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Is Fibromyalgia is a thyroid-related condition ?

By: Dr. John C. Lowe  & Dr. Gina Honeyman-Lowe

This  paper was presented and discussed in Grenoble, France, May 6 2000 (conference of the French Fibromyalgia Association of Région Rhône-Alpes) and in Toulon, France on May 11 (at the Centre Hospitalier Intercommunal). Scheduled for publication in Myalgies.
 
The clinical features of fibromyalgia syndrome (FMS) and hypothyroidism are virtually the same The most common symptoms of fibromyalgia are also common symptoms of hypothyroidism, and the objective abnormalities of FMS are also objective abnormalities of hypothyroidism. The symptoms and objective abnormalities of hypothyroidism are mediated by inadequate thyroid hormone regulation of cell function. Inadequate thyroid hormone regulation also plausibly mediates the documented features of FMS
Hypothyroidism in FMS Primary Hypothyroidism.
The estimated incidence of hypothyroidism in FMS is higher than in the general public. The reported incidence of primary hypothyroidism in the general non-elderly USA population varies between 1% and 5%. Laboratory thyroid function testing suggests that the incidence of primary hypothyroidism in FMS is 10% to 13%.
Anti-thyroid Antibodies. Aarflot and Bruusgaard measured thyroid microsomal antibodies in 737 men and 771 women who ranged in age from 40-to-42. Subjects with chronic widespread musculoskeletal complaints had a significantly higher incidence of antibodies than did subjects without such complaints (16.0% versus 7.3%.
The prevalence of antibodies was significantly higher in women than men (20.4% versus 11.6%. It is noteworthy, however, that laboratory thyroid function test results did not differ significantly between the two groups. The investigators wrote that their results suggest that patients with microsomal thyroid anti-bodies may have symptoms due to subnormal thyroid hormone regulation of cell function before thyroid gland dysfunction is detectable by tests of thyroid hormone and TSH levels. The researchers implied that many patients diagnosed with FMS may in fact have chronic, widespread pain due to impaired thyroid gland function revealed only by increased titers of thyroid microsomal antibodies. If this is true, then the incidence of primary hypothyroidism among FMS patients may be higher than the 10% to 13% suggested by measures of TSH and thyroid hormone levels.
Central Hypothyroidism.
The incidence of central hypothyroidism, involving hypothalamic or pituitary dysfunction, in the USA population at large is about 0.00021%. My research group has found that of 92 sequential unselected FMS patients, 40 patients (43.5%) had laboratory test results consistent with central hypothyroidism. Other researchers have also reported high incidences of test results consistent with central hypothyroidism.
Thus, the incidence of primary hypothyroidism among FMS patients may be 2 to 10 or more times higher than in the population at large. The incidence of possible central hypothyroidism, however, may be 250,000 times higher. If we trust in the reliability of thyroid function test results, we are compelled to reach a conclusion: If 10% of FMS patients have primary hypothyroidism, and 44% have central hypothyroidism, the total percentage of FMS patients with hypothyroidism is 54%.
Thyroid Hormone Resistance
Many researchers and clinicians consider the term "thyroid disease" to include only pathological processes that occur 1) within the thyroid gland itself, or 2) in other tissues, such as the pituitary gland, and indirectly result in subnormal function of the thyroid gland. However, this definition may be too narrow. In 1967, Refetoff et al. provided convincing evidence of partial cellular resistance to thyroid hormone in humans. Since then, a great volume of studies of human thyroid hormone resistance has accumulated. Also, mutations have been shown to be the underlying mechanisms of general resistance to thyroid hormone. (The mechanisms of resistance in most afflicted patients remain unknown.) In some thyroidology textbooks, thyroid hormone resistance is grouped under "Special Topics in Thyroidology."
However, it can be argued that thyroid hormone resistance should be classified as a subset of thyroid disease. As in central hypothyroidism, which is classed as a thyroid disease, thyroid gland function is indirectly altered in two classifications of thyroid hormone resistance. Also as in primary and central hypo-thyroidism, patients with symptoms and signs caused by thyroid hormone resistance can be effectively treated with thyroid hormone (albeit in higher than physiologic dosages, called "supraphysiologic" dosages).
Thyroid Hormone Resistance and FMS.
As far back as the late 1980s, I was puzzled as to why euthyroid FMS patients (those with normal thyroid test results) had identically the same hypothyroid-like symptoms and signs as did hypothyroid FMS patients. In searching for an answer, I came into communication with thyroid hormone resistance researchers. One of these, Steve Usala, had established a link between a gene and thyroid hormone resistance. He was also first to discover a mutation in the gene. (More than 100 different mutations in the gene have now been discovered. Based on communication with Usala and other thyroid hormone resistance researchers, in 1990, my colleagues and I treated 77 euthyroid female FMS patients with the active thyroid hormone called T3 (as part of more comprehensive metabolic treatment).
This treatment was based on our hypothesis that the patients had partial cellular resistance to thyroid hormone. Of the 77 patients, 19 (25%) did not feel that T3 had improved their status. They were withdrawn from the hormone. The remaining 58 patients (75%) reported that their symptoms were improved to varying degrees. For the group, the difference between pre- and post-treatment algometer scores (mean of the pressure/pain threshold of 18 tender points) was highly significant. The mean pressure/pain threshold of the 18 tender point sites was significantly higher (improved) after T3 treatment. Effective dosages of T3 ranged from 75 µg. to 150 µg. Most patients improved with dosages between 81.25 µg. and 100 µg. (Normal replacement dosages were reported to be from 25-to-75 µg.)
Since that early open trial, my colleagues and I have continued to treat euthyroid FMS patients on the assumption that they have thyroid hormone resistance. We find that approximately 75% of euthyroid FMS patients markedly improve or completely recover when treated with what we term "metabolic rehabilitation." The treatment involves the use of T3, exercise to tolerance, wholesome diet, nutritional supplements, physical treatment, and cessation of the use of metabolism-impeding medications.
Most patients improve only with supraphysiologic dosages of T3. We are convinced that the patients who improve or recover with supraphysiologic dosages of T3 have cellular resistance to thyroid hormone. We conclude that a patient has thyroid hormone resistance when four criteria are met. The patient:
(1) is euthyroid before beginning the use of T3, according to thyroid function test results, including a TRH stimulation test;
(2) markedly improves or completely recovers from hypothyroid-like FMS symptoms and signs with supraphysiologic dosages of T3;
(3) after beginning T3 therapy has an extremely high free T3 blood level;
(4) has no evidence of tissue thyrotoxicosis due to the high T3 level, according to the results of serial ECGs, serum and urine biochemical tests, and bone densitometry.
Most of our euthyroid patients who improve or recover with metabolic rehabilitation involving T3 therapy meet these four criteria. Clearly, this set of findings in many treated euthyroid FMS patients shows that they meet Refetoff’s definition of thyroid hormone resistance: "reduced responsiveness of target tissues to concentrations of thyroid hormone that under normal conditions would be excessive". According to the four criteria, we have documented the presence of thyroid hormone resistance in FMS patients in several double-blind, placebo-controlled, crossover studies. Also, in a case-control study, we found that the results of the treatment lasted long term. Throughout a 1-to-5 year follow-up period, 10 hypothyroid FMS patients maintained their improvement compared to untreated FMS matched control patients. Also, 10 euthyroid FMS patients treated with T3 maintained their improvement compared to control patients.
 
