Biological Systems as Mediators of Transactional Influences on Anxiety Risk in the Mother-Child Dyad During Infancy and will to NIMH

Project Summary/Abstract
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.

Grant Number: 3R01MH113669-04S1
NIH Institute/Center: NIH
Principal Investigator: Rebecca Brooker