Thyroid Science
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| Letters related to Dr. Lowe's rebuttal to British Thyroid Association |
| Readers responses to Dr. Najarian and Dr. Rowsemitt's two papers |

Subject: Are euthyroid patients harmed by thyroxine therapy
Date: June 20, 2010
From: Author prefers anonymity

June 20, 2010
I am a general practitioner in the UK. Many of my patients have told me that they recovered from their hypothyroid symptoms after they found a private doctor who treated them with thyroxine despite their normal TSH levels. These patients had been denied thyroxine treatment by doctors within the National Health Service because of their normal TSH levels. So many patients have told me this that I have developed reservations about ruling out hypothyroidism and the need for thyroxine therapy based on a normal TSH test.

Many more of my patients with normal TSH levels ask me to prescribe thyroxine or Armour Thyroid. I am hesitant to comply because of the Royal College of Physicians' statement about adverse effects from unnecessary thyroid hormone therapy. May I have your point of view on the potential for adverse effects from thyroxine treatment when patients do not actually need it?

Dr. Lowe: I'm familiar with the statement you refer to by the Royal College of Physicians. Specifically it is: ". . . some patients are inappropriately diagnosed as being hypothyroid (often outside the NHS) and are started on thyroxine or other thyroid hormones which will not only cause them possible harm . . ." (Italics and bold mine.)

Like too many other statements or implications by the Royal College of Physicians, when applied to the general population, this one is patently false.  

Unless you're a geriatric specialist whose patients are among the most fragile of human beings, even if they don’t need supplemental thyroid hormone, a trial of thyroid hormone therapy is harmless. If the hormone doesn’t help them, you can wean them off it and then have them stop it altogether. No harm done!

Proof of this is in the history of FDA-guided studies of the potency and stability of T4. To test T4 for potency and stability, researchers—using FDA test guidance!—have traditionally used volunteers who were "euthyroid," meaning, of course, that they subjects had normal thyroid function test results. Moreover, FDA test guidance has allowed researchers to use euthyroid volunteers to test higher-than-physiological (supraphysiologic) doses of T4.

I ask the Royal College of Physicians: If it were likely to harm euthyroid volunteers, why would FDA-test guidance allow researchers to use them for the testing? And why would institutional review boards approve the studies as not potentially harmful to the volunteers?

The answer is simple, of course: A trial of thyroid hormone therapy—even for people with perfectly normal thyroid function—is harmless, even when they use supraphysiologic doses.

Only recently have researchers suggested that rather than testing euthyroid volunteers, they would best use thyroidectomized patients. But the researchers'  reason for this suggestion has nothing whatever to do with any harm ever done to euthyroid volunteers in the studies. The testing hasn't harmed the euthyroid volunteers, nor will a trial of thyroid hormone therapy harm practically any of your euthyroid patients except possibly the most severely fragile of them. But, then, a cup of coffee is just as likely to harm those fragile folks.

I just don't understand something: How does the Royal College of Physicians (as with this particular issue) and the British Thyroid Association make scientifically false statements and stand by them in the face of proof that they are false, yet receive no official reprimands from regulatory authorities in the UK? To me, their false statements are an affront to the noble tradition of science, and the organizations sticking by their false statements in the face of refuting evidence reduces the statements to examples of pseudoscience.

At any rate, I hope this reply is helpful to you in providing your patients with harmless trials of thyroid hormone therapy, whether they truly need it or not.


1. Royal College of Physicians. The diagnosis and management of primary hypothyroidism. 2008.

2. Eisenberg, M. and DiStefano, III, J.J.: TSH-Based Protocol, Tablet Instability, and Absorption Effects on L-T4 Bioequivalence. Thyroid, 19(2):103-110, 2009.

(This Q&A was published simultaneously at

Letter to the Editor

Subject: Question about where to submit my paper
Date: June 12, 2010
From: Author prefers anonymity

June 12, 2010
I have a hypothesis paper that I’m considering submitting to Thyroid Science. I’m hesitant, however, because there may be advantages to publishing in major medical journals, such as the Journal of the American Medical Association. Of course, I may have a harder time getting my paper accepted because of competition. What are your thoughts for people who are new to submitting papers to journals? Can I submit my paper both to Thyroid Science and another journal and go with which ever journal accept it?

