Addendum 1
Fibromyalgia

We can’t doubt what Dr. Guttler believes about the relationship of fibromyalgia symptoms to thyroid disease; he’s hurled judgment down to us in the style of a sovereign’s edict: About fibromyalgia, he wrote, "There is no relationship between that entity and Hypothyroidism. End of story."[7] (Italics mine.)

Many researchers have noted that fibromyalgia symptoms are virtually identical to those of hypothyroidism.[56][57][58][59][60][61][62][63][64][65][66][67][68] Indeed, as my collaborator Jackie Yellin, has shown, the most well-documented features of fibromyalgia are exactly the same as features of hypothyroidism (see Table 1).

Studies by several research teams indicate that 90% of fibromyalgia patients have underlying thyroid diseases.[69][70] Studies by researchers in the U.S., France, Germany, and Italy show that these thyroid diseases include primary and central hypothyroidism and cellular resistance to thyroid hormone.[57][71][73][74][75][76][78] It’s important to note, however, that most patients’ fibromyalgia symptoms caused by thyroid disease are compounded by other metabolism-impeding factors. The most common factors are poor diet, nutritional deficiencies, poor physical fitness, and metabolism-impairing drugs.[25]

When fibromyalgia patients receive effective treatment for hypothyroidism or thyroid hormone resistance, most are fully and lastingly freed from their fibromyalgia symptoms. Several open but systematic trials and several blinded studies have shown that metabolic treatment including thyroid hormone completely relieves most patients’ symptoms.[16][72][77][79][80][81][82][83] In another double-blind crossover study, researchers reported a positive therapeutic effect on fibromyalgia from transdermal T3.[14] In a randomized double-blind, placebo-controlled study, clinicians used multiple therapies.[13] In that study, as Peter Warmingham noted in an article titled "Fibromyalgia has been solved,"[12] 90% of the fibromyalgia patients used thyroid hormone and 90% improved. These are the only studies in which patients have largely or fully recovered from fibromyalgia symptoms.

If Dr. Guttler doubts the relationship between fibromyalgia symptoms and too little thyroid hormone regulation, he should read three studies by our research team at the Fibromyalgia Research Foundation.[81][82][83] These were double-blind, placebo-controlled, crossover studies. In them, we tested the effects of T3 and placebos on fibromyalgia symptoms. We repeatedly turned the patients’ symptoms off and on by switching them from T3 to placebos, much like turning the flow of water off and on by switching a faucet handle one way and then the other.

We conducted another study that showed that thyroid hormone’s effectiveness at relieving fibromyalgia symptoms isn’t a placebo effect.[15] This study was the first to show long-term effectiveness of a fibromyalgia treatment. The study was a 1-to-5-year follow-up comparing untreated patients to patients treated with metabolic therapy including thyroid hormone. We matched 20 fibromyalgia patients who hadn’t undergone treatment, with 20 fibromyalgia patients who had. We matched them by sex, thyroid status, and the time since their first evaluation.

In addition to these studies, a huge body of evidence points to too little thyroid hormone regulation as the main underlying cause of fibromyalgia. For example, compared to other people, the fibromyalgia patient has an extremely high level of substance P in her spinal cord.[84] Substance P is a chemical that amplifies perception of pain.[85][86][87][88] It amplifies pain perception so much that the patient perceives as painful something that ordinarily is not, such as the pressure of a mattress on her back and buttocks.

Thyroid hormone inhibits the production of substance P in the spinal cord.[89][90] When researchers make animals hypothyroid, substance P production is no longer inhibited; the level then rises steeply in the animals’ spinal cords. The high level magnifies the animals’ perception of pain, and like fibromyalgia patients, the animals perceive as painful something that ordinarily is not,[85][86] such as a light squeeze of a rat’s tail. In humans, the increased pain perception is experienced as chronic widespread aches and pains.[91] Such aches and pains, of course, are the main symptoms fibromyalgia.

In our three blinded studies I mention above,[81][82][83] fibromyalgia patients’ pain dramatically decreased or stopped altogether when they took T3. In placebo phases, their pain returned. We assume that the thyroid hormone reduced or stopped our patients’ pain by lowering their substance P levels.

Studies indicate that fibromyalgia patients have the opposite ratio of receptors: (1) an increased density of alpha2-drenergic receptors,[6] and probably (2) a decreased density of beta-adrenergic receptors.[4] These changes slow the patients’ metabolism. When researchers treated fibromyalgia patients with a drug (salbutamol) that stimulates beta-adrenergic receptors, their symptoms markedly improved.[4] This evidence points directly to too little thyroid hormone regulation as the main underlying mechanism of fibromyalgia.

I could continue citing such evidence for hundreds of pages. I’ve already done that, however, in a 1260-page book titled The Metabolic Treatment of Fibromyalgia. I cited thousands of studies in the book that point directly to inadequate thyroid hormone regulation as the main underlying cause of fibromyalgia symptoms.[25]

Foremost among these irrelevant and incredible views of fibromyalgia is Dr. Guttler’s, expressed as a dictator’s decree—"There is no relationship between that entity [fibromyalgia] and Hypothyroidism. End of story."[7] (Italics mine.)

