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Decades of research indicate that individuals exposed to childhood adversity are at risk for poor physical and mental health across their life span. More recently, intergenerational transmission of trauma and prenatal programming frameworks suggest an even longer reach for adverse childhood experiences (ACEs), with consequences that extend to subsequent generations. Beyond the individual-level consequences typically observed by empirical studies of ACEs, mothers’ experiences of early adversity may also compromise the maternal–child dyadic relationship. We propose a conceptual model whereby mothers’ ACEs impact maternal–infant dyadic functioning and later biobehavioral health outcomes through heightened perinatal psychosocial risk. We provide support for the proposed paths and mechanistic processes in our model with data drawn from Las Madres Nuevas, a longitudinal study of low-income Mexican-origin families who participated in a series of home and laboratory visits from the prenatal period through early childhood. Higher ACEs exposure among Las Madres Nuevas participants was associated with numerous perinatal psychosocial risk factors, which predicted poorer mother–infant dyadic functioning. Compromised dyadic functioning during infancy was associated with later maternal mental health and child behavior problems. We conclude with discussion of prevention and treatment strategies that can buffer against proposed risk pathways, including perinatal assessment of maternal ACEs and psychosocial risk, perinatal treatment of maternal distress, and mother–infant therapy in the postpartum period. It is our hope that the proposed conceptual model will serve as a guide for future research to examine the lasting consequences of childhood adversities within and across generations among high-risk populations.

Parent-child relationships can critically affect youth physiological development. Most studies have focused on the influence of maternal behaviors, with little attention to paternal influences. The current study investigated father engagement with their adolescents in household (shopping, cooking) and discretionary leisure activities as a predictor of youth cortisol response to a challenging interpersonal task in young adulthood. The sample (N = 213) was roughly divided between Mexican-American (MA; n = 101) and European American (EA; n = 112) families, and included resident biological-father (n = 131) and resident stepfather families (n = 82). Salivary cortisol was collected before, immediately after, and at 20 and 40 minutes after an interpersonal challenge task; area under the curve (AUCg) was calculated to capture total cortisol output. Results suggested that more frequent father engagement in shared activities with adolescents (ages 11–16), but not mother engagement, predicted lower AUCg cortisol response in young adulthood (ages 19–22). The relation remained significant after adjusting for current mother and father engagement and current mental health. Further, the relation did not differ given family ethnicity, father type (step or biological), or adolescent sex. Future research should consider unique influences of fathers when investigating the effects of parent-child relationships on youth physiological development and health.

No abstract

Context-appropriate infant physiological functioning may support emotion regulation and mother–infant emotion coregulation. Among a sample of 210 low-income Mexican-origin mothers and their 24-week-old infants, dynamic structural equation modeling (DSEM) was used to examine whether within-infant vagal functioning accounted for between-dyad differences in within-dyad second-by-second emotion regulation and coregulation during free play. Vagal functioning was captured by within-infant mean and variability (standard deviation) of respiratory sinus arrhythmia (RSA) during free play. Infant emotion regulation was quantified as emotional equilibria (within-person mean), volatility (within-person deviation from equilibrium), carryover (how quickly equilibrium is restored following a disturbance), and feedback loops (the extent to which prior affect dampens or amplifies subsequent affect) in positive and negative affect during free play; coregulation was quantified as the influence of one partner's affect on the other's subsequent affect. Among infants with lower RSA variability, positive affect fluctuated around a higher equilibrium, and negative affect fluctuated around a lower equilibrium; these infants exhibited feedback loops where their positive affect dampened their subsequent negative affect. As expected, infants with higher mean RSA exhibited more volatility in positive affect, feedback loops between their positive and negative affect, and stronger mother-driven emotion coregulation. The results highlight differences in simultaneously occurring biological and emotion regulation.