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When I began to write this book several years ago, I did so because I knew it was essential if most fibromyalgia patients were ever to be relieved of their suffering. I had learned through clinical experience and research that most patients’ fibromyalgia is little more than the symptoms and signs of one or both of two underlying conditions: (1) undiagnosed or undertreated hypothyroidism, and/or (2) untreated partial cellular resistance to thyroid hormone. I say "little more" because various other metabolism-impeding factors also influence most patients’ signs and symptoms. Among the other factors are poor diet and nutritional deficiencies, physical deconditioning, various medications, and imbalances of other hormones. For patients to improve or recover, the influence of these other factors must be effectively reduced or eliminated. But for most patients, the use of the proper form and dosage of exogenous thyroid hormone is also indispensable. Slowly, through trial and error, meticulous record-keeping, and data analysis, my colleagues and I evolved a treatment protocol, now called metabolic rehabilitation, that was highly effective and safe in enabling most fibromyalgia patients to markedly improve or completely recover. Later, we conducted various controlled studies which confirmed that the effects we obtained in the clinical setting were real— they were not due to misperceptions, nor were they placebo effects. I gradually learned during this odyssey, which has lasted from 1986 until the present, that the greatest obstacle to the improvement or recovery of fibromyalgia patients (and other patients with too little thyroid hormone tissue regulation) is the adherence to four false yet dogmatic beliefs by most conventional medical clinicians: 1) that the only thyroid-hormone-related cause of the symptoms characteristic of thyroid hormone deficiency is hypothyroidism, 2) that no one should be permitted to use exogenous thyroid hormone unless laboratory test results confirm hypothyroidism, 3) that hypothyroid patients should be permitted to use only T4, and 4) that the T4 dosage should be adjusted according to TSH and possibly thyroid hormone blood levels. These four beliefs are mandates of the current endocrinology paradigm. Conventional endocrinology touts them as scientifically established facts that apply to the entire human population. This, however, is simply not true. I have seen a small minority of fibromyalgia patients improve using the diagnostic and treatment protocol dictated by the mandates. But most patients improve or recover only when treated by a protocol that violates the mandates. As a result, to be effective and safe in helping fibromyalgia patients improve or recover, metabolic rehabilitation (as I describe and advocate it in this book) is by necessity a transgression against the endocrinology mandates. Over the past 30 years, most conventional clinicians have unquestioningly accepted the endocrinology mandates. They obstinately believe that the mandates are true, and they comply with them as guidelines for diagnosis and treatment. Their doing so has created a major unrecognized public health problem—incalculable thousands of patients with chronic symptoms sustained by inadequate thyroid hormone regulation of their tissues. The epidemic of inadequate tissue regulation and chronic symptoms results from these clinicians undertreating patients with thyroid hormone or denying them treatment altogether. The clinicians’ imperious belief in the truth of the mandates has led them to erroneously interpret patients’ chronic symptoms as "new diseases." Of these new diseases, fibromyalgia and chronic fatigue syndrome are the two most publicized. Most medical researchers, like most conventional clinicians, have narrow-mindedly refused to consider that the mechanism underlying these "new diseases" may be inadequate thyroid hormone regulation of patients’ tissues. Blinded by their own beliefs, they have been unable—and will remain unable!—to solve the mystery before them. They remain baffled even though, as I describe in Section III, they themselves, through their studies, have generated a substantial body of evidence that points unequivocally to the mechanism I describe in this book. My efforts to communicate with members of the rheumatology fibromyalgia research community regarding our findings have been largely ignored over the years. The notable exception is the eminent French rheumatologist and fibromyalgia researcher, Professor J. Eisinger, whose work I extensively cite throughout this book. His finding of glycolysis abnormalities in fibromyalgia patients that resemble those of hypothyroid patients was a landmark discovery. It is a finding that the serotonin deficiency hypothesis (the unifying concept of the rheumatology fibromyalgia paradigm) cannot explain. It therefore raises doubt that a serotonin deficiency could be the main underlying causative factor in fibromyalgia. Over a 20-year period, the rheumatology paradigm was fruitful. It motivated researchers to conduct hundreds of studies of fibromyalgia patients, and the studies have provided vitally important information about the disorder. Gradually, however, progressively more studies have produced anomalies—research findings that the rheumatology paradigm cannot account for. Some of the anomalies are crucial blows to the paradigm, and show that it is inadequate for understanding fibromyalgia. The accumulation of anomalies has begun to dissolve the sense of cohesion the paradigm previously provided clinicians and researchers. Consequently, some researchers and clinicians have lost confidence in the paradigm. At the same time, the anomalies, one after another, have strengthened the hypothesis that inadequate thyroid hormone regulation of tissues is the cause of most patients’ fibromyalgia. During the years of my work on this