Common and Distinct Mechanisms of Social Anxiety and Alcohol Use

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Social anxiety disorder (SAD) co-occurs frequently with alcohol use disorder (AUD). Our project aims to disentangle common and specific behavioral and neuronal mechanisms of SAD and AUD to investigate potential shared vulnerabilities. Whereas SAD is associated with increased threat reactivity and performance monitoring, the risk to develop AUD is suggested to be enhanced under either altered threat reactivity or reward sensitivity and impulsivity. However, it remains unclear which combination of alterations in these mechanisms are associated with the comorbidity of SAD and AUD. Prior work suggests that there is an impulsive-anxious subtype among individuals with SAD which might account for problematic alcohol use and is associated with self-reported reward sensitivity and impulsivity. However, no study to date has investigated underlying mechanisms regarding this comorbidity. We will focus on markers robustly associated with anxiety or addiction. Threat reactivity will be assessed as startle response using electromyography in a no/predictable/unpredictable threat task. Markers for reward sensitivity will be striatal activity and reaction times in a monetary incentive delay task during functional magnetic resonance imaging. The error-related negativity will serve as a marker for performance monitoring and will be assessed in a flanker task using electroencephalography (EEG). Impulsivity will be examined with response inhibition and delay discounting. The N2 and P3 amplitude will serve as neuronal markers of response inhibition in a stop signal task during EEG. The discounting factor (k-value) will serve as a behavioral marker assessed in a delay discounting task. This multimethod study will be conducted in four groups of participants: Individuals with SAD, AUD, comorbid SAD + AUD and healthy controls. Besides dimensional and group comparison analyses for each mechanisms, we will conduct an overall latent class analysis to examine whether underlying behavioral and neuronal mechanisms explain across and beyond diagnoses the comorbidity of SAD and AUD. The results of this project would be highly relevant for understanding the comorbidity between the examined disorders and providing a basis for developing and improving tailored treatment procedures for individuals with SAD and AUD.