Stress protection by your group : increasing group size reduces physiological stress contagion

Abstract

Background & objectives: Stress contagion refers to the spread of stress from one person to another. We previously established a standardized, controlled experimental paradigm to study stress contagion in humans. While stress contagion effects have been characterized on a physiological level, potential modulating factors are beginning to be understood. Using our paradigm, we tested for the first time whether the number of observers, i.e. observer group size, modulates physiological stress contagion in stress observers.

Methods: Our experimental condition comprised three groups of stress observers varying in group sizes of two (“Group 1”, n=30), three (“Group 2”, n=31), or more observers (“Group 3”, n=31), with each group observing one stressed participant. The data assessment comprised up to 5 healthy young male participants, with one participant randomly assigned to undergo an adapted version of the Trier Social Stress Test (“TSST participants”, n=57) and the remaining participants observing him disguised as panel member(s) (“stress observers”, n=92) in addition to one panel confederate. We repeatedly assessed salivary cortisol, salivary alpha-amylase, and heart rate.

Results: The TSST induced significant increases in all physiological parameters under study (p´s<=.025) without reactivity differences between TSST participants of the three experimental groups (p´s>=.23). When comparing the physiological reactivity to direct stress observation, the stress-observer-groups significantly differed in terms of cortisol (p=.029) with overall higher reactivity in smaller observer groups. Further analyses confirmed a linear effect in terms of higher reactivity with lower observer group size (p=.046). There were no group-by-time interactions in salivary alpha-amylase and heart rate reactivity.

Discussion: Our results suggest that when directly observing stress in other individuals, observer group size has a differential effect on physiological stress contagion systems. While we found evidence for modulating effects on hypothalamic-pituitary-adrenal axis reactivity in terms of higher cortisol stress contagion reactivity with lower observer group size, observer group size did not relate to the sympathetic–adrenal–medullary axis. Potential implications remain to be elucidated.