Hashimoto's Disease was first described by a Japanese doctor in 1912. Hashimoto's disease is a description often levelled at anyone with hypothyroidism, in much the same way as Graves' Disease is with hyperthyroidism. The thing to understand about Hashimoto's disease is that it is basically a variant of hypothyroidism, caused specifically by autoimmunity; the thyroid gets infiltrated by white cells and slowly loses its function; it usually enlarges but may not, and may start with an over-active phase before becoming under-active.
In fact, both Graves' disease and Hashimoto's disease are forms of autoimmune thyroiditis, where the body's defence mechanisms overact or respond dysfunctionally, and cause damage to target tissues.
Hashimoto's disease is relatively common, and has several ways of presenting itself. Both Graves' and Hashimoto's disease can be triggered off by stress factors and also pregnancy. There is a genetic predisposition for both conditions, and both may involve the infiltration by white cells (lymphocytic infiltration), increased immunoglobulins within the gland, and increased blood levels of thyroid antibodies. Each can change into the other, although more commonly it is the over-active thyroid resulting from immune dysfunction that will revert to the under-active phase.
Hashimoto's disease should more properly be called chronic immune thyroiditis, and can be detected chemically by the presence of antibodies, the rise in TSH, and low blood levels of thyroid hormones. Where the TSH rises, but the thyroid hormone levels remain in range, the condition can be called subclinical hypothyroidism. It is worth noting that the antibody levels may diminish as hypothyroidism becomes established, or where treatment with thyroxine is given.
It frequently happens that Hashimoto's disease is missed because of undue reliance on blood tests. Usually the T4 is low, although it may not be out of range. So too, may be the T3. This will suggest poor thyroid hormone output. While in the normal course of events the TSH normally rises in this situation, it may actually be normal, or even low. The reason for this is a down-grading of the hypothalamic/pituitary axis due to the state of hypo-metabolism that the low thyroid function induces. (This also applies to adrenal function, which it may be remembered, can also be damaged by autoimmune disease.)
The hypothalamus responds poorly to the low thyroid blood levels, and may not produce a normal level of Thyrotrophin Releasing Hormone (TRH). In addition, the pituitary, also affected adversely by the state of hypo-metabolism, may not properly respond to the TRH, and not therefore produce a normal level of TSH.
The thyroid itself, being damaged by the white cell infiltration and with damaged TSH receptors, may well be less responsive to TSH anyway. So there is a chain reaction of failure, beginning with the hypothalamus and extending to the pituitary. The antibody test is usually pretty conclusive and any level of thyroid antibodies will suggest an autoimmune process at work; although as noted above, as the damage becomes chronic the levels may lessen.
Clinically, there is a range of features to be found in patients with autoimmune thyroiditis. Firstly, there may be nothing to show for it at all, and it is noticed during a general blood "work up" for something else. Sooner or later though, hypothyroidism becomes clearly evident. Of the various ways it shows itself, we can pick out two.
1. Goitrous Autoimmune Thyroiditis – here the progressive infiltration of white cells enlarges the thyroid, and this is the version Hashimoto first described. In addition to the white cells taking over the glandular tissue, the gland itself becomes a mass of fibrous tissue, with the follicular cells (where the thyroid hormone is made) disappearing. The gland itself, of course, becomes enlarged into a goitre. Sometimes the fibrous tissue takes over completely. It has been found also that an increase in dietary iodine has a tendency to worsen autoimmune thyroiditis.
2. Atrophic Autoimmune Thyroiditis – this is the most common form, and results in the thyroid gland shrinking with progressive loss of tissue. The antibodies block the TSH receptors in the thyroid and on the basis that what you don't use, you lose, the glandular tissue shrinks.
While Hashimoto's disease is simply a common cause of hypothyroidism, the term should not be used for hypothyroid conditions unless antibodies are present although the treatment remains the same as for any hypothyroid state.
by Dr. John C. Lowe
In this newsletter, I address a question I often receive from readers of drlowe.com. The writers’ words differ a bit, but over-and-over again, they ask the same question, so I thought it appropriate to publish my general answer here. The oft-asked question goes something like this:
"I have very high thyroid antibodies, but my TSH, T4, and T3 are normal. I have many hypothyroid symptoms and my basal body temperature is extremely low, usually 96.7 degrees Fahrenheit (35.94 degrees Celsius). But my doctor says the antibodies aren’t important and that I don’t need to take thyroid hormone. Do you agree with him or not?"
My answer is always the same: I resoundingly do not agree with the doctor. First, as my wife Tammy recently said, consider the prefix to the term "anti-bodies." The prefix means "against," and just like anti-freeze prevents your car’s radiator from freezing, anti-bodies against your thyroid gland, if they stay high, will, sooner or later, prevent the gland from working normally. Your symptoms and your extremely low basal body temperature strongly suggest to me that your gland is already impaired.
How do we know if the thyroid gland has been damaged? Not necessarily by measuring your TSH, T4, or T3 levels. The levels of these hormones may be in range or out. The blood levels just aren’t reliable enough to tell us whether a person has sufficient thyroid hormone for his or her cells to function normally. The endocrinology specialty and its corporate sponsors wish with all their might that these tests were the ultimate gauges. But, alas, they definitely are not!
