COVID-19 and Type 1 Diabetes: Exploring the Potential Link

Prior to the COVID-19 pandemic, the incidence of adolescent type 1 diabetes was steadily increasing at a rate of 1.9% per year in the United States and 3-4% per year in European countries (3,7). Since the pandemic, however, several studies have reported an unprecedented surge in type 1 diabetes in children and teenagers.

What is Type 1 Diabetes?

Type 1 diabetes is a chronic disease that occurs when damage to pancreatic beta cells results in insufficient or nonexistent production of insulin, a hormone that regulates the amount of glucose in the blood (6). Most cases of type 1 diabetes have an autoimmune basis (type 1A diabetes), meaning the body’s immune system attacks and destroys the pancreatic beta cells (1). However, a very small number of individuals with type 1 diabetes have a non-autoimmune form of the disease (idiopathic or type 1B diabetes). 

When the pancreas doesn’t make sufficient insulin, the body is unable to move glucose from the bloodstream to cells, leading to a buildup of glucose in the cells (6). As a result, type 1 diabetes can cause long-term health complications such as heart disease, stroke, circulation problems, blindness, nerve damage, kidney failure, and gum disease. 

Recent Data on COVID-19 & Type 1 Diabetes

On June 30th, 2023 a study was published in Jama Network Open which confirmed researchers’ earlier concerns that type 1 diabetes diagnoses rose significantly during the COVID-19 pandemic (4). The study, which consisted of a meta-analysis of data pooled from 17 previous studies and included over 38,000 children and teenagers, found that the incidence rate of type 1 diabetes was about 14% higher in the first year of the pandemic than the previous year. The incidence rate further surged in the second year of the pandemic, up 27% from the pre-pandemic rate. 

The research not only identified a rise in the occurrence of type 1 diabetes, but also revealed a significant increase in diabetic ketoacidosis, a serious and potentially life-threatening complication of type 1 diabetes. From 2019 to 2020, the incidence of ketoacidosis rose by 26%. Although diabetic ketoacidosis is preventable if symptoms are caught and treated early on, there are serious long-term effects if left untreated. 

Potential Causes

Despite these findings, researchers are still unsure what caused this rapid increase in type 1 diabetes. Some researchers suspect it is the result of direct effects from SARS-CoV-2 infection, while others believe it has to do with indirect environmental effects caused by the pandemic. 

If SARS-CoV-2 infection is directly to blame, researchers have proposed a few potential explanations. One theory is that the SARS-CoV-2 virus may be able to enter and damage the beta cells directly (8). Another theory is that SARS-CoV-2 triggers the release of a plethora of proinflammatory cytokines, which then injure the beta cells. If either of these explanations are correct, a simultaneous increase in idiopathic type 1 diabetes would be expected, as neither of these theories involve an autoimmune response. However, studies have not observed an increase in the prevalence of type 1 diabetes that develops without autoimmunity, making these explanations unlikely (5). Therefore, if COVID-19 is directly to blame, a more probable explanation would be that the SARS-CoV-2 virus triggers the immune system to attack the pancreas, as has been documented with other infections, such as enteroviruses and hepatitis B (9).  

Although the previous explanation makes sense in theory, there is still no conclusive research directly linking SARS-CoV-2 to type 1 diabetes. Because of this, some researchers believe it is more likely that the spike in type 1 diabetes is attributable to environmental or lifestyle changes related to the pandemic, rather than the virus itself (4). Researchers have hypothesized that these environmental or lifestyle changes, such as increases in consumption of processed foods, weight gain, or changes in the gut microbiome, may have merely accelerated the onset of type 1 diabetes in adolescents who were already at risk. If this explanation is accurate, a drop-off in newly diagnosed type 1 diabetes would be expected to follow the pandemic. 


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Another theory has to do with the hygiene hypothesis for autoimmune diseases. To put it simply, the hygiene hypothesis suggests that a reduction in the frequency of infections directly increases the frequency of autoimmune conditions (2). The underlying mechanisms behind this hypothesis are unclear, but there is strong epidemiological data to support it. With this in mind, some researchers have proposed that the lockdowns and physical distancing related to the pandemic may have reduced childrens’ exposure to certain infectious agents, removing some sort of protective mechanism against type 1 diabetes (4).  

