There is a fundamental gap in understanding the pathways, timing, and risk and protective factors that translate early environmental stressors into emerging cardiometabolic risk during childhood. Improved knowledge of the pathways through which early environmental stressors give rise to emerging dysregulation in cardiometabolic processes, the timing during childhood when impacts are observed, and the protective factors that foster resilience, is necessary to optimize interventions to prevent the development of cardiovascular and metabolic diseases. The proposed study will address this knowledge gap using a unique cohort of 534 racially/ethnically diverse, low income children who participated in a two-arm randomized controlled obesity prevention trial and have been followed since 2-4 years of age [The NET-Works Trial (U01HD068890; Sherwood/French PIs), part of the COPTR consortium (Child Obesity Prevention and Treatment Research, NIH/NHLBI/DCVS/PPSP)]. The goal of this prospective study is to characterize the emergence of dysregulation in cardiometabolic processes in this high-risk cohort of children at 7-9 years of age, and identify malleable factors that mitigate the deleterious impact of early environmental stressors on later cardiometabolic risk. State-of-the-art measures of environmental stressors (objective and perceived neighborhood and home environment), child and parent behavior patterns (gold standard measures of children's health behaviors, executive functioning skills, and parenting factors) and physiological mediators (cortisol levels from hair samples), have already been obtained at four time points during early childhood. New measurements at ages 7-9 will allow the most cutting-edge assessment of cardiometabolic risk, including cardiovascular and metabolic parameters, body composition, pubertal stage, and oxidative stress/inflammation. Specifically, this study will (1) examine whether longitudinal patterns of children's health behavior, executive functioning, and parenting practices during early childhood buffer the relationship between early environmental stressors and emerging cardiometabolic risk, (2) examine whether HPA-axis regulation is on the pathway to emerging cardiometabolic risk, and determine the extent to which child and parenting factors exert a buffering effect through modulating children's cortisol levels, and (3) explore whether participation in a multi-level behavioral obesity prevention intervention can enhance the buffering effects of children's health behaviors, executive functioning, and parenting factors on cardiometabolic risk by altering the trajectories of these modifiable factors. This approach is innovative, because it represents a substantial departure from the status quo by focusing on the pathways through which early environmental stressors give rise to cardiometabolic risk during middle childhood and the protective factors which buffer against this risk, and significant because it is expected to have direct implications for optimizing interventions for young children living in stressful early environments to prevent cardiovascular and metabolic diseases.
This study will elucidate the pathways through which environmental stressors impact emerging cardiometabolic risk and identify protective factors that mitigate this relationship and improve children's health outcomes. Results will aid the prevention science field by identifying key intervention targets to prevent the development of cardiovascular and metabolic diseases for children living in stressful environments.
