The immune system protects you from disease by killing germs and other foreign invaders. It does this largely through the action of white blood cells, or lymphocytes. T lymphocytes, or T cells, can attack foreign cells directly. B lymphocytes, or B cells, produce special proteins called antibodies that recognize the shapes of molecules on the surface of specific invaders.
B cells sometimes manufacture antibodies that recognize a person’s own cells. These self-recognizing antibodies are called autoantibodies. Autoantibodies are found in many people with autoimmune disorders, but three autoantibodies are especially common in people with type 1 diabetes. These antibodies recognize the following:
- islet cells (beta cells are just one type of islet cell in the pancreas)
- glutamic acid decarboxylase (GAD, or the 64K protein), a protein made by the beta cells in the pancreas
These three types of autoantibodies all seem to act as markers. Researchers believe that these antibodies contribute to the demise of the beta cells of the pancreas by identifying which cells are to be attacked. It is really the T cells that ultimately destroy the insulin-producing cells of the pancreas. Of people newly diagnosed with type 1 diabetes, 70 to 80 percent have antibodies to islet cells, 30 to 50 percent have antibodies to insulin, and 80 to 95 percent have antibodies to GAD.
What Is Diabetes?
The antibodies may be present several years before diabetes is diagnosed. The islet cell antibodies disappear later on.
Because these antibodies are so common in people with type 1 diabetes and because they so often appear before the symptoms of diabetes appear, researchers are finding that they are useful in screening people for type 1 diabetes who are at high risk for the disease. Although the risk for developing diabetes may only be 1 to 10 percent for people with a parent or sibling with the disease, a much higher percentage of people who also have antibodies to islet cells develop type 1 diabetes within 5 years. And for many, having combinations of these antibodies and certain HLA genes results in an even higher risk.
Perhaps surprisingly, many scientists also suspect that viruses may cause type 1 diabetes. This is because people who develop type 1 diabetes have often recently had a viral infection, and “epidemics” of type 1 diabetes often occur after viral epidemics.
Viruses, such as those that cause mumps and German measles and the Coxsackie family of viruses, which is related to the virus that causes polio, may play some role in causing type 1 diabetes.
A small region of the GAD molecule is almost identical to a region of a protein found in the virus known as Coxsackie B4.
The two similar protein regions probably have similar shapes and may be recognized by the same T cells. Thus, to a T cell hunting for foreign invaders, the GAD protein, which is part of the body, might look the same as the Coxsackie virus protein, which is part of an invading cell. After a viral infection by the Coxsackie virus, the T cell, bent on destroying the invading virus, might actually destroy the body’s own beta cells that bear the GAD protein. This would destroy the cells that produce insulin and result in type 1 diabetes.
Other theories may also explain how a viral infection might lead to diabetes. Some researchers believe that when a virus infects a body, it might somehow change the structure of the antigens on the surface of the islet cells. If this occurs, then the altered antigen might appear to be foreign to the immune system, and a person’s own insulin-producing islet cells might be destroyed.
Another well-known diabetes researcher has a different theory. He believes that diabetes is a relatively new disease caused by a slow-acting virus. Although such a virus has not been found, he holds that the virus causes the immune system to attack proteins in the pancreas. A drastic increase in the number of cases of type 1 diabetes occurred on the island of Sardinia, Italy, in the 1960s and in Finland in the 1970s, and he believes that such a slow-acting virus could be the culprit.
Although it seems unlikely, different kinds of food may play a role in the development of type 1 diabetes. For example, one group of researchers found a connection between being fed cow’s milk early in life (before 3 or 4 months old) and type 1 diabetes. They showed that children newly diagnosed with type 1 diabetes have higher amounts of antibodies that recognize a specific protein in cow’s milk. These autoantibodies appear to bind to a protein that sometimes appears on the surface of the insulin-producing beta cells in the pancreas after an illness. The researchers speculate that, after an illness, the transient protein may appear on the surface of beta cells. The immune response to the milk protein might be to then recognize the beta cell surface proteins and attack the beta cells, leading to a destruction of the insulin-producing cells of the pancreas and, thus, to type 1 diabetes.
However, other researchers have looked for but not found an increased risk of type 1 diabetes if cow’s milk is given early in life and if breastfeeding is done for a short period. Cow’s milk is only one kind of food that may play a role in the development of type 1 diabetes. Studies in diabetes-prone rats show that withholding wheat and soy helps delay or prevent diabetes.