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Dr. Lowe Q&A – Hypothyroidism & Fibromyalgia

Updated: Mar 30, 2023

Written by Thyroid Patient Advocacy, August 16, 2004

 

Question: My doctor doesnt believe fibromyalgia has anything to do with hypothyroidism. She said that the rheumatologists she knows tell her that if fibromyalgia exists at all, the cause isn’t known. I’ve always felt that my fibromyalgiais related to low thyroid, but I don't have studies to show her. Are there any studies showing a connection that I can share with her?


Dr. Lowe: Its obvious why your doctor doesn't understand the connection between hypothyroidism and what we call “fibromyalgia” symptoms, she gets her information from misguided rheumatologists. I trust that the rheumatologists she knows, as most, are well-intended. Largely, though, rheumatologists have been misled by the rheumatology researchers who originally and valiantly spearheaded the study of fibromyalgia.

Those rheumatology researchers, throughout their thirty-year study of fibromyalgia, made a crucial mistake: they unquestioningly accepted as true a false belief perpetrated and perpetuated by the endocrinology specialty. That belief is that measuring the TSH and thyroid hormone levels infallibly identifies patients whose bodies are under-regulated by thyroid hormone. According to this false belief, if a patients levels are “normal,” then too little regulation by thyroid hormone can’t possibly be the cause of any symptom he or she complains of.


The fact is, however, TSH and thyroid hormone levels are highly unreliable indicants of whose body is under-regulated by thyroid hormone. The levels are so unreliable that the testing should be abandoned as the standard method for identifying such patients.

If your doctor is receptive, I suggest that she read two sets of information we recently posted to www.drlowe.com.

In one, I refute the dogmatic belief of Dr. Richard Guttler that thyroid function testing is failsafe. In the other, I show that doctors are mistaken in their blind faith that thyroid function testing is reliable. (I provide more evidence in my forthcoming book Tyranny of the TSH.

If you want the publisher to notify you when the book is available, send an email to McDPubCo@mcdowellpublishing.com with “Tyranny” in the subject line.)

I also suggest that your doctor read my most recent brief summary of the evidence that too little thyroid hormone regulation is the main underlying cause of “fibromyalgia.” Please let her know, however, that we always follow that causative proposition with a qualification: typically, several metabolism-impairing factors contribute to patients fibromyalgia symptoms. The most common ones are nutritional deficiencies, unwholesome diet, low physical fitness, and drugs that slow metabolism.

If your doctor reads my brief summary of the evidence, she may understand that the rheumatologists she knows are mistaken about fibromyalgia. She’ll also see that the UKs Peter Warmingham was correct two years ago when he succinctly wrote: “Fibromyalgia has been solved.”[1]


Reference: [1] Warmingham, P.: Fibromyalgia has been solved. Fibro Focus Supporter, 3:1-3, 2002.



November 13, 2002

Question: HELP! My 15-year-old has gone from being happy and healthy to being almost bed ridden. After our family doctor found a positive ANA blood test, we’ve gone to many doctors. This is what we know: She has Hashimotos thyroiditis and severe fibromyalgia. What we dont know is why her body is in so much pain all the time, to the point of her being in bed almost all day. At times she cries out in pain. Her body aches all over and at times she says it feels like a certain joint is being attacked. Her pain pills do no good. Her other symptoms are hair loss, not sleeping at night, swelling that comes and goes, and fatigue. Her exhaustion sometimes is so bad she can’t stand up and needs help walking to the bathroom. The severe fatigue we understand is from the Hashimotos thyroiditis. But since she tests negative for lupus and arthritis, why the awful pain?


Dr. Lowe: I’m terribly sorry your daughter is suffering so severely. If the cause of her symptoms is hypothyroidism due to Hashimoto’s, her suffering is correctable and unnecessary.


