This website is dedicated to the millions of thyroid patients who are being ignored and left to suffer unnecessarily, and to healthcare practitioners, who want to better serve those patients.

The Linguistic Etiologies of Thyroxine-Resistant Hypothyroidism

The victims of hypothyroidism who are thyroxine resistant are not suffering because there is no treatment available the Food and Drug Administration approved and indicated them long ago. These victims are suffering because the proper treatments are proscribed by the endocrine establishment, its paradigm, and its treatment guideline. Consequently, they are rarely considered. The proper treatments are not considered because linguistic etiologies keep the medical science of exo-endocrine hypothyroidism (hypothyroidism caused by etiologies outside of the endocrine system) beyond the rationale of the practicing physician by improperly (over) including them with endo-endocrine hypothyroidism (hypothyroidism caused by etiologies within the endocrine system). The first etiology is in the title: Thyroxine-Resistant Hypothyroidism. The second is in the description: exo-endocrine hypothyroidism. The endocrine establishment would claim that both are oxymorons. But are they? That depends upon the definition of hypothyroidism. Is it thyroid-centric or symptom-oriented? This essay explores the consequences of these choices in the light of the physiology to show that the thyroid-centric is only applicable to the recognized class of endo-endocrine hypothyroidism, while the symptom-oriented definition is applicable to both endo-endocrine hypothyroidism and the unrecognized class of exo-endocrine hypothyroidism.

Patient suffering should be sufficient to demand the linguistic treatment of these etiologies. But it has not. Many respondents to a minuscule outreach effort [32] have been suffering for decades. However, since medical guidelines are used by state boards of medicine to regulate, discipline, and prosecute physicians, the notion of Overinclusion, a derivative of the Equal Protection Clause of the Fourteenth Amendment and the antithesis of Due Process, appears to be applicable and compelling. [see the definitions below]

The physiology of hypothyroidism begins within the endocrine system (the hypothalamus, the pituitary, and the thyroid) continues through the exo-endocrine peripheral metabolism sites in various organs (predominately, the liver) to the hormone receptors of the peripheral cells, where the hormones are used and the symptoms begin to be sensed. Certainly, symptoms are not produced directly by any hormone when in the serum. Since the assays are serum based, they are indirect measurements. The subsequent conclusions, then, depend upon inferences and correlations.

The history of hypothyroidism begins after the discovery of hyperthyroidism with the discovery of thyroid extract in 1891, the realization that the thyroid controlled the metabolic rate in 1895, and Hashimotos disease in 1912. The structure of thyroxine (T4) was discovered in 1926 and triiodothyronine (T3) was identified in 1952. Thus, by the time that the exo-endocrine peripheral conversion of T4 to T3 was discovered in 1970, sufficient time had passed for the hypothyroidism paradigm to form and solidify. This paradigm includes the rigid belief that there was an intimate connection between the thyroid secretion and symptoms. Thus, all hypothyroidism etiologies belong to the same class. However, the thyroid and symptoms were separated by the discoveries, in 1967 and 1970, of two intervening hormone operations, the exo-3 endocrine peripheral conversion of T4 to T3 and the identification of T3-binding receptors in tissue. Then in 1989 and 1990, mutations in the thyroid-hormone receptor accounted for increasing hormone reception resistance. [1] Thus, there are exo-endocrine etiologies for the symptoms of hypothyroidism. Unfortunately, they are substantially ignored and hypothyroidism remained singularly classed in spite of significantly different etiologies, different diagnostics, and different hormone supplements.
Multiple, Undeclared Definitions for Hypothyroidism The inevitable tension created by the peripheral conversion and subsequent exo-endocrine discoveries are reflected in the once believed similar, but now distinct definitions for hypothyroidism. The thyroid-centric definition is quite similar to the definition of hypothyroid: The clinical consequences of inadequate secretion of hormones by the thyroid. The symptom-oriented definition removes the intimate connection between the thyroid gland and symptoms: The clinical consequences of inadequate levels of thyroid hormones in the body. (Tabers Cyclopaedia Medical Dictionary) And that definition may be reasonably and should be extended to The clinical consequences of inadequate usage of thyroid hormones by the body particularly in the light of Baisier, et al., finding that a 24-hour urine diagnostic correlates best [2] or Bradys preference for the rT3 test. [3]

