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Dr. Lowe How to Prepare Patient-to-Patient Fibromyalgia Research Foundation
The Metabolic Treatment
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In the April 2002 issue of the American Journal of Pain Management, Dr. Hal Blatman[1] applauded Dr. Jacob Teitelbaum’s recent randomized, double-blind, placebo-controlled study of the metabolic treatment of fibromyalgia.[2] Dr. Blatman wrote that the study confirms what years of clinical experience have shown—that comprehensive metabolic treatment of fibromyalgia can be successful. He stated that this shows that fibromyalgia is a highly treatment-responsive disorder. We enthusiastically echo Dr. Blatman’s praise of the Teitelbaum study, which is important for several reasons. First, with its results, Dr. Teitelbaum joins the chorus long sung by Professor J.B. Eisinger and coworkers[3] and Lowe and colleagues[4][5][6][7][8][9][10][11][12]—that (1) fibromyalgia is a set of symptoms and signs underlain by impaired metabolism, and (2) patients improve or recover only with metabolic treatment that corrects the impaired metabolism. As Lowe detailed in The Metabolic Treatment of Fibromyalgia[9] and Your Guide to Metabolic Health,[12] and Teitelbaum’s study[2] confirms, appropriate metabolic treatment integrates several metabolism-normalizing approaches: diet modification, nutritional supplementation, exercise to tolerance, the non-conventional use of sex and adrenal hormones when appropriate, and especially non-conventional thyroid hormone therapy. All involved researchers—Eisinger, Lowe, and Teitelbaum—concur that the integration of a variety of metabolism-normalizing treatments is essential. In his praise of the Teitelbaum study, Dr. Blatman highlighted an extremely important aspect of the treatment used in the study. "It is exciting," Dr. Blatman wrote, "that this research helps to usher in a new, more effective era in medical care by treating the patient and not only the laboratory tests."[1] (Italics ours.) This aspect warrants emphatic repetition: the focus of the treatment was the patients’ clinical responses rather than laboratory test results. This aspect of the Teitelbaum study confirms our finding in several double-blind, placebo-controlled and case-controlled studies[4][5][6][13] and extensive clinical experience. That finding is that our fibromyalgia patients improve or recover only when we ignore their laboratory test results—especially thyroid function test results—during treatment, and base our clinical decisions on patients’ tissue responses to treatment. (By tissue responses, we refer to various indirect measures of tissue metabolic status. These include, but are not limited to, visual analog scales of symptom intensities, pain distribution as a percentage of the body areas containing pain, speed of the relaxation phase of the Achilles reflex, voltage of the QRS complex of the electrocardiogram, and objective changes in pressure/pain threshold at tender points.) Using response-driven treatment, 85% of our fibromyalgia patients fully recover and no longer meet the American College of Rheumatology (ACR) criteria for fibromyalgia. In stark contrast, when our patients’ previous doctors based their treatment decisions on the results of thyroid function tests, these same patients remained ill. This finding illuminates a common cause of the continuation of fibromyalgia patients’ suffering: under-treatment with thyroid hormone due to the conventional approach of T4 replacement therapy—that is, restricting patients to the use of T4 and adjusting the dosage to keep the TSH within the reference range. Little thought is needed to understand the potential disastrous consequences for the public health from steadfast confidence in laboratory reference ranges for hormone levels. A lesson in this regard is the recent change in the implications of the reference range for the TSH.[14][15] Thyroid Function Testing During Treatment Hypothyroidism Among Fibromyalgia Patients We want to emphasize that most (albeit not all) hypothyroid fibromyalgia patients recover only with thyroid hormone dosages that lower their TSH levels below the lower end of the currently accepted reference range. Most often, effective dosages are equivalent to or higher than the 200-to-400 µg of T4 that hypothyroid patients used without harm through most of the 20th century.[26] (Suppression of the TSH below the reference range occurs on average with the equivalent of 145-to-171 µg of T4.[27][28]) Because our patients engage in a comprehensive program of metabolic rehabilitation, they do not have symptoms of thyrotoxicosis. (See below: "Potential Adverse Effects.") We find no evidence of tissue thyrotoxicosis with bone densitometry, serial electrocardiograms, and a variety of serum and urine biochemical tests. In fact, after 1-to-10 years of TSH-suppressive dosages of thyroid hormone therapy, bone densitometry has shown that our tested patients’ have bone mineral densities higher than other individuals of the same age and sex. (In this paper, we refer to dosages of thyroid hormone that lower TSH levels below the lower end of the reference range as "TSH-suppressive" dosages. We use this term for the sake of simplicity, and we caution clinicians to understand that a low TSH level is not synonymous with thyrotoxicosis. As we explain below, multiple objective measures show that our recovered hypothyroid and thyroid hormone resistance patients with low TSH levels clearly are not thyrotoxic.[9,p.812]) Thyroid Hormone Resistance
