We are very excited to begin sharing this 2 part blog series with you.
This series comes from Dr. Dana Gibbs, a specialist in all things thyroid! As many of you already know, autoimmune disorders usually come in clusters. For example, patients with rheumatologic conditions often also have autoimmune thyroid disorders.
We hope you find interest in this series and are able to learn valuable information from it.
Part 1 -
What is Hashimoto’s disease?
Hashimoto’s disease is one name for one of the two varieties of autoimmune thyroid disease. It is also known as chronic lymphocytic thyroiditis or autoimmune thyroiditis (AIT). It is the most common disorder of the thyroid gland in the U.S. It is also the world's most common autoimmune disorder (by far!) It affects 15% of all Americans and some 24% of allergic women. It is much more common in women than men, and can occur at any age, though the most common onset seems to be teenage to 30’s. It runs in families, but about half of patients don't know of any relatives with the problem.
Some triggers of this condition are: taking high levels of iodine, pregnancy, or viral illnesses, but in most cases, we don’t know what the trigger is. Frequently the disease process is well advanced before it is even discovered. It is frequently the first autoimmune disease that presents in a person, who may then tend to develop more severe autoimmune diseases later in life.
Hashimoto’s is also the most common cause of hypothyroidism - low thyroid function. But, it can also cause elevated thyroid hormone levels - hyperthyroidism - that come and go as the disease flares and remits. Because of these bouts of hyperthyroidism, people who have it are frequently misdiagnosed with Graves’ disease (another autoimmune thyroid condition) (see link to graves disease post HERE) and is mistakenly treated with surgical removal or Iodine 131 radiation treatment. At first glance, this can sometimes present as “subclinical hypothyroidism”, which is the common term for seemingly normal levels of thyroid hormones. I don’t like this name because it implies that the people who have it don’t have symptoms which, as you will see, is not true.
In Hashimoto's thyroiditis, the immune system has (for a variety of reasons) become "allergic" to the thyroid gland. It attacks it by sending destructive antibodies to target against the gland. The intended normal purpose of an antibody is to flag disease-causing foreign agents that need to be destroyed by other cells and components in the immune system. In an autoimmune disorder, the immune system produces rogue antibodies and immune cells that target healthy organs, cells or proteins in the body.
In Hashimoto's disease, the immune system produces an antibody to thyroid peroxidase (TPO), a protein that plays an important part in thyroid hormone production. Most people with Hashimoto's disease will have thyroid peroxidase (TPO) antibodies in their blood. The other main antibody that is seen in Hashimoto’s is Thyroglobulin antibody. Thyroglobulin is a protein that binds and helps store thyroid hormones. These antibodies and the immune cells that accompany them cause destruction of the tissues of the thyroid gland, sometimes releasing large amounts of thyroid hormone in the process.
Symptoms and Presentation of Hashimoto’s disease:
If you know anything about thyroid problems, you probably know that our thyroid hormones set the rate of our metabolism (how our body produces and uses energy). So, a person with Hashimoto’s can be hyperthyroid (too much thyroid hormone) for periods of time. This is called "Hashitoxicosis." They can then become euthyroid (just enough) briefly, before they finally become hypothyroid (not enough) as the destruction of the gland progresses. In about 50% of people, the immune attack remits after a few months, meaning it goes away as quietly as it started. The other half will gradually end up with hypothyroidism - a defunct gland. (see this other blog post for symptoms of inadequate thyroid function). This is when most doctors step in to treat by using thyroid hormone. However, Hashimoto's causes many symptoms before the gland becomes nonfunctional.
These symptoms can include inflammation of the thyroid gland itself, as well as all the symptoms of low thyroid function that we associate with a damaged or non-functioning gland. This seems to occur by the infiltration of lymphocytes into the thyroid gland, replacing normal thyroid tissue with scar tissue. If the gland recovers, frequently there will be a nodular pattern and even frank swelling (goiter). These can get quite large and can be mistaken for thyroid cancer. Or, the antibodies can block the action of TSH causing the gland to shrivel away, otherwise known as “atrophy”.
What is “subclinical Hypothyroidism”?