A fallacious attempt was made to mitigate this tension by contextually assuming the infallibility of exo-endocrine hormone operations. [4] However, not only is this somatic infallibility quite counter intuitive, but pre-dating research [5, 6] disputes this contextually alleged perfection. The tension is valid since the definitions have different associations. The thyroid-centric definition, being similar to hypothyroid, is more related to the secretion of thyroxine (T4). On the other hand, the symptom-oriented definition is more related to the availability or usage of triiodothyronine (T3) as suggested by the following quotation [7]:

T4 . . . is not the active ingredient. T3 is the active ingredient, and it’s the thing that accounts for the thyroid hormone action. As I’ve been reminded many times, there are no intracellular events that we know that can be described by T4 at the level of the nucleus. Only T3. T4 is not the active compound. Likewise, the site of action is in the nucleus. The site of action is not T4 in the plasma. Dr. E. Chester Ridgway

As a consequence of no intracellular events being directly related to thyroxine, the implications of the apparently similar definitions are significant. The thyroid-centric definition ignores the potential of exo-endocrine etiologies while the symptom-oriented definition is inclusive of both endo- and exo-endocrine etiologies. Thus, the following lament by Anthony Taft and Geoffrey Beckett [8] is, then, quite understandable:

It is extraordinary that more than 100 years since the first description of the treatment of hypothyroidism and the current availability of refined diagnostic tests, debate is continuing about its diagnosis and management.

This lament is even more understandable by the authors research of dictionary definitions of hypothyroidism. There were 29 citations for the thyroid-centric version and 22 citations of the symptom-oriented. However, to seemingly sustain the confusion, 11 of each were cited simultaneously. Confusion reigns.

Overinclusion reigns. Since the dominate endo-endocrine hormone is thyroxine (T4) and the dominate exo-endocrine hormone is triiodothyronine (T3) and since their etiologies are different, the treatment of these etiologies are different, these forms of hypothyroidism should be divided into two classes: endo-endocrine and exo-endocrine hypothyroidism. There is precedent for this concept, type 1 diabetes which suffers from the lack of insulin and type 2 which suffers from the inability to use it. This is quite similar to endo-endocrine hypothyroidism not producing sufficient thyroxine and exo-endocrine hypothyroidism not being able to use it by deficient peripheral metabolism or deficient hormone reception.

Then, this dense fog of overinclusion confusion is maintained. Inspect the only closest applicable guideline. [9] The choice of definitions for hypothyroidism is not indicated (or stipulated, see definitions), but the text implies both. The guideline description of symptoms implies the broad, symptom-oriented definition. But, the limited diagnostics and treatments in the guideline imply the narrow thyroid-centric definition. If the practicing physician has a thyroxine-resistant patient with persistent symptoms of hypothyroidism in spite of thyroxine treatment and euthyroid-indicating serum levels, the physician is left in a quandary. There is no other recommended treatment. This leaves the physician with two choices:

1. Adapt the standard practice excuses provided by the admonition against any treatment containing T3 [4, 9], deny the existence of continuing hypothyroidism, and deny the potential existence of a second class of hypothyroidism exo-endocrine hypothyroidism. In this way, the physician avoids the potential wrath of a board of medicine inquiry. The physician wins, but the suffering patient loses.

