It’s well-established that patients with pre-existing diabetes have a much greater risk of severe COVID-19 outcomes and death. A new line of research, however, is investigating the question “Can SARS-CoV-2 virus (which causes COVID-19) actually trigger the onset of diabetes?” 

Physicians are starting to notice and report the sudden and new occurrence of high blood sugars and even diabetic ketoacidosis in some COVID-19 patients. In a letter to the New England Journal of Medicine, several leading diabetes researchers have noted that some such patients are in states “for which exceptionally high doses of insulin are warranted.” They note that these effects go beyond what could be attributed to stress.

This is not a new idea – several studies have suggested that other viral infections may cause Type I diabetes. The first coronavirus known to cause sudden acute respiratory syndrome in humans, “SARS”, was also correlated with a higher incidence of diabetes than was seen in patients with pneumonia due to non-SARS pathogens. SARS is also associated with other autoimmune conditions. In fact, a number of other viruses are known to trigger autoimmunity.

COVID-19 is believed to use the angiotensin-converting enzyme 2 (ACE2) receptors to enter and infect human cells. These receptors exist in various tissues, including pancreatic beta cells (which produce the body’s insulin), adipose (fat) cells, etc.

It is unclear at this point whether the virus destroys the insulin-producing beta cells of the pancreas outright, or if it triggers an immune response in which the body’s defenses attack its own cells.

If evidence continues to build that this virus can cause diabetes, other questions to be researched include:

  • Can the diabetes be reversed in these patients once they have recovered from the infection?
  • How commonly do COVID-19 patients develop diabetes?
  • What type of diabetes is developed in COVID-19 patients? Type I, II, LADA (latent autoimmune diabetes of adulthood) or a new variant? 
  • Which treatments may be effective?
  • Do COVID-19 patients have increased risk of ketoacidosis?
  • Does COVID-19 worsen existing cases of diabetes or alter the course of the condition?
  • Do risk factors for diabetes prior to infection increase risk of the development of diabetes due to the coronavirus?

Details of a key in vitro study

Last week, the journal Cell published a study investigating the interaction of the SARS-CoV-2 virus with various cells and tissues. The researchers, Yang et al, developed various types of tissues from human pluripotent stem cells (hPSCs) and verified their results with adult cell types and humanized mouse model tissues. Their work confirmed:

  • ACE2 receptors exist in pancreatic alpha and beta cells, as well as in at least one type of liver cell (ALB+ hepatocytes);
  • Some cell types (including pancreatic beta cells) are more vulnerable to the SARS-CoV-2 virus than others;
  • Infection of these cells was associated with increased production of inflammatory chemokines (signal molecules) that have been found in higher than normal concentrations in the tissues of diseased COVID-19 patients;
  • Not all cells with ACE2 receptors had the same permissiveness to the virus, suggesting there is one or more factor(s) involved in cell infection.

ACTION YOU CAN TAKE:

  • Please (continue to) take this virus very seriously and take every precaution to avoid contracting or spreading it. 
  • If you have been infected or suspect you may have been exposed to the virus and are experiencing symptoms such as excessive thirst/hunger, frequent urination, and significant fatigue, seek prompt medical assistance. Untreated diabetes can quickly become a life-threatening condition.
  • If you are a healthcare practitioner, keep in mind this possible sequela of COVID-19 and report cases to this global registry of patients with COVID-19-related diabetes.

BLOG POST AUTHOR

Cindy Beernink, ND, M.Ed. (June 2020) lives and works in Toronto, ON. She is a founding member of the Naturopathic Alliance.