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Although the Research Diagnostic Criteria (RDoC) framework proposes biological and environmental mechanisms intersect in the etiology of psychopathology, there is no guidance on how to define or measure experiences in the environment within the RDoC matrix. Interpersonal dynamics during caregiver–child interactions involve temporal coordination of interacting partners' biobehavioral functioning; repeated experiences of signaling to caregivers and responding to caregivers' signals shape children's subsequent socioemotional and brain development. We begin with a review of the extant literature on caregiver-child dynamics, which reveals that RDoC's units of analysis (brain circuits, physiology, behavior, and self-report) are inextricably linked with moment-to-moment changes in the caregiving environment. We then offer a proof-of-concept for integrating biobehavioral RDoC units and environmental components via caregiver-child dynamics. Our approach uses dynamic structural equation models to estimate within-dyad dynamics involving arousal, social, cognitive, and negative or positive affective processes based on second-by-second changes in parasympathetic activity (RSA) during a conflict discussion and a positive event-planning task. Our results illustrate variation in parent–child RSA synchrony, suggesting differences depending on the driver (i.e., child- or parent-led) and on the unique and intersecting domains involved (e.g., positive or negative affect valence systems). We conclude with recommendations for conducting robust, methodologically rigorous studies of interpersonal dynamics that advance the RDoC framework and provide a summary of the clinical implications of this research. Examining caregiver-child dynamics during and across multiple dyadic interaction paradigms that differentially elicit key domains of functioning can deepen understanding of how caregiver- and child-led interpersonal dynamics contribute to child psychopathology risk. [ABSTRACT FROM AUTHOR]

Given that noncompliance is the most common externalizing problem during middle childhood and reliably predicts significant conduct problems, innovations in elucidating its etiology are sorely needed. Evaluation of in-the-moment antecedents and consequences of child noncompliance improves traction on this goal, given that multiple theories contend that child noncompliance and parent behavior mutually influence each other through negative reciprocation as well as contingent praise processes. Among a sample of 140 families (child age: 6–10 years; 32.1% female), the present study capitalized on intensive repeated measures of observed child noncompliance and parent negative talk and praise objectively coded during three unique tasks. We employed dynamic structural equation modeling to evaluate within-dyad parent–child behavioral dynamics and between-dyad differences therein. Results provided mixed support for hypotheses and suggested that antecedents and consequences of child noncompliance differed according to task demands and child ADHD symptoms. Contrary to models of coercive cycles, during child-led play, parent negative talk was more likely following prior child noncompliance, but child noncompliance was less likely following prior parent negative talk. As expected, during parent-led play, parent praise was less likely following prior child noncompliance, which was also less likely following prior parent praise. Relative to youth with fewer symptoms, for children with elevated ADHD symptoms, during a challenging clean-up task, child noncompliance was less stable and less contingent on prior parent negative talk. Results are discussed in terms of their implications of real-time parent–child interactions for typical and atypical development of externalizing problems. [ABSTRACT FROM AUTHOR]

Early life adversity is a potent risk factor for poor mental health outcomes across the lifespan, including offspring vulnerability to psychopathology. Developmentally, the prenatal period is a sensitive window in which maternal early life experiences may influence offspring outcomes and demarcates a time when expectant mothers and offspring are more susceptible to stressful and salutary influences. This prenatal plasticity constituted the focus of the current study where we tested the association of maternal early life adversity with infant stress regulation through maternal prenatal internalizing symptoms and moderation by prenatal social support. Mother-infant dyads (n = 162) were followed prospectively and mothers completed assessments of social support and depressive and anxiety symptoms across pregnancy. Infants completed standardized stress paradigms at one month and six months. There were several key findings. First, maternal prenatal depressive symptoms significantly mediated predictions of infant cortisol reactivity to the heel stick at one month from maternal early life adversity: specifically, maternal early life adversity positively predicted depressive symptoms in pregnancy, which in turn predicted dampened infant cortisol reactivity. Second, prenatal social support did not significantly moderate predictions of depressive or anxiety symptoms in pregnancy from maternal early life adversity nor did it alter the associations of maternal depressive or anxiety symptoms with infant stress regulation. These results suggest that maternal prenatal mental health is a key mechanism by which maternal early life adverse experiences affect offspring risk for psychopathology. We discuss potential clinical and health implications of dysregulated infant cortisol reactivity with respect to lifespan development. [ABSTRACT FROM AUTHOR]

Despite its transdiagnostic significance, there is modest evidence with respect to the predictive validity of childhood irritability, especially across developmental periods; similarly, little is known about explanatory factors underlying these predictions. This study had two goals: (1) to test the predictive validity of childhood irritability with respect to adolescent internalizing and externalizing problems, controlling for baseline ADHD and related psychopathology and (2) to test theoretically-derived family (i.e., parenting behavior, parenting stress) and social (i.e., peer status, social skills) constructs as explanatory factors of adolescent psychopathology. Two hundred thirty ethnically diverse (51.5% White) 5–10-year-old youth (32% female) with (n = 121) and without (n = 110) ADHD completed three separate laboratory-based assessments across six to seven years. Temporally-ordered predictors, putative mediators, and psychopathology outcomes were assessed using multiple informants (i.e., parent, teacher, youth) and methods (i.e., structured interviews, normed rating scales). Controlling for demographic factors, clinical correlates, and baseline psychopathology, childhood irritability uniquely predicted adolescent externalizing problems, but not internalizing problems. Next, analyses revealed that low social skills partially explained predictions of adolescent internalizing problems. However, family or social factors did not underlie predictions of adolescent externalizing problems. These preliminary findings support the predictive validity of childhood irritability with respect to early adolescent externalizing problems and implicate low social skills as a potentially unique mediator of internalizing outcomes. Intervention-induced improvements in social skills may minimize emergent psychopathology initiated by significant childhood irritability. [ABSTRACT FROM AUTHOR]

Given the increasing prevalence of adolescent depression, identification of its early predictors and elucidation of the mechanisms underlying its individual differences is imperative. Controlling for baseline executive functioning (EF), we tested separate ADHD dimensions (i.e., inattention, hyperactivity-impulsivity) as independent predictors of early adolescent depression, including temporally-ordered causal mediation by academic functioning and social problems, using structural equation modeling. At baseline, participants consisted of 216 children (67% male) ages 6–9 years old with (n = 112) and without (n = 104) ADHD who subsequently completed Wave 2 and 3 follow-ups approximately two and four years later, respectively. Predictors consisted of separate parent and teacher ratings of childhood ADHD and laboratory-based assessments of key EF domains. At Wave 2, parents and teachers completed normed rating scales of youth academic and social functioning; youth completed standardized assessments of academic achievement. At Wave 3, youth self-reported depression. Baseline inattention positively predicted early adolescent depression whereas childhood hyperactivity-impulsivity and EF did not. Neither academic nor social functioning significantly mediated predictions of depression from baseline ADHD and EF. We consider prediction of early adolescent depression from inattention, including directions for future intervention and prevention research. [ABSTRACT FROM AUTHOR]