2. Recognize that the excuses for thyroxine-only treatment failures are fallacious, exercise the treatment disclaimer (In general , page 6, left-hand column of [9]) and the completeness disclaimer at the end of the guideline (page 9 of [9]), and successfully treat the patient with a hormone replacement that is specifically discouraged and proscribed, but is applicable to a second class of hypothyroidism exo-endocrine hypothyroidism. While the patient wins, the physician loses to the liability of the draconian wrath of a board of medicine for unnecessarily exceeding the recommended treatment (as measured by inconclusive diagnostics, see below) and endangering the patient since they believe that there is only one class of hypothyroidism victims.
Linguistic etiologies create this quite unprofessional win-lose situation. First, the guideline [9] does not specify or stipulate which definition is operative. If the definition were specified, as required by protocol [27], the patient-physician relationship would become win-win for either of the following two reasons:

1. If the thyroid-centric endo-endocrine-only definition were specified in the guideline [9] then the physician and the board of medicine would realize that the guideline did not apply to the thyroxine resistant, exo-endocrine patients. The physician could then treat the patient properly without fear of fallacious hypothyroidism guideline action by a board of medicine.

2. If the symptom-oriented definition were specified in the guideline [9] and the guideline maintained logical consistency, then the physician would be appropriately guided by an expanded and revised guideline that addressed both classes of hypothyroidism. The patient would be treated properly without fear of fallacious action by a board of medicine.
Logical Faux Pas The lack of definition for hypothyroidism and the lack of recognition of a second class of hypothyroidism are hardly the last linguistic faux pas in this realm. For example, the guideline (the lower, right-hand column of page 6 of [9]) refers to a dispute between studies of combinations of thyroid hormones. Some studies [10-13] take advantage of the lack of definition of hypothyroidism, to form the studies and then to make overly broad conclusions or inspire overly broad interpretations. Using subjects with primary hypothyroidism is not representative of subjects with deficient peripheral metabolisms or increased peripheral hormone receptor resistance because they are physiologically different. Concluding that a T3-containing treatment is of no use is not proper when only most showed no improvement. The difference between all and most is rare or few, precisely the occurrence rate of thyroxine-resistant, exo-endocrine hypothyroidism, the other class of hypothyroidism victims. Thus, in either case, professionalism and patients are not served properly.

If the definitions were known, then those studies could be properly categorized according to the classes of hypothyroidism. The detractions to combination hormone treatments are formulated under a narrow definition of hypothyroidism, endo-endocrine hypothyroidism, and their conclusions must be so treated and limited. The proponents of combination hormone treatments [14-18] are formulated under a broad definition of hypothyroidism and their conclusions must be examined in a different, inclusive light.

For example, Thyroid Insufficiency? Is Thyroxine the Only Valuable Drug? [2] primarily deals with the thyroxine-resistant patient, i.e., those that fall within the broad, symptom-oriented definition of hypothyroidism but that fall outside of the narrow, thyroid-centric definition, i.e., exo-endocrine hypothyroidism. As a consequence, the conclusion of successful treatment for the thyroxine-resistant patients should only apply to the thyroxine-resistant, although this particular study also treated undelineated patients in the same way with success. Baisier, et al., had success with both classes of hypothyroidism because they used natural desiccated thyroid, which does address both classes of hypothyroidism.

In spite of the success by Baisier, et al. [2] in diagnosing and treating thyroxine-resistant patients, the expression of the paradigm [4], made the errant assumption that no one could be thyroxine resistant because the peripheral metabolism was regulated and contextually infallible. Although this regulation was refuted by counter examples in the literature [2 (by inference), 5, 6], these counter examples are simply ignored. They are ignored because it is human nature to preserve paradigms. [19] People want the consistency of prior decisions, i.e., starie decisis.

The expression of the hypothyroidism paradigm [4] also takes advantage of other logical faux pas to cover up or explain away the failures of thyroxine (T4) only therapies. The first cover up discredited the basal temperature diagnostic found by Barnes [14] and used by many others. However, this was falsely discredited by citing a study by Mackowiak. [20] Mackowiak had not excluded subjects with hypothyroidism. Thus, the lower basal temperature diagnostic was attempted to be dissociated from hypothyroidism with a conclusion influenced by hypothyroidism. This logical faux pas is a form of a circular argument and consequently proves nothing.

