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The Expert Report Interview With Dr John Lowe Written by Mark Swanson, ND This segment of The Expert Report pulls no punches. My interview guest is Dr John Lowe, author of The Metabolic Treatment of Fibromyalgia (1), an extraordinary and comprehensive 1100-page text, which I found to be a fascinating journey through thyroid science. His groundbreaking work makes for a compelling link between fibromyalgia and the functional disorder of thyroid hypometabolism and tissue resistance to triiodothyronine (T3). Herein, he continues his outspoken views by taking aim directly at the endocrine establishment on thyroid metabolics and the usefulness of assessing thyroid status as now adopted under the standards of care. His extensive body of works, research, treatment discussions, and “everything thyroid” can be found on his website, www.drlowe.com. Dr Lowe, I am very excited about this opportunity for our interview. I know that you will have a lot to share with our NDNR colleagues. The challenge will be to capture some of your outspoken brilliance, insight, and clinical pearls as one of the leading functional and authoritative thyroid intellects. Our ears and eyes are open, and we are taking notes. Try to keep it short, but don’t leave anything out! What is your educational background and current position? I received my chiropractic degree from Southern California University of Health Sciences [Whittier] in 1977. I also have an undergraduate and graduate degree in research psychology from University of West Florida [Pensacola]. I am currently the director of research at the Research Foundation in Houston, Texas. Our foundational research was in the use of T3 in fibromyalgia patients and longer-term follow-up studies on the effects of thyroid hormone in this patient group. Let’s start off with this quote from your website: “I learned early during the last 16 years that the endocrinology specialty’s judgment is corrupted by financial inducements from drug companies that profit from the TSH [thyrotropin] test and T4 [thyroxine] replacement.” You’re really taking on The Endocrine Society here. Why? The simple reason for my taking on the endocrine community is that my mission in life is to relieve as much human suffering as I can. We have long had ample research evidence that T4 replacement simply doesn’t work for and is harmful for too many patients. Consider a large community study (2) of T4 replacement conducted in 2002 in England. Hundreds of patients from numerous clinics taking T4 replacement were matched with other patients who were not hypothyroid and not taking thyroid hormone products. The noteworthy results of this study were 3-fold: a hair short of 50% of the hypothyroid patients on T4 replacement still suffered from hypothyroid symptoms, they had a significantly higher incidence of 5 potentially fatal diseases associated with underregulation with thyroid hormone, and patients on T4 replacement had to take more drugs than did the matched controls to lower hypothyroid symptoms and better control other diseases that afflicted only the hypothyroid patients. We have many such studies that bring into question the safety and effectiveness of T4 replacement for many hypothyroid patients. Whenever such studies are published, endocrinologists often resort to warped thinking to encourage hypothyroid patients to continuing T4 replacement as the only preferable approach. To me, it’s obvious that something other than the scientific findings drive these endocrinologists to advocate the use of only T4 replacement, despite its lack of safety and confirmed harm. What led you to become so passionate about the thyroid, its misconceptions, and the need for management revision? I entered this passionate dispute for a clear-cut reason: I was overwhelmed by evidence that conventional [allopathic] endocrinologists and drug companies that profit hugely from their mutual interaction were depriving thyroid patients of good health and well-being. My own personal experiences, of course, were only a series of countless hundreds of others I observed in clinical practice. The endocrinology specialty, however, was adamant: “If you’re on T4 replacement and still have hypothyroid-like symptoms, that proves that something else must be the cause of your symptoms.” Despite the endocrinologists’ assurances, I’ve been fully well on 150 mcg of T3 for some 25 years now. After all those years, in 2011, I had the pleasure of writing the Foreword to a book, Recovering with T3: My Journey from Hypothyroidism to Good Health Using the T3 Thyroid Hormone, by the British writer Paul Robinson (3). In the book, he describes being free from hypothyroid symptoms for 10 years by using T3 therapy alone. Keep in mind that this therapy, in the view of many endocrinologists, couldn’t possibly have helped Mr Robinson, although it dramatically did after T4 replacement and other forms of thyroid therapy had failed him. You research and write extensively on the inadequate thyroid hormone regulation hypothesis. What does this encompass? The hypothesis simply says this: a wide variety of symptoms and signs that clinicians deal with are caused mainly by too little thyroid hormone regulation of cell and tissue function. Of course, one might reasonably ask, “Too little cell and tissue regulation of exactly what?” The answer to that question varies widely. Inadequate thyroid hormone regulation of different biological compounds may give rise to different symptoms and signs. The resulting symptoms and signs aren’t necessarily the same from individual to individual. This requires that clinicians stay open-minded and diverse in their approaches to differential diagnosis. This clinical approach was used widely around the turn of the 20th century by the famed Dr William Osler and his colleagues. I’ve found that studying their publications encourages the proper orientation, which many of us call “clinical medicine.” Explain the treatment rationale of metabolic rehabilitation. When I first devised metabolic rehabilitation, my intention was to create a diagnostic and treatment approach that resembled the systematic approaches to physical and cardiovascular rehab. I did my best to compare rehabilitating metabolic functions of patients’ bodies and minds to the 2 better-known methods for rehabilitating patients: physical and cardiovascular health and well-being. In the case of metabolic rehab, the purpose was to help patients recover their full biochemical and physiological health and well-being. Our approach was to systematically correct any and all impediments to normal cellular and physiological metabolism. What is the difference (and misconceptions) between hypothyroid and thyroid resistance? The main misconception I hear comes from patients, although also from a few physicians. The conception usually expressed is, “I didn’t get over my symptoms even after being on 1 grain of desiccated thyroid for 6 months. Does that mean I’m thyroid hormone resistant?” Researchers have studied the 95th percentile in which most hypothyroid patients safely got well before the TSH became problematic in the early 1970s. That 95th percentile was 2 to 4 grains of desiccated thyroid, or 120 to 240 mg; in terms of the l-thyroxine, the 95th percentile was 200 to 400 mg. Partly because of these 95th percentiles, my treatment and research team traditionally hasn’t considered that a patient may have partial cellular resistance to thyroid hormone except under one condition: that is, over several weeks, the patient reached 4 grains of desiccated thyroid or 400 mg of T4 with no improvement whatever and no thyrotoxicosis. At that dosage, the typical hypothyroid patient has begun to benefit from the dosage, and some have adverse effects. But if the patient has had no improvement of thyrotoxicity, we have traditionally begun the protocol proper for patients partially resistant to thyroid hormone. When it comes to the thyroid, it seems physicians are not listening to many of their patients. They drive the laboratory results to a desired target as primary treatment criteria and insist that is where it needs to remain for symptom improvement. Yet, this often fails to improve or eliminate the ongoing hypothyroid symptoms. How has your research helped bridge that treatment gap? My research group and others have measured the resting metabolic rates (RMRs) of hundreds of patients; in general, we’ve found that in the majority of cases RMR levels don’t correlate with TSH levels. The free T4 never correlates—ever! The free T3 does correlate weakly, but only after we’ve included around 100 patients in a study. This finding with the free T3 means that it’s statistically interesting but of no clinical value. The main aim of using thyroid function test results should be to normalize oxidative metabolism. That’s what the RMR and basal metabolic rate (BMR) measure—the status of a patient’s oxidative metabolism. But, studies show that we can’t accurately tell what a patient’s oxidative metabolism is from the free T3, free T4, or the TSH. The result of our studies is that reaching conclusions about a patient’s metabolic status based on thyroid function tests is simply foolishness and almost always flat wrong. What is most worthy of note is this: as early as 1989, conventional [allopathic] endocrinologists had been avidly promoting thyroid function blood tests, without justification, as the “gold standard” of diagnosis. This was a presumption never scientifically warranted, nor is it any more today than it was in 1989. You state that thyroid laboratory test results “are of no value in finding an effective dose.” Should we throw testing out the window? My belief is that thyroid function tests are of value only when way out of range. Studies show that when the free T3, free T4, and TSH are within range, or close to it, their levels vary, as Japanese researchers have written, “dramatically”. Finding distinctions in the levels are, in general, a waste of time. The reason is that the levels vary statistically significantly about every 30 minutes. And, the levels don’t reliably correlate at 30-minute intervals from day to day, nor from week to week. How is thyroid resistance and rehabilitation distinguished from Wilson syndrome? I would like to say that I’m grateful to Dr Dennis Wilson for advocating and garnering support for clinicians using T3 rather than T4 alone. I must emphasize, though, that based on systematic examination I cannot agree with most of Dr Wilson’s positions that relate to health and thyroidology. I’ve known many hundreds of resistance patients who recovered with high T3 dosages. Yet, I don’t know a single one who has maintained their recovery upon lowering their T3 dosages all or most of the way back down. Maybe some such patients exist. However, Richard Garrison, MD, of Baylor Medical College [Houston, Texas], and I spent a year diligently searching for cases and came up completely empty handed. I can’t identify a single one out of the many hundreds of resistance patients I’ve treated over the years. Is reverse T3 a strong component of thyroid resistance? Should we be measuring it as routinely as is being advocated by many functional medicine labs and practitioners? Measuring reverse T3 has some diagnostic value in the realm of thyroid hormone resistance. It can be useful in identifying some conditions, especially those that interfere with the activity of 5-deiodinase, the enzyme that converts T4 into the metabolically active hormone T3. The conditions include high mercury levels, as in some dental workers. They also include excess cortisol production during dental and surgical procedures. Say, for example, that someone acquires a permanent lock on 5-deiodinase. This would increase the activity of 5-diodinase, resulting in excessive production of reverse T3. As reverse T3 appears to be metabolically inactive, this mechanism could have a devastating effect by slowing thyroid metabolism. Obviously, it would be important to identify this problem for the sake of correcting the patient’s mechanism of thyroid hormone resistance. Dr Swanson’s comment: Dr Lowe suggests here that reverse T3 elevation is a less common occurrence and is mostly limited to certain groups. This would be in disagreement with the widely held view described by Dr Dennis Wilson (Wilson syndrome) that it is a much more common finding, resulting from chronic stress and excess cortisol production. Thus, their evaluation workup, diagnostic interpretation, and therapy approach would likely be different for the same patient. With thyroid resistance treatment, elevations in serum T4/T3 will often exceed the upper reference limit. Reassure us on the adverse effect and safety management of thyroid rehabilitation therapy. Over the decades, my treatment and research team has compared the TSH, free T4, and free T3 with measures clearly controlled by thyroid hormone: oxidative metabolic rates, ECG [electrocardiogram] voltages, basal temperatures, Achilles reflexes speeds, daily variances of cortisol and glucose, and many other biochemical and physiological measures. What we’ve found is this: the TSH, free T4, and free T3 do not reliably predict the other measures. In fact, the thyroid test results, as Japanese researchers have confirmed, are extremely poor predictors of biochemical and physiological measures of the effects of thyroid hormone. This has understandably led to a high level of distrust in the usefulness of thyroid function test results. Among many researchers who conduct such studies, the conventional [allopathic] endocrinology specialty’s trick is divulged and over. Good riddance to the harm the test results have done. Please update us on your landmark text The Metabolic Treatment of Fibromyalgia1 and its related chapter in the Textbook of Natural Medicine(4). In 2000, McDowell Publishing Company published my textbook The Metabolic Treatment of Fibromyalgia (1). In the book, I covered what I considered—and still consider!