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Fibromyalgia - A Medical Mystery Solved

by Dr John Lowe

 

NB The website mentioned in this text, and any
references pertaining to this article are no longer available.

Dr John C Lowe
Diplomate: American Academy of Pain Management
Director of Research: Fibromyalgia Research Foundation
January 25, 2007

Nowadays, when patients complain to their doctors that they suffer from chronic widespread pain and abnormal tenderness, the diagnosis they usually get is "fibromyalgia syndrome." The doctors usually tell the patients, "We don't know what causes this condition, and treatments don't work well, so you're going to have to learn to live with it."

Most patients don't just live with it. They try various treatments, none of which—as their doctors told them—work well. Some use antidepressants, others narcotics. But researchers tell us that patients most often say that two treatments at least make their symptoms more tolerable; these treatments are massage therapy and chiropractic care. Many patients also take nutritional supplements and say these make them feel better, but not fully well.

For almost forty years now, most fibromyalgia researchers have repeatedly said they don't know the cause of fibromyalgia. They also say publicly that they've never gotten a patient well, and they have nothing but drugs to offer. (At best, the drugs slightly reduce the severity of some patients' symptoms. More often, the drugs make patients feel worse, so they stop taking them.)

These researchers often make these statements in journals, at professional conferences, and at public presentations. Each time they do, they ignore a line of evidence that points directly—and conclusively—to the main underlying cause of fibromyalgia. That cause is too little thyroid hormone regulation of patients' bodies. The deficient thyroid hormone regulation results from two conditions. First is an undiagnosed or undertreated deficiency of thyroid hormone. Second is the resistance of patients' tissues to thyroid hormone. "Resistance" means that patients' tissues need higher than "normal" amounts of thyroid hormone to maintain normal metabolism.

Several factors in addition to deficient thyroid hormone regulation complicate many patients' conditions. The four most common are nutritional deficiencies, an unwholesome diet, poor physical fitness, and drugs that slow metabolism. Some patients also have deficiencies or imbalances of other hormones, such as cortisol, estrogen, and progesterone.

How do we know now that too little thyroid hormone regulation is the major cause of fibromyalgia? Because our two new studies provide the final pieces of the puzzle. With these pieces in place, the proof that too little thyroid hormone regulation is the main underlying cause of fibromyalgia becomes irrefutable, as I show in the technical document at
http://www.fibromyalgiaresearch.org/solved/index.htm (NB This website is no longer available)

In this short article, I don't attempt to explain that proof. My reason is that the explanation is extremely complicated. To enable readers to comprehend the proof, I had to use more words and categorical displays of evidence than space here allows. Showing that the proof is indisputable requires that we examine it within the context of a field of logical discourse—deductively formulated theory—familiar for the most part only to philosophers of science, deductivist logicians, and genuine scientists such as mathematical physicists. My editor, Jackie Yellin, and I worked hard to make the technical document as understandable as possible. We've done this so that physicians, medical researchers, and inquisitive patients can see that the premises of my argument are true, that the argument itself is valid, and that the overall proof is, indeed, incontestable.

Here, however, I simply present the line of evidence—evidence that most fibromyalgia researchers have entirely ignored. And because they've ignored the evidence, they've failed to understand the nature of and the solutions to fibromyalgia. I trust that most patients and doctors who open-mindedly look at the evidence will clearly see a tragic historical fact: other fibromyalgia researchers, through their studies over forty years, have unwittingly unearthed the holy grail of fibromyalgia; yet throughout those forty years, they've uniformly failed to realize what they found. They've failed to recognize what the evidence compels open-minded individuals to understand - that the problem of fibromyalgia is solved.

Line of Evidence
The evidence that too little thyroid hormone regulation is the main cause of fibromyalgia falls into four categories. These are: (1) symptoms, (2) studies of thyroid test results, (3) objectively verified abnormalities among patients, and (4) of most importance to patients, clinical trials with thyroid hormone therapy.

Symptoms. Fibromyalgia patients' symptoms are exactly the same as those of patients who have hypothyroidism and the "peripheral" form of thyroid hormone resistance. Many medical writers have reported this, as the following list of references shows.[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17]

Table 1 lists the symptoms that fibromyalgia researchers call "associated symptoms" of fibromyalgia. These symptoms, of course, are classic symptoms of hypothyroidism and peripheral thyroid hormone resistance.

Table 1. Typical symptoms of fibromyalgia patients.

