Pediatric patients aged 10 to 19 years old diagnosed with COVID-19 have a higher risk of new-onset type 2 diabetes within six months compared to those diagnosed with other respiratory infections, according to researchers at Case Western Reserve University School of Medicine.

The research is a follow-up of meta-data analysis showing an increased risk of type 2 diabetes in adults. The meta-analysis revealed a 66% higher average risk of new-onset diabetes after SARS-CoV-2 infection in adults. In the current retrospective study, “SARS-CoV-2 Infection and New-Onset Type 2 Diabetes Among Pediatric Patients, 2020 to 2022,” published in JAMA Network Open, researchers looked to see if a similar pattern existed in children.

The study analyzed a cohort of 613,602 pediatric patients aged 10 to 19 years. After propensity score matching, this cohort was divided equally into two groups: 306,801 patients diagnosed with COVID-19 and 306,801 patients diagnosed with other respiratory infections (ORI).

A subset of the cohort with obesity and COVID or ORI was also analyzed, with two groupings of 16,469 patients.

The research compared the incidence of new type 2 diabetes diagnoses at one, three, and six months after the initial respiratory infection. The risk ratios (RR) for developing type 2 diabetes after COVID-19 were found to be significantly higher than for those with ORI.

Specifically, the RR was 1.55 (95% CI, 1.28–1.89) at one month, 1.48 (95% CI, 1.24–1.76) at three months, and 1.58 (95% CI, 1.35–1.85) at six months post-infection.

The smaller subgroup analyses revealed even greater elevated risks among children classified as overweight, with RRs of 2.07 at one month, 2.00 at three months, and 2.27 at six months. Hospitalized patients also showed increased risks, with RRs of 3.10 at one month, 2.74 at three months, and 2.62 at six months after COVID-19 diagnosis.

The study concluded that SARS-CoV-2 infection is associated with a higher incidence of type 2 diabetes diagnoses in children than those with other respiratory infections. Further research is necessary to determine whether the diabetes persists or is a recoverable condition that reverses later in life.

While COVID-19 may seem an unintuitive cause of type 2 diabetes, we currently do not understand what initiates the condition. It is often linked to being overweight, being less active, eating processed foods or having a family history of type 2 diabetes, indicating both an environmental and a possible genetic basis.

Insulin resistance is what type 2 diabetes essentially does within the body. Insulin is a hormone made in the pancreas that is essential for removing glucose from the blood by binding it to receptor sites of cells, where the glucose is absorbed and used as energy to power the cell.

Insulin resistance on a physiological level usually means that the cells have down-regulated binding site availability. This resistance can come about if cells have encountered too much insulin. The downregulation of binding sites leaves more unbound glucose in the bloodstream, which the brain interprets as needing the pancreas to produce more insulin. This negative feedback loop often progresses the disease.

The current retrospective analysis can only see past correlations between COVID-19 and the study cohort and cannot identify causation. Future research will be needed to determine if COVID-19 is interfering directly with any of the systems related to glucose sensing and insulin regulation by the brain, insulin production in the pancreas or the binding ability of cells.

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