—the folly of conventional [allopathic] medical groups concerning the diagnosis and treatment of too little thyroid hormone regulation of the human body and mind. I also included what I consider the rational alternative to the irrational conventional [allopathic] view. Then, in 2005, Joseph E. Pizzorno Jr, ND, and Michael T. Murray, ND, approached me with an extraordinary offer. They asked that I write the chapter on fibromyalgia for the sagacious third edition of their Textbook of Natural Medicine (4). Much to my privilege, when the fourth edition of the textbook came due, they asked that I update and revise the fibromyalgia chapter, which I happily did. Tell us a little about your current involvement with the online journal www.ThyroidScience.com. My publisher started Thyroid Science (5) at my request 6 years ago. My purpose was to provide a peer-reviewed journal of the thyroid field for clinicians, unfettered by the commercial and political motivations that dominate publications in the conventional [allopathic] endocrinology field. I’ve learned a great deal by reading and editing the widely diverse papers. We have an open invitation for naturopathic physicians to submit papers. There is no other discipline with which I feel a stronger brotherhood, and I wish this were shown in the pages of Thyroid Science. Dr Lowe, this has been a short but fascinating insight to he understanding, evaluation, and management of human thyroid resistance. Before we close the interview, please give us one final thought and another clinical pearl from your vast thyro–treasure chest. Clearly to me, the most important consideration is this: each clinician should understand that, by far, the free T4, free T3, and TSH are the most useless tests clinicians can employ in trying to identify patients who are hypothyroid or thyroid hormone resistant. These tests are little more than a 40-year-old financial enterprise, whose uselessness and harm are now scientifically too conspicuous. Dr Swanson’s closing comment: Thank you, Dr Lowe. Our NDNR readers will be thirsting for much more of you after this interview. I will simply direct that in-depth learning and education experience, along with the sheer pleasure of reading and listening to Dr Lowe’s brilliant thyroid intellect, to www.drlowe.com and to the additional references herein(6-21). There are so many who have benefited by your research and therapy protocols. Let me be the first to nominate you to the Thyroid Hall of Fame. Mark Swanson, ND, writes “The Expert Report” column, which is featured in NDNR. Dr. Swanson has over 25 years experience as chief medical advisor, research and technical consultant, and products formulations expert to leading practitioner brand supplement manufacturers. He is a former associate editor for the American Journal of Naturopathic Medicine, national product director, and published researcher. He is a pioneer graduate of Bastyr University, 1984. Dr. Swanson has his private practice specializing in Preventics Care and Functional Medicine, in Sequim, Washington. Contact: drmarkswanson@gmail.com References 1. Lowe JC. The Metabolic Treatment of Fibromyalgia. Boulder, CO: McDowell Publishing Co; 2000. 2. Saravanan P, Chau WF, Roberts N, et al. Psychological well-being in patients on “adequate” doses of l-thyroxine: results of a large, controlled community-based questionnaire study. Clin Endocrinol (Oxf). 2002;57(5):577-585. 3. Robinson P. Recovering with T3: My Journey from Hypothyroidism to Good Health Using the T3 Thyroid Hormone. Elephant in the Room Books; 2011. 4. Lowe JC. Fibromyalgia syndrome. In: Murray MT, Pizzorno JE Jr, eds. Textbook of Natural Medicine. 3rd ed. London, England: Elsevier; 2005. 5. Thyroid Science: an open-access journal for truth in thyroid science and thyroid clinical practice. http://www.thyroidscience.com. Accessed January 23, 2012. 6. Lowe JC. Your Guide to Metabolic Health. Boulder, CO: McDowell Health-Science Books; 2002. 7. Lowe JC. Thyroid dysfunction and fibromyalgia. In: Chaitow L, ed. Fibromyalgia Syndrome: A Practitioner’s Guide to Treatment. Edinburgh, Scotland: Churchill Livingston; 1999. 8. Lowe JC. Improvement in euthyroid fibromyalgia patients treated with T3 (tri-iodothyronine). J Myofascial Ther. 1994;1(2):16-29. 9. Lowe JC. T3-induced recovery from fibromyalgia by a hypothyroid patient resistant to T4 and desiccated thyroid. J Myofascial Ther. 1995;1(4):21-30. 10. Lowe JC, Garrison RL, Reichman AJ, Yellin J, Thompson M, Kaufman D. Effectiveness and safety of T3 (triiodothyronine) therapy for euthyroid fibromyalgia: a double-blind placebo-controlled response-driven crossover study. Clin Bull Myofascial Ther. 1997;2(2-3):31-58. 11. Lowe JC, Reichman AJ, Yellin J. The process of change during T3 treatment for euthyroid fibromyalgia: a double-blind placebo-controlled crossover study. Clin Bull Myofascial Ther. 1997;2(2-3):91-124. 12. Lowe JC, Garrison RL, Reichman AJ, Yellin J. Triiodothyronine (T3) treatment of euthyroid fibromyalgia: a small-N replication of a double-blind placebo-controlled crossover study [abstract]. Clin Bull Myofascial Ther. 1997;3(14):23-24. 13. Lowe JC. Thyroid status of 38 fibromyalgia patients: implications for the etiology of fibromyalgia. Clin Bull Myofascial Ther. 1997;2(1):47-64. 14. Lowe JC. Results of an open trial of T3 therapy with 77 euthyroid female fibromyalgia patients. Clin Bull Myofascial Ther. 1997;2(1):35-37. 15. Lowe JC. A case-control study of metabolic therapy for fibromyalgia: long-term (1-to-5 year) follow-up comparison of treated and untreated patients. Clin Bull Myofascial Ther. 1997;2(2-3):91-124. 16. Lowe JC, Reichman AJ, Yellin J, et al. Thyroid status of fibromyalgia patients. Clin Bull Myofascial Ther. 1998;3(1):47-53. 17. Lowe JC. Thyroid hormone replacement therapies: ineffective and harmful for many hypothyroid patients. May 4, 2004. http://www.drlowe.com/frf/t4replacement/intro.htm. Accessed January 22, 2012. 18. Lowe JC. Introduction: Dr. Richard Guttler and the “real thyroid experts”: their false and potentially harmful beliefs. August 14, 2004. http://www.drlowe.com/frf/guttler/intro.htm. Accessed January 22, 2012. 19. Lowe JC. Dr. Kenneth Blanchard’s false beliefs about T3 therapy. Thyroid Sci. 2008;3(1):1-2. 20. Lowe JC. Stability, effectiveness, and safety of desiccated thyroid vs. levothyroxine: a rebuttal to the British Thyroid Association. Thyroid Sci. 2009;4(3):C1-C12. 21. Lowe JC, Yellin JG. Inadequate thyroid hormone regulation as the main mechanism of fibromyalgia: a review of the evidence. Thyroid Sci. 2008;3(6):R1-R14.

Written by Dr. John C. Lowe In this newsletter, I address a question I often receive from readers of drlowe.com” target=”_blank” class=”bb-url”>http://www.drlowe.com”>drlowe.com The writers’ words differ a bit, but over-and-over again, they ask the same question, so I thought it appropriate to publish my general answer here. The often asked question goes something like this: “I have very high thyroid antibodies, but my TSH, T4, and T3 are normal. I have many hypothyroid symptoms and my basal body temperature is extremely low, usually 96.7 degrees Fahrenheit (35.94 degrees Celsius). But my doctor says the antibodies are not that important and that I do not need to take thyroid hormone. Do you agree with him or not?” My answer is always the same: I resoundingly do not agree with the doctor. First, as my wife Tammy recently said, consider the prefix to the term “anti-bodies.” The prefix means “against,” and just like anti-freeze prevents your car’s radiator from freezing, anti-bodies against your thyroid gland, if they stay high, will, sooner or later, prevent the gland from working normally. Your symptoms and your extremely low basal body temperature strongly suggest to me that your gland is already impaired. How do we know if the thyroid gland has been damaged? Not necessarily by measuring your TSH, T4, or T3 levels. The levels of these hormones may be in range or out. The blood levels just aren’t reliable enough to tell us whether a person has sufficient thyroid hormone for his or her cells to function normally. The endocrinology specialty and its corporate sponsors wish with all their might that these tests were the ultimate gauges. But, alas, they definitely are not! The TSH, T4, and T3 levels vary dramatically every thirty minutes(1, 2, 3, 4). Because of this extreme variance, unless the levels are far out of range, they are inaccurate criteria for inferring whether your tissues have enough thyroid hormone regulation. I have done hundreds of measurements of patients’ resting metabolic rates. Some patients were taking thyroid hormone and others not. For patients with low metabolic rates, I have done differential diagnoses to learn the most likely cause of the low rates. The most likely cause for most of them has been too little thyroid hormone regulation. I know from statistical analyses of the data from these evaluations that the TSH, T4, and T3 levels do not reliably predict which patients do and do not have too little thyroid hormone regulation. High thyroid antibodies are important in and of themselves. Because yours are high, you should be motivated to get them back down into their reference ranges. If a patient’s antibodies stay high, they may eventually cross-react with a tissue other than the thyroid gland. The patient will then have autoimmune disease of both the thyroid gland and the other tissue. I find antibody tests much more useful than the TSH, T4, or T3. High antibodies indicate that a patient’s symptoms are from too little thyroid hormone regulation when the TSH, T4, or T3 fail to do so. Consider a 1996 study by Aarflot and Bruusgaard (5). They included 737 men and 771 women in their study. Men and women who had chronic widespread musculoskeletal pain (often diagnosed as “fibromyalgia”) had a higher incidence of thyroid antibodies than men and women who didn’t have pain. But the TSH, T4, and T3 levels of the two groups of men and women did not differ. My research is now complete in showing that fibromyalgia symptoms are caused mainly by too little thyroid hormone regulation. In view of this, Aarflot and Bruusgaard’s finding indicates that antibody tests show too little thyroid hormone regulation while the TSH and thyroid hormone levels often fail to do so. As the well-known thyroid specialist Dr. Robert Volpé has written, the TSH, T4, and T3 levels may be “normal” for years despite patients having autoimmune thyroiditis the whole time (6). You can have more confidence in your need for thyroid hormone therapy if you have one or more of the physiological abnormalities common among hypothyroid patients. The abnormalities include - 1 a low basal body temperature, which you have; - 2 a basal pulse rate too low for your level of cardiovascular conditioning; - 3 a slow relaxation phase during your Achilles reflex; and - 4 a low voltage R wave in the QRS complex of your EKG. Of course, you can measure your temperature and pulse rate at home. Hopefully your doctor will cooperate by testing your Achilles reflex and measuring the voltage of your R wave. When patients come to our clinic, we also do the most important test of all the resting metabolic rate, and we measure the composition of their bodies. We measure body composition so that I know the patients’ lean body weight. I use the measurement in an equation to learn what his or her metabolic rate should be. Then, when we measure the patient’s actual metabolic rate, I can calculate how low it is compared to what it should be. The body composition measurement is important for another reason: so that I can decide whether the patient has a sign common among hypothyroid patients. This sign is too much body fat for the patient’s diet and physical activity level. When patients come to our clinic, we have the advantage of being able to observe them in person. The reason this is valuable is that if a doctor has learned the physical signs of hypothyroidism (7), he or she can usually tell a lot about a patient’s thyroid status just by observing the patient first hand. Considering what I said above, I hope that one thing is clear: whether you come to our clinic or not, you can accumulate evidence that should convince any reasonable doctor that you probably have too little thyroid hormone regulation. If that evidence exists, then a trial of thyroid hormone therapy – although not T4 – replacement is in order. Remember that the TSH, T4, or T3 don’t reliably tell you whether you do or don’t need treatment. So, if you let your doctor deny you a trial of thyroid hormone therapy because of reference range levels of these tests, you’ll be allowing him or her put your health and well-being at risk. I personally wouldn’t let an uninformed doctor subject me to that. References 1. Kraus, R.P., Phoenix, E., Edmonds, M.W., et al.: Exaggerated TSH responses to TRH in depressed patients with ‘normal’ baseline TSH. J. Clin. Psychiatry, 58(6):266-270, 1997. 2. Baumgartner, A., Dietzel, M., Saletu, B., et al.: Influence of partial sleep deprivation on the secretion of thyrotropin, thyroid hormones, growth hormone, prolactin, luteinizing hormone, follicle stimulating hormone, and estradiol in healthy young women. Psychiatry Res., 48(2):153-178, 1993. 3. Ain, K.B., Pucino, F., Shiver, T.M., et al.: Thyroid hormone levels affected by time of blood sampling in thyroxine-treated patients. Thyroid, 3(2):81-85, 1993. 4. Sakaue, K.: Studies on the factors affecting serum thyrotropin levels in healthy controls and on the thyroid functionin depressed patients using a highly sensitive immunoassay. Nippon Naibunpi Gakkai Zasshi, 66(10):1094-1107, 1990. 5. Aarflot, T. and Bruusgaard D.: Association between chronic widespread musculoskeletal complaints and thyroid autoimmunity. Results from a community survey. Scand. J. Prim. Health Care, 14(2):1111-1115, 1996. 6. Volpé, R.: Autoimmune thyroiditis. In Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text, 6thedition. Edited by L.E. Braverman and R.D. Utiger, New York, J.B. Lippincott Co., 1991, pp.921-933. 7. Lowe, J.C.: The Metabolic Treatment of Fibromyalgia. Boulder, McDowell Publishing Co., 2000.