Widespread pain

Cold intolerance

Abnormal tenderness

Bowel disturbance

Chronic fatigue

Exercise intolerance

Stiffness

Sleep disturbance

Depression

Numbness/tingling

Poor memory & concentration

Dry skin, hair, & mucous membranes

Anxiety

Headaches

 

Studies of Thyroid Test Results. A large percentage of fibromyalgia patients have high anti-thyroid antibodies.[18][19] A significant percentage of female patients with high anti-thyroid antibodies but "normal" TSH and thyroid hormone levels have chronic, widespread pain that is often diagnosed as "fibromyalgia."[15] Fibromyalgia patients as a group also have a high incidence of thyroid function test results showing "primary" and "central" hypothyroidism.[20][21][22][23][24][25][26]
In primary hypothyroidism, a thyroid hormone deficiency results from failure of the thyroid gland to produce enough thyroid hormone. In central hypothyroidism, the patient's thyroid gland produces too little thyroid hormone for another reason: one of the two structures in the brain that regulate the thyroid gland (either the hypothalamus or the pituitary) is malfunctioning. As a result, the thyroid gland doesn't produce an optimal amount of thyroid hormone.

The incidence of primary hypothyroidism in the general population is 1%-to-5%.[27][28] Among fibromyalgia patients, the reported incidence is 10%-to-24%.[20][23][24][29][32] The estimated incidence of central hypothyroidism among fibromyalgia patients (44%[21]) is some 250,000 times that in the general population.

Objectively Verified Abnormalities Among Fibromyalgia Patients. Theories about the cause of fibromyalgia abound. However, only a few have any backing by credible scientific evidence. Of the theories supported by some plausible evidence, none (except the inadequate thyroid hormone regulation theory) account for more than a few of the objectively verified abnormalities of fibromyalgia patients.

In stark contrast, our theory—that too little thyroid hormone regulation is the main cause—credibly accounts for at least 40 objective abnormalities of fibromyalgia patients. As I documented in 'The Metabolic Treatment of Fibromyalgia', studies show that these same abnormalities occur in both hypothyroidism and peripheral thyroid hormone resistance.[1]

Table 2. Lower Resting Metabolic Rates

Study
Number

Patients’ Average Resting Metabolic Rate*

Controls’ Average Resting Metabolic Rate*

1

28.81% below normal

7.98% below normal

2

29.68% below normal

7.98% below normal

* Averaged from different methods of calculation.

 

Table 3. Lower Basal Body Temperatures

Study
Number

Patients’ Average Basal Body Temperature

Controls’ Average Basal Body Temperature

1

96.95°F

97.54°F

2

96.38°F

97.54°F

 

Table 4 lists the 40 abnormalities found in fibromyalgia. The table is important because the cited studies show that each abnormality also occurs in hypothyroidism, peripheral thyroid hormone resistance, or both.

Could the 40 abnormalities occur in all three disorders if the disorders didn't have the same underlying cause? Possibly. But it's not likely. It's especially unlikely considering our recent findings that women with fibromyalgia had low resting metabolic rates and low basal body temperatures. These two objective abnormalities are highly characteristic of too little thyroid hormone regulation. Of most importance, in the two studies, we ruled out any likely cause of patients' low resting metabolic rates other than inadequate thyroid hormone regulation.

I've included those two study findings in Table 2 and Table 3. The findings—typically caused by too little thyroid hormone regulation—are the last pieces of the puzzle of fibromyalgia. They illuminate, objectively, the full picture of the disorder; we can now see clearly and completely that the major cause of fibromyalgia is inadequate thyroid hormone regulation.

Low Resting Metabolic Rates of Fibromyalgia Patients (Table 2). In the first study, patients' average resting metabolic rate was 29% below normal. The healthy women's metabolic rates were only 8% below normal. (We consider a "reasonable reference range" for resting metabolic rates to be 10% below the predicted average.)

In the second study, the average resting metabolic rate for patients was 30% below normal. The average metabolic rate of healthy women was, again, 8% below normal.

Low Basal Body Temperature of Fibromyalgia Patients (Table 3). In the first study, patients' average basal temperature was 96.95 F. The average for healthy women was 97.54 F. In the second study, the average temperature of patients was 96.38 F. The average for healthy controls was 97.54 F. Statistically, the patients' temperatures in both studies were significantly lower than those of controls.

Why are these results so important? Because they show that the differences between patients and controls were highly statistically significant for both temperatures and resting metabolic rates. The bottom line is that compared to matched healthy controls, women with fibromyalgia had significantly lower resting metabolic rates and basal body temperatures—objective findings entirely consistent with too little thyroid hormone regulation.

Clinical Trials with Thyroid Hormone Therapy. Most fibromyalgia patients and their cooperative doctors want to know mainly one thing: Do we have an effective treatment? The answer is yes, although most fibromyalgia researchers have totally ignored the studies that show what the effective treatment is.

