Common and Distinct Mechanisms of Social Anxiety and Alcohol Use

社交焦虑症(SAD)经常与酒精使用障碍(AUD)并存。我们的项目旨在理清SAD和AUD共同和特定的行为和神经机制，以调查潜在的共同漏洞。虽然SAD与更高的威胁反应性和绩效监控相关，但建议在威胁反应性或奖励敏感度和冲动性改变的情况下增加发生AUD的风险。然而，目前尚不清楚这些机制中的哪种改变组合与SAD和AUD的共病有关。先前的研究表明，在SAD患者中有一种冲动焦虑的亚型，这可能是酗酒问题的原因，并与自我报告的奖励敏感性和冲动有关。然而，到目前为止，还没有研究调查与这种共病有关的潜在机制。我们将重点关注与焦虑或成瘾密切相关的标记。在无/可预测/不可预测的威胁任务中，威胁反应性将被评估为惊吓反应。奖励敏感性的标记将是在功能磁共振成像期间的金钱激励延迟任务中的纹状体活动和反应时间。错误相关的负波将作为性能监测的标志，并将在侧翼任务中使用脑电(EEG)进行评估。冲动将通过反应抑制和延迟折扣来检验。在脑电的停止信号任务中，N_2和P_3波幅将作为反应抑制的神经元标志物。贴现因子(k值)将作为延迟贴现任务中评估的行为标记。这项多方法研究将在四组参与者中进行：患有SAD、AUD、合并SAD+AUD的个体和健康对照组。除了每种机制的维度和组比较分析外，我们还将进行总体潜伏类分析，以检查潜在的行为和神经机制是否可以解释SAD和AUD的共病。该项目的结果将对了解所检查的疾病之间的共病情况具有高度相关性，并为为SAD和AUD患者制定和改进量身定制的治疗程序提供基础。

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.