According to current theory, Graves’ disease, like most autoimmune disorders, is caused by a combination of genetic and environmental factors. There are several different genes associated with Graves’ disease, although there is no specific gene linked to this disorder. In other words, people who develop Graves’ disease have a certain combination of genes that are also seen in several different autoimmune disorders. The most significant genes, the immune system genes HLA B8 and D3, are seen in the majority of Caucasians with Graves’ disease, lupus, diabetes, pernicious anemia, and celiac disease. Then again, not all patients with Graves’ disease have these genes, and different immune system genes are associated with Asians and other ethnic groups.
Furthermore, the presence of HLA B7 appears to offer protection against developing Graves’ disease. Patients with HLA B8, D3 and B7 may develop one of the other associated autoimmune disorders, but it’s unlikely that they’ll develop Graves’ disease. Other genes, particularly those that govern the TSH receptor or the development of immunoglobulins, also play a role in Graves’ disease development.
What’s important here is that individuals who develop Graves’ disease have a certain genetic make-up that makes them susceptible to developing Graves’ disease…in the presence of certain environmental triggers. There is no one specific environmental trigger that causes Graves’ disease in all patients. If there were, the most likely culprit would be iodine. Besides iodine, other environmental agents known to trigger Graves’ disease include stress, viruses, estrogens and certain interferons and monoclonal antibodies used to treat other disorders such as multiple sclerosis.
What these environmental agents have in common is that they all cause immune system changes. By altering the amounts of immune system chemicals and white blood cells, these agents promote autoantibody development. Normally, the immune system produces antibodies against infectious agents in an effort to protect us from later developing disease. For instance, when we’re exposed to the polio virus or the polio vaccine, our immune systems produce antibodies against polio. If we were later exposed to polio, these antibodies would fight off the virus and protect us from developing polio.
