How Does Cortisol Affect Insulin and Blood Sugar?

Cortisol raises blood sugar by triggering the liver to produce glucose and by making your cells less responsive to insulin. In short bursts this is useful, keeping fuel available when your body faces a threat. But when cortisol stays elevated for weeks or months, it can push blood sugar chronically higher and contribute to insulin resistance, a state where your cells need more and more insulin to do the same job. The interplay between cortisol and insulin is central to understanding everything from stress-related blood sugar spikes to why long-term steroid medications so often cause diabetes.

How Cortisol Pushes the Liver to Make Glucose

Your liver is a glucose factory, and cortisol is one of its strongest activators. When cortisol levels rise, the liver ramps up a process called gluconeogenesis, essentially building new glucose from raw materials like amino acids and lactate. In lab studies, cortisol roughly doubled the rate at which liver tissue converted the amino acid alanine into glucose and glycogen, the stored form of sugar.¹ At the same time, cortisol stimulates the breakdown of fat stores. When researchers infused cortisol into healthy volunteers at levels mimicking a physiological stress response, fat breakdown in both abdominal and thigh tissue increased substantially, releasing fatty acids into the bloodstream that the liver can use as additional fuel for glucose production.²

The net result is a two-pronged assault on blood sugar control. More glucose gets dumped into the bloodstream from the liver, and the free fatty acids floating around simultaneously interfere with how well muscles take up that glucose. Even if your pancreas cranks out extra insulin to compensate, the glucose keeps piling up faster than your tissues can clear it.

Cortisol Alone Is Mild, but Together with Other Stress Hormones It Gets Extreme

Here is what surprises a lot of people: cortisol by itself produces only a modest bump in blood sugar. The real trouble begins when it teams up with the other “counter-regulatory” hormones your body releases during stress, namely epinephrine (adrenaline) and glucagon. When researchers infused each of these hormones individually into healthy fasting volunteers at stress-level doses, blood sugar rose only mildly, staying below about 120 mg/dL or climbing only briefly. But when all three were infused at the same time, glucose soared above 200 mg/dL despite the fact that insulin levels also doubled.³

The combined blood sugar spike was about three times larger than you would get by simply adding together the individual effects of each hormone. That synergy is not a small detail. It means that during a severe illness, a car accident, major surgery, or any situation where your body mounts a full-blown stress response, blood sugar can skyrocket even if your pancreas is working perfectly. The division of labor among the hormones is instructive: epinephrine and glucagon stimulate the liver to pour out glucose, while cortisol sustains that output over time and blocks peripheral glucose disposal.⁴ Cortisol’s job in this trio is less about starting the fire and more about keeping it burning.

This explains a phenomenon that hospital staff see routinely: “stress hyperglycemia.” A patient admitted for pneumonia or a broken hip who has never had diabetes may suddenly show blood sugars in the diabetic range. It is not that their pancreas failed overnight. It is that the combined hormonal surge overwhelmed insulin’s ability to keep up.

What Happens Inside the Pancreas

Cortisol does not simply overpower insulin from the outside. It also tinkers with the cells that make insulin. Research on both rodent and human beta cells (the insulin-producing cells in the pancreas) shows that cortisol suppresses voltage-dependent calcium channels, which are part of the normal machinery beta cells use to sense blood sugar and release insulin. You would expect that to cripple insulin output, but the beta cells partially compensate by ramping up alternative signaling pathways and docking more insulin-containing granules at the cell membrane, essentially staging more insulin for quick release.⁵

In a healthy person, this workaround keeps insulin secretion mostly intact during temporary cortisol surges. But the adaptation has limits. If cortisol remains elevated for a long time, or if the beta cells are already stressed (as in someone with prediabetes or a family history of type 2 diabetes), the compensatory mechanisms can fall short. That is when you start seeing chronically elevated blood sugar. Early studies on this used the synthetic steroid prednisone and found that just one day of treatment at moderate doses raised fasting blood glucose in healthy people from normal levels to around 137 mg/dL during a glucose infusion, a range that would raise clinical concern.⁶

Chronic Cortisol, Belly Fat, and Insulin Resistance

Short-lived cortisol spikes are one thing. The metabolic landscape changes when cortisol stays elevated for months or years, whether from chronic psychological stress, sleep deprivation, or a medical condition. Persistently high cortisol pushes energy storage preferentially toward abdominal visceral fat, the deep fat that wraps around organs, rather than the subcutaneous fat under the skin. That matters because visceral fat is metabolically active tissue that releases inflammatory signals which worsen insulin resistance.