Criticisms
Eisinger (rheumatologist) and Fontaine and Rinaldi (thyroid specialists) have given several criticisms of the hypothesis we present here. We agree with most of the criticisms. For example, we know that a small amount of the available evidence contradicts the hypothesis. Despite this, the hypothesis is supported by far more of the available evidence than is any competing hypothesis of the etiology of FMS. Also, rigorous logical analyses show that the hypothesis is the most useful at this time for stimulating further fruitful exploration of FMS.
Eisinger, Fontaine, and Rinaldi also argued that the hypothesis applies only to a subgroup of FMS patients. We maintain that the subgroup is large—close to 90%. We agree with them, however, that patients should be treated with precaution. We also agree with an astute observation of theirs: that when the peripheral cellular effects of thyroid hormone can be normalized by agents such as selenium (which may increase the deiodination of T4), this therapy is preferable to the use of exogenous thyroid hormone. (The American FMS researcher Richard Garrison has made a similar argument.) We should rigorously study the treatment of FMS patients with agents such as thiol and selenium to learn whether some of them benefit more from these than from the use of T3. Even when patients do benefit from such agents, however, the benefits are mediated by an improvement in thyroid hormone regulation of cell function. This outcome further supports the hypothesis that in the involved patients, inadequate thyroid hormone regulation of cell function underlies their FMS.
 
