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The Metabolic Treatment Your
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The scientific evidence available today makes it possible for clinicians to provide more effective patient care overall than they generally do. A major reason for clinicians’ less-than-possible performance is obvious upon critical scrutiny. Clinicians’ treatment decisions are based largely on their beliefs about causative mechanisms. Many of these beliefs are false, however, because those who create and promote them have misled themselves through poor scholarship, logical faults, and factual errors. This triple-flawed foundation is the source of a false belief recently espoused by Drs. Michael Schneider and David Brady (the authors). Their belief is that patients will benefit from clinicians reclassifying fibromyalgia into "true" and "pseudo" forms and providing treatment based on the reclassification. But the authors’ proposal, and their rebuttal to my critique of it, contain a violation of a basic rule of scholarship, logical fallacies, and factual errors. Founded on these flaws, their proposal only echoes outmoded concepts of the failed rheumatology paradigm of fibromyalgia. The proposal is thus irrelevant to our current, advanced understanding of fibromyalgia. The proposal does not further our understanding of fibromyalgia, nor is it likely to benefit fibromyalgia patients. Any of us who propose and promote causative mechanisms can avoid the mistakes Drs. Schneider and Brady committed. We can do so by tenaciously abiding by high standards of scholarship, painstaking use of correct logic, and scrupulous precision in reporting facts. And when we fail at these requirements for quality intellectual work, the hope is that readers will detect the failure and thereby avoid unwittingly absorbing the resulting false beliefs into their frames of reference. Violation of a Rule of Scholarship Neglect of Pertinent Evidence. As I wrote in my critique[1] of the authors’ proposal, a substantial body of credible thyroid research argues against their belief that a "true" form of fibromyalgia can be distinguished from a "pseudo" form. By misrepresenting most of this research as "anecdotal success stories," "case reports," and "nonpeer-reviewed,"[2][3] the authors dismissed it as irrelevant. In that their proposal fails to account for this crucial research, their reclassification scheme is incomplete and unimportant as a scientific hypothesis.[16] Why the authors brushed aside my research team’s work puzzles me. In an e-mail to Dr. Schneider before the Brady/Schneider proposal was published, I informed him of the relevance of our scientific work. I wrote to him (edited slightly for brevity): "We have a scrupulously documented full and lasting recovery rate [from fibromyalgia] of 85%. No other theorist I've communicated with or read has documentation that his hypothesis meets the most important criterion of being accurate—providing patients with full and long-term recovery. No research group other than mine has this form of documentation. We are the only group, for example, that has done a 1-to-5 year follow-up study and found that patients who underwent our treatment continued to be statistically and clinically better off than untreated matched controls." [25] To directly quote Dr. Schneider’s private reply to me would be a violation of noblesse oblige. It is relevant, however, that he acknowledged[24] previously reading an article by Dr. Gina Honeyman-Lowe and me[27] that summarizes results of our controlled clinical trials. He also has a copy of my textbook[4] that contains reprints of all our research reports. Despite this, he and Dr. Brady neglected our research in their proposal in JMPT.3 After I brought the neglect to their attention in my critique of their proposal,1 they repeated their error in their rebuttal.2Despite the authors’ misrepresentation, our published reports are far from anecdotal. Even our open trials were rigorously systematic, [32][33][34][35][36] and only those naive about research methodology and the nature of objective data would label them anecdotal. Three of our studies were double-blind, placebo-controlled,[29][30][31] and two were conducted in conjunction with researchers at Baylor University Medical School and the University of Texas Health Science Center, respectively.[29][30] Despite Schneider and Brady’s implications to the contrary, these papers were published in a peer-reviewed, indexed journal. The same is true of our 1-to-5 year follow-up study.[36] Our paper on fibromyalgia and mutations in the c-erbA-ß gene (that codes for the beta thyroid hormone receptor) was published in the world’s most respected peer-reviewed, indexed journal on theoretical medical science.[37] And our logical analysis of the available evidence arguing for a 90% incidence of thyroid disease among fibromyalgia patients was peer-reviewed by two French thyroidologists and France’s foremost rheumatology fibromyalgia researcher, Prof. J.B. Eisinger. The paper was further critiqued by scientists in separate meetings in Grenoble and Toulon, France,[38] and was published in France’s major peer-reviewed, indexed rheumatology journal devoted to fibromyalgia.