Keywords: Anxiety | Stress | Longitudinal
Presentation Type: Symposium
Background: Research suggests that social pain experiences in childhood and adolescence (e.g., rejection from peers) are related to the onset of Social Anxiety Disorder (SAD), but little is known about the nature of this relationship. The conditioning-based model of SAD posits that social pain experiences are aversive events that produce conditional fear to socially relevant stimuli. Over time, this fear becomes overly generalized and leads to clinically significant distress and impairment. This hypothesis has been prevalent in the literature and is it the foundation of cognitive behavioral therapy for SAD, but little research has subjected it to rigorous evaluation. In the present study, we tested the following hypotheses: 1) Social stress is a stronger predictor of subsequent SAD severity than non-social stress and 2) Social stress is a stronger predictor of subsequent SAD severity than subsequent severity of other anxiety disorders.
Methods: Participants were 627 high school students who were predominantly female (69%) and racially and ethnically diverse (48% Caucasian). Participants were administered well-validated clinician-administered assessments of DSM diagnoses and acute and chronic life stress at two time points one year apart. Path analyses were run using structural equation modeling.
Results: Consistent with hypotheses, chronic social group stress (β = 0.22, p < .05), but not equally severe chronic stress in a non-social domain (i.e., finances; β = -0.02, p > .05), predicted SAD severity one year later. Additionally, chronic social life stress significantly predicted SAD severity one year later (β = 0.23, p < .01), but not the severity of equally prevalent and impairing anxiety disorders not based in social evaluative concerns (e.g., generalized anxiety disorder; β = 0.10, p > .05).
Conclusions: The present findings provide support for the widely espoused conditioning-based etiological model of SAD by demonstrating a unique relationship between chronic social pain experiences and subsequent SAD. Although replication is needed, the present study marks an important contribution to the literature regarding the etiology of SAD.
Sunday, November 19
10:15 AM – 11:45 AM
The asset you are trying to access is locked. Please enter your access key to unlock.