A subset of patients with thyroid hormone deficiency caused by Hashimoto’s has a lowered pain threshold. The susceptible patient perceives as painful stimuli that aren’t painful to other people. The pain results from too little thyroid hormone regulation of certain nerve cells. Some of the cells, mainly in her spinal cord, when under-regulated by thyroid hormone, release excess amounts of “substance P.” The excess substance P then amplifies the transmission of “pain” impulses in the central nervous system.


Too little thyroid hormone regulation of other cells in the brain stem decreases the release in the spinal cord of a nerve transmitting substance called “noradrenaline.” The decreased noradrenaline in turn reduces the amount of opiates (morphine-like chemicals) released into the spinal cord. These opiates normally reduce the number of sensory impulses that enter the spinal cord and brain stem. When too few of the opiates are released, more sensory impulses make their way into the spinal cord and brain stem. As a result, the patient’s perception of pain is heightened.


The combination of high substance P and low noradrenaline (and hence low opiates) causes the patient to perceive pain in the absence of painful stimuli. For example, the patient might perceive as painful the mere movement of some joints. She might experience pain from the pressure on her underside when she is sits or lies on a well-padded surface. And her pain threshold might be so low that she experiences aches and pains despite no apparent stimulus such as movement or pressure.


My impression is that most doctors and researchers dont know that too little thyroid hormone regulation of cells in the brain stem and spinal cord can induce and sustain pain. When a hypothyroid patient is under-treated or denied treatment with thyroid hormone (the standard provisions of conventional medicine), and her main hypothyroid symptom is chronic, widespread pain, her doctor is likely to diagnose her pain as “fibromyalgia.”

After the fibromyalgia diagnosis, conventional treatment will follow. This will entail various medications that dont correct the underlying cause of her pain (hypothyroidism) and that are largely ineffective.


Through conventional care, her health is likely to deteriorate further over timepartly from her continuing hypothyroidism and partly from the adverse effects of conventional medications. To avert this from happening, I suggest that you and your daughter promptly abandon conventional medical care, and at the same time, get her under the care of an alternative doctor who'll competently treat her for her hypothyroidism. I wish her the very best.



February 15, 1999

Question: Two years ago a car crashed into the back of my car and caused my neck to have a whiplash injury. I developed fibromyalgia within a month after the accident. I talked with my doctor about the accident maybe causing me to become hypothyroid. He told me that my fibromyalgia may seem like hypothyroidism, but they are two separate conditions. He doesn’t believe it is necessary to order tests for hypothyroidism. Instead, he insists that I continue my treatment with amitriptyline for fibromyalgia. He also says that a car wreck may cause fibromyalgia but not hypothyroidism. What bothers me is that my fibromyalgia symptoms are the same as my mother’s symptoms, but the same doctor gave her the diagnosis of hypothyroidism. Is it possible that my whiplash caused both fibromyalgia and hypothyroidism?


Dr. Lowe: Keep in mind that many patients’ fibromyalgia symptoms are actually the symptoms of untreated or undertreated hypothyroidism. Your fibromyalgia may actually be hypothyroidism your doctor has failed to diagnose and properly treat. This is certainly possible because neck trauma often induces partial thyroid gland failure. The gland is then incapable of making and releasing enough thyroid hormones.

As a result, the patient develops the symptoms of hypothyroidism. If the patient is a woman and her main symptoms are widespread pain and abnormal tenderness, she is likely to get the diagnosis of fibromyalgia. Tragically, her doctors are likely to ignore the hypothyroidism and have her to use various antidepressants – medications that are useless and dangerous for many fibromyalgia patients.


Several research groups have found that trauma to the thyroid gland induces hemorrhaging in the gland.[1][2][3] The thyroid gland may be damaged even by adoctor examining it by touch (palpation). The palpation may cause inflammation and structural damage of the gland. The diagnosis of this condition is “palpatorythyroiditis.”[4]


Directly relevant to your case is a study by Sehnert and Croft. They found that somepatients develop primary hypothyroidism after whiplash injuries.[5] They studied 101 consecutive whiplash patients. The basal temperatures of 86% of the patients were below normal. Of these patients, 30% had thyroid function test results indicating hypothyroidism. Of the 14% of patients whose temperatures were normal, 33% had abnormal laboratory thyroid test results. Sehnert and Croft diagnosed 30% of the101 patients as having post-traumatic hypothyroidism. They concluded that whiplash can result in a form of hypothyroidism due to direct injury to the thyroid gland.