Written by Dr. Barry Durrant-Peatfield The body has a remarkable ability to heal itself, and should be given a chance to do so. The most successful early physicians knew their subject so well that the natural cause, and eventually self-healing of the illness, was often quite predictable. So the Vital Elixir was given just before the patient showed clear signs of getting better, with, of course, miraculous results. This incidentally, is not the same as the placebo effect (often cited as the result of thyroid and adrenal therapy), which occurs for a limited time as a result of strong suggestions by the prescriber or high expectation by the patient. Sometimes, a remarkable and dramatic recovery occurs using eye of newt and toe of frog. This bedevils a balanced judgement of cause and effect. Sorry, I digress. So the first approach is an alert and informed assessment of progress, intervening only when necessary. Over-intervention is the curse of modern medicine in almost any illness you can imagine; we should take to heart that sometimes a policy of masterly inactivity is much better for the patient and may even spare his life. The second line of approach is to relieve symptoms until it is clear that the illness is either going to resolve itself in time or will recall sterner measures. There are two medical weapons in most common use. First, simply anxiolytics. These are basically tranquillisers, and are acceptable for a limited time where the degree of over activity causes nervous tremor, worry, panic and palpitations. The old fashioned and much derided Valium has a use here not a large dose, say 5 mgs twice or three times a day can make life bearable. Along with this, or possibly instead beta blockers may be used. These are a group of compounds which prevent high levels of nervous activity reaching the tissues, and have a general calming effect on anxiety, nervous shaking and rapid pulse, in addition to their other therapeutic effects like reducing blood pressure, slowing down heart action (helping angina) and preventing migraines. The one most widely used is Propranalol, often 10 to 40 mgs 2 or 3 times a day according to need. Even with extensive use, there are very few either short term or long term side effects, although asthma is sometimes a problem. Many doctors have found that a combination of an anxiolytic and a beta-blocker, in really small doses, works better than high doses of either by themselves and may control mild hyperthyroidism for extended periods of time. When things are getting tougher, the next approach is the use of a chemical block on the production within the thyroid of thyroxine, which prevents the iodine molecules from attaching themselves normally to the thyronine molecule. Two preparations have been in use for years; the commonest is Carbimazole (usually in multiples of 5 mgs) and the other is Propyl-thiouracil (20 mgs). They are both widely used as a bulwark against invasive surgical or medical attack, as I will discuss in a moment. There are of course, difficulties; they have been found to cause problems with the growth of white blood cells, suddenly and unexpectedly, and the immune system may be so compromised that a major or minor infection may suddenly appear. Sometimes, of course, the patient is simply intolerant of the medication and becomes ill. A regular daily dose is chosen; rapidly, the amount of thyroid hormone production starts to fall and the circulation of thyroid hormones starts to decline. The trick, of course, is to ensure the dose is neither too much, nor too little, remembering that thyroid production and thyroid hormone requirement may vary quite a lot. If this isnt born in mind, the result would be that the patient may be out of balance, either over or under active. Most physicians fall back upon the blood test to adjust dosage, but I think it is tiresome to have repeated tests, when the patient who after all, knows how they fell better than anybody may often have a much better idea of their requirements than any blood tests. I have always taught my patients to check their pulse rate once or twice a day and their resting temperature; and to make an overall assessment as to whether they fell well or not. If too much of the medicine is given, the thyroid activity will be low and the patient will feel tired, cold and sluggish; the pulse may be low, say 60 bpm; the resting temperature below 36.6 degrees centigrade or 97.8 degrees Fahrenheit. (Of this resting temperature, more anon). The patient should, in my view, with ordinary common sense, then adjust the dose downwards, (or have a day or so off) until things have put themselves right. And, of course, vice versa. This treatment may be used for an extended time, certainly a year or so so long as the self-monitoring and the advice from an understanding doctor or health care practitioner provide for virtual normality. Most commonly, the over active state will, with ups and downs, tend to correct itself; and the patient may find in time the medication becomes unnecessary. A life event or illness may, however, start it all over again, but the patient by now will recognise the symptoms and be able to deal with them. Another common sequel however, is that having normalised for a while, the thyroid activity may start running below normal. This, as we noted before, occurs with Hashimotos disease. The management problem is that this running down may be slow and insidious the loss of energy and well being, the weight gain, may go more or less unnoticed, may be put down to age, over-work, worry, or bad eating, before it becomes obvious that all is not well. Informed patients will alert themselves to this and seek advice. This may or may not be helpful, and patients may have to take matters into their own hands, using available natural thyroid support, not requiring a prescription. Popular in some quarters is the block and replace approach to treatment. A dose of Carbimozole (Neomercazole) or Propyl-thiouracil is chosen to be deliberately in excess of the actual requirements enough more or less to shut the whole thing down. Then, thyroxine is added to bring it all back to normal. Yes I know what youre thinking. However, the idea is to shut the thyroid down so thoroughly that it is sufficiently shocked by it all not to relapse when the anti-thyroid treatment is withdrawn. It is claimed that control is smoother, and there is a lower relapse rate. All I can say is that it may work like this way sometimes, but it is difficult to be convinced. What should be the final solution is, in my view, all too rapidly turned to by doctors and surgeons, who may consider their solution the treatment of choice right from the start. It has the merit of usually having an immediate effect, but may bring in its train other problems, and simply exchange one therapeutic master for another, with no hope of a normal thyroid function without continuous and long-term medication. This final solution is thyroid ablation, which means the thyroid is knocked out finally and forever. Two approaches are chosen; the first is radioactive iodine. Here the iodine is given to the patient as a drink. The radioactive iodine concentrates in the thyroid tissue and nukes it. The second is surgery, where a proportion of thyroid tissue is removed. The problem with these two solutions lies in their permanence; they cannot be undone, and getting it right that is nuking or removing the right amount, can only be a matter of guess work. More often than not, the amount destroyed or removed is not right to begin with; furthermore, it obviously cannot allow for changes in thyroid function, which will occur within the passage of time. With radioactive iodine ablation there is the merit of simplicity. A solution is prepared of the radioactive isotope of iodine, which is swallowed in one draught. The thyroid uses iodine as its main raw material, and so this radioactive form concentrates in the colloid (hormone forming) tissue in the thyroid gland. (Of course, it goes elsewhere in the body, especially the breast, but you may not be told this). We all know that radioactivity destroys cell and Chernobyl showed us how terrible its uncontrolled effects are. Radioactive iodine concentrates itself in the cells and this radioactivity destroys them. The severity of cellular damage depends, of course, on how much is initially given. This amount is calculated by body weight and the presumed severity of the over activity of the thyroid forming cells. You hope it is about right. You have undergone all the blood tests after all. And we know blood tests are wonderful and right- Or do we? There are 3 possible scenarios. One is that the calculation is right it does happen. The amount of thyroid tissue left is just right to produce the right level of hormones in the blood stream. (Of course, the cells may later partly recover, and then it may have to be done all over again, or further damage and loss of function may occur and the thyroid as a whole may become under active). The second scenario is that the patient continues to have an over active thyroid in spite of treatment, and a further dose of radioactive iodine or doses may have to be given at once. In this circumstance, getting it right becomes more and more unlikely. The third scenario is a good deal more common. Overkill becomes evident in a few days, and thyroid hormone in the blood stream falls pretty quickly. Very soon, thyroid replacement (usually thyroxine) becomes necessary. So long as the physician is convinced that this is what has happened admits it, in spite of blood tests, which may or may not confirm the situation and prescribes thyroxine, the resulting hypothyroidism can be sorted out. However, as we shall see later, diagnosis is most likely to be based on blood levels, and not on what the patient is saying. So the hapless patient, bewildered by this perfect high-tech wonder treatment, repeatedly assured how much better they must be, but feeling more or less terrible, exchanged one sort of pill for another, this time for the rest of his or her life. As I have found with many hundreds of patients, it may now be very difficult to get the reasons not entirely clear, problems arise with the uptake of the synthetic thyroxine (we know the other thyroid hormones will assuredly not be given) and the conversion T4 to T3 doesnt work as it should, and tissue uptake doesnt take place as it should. It would seem logical, having wrecked thyroid function, that if replacement is required it should be provided as close to natural thyroid hormone as possible. What seems to happen, however, is that our unfortunate patient, having repeated blood tests finds blood levels swinging about from one extreme to another, as the physician constantly tries to get it right by altering the thyroxine doses. The patient, of course, never feels really well, sometimes ever again. The second ablative approach we saw is thyroid surgery. Let it be said at once that growths or cysts in the thyroid must be treated by surgical removal or a draining procedure, and a much-enlarged thyroid which interferes with breathing or swallowing leaves no option. But partial thyroidectomy to reduce the amount of thyroid hormone forming tissue is a popular, if in some eyes, barbaric procedure. It is popular with surgeons, if only because, their job done, they may then refer the patient back to the physician for subsequent management. My view is that as a procedure, it should be the last resort only; and not as is so often and regrettably the case, almost the first option. Apart from all the normal objections to surgery, and a lasting reminder from the scar that one has had ones throat cut, the objection has to be the same as with nuking; however, can one make a good enough guess to get it right? Well, usually it isn't possible. Too little means the surgery may have to be done again or suppressant drugs continued with; too much and one falls back on thyroxine replacement. Sometimes, the abused thyroid tissue may recover some function, so that the result of an over enthusiastic surgical removal may, in time, largely correct itself. But many patients, who have passed through my surgery doors, have found themselves under active sooner or later. Once again, the patient is obliged to join the seesaw of more or less replacement therapy ever after, being told that they are perfectly well whatever they say since the blood tests show they are. Inevitably, I have seen many patients who are hypothyroid in consequence of this treatment. They are told that thyroxine will solve all their problems, resulting in now being hypothyroid. Sometimes, sometimes, it does. But it doesnt do any such thing for a very large number of people. The thyroid produces T4, T3, T2, T1 and calcitonin (and possibly another hormone suspected by Broda Barnes) this is how it works. Perhaps someone can tell me how one of the hormones, a synthetic precursor hormone, can do as well as the natural product. Well, largely I find it cant, and doesnt. I find many people never recapture their original health, in spite of the constant adjustment of dose; and more over, they often turn out to be suffering from symptoms and signs of low adrenal function. Getting them right can be very difficult but a combination of adrenal support, often natural, together with thyroid support, can go a very long way to restoring normal health.

