Diabetes has no single cause. It develops through different mechanisms depending on the type, and often multiple factors converge at once. Some causes are genetic, some are metabolic, and some are environmental or even triggered by medications or other medical conditions. Globally, about 589 million adults were living with diabetes in 2024, roughly one in nine people, making it one of the most common chronic diseases on earth.
Type 1: The Immune System Attacks Insulin-Producing Cells
Type 1 diabetes occurs when the immune system destroys the cells in the pancreas responsible for making insulin. These cells, called beta cells, sit inside clusters known as pancreatic islets. The destruction is carried out by a type of white blood cell (T cells) that mistakenly identifies beta cells as a threat.
What triggers this attack isn’t fully understood, but current evidence points to a two-step process. First, the beta cells come under stress from some combination of genetic susceptibility and environmental exposure. That stress changes the cells in ways that make them visible to the immune system. Inflammation then drives deeper changes in the beta cells, essentially putting a target on them. Once the immune response ramps up, it progressively wipes out the body’s ability to produce insulin, sometimes over months, sometimes over years.
Type 1 diabetes accounts for roughly 5 to 10 percent of all diabetes cases and is most commonly diagnosed in children and young adults, though it can appear at any age.
Type 2: Insulin Resistance and Metabolic Overload
Type 2 diabetes is by far the most common form, making up about 90 percent of cases. It develops when the body’s cells stop responding properly to insulin, a condition called insulin resistance. The pancreas compensates by producing more insulin, but eventually it can’t keep up, and blood sugar rises.
The core driver of insulin resistance in most people is excess body fat, particularly fat stored around the organs (visceral fat). Fat tissue isn’t just passive storage. It actively releases inflammatory signals, notably TNF-alpha and IL-6, that interfere with insulin’s ability to move sugar from the bloodstream into cells. These molecules essentially jam the lock-and-key mechanism insulin uses to open cells to glucose. The more visceral fat a person carries, the louder this inflammatory signal becomes.
Genetics Play a Major Role
Having a parent or sibling with type 2 diabetes significantly raises your risk, and researchers have identified specific genes involved. The most influential is a gene variant called TCF7L2, which increases the odds of developing type 2 diabetes by 30 to 50 percent for each copy inherited. That’s roughly double the risk associated with most other diabetes-related gene variants. But genetics alone rarely cause type 2 diabetes. They load the gun; lifestyle and environment pull the trigger.
The Liver’s Role in Rising Blood Sugar
The liver is a key player in blood sugar regulation. After a meal, insulin signals the liver to store excess glucose. Between meals, the liver releases glucose back into the blood to keep energy available. When the liver becomes resistant to insulin, it loses the ability to respond to that “stop releasing glucose” signal. The result is a liver that keeps pumping sugar into the bloodstream even when levels are already high.
Fatty liver disease accelerates this problem. Fat buildup in the liver triggers stress and inflammatory pathways that further weaken insulin signaling. This creates a feedback loop: insulin resistance promotes fat accumulation in the liver, and a fatty liver worsens insulin resistance. Fatty liver disease is now recognized as both a consequence and a driving factor of the metabolic dysfunction behind type 2 diabetes.
Gestational Diabetes: Hormonal Shifts During Pregnancy
Gestational diabetes develops during pregnancy, typically in the second or third trimester, and affects roughly 2 to 10 percent of pregnancies. The cause is primarily hormonal. The placenta produces hormones that are essential for the baby’s growth but also make the mother’s cells less responsive to insulin.
Two placental hormones are central to this process. Placental growth hormone reduces levels of a protective protein called adiponectin and directly blocks insulin’s ability to shuttle glucose into cells. Human placental lactogen (hPL) has similar effects. On top of this, the placenta during pregnancy becomes a major source of leptin and resistin, two hormones that further dampen insulin sensitivity. Resistin, for example, interferes with insulin release from the pancreas while also reducing how well muscles, fat, and the liver respond to insulin.
