Family aggression and attachment avoidance influence neuroendocrine reactivity in young adult couples.

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. The 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. This study measured 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. A total of 112 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. Multilevel structural equation models revealed that FOA did not predict either the actor's or the 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. The results support the conjecture 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. Because 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. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

SUBMITTER: Kazmierski KFM 

PROVIDER: S-EPMC7416485 | biostudies-literature |

REPOSITORIES: biostudies-literature