Similarly, the paradigm expression [4] attempts to reassign somatic symptoms when the thyroxine treatment for hypothyroidism fails by describing them as nonspecific. This attempt cited Barsky [21] who also did not exclude subjects with hypothyroidism and consequently used a conclusion influenced by hypothyroidism to dissociate a connection with hypothyroidism. Additionally, Baisier, et al., [2] presents a counterexample in the form of an accurate somatic diagnostic technique based upon a combination of coarse evaluations of each of eight somatic symptoms. First, this clinical evaluation values each of the eight symptoms with 0, 1, or 2 for none, some, and substantial presence. Second, these valuations are summed for an overall value between 0 and 16 inclusive. Finally, the sum of these eight clinical evaluations is compared to limits. The ranges of values for euthroid subjects and those with hypothyroidism are substantially separated. Therefore, symptoms, although in combination, can successfully diagnose hypothyroidism a substantial counter-example to the hypothyroidism paradigm.

Thus, the establishment deflection of blame for the failures of the single-class, thyroxine-only prescription [9] is both illogical and disproved.

Further, neither the guideline [9] nor the paradigm expression [4] acknowledges the existence of any syndrome of the resistance to thyroid hormones [22, 23] or its potential for treatment. [24] There are hormone receptors everywhere. Any abnormality in the reception at the glands or organs is indistinguishable from immediately subsequent hormonal operation abnormalities. However, in the peripheral cells, the abnormality is the basic operation of the cell and the creation of symptoms.

Medical Failures Hidden by the Corruption of Evidence-Based Medicine
The failure of the thyroxine-only treatment prescription is made more confusing by enshrining its short comings in the gold standard of a laboratory assay protocol. This corrupts the vaunted Evidence-Based Medicine protocol. [25] Such a corruption is promoted by the now-discredited, mind-distrusting Behaviorist philosophy [26] and ignores the checks and balances counsel of governance of the great James Madison:

That if all men were angels, no government would be necessary. If angels were to govern men, neither external nor internal controls on government would be necessary. In framing a government which is to be administered by men over men, the great difficulty lies in this: you must first enable the government to control the governed and, in the next place, oblige the government to control itself. The Federalist Papers

This corruption of Evidence-Based Medicine defies the non-angelic fallibility of mankind as it assumes that every element of the test from its creation and the establishment of normality to the delivery of test data is always perfect. The excessive faith in this illogical corruption is a substantial component in the systemic maltreatment of the victims of thyroxine-resistant, exo-endocrine hypothyroidism. It improperly keeps physicians from listening to their patients and considering the validity of their symptoms. It improperly claims people do not have thyroid hormone issues when it does not measure the results of where the action is [7]: in the intracellular spaces or any result or indication thereof.

Counter Examples
The author knows of two people presenting counterexamples to the thyroid-stimulating hormone concepts:

1. A subject with an extreme hyperthyroidism indicating TSH level of .002 exhibits clinical hypothyroidism.
2. A subject with a substantial hypothyroidism indicating TSH level of 60 exhibits clinical hyperthyroidism.
The thyroid paradigm cannot explain these characteristics, however, deficiencies and excesses in the exo-endocrine behaviors can. The failure of the thyroid-stimulating hormone paradigm to explain these counterexamples demands consideration of a second class of thyroid etiologies exo-endocrine etiologies.

The Etiologies of Linguistic Etiologies Non-Compliant Guidelines The etiologies of linguistic imprecision stem from the apparent assumption that the problem does not exist. The immediate guide to medical authors, The Manual of Style, produced by the American Medical Association, does not mention the concept beyond a single sentence admonition for clarity. It spends scores of pages upon abbreviations and statistics but only one sentence for clarity. Unfortunately, The Manual of Style is not alone. Other such manuals are also quite lacking in lessons of clarity. More unfortunately, the etiologies of vagueness are generally not explored in the classroom. Somehow, clarity is supposed to arise in the mind like wild flowers in the spring naturally.

