People get diabetes when their body either stops making insulin, stops responding to it properly, or both. The specific cause depends on the type of diabetes, but every form comes down to the same core problem: glucose builds up in the blood instead of entering cells where it’s needed for energy. About 90-95% of cases are type 2 diabetes, driven largely by lifestyle and genetic factors. The remaining cases are mostly type 1, an autoimmune condition, or gestational diabetes during pregnancy.
How Type 1 Diabetes Develops
Type 1 diabetes is an autoimmune disease. The immune system mistakenly attacks the insulin-producing cells in the pancreas, eventually destroying them. Without these cells, the body can’t make insulin at all, and blood sugar rises uncontrollably. This process can unfold over months or years before symptoms appear, and by the time someone is diagnosed, most of those cells are already gone.
Genetics play a significant role. Variations in a group of immune-system genes called the HLA complex account for roughly 40% of the genetic risk for type 1 diabetes. These genes help the immune system distinguish the body’s own cells from foreign invaders. Certain inherited combinations of these gene variants make the immune system more likely to turn on the pancreas. Other HLA variations actually appear to protect against the disease, which partly explains why type 1 runs in some families but skips others.
Environmental triggers also matter, though they’re less well understood. Viral infections, early dietary exposures, and other factors are thought to set off the autoimmune attack in genetically susceptible people. Type 1 can develop at any age but most often appears in children, teens, and young adults. In the United States, white people are more likely to develop it than Black or Hispanic populations.
How Type 2 Diabetes Develops
Type 2 diabetes starts with insulin resistance. Your muscle, liver, and fat cells gradually stop responding to insulin the way they should. The pancreas compensates by producing more insulin, sometimes for years, but eventually it can’t keep up. Blood sugar begins to creep upward, first into the prediabetes range (a fasting blood sugar of 100 to 125 mg/dL, or an A1C of 5.7% to 6.4%), and then into full diabetes territory (fasting blood sugar of 126 mg/dL or higher, or an A1C of 6.5% or above).
At the cellular level, insulin resistance involves real physical changes. In people with obesity, the cells have fewer insulin receptors, and the receptors that remain don’t activate properly. At the same time, excess body fat, especially the deep visceral fat around the organs, triggers a state of chronic low-grade inflammation throughout the body. Fat tissue releases inflammatory signaling molecules that interfere with insulin signaling in the muscles, liver, and fat cells themselves. Population studies consistently link insulin resistance to elevated levels of these inflammatory molecules in the blood.
The liver plays a key role in making things worse. Normally, insulin tells the liver to stop releasing stored glucose into the blood after a meal. When the liver becomes insulin resistant, it keeps pumping out glucose even when blood sugar is already high. This is a major reason people with type 2 diabetes have elevated fasting blood sugar first thing in the morning, before they’ve eaten anything.
The Biggest Risk Factors
Excess weight is the single most common cause of insulin resistance. But weight alone doesn’t tell the whole story. Your risk of type 2 diabetes also increases if you:
- Are 45 or older
- Have a family history of type 2 diabetes
- Are physically inactive
- Belong to certain ethnic groups, including Black, Hispanic or Latino, American Indian, Alaska Native, and some Asian American and Pacific Islander populations
These risk factors compound each other. A 50-year-old with a family history, a sedentary job, and 30 extra pounds of visceral fat faces a very different risk profile than someone with just one of those factors.
How Gestational Diabetes Develops
Gestational diabetes follows a specific biological script tied to pregnancy. The placenta produces hormones, including estrogen, cortisol, and human placental lactogen, that naturally block insulin’s effects. This “contra-insulin effect” typically kicks in around 20 to 24 weeks of pregnancy and intensifies as the placenta grows larger. In most pregnancies, the pancreas simply ramps up insulin production to compensate. Gestational diabetes develops when the pancreas can’t produce enough extra insulin to overcome the hormonal blockade.
Risk factors include being over 25 years old, having excess weight before pregnancy, and belonging to populations with higher overall diabetes risk, including Black, Hispanic or Latino, American Indian, Alaska Native, Native Hawaiian, and Pacific Islander women. Gestational diabetes usually resolves after delivery, but it significantly raises the mother’s lifetime risk of developing type 2 diabetes later.
Medications That Can Raise Blood Sugar
Certain medications can push blood sugar high enough to trigger diabetes in people who are already on the edge. Corticosteroids (commonly prescribed for inflammation and autoimmune conditions) are the best-known culprits, but the list is longer than most people realize. Antipsychotic medications, certain blood pressure drugs (thiazide diuretics and beta-blockers), some antibiotics, and immunosuppressants can all contribute.
Statins, one of the most widely prescribed drug classes in the world, carry a 9 to 33% higher risk of new-onset diabetes depending on the specific drug and dose. These medications cause problems through several routes: they can reduce insulin sensitivity, directly damage pancreatic cells, or increase the liver’s glucose output. If you’re taking any of these medications and have other risk factors for diabetes, your doctor will likely monitor your blood sugar more frequently.
Why Some People Get Diabetes and Others Don’t
Diabetes is never caused by a single thing. It results from a collision between genetic predisposition and environmental or lifestyle pressures. Two people can carry the same genetic risk, but the one who gains significant visceral fat, stays sedentary, and experiences chronic stress is far more likely to develop type 2 diabetes. Similarly, two siblings can inherit the same immune-system gene variants, but only one develops type 1 diabetes, likely because of differences in environmental exposures.
The prediabetes stage is where this matters most practically. At that point, the body is struggling but hasn’t yet lost the battle. Modest weight loss (even 5 to 7% of body weight), regular physical activity, and dietary changes can restore enough insulin sensitivity to delay or prevent the progression to type 2 diabetes. By the time blood sugar crosses the diabetes threshold, the pancreas has typically lost a significant portion of its insulin-producing capacity, making reversal much harder.