What Happens When a Diabetic Stops Taking Insulin?

When a person with diabetes stops taking insulin, blood sugar begins climbing within hours, and the body shifts into an increasingly dangerous state of metabolic crisis. For someone with type 1 diabetes, who produces no insulin at all, this can become life-threatening in less than a day. For someone with type 2 diabetes who relies on insulin, the timeline is usually slower but the endpoint can be just as severe. The specifics depend on the type of diabetes, how much insulin the body still makes on its own, and what triggers the stoppage, but the trajectory without intervention always points in the same direction.

The First Hours Without Insulin

Insulin does two essential jobs: it lets cells absorb glucose from the bloodstream for energy, and it tells the liver to stop releasing stored glucose. When insulin disappears, both systems fail at once. Cells can no longer take up the glucose circulating in the blood, and the liver starts dumping even more glucose into a system already overloaded with it. Hepatic glucose production, driven primarily by a process called gluconeogenesis, ramps up in proportion to the rising blood sugar levels.¹ The result is blood sugar that climbs rapidly, often exceeding 300 or 400 mg/dL within a matter of hours in someone with type 1 diabetes.

At the same time, without insulin signaling fat cells to hold onto their stores, the body begins breaking down fat at an accelerated rate. This process, called lipolysis, floods the bloodstream with free fatty acids. In people with severe insulin deficiency, lipolysis can be dramatically elevated compared to those who retain even partial insulin signaling.² Those fatty acids head to the liver, where they are converted into ketone bodies as an emergency fuel source. Under normal circumstances, ketones serve as a backup energy supply when glucose is scarce. But when insulin is absent, ketone production spirals out of control because the usual brake on the process is missing.

Diabetic Ketoacidosis

The most acute and dangerous consequence of stopping insulin, particularly for people with type 1 diabetes, is diabetic ketoacidosis, or DKA. As ketone bodies accumulate in the blood, they make it increasingly acidic. The body tries to compensate: breathing becomes fast and deep as the lungs attempt to blow off carbon dioxide to counteract the acid. The kidneys work overtime trying to excrete excess glucose and ketones, pulling water and electrolytes along with them. This creates a vicious cycle of dehydration that concentrates the blood sugar and ketones even further.

During DKA, the predominant ketone in the blood is beta-hydroxybutyrate, which accumulates as the liver converts the surge of free fatty acids into ketone bodies.³ The symptoms escalate in a predictable pattern: excessive thirst, frequent urination, nausea and vomiting, abdominal pain, fruity-smelling breath (from acetone, a byproduct of ketone metabolism), confusion, and eventually loss of consciousness. DKA commonly occurs in type 1 diabetes because of the absolute insulin deficiency, though it can also develop in people with type 2 diabetes under certain circumstances.⁴

Untreated DKA is fatal. Before insulin was discovered in the 1920s, type 1 diabetes was a death sentence, and DKA was typically how it ended. Even today, with modern emergency care, DKA carries a mortality rate that demands urgent treatment. It remains one of the leading causes of death in young people with type 1 diabetes.

How Type 2 Diabetes Differs

People with type 2 diabetes who stop insulin face a different, though still serious, trajectory. Because most people with type 2 diabetes still produce some insulin on their own, full-blown ketoacidosis is less common. Their pancreas may be producing enough insulin to partially suppress ketone production but not enough to keep blood sugar under control. Instead of DKA, they are more likely to develop a condition called hyperosmolar hyperglycemic state, or HHS.

In HHS, blood sugar climbs to extreme levels, sometimes above 600 mg/dL, without the dramatic acid buildup seen in DKA. The severe hyperglycemia causes massive fluid loss through the kidneys, leading to profound dehydration. Symptoms range from lethargy to confusion and coma, with mental status declining in direct proportion to how concentrated the blood becomes.⁵ HHS develops more slowly than DKA, often over days to weeks, which can make it deceptively dangerous. By the time symptoms become obvious, the person may already be severely dehydrated and close to organ failure. HHS actually carries a higher mortality rate than DKA in many clinical settings, partly because it tends to affect older adults with other health problems.

When people with type 2 diabetes do develop DKA, it tends to look somewhat different from the type 1 version. A study comparing DKA in adults with type 1 and type 2 diabetes found that type 2 patients had significantly higher creatinine levels during DKA episodes, suggesting greater kidney stress.⁶ This makes sense given that type 2 patients are generally older and more likely to have pre-existing kidney disease.