Written by Dr. Barry Durrant-Peatfield In his article mysteriously entitled, "Whose thyroid replacement is it anyway?" Professor Weetman starts the discussion by taking the view that there seems nothing more straightforward than the treatment of hypothyroidism. One certainly wishes that this simplistic view were true. Sadly, this is very far indeed from the case. Thyroid deficiency affects every organ, every tissue, every cell of the body, and in an degree from a mild dysfunction to complete failure; moreover, being human necessarily implies that sufferers are going to react differently. This makes, on the contrary, for very great complexity in the management of hypothyroid dysfunction. It would be a great help if present assays, however robust, could be relied upon; but they cannot. The gold standard of measurement, the TSH, is subject to extreme error. The tissue thyroid receptors, the alpha 1 and 2 receptors and the beta 1 and 2 receptors provoke a differing TSH response to cellular thyroid hormone deficiency; and a pituitary, affected by a period of hypometabolism, will have a dysfunctional response so that its TSH production may be down-regulated. The measurements of serum thyroxine and serum liothyronine levels are similarly full of hazard. They are, as it were, a snapshot of blood levels, which may have a very limited relationship to the amount of T3 binding to tissue receptors, or the viability of T4 to T3 conversion, or indeed the availability of T4 from the transport protein. One reliable way of overcoming these problems is the assay of T3 and T4 excreted over 24 hours in the urine, a technique described by Baisier and Hertoghe; but, almost unbelievably, endocrinologists, if they are aware of this assay, unite in condemnation of it. Nowhere has Prof Weetman given any credence to the clinical appraisal of the hypothyroid state. A proper history and physical examination can make the diagnosis obvious to the physician. We have the examples of Murray and Hertoghe in the first two decades of the last century, whose descriptions of their clinical approach are without peer; and are just as true today as they were then. In this world of evidence based medicine this has come to mean that the evidence is narrowed down to clinical assays only. It should go without dispute that the physicians observation should not only be included in this evidence, but, indeed, have precedence over the tests. In this connection the Barnes Basal temperature test does not deserve the implied opprobrium heaped on it by Prof Weetman. It is a most valuable tool as a screening test, and Prof Weetman misunderstands its role when he suggests that it is used to make the diagnosis. In fact a low basal temperature points the way to a fuller clinical appraisal, and it is here that its great value lies. The dissatisfaction of patients as described in the listed submissions is clearly extreme. Indeed, it is difficult to find a parallel anywhere else in medicine. There are really only two possible explanations for the anger and depth of feeling thus expressed. That there are disaffected pressure groups intent on torpedoing the proper practice of medicine for an agenda of their own. That the standard of care, diagnosis and treatment offered by practitioners falls so far short of reasonably expected standards that desperate patients want something done. Prof Weetman clearly discounts the second alternative, refusing to countenance the possibility that the conduct of himself and his like minded colleagues could possibly be at fault. Patients who have the temerity to conduct their own research and so question the rigidly held conclusions of their medical advisors are, it would seem, straying into fields of knowledge they have no right to go. In fact, these disaffected, and, be it said, ungrateful folk, are quite as bright as many of the doctors, and can work things out for themselves, successfully and correctly too. It is the fact that they do so which offends Prof Weetmans sensibilities. These are matters, he feels, for only the informed and elected cognoscenti; not for the vox populi. It would perhaps be disingenuous to point out that one of the most serious, and least considered, complications of thyroid illness is consequent adrenal dysfunction, which explains why so many patients stubbornly refuse to admit they are cured when the blood tests say they are. This brings us to the quite outrageous and sweeping assertion that the majority of these patients have functional somatoform disorders. This fine new description, thanks to Prof Wellesleys efforts, is a neologism for hysteria. It implies that this majority of patients have personality disorders which make it impossible for them to accept, with good (and uncomplaining) grace, their illness. While no illness in medicine can ever be entirely without this pathology, this sweeping assertion is very much open to question. Indeed, one could be forgiven for wondering, perhaps, if these are the patients who havent played the game by the rules, and so remain ill, and it brings the whole of Prof Weetmans argument into a reductio ad absurdum. No wonder we on the inside cannot adequately describe these somatoform disorders. Could it be, it must be asked, that on the contrary, these patients really are ill? We are also asked to accept that healthism is a modern evil. The disgraceful fact, it would seem, is that the mob, distrustful of their doctors and a multiplicity of new and more lethal drugs, is actually out to improve its own health. This, of course, is the new curse of the age which should be stamped out by Prof Weetman and his colleagues. The manifest absurdity of this view is beyond comment. Perhaps it should be made clear why this flood of angry and disaffected patients seek out knowledge about their illness. Taking on board, for the sake of arguments, that a) they really are ill, b) they have through their researches learnt about their illness, and c) know the broad outlines of their treatment, if whatever they say is ignored, or put down to a functional somatoform disorder, then would not this response to their fate be entirely expected? Broda Barnes, whose pioneering and carefully researched work receives a passing mention in Prof Weetmans article was of the opinion that perhaps 30% of folk by mid-life may have some level of thyroid dysfunction. The present writer who can lay claim to more than 40 years of practical experience with hypothyroidism and hypoadrenalism, sees no reason to disagree with this admittedly alarming statistic. Yet Prof Weetman would have us believe that the majority of such sufferers are, basically, making the whole thing up. They cannot really be ill because the standard evidence gives them no support, and because they are told they are not. It is no help asking either, it would seem. They wont be listened to, and they wont be answered. The new guidelines suggesting that patients should not be treated unless the TSH is over 10, is not only totally out of step with thinking elsewhere in the world and especially the American Association of Clinical Endocrinologists but is actually bizarre. There is a reference to the risks of a suppressed TSH, which are very much more imagined than real. What these new guidelines suggests, will condemn, certainly, thousands of patients to being refused treatment; and their consequent illness the result of their functional somatoform disorder. Already, these guidelines have elicited a storm of protest, and it is to be deeply regretted that Prof Weetman allies himself to this position. Quite what the agenda is that condemns so many patients to perhaps decades of ill-health, can only be wondered at. Worse, guidelines have a way of being set in stone, and then doctors who think outside the envelopes, will find themselves proceeded against, led perhaps by Prof Weetman himself. As we know, hypothyroidism may be manifest by a large number of symptoms and signs; and it may be instructive to pick out certain of them. We can include weight gain, depression and anxiety, arthralgia and rheumatic illness, and raised cholesterol. If the diagnosis of hypothyroidism is discounted even forbidden then the functional somatoform disorders must receive attention, and the caring practitioner, anxious to help, may find himself prescribing antidepressants, non-steroidal anti-inflammatories, statins, and weight loss agents. The disadvantages of this approach lie in the cumulative expense and multiplicity of side effects, apart from the fact that it is symptoms being dealt with and not cause. Should the practitioner be able to overcome the hurdle of the diagnosis, then all the symptoms and signs could be treated using thyroxine, for a few pounds a month and usually with great success. There are certain precepts in medicine to which attention should be drawn with which perhaps Prof Weetman is no longer familiar. The first is to remember the value of Occams razor in medicine: that is, common things commonly occur. Then the importance of listening to the patient: 9 times out of 10 they will tell you the diagnosis and often the treatment. Finally: if the lab tests dont match your clinical intuition, back your intuition. Armed with these simple but valuable precepts, the diagnosis of functional somatoform disorder can be relegated to where it belongs, and the correct and perhaps obvious diagnosis made. The great fear is that the example of Prof Weetman and the guidelines suggested by him (and recently in other quarters) will become establishment medicine, and doctors will not dare to make the correct diagnosis. To do so may be more than their career is worth. Only a handful of independent, and independent minded, practitioners, will be prepared to shoulder this risk on behalf of their patients. And their number diminishes steadily. So one must ask what is it all about? Recently we learned that osteopaths and chiropractors dont help us in the way we all believe; that omega-3 supplements are no help to our cardiovascular health and that we should cheerfully accept very large doses of statins; and now that hypothyroidism is actually quite rare and its diagnosis likely to be evidence of a doctors incompetence in the face of pressure from his patients.