The protocols for the authorship of the guidelines have been written, even by the authoring organization of the hypothyroidism guideline [27, 9] but were ignored. The most important admonition to this case that is in the protocol [27] but is not written into the guideline [9]: the stipulation of definitions of critical and readily misunderstood words and terms [see the definitions].

Studies of the authorship of medical guidelines have shown them to be substantially lacking. Dr. Shaney et al., gave an average grade of 43% to 279 medical guidelines. [28] Dr. Grilli, et al., found that only 5% of 431 guidelines met all three criteria of their grading system and that most were unsatisfactory. [29] Dr. Burgers, et al., graded 100 guidelines and found that oncology guidelines were better (42.2%) than other guidelines (29.4%). [30]

Additionally, a study [31] estimates that 4% of all hospital patients will suffer from an adverse event that produces an estimated 200,000 deaths annually. Since half were preventable and a fourth are negligent, then the remaining causes are either beyond medical science or merely beyond practice guidelines, or in the confusion within practice guidelines.

Since it appears that human suffering is an inadequate motivation to transform vagueness to clarity, perhaps the civil rights guaranteed by the Constitution of the United States will. When medical missives meet the law at the governments boards of medicine, the concept of Overinclusion, a derivative of the Equal Protection Clause of the Fourteenth Amendment, becomes applicable. (See the definitions, below.) Overinclusion occurs when two distinct classes, of different etiologies that require different treatments, are included in the same class and the treatment for one of these classes is improper and consequently places undue and excessive burden upon the members of that class.

Certainly, the inconsistent implications of the two implied definitions of hypothyroidism in the guideline [9] and the expression of the paradigm [4] creates two classes, those people included in the narrow definition and those included in the broad definition but not included in the narrow definition. There is an endocrine precedent: While excessive urination is a general symptom of diabetes, its somatic nature separates the various distinct subclasses. The major subclasses, type 1 and type 2, are similar to the classes of hypothyroidism: the inability to produce and the inability to use respectively.
Conclusions and Final Implications Baisier, et al. [2], have empirically shown that thyroxine-resistant patients exist, can be treated properly, and regain their former selves with natural desiccated thyroid. This original treatment for hypothyroidism [1] has served many quite well [14, 18] in the past and presently. Other forms of combination therapies have been used successfully as well. [16, 17] The Baisier, et al., empirical results are not flukes. Physiological theory agrees. The exo-endocrine hormone operations, peripheral metabolism and peripheral hormone receptors, exist and are fallible. [5, 6, 22 – 24]

Accepting the fallibility of exo-endocrine operations upon the thyroid hormones, which common sense and science demands, also demands acceptance of the treatment with the active exo-endocrine hormone, triiodothyronine (T3), simply because that is the hormone that requires replacing in case of such failings. Unfortunately, the oligarchical powers bestowed on the medical associations via the state boards of medicine have far greater influence over physicians than truth and reality. Of the 120 plus thyroxine-resistant sufferers found by our minuscule outreach effort letters to the editors of West Virginia newspapers [32], only six have been able to use our research to persuade their physician to prescribe any physiologically necessary T3-containing therapy.

Hopefully, the Equal Protection of the citizens of the United States, guaranteed by the Fourteenth Amendment to the Constitution and Due Process, will, as it should, prevail. Hopefully, the existing Overinclusion of all hypothyroidism victims into a single class will demand an end to the linguistic etiologies that imprecisely treat all types of victims in the same way. Hopefully, the seemingly endless suffering by thyroxine resistant patients will end with their return to energetic lives by the proper treatment of exo-endocrine hypothyroidism.

Hopefully too, the linguistic methodology shown herein will spread throughout medicine to improve guidelines and medical care.