Patients with Hashimoto's generally do not efficiently activate and process their thyroid hormones to active thyroid hormone T3. (for a primer on the different thyroid hormones click here) This can be the case with normal or elevated TSH, and normal FreeT4 levels. This is “Subclinical Hypothyroidism”. Patients with subclinical hypothyroidism will frequently have some, or many, hypothyroid symptoms, and will frequently feel worse if given Levothyroxine (synthetic T4). The reason for this is that high T4 (the storage form of thyroid) levels feed back to the control mechanisms in the brain and pituitary gland, and reduce the conversion to T3 even more. And T3 is what drives the metabolic processes and makes us feel well. (See my Subclinical hypothyroidism video/blog)
Or, because of the large fluctuations in thyroid hormone early on in the disease, these patients can end up with high levels of Reverse T3, an inhibitor of T3, even if they do have “enough” of the active hormone T3. The production of Reverse T3 (a blocker of thyroid hormone function) is a natural defense mechanism by the body to guard against wasting body energy stores from excess metabolic function in times of famine, extreme physical illness, or the high levels of thyroid hormones seen in the setting of thyrotoxicosis (another name for hyperthyroidism). In the setting of Hashimoto’s disease, elevated reverse T3 will cause all the same hypothyroidism symptoms, even when the rest of the labs are completely normal!
Diagnosis of Hashimoto’s disease:
If a patient exhibits several symptoms of either hypo- or hyperthyroidism, a thorough exam and lab testing should be performed. Hashimoto’s disease can have a variety of clinical presentations including pain, swelling and redness at the point of the thyroid gland, a lumpy or nodular feel to the gland, significant enlargement of the gland with a rubbery feel, or even a gland that feels like it is missing (atrophic gland). There are other physical signs of low thyroid that should be checked as well.
Lab tests for suspected Hashimoto’s disease and thyroid dysfunction:
FreeT3, FreeT4, TSH, Total T3, ReverseT3 - These should all be tested together, and at the same time of day each time the tests are repeated. My preference is midday for someone who is already taking thyroid replacement. FreeT3, Free T4 and TSH in my clinic all have very tight ideal ranges within the “normal” reference range as given by the lab. The Ratio of Total T3 divided by Reverse T3 is an excellent indicator of healthy thyroid FUNCTION. Levels between 10 and 14 are ideal, but some people feel better even higher than that. Lower than 10 indicate inadequate action and availability of FreeT3.
Thyroid peroxidase antibody, and Thyroglobulin antibody - These should be tested once to verify the presence of Autoimmune thyroid antibodies. However, a negative antibody test does not completely rule out AIT, because it is primarily a cellular process. Frequent repetition of these tests is not required, but can give a rough indicator of whether your lifestyle changes are helping to control autoimmune inflammation.
TRAB and/or TSI - If there is hyperthyroidism, testing for Graves’ antibodies is also recommended.
Treatment of Hashimoto’s disease:
There are a variety of options for treating Hashimoto's thyroiditis. Most internet sources sponsored by major medical institutions will say there is no need to treat until the thyroid hormone function is inadequate. This is a huge problem because many doctors still believe that you can determine thyroid function with TSH (thyroid stimulating hormone) alone or with FreeT4 levels. Newer studies show this is not the case. Details and controversies in treatment of Hashimoto’s disease will be presented in an upcoming blog post.
If you are reading this and are not a physician, please keep in mind:
Scientific proof is not nearly as black and white as people think, and in order to make treatment decisions for individual people, sometimes we have to consider evidence that is not nearly as absolute as we would like.
This is not meant to be medical advice, and you should consult your own physician for any medical issues or diagnosis you may have.
Dana Gibbs, MD, is an integrative physician in North Texas. She is a Hashimoto’s expert who helps people address thyroid and other hormone imbalances. You can read more of her blog posts about hormone issues HERE. If you’re a thyroid or chronic fatigue sufferer in Texas or Iowa and you want a caring doctor to help you finally resolve your exhaustion, joint and muscle aches, poor sleep issues, and weight gain, you can sign up for a new patient evaluation with Dr. Gibbs at www.danagibbsmd.com
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