Anxiety is one of the most prevalent and costly problems facing mothers and their young children. Theoretical models about the etiology of anxiety risk, reflecting bidirectional associations between mothers and offspring, have gone largely without direct empirical testing. This has left a critical gap in knowledge regarding the nature of familial risk that will be necessary for a full understanding of the etiology of anxiety problems, one of the most prevalent, pervasive, and costly public health concerns in the present day. Two specific barriers to the successful prevention and treatment of anxiety problems include (1) an absence of empirically validated models that elucidate bidirectional influences between mothers and children, and (2) a lack of knolwedge of the neurobiological mechanisms that may serve as mediators for the bidirectional transmission of anxiety risk in mothers and offspring. Results from this project will contribute to the scientific knowledge base of anxiety risk in children and mothers across infancy and toddlerhood. This projects adopts a unique longitudinal multi-trait, multi-method design to test three biological systems as mediators of bidirectional effects of anxiety risk in mother-child dyads between child ages 1 and 3 years. Multiple aspects of negative valence systems are used to represent risk for anxiety in both children and mothers, and multiple biological arousal and regulatory systems are studied as mechanisms. Consistent with an RDoC framework, the project adopts a dimensional approach and utilizes both targeted and general sampling methods. The work proposed uncludes simultaneously testing maternal-based effects on child anxiety risk and child-based effects on maternal postpartum anxiety symptoms (Aim 1). Neural and neuroendocrine function in mothers and children will be tested as systems through which anxiety risk may be transmitted within the dyad (Aim 2). Children and mothers will be assessed via observation and surveys for levels of anxiety risk (fear, worry, anxious behaviors) and anxiety (anxiety symptoms) at each of three time points (child age 1, 2, and 3 years). This model will allow for the analysis of both concurrent and longitudinal associations between mother and child anxiety risk while accounting for individual stability in these systems.
Aim 2 tests biological systems of neural (EEG, ERP) and neuroendocrine (cortisol) reactivity as mediators of transactional links between maternal and infant anxiety risk. Results will not only empirically test long-standing theories of child development, but will also inform the timing and framework for future family-based interventions aimed at preventing or ameliorating long-term anxiety problems in both mothers and young children, aligning with the National Institute of Mental Health?s mission to chart trajectories of mental illness and inform their prevention.
This project contributes to public knowledge about the mechanisms that simultaneously influence the development of risk for anxiety problems in infants and postpartum mothers. Our findings can aid in the identification of risk factors that may put individuals at greatest risk for disorder and suggest ways to boost the efficacy of current programs of prevention and intervention.