Among Fibromyalgia Patients Despite these patients’ use of supraphysiologic dosages of T3, they do not have the syndrome of tissue overstimulation with T3 (termed "T3-thyrotoxicosis"). We determine this by the absence of symptoms of thyrotoxicosis and through patients’ normal results on bone densitometry, serial electrocardiograms, and a variety of serum and urine biochemical tests. Laboratory testing after the patients have fully recovered shows that they do not have increased clearance of T3 from their bodies; their serum free T3 levels are extremely high according to the current reference range. The absence of thyrotoxicosis, complete relief of symptoms and signs, high free T3 levels, and low TSH levels, demonstrate that the patients have partial peripheral cellular resistance to thyroid hormone.[9][29] (The designation "peripheral" means that the thyrotrophs of the patients’ anterior pituitary glands appear normally responsive to thyroid hormone.[29]) Potential Adverse Effects from Having studied the relevant scientific literature, we are astonished that endocrinologists persist in publishing and stating these warnings. They are among the best examples we can site of the extraordinarily bad science that prevails within the endocrinology specialty. Specifically, the warnings concern osteoporosis, acute adrenal crisis, and atrial fibrillation. We would like to briefly respond to each of these warnings based on our analysis of the available scientific literature and our clinical and research experience. Potential Adverse Effects on Bone. In the 1970s and 1980s, many faulty studies were published that led to the erroneous conclusion that TSH-suppressive dosages of thyroid hormone decrease bone mineral density in most patients. Some conventional endocrinologists wrongly extrapolated from these studies that TSH-suppressive dosages lead to osteoporosis and increased risk of bone fracture. Better designed studies have shown that these conclusions were wrong, and the only group of patients really at risk for substantial loss of bone density from the use of TSH-suppressive dosages are post-menopausal women who previously had Graves’ disease. Still, however, despite contrary scientific evidence, endocrinologist Daggett recently warned, "Although the evidence is not strong, there remains concern . . ."of osteoporosis. With a complete lack of evidence, he also stated, "This is particularly true of tri-iodothyronine (which is contained in ‘natural thyroid’)."[30] Among our patients who have used TSH-suppressive dosages of T3-containing preparations from 1-to-10 years, bone densitometry has shown that their density is higher than other men and women of the same age. Whybrow reported a similar finding.[31] He reported that TSH-suppressive dosages of T4 reduced the amplitude and frequency of patients’ manic and depressive episodes. Careful evaluation also showed that these patients had higher bone density than patients not treated with TSH-suppressive dosages of thyroid hormone. Inferring from a variety of studies, the most likely mechanism of the higher bone density in patients taking high-end dosages of thyroid hormone is the nutritional supplementation and exercise to tolerance we require them to engage in. It is worth emphasizing that our patients can engage in vigorous exercise because their dosages of thyroid hormone are high enough to give them sufficient motor drive and metabolic capacity. Clearly, the warnings about the bone demineralizing effects of TSH-suppressive dosages of thyroid hormone are grossly exaggerated. The finding of higher bone density among patients taking higher-end dosages of thyroid hormone suggests that under-treatment with thyroid hormone can contribute to lower bone density. The lower bone density is likely to result from patients being unable to engage in weight bearing exercise due to low motor drive and decreased metabolic capacity. Hypothyroid patients using T4 replacement dosages commonly lack the drive to engage in weight bearing exercise, indicating that replacement dosages are often tantamount to gross under-treatment. Acute Adrenal Crisis. The warnings of acute adrenal crisis among patients taking thyroid hormone are based on several published case reports. We have carefully studied these reports but have found no controlled studies of the subject. During our extensive clinical experience with patients using TSH-suppressive dosages of thyroid hormone, some of our patients developed symptoms suggesting adrenal insufficiency, especially muscle weakness. Laboratory tests confirmed that some patients had decreased adrenocortical reserve or frank cortisol deficiency. None of these patients, however, suffered the acute adrenal crises described in the case reports and that endocrinologists so often warn of.[36] In addition, many patients first consulted us when they were thyrotoxic from dosages of thyroid hormone that were excessive for them. Some of these patients had symptoms due to decreased adrenocortical reserve or cortisol deficiency, yet none suffered an acute adrenal crisis. Neither have any of these patients suffered the T4-induced "collapse" of which endocrinologist Daggett warned."