Social anxiety disorder (SAD) is characterised by a marked and persistent fear of social/performance situations, and a number of key environmental factors have been implicated in the aetiology of the disorder. Hence, the current article reviews theoretical and empirical evidence linking the development of SAD with parenting factors, traumatic life events, and aversive social experiences. Specifically, research suggests that the risk of developing SAD is increased by over-controlling, critical and cold parenting, an insecure attachment style, aversive social/peer experiences, emotional maltreatment, and to a lesser extent other forms of childhood maltreatment and adversity. Moreover, these factors may lead to posttraumatic reactions, distorted negative self-imagery, and internalised shame-based schemas that subsequently maintain SAD symptomatology. However, further research is necessary to clarify the nature, interactions, and relative contributions of these factors. It is likely that SAD develops via a complex interplay of biological and environmental factors, and that multiple aetiological pathways underlie the development of the disorder.

Social anxiety disorder (SAD) is characterised by a marked and persistent fear of social or performance situations. Cognitive models suggest that self-focused cognitive processes play a crucial role in generating and maintaining social anxiety, and that self-focused cognition occurs prior to, during, and following social situations (Clark & Wells, 1995; Rapee & Heimberg, 1997). There is a substantial body of empirical evidence demonstrating that socially anxious individuals engage in self-focused cognition during and following a social or performance situation. A smaller but growing body literature suggests that a similar process occurs prior to such situations, and that these three processes are interdependent. Furthermore, the vast majority of research to date indicates that self-focused cognitive processes are detrimental, and that they generate and maintain social anxiety in a variety of ways. However, there remains considerable scope for research to further explicate the role of these processes in the maintenance of SAD, and to enhance interventions designed to ameliorate their negative effects.