[39]Why, then, would Schneider and Brady persist in misrepresenting our scientific work as "anecdotal success stories," "case reports," and "nonpeer-reviewed," [2][3]—despite my having duly informed Dr. Schneider of the pertinence of our work to their proposal? I can only speculate, and doing so provides a plausible explanation for the failure of their proposal to be of any value in the field of fibromyalgia.Logical Fallacies Committed by the Authors In committing this fallacy, as did Schneider and Brady, one ignores or neglects—usually inadvertently—evidence that would support an opposing belief and undermine his own. Hurley wrote, "The fallacy consists of passing off what are at best half-truths as if they were the whole truth, thus making what is actually a defective argument appear to be good." [12] "As might be expected," wrote Kahane, "politicians frequently try to get us to commit the fallacy of suppressed evidence by furnishing only the evidence that favors the positions they champion, neglecting the unfavorable." He also wrote, "Lawyers refer to this kind of concealment of relevant evidence as a material omission." "It is important," he concluded, "that we learn how to bring relevant evidence to bear on an argument, how not to suppress evidence in our own reasoning, and how not to be taken in by others when they suppress evidence."[14]Kahane gave an illustration of the use of this fallacy that is relevant to the logical faults committed by Schneider and Brady. He noted that a trial attorney will often use innuendo to try to discredit an opposing witness’s testimony. In doing so, the attorney uses verbal ploys to misrepresent the testimony as having little importance when in fact it is quite damaging to his client’s case. [14] (Italics mine.) Schneider and Brady used this approach when they brushed aside our research as "anecdotal success stories," "case reports," and "nonpeer-reviewed,"[2][3] I trust, however, that they used the approach thoughtlessly as an instinctive defense of their proposal.I cannot overemphasize the importance of the authors neglecting our published work in the formulation and defense of their proposal. Only by failing to duly account for the study results of researchers in Italy, France, England, Germany, and the United States, and my group, can they confidently propound their proposal—that there exists a "true" form of fibromyalgia, and all other cases with overlapping symptoms and signs are "pseudo" fibromyalgia. Two points deserve emphasis. First, the overwhelming evidence indicates that inadequate thyroid hormone regulation is the main mechanism of all symptoms and virtually all objective abnormalities in fibromyalgia; no other hypothesis comes even close to this hypothesis/data fit. Second, inadequate thyroid hormone regulation plausibly accounts for all the evidence upon which other theorists base their competitive causative hypotheses of fibromyalgia. Most significantly for our purposes here, this is true of the central nervous system abnormality hypothesis that, according to the authors’ fallacious thinking, argues for a "true" form of fibromyalgia (see below: "Factual Errors"). These two points make the thyroid hypothesis of the cause of fibromyalgia far preferable to any other scientific hypothesis. [15] That this hypothesis—ignored by the authors—is tentatively the victorious competitor in the field renders it unlikely that the authors’ proposal is relevant to the study and treatment of fibromyalgia.Availability of Neglected Evidence. I wrote above that the evidence the authors grossly neglected is well-known in the fibromyalgia field. Let me clarify what I mean by this. They wrote, "Dr. Lowe believes that he cures virtually all patients diagnosed with fibromyalgia by administering T3 thyroid replacement." (This statement is patently false; some 60% of our fibromyalgia patients use desiccated thyroid and not T3 alone.) After making this statement, they used another logical fallacy, appeal to authority. They wrote, "Are we supposed to accept this as fact when the major researchers in the field have certainly not arrived at this conclusion?" (Italics mine.) I do not suppose I have to explain to most readers the foolishness in suggesting that we reject a scientific hypothesis because "major researchers" do not agree with it. And even if most major authorities in the fibromyalgia field did not agree with our hypothesis, rejecting it because of this majority opinion would itself be a logical fallacy. As science philosopher David Miller wrote, "Consensus is not correctness." [28] There is, however, no consensus of disagreement against our thyroid hypothesis of fibromyalgia.Buried within the authors’ appeal to authority—that "major researchers" do not agree with our thyroid hypothesis—is an implication: that our study results are arcane and my research team is of such minor importance in the field that few, other than ourselves, are aware of our work. Minimal open-eyed inquiry shows this to be false. A criterion of a research team’s success in its scientific field is explained by Candace Pert, Ph.D., discoverer of opiate receptors. She wrote that the criterion is the number of times publications cite the team’s work and the importance of the citing publications. [40] My colleagues and I have given up trying to keep track of the number of published papers and articles that cite or describe our scientific and clinical work. The number of books that do so are easier to track.At this time, the authors of at least fourteen published or forthcoming books have cited our work or devoted entire chapters to it. [6][7][9][10][11][18][26][41][42][43][44][45][46][49] Most of the books are widely considered important, especially the famous Travell and Simons’ Trigger Point Manual,[18] Simons and Menses’ Muscle Pain,[10] Pizzorno and Murray’s Textbook of Natural Medicine,[41] and Chaitow’s Fibromyalgia Syndrome.