Neurovisceral Model of Social Anxiety Disorder: An Integrative Review

Social anxiety involves persistent fear of negative evaluation that causes significant distress or avoidance in social situations and, when lasting at least six months with meaningful impairment across life domains, meets diagnostic criteria for social anxiety disorder (SAD). The origins and maintenance of SAD have been described by disparate models as dysregulation of central and peripheral networks involved in emotion regulation and threat appraisal. However, studies integrating central and peripheral levels of analysis remain scarce and lack integration, leaving our understanding of the neurobiology of SAD fragmented. Here we review these models and extant evidence. This review proposes an integrated neurovisceral model in which SAD reflects context-sensitive dysregulation among cortical regulation, limbic threat signaling, insular interoception, vagal and autonomic regulation, cardiac flexibility, HPA-axis output, and behavior. Genetic liability and behavioral inhibition are conceptualized as probabilistic influences on threat sensitivity and regulatory capacity. While environmental experience, developmental timing, sex-related factors, and stress sensitization shape the calibration of these systems. The model predicts heterogeneity along activation threshold, response magnitude, recovery, and central-peripheral coordination, which may give rise to acute hyperreactive, persistent sensitized/inflexible, and compromised/blunted SAD configurations. The model also generates testable predictions for longitudinal, multimodal research, and supports profile-sensitive approaches to assessment and treatment.