When my type 1 diabetes (T1D) was diagnosed in 1962, scientists couldn’t explain the cause of the disease or what triggered it. Fifty-seven years later, I’m still waiting for researchers to tell me precisely why my pancreas stopped making insulin and my blood sugar shot up so high that I needed to be hospitalized.

Still, while researchers continue to search for a full explanation of what causes T1D, they’ve solved more than a few diabetes-related mysteries. They’ve identified specific risk factors and come up with evidenced-based theories about what triggers this disease.

Many of the scientific detectives trying to track down culprits for T1D are also trying to explain why it is surging: T1D is increasing at a rate of 5.3 percent globally every year, by one estimate. Read on to learn more about what we know — and don’t know — about why.

If you or someone you love has T1D, you probably know the basic explanation for the disease: it occurs when the body’s immune system destroys the insulin-producing cells (beta cells) in the pancreas. It can occur at any age, although it’s much more common in kids.

It’s less well-known that T1D starts developing before symptoms appear. In fact, the national experts at JDRF, the American Diabetes Association, and the Endocrine Society now agree that there are three distinct stages of T1D development:

  • Stage 1: Biochemical signs of an attack on insulin-producing cells, called “autoantibodies,” start showing up. But at this stage the patient feels no symptoms and the blood sugar remains normal.
  • Stage 2: The immune system has destroyed enough insulin-producing cells to cause abnormal blood sugar levels, but there are still no symptoms. Most people have no idea that they have diabetes at this stage.
  • Stage 3: Enough insulin-producing cells have been destroyed for symptoms to start showing up. They include increased thirst, frequent urination, extreme hunger, weight loss, fatigue, irritability, blurred vision, and a fruity smell on the breath from ketones (which the body produces when it burns fat to get energy).

There are several risk factors that make it more likely that someone will develop T1D, including:

Genes and family history

Several specific genetic markers have been identified, and if you have one or more of them, you might develop T1D. Since genes are inherited, family history is an important predictor for T1D. If you have a relative with T1D, your risk of developing it is 1 in 20.

But according to researchers, less than 10 percent of people with these genetic markers develop T1D. So it’s clear that other factors besides genes put people at higher risk for developing the disease.


Certain ethnic groups have a higher rate of T1D. In the United States, for example, whites are more likely to develop T1D than African Americans and Hispanic Americans.


Where you live influences your chances of developing T1D as well. In China, T1D rates are 10 to 20 times lower than in North America, Europe, and Australia. Finland has the highest incidence of T1D in the world.

The American Diabetes Association acknowledges that “Type 1 diabetes develops more often in winter than summer and is more common in places with cold climates.” And on the flip side, “people who live in southern climates — such as South America — are less likely to develop type 1.” There is a related theory that because people in less sunny regions are more prone to T1D because they get less vitamin D — which comes directly from the sun.

Other autoimmune conditions

Autoimmune conditions often seem to come in pairs. So if someone has Graves’ disease, multiple sclerosis, pernicious anemia, or other autoimmune conditions, they are more likely to develop T1D.

Clearly, some kind of trigger is needed for the immune system to attack insulin-producing cells in people who are genetically susceptible to T1D. Here are a few of the potential triggers that have been identified:

Viral infections and type 1 diabetes

There is a lot of anecdotal evidence that people are diagnosed with T1D after experiencing some kind of viral infection.

“Scientists believe that certain viruses may target beta cells, and as the immune response ramps up to fight those viruses, it goes awry and attacks uninfected beta cells by mistake,” according to JDRF.

Animals and people with specific strains of infectious viruses, called “enteroviruses,” are more likely to get diabetes. It’s long been known that epidemics of mumps, rubella, and coxsackie viruses have been associated with increased frequency of type 1.

Toxins and type 1 diabetes

Other research indicates that toxins in the air, water, and food might trigger T1D in people who are genetically prone to it. Some studies reveal a higher incidence of the disease in people exposed to arsenic, while others have linked it to nitrates, ozone, sulfates, and other chemicals and pollutants.

