Therapists' oxytocin response mediates the association between patients' negative emotions and psychotherapy outcomes. Academic Article uri icon

Overview

abstract

  • BACKGROUND: Existing literature suggests that patients' experiences of emotions, especially negative emotions, predict outcomes in psychotherapies for major depressive disorder. However, the specific mechanisms underlying this effect remain unclear. Based on studies pointing to the role of oxytocin (OT) in attachment relationships, we proposed and tested a mediation model where the therapists' hormonal responses, as represented by increases in their OT levels, mediates the association between negative emotions and symptomatic change. METHOD: OT saliva samples (pre- and post-session, N = 435) were collected on a fixed schedule over 16 sessions from the therapists of 62 patients receiving psychotherapy for major depression. The Hamilton Rating Scale for Depression was administered to the patients before the sessions, and the patients reported their in-session emotions after the sessions. RESULTS: The findings support the proposed within-person mediation model: (a) higher levels of negative emotions in patients predicted greater increases in therapist OT levels pre- to post-session throughout treatment; (b) greater OT levels in therapists, in turn, predicted reduction in patients' depressive symptoms on the subsequent assessment; and (c) the therapists' OT levels significantly mediated the association between patients' negative emotions and reduction in their depressive symptoms. LIMITATIONS: This design precluded establishing a time sequence between patients' negative emotions and therapists' OT; thus, causality could not be inferred. CONCLUSION: These findings point to a possible biological mechanism underlying the effects of patients' experiences of negative emotions on treatment outcomes. The findings suggest that therapists' OT responses could potentially serve as a biomarker of an effective therapeutic processes.

publication date

  • June 7, 2023

Identity

Digital Object Identifier (DOI)

  • 10.1016/j.jad.2023.06.013

PubMed ID

  • 37295654

Additional Document Info

volume

  • 338