Graves Disease treatment and natural therapy

In Graves' disease, the thyroid gland goes into overdrive, producing excess levels of hormone that attack the tissue behind the eye, causing them to protrude. In extreme cases, patients experience trouble closing their eyelids, severe double vision, corneal scarring, optic nerve damage and even blindness.

Grave's disease treatment
The purpose of treatment is to control the overactivity of the thyroid gland. Beta-blockers such as propranolol are often used to treat symptoms of rapid heart rate, sweating, and anxiety until the hyperthyroidism is controlled. The overactive thyroid is treated with one or more of the following:

Antithyroid medications such as propylthiouracil and methimazole (Tapazole) interfere with thyroid hormone production. In June 2009 an alert by the FDA announced that propylthiouracil, used in the treatment of hyperthyroidism due to Graves' disease, has been associated with serious liver injury, including 13 deaths and 11 liver transplants.

Radioactive iodine

Surgery

Those who have radiation and surgery will need to take replacement thyroid hormones because these treatments destroy or remove the gland. Some of the eye problems related to Graves disease usually improve when hyperthyroidism is treated with medications, radiation, or surgery.

Graves Disease and eye bulging
Graves' disease attacks the muscle tissue behind the eyes, often causing them to bulge painfully from their sockets.
Scientists at UCLA's Jules Stein Eye Institute and Harbor-UCLA Medical Center discovered defects in the infection-fighting T-cells of Graves' disease patients' immune systems. Earlier research found that Graves' disease patients' immune systems produce an antibody that other people do not. The antibody mistakenly mounts an attack against the organ, causing inflammation and damage to the thyroid, including eye tissue. In the current study, UCLA researchers discovered that T-cells taken from these patients contain an abnormal surplus of the receptor targeted by this antibody. An antibody must latch to a specific receptor – like a key into a lock -- in order to elicit a cellular response. The receptors mobbed the patients' immune systems, even on T-cells that normally would not produce them. Raymond Douglas, MD, first author and assistant professor of ophthalmology at the Jules Stein Eye Institute,  tested Graves' disease patients' blood for the antibody and compared their findings to samples from healthy people, with about 100 subjects in each group. The new antibody was found in almost all of the Graves' disease patients' blood. The new antibody binds to the excess receptors on the T-cells, mimicking the actions of a hormone called IGF-1, or insulin-like growth factor 1. Similar to insulin, IGF-1 stimulates cell growth while suppressing normal cell death. The team suspects that this mechanism prolongs the survival of older T-cells, causing a cascade of autoimmune problems that spur the body to attack its own tissue. "We think that the extra receptors allow the new antibody and IGF-1 to disrupt the programming of the T-cells," said principal investigator Terry Smith, MD, professor of medicine at the David Geffen School of Medicine and chief of molecular medicine at Harbor-UCLA Medical Center. "The antibody provokes the receptor to signal the T-cell to grow and multiply – long after the cell was programmed to die," he explained. "After two or three generations of this process, we suspect that the high-jacked T-cells mutiny over the normal T-cells, sparking the body's immune reaction against itself." The next step is to identify what the T-cells are reacting to and how the receptor enables the cells to survive beyond their normal lifespan. The team plans to develop an antibody drug to block the receptor from interacting with the T-cells and slow down the disease. Andrew Gianoukakis, MD, assistant professor of endocrinology at Harbor-UCLA Medical Center, was a coauthor of the study, which received funding from the National Eye Institute, National Institute of Diabetes and Digestive and Kidney Diseases, American Thyroid Association and Bell Charitable Foundation.

Emails
I cam across a product called ThyroSoothe. This is what the website says, "ThyroSoothe is a unique blend and includes herbs such as Bugleweed, which helps relieve Graves' disease symptoms -like fatigue and insomnia, and Motherwort that is used to soothe heart palpitations. It is manufactured under strict regulations to provide a therapeutic benefit without negative side effects." Is there any evidence that it works?
   I have not seen any clinical studies with this product. A Medline search in 2011 came up with: The following term was not found in PubMed: ThyroSoothe.

My question is regarding R-Alpha lipoic acid and Graves disease. My son developed an autoimmune disease after receiving a CAT scan. He had a reaction to the contrasting material and developed an autoimmune problem that effects is thyroid. Is there any studies on alpha lipoic acid controlling the systems?
   Not that I am aware of as of 2011.