Albert Einstein recommends that problems be simplified to clarify them. However, they cannot be overly simplified, since that creates a different type of confusion. The early lack of knowledge plus the use of universally applicable natural desiccated thyroid gave single-class hypothyroidism credence. This over simplification became evident with the advent and use of levothyroxine sodium. Levothyroxine sodium left some hypothyroidism (broad, symptom-oriented definition) victims untreated, thereby demonstrating the confusion of over-simplification and overinclusion. Thus, the use of levothyroxine sodium exposed the existence of a second class of hypothyroidism victims those with exo-endocrine hypothyroidism, who have different physiological etiologies that physiologically, rightfully, and lawfully demand different treatments.


due process The conduct of legal proceedings according to established rules and principles for the protection and enforcement of private rights, including notice and the right to a fair hearing before a tribunal with the power to hear the case.

endo- A prefix meaning within or inside of.

exo- [Gr. exo, outside] Combining form meaning without or outside of.

equal protection The constitutional guarantee under the 14th Amendment that the government must treat a person or class of persons the same as it treats other persons or classes in like circumstances.

hypothyroidism Thyroid-centric meaning: the clinical consequences of inadequate secretion by the thyroid. Symptom-oriented meaning: the clinical consequences of inadequate levels or usage of thyroid hormones. Potential future meaning: The clinical consequences of inadequate usage of thyroid hormones. [This definition encompasses all etiologies of hypothyroidism.]

overinclusion Extention beyond the class of persons intended to be protected or regulated; burdening more persons than necessary to cure the problem. [Legally this concept requires judgement based upon the percentage of 10 persons overincluded, the extent of their burden, and the potential for removing the burden}

proscribe – Outlaw or prohibit; to forbid
starie decisis – [Latin for to stand by things decided] The doctrine of precedent, under which it is necessary for a court to follow earlier judicial decisions when the same points arise again in litigation.

stipulative definition A definition that, for the purposes of the document in which it appears, arbitrarily clarifies a term with uncertain boundaries or that includes or excludes specified items from the ambit of the term.

vagueness – Uncertain depth of meaning. Vagueness raises due-process concerns if legislation does not provide fair notice of what is required or prohibited, so that enforcement may well become arbitrary. [However, amazingly, vagueness can be eliminated if there is a consensus in the community of the meaning.]
References and Footnotes

