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Mitochondrial Dysfunction and Autoimmune Disease
2/23/2019 3:00 PM | Elaine Moore
Westhroid and Naturethroid Shortages
12/5/2018 12:43 PM | Elaine Moore
Clues to Understanding Autoimmune Disease
8/19/2018 5:06 PM | Elaine Moore
Autoimmune Pancreatitis Subtypes
6/18/2018 5:26 PM | Elaine Moore
Cell Mitochondria VS TSH Values
4/18/2018 1:00 PM | Elaine Moore
Shingles and Autoimmune Disease
3/8/2018 11:36 AM | Elaine Moore
Low Vitamin D levels Associated with Relapses in Graves Disease
2/1/2018 2:17 PM | Elaine Moore
Autoimmune Component in Parkinson's Disease Found
8/23/2017 6:13 PM | Elaine Moore
Thyroid Disorders That Come and Go
4/29/2017 7:04 PM | Elaine Moore
The TSH Conundrum in Thyroid Disease
4/26/2017 10:18 PM | Elaine Moore

Graves' disease & autoimmune disease education

This site supports and educates patients with Graves’ disease and other autoimmune disorders. It provides information on autoimmune diseases, their symptoms, diagnosis and treatment, including integrative therapies to help support the immune system.

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Mitochondrial Dysfunction and Autoimmune Disease 

Excerpt: "...mitochondrial dysfunction has found to be a cause of cardiac disease, autoimmune disease, amyotrophic lateral sclerosis, Alzheimer's disease, bipolar and mood disorders, vascular disease, and many other conditions..."


What is Graves’ Disease?

Graves' disease (GD) is an autoimmune thyroid disorder that primarily affects the thyroid gland, causing hyperthyroidism. It may also affect the eyes, causing Graves' ophthalmopathy (thyroid eye disease or TED); the skeletal muscles causing myopathy or muscle weakness; and the skin, causing pretibial myxedema and acropachy. There are many GD variants or subtypes, and each individual case of GD is unique.

Graves' disease is caused by stimulating TSH receptor antibodies or thyroid stimulating immunoglobulins (TSI). TSI activate the TSH receptor on thyroid cells, mimicking the action of TSH, the latter a pituitary hormone which regulates thyroid hormone levels in the blood. 

The concentration of TSH present in the blood is generally a good indicator of thyroid status, and levels of TSH are often used to diagnose thyroid disorders. Normally, TSH stimulates the thyroid gland to produce and release thyroid hormone. But bypassing all normal regulatory controls, TSI causes the thyroid gland to release excess thyroid hormone, causing hyperthyroidism. TSI also stimulates orbital cells, causing Graves' ophthalmopathy and they stimulate dermal cells, causing pretibial myxedema.

When thyroid hormone levels in the blood are low, the hypothalamus orders the pituitary to secrete more TSH and TSH levels are high. When thyroid hormone levels are elevated, the hypothalamus halts TSH release. 

Thyroid hormones include thyroxine (T4)and triiodothyronine (T3). Normally, the thyroid primarily produces T4 along with a small amount of T3. T3, which is 10 times more active than T4, is mainly produced in the body by conversion (or losing one iodine molecule) from T4. Thyroid hormone is 65% iodine. Thus, in hyperthyroidism, levels of TSH are low, frequently lower than the detection level (usually <0.01 IU/L). 

T4 has 4 iodine atoms, whereas T3 has 3 iodine atoms. However, in GD the thyroid gland produces more T3 relative to T4 than usual. This results in a condition known as T3 toxicosis. Despite it's ominous sound, T3 toxicosis is a good indicator of a favorable response to anti-thyroid drug therapy.

The true prevalence of GD is unknown, but it has been estimated to be slightly less than 1% of the U.S. population. In additon, as many as 3% to 4% of the population is thought to have subclincial Graves' disease, a condition in which the patient has no symptoms although lab tests paint a picture of hyperthyroidism. Graves' disease affects many times more women than men. The peak age for GD is 20-40 years, although young children and the elderly are also affected, i.e. GD can affect individuals of any age.  Symptoms of GD in males are often more severe and men are more likely to develop muscle disorders.

For the complete article...


Advances in
Graves' Disease

Graves' Disease:
A Practical Guide


Werner & Ingbar's
The Thyroid



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