book, the accumulating anomalies and continued suffering of fibromyalgia patients have kept me aware of the importance of making the information in the book available for patients and their clinicians. Now, however, just before the book goes to press, I realize that it is not only important—it is imperative! The accumulating anomalies are conspicuous signs that the rheumatology paradigm is crumbling. But it is the potentially ominous outcome of the fall of the paradigm that concerns me. In conventional medicine, when there is no strong biologically-oriented paradigm to explain a disorder, many clinicians and researchers irrationally conclude that the symptoms of the disorder are psychogenic. This means, of course, that they come to believe, by default, that the symptoms are of mental or emotional origin. In recent years, in the field of fibromyalgia, this line of thinking has been developing into a trend. As the history of medicine teaches, this turn of events will not favor the interests of fibromyalgia patients. If the trend is not curtailed, their plight is likely to markedly worsen in years to come. What has led to this trend? My assessment is as follows. Long-term studies show that rheumatology treatments, mainly the use of antidepressants, are ineffective—they have no beneficial effect whatever on the long-term status of fibromyalgia patients. In addition, the long-term use of the medications is far from benign for some patients. For example, amitriptyline, probably the most prescribed medication for fibromyalgia, may cause coronary artery constrictions. This is an adverse effect that could devastate some fibromyalgia patients who have, as most do, extremely low cardiovascular fitness levels. But such adverse effects from medications are not the only dangers patients face. The cost of these currently prescribed medications is substantial. And so are the costs of other health care services fibromyalgia patients continue to use because they remain ill, even while taking the medications. Many patients remain so ill that they are unable to work, and as a result, a considerable percentage of them apply for and receive disability payments. The overall cost of the medications, other health care services, and disability has increased as fibromyalgia has become popularized (progressively more clinicians are diagnosing the disorder). Some members of the rheumatology research community continue to incorrectly report that amitriptyline and cyclobenzaprine are "effective" treatments for fibromyalgia. These reports influence clinicians to prescribe the medications for their newly diagnosed patients. Such patients have swollen the ranks of those using the medications on an indefinite basis and of those on the disability rosters. Hence, cumulative costs continue to escalate. It should not come as a surprise that third party payers (mainly insurance companies) have become concerned about escalating costs for fibromyalgia treatments. Third party payers, whose job it is to pay the bills, are in business. All businesses, to succeed, must effectively curb costs that threaten to endlessly rise. But when the "business" of a business is paying health-care costs, cutting those costs is crucial to making a profit. An effective tool for cost-containment is the accusation that the symptoms of the patients in question are psychogenic. There is no shortage of clinicians and researchers willing to brandish this sword against patients—and literally brand into the patients’ records labels from the Diagnostic and Statistical Manual (DSM) of the American Psychiatric Association. The DSM label transmutes the accusation of psychogenesis into a "diagnosis," although a spurious one. Probably most clinicians today earnestly believe that DSM labels are genuine diagnoses. Despite this, the labels are nothing more than descriptive terms applied to patients who have certain sets of symptoms, with no regard for the underlying biological causes. The labels are profitable to third party payers. Patients who use health care services based on the labels receive minimal third party reimbursement or none at all. The payoff from DSM labels is substantial enough to motivate third party payers to employ clinicians (usually called expert witnesses or independent medical evaluators) willing to ignore their Hippocratic or chiropractic oaths and assign these labels to patients. Thus, for third party payers, DSM labels are an effective remedy for the rising costs of the care of fibromyalgia patients. Most clinicians and researchers who use DSM labels do not do so for this strategic financial purpose, as I explain in Chapter 1.2. It is my belief that for some researchers, resorting to the use of DSM labels serves as a psychological refuge from the harsh realization that they have failed to learn the biological basis of a health problem such as fibromyalgia. After all, if fibromyalgia is psychogenic, as DSM labels imply, one cannot be responsible for failing to have found a biological cause for the condition. One can stop searching without chagrin. It is crucial that fibromyalgia patients, and the clinicians who are committed to care for them, not forget the facts about DSM labels and the putative psychogenic mechanisms they imply. No credible scientific study has ever verified a purely psychogenic cause of any disease, including fibromyalgia. There is no logical or scientific reason patients should ever receive these counterfeit "diagnoses." Fibromyalgia patients and concerned clinicians would best steadfastly refuse to accept DSM labels and take to task (based on information I provide in Chapter 1.2) any clinician who dares try to apply one. Ultimately, it is the cost concerns of third party payers that make it imperative that a truly effective treatment for fibromyalgia come into widespread use. I describe that treatment, metabolic rehabilitation, in this book. Most fibromyalgia patients who have