An Interview With Dr. Raymond Peat who offers his thoughts about Thyroid Disease Mary Shomon: Why do women with treated hypothyroidism frequently still have inappropriately high levels of cholesterol and high triglycerides, and what can they do to help lower these levels? Dr. Ray Peat: Often it’s because they were given thyroxine, instead of the active thyroid hormone, but hypertriglyceridemia can be caused by a variety of things that interact with hypothyroidism. Estrogen treatment is a common cause of high triglycerides, and deficiencies of magnesium, copper, and protein can contribute to that abnormality. Toxins, including some drugs and herbs, can irritate or stimulate the liver to produce too much triglyceride. T3, triiodothyronine, is the active thyroid hormone, and it is produced (mainly in the liver) from thyroxine, and the female liver is less efficient than the male liver in producing it, as is the female thyroid gland. The thyroid gland, which normally produces some T3, will decrease its production in the presence of increased thyroxine. Therefore, thyroxine often acts as a “thyroid anti-hormone,” especially in women. When thyroxine was tested in healthy young male medical students, it seemed to function “just like the thyroid hormone,” but in people who are seriously hypothyroid, it can suppress their oxidative metabolism even more. It’s a very common, but very serious, mistake to call thyroxine “the thyroid hormone.” High cholesterol is more closely connected to hypothyroidism than hypertriglyceridemia is. Increased T3 will immediately increase the conversion of cholesterol to progesterone and bile acids. When people have abnormally low cholesterol, I think it’s important to increase their cholesterol before taking thyroid, since their steroid-forming tissues won’t be able to respond properly to thyroid without adequate cholesterol. Mary Shomon: You feel that progesterone can have anti-stress effects, without harming the adrenal glands. Is progesterone therapy something you feel is useful to many or most hypothyroid patients? How can a patient know if she needs progesterone? Do you recommend blood tests? And if so, at what point in a woman’s cycle? Dr. Ray Peat: Estrogen blocks the release of hormone from the thyroid gland, and progesterone facilitates the release. Estrogen excess or progesterone deficiency tends to cause enlargement of the thyroid gland, in association with a hypothyroid state. Estrogen can activate the adrenals to produce cortisol, leading to various harmful effects, including brain aging and bone loss. Progesterone stimulates the adrenals and the ovaries to produce more progesterone, but since progesterone protects against the catabolic effects of cortisol, its effects are the opposite of estrogen’s. Progesterone has antiinflammatory and protective effects, similar to cortisol, but it doesn’t have the harmful effects. In hypothyroidism, there is a tendency to have too much estrogen and cortisol, and too little progesterone. The blood tests can be useful to demonstrate to physicians what the problem is, but I don’t think they are necessary. There is evidence that having 50 or 100 times as much progesterone as estrogen is desirable, but I don’t advocate “progesterone replacement therapy” in the way it’s often understood. Progesterone can instantly activate the thyroid and the ovaries, so it shouldn’t be necessary to keep using it month after month. If progesterone is used consistently, it can postpone menopause for many years. Cholesterol is converted to pregnenolone and progesterone by the ovaries, the adrenals, and the brain, if there is enough thyroid hormone and vitamin A, and if there are no interfering factors, such as too much carotene or unsaturated fatty acids. Progesterone deficiency is an indicator that something is wrong, and using a supplement of progesterone without investigating the nature of the problem isn’t a good approach. The normal time to use a progesterone supplement is during the “latter half” of the cycle, the two weeks from ovulation until menstruation. If it is being used to treat epilepsy, cancer, emphysema, migraine or arthritis, or something else so serious that menstrual regularity isn’t a concern, then it can be used at any time. If progesterone is used consistently, it can postpone menopause for many years. Mary Shomon: What supplements do you feel are essential for most people with hypothyroidism? Dr. Ray Peat: Because the quality of commercial nutritional supplements is dangerously low, the only supplement I generally advocate is vitamin E, and that should be used sparingly. Occasionally, I will suggest limited use of other supplements, but it is far safer in general to use real foods, and to exclude foods which are poor in nutrients. Magnesium is typically deficient in hypothyroidism, and the safest way to get it is by using orange juice and meats, and by using epsom salts baths; magnesium carbonate can be helpful, if the person doesn’t experience side effects such as headaches or hemorrhoids. Mary Shomon: Do you feel that there are any special considerations, issues, or treatments for men with hypothyroidism? Dr. Ray Peat: Thyroid supplements can be useful for prostate hypertrophy and some cases of impotence and infertility. Occasionally, a man who can’t put on a normal amount of weight finds that a thyroid supplement allows normal weight gain. Leg cramps, insomnia and depression are often the result of hypothyroidism. Heart failure, gynecomastia, liver disease, baldness and dozens of other problems can result from hypothyroidism. Mary Shomon: Many people describe how they are clinically hypothyroid, with elevated TSH levels, but have extremely high pulse rates. Do you have any thoughts as to what might be going on in that situation? Dr. Ray Peat: In hypothyroidism, thyrotropin-release hormone (TRH) is usually increased, increasing release of TSH. TRH itself can cause tachycardia, “palpitations,” high blood pressure, stasis of the intestine, increas of pressure in the eye, and hyperventilation with alkalosis. It can increase the release of norepinephrine, but in itself it acts very much like adrenalin. TRH stimulates prolactin release, and this can interfere with progesterone synthesis, which in itself affects heart function. I consider even the lowest TSH within the “normal range” to be consistent with hypothyroidism; in good health, very little TSH is needed. When the thyroid function is low, the body often compensates by over-producing adrenalin. The daily production of adrenalin is sometimes 30 or 40 times higher than normal in hypothyroidism. The adrenalin tends to sustain blood sugar in spite of the metabolic inefficiency of hypothyroidism, and it can help to maintain core body temperature by causing vasoconstriction in the skin, but it also disturbs the sleep and accelerates the heart. During the night, cycles of rising adrenalin can cause nightmares, wakefulness, worry, and a pounding heart. Occasionally, a person who has chronically had a heart rate of 150 beats per minute or higher, will have a much lower heart rate after using a thyroid supplement for a few days. If your temperature or heart rate is lower after breakfast than before, it’s likely that they were raised as a result of the nocturnal increase of adrenalin and cortisol caused by hypothyroidism. Mary Shomon: You have written that for some people, there is a problem converting T4 to T3, but that diet can help. You recommend a piece of fruit or juice or milk between meals, plus adequate protein, can help the liver produce the hormone. Can you explain a bit more about this idea and how it works? Dr. Ray Peat: The amount of glucose in liver cells regulates the enzyme that converts T4 to T3. This means that hypoglycemia or diabetes (in which glucose doesn’t enter cells efficiently) will cause hypothyroidism, when T4 can’t be converted into T3. When a person is fasting, at first the liver’s glycogen stores will provide glucose to maintain T3 production. When the glycogen is depleted, the body resorts to the dissolution of tissue to provide energy. The mobilized fatty acids interfere with the use of glucose, and certain amino acids suppress the thyroid gland. Eating carbohydrate (especially fruits) can allow the liver to resume its production of T3. Mary Shomon: You have recommended if supplemental T3 is used, a thyroid patients “nibble on a 10-15 mg Cytomel tablet throughout the day.” Can you explain why? Would compounded time-released T3 as available in some compounding pharmacies do the same? Dr. Ray Peat: Most hypothyroid people can successfully use a supplement that contains four parts of thyroxine for each part of T3, but some people need a larger proportion of T3 for best functioning. The body normally produces several micrograms of T3 every hour, but if a large amount of supplementary thyroid is taken in a short time, the liver quickly inactivates some of the excess T3. Taking a few micrograms per hour provides what the body can use, and doesn’t suppress either the liver’s or the thyroid’s production of the hormone. I have only rarely talked to anyone who had good results with the so-called time-release T3, and I have seen analyses of some samples in which there was little or no T3 present. It is hard to compound T3 properly, and the conditions of each person’s digestive system can determine whether the T3 is released all at once, or not at all. I don’t think there is a valid scientific basis for calling anything “time-release T3.” I have been told that the company which now owns the Armour name and manufactures “Armour thyroid USP” has added a polymer to the formula, and I think this would account for the stories I have heard about its apparent inactivity. Some people have found that the tablets passed through their intestine undigested, so I think it’s advisable to crush or powder the tablets. Mary Shomon: You feel that excessive aerobic exercise can be a cause of hypothyroidism. Can you explain this further? How much is too much? Dr. Ray Peat: I’m not sure who introduced the term “aerobic” to describe the state of anaerobic metabolism that develops during stressful exercise, but it has had many harmful repercussions. In experiments, T3 production is stopped very quickly by even “sub-aerobic” exercise, probably becaue of the combination of a decrease of blood glucose and an increase in free fatty acids. In a healthy person, rest will tend to restore the normal level of T3, but there is evidence that even very good athletes remain in a hypothyroid state even at rest. A chronic increase of lactic acid and cortisol indicates that something is wrong. The “slender muscles” of endurance runners are signs of a catabolic state, that has been demonstrated even in the heart muscle. A slow heart beat very strongly suggests hypothyroidism. Hypothyroid people, who are likely to produce lactic acid even at rest, are especially susceptible to the harmful effects of “aerobic” exercise. The good effect some people feel from exercise is probably the result of raising the body temperature; a warm bath will do the same for people with low body temperature. Mary Shomon: You feel that chronic protein deficiency is a common cause of hypothyroidism. How much protein should people get (as much as 70-100 grams a day?) and what types of protein, in order to prevent hypothyroidism? Dr. Ray Peat: The World Health Organization standard was revised upward by researchers at MIT, and recently the MIT standard has been revised upward again by military researchers; this is described in a publication of the National Academy of Sciences (National Academy Press, The Role of Protein and Amino Acids in Sustaining and Enhancing Performance, 1999). When to little protein, or the wrong kind of protein, is eaten, there is a stress reaction, with thyroid suppression. Many of the people who don’t respond to a thyroid supplement are simply not eating enough good protein. I have talked to many supposedly well educated people who are getting only 15 or 20 grams of protein per day. To survive on that amount, their metabolic rate becomes extremely low. The quality of most vegetable protein (especially beans and nuts) is so low that it hardly functions as protein. Muscle meats (including the muscles of poultry and fish) contain large amounts of the amino acids that suppress the thyroid, and shouldn’t be the only source of protein. It’s a good idea to have a quart of milk (about 32 grams of protein) every day, besides a variety of other high quality proteins, including cheeses, eggs, shellfish, and potatoes. The protein of potatoes is extremely high quality, and the quantity, in terms of a percentage, is similar to that of milk. Mary Shomon: You talk about darkness and shorter days of winter as a stress. It’s known that more thyroid hormone is needed by some patients during colder weather. Are there other things you recommend patients do to “winterproof” their metabolism? Dr. Ray Peat: Very bright incandescent lights are helpful, because light acts on, and restores, the same mitochondrial enzymes that are governed by the thyroid hormone. In squirrels, hibernation is brought on by the accumulation of unsaturated fats in the tissues, suppressing respiration and stimulating increased serotonin production. In humans, winter sickness is intensified by those same antithyroid substances, so it’s important to limit consumption of unsaturated fats and tryptophan (which is the source of serotonin). When a person is using a thyroid supplement, it’s common to need four times as much in December as in July. Mary Shomon: You have reported that pregnenolone can be helpful for Graves’ patients with exophthalmus. Can you explain further? Dr. Ray Peat: Graves’ disease and exophthalmos can occur with hypothyroidism or euthyroidism, as well as with hyperthyroidism. Pregnenolone regulates brain chemistry in a way that prevents excessive production of ACTH and cortisol, and it helps to stabilize mitochondrial metabolism. It apparently acts directly on a variety of tissues to reduce their retention of water. In the last several years, all of the people I have seen who had been diagnosed as “hyperthyroid” have actually been hypothyroid, and benefitted from increasing their thyroid function; some of these people had also been told that they had Graves’ disease. Mary Shomon: You are a proponent of coconut oil for thyroid patients. Can you explain why? Dr. Ray Peat: An important function of coconut oil is that it supports mitochondrial respiration, increasing energy production that has been blocked by the unsaturated fatty acids. Since the polyunsaturated fatty acids inhibit thyroid function at many levels, coconut oil can promote thyroid function simply by reducing those toxic effects. It allows normal mitochondrial oxidative metabolism, without producing the toxic lipid peroxidation that is promoted by unsaturated fats. Mary Shomon: Do you have any thoughts for thyroid patients who are trying to do everything right, and yet still can’t lose any weight? Dr. Ray Peat: Coconut oil added to the diet can increase the metabolic rate. Small frequent feedings, each combining some carbohydrate and some protein, such as fruit and cheese, often help to keep the metabolic rate higher. Eating raw carrots can prevent the absorption of estrogen from the intestine, allowing the liver to more effectively regulate metabolism. If a person doesn’t lose excess weight on a moderately low calorie diet with adequate protein, it’s clear that the metabolic rate is low. The number of calories burned is a good indicator of the metabolic rate. The amount of water lost by evaporation is another rough indicator: For each liter of water evaporated, about 1000 calories are burned. Mary Shomon:You have talked about internal malnutrition as a problem for many thyroid patients, due to insufficient digestive juices and poor intestinal movements. Are there ways patients who are treated for hypothyroidism can help alleviate this problem. Dr. Ray Peat: The absorption and retention of magnesium, sodium, and copper, and the synthesis of proteins, are usually poor in hypothyroidism. Salt craving is common in hypothyroidism, and eating additional sodium tends to raise the body temperature, and by decreasing the production of aldosterone, it helps to minimize the loss of magnesium, which in turn allows cells to respond better to the thyroid hormone. This is probably why a low sodium diet increases adrenalin production, and why eating enough sodium lowers adrenalin and improves sleep. The lowered adrenalin is also likely to improve intestinal motility. Mary Shomon: You’ve mentioned eggs, milk and gelatin as good for the thyroid. Can you explain a bit more about this? Dr. Ray Peat: Milk contains a small amount of thyroid and progesterone, but it also contains a good balance of amino acids. For adults, the amino acid balance of cheese might be even better, since the whey portion of milk contains more tryptophan than the curd, and tryptophan excess is significantly antagonistic to thyroid function. The muscle meats contain so much tryptophan and cysteine (which is both antithyroid and potentially excitotoxic) that a pure meat diet can cause hypothyroidism. In poor countries, people have generally eaten all parts of the animal, rather than just the muscles==feet, heads, skin, etc. About half of the protein in an animal is collagen (gelatin), and collagen is deficient in tryptophan and cysteine. This means that, in the whole animal, the amino acid balance is similar to the adult’s requirements. Research in the amino acid requirements of adults has been very inadequate, since it has been largely directed toward finding methods to produce farm animals with a minimum of expense for feed. The meat industry isn’t interested in finding a diet for keeping chickens, pigs, and cattle healthy into old age. As a result, adult rats have provided most of our direct information about the protein requirements of adults, and since rats keep growing for most of their life, their amino acid requirements are unlikely to be the same as ours. Mary Shomon: Do you think the majority of people with hypothyroidism get too much or too little iodine? Should people with hypothyroidism add more iodine, like kelp, seaweeds, etc.? Dr. Ray Peat: 30 years ago, it was found that people in the US were getting about ten times more iodine than they needed. In the mountains of Mexico and in the Andes, and in a few other remote places, iodine deficiency still exists. Kelp and other sources of excess iodine can suppress the thyroid, so they definitely shouldn’t be used to treat hypothyroidism. Mary Shomon: What are your thoughts for Graves’ disease/hyperthyroidism patients? Should they move ahead quickly to get radioactive iodine treatment, or are there natural things they might be able to try to temporarily or even permanently get a remission? Dr. Ray Peat: Occasionally, a person with a goiter will temporarily become hyperthyroid as the gland releases its colloid stores in a corrective process. Some people enjoy the period of moderate hyperthyroidism, but if they find it uncomfortable or inconvenient, they can usually control it just by eating plenty of liver, and maybe some cole slaw or raw cabbage juice. Propranolol will slow a rapid heart. The effects of a thyroid inhibitor, PTU, propylthiouracil, have been compared to those of thyroidectomy and radioactive iodine. The results of the chemical treatment are better for the patient, but not nearly so profitable for the physician. Besides a few people who were experiencing the unloading of a goiter, and one man from the mountains of Mexico who became hypermetabolic when he moved to Japan (probably from the sudden increase of iodine in his diet, and maybe from a smaller amount of meat in his diet), all of the people I have seen in recent decades who were called “hyperthyroid” were not. None of the people I have talked to after they had radioiodine treatment were properly studied to determine the nature of their condition. Radioiodine is a foolish medical toy, as far as I can see, and is never a proper treatment.