A study measuring cortisol production rates and visceral fat in men found that higher cortisol output correlated with more visceral fat and greater insulin resistance. The researchers concluded that increased activity in the hormonal stress axis promotes selective visceral fat accumulation and insulin resistance, and may even promote weight regain after dieting.⁷ A broader review of how insulin and cortisol interact in the metabolic syndrome describes this as a reinforcing loop: high insulin and what researchers call “functional hypercortisolism” work together to shift energy toward abdominal fat stores, which in turn worsens both insulin resistance and cortisol dysregulation.⁸

From an evolutionary standpoint, this system made sense. In a world of intermittent famine and physical danger, mobilizing glucose and fat stores during a crisis helped ancestors survive. Stress hormones like cortisol temporarily blocked insulin action so that energy would be available for muscles and the brain. The problem is that our biology still runs this program even when the “threat” is a demanding job or chronic sleep loss, situations where the mobilized energy just circulates in the blood without being burned off.⁹

Cushing’s Syndrome and Steroid-Induced Diabetes

Cushing’s syndrome is what happens when cortisol is dramatically and persistently elevated, either because of a tumor in the pituitary or adrenal glands, or from taking glucocorticoid medications like prednisone for a long time. It is the clearest clinical demonstration of what cortisol does to blood sugar when left unchecked. Roughly 20 to 45 percent of people with Cushing’s syndrome develop outright diabetes, and another 10 to 30 percent have impaired glucose tolerance, bringing the total rate of glucose metabolism problems close to 70 percent.¹⁰ That tells you something about the potency of cortisol’s metabolic effects: given enough exposure, most people’s glucose regulation will buckle.

The mechanism in Cushing’s syndrome mirrors what we see in acute stress, just stretched over months or years. Insulin action is markedly impaired, glucose disposal by muscles drops, and the pancreas cannot secrete enough extra insulin to keep pace.¹¹ The good news is that when the source of excess cortisol is removed, whether by surgery or by tapering off steroid medications, blood sugar often improves substantially or returns to normal.

Steroid-induced diabetes is the more common version of this problem in everyday medicine. Glucocorticoid drugs are prescribed widely for asthma, rheumatoid arthritis, inflammatory bowel disease, organ transplant rejection, and dozens of other conditions. Since their introduction in the 1940s, the side effect of unexpected high blood sugar has been a persistent problem, sometimes leading to hospital admissions, prolonged stays, and increased infection risk.¹² If you are starting a course of steroids and you have risk factors for diabetes, your doctor will often monitor your blood sugar more closely for exactly this reason.

The Morning Cortisol Surge and the Dawn Phenomenon

Cortisol follows a 24-hour rhythm. It peaks in the first hour after waking, sometimes doubling or tripling from overnight lows, then gradually declines through the afternoon and evening. That morning spike is part of what gets your body ready for the day. People with diabetes are familiar with a related annoyance called the “dawn phenomenon,” where blood sugar rises in the early morning hours even before eating. Given cortisol’s glucose-raising properties, a reasonable assumption would be that the morning cortisol surge is the main driver.

The evidence is more nuanced. A study specifically looking at the morning cortisol response found no correlation between the size of the cortisol rise and blood glucose levels upon waking. Even people whose blood glucose sat at the low end of normal showed a full cortisol response.¹³ That suggests morning cortisol is doing other things besides cranking up blood sugar in healthy people, probably tuning the immune system, alertness, and blood pressure. In someone who already has impaired insulin signaling, though, that same cortisol burst can push blood sugar higher than it should go, because their system lacks the buffer that a healthy insulin response provides. So the dawn phenomenon is not purely a cortisol story, but cortisol contributes to it when the rest of the metabolic machinery is compromised.

Night-Shift Work and Disrupted Cortisol Patterns

If the normal cortisol rhythm matters, what happens when you scramble it? Night-shift workers routinely experience a flattened or inverted cortisol curve, with cortisol levels that are relatively high when they should be low and sluggish when they should be peaking. A review examining the metabolic consequences of this disruption found that altered cortisol rhythms in night-shift workers contribute to metabolic disorders and cardiovascular disease.¹⁴

This is consistent with the broader epidemiological finding that chronic night-shift work is associated with higher rates of type 2 diabetes. The explanation likely involves more than just cortisol: disrupted sleep, mistimed meals, and changes in melatonin all play roles. But the cortisol angle is particularly relevant because it connects the hormonal stress system directly to glucose regulation. If your cortisol is elevated at 3 a.m. when it should be at its daily nadir, you are getting an unwanted glucose-production signal at a time when your body is supposed to be in a quiet metabolic state.

