UCLA

The widely accepted theory regarding the etiology of social anxiety disorder (SAD) is rooted in learning theory. In line with Pavlovian conditioning models, the fear and arousal experienced in response to aversive social experiences are believed to generalize, thus producing conditioned fear responses to formally neutral stimuli. Although there is overwhelming evidence for the role of conditioning in the onset of anxiety disorders, there is a paucity of research regarding fear conditioning to aversive social experiences. The present studies aimed to address key questions regarding this significant gap in the literature. The first two studies aimed to develop a socially relevant unconditioned stimulus (US) that is theoretically grounded, sufficiently potent to elicit fear responding, and feasible for use in conditioning paradigms. Study 1 examined the unconditioned response (UR) to this social US by measuring subjective and physiological reactions to a range of intensities of the stimulus and comparing these reactions to those of a well-established physical stimulus. Results suggested that the social US elicited significant subjective and physiological fear responses, but that increasing responding did not occur at increasing levels of intensity and SAD severity did not moderate reactions to the social US. Study 2 aimed to enhance the social US from Study 1 and test its ability to produce a conditioned fear response in a differential classical conditioning paradigm. The paradigm allowed for the comparison of acquisition, extinction, and return of fear to conditioned stimuli paired with the social US, a physical US, and a control stimulus. Preliminary results from a small pilot sample suggest that fear conditioning to stimuli associated with the social US occurred as hypothesized. Study 3 moves out of the laboratory by examining how social pain and SAD symptoms are related over time in a longitudinal sample of adolescents. Results replicated prior research by finding that chronic stress in an individuals' social group prospectively predicted SAD severity one year later, but did not support the specific relationship between social stress and SAD that etiological model of SAD hypothesizes. The limitations and implications of these studies are discussed and directions for future research are outlined.