[6] Other less academic books that devote sections or chapters to our work were written by best selling authors, including Mary Shomon,[42][43] Devin Starlanyl, MD,[44][45] Jim Scheer and Steven Langer, MD,[46] Leon Chaitow, ND, DO,[7] Jacob Teitelbaum, MD,[26] and Ridha Arem, MD.[11] Regardless of whether Schneider and Brady consider our treatment team among "major researchers" in the field, the prominent authors of these books consider our work of major importance. Obviously, no consensus exists against our view of fibromyalgia.Further evidence of the impact of our scientific work in the fibromyalgia field is that other researchers, inspired by our findings, have begun conducting fibromyalgia studies as offshoots of our work. [8][21][47]48[] The research activities of these other investigators are the makings of an emerging new fibromyalgia paradigm of which our work is the scientific foundation.For me to have to bring all this to the authors’ attention is more evidence of their failure to properly apprize themselves of the current state of the fibromyalgia field and what research is impacting it. Their proposal, formulated without consideration of this information, is therefore irrelevant to the field. Factual Errors The authors defined "true" fibromyalgia as widespread pain and tenderness in patients who have a "dysfunction of the descending anti-nociceptive system, such that sensory stimuli that are normally not painful are perceived at the cortical level as being ‘painful.’"[3] They followed this true statement with a false one in the next paragraph: "This data [sic] clearly indicates some type of central or systemic process is at the root cause of this condition of abnormal pain perception that has been called primary fibromyalgia when no other medical condition can explain the situation."[3] (Italics mine.) This last sentence of theirs contains a factual error. The error is based on their neglect of the pertinent evidence of the relation of thyroid hormone regulation to pain. My coauthors and I have explained the relationship in several publications.[4] The research literature is clear that one disorder can plausibly "explain the situation."[3] Too little thyroid hormone regulation of three types of central nervous system nerve cells can account for all the biochemical abnormalities in fibromyalgia that appear to mediate widespread pain and tenderness. Measurements of metabolites in the cerebrospinal fluid of fibromyalgia patients indicate that the fluid contains high levels of substance P and low levels of norepinephrine. Thyroid hormone regulates the levels of both of these substances in the central nervous system. In hypothyroid patients, substance P levels in the cerebrospinal fluid enormously increase,[4] just as they do in fibromyalgia patients. The increased substance P can markedly augment peripheral sensory input to the central nervous system, rendering normally non-painful nerve signals painful. Also in hypothyroid patients, norepinephrine production markedly decreases.[4] Decreased norepinephrine secretion by descending inhibitory neurons can reduce opioid secretion by dorsal horn interneurons. Reduced opioid secretion increases the entry of sensory signals from primary sensory fibers into the dorsal horns. This increase in sensory input can combine with the signal-facilitating effects of substance P and heighten perception of pain.[4] Correction of the high substance P and low norepinephrine by thyroid hormone therapy probably explains the complete pain relief experienced by our fibromyalgia patients[29][30][31][32][33][34][35] and continuation of that relief for at least 1-to-5 years.[36] The authors wrote, "It has been shown conclusively in the FMS [fibromyalgia} literature that classic FMS patients have profound alterations in the amounts of serotonin (decreased) . . . circulating within the cerebrospinal fluid (CSF)." [3] This statement is false; two studies have failed to find low serotonin levels in the cerebrospinal fluid of fibromyalgia patients.[5][17] The failure to find low cerebrospinal fluid serotonin levels has contributed to the demise of the serotonin deficiency hypothesis of fibromyalgia.[4] Here again, the failure of the authors to study the relevant literature has resulted in their making another factual error.Serotonin levels in peripheral blood platelets were low in fibromyalgia patients. [19][20] The low level is possibly explained by too little thyroid hormone regulation of the ß-adrenergic receptor gene, resulting in a low density of the receptors on fibromyalgia patients’ platelets. The low ß-adrenergic receptor density may favor the release of serotonin from platelets, lowering the platelet concentration.[22][23]Conclusion References 1. Lowe J. The Brady/Schneider proposal: a misdirected reclassification
of fibromyalgia. Dyn. Chir., 2002;20(4):12,14,25,26,27. |
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