Rosenström Tom H, Torvik Fartein Ask
Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Helsinki, Finland; Department of Psychiatry, University of Helsinki and HUS Helsinki University Hospital, Helsinki, Finland.
Centre for Fertility and Health, Norwegian Institute of Public Health, Oslo, Norway; PROMENTA Research Center, Department of Psychology, University of Oslo, Oslo, Norway.
Drug Alcohol Depend. 2023 Aug 1;249:109945. doi: 10.1016/j.drugalcdep.2023.109945. Epub 2023 May 26.
According to the self-medication and biopsychosocial models, individuals with social anxiety disorder (SAD) are at increased risk of developing an alcohol use disorder (AUD) as alcohol represents a maladaptive coping mechanism for some sufferers of SAD. The SAD-to-AUD causation was earlier supported in Norwegian longitudinal twin data and later questioned using longitudinal data from the USA.
We re-analyzed partly the same USA-based data (National Comorbidity Surveys, n = 5001), conducting theoretical and simulation analyses on different formulations of temporality and using real-data Logistic regression analysis to investigate whether baseline SAD was associated with AUD at the follow-up.
Upon proper analysis of temporality, SAD preceded AUD. Specifically, SAD was the only one of the seven anxiety disorders that predicted 10-year later AUD after adjusting for all other anxiety disorders and AUD at the baseline (odds ratio was 1.70% and 95% confidence interval 1.12-2.57). SAD was also associated with incident AUD (OR = 1.64, 95% CI = 1.14-2.37). We provide formal, simulation-based, and data-based arguments on how certain flawed models of incidence attenuate the temporal association.
We demonstrated temporality and specificity in SAD-to-AUD association, which are considered signs of causation. We further identified and discussed problems in previous statistical analyses with different conclusions. Our findings add support for models positing causal effects of SAD on AUD, such as the self-medication and biopsychosocial models. The available evidence suggests that treating SAD should incur better chances of preventing AUD compared to treating other anxiety disorders, which lack comparable evidence on causation.
根据自我药疗和生物心理社会模型,社交焦虑障碍(SAD)患者患酒精使用障碍(AUD)的风险增加,因为酒精对一些SAD患者来说是一种适应不良的应对机制。SAD导致AUD这一因果关系早期在挪威纵向双胞胎数据中得到支持,后来在美国的纵向数据中受到质疑。
我们对部分相同的基于美国的数据(全国共病调查,n = 5001)进行了重新分析,对不同的时间性表述进行了理论和模拟分析,并使用实际数据进行逻辑回归分析,以研究基线时的SAD是否与随访时的AUD相关。
在对时间性进行恰当分析后,SAD先于AUD出现。具体而言,在对所有其他焦虑障碍和基线时的AUD进行调整后,SAD是七种焦虑障碍中唯一能预测10年后AUD的障碍(优势比为1.70%,95%置信区间为1.12 - 2.57)。SAD也与新发AUD相关(OR = 1.64,95% CI = 1.14 - 2.37)。我们提供了基于形式、模拟和数据的论据,说明某些有缺陷的发病率模型如何削弱时间关联。
我们证明了SAD与AUD关联中的时间性和特异性,这被认为是因果关系的标志。我们进一步识别并讨论了先前得出不同结论的统计分析中存在的问题。我们的研究结果为认为SAD对AUD有因果作用的模型提供了支持,如自我药疗和生物心理社会模型。现有证据表明,与治疗其他缺乏类似因果关系证据的焦虑障碍相比,治疗SAD应该更有可能预防AUD。