Dr. Lowe: Many people have asked us this same question. Of course, we would like a chance to publish your paper if our reviewers believe it has merit in the field of thyroidology. However, if your paper may contribute to changing the current “T4 replacement paradigm” for hypothyroidism, we really don't care which journal first publishes it, as long as you get it published.

To some, that policy may seem self-sabotaging to Thyroid Science, but it really isn't. If we feel that a paper published elsewhere is important enough, we'll ask the author(s) to write a summary of the paper for our journal, possibly further articulating the thesis and providing more supporting evidence. And if the author won’t cooperate, we may compose a paper based on the author(s)' that provides the important information for our readers.

In deciding where to submit your paper, you might keep in mind a few points I wrote to another potential author this morning. What I wrote to him is essentially the following.

Long ago, when I was being educated in research psychology (I think Galileo sat two rows in front of me), I took courses that dealt with the ethics of scientific conduct. We were taught that it's unethical to publish exactly the same paper in more than one journal, even if years have passed since the first publication. That policy is an old one, and it still applies. Because of this, you should submit your paper only to one journal at a time. If the first journal rejects your paper, then, and only then, submit it to the next one.

If you want to spread your hypothesis wider than one journal would allow, you can easily do that. First, publish your paper in one journal, and write as many other papers as you want for other journals. This is perfectly ethical as long as your other versions of your paper are indeed other versions; that is, in subsequent papers, you should express your hypothesis exactly as it was originally published, but in different terms. Expressing the same thoughts in different terms is ethical. In my view, in fact, if you feel that your hypothesis can lead to the relief of suffering of human beings, you have a humanitarian responsibility to publish it as many times as needed to accomplish that worthy end.

If you can get your paper accepted by a major traditional print journal, you'll have some important advantages. For example, you're likely to have more prestige in the eyes of the typical practicing conventional clinician, and your paper will be included in the traditional major indexing systems, such as Medline.

On the other hand, the print journal may fail to publish your paper in an open-access electronic version of the journal. If so, only those who subscribe to the print version of the journal are likely to read your full paper. As time passes, the only part of your paper that most interested people will have access to will be the abstract that is online. They can access your abstract through most search engines, such as Google and Yahoo.

Otherwise, if anyone is interested enough in arrange to get a copy of your full paper, he or she will have one of two options: First, he or she can buy a copy online from the closed-access journal. This can be expensive, and it can be prohibitive if one does a great deal of journal research. Second, he or she can travel to a medical library, track down your paper in a bound volume of all the papers published in that journal during the year, and photocopy it. This option is inconvenient for most people. This may account for me seeing in recent years fewer and fewer people in medical libraries copying journal papers.

Another downside of traditional print journals is something that frustrated  many of us who used to publish in traditional print journals: the “publication lag.” I know of some journals that had a lag of two years. This meant that by the time one’s paper was published, it was more history than news. Because of the publication lag, I encourage you talk or write to an editor of the journal you decide to submit to. As whether in addition to publishing a print version, the journal will also rapidly publish an electronic version online.

Another important issue is whether the journal is available only to subscribers ("closed-access") or is "open-access." Open-access means that most publications in the journal are free to read without a subscription. Steadily more open-access journals are being published, and they are impacting traditional print journals. When I've inquired, medical librarians, who work where traditional print journals are stored, have told me, “open-access journals are killing us.”

One advantage of electronic publishing, especially in open-access journals such as Thyroid Science, is that we have virtually no publication lag. We publish papers are rapidly compared to print journals. In addition, with open-access journals, anyone in the world with access to the Internet can find and read your paper using Google, Yahoo, or most any other search engines. One doesn't even need to use Medline, PubMed, or any of the other traditional indexing system. In fact, I believe these systems are on the verge of being obsolete. Most search engines such as Google also index the papers that formerly were indexed only in the traditional indexing systems. Plus, Internet search engines also indexe publications not included in PubMed.

If you publish in another journal for whatever advantage, we fully support you in it. And if you'll send us an advanced copy of your paper, after the  other journal publishes it, we may ask you to summarize your hypothesis and elaborate on it in a second paper for Thyroid Science.

Best of luck in getting your hypothesis published, wherever you decide to submit your paper.

