ArticleDiabetologia2026
SARS-CoV-2 infection and COVID-19 vaccination and the risk for new-onset type 1 diabetes: a register-based population study in Sweden.
Article in Diabetologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aims/hypothesisReports from several countries suggested increased incidence of type 1 diabetes during the COVID-19 pandemic, but causality has remained unclear. We investigated incident type 1 diabetes related to SARS-CoV-2 infection and vaccination in Swedish children and adults and assessed whether vaccination modified infection-related risk.
methodsWe assembled a register-based cohort of all residents aged <80 years on 1 January 2020 and births during follow-up (1 January 2020-31 December 2023). Risk windows after infection (and after each vaccine dose) were 0-30 days, 31-180 days, 181-365 days, and 1-2 years. Incident type 1 diabetes was defined by the earliest ICD-10 diagnosis E10 in the National Diabetes Register or in the National Patient Register. Cox regression with calendar time as the timescale was used with time-varying exposures; analyses were stratified by age (children <18 years; adults 18-79 years), with age-appropriate covariate adjustment. Sensitivity analyses for children were restricted to ages 12-17 years.
resultsThe cohort included 2,650,492 children (3813 incident type 1 diabetes) and 6,870,328 adults (4453 incident type 1 diabetes). SARS-CoV-2 infection was associated with increased type 1 diabetes risk within 2 years in children (hazard ratio [HR] 1.22; 95% confidence interval 1.10, 1.36) and adults (1.10; 1.00, 1.20), driven largely by the 0-30-day window (5.41; 4.34, 6.74 in children, 3.33; 2.69, 4.12 in adults). Vaccination did not modify infection-associated risk (interaction p>0.5). When vaccination was investigated as the exposure, children showed lower HRs (0.77; 0.67, 0.88) within 2 years, but this association was not observed in ages 12-17 (1.00; 0.80, 1.26); adults showed a small excess risk within 0-30 days after dose 1 (1.32; 1.07, 1.62), but not in later windows or doses. CONCLUSIONS/
interpretationShort-term elevations in incident type 1 diabetes diagnoses were observed in the first 30 days after infection and after first vaccination, and did not persist, supporting detection/diagnostic acceleration rather than a sustained causal effect of SARS-CoV-2 infection or vaccination on type 1 diabetes.
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