Written by Dr. John C. Lowe, MA, DC, Director of Research, Fibromyalgia Research Foundation, August 20, 2010 The case report we present here was originally published in 1995. The case study was not blinded, but it was highly systematic. Three clinicians (a neuropsychiatrist; a physical therapist; and myself, a chiropractic physician) working in our separate clinical practices in different locations, evaluated the patient using objective measures. The data that I presented in the report of this case report fifteen years ago, and again now, was collected by the three independent clinicians each of whom worked simultaneously with the patient. This systematic single case shows three noteworthy features of the patient: First, she was hypothyroid; second, she met the American College of Rheumatology criteria for fibromyalgia; and third, she no longer met those criteria and fully recovered when we switched her to T3 therapy after T4 and desiccated thyroid had failed to benefit her. It is worth emphasizing that the patient continued to meet the criteria for fibromyalgia when being treated with T4 (Synthroid) and then with desiccated thyroid (Armour). However, she quickly and dramatically recovered—no longer meeting the criteria for fibromyalgia—when we switched her treatment to plain T3 (Cytomel) with her daily dose well within the physiologic range. I asked that Thyroid Science republish this case report for two reasons: First, many people have requested reprints of the original case report. To get reprints, these patients and clinicians had to contact my office. The reason is that the paper is no longer available online or in an accessible journal. In 1996, McDowell Publishing Company, LLC, who owned the journal that first published the report, sold the journal to Haworth Medical Press. The latter publisher, however, did not make available the journal issue that the case report had been published in. Thyroid Science's open-access republishing of the paper now makes it perpetually available to anyone who finds its contents of interest. My second reason for asking that Thyroid Science republish the report is the utter failure of fibromyalgia researchers in general to open their eyes to an obvious truth: that inadequate thyroid hormone regulation is the main underlying mechanisms of most patients so-called fibromyalgia. That I say that this is an obvious truth does not mean that all cases of fibromyalgia are easily solved simply by treating treating the patient with the proper form and dosage of thyroid hormone. As my colleague David Derry, MD, long ago pointed out in the British Journal of Medicine, living long years with untreated or undertreated hypothyroidism causes most patients to accrue secondary, tertiary, and other health complications that also must be disentangled from the enlarging clinical knot that further encumbers the patients. That a patient's fibromyaliga is long-standing usually means that successful recovery is a more complicated process. Nonetheless, deductively formulated theory (the mathematical physicist's tool of victory that is absent from the intellectual armamentarium of the fibromyalgia establishment) shows unequivocally that the main underlying mechanism of fibromyalgia is too little thyroid hormone regulation. The inadequate thyroid hypothesis accounts for virtually all objective evidence we have on fibromyalgia. In stark contrast, no other hypothesis accounts for more than a minute fraction. Ignoring this fact forsakes fibromyalgia patients the world over, but it brings in a king's ransom from the purchase of ineffective and potentially harmful "fibromyalgia drugs" such as Lyrica and Cymbalta. Why do fibromyalgia researchers in general ignore the obvious? Through more than two decades of involvement in this field, I have learned a list of disreputable reasons: prejudice against the possibility of a causative thyroid connection, ignorance of basic and clinical thyroidology, egotistical pursuit of failed pet theories, and corruption through acceptance of judgment-forming grants and other perks from Big Pharma to develop drugs for fibromyalgia that are palliative at best and harmful at worst. Despite many prominent fibromyalgia researchers claiming to be pursuing the underlying mechanism(s) of what we call fibromyalgia, they look everywhere but in the right direction. But while the researchers have spent decades looking in all the wrong directions, countless fibromyalgia patients—such as the female I describe in the case report—have recovered full health by the intelligent use of thyroid hormone as part of a comprehensive program of metabolic rehabilitation. Many have accomplished this by taking their health care into their own hands, while others have had the help of enlightened and collaborative clinicians. My friend and colleague Richard L. Garrison, MD, for example, with T3 therapy and other assertive thyroid therapies, helped countless fibromyalgia patients to recover their health. This infuriated jealous physicians who had gaven the patients quack diagnoses of psychiatric disorders. Dr. Garrison was brutally punished for his crime of being scientific, humanitarian, and effective with patients. But emails I still receive some 3 years after his death tell me that for every physician who detested his clinical successes with fibromyalgia patients is at least matched by recovered patients who still adore him for enabling them to recover their health. I republish this 1995 report with sorrow in my heart over the persecution of courageous physicians such as Dr. Richard L. Garrison who relieved so many patients suffering with the intelligent use of thyroid hormone. My sorrow is even deeper, however, over the millions of fibromyalgia patients who today are improperly treated for profit with Big Pharma's drugs. As my colleagues and I showed many years ago (and typified by the case we republish today in Thyroid Science), the continued suffering of most of those people is avoidable. But sadly, we now live in a world where drug companies and researchers they fund steadily more make their fortunes from sustaining the suffering of other human beings. I find it more than difficult at times to live with the awareness that millions of fibromyalgia patients spend their lives suffering needlessly. But I find some solace in a famous statement by physicist Max Planck, the founder of quantum theory: "A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it." And happily, a new generation appears to me to be sprouting in the field of fibromyalgia. At this time, Ian R. Carroll, MD at Stanford University School of Medicine is conducting a study of T3 for fibromyalgia patients. The title of his study is, "T3 for Fibromyalgia: a Pilot Double-blind Non-randomized Clinical Trial." I have no idea yet how this study will unfold. No research team I am aware other than mine has extensive research and clinical experience in treating fibromyalgia patients effectively with T3. But Dr. Carroll was unaware of my research team and our work until recently, when I learned of his study and sent him a copy of my book The Metabolic Treatment of Fibromyalgia. As his pilot study nears its end, he and I have just begun to correspond. With no intent of malice, but only the hope of seeing the relief of untold and unnecessary human suffering, I am impatient for the passing of that generation of closed-minded fibromyalgia researchers. Before much more time passes, I hope to see a new and enlightened generation of researchers and clinicians that declines to assign the label "fibromyalgia" to people with chronic widespread pain and simply treats them effectively for their hypothyroidism or thyroid hormone resistance. In the mean time, if the case we republish today leads to even one patient's pain relief tomorrow, I will be pleased indeed that I wrote the report fifteen years ago.

Written by: Mary Shomon Dr. Teitelbaum believes that an underlying hypothalamic-pituitary dysfunction – potentially caused by viral damage -- could be common to many cases of both CFS and hypothyroidism. His conclusion that CFS and hypothyroidism are connected is borne out by a number of studies that have shown various links between underlying infections common to both CFS patients, and patients with subclinical or overt hypothyroidism. For example, several studies have found higher-than-normal incidence of human herpesvirus 6 (HHV-6) infection and Epstein Barr Virus (EBV) in both CFS and patients with Hashimoto’s thyroiditis, the autoimmune disease that causes hypothyroidism. One of the most groundbreaking studies was released in 2018. Titled “Higher Prevalence of “ Low T3 Syndrome” in Patients With Chronic Fatigue Syndrome: A Case–Control Study, the study was published in the journal Frontiers in Endocrinology. The researchers reported that CFS, like hypothyroidism, is characterized by low levels of most – but not all – thyroid hormones. Researchers found that most CFS patients had low or low-normal levels of the two key thyroid hormones -- triiodothyronine (T3) and thyroxine (T4). A significant number of the CFS patients also had levels of free T3 – the active and available thyroid hormone that helps oxygen and energy reach cells – that were below the reference range. The CFS patients also tended to have lower iodine levels and higher Reverse T3 levels. Surprisingly, despite all these markers for hypothyroidism, the CFS patients had normal levels of thyroid stimulating hormone (TSH). This meant that conventional guidelines would exclude a diagnosis of hypothyroidism. Instead, according to the researchers, “the low T3 levels found in CFS patients coupled with this switchover to Reverse T3 could mean that T3 levels are severely reduced in tissue.” To that end, the study authors concluded that CFS could be characterized as a “nonthyroidal illness syndrome (NTIS)” or “low T3 syndrome.” According to the researchers, while more studies are needed to confirm their findings, trials of treatment with T3 medication and iodine supplements might be indicated in CFS patients. Interestingly, the researchers also found that the metabolic profile of the CFS patients closely resembled those of hypothyroid patients on levothyroxine (T4) treatment who had persistent and unresolved symptoms, including fatigue. This led the researchers to conclude that T3 treatment may be effective not only in CFS patients, but also in hypothyroid patients with continued symptoms on levothyroxine.