The “accelerator hypothesis” and “double diabetes”

The notion of an overlap between type 1 and type 2 diabetes has been a topic of research since the 1990s. From this work comes the “accelerator hypothesis,” which posits that obesity-associated insulin resistance can accelerate the onset and progression of T1D. The idea is that the beta cells are further stressed, which makes them more susceptible to autoimmune attack.

Also, with the incidence of diabetes in obese young people on the rise — and growing difficulty distinguishing type 1 from type 2 in some patients — scientists have also coined the term “double diabetes” to refer to coexistence of autoimmunity and insulin resistance.

Diet and type 1 diabetes: Is there a connection?

Despite some public misconception, the onset of T1D has never been linked to consuming too many sweets or even overeating in general. But there are some specific foods that researchers suspect may play a role.

In the 1980s, there was a lot of excitement among researchers about studies showing that kids who ate cow’s milk-based foods at a very young age ran a higher risk of developing T1D. One long-term study tested the idea that weaning infants to a special kind of formula would reduce the risk. Alas, that didn’t work!

But the role of cow’s milk is still being investigated. There is also some evidence linkingcereals,gluten (wheat protein), root vegetables, and omega-3 fatty acids to an elevated risk of T1D.

Also, as noted above, some studies indicate that people who get more vitamin D from sunshine are less prone to T1D. Dan Hurley calls this theory “the sunshine hypothesis” in his very enlightening book, “Diabetes Rising.”

If that’s true, would taking vitamin D supplements help prevent the disease? A review of relevant research in Lancet notes that “there is surprisingly little supporting evidence” for this idea.

Other physical and psychological triggers

Unfortunately, we’ve just scratched the surface here, as scientists are still investigating a whole array of other factors that might also influence the development of T1D:

  • frequent early childhood respiratory or gastrointestinal infections
  • Rapid growth and weight gain in children
  • low physical activity during puberty
  • trauma or serious life events, such as divorce or death in the family
  • stress (via increased cortisol concentrations)

Weakened immune systems?

While trying for decades to identify the risk factors for T1D, scientists have also been struggling to understand its underlying causes and why its incidence is increasing, especially in developed countries.

One idea that got tons of publicity in the 1990s is the “hygiene hypothesis,” which proposes that people in the developed world are too clean for our own good. The idea is that advanced sanitation has weakened our immune systems, because they no longer have to fight off so many germs and infections. So instead, the theory proposes, the immune system goes haywire and attacks healthy cells in the body.

There hasn’t been conclusive evidence to support a direct connection between improved hygiene and T1D, but one current hypothesis is a closely related notion. It poses that as children, we need to be exposed to a broad range of little microbes to teach the immune system to distinguish between the body’s friends and foes. If kids don’t get enough contact with these harmless microorganisms that have been present throughout human evolution, their immune systems may not get properly trained. And one consequence could be T1D.

There is also emerging evidence of a link between the so-called “microbiome” — the tiny organisms inside of the gut — and T1D. Scientist pose that people might need the right combinations of these little organisms for the immune system to function properly and not turn against insulin-producing cells.

None of this is yet conclusive, so the quest to understand why T1Ds’ immune systems are compromised continues.

Unfortunately, no one has come up with a unified theory that convincingly explains the possible interactions between genes, viruses, the environment, diet, microbes, and other potential contributors to T1D.

Without nailing the causes, science hasn’t been able to offer us convincing steps people can take to prevent T1D. Not yet, that is.

Two long-term studies are underway to sort some of this out. The first is called TrialNet, a network of leading T1D research clinic sites around the world that is testing children who are a direct relative of someone with T1D — a parent, sibling, aunt, uncle, cousin, or grandparent — to learn about how this disease may be inherited.

The second is called The Environmental Determinants of Diabetes in the Young (TEDDY) study, which is keeping track of children with genetic markers of T1D and trying to determine what prompts some of them to get the disease while others remain diabetes-free.

Let’s keep hoping that researchers will eventually unravel the mystery of what causes T1D. That might help them come closer to finding a way to prevent and even cure it.

This article has been medically reviewed by Maria Basina, MD, on 11/19/2019.