Adverse childhood experiences (ACEs), parenting, and social determinants of health (SDH) contribute to early life adversity (ELA), which can disrupt development in the brain, cardiovascular, metabolic, and immune systems to increase the risks for chronic non-communicable diseases, substance abuse, or other detrimental outcomes. In contrast, positive childhood experiences (PCEs) can build resilience, and improve physical and mental health outcomes. We have validated the assays for hair cortisol concentrations (HCC) to assess chronic stress and hair oxytocin concentrations (HOC) to assess social bonding in over 1200 children. We found significant differences in HCC/HOC by age, sex, race/ethnicity, parent income, the child’s health and ACEs exposures. We also measured hair growth rates and hair composition, and found no effects of hair composition on HCC/HOC. The social psychology of childhood flows from parenting and family factors, with ACEs and PCEs reflecting the negative vs. positive experiences in the child’s social ecology. We propose an identity disruption model to study how early social psychology and health are altered by their social ecology, using hair biomarkers to define the role of HPA-axis (dys)regulation in mediating these outcomes. We will derive a measure of toxic stress (TS) from ACEs, PCEs, and family factors in a prospective longitudinal study, evaluating 450 children at 6-month intervals to see how TS affects HCC/HOC trajectories and to develop HCC criteria for HPA-axis dysregulation. AIM 1 examines how ACEs exposures in preschool children are related to a chronic stress biomarker (HCC). AIM 2 examines how the PCEs are related to a social bonding biomarker (HOC), and if the PCEs can protect children from developing HPA-axis dysregulation. The degree and timing of child exposures to toxic stress will be related to the adaptive, hyperresponsive, maladaptive, and exhaustive phases of HPA-axis (dys)regulation. We will examine how the ACEs, PCEs, and