  1. Gossel, Thomas A., RPh, PhD, Professor of Pharmacology and Toxicology, Emeritus, Endocrinology Continuing Education accredited by the Accreditation Council for Continuing Medical Education (ACCME), 2005
  2. Baisier, WV, Hertoghe, J., Beekhaut, W., Thyroid Insufficiency? Is Thyroxine the Only Valuable Drug?, Journal of Nutritional and Environmental Medicine, Vol 11, No. 3, September 2001, pages 159-166
  3. Brady, David, DC, CCN, DACBN, Functional Thyroid Disorders, Part I, Dynamic Chiropractic, March 20, 2000, Volume 18, Issue 07, Table 2
  4. Wilsons Syndrome, American Thyroid Association, November 1999 and updated May 2005, 6066 Leesburg Pike, Falls Church, VA 22041, Barbara Smith, CAE, Executive Director
  5. Nomura S., et al. Reduced Peripheral Conversion of Thyroxine to Triiodothyronine in Patients with Hepatic Cirrhosis, J of Clinical Investigation, Sept 1975, 56(3): 643-652.
  6. Bianchi R, Mariani G, Molea N, Vitek F, Cazzuola F, Carpi A, Mazzuca N, Toni MG, Peripheral Metabolism of Thyroid Hormones in Man. Direct Measurement of the Conversion Rate of Thyroxine to 3,5,3′-Triiodothyronine (T3) and Determination of the Peripheral and Thyroidal Production of T3., J. Clinical Endocrinol Metab., 1983 June; 56(6):1152-63
  7. Dr. E. Chester Ridgway, Director of Endocrinology at the University of Colorado Health Sciences Center, Equivalence of Levothyroxine Sodium Products, Joint Public Meeting (Cosponsored with the American Thyroid Association, The Endocrine Society, and the American Association of Clinical Endocrinologists) Monday, May 23, 2005, pages 144-11 145
  8. Anthony Taft and Geoffrey Beckett, British Medical Journal 2003 (8 Feb); 326:295-296
  9. Baskin, HJ, MD, Medical Guidelines for Clinical Practice for the Evaluation and Treatment of Hyperthyroidism and Hypothyroidism, American Association of Clinical Endocrinologists, Revised 2006.
  10. Sawka, AM, Gerstein, HC, Marriott, MJ, MacQueen GM, and Joffe, RT, Does a Combination Regimen of Thyroxine (T4) and 3,5,3′-Triiodothyronine Improve Depressive Symptoms Better Than T4 Alone in Patients With Hypothyroidism? Results of a Double-Blind, Randomized, Controlled Trial, Journal of Clinical Endocrinology and Metabolism, March 2004, 89(3); 1486-7
  11. Siegmund W, Spieker K, Weike AI, Giessmann T, Modess C, Dabers T, Kirsh G, Sanger E, Engle G, Hamm AO, Nauck M, Meng W., Replacement Therapy with Levothyroxine Plus Triiodothyronine (Bioavailable Molor Ratio 14:1) is not Superior to Thyroxine Alone to Improve Well-Being and Cognitive Performance in Hypothyroidism, Clin Endocrinol, 2004 June;60(6);750-757
  12. Walsh, Dr. John P., Combined Thyroxine/Liothyronine Treatment Does Not Improve Well-Being, Quality of Life, Or Cognitive Function Compared to Thyroxine Alone: A Randomized Controlled Trial in Patients with Primary Hypothyroidism, The Journal of Clinical Endocrinology and Metabolism, Vol 88., No 10, pgs 4543-4550.
  13. Clyde, Patrick W, MD, Combinination Levothyroxine/Liothyronine Shows No Obvious Benefit Over Levothyroxine Alone in Patients With Primary Hypothyroidism, Journal of the American Medical Association, December 2003 as reported by Joene Hendry of Doctors Guide.
  14. Barnes, B MD, Hypothyroidism: The Unsuspected Illness, Harper & Row, 1976
  15. Bunevacius, R MD PhD, Kacanavicius, G MD PhD, Zalinkinevicius, R MD, Prange, A MD, Effects of Thyroxine as Compared with Thyroxine plus Triiodothyronine in Patients with Hypothyroidism, New England Journal of Medicine, Feb 11, 1999, 340:424-429
  16. The second patients case was reported in a March 16, 2003 letter to the British Medical Journal. She presented Dr. Henk de Vries with hypothyroidism symptoms and tests revealed a TSH of 100 mIU/mL. Subsequent thyroxine therapy reduced the TSH to only 12 mIU/mL with the substantial daily dose of 175 micrograms OD. Since she was still symptomatic, she was given a combination therapy with success.
  17. Toft, Dr. AD, T3/T4 Combination Therapy, 21st Joint Meeting of the British Endocrine Societies, April 2002.
  18. Starr, Mark MD, Hypothyroidism Type 2, Mark Starr Trust, Columbia, MO, 2005
  19. Kuhn, Thomas S., The Structure of Scientific Revolutions, University of Chicago Press, 1962
  20. Mackowiak, et al., A Critical Appraisal of 98.6 Degrees F, the Upper Limit of the Normal Body Temperature, and other Legacies of Carl Reinhold August Wunderlich, Journal of the AMA, 1992, Volume 268, pgs 1578-1580
  21. Barsky, Arthur J, MD and Borus, Jonathan F. MD, Functional Somatic Syndromes, Annals of Internal Medicine, June 1999, Volume 130, Issue 11, pages 910-921.
  22. Sakurai A, Takeda K, Ain K, et al., Generalized Resistance to Thyroid Hormone Associated with a Mutation in the Ligand-Binding Domain of the Human Thyroid Hormone Receptor ?, Proc. Natl. Acad. Science, November1989, Vol. 86, pgs 8977-8981. Refetoff S, Weiss RE, Usala SJ, The Syndromes of Resistance to Thyroid Hormone, Endocrine Review, 1993, Volume 14, No. 3, pgs 348-399
  23. Weiss RE, Refetoff S, Treatment of Resistance to Thyroid Hormone Primum Non Nocere, Journal of Clinical Endocrinology and Metabolism, Vol 84, No 2, pgs 401-404.
  24. Sackett, et al, Evidence-Based Medicine: What it is and What it isnt, Centre for Evidence-Based Medicine and based upon an editorial in the British Medical Journal 1996; 312: 7-12.
  25. Pinker S, The Blank Slate The Modern Denial of Human Nature, 2002, page 19, Viking, Penguin Group, New York, NY.
  26. American Association of Clinical Endocrinologists Protocol for Standardized Production of Clinical Practice Guidelines, Endocrine Practice, Vol. 10, No. 4, 2004
  27. Shaneyfelt TM, Mayo-Smith MF, Rothwangl, J, Are Guidelines Following Guidelines?, Journal of the American Medical Association, Vol. 281, No. 20, May 26, 1999.
  28. Grilli R, Magrini N, Penna A, Mura G, Liberati A, Practice Guidelines Developed by Specialty Societies: The Need For a Critical Appraisal, Lancet, Jan 8, 2000.
  29. Burgers JS, Fervers B, Haugh M, Brouwers M, Browman G, Cluzeau PFA, Internatinal Assessment of the Quality of Clinical Practice Guidelines in Oncology Using the Appraisal of Guidelines and Research and Evaluation Instrument, Journal of Clinical Oncology, Vol. 22, No 10, May 15, 2004.
  30. Acknowledgements
    The author appreciates the legal observations by Dr. Christine Kellett, Professor Emeritus of Constitutional Law. The author also appreciates the interest shown by Dr. Jon Sterngold, Dr. Joseph De Soto, and Dr. Paul Quarantillo.
    About the Author Eric K. Pritchard has degrees in mathematics and electrical engineering and more than forty years of experience in these fields. He has thirty-nine U.S. Patents in seven disciplines, some of which also have foreign counterparts. After researching and designing circuits to operate through a strategic nuclear threat, he began researching and designing solutions for specialized production problems. The impossible task of translating the artistry of vacuum tube amplifiers to solid state, a task that many had tried and all failed, intrigued him and ultimately demanded a reinspection of engineering theory.

