T1D has genetic, environmental and immune components

Type 1 diabetes (T1D) is an autoimmune disease in which a person’s pancreas stops producing insulin, a hormone that controls blood-sugar levels. T1D develops when the body’s immune system mistakenly attacks the cells in the pancreas that produce insulin, called beta cells. Research is underway to find out what causes T1D—and how to stop it—but we already know that there are multiple components in play.

Genes and family history

Certain genes increase a person’s risk of developing T1D, as does family history. If you have a relative with T1D, your risk of developing it is 1 in 20, which is 15 times greater than the general population. The genetic coding that puts you at higher risk for T1D is in a large part related to your body’s immune response.

Environmental triggers

Although genes are important in determining risk, they aren’t the whole story. Environmental factors, such as viruses, may trigger T1D in people who are genetically at risk. 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.

Immune response

Once T1D is triggered, biochemical signs of the immune attack on beta cells can be detected. These signs, called autoantibodies, appear well before T1D symptoms do. As the immune attack continues and more beta cells are destroyed, insulin production decreases and blood-sugar levels become abnormal. Eventually, so many beta cells are destroyed, and insulin production drops so low, that symptoms of T1D appear.

What doesn’t cause T1D?

Onset of T1D has nothing to do with diet or lifestyle. Today, there is nothing you can do to prevent it or get rid of it.

But JDRF is working to change that. We are unlocking the science behind new therapies to prevent or stop the autoimmune attack and restore beta cells. We are changing the future for the 1.25 million Americans living with this disease and the 5 million who are expected to have it by 2050. Join us!