Another study done in Israel is relevant to your case. Buskila and colleagues found that a significant percentage of patients with neck injury develop fibromyalgia.[6] The researchers studied 102 patients with neck injuries and 59 patients with leg fractures. They examined all the patients for nonarticular (soft tissue) tenderness and the presence of fibromyalgia. None of the patients had a chronic pain syndrome before the trauma. Of the patients with neck injuries, 21.6% met the criteria for fibromyalgia. Only 1.7% of patients with leg fractures met the criteria.

The incidence of fibromyalgia among patients with neck injuries was 13 times that of patients with leg fractures. Fibromyalgia developed at an average of 3.2 months after the trauma. Virtually all fibromyalgia symptoms were more common and severe among the 22 neck injury fibromyalgia patients. They had more tenderness, reported a lower quality of life, and had more impaired physical functioning than did patients without fibromyalgia.


Because it is possible that your whiplash injury damaged your thyroid gland, you should have laboratory thyroid function tests. The results of the tests may provide evidence that you have hypothyroidism. If your present physician refuses to order the proper tests, I suggest you find another physician who will. It is critical that you do; undiagnosed and untreated hypothyroidism can have a devastating impact on one’s life.


References: 1. Armstrong, W.B., Funk, G.F., and Rice, D.H.: Acute airway compromise secondary to traumatic thyroid hemorrhage. Archives of Otolaryngology: Head and Neck Surgery, 20(4):427-430, 1994. 2. Oertli, D. and Harder, F.: Complete traumatic transection of the thyroid gland. Surgery, 115(4):527-529, 1994. 3. Rupprecht, H., Rumenapf, G., Braig, H., and Flesch, R.: Acute bleeding caused by rupture of the thyroid gland following blunt neck trauma: case report. Journal of Trauma, 36(3):408-409, 1994. 4. Oertel, J.E. and LiVolsi, V.A.: Pathology of thyroid diseases. 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.609 610. 5. Sehnert, K.W. and Croft, A.C.: Basal metabolic temperature vs. laboratory assessment in “posttraumatic hypothyroidism.” Journal of Manipulative and Physiological Therapeutics, 19(1):6-12, 1996. 6. Buskila, D., Neumann, L., Vaisberg, G., Alkalay, D., and Wolfe, F.: Increased rates of fibromyalgia following cervical spine injury. A controlled study of 161 cases of traumatic injury. Arthritis and Rheumatism, 40(3):446-452, 1997.



December 15, 1998

Question: I have both fibromyalgia and hypothyroidism. Recently, an endocrinologist answered a question I sent to him through the Internet. In his answer, he made the following statement: “Muscle pain is a very unusual MAJOR symptom of hypothyroidism…” Will you comment on his statement?


Dr. Lowe: This is not the first time I have heard this statement made by an endocrinologist. The statement is false. This misbelief of theirs has resulted from their restricting hypothyroid patients to “replacement” dosages of thyroid hormone dosages that keep the TSH level within the range of “normal.”


Many hypothyroid patients have widespread and severe muscle pain. And many of these patients continue to have muscle pain as a residual symptom even after their endocrinologists place them on (and restrict them to) “replacement” dosages of thyroid hormone. When a patient continues to complain of muscle pain, the endocrinologist typically concludes that the pain must be caused by “something other than a thyroid hormone deficiency.” The endocrinologist thinks that if the pain were caused by a thyroid hormone deficiency, then it would disappear since the patient is on a “replacement” dosage.


The replacement dosage the endocrinologist refers to is a dosage that “replaces” the TSH level back to normal. Unfortunately, in general, this dosage does not adequate accomplish what’s really important==replace the patient’s tissue metabolism back to normal. Typically, the endocrinologist refers the patient who continues to complain of muscle pain to a rheumatologist for a fibromyalgia evaluation.