In most women, the pancreas ramps up insulin production enough to compensate. When it can’t, blood sugar rises and gestational diabetes results. The condition usually resolves after delivery, but it significantly increases the mother’s lifetime risk of developing type 2 diabetes.
Sleep Disruption and Circadian Misalignment
Chronic sleep deprivation does more than make you tired. It measurably reduces your body’s ability to handle sugar. In one study, restricting sleep to five hours per night reduced insulin sensitivity by 34 percent when participants slept at night. When sleep was both restricted and shifted to daytime hours (mimicking shift work), insulin sensitivity dropped by 47 percent.
This matters because millions of people routinely sleep fewer than six hours or work rotating shifts. Over months and years, even a moderate reduction in insulin sensitivity forces the pancreas to work harder. Combined with other risk factors like excess weight or a family history of diabetes, poor sleep can be the factor that tips the balance.
Medications That Raise Blood Sugar
Certain medications can push blood sugar into diabetic ranges, especially in people who are already at risk. Corticosteroids (commonly prescribed for asthma, autoimmune conditions, and inflammation) are the most well-known culprits. Doses equivalent to more than 20 mg of prednisolone per day are considered high risk for triggering steroid-induced high blood sugar. The risk increases with both higher doses and longer duration of use.
Other medications linked to elevated blood sugar include some antipsychotics, certain blood pressure medications (thiazide diuretics, beta-blockers), and immunosuppressants used after organ transplants. In many cases, blood sugar returns to normal after the medication is stopped, but not always, particularly if underlying insulin resistance was already present.
Environmental Chemicals
A growing body of evidence links certain industrial chemicals to diabetes risk. Bisphenol A (BPA), found in plastics and food container linings, initially causes the pancreas to pump out extra insulin. But with longer exposure, this effect reverses: insulin-producing cells become damaged and lose their ability to respond to rising blood sugar. Animal studies show BPA can even trigger cell death in insulin-producing cells through damage to their energy-generating structures.
Phthalates, another group of chemicals common in plastics, personal care products, and food packaging, are associated with reduced insulin-producing cell mass and altered expression of genes involved in insulin production. Studies in pregnant women have found that higher exposure to both BPA and phthalates correlates with elevated blood sugar and reduced glucose tolerance.
Other Medical Conditions
Several diseases can damage the pancreas or disrupt metabolism enough to cause diabetes independent of the usual type 1 or type 2 pathways.
- Iron overload (hemochromatosis): Excess iron deposits selectively damage the insulin-producing beta cells in the pancreas, impairing both insulin production and release. Iron accumulation in the liver also causes scarring that worsens insulin resistance. This was historically called “bronze diabetes” because of the skin discoloration that accompanies the condition.
- Chronic pancreatitis: Repeated inflammation of the pancreas from alcohol use, gallstones, or genetic conditions gradually destroys the tissue that produces insulin.
- Cushing’s syndrome: The body produces excess cortisol, a hormone that raises blood sugar and promotes insulin resistance. The effect is similar to taking high-dose corticosteroid medications.
- Polycystic ovary syndrome (PCOS): Strongly associated with insulin resistance, PCOS significantly raises the risk of type 2 diabetes in women, particularly when combined with excess weight.
Physical Inactivity and Diet
Sedentary behavior independently increases diabetes risk even in people who aren’t overweight. Muscle tissue is the largest consumer of blood sugar in the body, and regular contraction during physical activity keeps muscle cells sensitive to insulin. When muscles sit idle for most of the day, their insulin sensitivity drops, forcing the pancreas to produce more insulin to achieve the same effect.
Dietary patterns matter too, though in more nuanced ways than simple sugar intake. Diets high in ultra-processed foods, refined carbohydrates, and sugary drinks are consistently linked to higher diabetes risk. These foods cause rapid spikes in blood sugar that stress the pancreas over time. They also tend to promote visceral fat gain, feeding into the inflammatory cycle that drives insulin resistance. Conversely, diets rich in whole grains, fiber, and unsaturated fats are associated with lower risk, likely because they produce slower, more manageable rises in blood sugar and reduce chronic inflammation.