The TSH, T4, and T3 levels vary dramatically every thirty minutes. Because of this extreme variance, unless the levels are far out of range, they are inaccurate criteria for inferring whether your tissues have enough thyroid hormone regulation. I have done hundreds of measurements of patients’ resting metabolic rates. Some patients were taking thyroid hormone and others not. For patients with low metabolic rates, I’ve done differential diagnoses to learn the most likely cause of the low rates. The most likely cause for most of them has been too little thyroid hormone regulation. I know from statistical analyses of the data from these evaluations that the TSH, T4, and T3 levels do not reliably predict which patients do and do not have too little thyroid hormone regulation.
High thyroid antibodies are important in and of themselves. Because yours are high, you should be motivated to get them back down into their reference ranges. If a patient's antibodies stay high, they may eventually cross-react with a tissue other than the thyroid gland. The patient will then have autoimmune disease of both the thyroid gland and the other tissue.
I find antibody tests much more useful than the TSH, T4, or T3. High antibodies indicate that a patient's symptoms are from too little thyroid hormone regulation when the TSH, T4, or T3 fail to do so. Consider a 1996 study by Aarflot and Bruusgaard. They included 737 men and 771 women in their study. Men and women who had chronic widespread musculoskeletal pain (often diagnosed as "fibromyalgia") had a higher incidence of thyroid antibodies than men and women who didn’t have pain. But the TSH, T4, and T3 levels of the two groups of men and women did not differ.
My research is now complete in showing that fibromyalgia symptoms are caused mainly by too little thyroid hormone regulation. In view of this, Aarflot and Bruusgaard’s finding indicates that antibody tests show too little thyroid hormone regulation while the TSH and thyroid hormone levels often fail to do so. As the well-known thyroid specialist Dr. Robert Volpé has written, the TSH, T4, and T3 levels may be "normal" for years despite patients having autoimmune thyroiditis the whole time.
You can have more confidence in your need for thyroid hormone therapy if you have one or more of the physiological abnormalities common among hypothyroid patients. The abnormalities include (1) a low basal body temperature, which you have; (2) a basal pulse rate too low for your level of cardiovascular conditioning; (3) a slow relaxation phase during your Achilles reflex; and (4) a low voltage R wave in the QRS complex of your EKG. Of course, you can measure your temperature and pulse rate at home. Hopefully your doctor will cooperate by testing your Achilles reflex and measuring the voltage of your R wave.
When patients come to our clinic, we also do the most important test of all—the resting metabolic rate. And we measure the composition of their bodies. We measure body composition so that I know the patient’s lean body weight. I use the measurement in an equation to learn what his or her metabolic rate should be. Then, when we measure the patient’s actual metabolic rate, I can calculate how low it is compared to what it should be.
The body composition measurement is important for another reason: so that I can decide whether the patient has a sign common among hypothyroid patients. This sign is too much body fat for the patient’s diet and physical activity level.
When patients come to our clinic, we have the advantage of being able to observe them in person. The reason this is valuable is that if a doctor has learned the physical signs of hypothyroidism, he or she can usually tell a lot about a patient’s thyroid status just by observing the patient first hand.
Considering what I said above, I hope that one thing is clear: whether you come to our clinic or not, you can accumulate evidence that should convince any reasonable doctor that you probably have too little thyroid hormone regulation. If that evidence exists, then a trial of thyroid hormone therapy—although not T4-replacement!—is in order. Remember that the TSH, T4, or T3 don't reliably tell you whether you do or don't need treatment. So, if you let your doctor deny you a trial of thyroid hormone therapy because of reference range levels of these tests, you’ll be allowing him or her put your health and well-being at risk. I personally wouldn't let an uninformed doctor subject me to that.
1. Kraus, R.P., Phoenix, E., Edmonds, M.W., et al.: Exaggerated TSH responses to TRH in depressed patients with 'normal' baseline TSH. J. Clin. Psychiatry, 58(6):266-270, 1997.
2. Baumgartner, A., Dietzel, M., Saletu, B., et al.: Influence of partial sleep deprivation on the secretion of thyrotropin, thyroid hormones, growth hormone, prolactin, luteinizing hormone, follicle stimulating hormone, and estradiol in healthy young women. Psychiatry Res., 48(2):153-178, 1993.
3. Ain, K.B., Pucino, F., Shiver, T.M., et al.: Thyroid hormone levels affected by time of blood sampling in thyroxine-treated patients. Thyroid, 3(2):81-85, 1993.
4. Sakaue, K.: Studies on the factors affecting serum thyrotropin levels in healthy controls and on the thyroid function in depressed patients using a highly sensitive immunoassay. Nippon Naibunpi Gakkai Zasshi, 66(10):1094-1107, 1990.
5. Aarflot, T. and Bruusgaard D.: Association between chronic widespread musculoskeletal complaints and thyroid autoimmunity. Results from a community survey. Scand. J. Prim. Health Care, 14(2):1111-1115, 1996.
6. Volpé, R.: Autoimmune thyroiditis. In Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text, 6th edition. Edited by L.E. Braverman and R.D. Utiger, New York, J.B. Lippincott Co., 1991, pp.921-933.
7. Lowe, J.C.: The Metabolic Treatment of Fibromyalgia. Boulder, McDowell Publishing Co., 2000.
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