undergone metabolic rehabilitation have markedly improved or completely recovered. My research colleagues and I have decisively demonstrated patient recovery in stringently controlled clinical trials. And we found in a 1-to-5-year follow-up study that patients maintained their improvement long term. Fibromyalgia patients who have improved or recovered with metabolic rehabilitation require either minimal or no further health care services under the diagnosis of fibromyalgia. In the clinical sections of this book, I provide clinicians and their patients with a "how to" manual of metabolic rehabilitation. This includes a precise and detailed description of the treatment protocol. I am convinced that the widespread and proper use of this treatment will halt the rising costs for the clinical care of fibromyalgia patients and end the need for most disability applications. These results will remove the main motive for branding fibromyalgia patients with DSM labels. My professional credentials are different from those of most researchers who are members of the rheumatology fibromyalgia community. On this basis, most of them (with a few notable exceptions), à la ad hominem, have dismissed the possibility that my view of fibromyalgia could possibly have merit. Quite the contrary—it is because of the differences in my educational background and clinical practice that I have been able to sidestep what Peter Duesberg called "the biggest obstacle in finding the truth"; that is, "the bias of investigators on what data to chase and how to interpret them." When Duesberg wrote, "As often in the history of science, the biggest obstacle in finding the truth is not the difficulty in obtaining data," he could have been referring to the field of fibromyalgia. A quick glance at the thousands of published papers I cite in this book will show that we have no shortage of data to interpret. My detractors may argue that most of the references are not to studies of fibromyalgia patients but to those of hypothyroid and thyroid hormone resistant patients. In retort, I conjecture that if these detractors were to scrupulously look for the differences between fibromyalgia patients and the other two groups (as I have been doing for well over a decade), they would soon discover that fundamentally, there are none. I want to emphasize the most important feature of the clinical sections of this book. As I wrote above, the clinical sections are a manual on the proper use of metabolic rehabilitation. The clinical success rate is the same when different clinicians use precisely the same protocol. Using the protocol properly will require that most clinicians change their customary mode of practice to one of a rehabilitation model, even if they do so only with their fibromyalgia patients. To vary from the protocol as I describe it, is to compromise the therapeutic outcome. The most critical component of the protocol is the feedback from objective measures of fibromyalgia status. The clinician must monitor the patient’s fibromyalgia status at close intervals using objective measures, which I describe in Chapters 4.1, 4.3, and 5.2. He must also post the scores from the measures as data points to line graphs, which we provide in Appendix A. He must base therapeutic decisions on clinical judgment integrated with the trends of the data points on the graphs. Informative feedback is currently used in conventional medicine in places such as post-surgery and critical care wards, and in the care of patients with conditions such as hypertension. Otherwise, clinical practice usually lacks the use of informative feedback. As John Gedye explains in the Foreword, however, the use of such feedback is essential to the effective control of most any phenomena in our world, including fibromyalgia. In Section IV, I describe the diagnostic protocol of metabolic rehabilitation. Chapter 4.1 includes information on diagnosing fibromyalgia and monitoring the fibromyalgia status of patients. The methods I describe in the chapter for quantifying the patient’s status are critically important. Only by using these methods precisely is the clinician likely to effectively guide the patient through the rehabilitation process. For most patients, maximum improvement—which I consider complete and lasting relief from fibromyalgia symptoms—is possible only when the methods are used properly. In Chapter 4.2, I describe and comment on the currently available laboratory tests for assessing the patient’s thyroid status. My view is that: 1) these tests are useful only for initially establishing the thyroid status of the patient who appears to have inadequate thyroid hormone regulation of cell function, 2) the tests are useless for determining the patient’s effective dosage of exogenous thyroid hormone, and 3) while some clinicians may use the tests during patients’ treatment to comply with the current "standard of care," the cost of the tests during that time cannot be justified logically or scientifically. What makes laboratory thyroid function tests useless for adjusting the thyroid hormone dosage? Simply that they do not measure what is most important in the treatment of hypothyroid and thyroid hormone resistant patients—that is, how patients’ tissues are responding to the hormone. In Chapter 4.3, I describe how to measure the responses of different tissues. Essentially, the chapter is an effort to revive a rational, safe, and highly effective clinical method of guiding patients to recovery. To the detriment of patients with inadequate thyroid hormone tissue regulation, conventional clinicians discarded this method some 30 years ago. On behalf of patient welfare, clinicians should resume use of the method. I devote Chapter 4.4 to the possible adverse effects of the patient using dosages of exogenous thyroid hormone that are excessive for her. The chapter is an overview of available studies. One of the most pertinent points of the