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 childrens subsequent socioemotional and brain development. We begin with a review of the extant literature on caregiver-child dynamics, which reveals that RDoCs 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.

Peer victimization during high school is a common experience associated with engagement in risky health behaviors and elevated depressive symptoms. Mechanisms linking peer victimization to health outcomes remain inadequately understood. In the current study, latent class analysis was used to identify latent subclasses of college students who display similar patterns of responses to frequent peer victimization experiences during high school. We also examined moderating and mediating effects of coping (approach/avoidance) on relationships between victimization class and health outcomes (i.e., binge drinking, current smoking, depressive symptoms). College students completed questionnaire measures of peer victimization, approach and avoidance coping, binge drinking, smoking, and depressive symptoms. Four distinct patterns of peer victimization were identified among college students (Low, High, Moderate, and Social/Verbal). Moderation models revealed significant interactions of moderate victimization x approach coping on depressive symptoms and high victimization x avoidance coping on binge drinking. Mediation models revealed a significant indirect effect of avoidance coping on depressive symptoms for those in the high victimization class. Findings provide a greater understanding of the complex patterns of peer victimization. Coping efforts among varying peer victimization classes had different relationships with health outcomes during the college years. Interventions aimed at reducing health-risk and depressive symptoms among college student might benefit from increased attention to high school victimization experiences and current coping processes.Supplemental data for this article is available online at https://doi.org/10.1080/08964289.2021.1946468 .

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.

Background

Maternal depressive symptoms in pregnancy may affect offspring health through prenatal programming of the hypothalamic-pituitary-adrenal (HPA) axis. The biological mechanisms that explain the associations between maternal prenatal depressive symptoms and offspring HPA axis regulation are not yet clear. This pre-registered investigation examines whether patterns of maternal depressive symptoms in pregnancy are associated with infant cortisol reactivity and whether this association is mediated by changes in placental corticotropin-releasing hormone (pCRH).

Method

A sample of 174 pregnant women completed assessments in early, mid, and late pregnancy that included standardized measures of depressive symptoms and blood samples for pCRH. Infant cortisol reactivity was assessed at 1 and 6 months of age.

Results

Greater increases in maternal depressive symptoms in pregnancy were associated with higher cortisol infant cortisol reactivity at 1 and 6 months. Greater increases in maternal depressive symptoms in pregnancy were associated with greater increases in pCRH from early to late pregnancy which in turn were associated with higher infant cortisol reactivity.

Conclusions

Increases in maternal depressive symptoms and pCRH over pregnancy may contribute to higher infant cortisol reactivity. These findings help to elucidate the prenatal biopsychosocial processes contributing to offspring HPA axis regulation early in development.

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.

Objective

High pregnancy anxiety is a consistent predictor of earlier labor and delivery. Placental corticotropin-releasing hormone (pCRH) predicts earlier delivery consistently and it has been identified as a biological mediator of the association between pregnancy anxiety and gestational length. However, studies have not examined whether changes in pregnancy anxiety are associated with earlier birth as mediated by changes in pCRH during pregnancy. Accordingly, this study tests whether linear changes in pregnancy anxiety are associated with length of gestation indirectly through nonlinear increases in pCRH over pregnancy.

Methods

A sample of pregnant women (n=233) completed prenatal assessments in early pregnancy, second trimester, and third trimester that included a 4-item assessment of pregnancy anxiety and collection of blood samples assayed for pCRH using radioimmunoassay. Length of gestation was abstracted from medical records after birth.

Results

Increases in pregnancy anxiety from early pregnancy to third trimester predicted shorted length of gestation, as did nonlinear increases in pCRH over pregnancy. However, there was no evidence of an indirect effect of changes in pregnancy anxiety on length of gestation via changes in pCRH.

Conclusions

These results indicate that linear changes in pregnancy anxiety and nonlinear changes in pCRH during pregnancy are independent risk factors for shortened gestational length. This study adds to a small but growing body of work on biopsychological processes in pregnancy and length of gestation. Modeling changes in psychological and biological processes during pregnancy could provide more insight into understanding risk for adverse pregnancy outcomes.

Although maternal stress during pregnancy and even before conception shapes offspring risk for mental health problems, relatively little is known about the mechanisms through which these associations operate. In theory, preconception and prenatal stress may affect offspring mental health by influencing child responses to postnatal caregiving. To address this knowledge gap, this study had two aims. First, we examined associations between preconception and prenatal stress with child temperament profiles at age four using multilevel assessment of maternal perceived stress and stress physiology. Second, we tested child temperament profiles as moderators of associations between observed parenting behaviors during a parent-child free-play interaction when children were 4 years old and child behavior problems 1 year later. Latent profile analyses yielded four distinct child temperament profiles: inhibited, exuberant, regulated low reactive, and regulated high reactive. Consistent with hypotheses, preconception, and prenatal stress each independently predicted the likelihood of children having temperament profiles characterized by higher negative emotionality and lower regulation. Specifically, preconception perceived stress and prenatal cortisol predicted likelihood of children having an exuberant temperament, whereas prenatal perceived stress predicted likelihood of children having an inhibited temperament. Contrary to hypotheses, temperament profiles did not moderate predictions of child behavior problems from observed parenting behaviors; however, responsive parenting behaviors inversely predicted child behavior problems independently of child temperament. These findings add to growing evidence regarding effects of preconception factors on child outcomes and underscore a central role for responsive parenting behaviors in predicting more favorable child mental health independent of child temperament. (PsycInfo Database Record (c) 2024 APA, all rights reserved).