Sex Differences in Cortisol Metabolism

Men and women handle cortisol somewhat differently, and those differences change again with body weight. Your body does not just produce cortisol and let it circulate forever; it also deactivates cortisol by converting it to cortisone, and reactivates it again in tissues like the liver, fat, and muscle. The enzymes that manage this conversion are influenced by sex hormones like estrogen. A study of middle-aged men and postmenopausal women found that in obese individuals of both sexes, cortisol metabolism shifted in ways that favor keeping cortisol active in tissues rather than deactivating it.¹⁵ This could partly explain why obesity and insulin resistance so often travel together: extra body fat alters cortisol handling in a way that generates more cortisol activity in exactly the tissues where you do not want it.

Interestingly, estrogen replacement therapy in the postmenopausal women in that study did not significantly change these cortisol metabolism ratios, suggesting the relationship between fat and cortisol processing may be more about body composition itself than about estrogen levels per se. For men, the pattern of favoring active cortisol over inactive cortisone was more pronounced in those who were obese, reinforcing the vicious cycle of visceral fat, cortisol, and insulin resistance described earlier.

Can Stress Reduction Actually Lower Blood Sugar?

If cortisol is the bridge between stress and high blood sugar, it follows logically that reducing stress should help with glucose control. The evidence suggests this is true, though the effect sizes are modest. A meta-analysis of mindfulness-based interventions in people with diabetes found that these programs lowered HbA1c (a three-month average blood sugar marker) by about 0.25 percentage points. They also produced moderate reductions in depression and stress levels.¹⁶ A quarter-point drop in HbA1c is clinically meaningful. It is smaller than what you get from adding a diabetes medication, but it is a real change and it comes with improvements in mood that medication does not always deliver.

A more targeted study tested an eight-week mindfulness-based stress reduction program specifically in older adults with type 2 diabetes during the COVID-19 pandemic, a period when stress was unusually high. The intervention group showed significant reductions in cortisol levels, anxiety, depression, and stress scores compared to controls, and the benefits persisted at a three-month follow-up.¹⁷

None of this means you can meditate your way out of type 2 diabetes. Diet, exercise, and medication remain the heavy hitters for glycemic control. But if you are someone whose blood sugar runs higher during stressful periods, or if your glucose seems disproportionately hard to manage despite doing everything right with food and exercise, the cortisol connection is worth taking seriously. Consistent sleep, regular physical activity, and structured stress-management techniques all lower cortisol. They will not eliminate the underlying metabolic problem, but they can take the edge off the hormonal headwind that makes blood sugar control harder than it needs to be.

When Low Blood Sugar Triggers Cortisol

The relationship between cortisol and blood sugar is not one-directional. Just as cortisol raises blood sugar, low blood sugar triggers cortisol release. This is a safety mechanism: when glucose drops too low, the brain detects the threat and activates the stress axis to push sugar back up. In a study of patients with insulinomas (tumors that secrete excess insulin and drive blood sugar dangerously low), cortisol levels at the end of a prolonged fast were nearly double those seen in healthy controls. Patients with the tumors had a median cortisol of 19 µg/dL compared with 11 µg/dL in controls, despite their blood sugar being far lower.¹⁸

This feedback loop matters for people with diabetes who experience hypoglycemia from insulin or certain oral medications. Their cortisol response to a low blood sugar event can cause a rebound spike hours later, a pattern known as the Somogyi effect (though its clinical prevalence is debated). It also matters for anyone practicing prolonged fasting or very-low-carbohydrate diets: some of the jitteriness and elevated morning glucose that people report during fasting may be cortisol doing its job of defending the brain’s glucose supply.

The broader takeaway is that cortisol and insulin exist in a constant tug of war. Insulin drives glucose into cells for storage; cortisol pulls it back out for immediate use. In health, these two forces balance each other elegantly, responding to meals, fasting, exercise, and sleep in a coordinated rhythm. Problems emerge when the balance tips too far in either direction for too long, or when the body loses its ability to toggle between the two states cleanly.