What High Blood Sugar Does to Your Blood Vessels

Even before someone reaches a full metabolic crisis, the sustained high blood sugar from missing insulin inflicts damage on blood vessels. Acutely elevated glucose harms the lining of blood vessels, impairing their ability to dilate and regulate blood flow.⁷ Over time, this kind of vascular injury is what drives the classic complications of poorly controlled diabetes: damage to the small vessels in the eyes, kidneys, and nerves, along with accelerated atherosclerosis in larger arteries.

Someone who stops insulin for days or weeks without dying from DKA or HHS is essentially fast-tracking these complications. The retina, the kidneys, and the peripheral nerves are exquisitely sensitive to chronic hyperglycemia. Weeks of uncontrolled blood sugar can cause damage that would normally take months or years of moderately elevated glucose. The vascular injury compounds: each episode of severe hyperglycemia makes the next one more damaging because the repair mechanisms are themselves impaired by the high-sugar environment.

The Immune System Takes a Hit

Uncontrolled diabetes weakens the immune system in ways that create real vulnerability to infection. The white blood cells responsible for finding, engulfing, and killing bacteria and fungi all perform worse when blood sugar is high. Studies show that the movement, engulfing ability, and killing capacity of these immune cells are all decreased in people with poorly controlled diabetes compared to those with well-managed blood sugar.⁸ Better glucose control improves these functions, which is one of the reasons infections can become a runaway problem when someone stops taking insulin. Urinary tract infections, skin infections, and fungal infections are commonly the first signs of trouble, and in a severely hyperglycemic state, even minor wounds can spiral into serious infections that resist treatment.

The Dangers of Restarting Treatment

An underappreciated risk comes not just from stopping insulin but from what happens when treatment resumes after a crisis. Treating DKA requires carefully reintroducing insulin and fluids, and doing it too aggressively can cause a dangerous complication: cerebral edema, or brain swelling. Research in animal models of DKA has shown that brain water content increases by about 8% after treatment, driven primarily by the rapid reduction in blood sugar and blood concentration rather than by the acidosis itself.⁹ Using isotonic rather than hypotonic fluids during treatment produced significantly less brain swelling in these studies.

This is why DKA treatment in a hospital follows strict protocols for how quickly blood sugar is brought down and what type of fluids are given. It is also why someone who has been in DKA should never simply inject a large dose of insulin at home and hope for the best. The correction itself is a medical procedure that requires monitoring of blood chemistry, electrolytes (especially potassium, which shifts dramatically during insulin treatment), and neurological status. Cerebral edema during DKA treatment is particularly dangerous in children and young adults, and it remains one of the leading causes of DKA-related death in pediatric patients.

When People Stop Insulin on Purpose

Not everyone who stops insulin does so accidentally or because they ran out. Deliberate insulin omission is a recognized and serious problem, particularly among young women with type 1 diabetes. When someone with type 1 skips insulin, they lose weight rapidly because the body cannot store the calories it consumes and instead excretes glucose in the urine. This behavior, sometimes called “diabulimia” in popular media, is increasingly recognized as a distinct and dangerous pattern that can lead to severe vascular complications and premature death.¹⁰

Detecting this behavior is challenging, but certain patterns raise red flags. Adolescents who intentionally omit insulin tend to be female, have persistently high HbA1c values (above roughly 9%), and show a pattern of wildly fluctuating blood sugar control over time.¹¹ The weight loss can be dramatic and rapid, which reinforces the behavior even as the person becomes increasingly sick. Clinicians who treat type 1 diabetes are trained to look for these patterns, but the behavior often goes undetected for months or years because the person may not volunteer that they are skipping doses, and the symptoms of chronic hyperglycemia build gradually.

The long-term consequences of repeated insulin omission for weight control are devastating. The combination of chronically high blood sugar, repeated episodes of DKA, dehydration, and electrolyte imbalances accelerates every diabetes complication. Retinopathy, neuropathy, and kidney damage develop at younger ages and progress faster. Addressing the behavior requires treating both the diabetes and the underlying eating disorder, which makes it one of the more complex clinical situations in diabetes care.

Insulin Rationing Due to Cost

In the United States, a significant number of people stop or reduce insulin not by choice but because they cannot afford it. A study comparing insulin rationing in 2017 and 2024 found that roughly one in four insulin-dependent individuals reported cost-related rationing, and this rate did not significantly improve over the seven-year period despite policy changes aimed at lowering insulin prices. In 2024, about 24% reported rationing due to cost, 17% due to insurance delays, and 19% due to pharmacy shortages, with nearly 38% experiencing rationing from at least one of these causes.¹²

Rationing looks different from a sudden stop. People stretch their vials by taking smaller doses, skipping meals, or using rapid-acting insulin less frequently. The result is a slow, grinding deterioration rather than an acute crisis. Blood sugar runs high for weeks or months, silently damaging vessels, nerves, and organs. Occasionally, someone rationing insulin tips over into full DKA, which is how the problem comes to medical attention. These cases are particularly tragic because they are entirely preventable with adequate access to medication.

