Keywords: Alcohol | Social Anxiety
Presentation Type: Symposium
Internalizing syndromes (anxiety/depression; INTDs) frequently co-occur with alcohol use disorder (“comorbidity”). In a previous study of 363 alcohol use disorder (AUD) treatment inpatients with a co-occurring INTD, we applied a network analytic approach to conceptualize INTD-AUD comorbidity as a complex system of interacting INTD syndromes and extra-diagnostic constructs. This earlier work identified drinking to cope (DTC) with negative affect and perceived stress as central processes in the comorbidity network. In the present study, we extend these findings within a causal framework by identifying probabilistic pathways of influence underlying these network connections. Toward this end, we computed a directed acyclic graph (DAG) (via a Bayesian hill-climbing algorithm) to model causal relationships between measures corresponding to the following: syndrome-specific groupings of INTD symptoms, alcohol craving, drinking behavior, perceived stress, DTC, and self-efficacy to resist DTC. The DAG placed social phobia and perceived stress at the top and alcohol craving and drinking behavior at the bottom of a causal hierarchy. Within the hierarchy, DTC served as a central hub for two distinct causal pathways leading to drinking behavior; 1) a syndromic pathway originating with social phobia and 2) a stress pathway originating with perceived stress comprised of direct and indirect (through self-efficacy) causal connections to DTC. Notably, perceived stress also directly influenced internalizing conditions (depression, generalized anxiety, and panic) that were not a part of the direct causal drinking pathway, indicating that stress held prominence across multiple domains within the causal hierarchy. An important and novel implication of these findings is that social phobia directly influences DTC whereas stress serves as the common cause of DTC in addition to other anxiety/depression states. These findings further our understanding of the intricate inter-play between multiple constructs and pathways in maintaining comorbidity and provide novel treatment implications.
University of Minnesota
Sunday, November 19
10:15 AM – 11:45 AM
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