We have had many years of experience treating hypothyroid patients who also meet the criteria for fibromyalgia. The distinguishing symptom of fibromyalgia, of course, is muscle pain. When we permit these patients to use TSH-suppressive (but non-thyrotoxic) dosages of thyroid hormone, virtually all of them have complete relief from their muscle pain.

These patients’ complete relief from muscle pain is not merely an anecdotal observation; we have documented the finding by objective measures under both clinical and experimental conditions. For some patients, it is necessary that we also use effective physical treatment (especially trigger point myofascial therapy) before the pain completely disappears.


It is important to note, however, that without the TSH-suppressive dosages of thyroid hormone, the patients’ pain persists despite the physical treatment.

By forcing patients to use only what they call “replacement” dosages of thyroid hormone, endocrinologists deprive themselves of valuable clinical experience. In effect, they rob themselves of the opportunity to witness the relief of hypothyroid patients’ muscle pain through sufficiently high dosages of thyroid hormone.


As a pain management specialist, fibromyalgia researcher, and thyroidologist, I offer firm testimony: The belief of endocrinologists that muscle pain is not a common major symptom of hypothyroidism is simply a self-imposed and self-perpetuated false belief.



December 13, 1998

Question: I have both hypothyroidism and severe fibromyalgia. My fibromyalgiasymptoms improved when my family doctor let me increase my Synthroid (T4) dose from 0.10 mg to 0.15 mg per day. However, he won’t let me increase the dose any further. I also see a nutritional doctor. This doctor recently tested my blood for betacarotene and found that it is high. I take only 25 mg of beta carotene each day. Despite the low intake of beta carotene, the nutritional doctor suggested that I reduce my dose even further to get my blood level down to normal. I haven’t lowered the dose yet. My reason is that I read somewhere that hypothyroid patients have high beta carotene levels in the blood. Does my high blood level of betacarotene mean that I am not taking enough Synthroid? Or should I lower my betacarotene dose?


Dr. Lowe: First, your fibromyalgia symptoms are most likely nothing more than hypothyroid symptoms. This is indicated by the improvement in your fibromyalgia symptoms with the increased dosage of thyroid hormone. We find that fibromyalgia symptoms completely disappear when most hypothyroid patients take dosages of thyroid hormone that suppress the TSH level. Dosages that suppress the TSH level are larger than the “replacement” dosages mandated by conventional endocrinologists.

In most cases such as yours, the elevated blood beta carotene level results from the hypothyroid patient taking too little thyroid hormone. High serum levels of beta carotene are found in many hypothyroid patients. In fact, a high carotene level is the best-known example of abnormal vitamin metabolism in hypothyroidism. There are two mechanisms that account for the high carotene levels. One of these is not a serious concern, but the other raises ominous possibilities.


The first mechanism is reduced conversion of carotene to vitamin A in hypothyroidism.

The reduced conversion leaves more carotene to circulate in the blood. This may prove annoying in that it may cause a slightly yellowish tint of your skin, especially of your palms and soles. The second mechanism is elevated “lipoproteins.” Lipoproteins are compounds in the blood that contain fat and protein. The low density lipoproteins (also called LDL) are rich in cholesterol and triglycerides. The compounds are called “bad” lipoproteins for good reason: When these lipoproteins elevated (as they are in untreated and under-treated hypothyroid patients), they are a risk for cardiovascular disease. Carotene is transported in the blood by lipoproteins, and a high carotene level indicates that the patient also has high lipoprotein levels.


There is considerable evidence that the dosage of thyroid hormone that conventional doctors allow hypothyroid patients to use is too low to reduce lipoprotein levels to normal. As a result, patients taking these inadequate thyroid hormone dosages may also have elevated circulating carotene levels. In that the inadequate dosages increase the patients’ risk for cardiovascular disease, heart attacks, and strokes, the conventional treatment protocol is a public health menace. Patients and informed physicians should aggressively oppose the conventional protocol being imposed on hypothyroid patients. (For more detailed information on this, see my rebuttal to thyroidologist Dr. Robert Volpe.)


