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Reactivity to acute social threat, commonly elicited by the Trier Social Stress Test (TSST; Kirschbaum et al., 1993), is related to adolescent internalizing symptoms. Social anxiety involves dysregulation at both biological (hypothalamic-pituitary-adrenal, HPA; autonomic nervous system, ANS) and behavioral levels (Crisan et al., 2016; Lanteigne, 2012), and the NIMH RDoC initiative advocates the integration of multiple units of analysis to characterize constructs of clinical importance. Nevertheless, most prior research on stress reactivity focuses on isolated biological stress response systems rather than examining how multiple systems operate together. The few studies that do assess stress reactivity across HPA, ANS, and behavioral systems have yielded mixed findings regarding their coordination, suggesting that these reactivity systems are sometimes, but not always, concordant (Burkholder et al., 2016; Quas et al., 2018). Moreover, coordination of stress response systems may affect risk or resilience for psychopathology (Lucas-Thompson et al., 2018; McKernan et al., 2018), however, little research has explicitly tested this idea. Limited research and mixed findings regarding the concordance of stress response systems across levels of analysis has limited our understanding of the relation between stress reactivity and social anxiety, underscoring a critical gap in the literature.
To address this gap, the current study aims to examine (1) the unique associations between behavioral, autonomic, and HPA reactivity to the TSST and adolescent social anxiety symptoms and (2) patterns of concordance across these three levels of analysis. Data comes from the first timepoint of a longitudinal study of anxiety symptom development and temperament in adolescents (projected N=60). During an in-person laboratory session, adolescents (aged 13-15) completed the TSST. Adolescents' behavioral displays of stress across the TSST were coded, and both ANS and HPA activity were collected throughout the laboratory session.
Behavioral reactivity was computed as the sum of stress-related behaviors observed across the task. Autonomic reactivity is operationalized as the difference between baseline RSA and the mean RSA value across the TSST. HPA reactivity is operationalized as the difference between baseline cortisol and the peak cortisol value across the laboratory session. Finally, adolescents reported social anxiety symptoms using the Screen for Child Anxiety-Related Disorders (SCARED; Birmaher et al., 1997).
To examine the overall concordance between HPA, autonomic, and behavioral reactivity to the TSST, we will test bivariate correlations between the three reactivity scores. Second, we will conduct a multiple regression analysis to examine the relations between HPA, ANS, and behavioral reactivity and social anxiety. Finally, we will conduct exploratory person-centered analyses of the three reactivity scores using cluster analysis to identify patterns of biobehavioral concordance. Clusters identified will inform future analyses and examinations of reactivity in the TSST.
We expect that higher ANS, behavioral, and HPA reactivity will each predict higher social anxiety. Further, we expect a positive relation between behavioral and HPA reactivity and negative relations between ANS and HPA reactivity, and RSA and behavioral reactivity. Finally, we expect to identify multiple clusters of reactivity with some individuals showing high concordance across levels of analysis, and others showing low concordance.
Nora Anne Tucker, Pennsylvania State University, University Park
Presenting Author
Madison Alexandra Politte-Corn, Pennsylvania State University, University Park
Jianing Sun, Pennsylvania State University, University Park
Sarah Myruski, Pennsylvania State University, University Park
Kristin A. Buss, Pennsylvania State University, University Park