The “conflict avoidance theory of inflammation-induced anxiety” (CATIA): A psychoneuroimmunologic hypothesis

Abstract

Anxiety and inflammation are complex, interconnected physiological processes. The “Conflict Avoidance Theory of Inflammation-Induced Anxiety” (CATIA) hypothesizes that inflammation-induced anxiety confers an evolutionary advantage by promoting harm-avoidance and recovery-promoting behaviour. Inflammatory cytokines act as signalling molecules to anxiety-related brain regions, primarily limbic structures such as the amygdala, thus influencing decision-making and behaviour. This is archieved by priming these structures for exaggerated fear-responses counteracting conflict engagement, when adaptive physiological readiness is impaired.

This adaptive mechanism prioritizes recovery and survival during illness or injury. However, in modern contexts, inflammation driven by lifestyle factors or chronic conditions may perpetuate anxiety symptoms, contributing to psychiatric disorders like generalized anxiety disorder (GAD) and major depressive disorder (MDD). Understanding the psychoneuroimmunologic underpinnings of CATIA may inform screening, prevention, and treatment strategies for anxiety-associated disorders.

Therefore, we propose clinical applications particularly for clearly defined vulnerable populations affected by inflammation-induced anxiety. These vulnerable populations could be detected using a “screening & scoring system”, and personalized treatment options could then be applied according to a defined algorithm. Although the literature widely supports the theoretical background of CATIA, the hypothesis is thus far untested and needs further investigation. We outline specific suggestions how this could be achieved in a clinical context.