Anxiety sensitivity and impairment: Evidence for a direct association and partial mediation by subclinical anxiety symptoms

BackgroundMounting evidence suggests that specific psychological risk factors increase the likelihood for the development of anxiety psychopathology. Anxiety sensitivity (AS), the fear of the consequences of anxiety, is one such risk factor. However, very little is known about the consequences of having elevated AS prior to the development of diagnosable psychopathology. We hypothesized that elevated AS may create impairment among premorbid individuals. The aims of the present study were twofold. The first aim was to examine whether having elevated AS would be predictive of impairment in a nonclinical sample. The second aim was to examine whether subclinical anxiety symptoms would partially mediate the association between AS and impairment in daily life.MethodThese aims were examined in two studies utilizing samples of individuals with elevated levels of AS. Study 1 (N=387) and Study 2 (N=79) were comprised of participants with elevated AS. Participants completed a battery of questionnaires and a diagnostic interview to assess for risk status. Only participants without an anxiety disorder were eligible to participate in the study to ensure that they were in the premorbid stage.ResultsIn Study 1, there was a direct effect of AS on impairment. Additionally, there was evidence for anxiety symptoms acting as a partial mediator in the relation between AS and impairment. Study 2 revealed the same pattern of results, with AS having a significant direct effect on impairment that was partially mediated by anxiety symptoms.LimitationsThe samples utilized in the present sample were primarily Caucasian females, thereby potentially limiting the generalizability of these findings.ConclusionsThis study provides evidence that a premorbid risk factor is associated with impairment before the actual development of an anxiety disorder. Implications of the present investigation and future directions are discussed.