Conclusion

Despite all of these hypotheses, researchers are still not confident in what is behind the rapid increase in type 1 diabetes. Additional, long-term research is needed to help researchers to identify if COVID-19 or environmental and lifestyle changes are to blame. Nevertheless, this rapid increase certainly offers an important opportunity for researchers to investigate what is not only causing this recent spike, but the decades-long rise in type 1 diabetes as well.

References

  1. Anaya, J.-M., Shoenfeld, Y., Rojas-Villarraga, A., Levy, R. A., Cervera, R., Echeverri, A. F., & Tobón, G. J. (2013). Autoimmune Diabetes Mellitus (Type 1A). In Autoimmunity: From Bench to Bedside. essay, El Rosario University Press. 
  1. Bach, J.-F. (2017). The hygiene hypothesis in autoimmunity: The role of pathogens and commensals. Nature Reviews Immunology, 18(2), 105–120. https://doi.org/10.1038/nri.2017.111 
  1. Centers for Disease Control and Prevention. (2022, December 30). Rates of new diagnosed cases of type 1 and type 2 diabetes continue to rise among children, teens. Centers for Disease Control and Prevention. https://www.cdc.gov/diabetes/research/reports/children-diabetes-rates-rise.html#:~:text=The%20rate%20of%20new%20cases,of%20CDC’s%20Morbidity%20and%20Mortality 
  1. D’Souza, D., Empringham, J., Pechlivanoglou, P., Uleryk, E. M., Cohen, E., & Shulman, R. (2023). Incidence of diabetes in children and adolescents during the COVID-19 pandemic. JAMA Network Open, 6(6). https://doi.org/10.1001/jamanetworkopen.2023.21281 
  1. Kamrath, C., Rosenbauer, J., Eckert, A. J., Siedler, K., Bartelt, H., Klose, D., Sindichakis, M., Herrlinger, S., Lahn, V., & Holl, R. W. (2022). Incidence of type 1 diabetes in children and adolescents during the COVID-19 pandemic in Germany: Results from the DPV registry. Diabetes Care, 45(8), 1762–1771. https://doi.org/10.2337/dc21-0969 
  1. Mayo Foundation for Medical Education and Research. (2023, September 15). Type 1 diabetes. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/type-1-diabetes/symptoms-causes/syc-20353011 
  1. Patterson, C. C., Harjutsalo, V., Rosenbauer, J., Neu, A., Cinek, O., Skrivarhaug, T., Rami-Merhar, B., Soltesz, G., Svensson, J., Parslow, R. C., Castell, C., Schoenle, E. J., Bingley, P. J., Dahlquist, G., Jarosz-Chobot, P. K., Marčiulionytė, D., Roche, E. F., Rothe, U., Bratina, N., … Green, A. (2018). Trends and cyclical variation in the incidence of childhood type 1 diabetes in 26 European centres in the 25 year period 1989–2013: A multicentre prospective registration study. Diabetologia, 62(3), 408–417. https://doi.org/10.1007/s00125-018-4763-3 
  1. Sathish, T., Tapp, R. J., Cooper, M. E., & Zimmet, P. (2021). Potential metabolic and inflammatory pathways between COVID-19 and new-onset diabetes. Diabetes & Metabolism, 47(2), 101204. https://doi.org/10.1016/j.diabet.2020.10.002 
  1. Watson, C. (2023). As covid-19 cases rose, so did diabetes — no one knows why. Nature, 619(7971), 677–678. https://doi.org/10.1038/d41586-023-02322-0  
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Sara Christenson

Sara Christenson

YouTube Optimization & Social Media Intern at Promega Corporation
Sara is a Marketing Coordinator at Promega. She earned her B.S. in Life Sciences Communication and a certificate in Digital Studies at the University of Wisconsin-Madison.

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