In making treatment decisions, your physicians and you must consider the peculiarities of your case. In doing so, I would urge them and you to consider a potentially serious possibility==that your elevated beta carotene level indicates that your thyroid hormone dosage is too low to adequately protect your cardiovascular health. A higher dosage may provide cardiovascular protection, and it may also lower your blood carotene level.



November 5, 1997

Question: My wife had cancer (papillary w/ follicular variants) of the thyroid. Her thyroid was removed in March of 1997, and so she’s now on Synthroid, 0.150 mg daily. She also underwent post surgical oblation with I-131, I think it was 120 millicuries (something like 80% of the max dose which if I recall was 150 mc). Anyway, she has had CFIDS/CFS symptoms since 1991, and pretty severe FM. Can she be put on your protocol and if so, what adjustments would have to be made given the missing gland? Her cancer prognosis is great, no sign of metastases.


Dr. Lowe: If your wife meets the criteria for fibromyalgia, the medical history you’ve given indicates that she is a good candidate for our treatment protocol. You may know that surgical removal and radioactive iodine (I-131) treatment of the thyroid gland are “antithyroid” therapies. This means that they decrease the amount of thyroid gland tissue.


A consequence is that the amount of thyroid hormone produced in the thyroid gland, leaving the patient hypothyroid to some degree. Anyone who has undergone antithyroid therapy should take thyroid hormone orally, as your wife does. The thyroid hormone medication serves two purposes. First, it decreases the likelihood of recurrence of the cancer. Second, it should compensate for the thyroid hormone the patient is no longer able to produce internally.


Unfortunately, many of such patients take too little thyroid hormone to maintain normal metabolism in the tissues that give rise to fibromyalgia symptoms. For many people, fibromyalgia begins after the antithyroid treatment, despite the use of thyroid hormone medication at the typically prescribed dosage. These patients usually join the fibromyalgia roles as victims of the “tyranny of the TSH.”


By this, I mean that their doctors dictate the patients’ thyroid hormone dosages according to the patients’ serum TSH levels. The TSH level tells us only how the anterior pituitary gland is responding to the dosage of thyroid hormone. It tells us absolutely nothing about how all the other tissues of the body are responding. Yet, there is considerable variability in how different tissues respond. (A recent paper that deals with this phenomenon is: Hector, F., et al.: “Replacement therapy for hypothyroidism with thyroxine alone does not ensure euthyroidism in all tissues, as studied in thyroidectomized rats. Journal of Clinical Investigation, vol. 96, pages 2828-2838, 1995.) As a result, in many patients, certain metabolically understimulated tissues give rise to fibromyalgia symptoms.


Many years of clinical and experimental experience with hypothyroid fibromyalgia patients have made one thing clear: few improve or recover from their fibromyalgia symptoms with a Synthroid (or other T4 product) dosage as low as 0.15 mg. We have had a high rate of improvement and recovery with hypothyroid fibromyalgia patients. Our protocol is to (1) ignore the patient’s TSH level, (2) increase her T4 dosage based on the metabolic responses of tissues other than the anterior pituitary (which secretes TSH), and (3) have her take nutritional supplements and exercise to tolerance. We’ve carefully monitored patients for the adverse effects many doctors fear from patients taking relatively high dosages (0.2 mg-to-0.4 mg) of thyroid hormone. The results do not justify the fear.


That your wife had fibromyalgia symptoms some six years prior to having antithyroid treatment may indicate that she had a thyroid hormone deficiency before developing thyroid cancer. If she had thyroiditis, which increases the risk of thyroid cancer, she could have had fibromyalgia symptoms from an associated thyroid hormone deficiency. On the other hand, she may have had impaired responsiveness of fibromyalgia-related tissues to normal thyroid hormone levels. If this is this case, she will most likely require T3 rather than T4 (and a fairly large dosage).


Thyroid Patient Advocacy



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