Conclusions
If cellular resistance to thyroid hormone is accepted as a subset of thyroid disease not directly involving the thyroid gland, then our findings suggest that most FMS patients have thyroid disease. About 10% have laboratory test results consistent with primary hypothyroidism, and about 45% have results consistent with central hypothyroidism. This is a total of 55% of FMS patients who may have hypothyroidism.
Of the remaining 45% who have test results consistent with euthyroidism, 75% on average improve or recover when treated on the assumption that they have thyroid hormone resistance. This 75% is about 34% of our total sample of FMS patients. For a total percentage of FMS patients with possible thyroid disease, we can add this 34% of patients with thyroid hormone resistance (according to the four post-treatment criteria) to the 55% of hypothyroid patients (according to thyroid function test results). The result is 89% of FMS patients with possible thyroid disease.
This estimate is consistent with previous findings such as glycolysis abnormalities and T3-induced improvement in FMS patients with the polymyalgia-hypothyroid intractability syndrome described by Eisinger. In fact, as I (JCL) recently argued, virtually every symptom and abnormal finding in FMS is plausibly explained by inadequate thyroid hormone regulation. This proposed mechanism is unique in this respect.
 
Percentage of FMS patients with thyroid disease.
Class of Thyroid Disease% of Patients
Primary hypothyroid 10%
Central hypothyroid 45%
Thyroid hormone resistant 34%
Total % with thyroid disease 89%
The remaining 11% of FMS patients also have symptoms and signs that resemble those of hypothyroidism. Our conjecture is that these patients’ symptoms and signs result from pathophysiological processes not related directly to thyroid hormone. However, we believe the pathophysiological processes in these patients impede metabolism in a set of tissues that generate symptoms and signs resembling those of hypothyroidism or thyroid hormone resistance.
 
References
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Golding DN. Hypothyroidism presenting with musculoskeletal symptoms. Ann. Rheumatic. Dis. 1970; 29:10-41.
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Delamere JP, Scott DL, and Felix-Davies DD. Thyroid dysfunction and rheumatic diseases. J. Royal Soc Med., 1982; 75:102.
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Awad EA. Histopathological changes in fibrositis. In Advances in Pain Research and Therapy, vol. 17. Edited by J.R. Fricton and E.A. Awad, New York, Raven Press, 1990, pp.249-258.
Sonkin LS. Endocrine disorders and muscle dysfunction. In Clinical Management of Head, Neck, and TMJ Pain and Dysfunction. Edited by B. Gelb, Philadelphia, W.B. Saunders Co., 1985, pp.137170
Lowe JC. The Metabolic Treatment of Fibromyalgia. Boulder, McDowell Publishing Co., 2000.
Hershman JM. Hypothalamic and pituitary hypothyroidism. In Progress in the Diagnosis and Treatment of Hypothyroid Conditions. Edited by P.A. Bastenie, M. Bonnyns, and L.VanHaelst, Amsterdam, Excerpta Medica, 1980, pp.40-50.
Tunbridge WMG, Evered DC, and Hall R. The spectrum of thyroid disease in a community survey. Clin. Endocrinol., 1977; 7:481-493.
Eisinger J. Hypothyroïdie et fibromyalgie: indications d’une double hormonothérapie thyroïdienne. Lyon Med. Med., 1999, 35 : 31-36.
Gerwin R. A study of 96 subjects examined both for fibromyalgia and myofascial pain. J. Musculoskel. Pain, 1995; 3:(Suppl.)1:121.
Lowe JC. Thyroid status of 38 fibromyalgia patients: implications for the etiology of fibromyalgia. Clin. Bull. Myofascial Ther., 1997; 2(1):36-41.
Shiroky JB, Cohen M, Ballachey M-L, and Neville C. Thyroid dysfunction in rheumatoid arthritis: a ontrolled prospective survey. Ann .Rheumat. Dis., 1993; 52:454-456.
Lowe JC, Reichman AJ, Honeyman GS, and Yellin J. Thyroid status of fibromyalgia patients (Abst.). Clin. Bull. Myofascial Ther., 1998; 3(1): 69-70.
Neeck G, and Riedel W. Thyroid function in patients with fibromyalgia syndrome. J. Rheumatol., 1992; 9:1120-1122.
Ferraccioli G, Cavalieri F, Salaffi F, et al. Neuroendocrinologic findings in primary fibromyalgia (soft tissue chronic pain syndrome) and in other chronic rheumatic conditions (rheumatoid arthritis, low back pain). J. Rheumatol., 1990; 17:869-873.
Aarflot T, and Bruusgaard D. Association between chronic widespread musculoskeletal complaints and thyroid autoimmunity:results from a community survey.Scand.J. Prim. Health Care, 1996; 14(2):111-115
Refetoff S, Dewind LT, and DeGroot LJ. Familial syndrome combining deaf-mutism, stippled epiphyses, goiter and abnormally high PBI: possible target organ refractoriness to thyroid hormone. J. Clin. Endocrinol. Metab., 1967; 27:279.
Refetoff S. Resistance to thyroid hormone: an historical overview. Thyroid, 1994; 4(3):345-349.
Usala SJ, Bale AE, Gesundheit N, et al. Tight linkage between the syndrome of generalized thyroid hormone resistance and the human c-erbAß gene. Mol. Endocrinol., 1988; 2:1217-1220.
Usala SJ, Tennyson GE, Bale AE, et al. A base mutation of the c-erbAß thyroid hormone receptor in a kindred with generalized thyroid hormone resistance: molecular heterogeneity in two other kindreds. J. Clin. Invest., 1990; 85:93-100.
Lowe JC. Results of an open trial of T3 therapy with 77 euthyroid female fibromyalgia patients. Clin. Bull. Myofascial Ther., 1997; 2 (1):35-37.
Lowe JC, Reichman A, Yellin J. The process of change with T3 therapy for euthyroid fibromyalgia: a double-blind placebo-controlled crossover study. Clin. Bull. Myofascial Ther., 1997; 2(2/3):91-124.
Lowe, J.C., Garrison, R.L., Reichman, A.J., and Yellin, J.: Triiodothyronine (T3) treatment of euthyroid fibromyalgia: a small-N replication of a double-blind placebo-controlled crossover study. Clin.Bull.Myofascial Ther., 2(4): 71-88, 1997
Lowe JC, Reichman A, and Yellin J. A case-control study of metabolic therapy for fibromyalgia: long-term follow-up comparison of treated and untreated patients (abstract). Clin. Bull. Myofascial Ther., 1998; 3(1):23-24.
Eisinger, J, Fontaine, G, and Rinaldi JP (Toulon). Commentaires sur "Thyroid Disease and Fibromyalgia Syndrome" (J. Lowe and G. Honeyman-Lowe), April 20, 2000.
Lowe, J.C., Garrison, R., Reichman, A., Yellin, J., Thompson, M., and Kaufman, D.: Effectiveness and safety of T3 therapy for euthyroid fibromyalgia: a double-blind, placebo-controlled response-driven crossover study, Clin. Bull. Myofascial Ther., 2(2/3):31-57, 1997.
 
