Abstract
AIMS: Social anxiety disorder (SAD) is one of the most common anxiety disorders and is associated with significant impairment and societal costs. The association between SAD and mortality remains poorly understood, partly because in epidemiological research it is rarely studied independently from other anxiety disorders. In this population-based matched cohort and sibling control study, we estimated the risk of all-cause and cause-specific mortality in individuals with SAD. METHODS: From a population of individuals born from 1932 and living in Sweden between 1997 and 2020, we identified all cases of SAD (Swedish ICD-10 code F40.1) in the National Patient Register. Each of these individuals was matched on sex, birth year and county of residence with 10 individuals who had never received a diagnosis. Mortality data were extracted from the Cause of Death Register. Risks were estimated using Cox proportional hazards regression models. Models adjusted for sociodemographic covariates and other lifetime psychiatric disorders. We also identified all clusters of full siblings and conducted within-sibling comparisons to account for unmeasured familial confounding. RESULTS: The matched cohort included 57,360 individuals with SAD and 573,600 unexposed individuals. During the follow-up, 2355 deaths were registered within the exposed cohort vs. 7800 deaths in the matched cohort (crude mortality rates, 5.25 and 1.73 per 1000 person-years, respectively). The full cohort was followed up for a mean of 7.87 years (standard deviation 5.23). In models adjusting for sociodemographic variables, individuals with SAD had a 2.24-fold increased hazard of all-cause mortality (95% confidence interval [CI], 2.13-2.35). The increased risk was observed for both natural (adjusted hazard ratio [HR], 1.62; 95% CI 1.52-1.72) and unnatural causes of death (HR, 4.18; 95% CI 3.82-4.58). The results were robust to additional adjustment for psychiatric comorbidities, but the magnitude of the associations was attenuated, particularly when adjusting for substance use disorders. In the sibling cohort, 39,993 individuals with SAD were compared with their 64,640 unaffected siblings. While the estimates were also attenuated, they remained statistically significant (HR for all-cause mortality, 1.40; 95% CI 1.36-1.45). CONCLUSIONS: Individuals with SAD face an increased risk of mortality, attributable primarily to unnatural causes of death, such as suicide, but also to natural causes, even after adjusting for socioeconomic variables. Psychiatric comorbidities, particularly substance use disorders, and shared familial factors may also contribute to this excess death. Further study of underlying mechanisms may inform prevention and early intervention strategies to reduce mortality in this vulnerable population.