Effects of childhood adversity on physiology and health in emerging adulthood

Abstract

Paper 1 Abstract. Objectives: Childhood adversity is a risk factor for the development of obesity in adulthood. ❧ Dysregulated hypothalamic-pituitary-adrenal (HPA) activity, which has been associated separately with both adverse childhood experiences and obesity, has been posited as a mechanism by which stressful experiences influence body mass index (BMI); however, this mechanism has not yet been tested longitudinally. The present study uses multi-reporter, longitudinal data across three time points to test whether the adolescent cortisol awakening response (CAR), an index of diurnal HPA activity, mediates the association between adversity in childhood and BMI in adulthood. ❧ Methods: 82 youth, mothers, and fathers reported on adverse childhood experiences from middle childhood to late adolescence. During adolescence, youth provided saliva samples three times each morning across three days, which were assayed for cortisol to calculate CAR. During early adulthood, youth reported height and weight to calculate BMI. ❧ Results: Greater adversity predicted flatter CAR and higher young adult BMI. Flatter CAR partially mediated the association between childhood adversity and young adult BMI. ❧ Conclusions: Stress-related alterations to HPA activity account in part for the childhood adversity-adult obesity link. Findings are consistent with theoretical models implicating HPA alterations as linking childhood adversity to metabolic and behavioral determinants of BMI in adulthood. ❧ Paper 2 Abstract. Family of origin aggression (FOA) exposure is a chronic childhood stressor that has been linked to altered stress reactivity of the hypothalamic pituitary adrenal (HPA) axis in adulthood. Effects of FOA also spill over between partners in romantic couples, such that one partner’s FOA history influences the other’s HPA reactivity during couple interactions. However, the direction of these effects is inconsistent, with both heightened and blunted HPA reactivity observed; this heterogeneity suggests the presence of moderators. The present study measures HPA reactivity during emotionally vulnerable conversations between young adult romantic partners to assess whether romantic attachment avoidance accounts for this divergence by moderating actor- and partner-effects of FOA on HPA. One hundred-twelve opposite-sex couples (224 young adults) provided information on FOA and avoidance, completed dyadic interaction procedures, and provided saliva samples to assess HPA reactivity during interactions. Multi-level structural equation models revealed that FOA did not predict either own or partner’s HPA reactivity. However, FOA and avoidance interacted to produce both actor- and partner-effects, such that greater FOA exposure heightened HPA reactivity when avoidance was high but blunted reactivity when avoidance was low. Results support that proximal relationship-related characteristics, such as attachment avoidance, influence whether distal relationship-related stressors, such as FOA, amplify or attenuate physiological reactivity during emotionally vulnerable interactions. As HPA reactivity has been linked to a variety of health outcomes, identifying relationship-related buffers of associations between FOA and HPA response may inform future interventions to protect health for FOA-exposed youth. ❧ Paper 3 Abstract. Growing up in an aggressive family confers health risk life-long. However, less is known about how the romantic relationships young adults form may contribute to trajectories from family of origin aggression (FOA) to disease. The present study assesses whether health effects of FOA can be detected as early as young adulthood in a community sample, whether hypothalamic-pituitary-adrenal (HPA) axis reactivity during interactions with romantic partners mediates these associations, and whether this risk mechanism depends on young adults’ levels of romantic attachment avoidance. Eighty-five opposite sex couples reported on FOA and attachment avoidance, engaged in dyadic interaction tasks while providing saliva samples to index HPA reactivity, and had at least one partner complete a follow-up health visit. Inflammation was indexed by two pro-inflammatory cytokines: interleukin-1β (IL-1β) and interleukin-6 (IL-6). Results indicate that FOA is associated with greater IL-1β and IL-6 for men. The indirect effect of men’s FOA on IL-1β through HPA reactivity was conditional on men’s levels of attachment avoidance, such that greater FOA only conferred heightened reactivity for more avoidant men; heightened reactivity, in turn, predicted greater IL-1β. Low attachment avoidance buffered men from the total effect of FOA on IL-1β. No indirect or conditional indirect effects were detected for men’s IL-6. No predictors were associated with women’s inflammation. By identifying how attachment amplifies or attenuates risky health trajectories, we take an exploratory step toward identifying how young adults’ relationships can serve both as a disease mechanism and as a natural point of intervention.