Early life stressors, such as abuse and neglect, have been associated with poor physical and mental health outcomes in adulthood. Moreover, animal models suggest that caregivers\u27 early life stress can have intergenerational effects that then impact the health and well-being of their offspring. Although animal models are compelling, and inter-generationally transmitted and co-occurring risks are well-documented, proximal mechanistic explanations for how caregiver\u27s history of childhood adversity can result in changes to their child\u27s stress physiology and outcomes have not yet been systematically tested in humans. Thus, among a sample of low-income, predominantly Latino families participating in Early Head Start (EHS), the current study explored whether caregiver history of adversity predicted infant and toddler physiology, and if three pathways, one psychological (caregiver mental health), one physical/environmental (environmental instability), and one biological (epigenetic), mediated the effects of caregiver history of adversity on infant and toddler dysregulated stress physiology. I also explored whether caregiver warmth and responsivity either mediated or moderated the direct relationship between caregiver history of adversity and infant and toddler stress physiology. Results showed that after controlling for important covariates (income-to-needs, caregiver race and ethnicity, and child early life stress), higher caregiver history of adversity predicted infant and toddler diurnal cortisol (e.g., higher noon and bedtime values), but no relationship was found for infant and toddler stress reactivity cortisol. Mediation analyses demonstrated that current caregiver mental health symptoms partially mediated the relationship between caregiver history of adversity and infant and toddler noon and bedtime cortisol values. Further, environmental instability fully mediated the relationship between caregiver history of adversity and infant and toddler noon cortisol, but was non-significant for bedtime cortisol values. Caregiver adversity was not related to infant and toddler methylation rates of the human glucocorticoid receptor gene NR3C1, nor caregiver warmth and responsivity. However, caregiver warmth and responsivity moderated the effects of caregiver history of adversity on infant and toddler noon and bedtime cortisol such that when infants and toddlers experienced lower warmth and responsivity (both chronically and acutely) and high caregiver history of adversity they experienced particularly high noon and bedtime cortisol values. Results suggest proximal processes account for many of the effects of caregiver history of adversity on diurnal, but not stress reactive, cortisol in infants and toddlers in a sample of families experiencing significant current economic and psychosocial adversity