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Addendum 2
Blind Faith That Laboratory Thyroid Tests Are Infallible

I’ve extensively studied the scientific literature on thyroid function testing and consulted with many laboratory medicine specialists who are the ultimate experts on the tests. I’ve also written comprehensively on the merits and demerits of the tests.[25] And I’ve undoubtedly ordered and interpreted them for as many patients as Dr. Guttler has. Based on that cumulative experience, I’m convinced that reliably accurate clinical decisions cannot be made solely on the basis of thyroid function test results. I consider clinical decisions of doctors who rely exclusively on the tests to be dubious at best and harmful to many patients at worst.

Dr. Guttler argues that his beliefs about the T4 and TSH tests are scientifically-based. For example, he wrote to Mary Shomon, "Your motto should be We’re patients.... not lab values, we want our doctors to ignore 50 years of research, and treat us like they did in the 1940’s, when therapy was based on symptoms, not facts."[3] Although he suggests that science is the basis of his beliefs, his dogmatic assertions implying that thyroid function tests are infallible are more like evangelism.

In 1997, researchers reported that when they measured patients’ TSH levels week-to-week, the levels did not significantly correlate. The correlation is reported as an "r" value. 1.00 is a perfect correlation, and 0.00 is no correlation whatever. The r value for week-to-week TSH levels was a mere 0.17—just a teensy bit (17%) above no correlation at all. The r value was not statistically significant. This means that the very weak positive correlation week-to-week could have been due merely to chance similarities in the TSH levels, and there may actually have been no correlation at all.[38] Another way of looking at this is that patients’ TSH levels significantly differed week-to-week.

A Japanese researcher studied variations in TSH levels in normal and depressed men and women. He reported, "A large intra-individual variation [variations in the same person] of serum TSH levels determined on different days was found equally in both men and women." He also reported, "The present study demonstrated a large variation of TSH levels in various conditions, even in the same individuals . . . ."[42]

Still other researchers, Weete and colleagues, reported significant variations in the levels of the free T4 and TSH in normal men—levels Dr. Guttler assumes to be impeccably consistent. Variations in the levels of the hormones, however, are of great enough magnitude to lead to misdiagnoses of patients’ thyroid status. The researchers reported that from day to night, men’s TSH levels increased an average of 140%. Their free T4 levels increased by 7%. The researchers also took blood samples every five minutes in a six-to-seven hour period starting between 7 pm and 10 pm. On average, the free T4 level varied by 11%, the free T3 by 15%, and the TSH by 13%. The researchers reported that "a significant regular variation" in the levels of the hormones occurred every 30 minutes.[39]

Aside from natural variations in TSH levels, the levels may vary according to other factors, such as lost sleep or absorption of thyroid hormone into the blood. When normal women were partially deprived of sleep, their TSH concentrations increased significantly. The levels remained high through the following day.[40] Sleep deprivation is so common nowadays that it’s likely that many patients’ TSH levels are tested the day following a night of insufficient sleep. This study suggests that their TSH levels may be higher than they would be following a night of enough sleep. This variation in TSH levels could easily lead doctors to misdiagnoses[25] if they aren’t cognizant of the effect of too little sleep and inquire about it when they test a patient’s TSH level.

After a patient takes a dose of T4, her free T4 level remains elevated for some 9 hours. In patients taking T4-replacement, the T4 level was increased an average of 13%. The TSH level in these patients was decreased by 19%.[41] Obviously, if a patient’s blood is drawn during this 9-hour time, the decision her doctor makes about a dosage adjustment may be quite different from the one he would make if her blood is drawn after the 9-hour period.

Based on this finding, the following scenario is highly likely to occur in the clinic of an endocrinologist. Like a quasi-accountant, this endocrinologist bases his decisions strictly by the numbers—by the patient’s lab test levels.[25]

Contrast the above outcome with the following likely result had the man come in thirty minutes later. The endocrinologist measures the man’s TSH and free T4 levels. As the Weete study found,[39] the TSH may vary 13% every half-hour. In line with this, thirty minutes later the man’s TSH level is 13% less than in the first scenario; it is down from 3.05 to 2.65.

The endocrinologist also measures the man’s free T4 level. Recall that Weete found that men’s free T4 levels varied 11% in thirty-minutes.[39] The man’s level now—thirty minutes later than in the first scenario—is up by 11%; it’s no longer 59.0, but 64.9. Based on these TSH and free T4 levels, the technocratic doctor tells the man that he’s definitely not hypothyroid and that his symptoms must be caused by some other disorder. For the man’s depression, the endocrinologist recommends a psychiatrist; for his fatigue, more sleep; and for his weight gain, more exercise.

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Introduction | Full Paper | Addenda | Errors in Quotations from Dr. Guttler
Clarifications | Selected Response Letters | pdf format