COVID-19 can raise blood sugar substantially, even in people who had perfectly normal glucose levels before infection. The virus triggers a cascade of hormonal, inflammatory, and tissue-damaging effects that push blood sugar up during the acute illness and, in many cases, keep it elevated for months afterward. What makes COVID-19 unusual compared with other respiratory infections is the number of pathways it uses to disrupt glucose metabolism, from a massive stress-hormone surge to direct infection of the cells that produce insulin.
The Stress-Hormone Surge During Acute Infection
When your body fights a severe infection, it floods the bloodstream with stress hormones like cortisol, adrenaline, and glucagon. These hormones exist to mobilize energy for the fight, but they also tell the liver to dump stored glucose into the blood while making muscle and fat cells less responsive to insulin. The result is a spike in blood sugar that can happen regardless of whether you have diabetes. In critically ill COVID-19 patients, this stress-induced high blood sugar is common enough that researchers use a dedicated metric to measure it, and higher values consistently predict worse outcomes including death.1PubMed Central. Stress hyperglycemia ratio improves machine learning-based mortality risk prediction in critically ill COVID-19 patients: a multicenter retrospective study
This type of high blood sugar is not unique to COVID-19. Any serious illness, from sepsis to major surgery, can provoke the same hormonal storm. But the inflammatory response in severe COVID-19 tends to be unusually intense. The virus can trigger a cytokine storm, a runaway loop of immune signaling that amplifies insulin resistance well beyond what a typical respiratory infection would cause. That extra inflammatory push means blood sugar can climb higher and stay elevated longer than you might expect from the infection’s severity alone.
Direct Damage to Insulin-Producing Cells
Beyond the general stress response, SARS-CoV-2 appears to directly invade tissues that regulate blood sugar. The virus enters cells through a surface protein called ACE2, and that protein shows up in high concentrations on the insulin-producing beta cells of the pancreas. Lab studies have shown that SARS-CoV-2 can infect human pancreatic cells grown from stem cells, and viral material has been found in pancreatic tissue from deceased COVID-19 patients.2PubMed Central. ACE2 function in the pancreatic islet: Implications for relationship between SARS-CoV-2 and diabetes This strongly suggests the virus can damage or destroy beta cells, reducing the body’s ability to produce insulin right when demand for it is skyrocketing.
The pancreas is not the only metabolic tissue under attack. Research has found that SARS-CoV-2 can also infect fat cells. Infected adipose tissue showed a vigorous antiviral gene response along with reduced production of adiponectin, a hormone that helps cells respond to insulin. Patients with COVID-19 who had lower adiponectin levels showed more pronounced insulin resistance.3PubMed Central. Hyperglycemia in acute COVID-19 is characterized by insulin resistance and adipose tissue infectivity by SARS-CoV-2 So the virus hits you from two directions at once: it hobbles insulin production while also making your tissues less sensitive to whatever insulin you still produce.
How COVID-19 Treatments Can Push Blood Sugar Higher
One of the most effective treatments for severe COVID-19, the steroid dexamethasone, comes with a well-known side effect: it raises blood sugar. Steroids work by tamping down the dangerous overreaction of the immune system, but they simultaneously ramp up liver glucose production and reduce insulin sensitivity. For hospitalized COVID-19 patients, dexamethasone has been shown to increase blood glucose levels and raise insulin requirements.4PubMed Central. Considerations for management of patients with diabetes mellitus and acute COVID-19
The effect is dose-dependent and gets worse in people whose blood sugar is already poorly controlled. Even at the standard dose of 6 mg daily, dexamethasone causes enough hyperglycemia in COVID-19 patients that those with higher pre-treatment HbA1c levels need significantly more insulin to compensate.5Diabetes Epidemiology and Management. Dexamethasone use and insulin requirements in coronovirus-19 (COVID-19) infection stratified by Hemoglobin A1c This creates a clinical dilemma: the steroid reduces the risk of dying from the lung inflammation, but it simultaneously worsens the metabolic damage. Hospital teams typically manage this by increasing glucose monitoring and adjusting insulin doses, but the blood sugar swings can be dramatic.