Written by Cort Johnson Low T3 syndrome or nonthyroidal illness syndrome (NTIS) (or euthyroid sick syndrome ESS) is a debated illness found in some serious illness states including sepsis, starvation, surgery, heart attack, and others. Dr. Leslie J DeGroot, M.D., a top endocrinologist, reported in a 2015 review “The Non-Thyroidal Illness Syndrome” that this syndrome probably occurs in “any severe illness”. DeGroot starts off his review stating that NTIS, “refers to a syndrome found in seriously ill or starving patients” who have low free T3, increased reverse T3, normal or low TSH, and, if the condition becomes chronic, low free T4. DeGroot asserts that these findings indicate, as Dr. Holtorf asserts, that low tissue thyroid hormone levels are present, and thus tissue hypothyroidism is present. (Note that low total T4 was not found in the ME/CFS group.) In some ways, this syndrome is no surprise: serum thyroid hormone levels are known to drop during starvation and illness. Starvation (carbohydrate deprivation) inhibits the conversion of T4 to T3 (the active form of thyroid hormone) and prevents the metabolism of reverse T3 (which blocks the receptors for T3, thus reducing the production of T3.) The reduction of active thyroid hormone levels seems to make sense, given a similar reduction in the basal metabolic rate induced by starvation: the body appears to be hunkering down and attempting to conserve its resources until food is present. Starvation isn’t the only inducer of this process, though. DeGroot reports that a large proportion of people in intensive care also exhibit low T3 and T4 levels. They also tend to have increased sympathetic nervous system response – which is, of course, typical in ME/CFS. Various hypotheses have been put forward which propose that NTIS is beneficial or inconsequential and should not be messed with. They include the possibilities that the abnormalities are artifacts, that they do not reflect true free hormone findings, and that they reflect the body’s way of dealing with the situation. DeGroot, however, believes the findings reflect a pathological state. He does not appear to believe that pituitary thyroid hormone levels differ from those of the body in NTIS, but suggests that cortisol / cytokine levels / low O2 levels (hypoxia) / reduced leptin, etc. are likely responsible for the initiation of NTIS. The T4 Paradox – When Treatments Make Things Worse DeGroot’s personal experience is that treating patients with NTIS with T4 (unpublished) often results in significantly elevated rT3 levels (and T3 inhibition). Nunez-Ruiz et. al. also suggest that standard thyroid therapy (T4) in the NTIS-like ME/CFS subset could actually induce a state of NTIS, and point out that T3, recommended by Holtorf for ME/CFS and FM, has been suggested for severe NTIS. They referred to the NHANES cohort, which found that T4 administration resulted in higher T4 levels but 5–10% lower T3 and FT3 levels, and a 15–20% lower T3/T4 ratio. They believe tissue levels of those factors are probably far lower. "Low “T3 syndrome” in our study resembles the thyroid hormone profile of a subgroup of hypothyroid patients receiving T4 monotherapy." The authors Holtorf also has found T4 supplementation unproductive and even harmful at times in his ME/CFS and fibromyalgia population. When high levels of rT3 (>150) are found, or free T3/reverse T3 ratio is greater than 0.2 (measured in picograms per milliliter (pg/mL), instead of T4 (Synthroid and Levoxyl or Amour thyroid – a pig glandular product) Holtorf will prescribe free T3 (compounded) instead. The Worm (Dauer) Rides Again Ruiz-Nunez et. al. believe the metabolomic studies in ME/CFS may be providing a clue. The impaired mitochondrial production and hypometabolic state they suggest appears to fit with their findings of NTIS in a subset of ME/CFS patients (and one would think the general state of reduced thyroid activity in the group as a whole). Hypothyroidism is, after all, associated with decreases in metabolic and heart rates, oxygen consumption, body temperature and oxidation of glucose, fatty acids, and amino acids. They throw the whole kit and kaboodle into the mix (inflammation, infection, gut issues, psychological trauma (particularly during childhood) as they suggest that the cell danger response (aka Naviaux) could be behind the NTIS-like findings in some ME/CFS patients. Inflammation may or may not be the issue. The authors believe that ME/CFS probably represents a common pathophysiological state that can be reached in any number of ways. In a refreshingly direct manner, they reported that their study findings presented one possible way of reaching that state, “but do not get us closer to the cause(s).” Herpesviruses to the Fore? Could one answer – HHV-6 – be hiding in plain sight? Back in 2001, Wikiland reported in The Lancet that fine needle biopsies demonstrated that 40% of people with ME/CFS have lymphocytic thyroiditis. The fact that half of those found with diseased thyroid tissues had normal thyroid lab values suggests that lab values, as Holtorf believes, may not always tell the whole story. Could HHV-6A be contributing to the thyroid issues in ME/CFS? Hashimoto’s thyroiditis, the most common cause of hypothyroidism, occurs as a result of an autoimmune attack. Casselli’s 2012 study finding of a high incidence of HHV-6A DNA in Hashimoto’s thyroid tissues but not in controls (82% vs. 10%, p≤0.001), suggests that HHV-6 could be triggering Hashimoto’s. (HHV-6A was also active in the Hashimoto’s patients, but not in the healthy controls.) If HHV-6A is triggering Hashimoto’s, it might also be triggering the hypothyroidism that seems almost endemic in ME/CFS. The fact that Caselli found HHV – 6A, not HHV- 6B was notable because while virtually everyone is infected with HHV-6B early in life not everyone is infected with HHV-6A – and when they are it tends to be later in life, which is when most cases of ME/CFS begin. Kristin Loomis of the HHV-6 Foundation has tried for years to interest someone in examining the thyroid tissue of people with ME/CFS for pathogens. She’s noted that many of the suspected viral culprits in ME/CFS (HHV-6, parvovirus B19) can cause “smoldering” infections in the thyroid. Now enter Bhupesh Prusty, a Solve ME/CFS Initiative-funded researcher who found HHV-6 in about 60% of a small group of ME/CFS patients’ cells. Prusty found that one HHV-6 infected ME/CFS cell was able to alter the mitochondrial functioning of neighboring, or even distant cells – apparently by secreting mitochondrial inhibitors. Prusty will be speaking at the NIH ME/CFS conference in April. Kristin Loomis speculates that if HHV-6 is present in the thyroid, it may have found its way to the brainstem as well, where it could help produce the autonomic problems in ME/CFS. At the 2016 IACFS/ME Conference, Dr. Klimas presented evidence that indices of HHV-6 activation are correlated with symptom severity in ME/CFS. Learn more about HHV-6 here. Conclusion A fairly large Dutch study found evidence of low thyroid functioning in ME/CFS. The study needs to be replicated, but about 15% of the ME/CFS group met the criteria for Non-Thyroidal Illness Syndrome (NTIS) which occurs in starvation, sepsis and probably other serious illnesses. While most people with ME/CFS did not meet the criteria for NTIS, the overall findings – normal TSH levels, increased reverse T3, and reductions in a variety of thyroid tests – suggest the group as a whole trended in the direction of NTIS. The findings may call for the use of T3 instead of T4 for some people with ME/CFS/FM. While studies assessing the effectiveness of T3 are lacking, both Leslie DeGroot, a prominent endocrinologist, and Dr. Kent Holtorf, an ME/CFS/FM specialist, support using T3 (in Dr. Holtorf’s case, compounded T3) instead of the usual T4 preparation (such as Synthroid) in patients with NTIS (DeGroot) or ME/CFS/FM (Holtorf). The cause of atypical thyroid issues (normal TSH/low T3/high rT3) found in some people with ME/CFS/FM is unknown but could reflect an attempt by the body to conserve resources (Dauer state), could be produced by cytokines, cortisol, hypoxia, etc.) or possibly a pathogen such as HHV-6.

Written by John C. Lowe, MA, DC and The Thyroid Patient Advocacy UK One of the leading experts on hormonal health, Dr. John Lowe, has shared his thoughts about what constitutes optimal treatment for hypothyroidism, this series featuring practitioners with expertise in hormone balance and hypothyroidism diagnosis and treatment. In the course of successfully treating hypothyroidism (as well as most any other disease), Dr. John Lowe believes that relevant outcome measures are crucial. He says: “How else does the patient or clinician know with reasonable accuracy how well or whether at all the treatment regimen is working?” According to Dr. Lowe, diagnosis comes first. In some venues, the clinician is limited in the number of blood tests he or she can order. This may be true, for example, in managed care or socialized medicine. When this is the case, he believes the clinician should order antithyroid antibodies. Says Dr. Lowe: Endocrinologist Dr. Robert Volp made this clear to me. He wrote that a patient may be hypothyroid due to antithyroid antibodies for a few years before the TSH rises and thyroid hormone levels decline. Among people who consume enough iodine, the most common cause of hypothyroidism is autoimmune thyroiditis. Because the TSH and thyroid hormone levels may reveal the hypothyroidism only years after a person develops autoimmune thyroiditis, the proper protocol is clear to me: test thyroid peroxidase and thyroglobulin antibody levels before concerning oneself with the TSH and thyroid hormone levels. If the clinician is free to order these latter tests, thats fine, but the antithyroid antibodies, to me, are far more important. However, as Dr. Bo Wikland has shown in Thyroid Science, many patients with hypothyroid symptoms caused by autoimmune thyroid disease do not have high antithyroid antibody levels. These patients may also have inrange TSH and thyroid hormone levels. Yet thyroid fine-needle aspiration shows that the patients thyroid glands are festering with inflamed and antithyroid antibodies. Laboratory tests, then, including antithyroid antibodies, are not particularly reliable. Dr. Lowe still believes that clinicians or patients should order the tests, but if the tests are all in range, he feels a patient shouldn't accept that he or she is negative for hypothyroidism. If the patient has symptoms and signs characteristic of hypothyroidism, he feels that a trial of thyroid hormone therapy is proper. According to Dr. Lowe, many patients, after beginning thyroid hormone therapy, recover from their symptoms and have a higher level of well-being. They improve despite never having had any lab test results that were consistent with hypothyroidism. For many patients, that is enough for them; they are satisfied with their treatment results. According to Dr. Lowe, achieving optimal therapeutic results for many patients depends on them rejecting T4 replacement. Says Dr. Lowe: Instead of using that commercially-driven alternative, they should use one of the generally more effective alternatives. These include T4/T3 combination therapy (with either synthetic or natural thyroid hormones), or T3 alone. And they should ignore their TSH levels when searching for the dosages that are optimal for them; optimal in the sense of relieving their symptoms without overstimulation of their tissues. As I said, relief of symptoms and better well-being are sufficient for many patients. However, some patients get optimal results only when they also include physiological measures in their treatment regimen. I know some patients who obtain hand-held indirect calorimeters and actually measure their own basal metabolic rates. I know of no other physiological measurement that is more meaningful and useful. There are other relevant and useful measures, though, such as the basal body temperature, basal pulse rate, body weight, and perhaps the voltage of the R-wave on ones ECGs/EKGs. In finding their safe and effective (optimal) thyroid hormone dosage, some patients use all of these physiological measures and they estimate of the intensity of their hypothyroid symptoms at close intervals to learn whether a particular thyroid hormone dosage is moving them in the right direction. And if they started out with high antithyroid antibody levels, they measure these again at intervals to ensure that their thyroid hormone therapy has acceptably lowered the levels. For Dr. Lowe, patients monitoring their responses to thyroid hormone therapy with these tools constitutes the best of outcome testing, which, in his experience, is more likely to provide patients with optimal treatment results. Dr. John Lowe was a long-time thyroid and fibromyalgia researcher and practitioner, and Editor of the journal “Thyroid Science.” Dr. John Lowe’s websites: www.drlowe.com, www.thyroidscience.com Source: Email interview with John Lowe December 2010

