toward a better understanding of the development of personality pathology. The current study evaluated the interaction between an individual difference risk factor (i.e., temperament) and a biological risk factor for aggressive behavior (i.e., atypical [larger] rightward hippocampal asymmetry) in predicting the emergence of borderline personality disorder (BPD) and antisocial personality disorder symptoms during early adolescence. The sample consisted of 153 healthy adolescents (M = 12.6 years, SD = 0.4, range = 11.4–13.7) who were selected from a larger sample to maximize variation in temperament. Interactions between four temperament factors (effortful control, negative affectivity, surgency, and affiliativeness), based on the Early Adolescent Temperament Questionnaire—Revised, and volumetric measures of hippocampal asymmetry were examined as cross-sectional predictors of BPD and antisocial personality disorder symptoms. Boys were more likely to have elevated BPD symptoms if they were high on affiliation and had larger rightward hippocampal asymmetry. In boys, low affiliation was a significant predictor of BPD symptoms in the presence of low rightward hippocampal asymmetry. For girls, low effortful control was associated with elevated BPD symptoms in the presence of atypical rightward hippocampal asymmetry. This study builds on previous work reporting significant associations between atypical hippocampal asymmetry and poor behavioral regulation.

It has been suggested that biological factors confer increased sensitivity to environmental influences on depressive symptoms during adolescence, a crucial time for the onset of depressive disorders. Given the critical role of the hippocampus in sensitivity to stress and processing of contextual aspects of the environment, investigation of its role in determining sensitivity to environmental context seems warranted. This study prospectively examined hippocampal volume as a measure of sensitivity to the influence of aggressive maternal behavior on change in depressive symptoms from early to midadolescence. The interaction between aggressive maternal behavior and hippocampal volume was found to predict change in depressive symptoms. Significant sex differences also emerged, whereby only for girls were larger bilateral hippocampal volumes more sensitive to the effects of maternal aggressive behavior, particularly with respect to experiencing the protective effects of low levels of maternal aggressiveness. These findings help elucidate the complex relationships between brain structure, environmental factors such as maternal parenting style, and sensitivity to (i.e., risk for, and protection from) the emergence of depression during this life stage. Given that family context risk factors are modifiable, our findings suggest the potential utility of targeted parenting interventions for the prevention and treatment of adolescent depressive disorder.

This study examined the relations among temperament, emotion regulation, and depressive symptoms in early adolescents. Early adolescents provided self-reports of temperament on two occasions, as well as reports on emotion regulation and depressive symptomatology. Furthermore, 163 of these adolescents participated in event-planning and problem-solving interactions with their mothers. Adolescents with temperaments that were high in negative emotionality or low in effortful control displayed more emotionally dysregulated behaviors during the interaction tasks, reported having maladaptive responses to negative affect more often and adaptive responses less often, and had more depressive symptoms. In particular, adolescents with the high negative emotionality and low effortful control temperament combination reported the highest levels of depressive symptomatology. Sequential analyses of family interactions indicated that adolescents with more depressive symptoms were more likely to reciprocate their mothers' negative affective behaviors. Adolescents' adaptive and maladaptive responses to negative affect mediated the associations between their temperament and concurrent depressive symptoms.