New-Onset Diabetes After COVID-19
Perhaps the most alarming finding is that COVID-19 appears to trigger entirely new cases of diabetes in people who did not have the disease before. A growing body of research points in this direction, although the exact size of the risk is still debated. Large observational studies and meta-analyses have reported that the risk of developing diabetes after COVID-19 is roughly 30 to 70 percent higher than in people who were not infected.6PubMed Central. Glucose metabolism across COVID-19 and long COVID: a longitudinal study A review in the Journal of Clinical Endocrinology and Metabolism acknowledged that COVID-19 increases the risk of developing diabetes, while cautioning that the exact magnitude remains uncertain because of differences in study design, pandemic phases, variants, and vaccination status.7PubMed Central. New-Onset Diabetes After COVID-19
What stands out is how COVID-19 compares to other respiratory infections on this front. In one study, new-onset diabetes developed in nearly 23 percent of hospitalized COVID-19 patients, compared with only about 3 percent of those hospitalized with influenza.8PubMed Central. Incidence of new-onset in-hospital and persistent diabetes in COVID-19 patients: comparison with influenza That roughly sevenfold difference suggests something specific about SARS-CoV-2 is at work, not just the general metabolic stress of being seriously ill. The mechanisms discussed earlier, direct pancreatic damage, adipose tissue infection, and the unusually intense inflammatory response, likely explain much of that gap.
Not all researchers are convinced the risk is as high as the largest studies suggest. Some smaller longitudinal studies tracking patients over time have not found a significant jump in new diabetes diagnoses, and there is ongoing debate about whether some of the “new” cases were actually undiagnosed diabetes that surfaced because of increased medical attention during hospitalization. The consensus, though, leans toward a real increase in risk, especially for people who were severely ill.
Blood Sugar Problems That Persist with Long COVID
For some people, the metabolic disruption does not end when the acute infection clears. Long COVID, defined as symptoms lasting weeks to months after the initial illness, frequently includes worsening insulin resistance. A systematic review and meta-analysis found that people with long COVID had meaningfully elevated fasting blood sugar, random blood sugar, insulin levels, and insulin resistance scores compared with healthy controls.9PubMed Central. Increased Insulin Resistance and Hyperglycaemia in Long COVID: A Systematic Review and Meta-Analysis
Animal studies have corroborated this pattern. Research in non-human primates found that SARS-CoV-2 infection triggered a dysregulated immune signaling pattern during the acute phase that predicted persistent high blood sugar four months later.10PubMed Central. Non-human primate model of long-COVID identifies immune associates of hyperglycemia The implication is that the virus sets off a chain of immune events during the initial infection that continues to impair glucose regulation long after the virus itself is gone.
In one clinical study of hospitalized patients, those who went on to develop long COVID were substantially more likely to develop diabetes within a year of their acute infection. Among patients with long COVID, three-quarters developed diabetes within 12 months, compared with roughly 56 percent of those who recovered without lingering symptoms.11PubMed Central. Insulin Resistance in Long COVID-19 Syndrome These numbers came from a population of hospitalized patients who already carried risk factors like obesity, so they should not be generalized to everyone who catches COVID-19. But they illustrate how strongly the long-term metabolic trajectory can diverge depending on whether the acute illness fully resolves.
Diabetic Emergencies During COVID-19
When blood sugar climbs high enough, fast enough, it can lead to life-threatening emergencies. Diabetic ketoacidosis, a condition where the body starts breaking down fat for fuel and produces dangerous levels of acid in the blood, was observed frequently during the pandemic. Early data from China found that among COVID-19 patients admitted with ketosis, about a third had diabetes, and 20 percent of those developed full-blown DKA.12PubMed Central. Diabetic ketoacidosis precipitated by COVID-19: A report of two cases and review of literature Some of these patients had no prior diabetes diagnosis, meaning DKA was their first sign that something had gone wrong with their blood sugar.