Acknowledgements:
Dr. John Lowe’s book ‘The Metabolic Treatment of Fibromyalgia’ is published by
Boulder, McDowell Publishing Co., 2000. 

 

 

Yvonne Clark said,

October 5, 2008 @ 10:25 pm

Would there be significant weight gain with hypothyrodism that exercise and diet made no changes to. Also could it cause lumps of non pitting odema?

Eric Bakker ND said,

October 8, 2008 @ 9:59 am

Hi Yvonne,

Yes – as the thyroid decreases in function, so does your metabolic rate. Things “slow down” in your body, including your ability to burn fat, and many other problems can occur as well. Weight which does not shift inspite of strict adherence to diet and exercise is generally a thyroid issue in my clinical experience. The problem is, if the blood tests come back normal (TSH, T3 & T4) then the patient is deemed to by “normal”. I have found that many hypothyroids have bowel issues like a sluggish bowel including constipation, but also present with tiredness, cold hands & feet, weakness, some have pain in muscles or joints and yes, “puffiness” can certainly be adrenal or thyroid in origin. Many will complain of “brain fog”, poor memory, hair, skin or nail issues as well. With puffiness you have to exclude heart problems naturally, which may cause pitting oedema. It has been estimated that up to 40% of women in NZ have some type of thyroid issue, amazing !

Dr. Gina S. Honeyman said,

December 15, 2008 @ 6:22 pm

Hello Yvonne,

I agree with Dr. Bakker’s comments about symptoms of poor thyroid regulation. Many of my patients have also had the phenomenon you describe; despite consuming a wholesome diet and exercising to tolerance the weight does not drop. I encourage you to get your resting metabolic rate (RMR) measured to gather more information about your thyroid issues. People with thyroid hormone resistance usually have normal TSH, free T3 and free T4 levels. The value of RMR measurement is that it reflects tissue utilization of thyroid hormone; the blood tests do not. Feel free to use the self-tests for thyroid and adrenal problems on my website, http://www.drginahoneyman.com. The prevalence of people across the globe with thyroid problems is so vast that I consider it a global health epidemic!

