Communication and social interaction anxiety enhance interleukin-1 beta and cortisol reactivity during high-stakes public speaking

Background: Worry or fear related to speaking in front of others, or more broadly, communicating and interacting with others, is common. At elevated levels, however, it may contribute to heightened stress reactivity during acute speaking challenges. The purpose of this study was to examine multi-system physiological stress reactivity in the context of high-stakes public speaking while considering the impact of hypothesized individual difference risk factors. Methods: University student participants (n = 95) delivering speeches as a heavily-weighted component of their final grade had saliva samples collected immediately prior to speaking, immediately after, and 20 min after speech completion. Saliva samples were assayed for alpha amylase (sAA), cortisol, and interleukin-1 beta (IL-1 beta). Self-reported communication anxiety, social interaction anxiety, rejection sensitivity, and sex were assessed as risk factors for heightened stress reactivity. Results: Salivary sAA, cortisol, and IL-1 beta significantly changed following speech delivery. Multivariate analyses demonstrated that elevated levels of self-reported communication anxiety and social interaction anxiety were independently associated with increased cortisol and IL-1 beta responses and combined to enhance HPA axis and inflammatory cytokine activity further (i.e., cortisol and IL-1 beta AUC(I)). Sex and rejection sensitivity were unrelated to physiological stress reactivity. Conclusions: These findings suggest that individuals with elevated communication and interaction fears may be at increased risk of heightened neuroendocrine and inflammatory responses following exposure to acute social stressors. Both types of anxiety may combine to increase physiological reactivity further, with unknown, though likely insalubrious, health consequences over time.