chapter is that the possible adverse effects have been highly exaggerated. At the same time, I emphasize that the clinician must consider each patient on an individual basis. To effectively do so, he must use measures that can accurately detect adverse tissue effects. These measures do not include laboratory thyroid function tests. Instead, the measures are those that assess tissue responses to thyroid hormone, as I describe in Chapter 4.3. In Chapter 4.4, I also include a section on a tragically neglected subject: the adverse effects of too little thyroid hormone stimulation of tissues. The importance of this section is that the current practice of titrating thyroid hormone dosages by laboratory thyroid function tests typically restricts patients to dosages of thyroid hormone that are too low. The low dosages permit inadequate thyroid hormone regulation of tissues to continue apace. As a result, patients suffer from symptoms of hypometabolism, such as chronic fatigue, pain, stiffness, depression, and cognitive dysfunction. They are also at an increased risk for potentially lethal cardiovascular disease. As this section indicates, patient welfare is truly safeguarded only when clinicians have a balanced concern for excessive and deficient thyroid hormone tissue stimulation. Section V is devoted to treatment. In Chapter 5.1, I review the studies of fibromyalgia treatments. Most of the treatments are intended to control the symptoms of fibromyalgia without an appreciation of the underlying cause of those symptoms. Other treatments are intended to relieve fibromyalgia symptoms by compensating for an objective fibromyalgia abnormality, such as a low growth hormone level. Such treatments may reduce or relieve the particular features of fibromyalgia caused by that abnormality. However, the treatments do not address the underlying cause of fibromyalgia in most cases—inadequate thyroid hormone regulation of cell function. Inadequate thyroid hormone regulation can account not only for the particular abnormality such a treatment addresses, it can also account for all the other symptoms and objectively verifiable abnormalities of fibromyalgia. Thus, predictably, none of the treatments described in Chapter 5.1 (exempting metabolic rehabilitation) were effective enough to provide any noteworthy improvement in the status of the average fibromyalgia patient. Chapter 5.2 provides a detailed description of metabolic rehabilitation. Each component of the treatment protocol is included for one reason: trial and error and systematic testing have shown that the component is essential to most patients markedly improving or recovering. In Chapter 5.3, I describe and critique the mandates of the current endocrinology paradigm for deciding who might or might not benefit from the use of exogenous thyroid hormone. I contend that these mandates are false propositions that are the root cause of the "new diseases" such as fibromyalgia and chronic fatigue syndrome. I also explain why T4 alone is a poor choice for treating the hypothyroid patient, and I provide details on the therapeutic use of combinations of T4 and T3. In Chapter 5.4, I cover special considerations concerning the use of T3 alone. Chapter 5.5 addresses forms of treatment that are complementary to the use of exogenous thyroid hormone during metabolic rehabilitation. This chapter is a supplement to Chapter 5.2 (which describes the treatment protocol). In Section II, I cover the basic science foundations of clinical thyroidology. Reading the chapters in this section is not essential before the clinician begins to use metabolic rehabilitation. However, as with any other special area of clinical practice, an understanding of the basic science underpinnings will give the clinician the edge in helping patients improve or recover. The clinician is most likely to acquire that understanding as he selectively uses information from the chapters in Section II when that information is relevant to cases under his care. Learning more about the science behind clinical thyroidology can also help the clinician troubleshoot any puzzling cases. Section III is the bridge between the basic science foundations in Section II and the diagnostic and treatment protocols in Sections IV and V. In Section III, I interpret the main symptoms and objectively verified abnormalities of fibromyalgia as effects of inadequate thyroid hormone regulation of cell function. To the extent possible based on the available evidence, I describe and document plausible mechanisms by which fibromyalgia symptoms and objective findings develop from inadequate thyroid hormone tissue regulation. I suspect that most patients, clinicians, and researchers who read this book will take the most interest in this section. In some chapters, I show that it is plausible that the symptoms or objective findings are products of thyroid hormone deficiency or resistance. In most chapters, I show that this is highly probable. In the chapters in Section I, I provide details of the argument I make in this introduction: that the plight of fibromyalgia patients in the future is likely to be worse than now, unless we avert developing trends. In my view, the only way to ward off the trends is to influence patients, clinicians, and researchers to accept, based on the evidence I present, the basic thesis of this book: that hypometabolism due to inadequate tissue regulation by thyroid hormone is the cause of fibromyalgia. To justify acceptance of this thesis, an acceptance which would change the direction of fibromyalgia research and clinical care, has been my main purpose in writing this book. Only through the widespread acceptance of this thesis—scientifically-derived, scrupulously tested, and able to plausibly explain all we know about fibromyalgia—will the suffering of most fibromyalgia patients finally come to an end. McDowell
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