DKA is dangerous in any context, but it becomes harder to manage when a patient is also fighting a severe respiratory infection. The dehydration, electrolyte imbalances, and acidosis of DKA compound the lung and cardiovascular damage from COVID-19. Hospital teams had to develop specific protocols for managing the overlap, often involving aggressive insulin infusions alongside ventilator support and antiviral treatment.
Why Children Are Not Immune to These Effects
Adults were not the only ones affected. Pediatric data revealed an unsettling trend: new diagnoses of type 2 diabetes in children roughly doubled during 2020 compared with 2019, and children diagnosed with type 1 diabetes were more likely to present in DKA during the pandemic. A meta-analysis covering the first year of the pandemic found that worldwide, new-onset type 1 diabetes in children increased by about 10 percent, DKA at the time of type 1 diagnosis rose by about 25 percent, and severe DKA jumped by about 20 percent.13PubMed Central. COVID-19 induced type 1 diabetes: A systematic review of case reports and series
A large study comparing children who had COVID-19 with those who had other respiratory infections found that the risk of new type 2 diabetes was about 50 to 60 percent higher in the COVID-19 group across various follow-up windows. Among children who were hospitalized, the risk was roughly two to three times higher. And among children who already had overweight or obesity, the risk approximately doubled.14JAMA Network Open. SARS-CoV-2 Infection and New-Onset Type 2 Diabetes Among Pediatric Patients, 2020 to 2022 These findings are particularly concerning because type 2 diabetes in childhood carries decades of potential complications and is already rising for other reasons like increasing obesity rates.
When Standard Blood Sugar Tests Become Unreliable
An underappreciated wrinkle in all of this is that one of the most common tools for assessing blood sugar control, the HbA1c test, may give misleading readings during and shortly after COVID-19. HbA1c measures how much glucose has attached to red blood cells over the previous two to three months, which makes it a useful snapshot of longer-term blood sugar trends. But COVID-19 appears to interfere with the test itself.
Researchers observed that some severe COVID-19 patients without any history of diabetes had abnormally high HbA1c values during their illness, which then dropped to normal within just six weeks of recovery, far faster than genuine improvements in blood sugar would allow. One proposed explanation is that the heavily sugar-coated spike protein of SARS-CoV-2 binds to red blood cells, and the standard lab method for measuring HbA1c cannot distinguish between glucose attached to hemoglobin and viral spike proteins attached to the same cells. If that is correct, elevated HbA1c during acute COVID-19 may partly reflect viral damage to red blood cells rather than genuinely high blood sugar.15Diabetes. HbA1c Level in Severe COVID-19 Patients Is Not Only a Marker of Glycemic Status but Also of Acute Erythrocyte Damage
This matters for practical decisions. If a doctor sees a high HbA1c result in someone who was recently hospitalized with COVID-19, it might not mean that person needs long-term diabetes medication. Confirming the diagnosis with additional tests, like fasting glucose or an oral glucose tolerance test done after recovery, is important before starting treatment based on a potentially unreliable number.
How Pre-Existing Diabetes Makes COVID-19 Worse
The relationship between COVID-19 and blood sugar runs in both directions. The virus disrupts blood sugar, but high blood sugar also makes the virus more dangerous. A systematic review and meta-analysis found that higher pre-infection HbA1c was linearly associated with increased risk of dying from COVID-19 or experiencing worse outcomes. Patients with poorly controlled blood sugar before catching the virus had significantly higher odds of severe illness.16PubMed Central. Elevated HbA1c levels in pre‐Covid‐19 infection increases the risk of mortality: A systematic review and meta‐analysis
The reasons make biological sense. Chronically elevated blood sugar impairs white blood cell function, weakening the immune response. It also damages blood vessel linings and promotes clotting, both of which are already major problems in severe COVID-19. High blood sugar creates a vicious cycle: the infection worsens glucose control, which in turn weakens the body’s ability to fight the infection and increases the risk of cardiovascular complications like blood clots, heart attacks, and strokes.17Medical Journal of Clinical Trials & Case Studies. Hyperglycemia as a Risk Factor for Cardiovascular Disease Post- Acute Sequelae of SARS-CoV-2 Infection This cycle is a major reason why people with diabetes were consistently overrepresented among COVID-19 hospitalizations and deaths throughout the pandemic.
