Stopping insulin therapy is an extremely dangerous, life-threatening action that can lead to death within days or hours. Insulin is a foundational hormone responsible for managing the body’s primary energy source, and withholding it initiates a rapid metabolic collapse. For individuals with Type 1 diabetes, who produce virtually no insulin, this deprivation quickly becomes a medical emergency. While the crisis may progress slower for those with Type 2 diabetes who still produce some insulin, the outcome of uncontrolled high blood sugar and metabolic derangement remains severe and often fatal without immediate intervention.
Insulin’s Essential Role in Cellular Energy
Insulin is a peptide hormone that regulates energy metabolism, ensuring that glucose, the primary fuel derived from food, can be used or stored by cells. After a meal, the pancreas releases insulin, which acts like a key, unlocking receptors on muscle, fat, and liver cells. This allows circulating glucose to be transported from the bloodstream into the cells, where it is converted into usable energy or stored as glycogen or fat.
When insulin is absent or severely impaired, this process halts, leading to internal energy starvation despite abundant fuel. Glucose cannot enter the cells and accumulates to dangerously high levels in the blood, known as hyperglycemia. Hyperglycemia triggers excessive urination and dehydration as the body attempts to flush out the excess sugar through the kidneys, causing significant water and electrolyte loss.
Deprived of glucose, the body’s cells signal famine, prompting the release of counter-regulatory hormones such as glucagon, cortisol, and epinephrine. These hormones exacerbate the problem by stimulating the liver to produce even more glucose through gluconeogenesis and glycogenolysis. This metabolic shift forces the body to rapidly break down fat stores for an alternative energy source, a process called lipolysis.
This metabolic crisis is swift in people with Type 1 diabetes, whose pancreatic beta cells have been destroyed, resulting in an absolute insulin deficiency. People with Type 2 diabetes, who have insulin resistance, may experience a slower progression, but prolonged deprivation still results in a severe, life-threatening collapse of metabolic function.
The Acute Life Threat Diabetic Ketoacidosis
The most immediate life threat from severe insulin deprivation, especially for those with Type 1 diabetes, is Diabetic Ketoacidosis (DKA). DKA is a metabolic disorder driven by the body’s attempt to find fuel by breaking down fat stores. This rapid lipolysis releases large quantities of free fatty acids into the bloodstream.
The liver processes these fatty acids into acidic compounds called ketone bodies, primarily beta-hydroxybutyric acid and acetoacetic acid. These strong organic acids rapidly overwhelm the body’s natural buffering systems, leading to a profound drop in the blood’s pH, known as metabolic acidosis. The accumulation of these acids is the defining feature of DKA and makes the condition rapidly toxic to organs.
As acidosis progresses, the body attempts to compensate by increasing the rate and depth of breathing, known as Kussmaul respirations, in an effort to expel carbon dioxide and raise the blood’s pH. The presence of the ketone acetone, one of the ketone bodies, can also cause the breath to have a distinct, sweet, or fruity odor. Symptoms develop quickly, often over 24 hours, and include pronounced thirst, excessive urination, severe nausea, vomiting, and abdominal pain.
If DKA is not treated promptly, the combination of severe dehydration, electrolyte imbalances, and metabolic acidosis can lead to lethargy, confusion, cerebral edema, and coma. The mortality rate for DKA remains a serious risk, emphasizing the speed at which the body can fail without insulin.
Other Severe Systemic Consequences of Deprivation
While DKA is the most rapid acute threat, prolonged insulin deprivation also exposes the body to other severe systemic crises. One is the Hyperosmolar Hyperglycemic State (HHS), a severe complication more common in older adults with Type 2 diabetes. HHS is characterized by extremely high blood glucose levels, often exceeding 600 mg/dL, leading to extreme dehydration and a dangerously high concentration of particles in the blood, known as hyperosmolarity.
The key difference between HHS and DKA is that HHS involves a relative lack of insulin, which is sufficient to suppress the massive fat breakdown that causes significant ketosis and acidosis. Consequently, patients with HHS often present with more profound dehydration and severe neurological symptoms, including altered mental status, seizures, and coma, without the deep, rapid breathing seen in DKA. HHS develops more gradually, sometimes over days or weeks, but it carries a significant mortality rate, often higher than DKA, due in part to the older age and coexisting conditions of those affected.
Beyond these acute emergencies, sustained high blood sugar accelerates the microvascular and macrovascular damage characteristic of uncontrolled diabetes. This rapid deterioration affects multiple organ systems and contributes to long-term mortality. Within a short period, increased blood glucose levels begin to damage the delicate blood vessels in the eyes, potentially leading to retinopathy and vision loss.
The small blood vessels in the kidneys are also targeted, leading to accelerated kidney disease and progression toward kidney failure. Nerves are damaged, causing neuropathy that can result in pain, numbness, and an increased risk of severe foot ulcers and amputations. While these complications are usually associated with chronic diabetes, they accelerate dramatically when insulin is suddenly withheld.
Immediate Emergency Action and Medical Intervention
Stopping insulin is a medical emergency requiring immediate professional intervention to prevent irreversible organ damage or death. Anyone who has stopped taking prescribed insulin, or who is exhibiting symptoms of severe hyperglycemia, DKA, or HHS, must seek emergency medical care. Attempting to manage these conditions at home by simply resuming a normal insulin dose is insufficient and potentially dangerous without medical supervision.
Hospital treatment for these hyperglycemic crises focuses on three simultaneous goals: fluid replacement, insulin administration, and electrolyte correction. Aggressive administration of intravenous (IV) fluids, such as isotonic saline, is the first and most crucial step to correct severe dehydration and poor blood circulation caused by excessive urination. Adults with HHS, for example, may require an average of nine liters of fluid replacement over the first two days.
Insulin is administered intravenously as a continuous drip at a measured rate, such as 0.1 units/kg/h, to safely lower blood glucose levels and halt the production of acidic ketones. Careful monitoring and replacement of electrolytes, particularly potassium, are necessary, as insulin therapy can shift potassium from the blood into the cells, potentially causing hypokalemia. Treatment protocols require frequent monitoring of blood glucose, electrolytes, and acid-base balance until the metabolic crisis is fully resolved.