Cognitive Consequences of Repeated DKA

Each episode of DKA is not just a crisis that resolves once treatment is finished. Research suggests there is a cumulative toll, particularly on the brain. A study of older adults with type 1 diabetes found that those who had experienced recurrent DKA episodes scored lower on tests of overall cognitive function and significantly lower on measures of executive function and processing speed. People with recurrent DKA were more than three times as likely to fall into the lowest tier of executive function performance compared to those without recurrent episodes.¹³

The mechanism behind this cognitive decline likely involves a combination of factors. The severe metabolic derangement of DKA itself stresses brain cells. The rapid osmotic shifts during treatment can cause subclinical brain swelling even when full cerebral edema does not develop. Recurrent dehydration and electrolyte imbalances may also contribute. For someone who has experienced multiple DKA episodes due to insulin omission, cost-related rationing, or other reasons, the cognitive effects represent yet another layer of damage that may not be fully reversible.

Euglycemic DKA and Medications That Mask the Warning Signs

A newer wrinkle in the picture of insulin deficiency involves a class of diabetes medications called SGLT-2 inhibitors, which are widely prescribed for type 2 diabetes and sometimes used in type 1 as well. These drugs work by blocking glucose reabsorption in the kidneys, causing excess sugar to be excreted in the urine. The catch is that by constantly lowering blood glucose through the kidneys, they can mask the usual warning sign of DKA: extremely high blood sugar.

People taking SGLT-2 inhibitors can develop what is called euglycemic DKA, where dangerous ketoacidosis occurs with blood sugar levels that look normal or only mildly elevated. The mechanism involves several overlapping pathways. The drugs increase renal glucose clearance, which allows blood sugar to stay deceptively low. Meanwhile, they also raise glucagon levels through mechanisms that are not fully understood, and glucagon promotes ketone production. The fluid and sodium losses caused by the drugs worsen dehydration, which triggers stress hormones that further drive ketone production and insulin resistance.¹⁴

This matters for the question of stopping insulin because someone on an SGLT-2 inhibitor who reduces or stops their insulin may not see the dramatic blood sugar spike they expect. They might assume they are fine because their glucose readings look reasonable, while ketones are quietly building to dangerous levels. This is one reason why ketone monitoring, not just glucose monitoring, is recommended for anyone on SGLT-2 inhibitors who becomes ill, undergoes surgery, or makes changes to their insulin regimen. During DKA, beta-hydroxybutyrate is the dominant ketone in the blood, while urine ketone strips primarily detect acetoacetate, which becomes predominant only as DKA resolves.³ This means urine strips can underestimate the severity of early DKA, and blood ketone meters give a more accurate picture of what is actually happening.

How Quickly Things Go Wrong

The timeline varies enormously between individuals. A person with type 1 diabetes who uses an insulin pump and disconnects it can be in DKA within four to eight hours, because they have no long-acting insulin providing background coverage. Someone on long-acting injections who skips one dose may not feel much for 12 to 24 hours as the previous dose tapers off, but will likely be in trouble by the following day. For type 2 patients who still produce some insulin, the decline is more gradual. They might feel increasingly tired, thirsty, and foggy over days to weeks as blood sugar creeps higher. Some people with type 2 who stop insulin do not develop an acute crisis at all but instead settle into a state of chronic hyperglycemia that quietly erodes their health over months.

Several factors speed up the timeline. Illness or infection raises blood sugar and insulin requirements simultaneously, so stopping insulin while sick is especially dangerous. Dehydration, whether from vomiting, diarrhea, or simply not drinking enough water, concentrates the blood sugar faster. Stress, surgery, and certain medications (particularly steroids) also spike glucose and can push someone from uncomfortable to critical more quickly. Children and adolescents tend to develop DKA faster than adults, partly because they have higher metabolic rates and smaller fluid reserves.

For anyone who depends on insulin, the bottom line is that stopping is not something that can be safely experimented with. Even a brief interruption carries risks that escalate unpredictably, and the consequences, both immediate and cumulative, extend well beyond the acute episode.