    According to Pritchard, Like medicine, engineering predominately fails to maintain a tightly logical connection with firm knowledge. Unlike mathematics, both make sweeping assumptions and approximations, use imprecise arguments, and readily excuse failures. Although failures in engineering usually only cost money, failures in medicine cause or extend pain and suffering and can cause or hasten death.

    Mr. Pritchard began studying the etiologies of and treatments for hypothyroidism after his wife recounted to him visits with physicians that suggested an errant philosophical structure in the diagnosis and treatment of hypothyroidism. He writes, This suggestion was made by the excessive dependence upon the objective laboratory assay and the total depreciation of the subjective clinical presentation. The laboratory assay claimed euthroidism while the clinical presentation disagreed completely. From earlier research in audio, where the objective and subjective clash also and where the objective is overly glorified and the subjective is under appreciated, the existence of an errant technical assumption was probably being hidden by the excessive valuation of objective testing. Just as the audio paradigm assumes that the human hearing process does not produce harmonics of audible tones, the endocrine paradigm assumes that all somatic operations on thyroid hormones outside of the endocrine system are infallible. Just as the audio paradigm made the Total Harmonic Distortion test and the Intermodulation test the gold standard of objectivity, the endocrine paradigm made the thyroid-stimulating hormone (TSH) test its gold standard.

    Pritchard poignantly concludes: The difference between these situations is substantial. The audio debate does not adversely affect health.


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