Type 1 diabetes is an autoimmune disease, in which the body’s own immune system destroys the body's capacity to produce or use insulin. Insulin is the principal hormone that helps move glucose (blood sugar) into cells to be used for energy.

In a healthy person, the immune system protects the body by attacking foreign invaders. In patients with type 1 diabetes, the the immune system’s antibodies mistakenly attack the beta cells of the pancreas that produce insulin and other proteins involved in insulin production.

Because the antibodies can be present several years before the diagnosis of type 1 diabetes, researchers have found their identification helpful in screening high-risk individuals with autoantibody testing. Having certain antibodies means that person has a greater chance of developing type 1 diabetes.

Why this occurs is not completely understood, but researchers have found many factors that appear to be linked to type 1 diabetes. It is important to note that, although these factors may increase the risk of diabetes, researchers have not identified any single cause or characteristic. Risk factors and causes may include:

• Family history and genetics. Family medical history can contribute to the risk of developing the disorder. If a mother or father has diabetes, there is a greater chance their child will develop diabetes than a child without diabetic parents. The risk for diabetes also increases if a brother or sister has diabetes. This risk varies according to which relative has the disease.

Children born to women who experience high stress during pregnancy may be at higher risk of type 1 diabetes, according to recent research. The researchers suggested that maternal stress might, in offspring, increase stress hormones that damage the pancreas.

• Race and nationality. Type 1 diabetes is found more often in white people, particularly those of Northern European descent. In contrast, people of other races are more prone to type 2 diabetes, which is far more common. Places where above-average rates of type 1 diabetes are reported include Finland, Scandinavia, the Italian island of Sardinia, the United Kingdom, Canada, the United States, Puerto Rico, the Virgin Islands, Australia, New Zealand and Kuwait.
  
  

• Environmental factors. Many researchers suspect that free radicals may contribute to the development of type 1 diabetes. Free radicals are formed as a result of chemical reactions in the body. Smoke, air pollution and even genetics contribute to the formation of free radicals in the body. When these radicals build up, they can destroy the body’s own cells, including those involved in the production of insulin.

  Cold weather is another possible environmental trigger for this condition. Type 1 diabetes is more common in cold climates and develops more often in the winter than the summer. Researchers are unsure of the reason for this connection between the cold and type 1 diabetes.
  
  
• Viruses. Many scientists suspect that certain viruses may be a factor in type 1 diabetes. People are often diagnosed with type 1 diabetes after a viral infection. The viruses thought to be related to type 1 diabetes include:
  
  
• Mumps
• Rubella (German measles)
• Coxsackie virus (related to the virus family that causes polio and hepatitis)

It is suspected that virus cells share a protein or part of a protein found in the insulin-producing beta cells. The immune system attempts to destroy cells containing the virus, but it may mistakenly attack the beta cells, confusing them for the viral-infected cells. Instead of destroying bad virus cells, the body is destroying the good cells that produce insulin.

Another theory regarding the role of viruses and type 1 diabetes involves the way a virus affects cells. Some researchers suspect that when a virus infects the body, it changes the characteristics of the islet cells, which produce insulin. If this process occurs, the islet cells appear as foreign and are attacked by the immune system. If the cells are destroyed, insulin cannot be produced, leading to type 1 diabetes.

• Chemicals and drugs. Several chemicals have been shown to contribute to type 1 diabetes, such as a type of rat poison called pyriminal. In addition, some prescription drugs may cause or contribute to type 1 diabetes, such as pentamidine (used to treat pneumonia) and L-asparaginase (an anti-cancer drug).
  
  
• Other diseases. Some research has found higher rates of type 1 diabetes in people with conditions including celiac disease (gluten intolerance) and some forms of epilepsy. Cystic fibrosis has been linked to a form of diabetes that has some features of type 1 and type 2 diabetes.
  
  
• Diet. Scientists have studied certain foods and their possible role in the development of type 1 diabetes. Some researchers suspect that being fed cow’s milk early in life may be connected to the development of type 1 diabetes. Other scientists have been unable to support this association, and the role of cow’s milk in the development of type 1 diabetes remains controversial.

The studies that support this hypothesis appear to show that children with newly diagnosed type 1 diabetes have a higher amount of antibodies specific to cow’s milk. These antibodies may be responsible for inducing the immune system to destroy the beta cells that produce insulin. These researchers concluded that:

• Children who are fed cow’s milk before 3 or 4 months of age have a greater chance of developing type 1 diabetes.
  
  
• If a baby is breastfed for a short period and then given cow’s milk, there is no increased risk for type 1 diabetes.

Studies in diabetes-prone animals have shown that withholding wheat and soy helps delay or prevent diabetes. These studies have not demonstrated the same results in humans. Additional research must be completed to understand the role of diet and the development of type 1 diabetes.

Genetic or environmental factors by themselves probably do not cause type 1 diabetes. However, if an individual is at high risk for developing type 1 diabetes because of genetic reasons, exposure to other risk factors may trigger the disease.