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Graves' Disease Simplified and A New Warning Against Radioiodine

© Elaine Moore

Much has been learned about Graves’ disease in the past decade, making treatment protocols popular 50 years ago questionable today. Today we know that Graves’ disease is an autoimmune disease that targets one or more of the following: the thyroid gland, the eyes, skin, and muscles. The thyroid gland is the organ most often affected, and the resulting condition is one of over-activity or hyperthyroidism. Excess thyroid hormone causes a condition of thyrotoxicosis. Over time this leads to hyperthyroidism.

Autoimmune diseases are conditions that originate when the immune system errs in its efforts to protect us. The immune system refers to a network of organs, such as the spleen, tonsils, bone marrow, the lymph glands, and discrete patches of lymphoid scattered throughout the intestines and other organs. These organs store white blood cells. White blood cells, particularly lymphocytes, are the key players of the immune system.

Normally, lymphocytes watch out for foreign threats such as viruses and bacteria. And they destroy cancerous cells. Chemicals and stress can overburden these cells, and infectious agents can cause these cells to work overtime. This causes some of the white blood cells to err and target protein particles in the body’s own cells. These cells become auto-reactive or reactive against self molecules. If autoreactive cells are allowed to persist and proliferate, they form autoantibodies, which are antibodies that react against the body’s own tissues.

In Graves’ disease, the immune system produces autoantibodies that react with the TSH cell receptor. Normally, only the pituitary hormone TSH reacts with this receptor, activating the receptor and ordering thyroid cells to produce and release more thyroid hormone. In Graves’ disease, stimulating TSH receptor antibodies (also known as thyroid stimulating immunoglobulins or TSI) latch onto the receptor acting in place of TSH. The result is excess thyroid hormone. Realizing the levels of thyroid hormone in the blood are more than adequate, the pituitary gland stops releasing TSH.

Normally, without TSH, thyroid hormone would not be produced. But TSI in Graves’ disease ignore this normal feedback mechanism. Consequently, in Graves’ disease, blood levels of the thyroid hormones T3 and T4 are elevated and blood levels of the pituitary hormone TSH are low or suppressed. Also, TSI and other thyroid autoantibodies are also present in the blood.

The goal in treating Graves’ disease is palliative. This means that symptoms are reduced, but the disease is not cured. Graves’ disease runs its own course and eventually resolves on its own. In many instances, the antibodies produced by Graves’ disease patients change and blocking TSH receptor antibodies predominate. This is responsible for the hypothyroidism that eventually develops in about 20% of untreated patients.