Eric Bakker ND said,

December 15, 2008 @ 11:01 pm

Hi Dr. Honeyman,
Thanks for your coments.
Like in your country, many women in New Zealand suffer needlessly with fibromyalgia, hypo-thyroidism and adrenal fatigue. Your website is great, with plenty of useful and credible information, and like this website, hopefully, will allow free public access to useful and high quality information related to their condition. Keep up the good work!

Eric Bakker ND

Judith Philpott said,

January 2, 2009 @ 11:15 am

Hi Eric,
An anti-inflammatory diet may reverse symptoms. I have experienced fibromyalgia, and noticed that the fibromyalgia symptoms lessened and at times left for days on end when I ate GREEN BEANS. Most people with fibromyalgia experience the pain for a while and then the symptoms for some reason leave. When the consumption is anti-inflammatory it is when they are free of pain. I am free of firomyalgia as long as I eat GREEN BEANS at least three times a week in conjunction with the anti-inflammatory diet. Calciun Magnesium depletion is a problem.

Hi Judith,
Thanks for your comments. Green beans are high in beta-carotene and also vitamin C, both nutrients have strong anti-inflammatory effects. This may make green beans helpful for reducing the severity of diseases where inflammation plays a major role, such as fibromyalgia, osteo and rheumatoid arthritis.
Green beans are also an excellent source of vitamin B2, riboflavin, which has been shown to help reduce the frequency of various forms of pain in people who suffer with pain. Riboflavin’s protective role in energy production may explain why. The oxygen-containing molecules the body uses to produce energy can be highly reactive and can inadvertently cause damage the mitochondria (inside the cell) and even the cells themselves. In the mitochondria, such damage is largely prevented by a small, protein-like molecule called glutathione. Like many “antioxidant” molecules, glutathione must be constantly recycled, and it is vitamin B2 that allows this recycling to take place, and one cup of green beans supplies ore than 7 % of the DV for riboflavin. There is always a reason why one food can have such an amazing effect on one patient, and not necesarily another person. I can verify this in the clinic and have seen it time and again. “That raw potato juice did the trick with my heartburn” one person will tell me, whilst another person swore to me that “having a large pinch of Epsom salts is the magic potion” to lots of aches and pains. Sometimes a simple suggestion of 50 to 100 mcg of Molybdenum (not to be confused with Magnesium) can make all the difference in the world for the patient with certain forms of muscle, bone or joint pains.
You are also correct to mention Calcium and Magnesium, Magnesium deficiency within the muscle fibers is speculated to be a significant factor in the development of FM, and daily supplementation of 300 – 600 mg of Mg may result in significant improvements in the number of tender points in FM patients.
As far as calcium is concerned, I find it always worth mentioning for the FM patient to take in a few different forms. Calcium Malate as well as calcium phosphate are both wise choices, for too many biochemical reasons to mention! And, don’t forget the trace elements such molybdenum and manganese. They are very important and often overlooked as far as FM is concerned, and last but not least – get your vitamin B12 level checked, I have seen too many FM patients with rock bottom B12 levels.

Eric Bakker ND

Sharon said,

June 4, 2009 @ 9:16 am

I have had partial removal of the thyroid in 2000. I have now developed a goiter which has attached its self chest bone. I have got a pain in my upper breast and swallowing is bad. I am cold all the time, sweating, and have brain fog which is shocking. I’m depressed beyond belief and I also have no energy, my hands and feet are cold.
When the tests came back it said my thyroid was fine, but how can this be. I woke this moring with pain full nails which looked at the they are lifting. I am fed up with this and am awaiting surgery but there is a 9 months waiting list. I feel like I can’t cope with this much longer, am fed up and people dont understand the coldness issue!
I have spoken to my doctor who sent me for needle aspiration and scans but is not able to answer my questions. If I have full removal will I have weight issues? I have had this since puberty and at the moment cant seem to eat without putting on weight. I am fed up with this condition, I cant sleep very well and feel like my body is shutting down. I ache and feel so unwell all the time that people are always asking how I am: “you look ill” they say. I feel like shouting: “I’d rather be dead that have this pathetic quailty of life”.
constipated as well i hate feeling this way driving sometimes hard so bloody tired. How pathetis is this.
Cant be bothered to do anything i fake work just get through it to pay the mortgage and then days off sleep.
The latest issues apart from my nails is strange headaches. With premenstrual time my period is awful and heavy, I’m even more tired and depressed but feeling I have nothing to be depressed about!
I read “eat seaweed” and can’t seem to find a suitable diet for thyroid people. God help my kids if they get this of me!
I also have no iodine, but the doctor said “dont take supplements” I’m so fed up and confused and unhappy. Eric, please help me, the last time I emailed a web site I received no answer so here I’m hoping you will!

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