Patients have recovered from their fibromyalgia symptoms in two types of studies: open [172][173][174][175][176] and blinded [177][178][179][180][181] clinical trials. All these trials have included the use of thyroid hormone therapies other than T4-replacement.

In addition, a follow-up study showed the long-term effectiveness of treatment with thyroid hormone therapy other than T4-replacement. In that study, I evaluated patients 1-to-5 years after they had undergone treatment with thyroid hormone therapy other than T4-replacement. I compared these patients to matched controls—patients I had evaluated earlier but who did not undergo treatment. Compared to these matched controls, the treated patients had significantly improved. Morever, their improvement lasted for 1-to-5 years, depending on the time of follow-up since they began treatment.[182]

Summary. Is too little thyroid hormone regulation the main cause of fibromyalgia? The answer is a resounding yes! That the proof for this conclusion is irrefutable is clear only through one course of action—examining the evidence for the conclusion through the logic of science's most advanced state of inquiry, deductively formulated theory. Nonetheless, the line of evidence I've given here should make the reasonable conclusion crystal clear: the medical problem of fibromyalgia is solved.

This conclusion, however, despite its granite-hard logical and scientific grounding, is—as are all scientific conclusions—a conjecture. And as a devout critical rationalist, I welcome any well-thought-out challenges to the conjecture.

(For references, please see the paper in Thyroid Science that I've based this article on.)

Table 4. Same objectively verified abnormalities in fibromyalgia (FM) as compared to hypothyroidism (HO) or peripheral resistance to thyroid hormone (PRTH). (Numbers under "FM" and "HO or PRTH" refer to publications referenced in the published paper, A, cited below.)

Table 4. Same objectively verified abnormalities in fibromyalgia (FM) as compared to hypothyroidism (HO) or peripheral resistance to thyroid hormone (PRTH). (Numbers under "FM" and "HO or PRTH" refer to publications referenced in the published paper, A, cited below.)

ABNORMALITIES
FM
HO or PRTH
Histological
^ Hyaluronic acid 34,35 36
^ Ground substance proteoglycans 11,12,37-39 40-43
v Collagen  44,45 46,47
v Pyridinoline 48,49 50,51
v Procollagen III 52-54 36,55,56

v Hydroxyproline

44,45,48,49
47,50,57,58
^ Mast cells 37,38,59 46,60-64
Cerebrospinal fluid
^ Substance P 65-68 69-72
v Dopamine (homovanillic acid) 73 74,75
v Tissue norepinephrine 73 76-78
v Urinary 5-hydroxyindole acetic acid 79 80
v Brain 5-hydroxytryptophan 73,81 82
^ Nerve growth factor 83 84,85
Molecular
^ α-Adrenoceptors 86,87 88-95
Mitochondrial
Ragged red fibers 96,97 98,99
v Cytochrome-c-oxidase 100 98,99
Physiological
v Basal body temperature A,B (see below) 225,226,242,243
v Resting metabolic rate A,B (see below) 57,183,184
Exercise intolerance 101-104 105-108
v Muscle relaxation time 109 110
Blunted cortisol response to ACTH 111,112 113
Orthostatic hypotension 114,115 116
Joint hypermobility 117,118 119
v Brain blood flow 120-122 123
v Peripheral blood flow 124-126 127
Blunted sympathetic and end-organ response to stress 101,115,128-131 132-135
Excess urination 136,137 138,139
v Delta-wave and nonrestorative sleep 140,141 138,142-144
High-energy phosphates
v Adenosine triphosphate (ATP) 145 146-149
^ Phosphodiesters 150-152 153
^ Inorganic phosphate (Pi) 151 153,154
v Phosphocreatine (PCr) 145 146
v PCr/Pi ratio 145 154,155
Carbohydrate metabolism
^ Pyruvate 156-158 105,156,159
v Lactic dehydrogenase (LDH) 150,156 150,156
v Intracellular pH 150 153,154
v Skeletal muscle glucose use 160 161-163
Endocrine
v HPA axis function 131,164 165,166
v GH and IGF-1 167-169 170,171
^ Hypothyroidism 20-26 N/A


A. Lowe, J.C., Honeyman, G., and Yellin, J.: Lower resting metabolic rate and basal body temperature of fibromyalgia patients compared to matched healthy controls. Thyroid Science, 1:T1-T18, 2006.
B. Lowe, J.C., Yellin, J., and Honeyman-Lowe, G.: Female fibromyalgia patients: lower resting metabolic rates than matched healthy controls. Medical Science Monitor, 12(8):CR1-CR8, 2006.