[30] Daggett wrote, "If thyroxine is given to someone whose symptoms result from underactive adrenal glands, they may collapse."[30] In this warning, he appears to ignore the fact that low adrenocortical function in many patients results from under-regulation of the adrenal cortices by thyroid hormone. In such cases, the proper and most direct method of treatment is the judicious use of thyroid hormone. In that this is well established, we cannot determine whether Daggettt’s and similar warnings are merely carelessly formulated or whether they are intended to frighten rather than enlighten. From our study of the available literature and from our clinical experience, we conclude that while acute adrenal crisis is possible, it is extremely rare among patients with adrenocortical insufficiency who begin taking thyroid hormone. Clinicians must consider all patients, of course, on an individual basis. Our assessment, however, is that endocrinologists’ warnings of acute adrenal crisis are grossly exaggerated. Cardiac Effects. Today, the warning most responsible for clinicians keeping their patients’ thyroid hormone dosages ineffectively low is this: TSH-suppressive dosages of thyroid hormone cause a three-fold increase in the incidence of atrial fibrillation. This warning, as stated, is patently false, and as a study conclusion, it is invalid. The statement is false and invalid because it is not properly qualified. The studies the warning is derived from involved elderly, sedentary individuals, some of whom were bedridden in nursing homes. Moreover, the researchers did not distinguish the incidence of atrial fibrillation within subgroups of subjects based on objectively verified differences in cardiovascular status. Despite the highly probable poor cardiovascular status of the subjects in the studies, and the lack of adequate controls for differences in cardiovascular status, endocrinologists have carelessly generalized the results of the studies to all patients who have low TSH levels—without regard for age or cardiovascular status. Clearly, the results of these studies cannot rationally be extrapolated to individuals who are younger than those studied or even to elderly individuals with longstanding cardio-protective lifestyles. That this false and invalid conclusion is so often repeated is stunning, in that it clearly violates a most elementary rule of research methodology—to avoid generalizing a study result from one group of patients to other groups that distinctly differ in highly relevant respects. We screen patients at intake for cardiovascular conditions that might contraindicate the use of TSH-suppressive dosages of thyroid hormone, and we refer patients for evaluations by cardiologists if indicated. We require our patients who use TSH-suppressive dosages of thyroid hormone to (1) modify their diet so that it favors cardiovascular health, (2) take all known heart-protective nutrients, and (3) regularly engage in cardiovascular exercise to tolerance. Over the years, we have found it necessary to exclude a few patients with congenital cardiac abnormalities from our treatment program. But among other patients whom we treated and studied with serial electrocardiograms and occasional cardiology workups, none have developed arrhythmias—including atrial fibrillation—despite their use for many years of TSH-suppressive dosages of thyroid hormone. As prudence dictates, we caution clinicians not to permit sedentary patients with an atherogenic diet and poor nutrition to use TSH-suppressive dosages of thyroid hormone. With reasonable precaution, however, we have found no reason for the typical patient—who maintains a cardio-protective lifestyle—to abstain from using TSH-suppressive dosages of thyroid hormone. Hence, our extensive experience indicates that the unqualified warning that TSH-suppressive dosages of thyroid hormone cause a three-fold increase in atrial fibrillation is clearly false and invalid. Conventional endocrinologists almost uniformly ignore the potential adverse cardiovascular effects of under-treatment with thyroid hormone. However, under-treatment of hypothyroidism or thyroid hormone resistance may result in elevated cholesterol and triglycerides, coronary atherosclerosis, cardiac ischemia, and hypertension.[19][20] Some evidence indicates that higher-end thyroid hormone dosages may cause regression of the atherosclerosis of coronary arteries.[19][21] Conclusion Our clinical and research findings reveal an inimical impact of T4 replacement therapy on the population of fibromyalgia patients. Only rarely does a fibromyalgia patient improve with T4 replacement therapy. Most hypothyroid patients on T4 replacement therapy who consult us meet the ACR criteria for fibromyalgia; the symptoms of some are so severe that the patients are debilitated. Most of these patients fully recover when they abandon T4 replacement therapy and undergo comprehensive metabolic rehabilitation, including thyroid hormone therapy, as we have described it in this paper. The regularity of this finding forces us to conclude that T4 replacement therapy generally constitutes under-treatment of patients with thyroid hormone, and that specifically, this form of treatment is thus a major cause of the continued suffering of patients with a diagnosis of fibromyalgia. References
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