– additional conversations with your doctor Written By Keith Littlewood When I completed my master’s degree in endocrinology I put some effort into demonstrating the pitfalls of evaluating thyroid function via thyroid stimulating hormone and the thyroid hormones. It was useful to show how the somewhat crude but helpful variables of body temperature (Tb) and heart rate (Hr) can indicate a low metabolic state. It got me thinking about all the other useful potential markers of metabolic decline associated with hypothyroidism or a functionally hypothyroid state that a person could request to back up the suggestions of low thyroid function. First, it’s useful to clarify where an individual is at with aspects of Tb and Hr. I had a client who came back to me extremely annoyed because her doctor had laughed at her using a thermometer to establish metabolic function, yet the end result was that she was put on thyroid hormone. Understanding whether you as an individual or your client is in a sympathetic, compensatory state is essential to determining compensated versus actual Tb and Hr. In a compensatory state of low thyroid availability, assimilation or utilisation the body will increase adrenaline, noradrenaline and cortisol as a temporary response to maintain homeostasis (Peat,1999) (Fommei & Iervasi, 2002). If you’re eating well, consuming little anti-metabolic foods and eating on a regular basis this may not be the case and a functionally hypothyroid state can probably be ruled out. However long term subclinical or undetectable hypothyroidism will often go through a compensatory stage recruiting sympathetic hormones to maintain function. As thyroid hormone permeates every level of function, it’s useful to consider some of the systemic mechanisms that thyroid affects so that single use medications can be avoided. Blood glucose – increased then decreased in hypothyroidism Blood pressure – decreased then increased in hypothyroidism Cholesterol values – increased in hypothyroidism Energy production – decreased in hypothyroidism Digestion – decreased function then after chronic damage increased evacuation Fertility – decreased in hypothyroidism Heart rate – decreased in hypothyroidism but dependent on compensation Ovulation – decreased in hypothyroidism Tendon reflexes – decreased in hypothyroidism Systemic diseases tend to not spring up in isolation. Acquired inheritance, phenotype expressions, environmental stimulus and nutrition are just some of the factors that allow different losses of function to appear first, it’s never a neat and tidy ordered response with disorder. For some it might be blood pressure, in other cholesterol elevation or digestive disturbances. Albumin – Albumin Is a major blood protein that’s responsible for 80% of the colloid osmotic pressure between blood and tissue fluids and can also transport thyroid hormones. During states of hypothyroidism albumin metabolism is reduced an may often present with hyperalbuminemia. Hypothyroidism and combinations of excess estrogens often induce vascular leakage of albumin and this can also show up in an individual’s urine. Bicarbonate – Typically hypothyroid people can hyperventilate which increases the wastage of carbon dioxide. Bicarbonate is the alkaline ion that is converted via carbonic anhydrase to CO2 when regulating cellular pH levels .To acidic and carbon dioxide is expelled from the body, if chronic the base ion bicarbonate is converted and lost and therefore low levels of bicarbonate are a common finding of hyperventilation and a respiratory alkalosis can ensue to compensate for CO2 loss. From a blood pH perspective as carbon dioxide increases this facilitates the Bohr effect, increasing acidity and allowing respiratio to occur via release of oxygen from haemoglobin. As pH is restored to 7.4 or elevates beyond, an alkalosis can occur, decreasing respiration rate and attempts to retain CO2. It’s useful to think of the balance between bicarbonate and CO2 through evacuating functions. During vomiting hydrogen ions are lost and increased bicarbonate ratio. During diarrhoea bicarbonate ions are lost increasing hydrogen and acidosis. Blood pressure – Hypothyroidism is well known to exert negative cardiometabolic effects that extend to decreased blood volume, increased mean arterial pressure MAP, increased ST segment of ECG (electrocardiogram) and arterial stiffness. Hypertension is usually diagnosed at 140/90 mm/HG A simple blood pressure measurement can be useful combined with any of the discussed markers. Cholesterol – Broda Barnes presented the notion that elevated LDL cholesterol values were a classic sign of hypothyroidism (Barnes 1942), yet still many people are often prescribed statins due to poor evaluation of thyroid function. LDL receptors and liver regulation of cholesterol are reduced in hypothyroidism. The previous data on cholesterol values have shown vast differences on optimal LDL values and ranges these days are to suit financial criteria rather than lifesaving values. In neuro degenerative diseases those with higher cholesterol values generally have more positive outcomes than lower. Iron – You may have been told that you have low iron based upon some basic iron/ferritin blood tests and told to take additional iron. Feel better temporarily then present with constipation and more fatigue. Chances are you may have low thyroid function. There can be many reasons why you present with a low serum iron and these can include vitamin A deficiency, low thyroid and a stressed tissue response often called the CDR or Cell danger response. An iron test even with an RBC can be of little relevance. Many females are often misinformed that the menstrual cycle correlates with increased iron needs. The about of menstrual flow doesn’t appear to correlate with iron loss and most deficits can be maintained by red meat and an increased uptake facilitator like vitamin c. Often if experiencing an infection or illness a requirement of vitamin A is necessary to increase iron status. In order to adequately assess iron need additional test of ferritin, Total iron binding capacity (TIBC) and % transferrin saturation are necessary. It’s often rare that the anaemic states that everyone reports are related to an actual iron deficit. In overt states of hypothyroidism low levels of iron and ferritin are usual whereas TIBC is often elevated (Dahiya et al., 2016). This may be a useful tool in assessing a subclinical or undetectable state of hypothyroidism from regular thyroid biochemistry. Anaemia in many forms is a product of low thyroid function. Prolactin – Produced by the pituitary, usually from stimulation from the hypothalamus, decreased dopamine allows prolactin (PRL) stimulation. Equally an excess of estrogen stimulates both prolactin and TRH. Estrogen is well known to suppress thyroid hormone conversion and therefore PRL can be a useful reflection of estrogen stimulation of the lactotrophs, which secrete PRL. Those with hypothyroidism generally produce more PRL are associated with hyperprolactinemia and heart disease (Binita, Suprava, Mainak, Koner, & Alpana, 2009)(Reuwer et al., 2009) Red blood cell count – A variety of studies provide differing views on total red blood cell indices but a pattern found in hypothyroidism is decreased Red blood cell count (RBC), haemoglobin (H) and haematocrit (HCT). However increased red distribution width (RDW) correlates with increasing TSH. Increased RDW is often found elevated in cardiovascular disease (a well -known factor negated by Barnes’s original studies), and associated with a poorer outcome (Danese, Lippi, & Montagnana 2015). As this also seems to increase during subclinical hypothyroidism RDW increases and decreasing RBC count might be a useful observation. Sex Hormone Binding Globulin – SHBG is a protein that has been suggested as a useful marker for diagnosing peripheral resistance of thyroid hormone. This in itself is supposed to be quite rare but I generally think that increased rates of pollution will ultimately affect peripheral resistance not just by modulation of thyroid hormone and estrogen receptors (THR and ER) but conversion and transport. Optimal thyroid regulation is regulated by the deiodinase enzymes which also have an effect on monocarboxylate transporters 8 and 10 (MCT 8 and MCT 10. MCT 8 regulates thyroid hormone transfer to the nucleus of the cell. All of the above mentioned factors appear to be negatively affected by pollution such as polyaromatic hydrocarbons and many others (Annamalai & Namasivayam, 2015) (Oliveira, Chiamolera, Giannocco, Pazos-Moura, & Ortiga-Carvalho, 2018). Decreased SHBG (and failure to increase with additional TH) can be a marker of a peripheral resistance if THs are elevated (and yet clinical presentation may be hypothyroid). Usually many doctors would be quick to diagnose hyperthyroidism. This may also be clarified by the well documented increases in reverse T3 but represents an alternative to consider. Woltman’s sign – The tendon reflex was used effectively to observe low energy states. Poor thyroid regulation meant poor adenosine triphosphate production (ATP or energy compound). Low energy, slowed movement, poor muscle relaxation (Burkholder, Klaas, Kumar, & Boes, 2013)(HOUSTON, 1958). This test has been frowned upon by modern endocrinologists and I’ll add that perhaps even compensatory patterns of adrenaline production and nociceptive, mechanical and pain issues may make the test less than accurate but it still has value in context with the aforementioned tests. These tests are recommended for having better conversations about your thyroid function if blood tests come back as normal and yet you feel your blood tests are not reflective of your current health. I don’t for a minute suggest that these are fully diagnostic but hopefully lend to better discussions about thyroid evaluation. References: Annamalai, J., & Namasivayam, V. (2015). Endocrine disrupting chemicals in the atmosphere: Their effects on humans and wildlife. Environment International. https://doi.org/10.1016/j.envint.2014.12.006 Barnes, B. (1942). Basal temperature versus basal metabolism. Journal of the American Medical Association, 119(14), 1072–1074. https://doi.org/10.1001/jama.1942.02830310006003 Binita, G., Suprava, P., Mainak, C., Koner, B. C., & Alpana, S. (2009). Correlation of prolactin and thyroid hormone concentration with menstrual patterns in infertile women. Journal of Reproduction & Infertility. Burkholder, D. B., Klaas, J. P., Kumar, N., & Boes, C. J. (2013). The origin of Woltman’s sign of myxoedema. Journal of Clinical Neuroscience. https://doi.org/10.1016/j.jocn.2012.09.047 Dahiya, K., Verma, M., Dhankhar, R., Ghalaut, V. S., Ghalaut, P. S., Sachdeva, A., … Kumar, R. (2016). Thyroid profile and iron metabolism: Mutual relationship in hypothyroidism. Biomedical Research (India). Danese, E., Lippi, G., & Montagnana, M. (2015). Red blood cell distribution width and cardiovascular diseases. Journal of Thoracic Disease. https://doi.org/10.3978/j.issn.2072-1439.2015.10.04 Fommei, E., & Iervasi, G. (2002). The role of thyroid hormone in blood pressure homeostasis: Evidence from short-term hypothyroidism in humans. Journal of Clinical Endocrinology and Metabolism. https://doi.org/10.1210/jcem.87.5.8464 HOUSTON, C. S. (1958). The diagnostic importance of the myxoedema reflex (Woltman’s sign). Canadian Medical Association Journal. Oliveira, K. J., Chiamolera, M. I., Giannocco, G., Pazos-Moura, C. C., & Ortiga-Carvalho, T. M. (2018). Thyroid function disruptors: from nature to chemicals. Journal of Molecular Endocrinology. https://doi.org/10.1530/jme-18-0081 Peat, R. (1999). Thyroid Therapies, Confusion and Fraud. Retrieved from http://www.raypeat.com/articles/articles/thyroid.shtml Reuwer, A. Q., Twickler, M. T., Hutten, B. a, Molema, F. W., Wareham, N. J., Dallinga-Thie, G. M., … Khaw, K.-T. (2009). Prolactin levels and the risk of future coronary artery disease in apparently healthy men and women. Circulation. Cardiovascular Genetics, 2(4), 389–395. https://doi.org/10.1161/CIRCGENETICS.109.853572