Graves Disease treatment and natural therapy
January 25 2016

In Grave's 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.

Endokrynol Pol. 2014. Influence of cigarette smoking on thyroid gland - an update. Many studies have shown that cigarette smoking exerts multiple effects on the thyroid gland. Smoking seems to induce changes in thyroid function tests, like decrease in TSH and increase in thyroid hormones. However, these alterations are usually mild. In addition, tobacco smoking may also play a role in thyroid autoimmunity. Many studies have confirmed a significant influence of smoking on Graves' hyperthyroidism and particularly on Graves' orbitopathy.

Grave's disease treatment
The purpose of treatment is to control the overactivity of the thyroid gland.

Management of Graves disease includes treatment with antithyroid drugs, radioactive iodine RAI, or thyroidectomy. The optimal approach depends on patient preference and specific patient clinical features such as age, history of arrhythmia or ischemic heart disease, size of goiter, and severity of thyrotoxicosis.

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


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.

Autoimmun Rev. 2014 Jan 12. Diagnosis and classification of Graves' disease. GD is an autoimmune disorder involving the thyroid gland, typically characterized by the presence of circulating autoantibodies that bind to and stimulate the thyroid hormone receptor (TSHR), resulting in hyperthyroidism and goiter. Organs other than the thyroid can also be affected, leading to the extrathyroidal manifestations of GD, namely Graves' ophthalmopathy, which is observed in ~50% of patients, and Graves' dermopathy and acropachy, which are quite rare. Presumably, the extrathyroidal manifestations of GD are due to autoimmunity against antigens common to the thyroid and other affected organs. Although its exact etiology remains to be completely understood, GD is believed to result from a complex interaction between genetic susceptibility and environmental factors. Clinically, GD is characterized by the manifestations of thyrotoxicosis as well as by its extrathyroidal features when present, the latter making the diagnosis almost unmistakable. In the absence of ophthalmopathy, the diagnosis is generally based on the association of hyperthyroidism and usually diffuse goiter confirmed with serum anti-TSHR autoantibodies (TRAbs). Hyperthyroidism is generally treated with anti-thyroid drugs, but a common long term treatment strategy in patients relapsing after a course of anti-thyroid drugs (60-70%), implies the use of radioactive iodine or surgery.

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 2014.

Q. I had Graves disease, and had a total thyroidectomy ,with a tiny piece of thyroid remaining, 10 years ago. I have been on 100mcg (sometimes 112 mcg) of Levoxyl since then I feel around 75% normal, but I do have hair loss, weight gain issues (and I am very athletic, and eat right, trust me), fatigue, depression, etc. My menstrual cycle has been normal though. I have also had one successful pregnancy, and delivered a healthy baby boy last year. Post delivery, I have tried everything from Levoxyl 100 and Cytomel 5 (once a day) to increasing my dose of Levoxyl (to 112), with no success. The former caused me to become severely hyperthyroid, and I had horrible muscle fatigue, headaches, dizziness (this is the 3rd time I have tried Cytomel with similar problems each time)  The latter made my symptoms persist, despite fairly low TSH and normal free T3 / T4 levels Staying at Levoxyl 100 keeps my levels in the normal range, but symptoms as I mentioned above (hypothyroid symptoms) persist. The question I have is this : if I try a natural supplement like Ashwagandha or Guggal - will these supplements stimulate the small remnant piece of my thyroid and put me at risk of hyperthyroidism? Will they cause my Graves to flare up? I still show the antibodies present in my blood.
   A. Human research with ashwagandha, guggul, and many herbs is quite limited and little is known on how these supplements influence the thyroid gland let alone a small portion of a thyroid gland.

Q. I have an eye condition called Graves disease, it has to do with the muscles of my eyes. Can you tell me if Eyesight Rx will help the condition. My husband uses it and I was wondering if it would help me.
   A. Eyesight Rx was developed for those who have age related gradual vision loss, not for Grave's disease. We doubt it will help a thyroid condition but we have never tested it in this condition.

I am wondering if you can tell me if there is any research or user testimonials regarding how pregnenolone might impact those people who have Grave’s Disease (hyperthyroidism caused by autoimmune response)? Mine is stable on a low dose of anti-thyroid medication but I wondered if there is any contraindication for pregnenolone? I am wanting to try it as I am perimenopausal and cannot take progesterone directly as it is too stimulating for some odd reason and I wanted something that would balance all of my hormones.
   A. I am not aware of such studies, but it would be preferable to use only tiny amounts of the hormone.