Salivary oxytocin and testosterone in empathic stress responding: a pilot study.

Authors

Katja Heilmann, Martin Walter, Veronika Engert

Published in

Stress (Amsterdam, Netherlands). Volume 30. Issue 1. Pages 2720481. Dec 31, 2027. Epub Oct 09, 2026.

Abstract

Suffering the stress of others (termed empathic stress or stress contagion) may affect an individual's health and well-being. To understand the underlying hormonal processes of empathic stress, N = 108 opposite-sex dyads were tested, with one dyad partner passively observing the other undergoing a standardized psychosocial laboratory stressor. A positive link between oxytocin release and empathic stress response was hypothesized, while a negative relationship was expected for testosterone release. Associations of observer oxytocin and testosterone levels with two components of empathic stress were examined: stress resonance (i.e. synchronized observer-target responses) and vicarious stress (observer responses independent of target stress). During the passive observation of a stressed target, salivary oxytocin and testosterone levels increased by 16.64% and 23.00%, respectively, followed by a drop back to baseline levels. Supporting our hypotheses, increased observer oxytocin reactivity was linked to greater stress resonance in HF-HRV reactivity. This association was reversed in low oxytocin responders. Further, testosterone reactivity was negatively associated with stress resonance in heart rate activity. However, testosterone also showed a positive association with vicarious cortisol activity, which resembles the response pattern seen in first-hand stress exposure. We conclude that stress resonance may be the more empathy-dependent component of the empathic stress construct, aligning with previous work on the involvement of oxytocin and testosterone in empathy. To draw further conclusions about the role of oxytocin and testosterone in empathic stress response, future studies including a control group and hormone stimulation are needed.

PMID:
42855957
Bibliographic data and abstract were imported from PubMed on 10 Oct 2026.

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