Racial and Ethnic Disparities
The metabolic impact of COVID-19 did not fall equally across populations. Ethnic minority groups experienced both more severe COVID-19 outcomes and more pronounced blood sugar disruption. The reasons are layered: higher baseline rates of diabetes, greater exposure to the virus through essential-worker jobs and crowded housing, and reduced access to healthcare, all rooted in longstanding structural inequities.18PubMed Central. The Impact of the COVID-19 Pandemic on Ethnic Minority Groups With Diabetes
Among children, the disparities were stark. The number of youth diagnosed with type 2 diabetes doubled during 2020, and Black youth consistently presented with higher HbA1c levels and were more likely to be in DKA at diagnosis than White youth. These gaps persisted at one-year follow-up regardless of diabetes type or year of onset.19Diabetes. 1158-P: Racial Disparities in Youth with Diabetes and the COVID-19 Pandemic The pandemic amplified existing disparities in diabetes management, in part because lockdowns disrupted routine care, limited access to healthy food, and reduced physical activity in communities that already had fewer resources.
Monitoring Blood Sugar in Hospitalized COVID-19 Patients
The pandemic forced hospitals to rethink how they monitor blood sugar. Normally, hospitalized patients with high blood sugar get fingerstick glucose checks multiple times a day, with a nurse physically entering the room each time. During COVID-19 surges, every room entry required full protective equipment and increased the risk of viral transmission to healthcare workers. Continuous glucose monitors, small sensors placed under the skin that transmit readings wirelessly, offered a solution.
Early experience at tertiary care centers showed that continuous glucose monitoring with twice-daily calibration was safe for guiding insulin dosing decisions and significantly reduced the number of fingerstick checks needed.20PubMed Central. Continuous Glucose Monitoring for Patients with COVID-19 Pneumonia: Initial Experience at a Tertiary Care Center Hybrid protocols combining continuous monitors with occasional point-of-care checks proved to be a practical way to maintain good blood sugar control while keeping healthcare workers safer and preserving protective equipment during shortages.21PubMed Central. The Role of Remote Glucose Management Using Real-time Continuous Glucose Monitoring Systems in ICU-hospitalized Patients with COVID-19 This shift, born from pandemic necessity, has accelerated broader adoption of continuous glucose monitoring in hospital settings beyond COVID-19 care.
What to Watch for After Recovery
If you have had COVID-19, especially a moderate or severe case, paying attention to your blood sugar in the following months is a reasonable precaution. Classic symptoms of high blood sugar include increased thirst, frequent urination, unexplained fatigue, and blurred vision. But elevated blood sugar can also be entirely silent, which is why periodic lab work matters.
There is no universally agreed-upon screening protocol for post-COVID blood sugar surveillance. Some endocrinologists recommend checking fasting glucose and HbA1c at three months and again at twelve months after a hospitalized COVID-19 infection, particularly if you have additional risk factors like obesity, a family history of diabetes, or if you needed steroid treatment. For milder cases, standard annual checkups with routine metabolic panels should catch most new problems. The key point is awareness: COVID-19 recovery is not just about your lungs and energy levels. Your metabolic health deserves attention too, and catching insulin resistance early gives you the widest range of options, from lifestyle changes to medication, to prevent it from progressing to full-blown diabetes.