Letter to the Editor

Subject: What is prealbumin
Date: November 24, 2009
From: Author prefers anonymity

My doctor gave me my lab results yesterday. I know what most of the thyroid tests are, but I’ve never heard of one. It is the “prealbumin.” Do you know what this is? My level was 0.20 g/L, and the range is listed as 0.18-to-0.39 g/L. Do you know what this result means?

Reply by Dr. John C. Lowe, Editor-in-Chief (November 24, 2009)

Dear Bob:
We have a newer name for prealbumin, which is “transthyretin.” Transthyretin is a protein that is important to thyroid hormone regulation of the brain. The protein transports thyroid hormone across the blood-brain barrier; that is, from the blood outside the brain to the blood inside brain. Transthyretin that transports thyroid hormone in the blood is produced in the liver, but transthyretin that transports thyroid hormone across the blood brain barrier is produced in a structure called the “choroid plexus” at the base of the brain.

When I say that the protein transports thyroid hormone across the blood-brain barrier, I mean that it transports both T4 and T3. This is important to understand. The reason is that many clinicians mistakenly think that transthyretin transports only T4 into the brain. Based on this mistaken belief, these clinicians also mistakenly believe that normal brain function depends on patients including T4 in their thyroid hormone therapy. This, however, is patently false. (Elsewhere, I extensively documented that transthyretin transports both T4 and T3 into the brain. I published one article in 2005 and the second in 2006.)

You wrote that your transthyretin level was 0.20 g/L (20 mg/dL). With a range of 0.18-to-0.39 g/L (18-to-39 mg/dL), your level is very low; it’s in the lower 4th of the range.

Some diagnosticians would say this level means you’re not producing an optimal amount of transthyretin; others would say that you’re producing plenty. I don’t think we have enough studies to tell us which of those diagnosticians are right and wrong.

What we can tell from your level is that you’re producing the protein and your most likely getting thyroid hormone into your brain. We don’t have tests commercially available that measure the amount of thyroid hormone that is bound to one’s transthyretin. That piece of information would be valuable. The reason is that dioxins and PCBs can displace thyroid hormone from the protein. As a result, these chemical contaminants can ride into the brain on the protein. The more of the contaminants that ride the protein into the brain, the less T4 and T3 are likely to reach brain cells. Once inside the brain, dioxins and PCBs bind to T3 receptors on genes. The binding alters the pattern of codes that the genes send out to the work part of the cell for the production of proteins. I believe this phenomenon is responsible for some of the cognitive and mood problems of people contaminated with dioxins and PCBs, which toxicologists have told me is each of us. (I heavily documented the thyroid-disrupting effects of these pollutants in the “Environmental Contaminants” section in Chapter 2.4, “Thyroid Hormone Deficiency,” of The Metabolic Treatment of Fibromyalgia [available in the publisher's E-Chapter section].)

I assume that you wrote to me about your transthyretin level from concern about your thyroid hormone status. However, some clinicians order the test to learn whether a patient is ingesting enough protein. Transthyretin is a “glycoprotein,” which means it is a carbohydrate combined with a protein. Of all the proteins in the blood, it’s transthyretin that is most useful in telling whether a person has a protein deficiency. The half life of the protein is about two days, so it’s level in the blood changes quickly when someone markedly decreases or increases protein intake, digestion, and/or absorption.

You didn’t say whether you ate little to no protein for several days before your blood was drawn to measure your transthyretin. If you ate little to none, that might account for your low-range transthyretin level. If that is the case, you should talk with your clinician about measuring your transthyretin level again after you eat 50-to-75 grams of protein each day for several days. Your tranthyretin level might then be higher. But keep in mind that inflammation and infection can also lower transthyretin level, and severe kidney disease and the use of glucocorticoid (such as prednisone or prednisolone) can raise your level. I hope this is helpful to you.  

Letter to the Editor

Subject: Followup photo of goiter patient
From: Ned Fuller
Date: March 1, 2009 10:08 am

My mother has a goiter and it has been advised that she have it surgically reduced. I am a physician but have not had the opportunity to see the postsurgical appearance of the neck after  a patient's goiter has been removed. My mother is concerned about the appearance, although she is also concerned about the appearance of the goiter. Are there any postsurgical photos of the patient whose goiter Drs. De Sousa, Dilip, Mervyn removed.

Editor’s Reply (March 2, 2009)

Dear Dr. Roberts:
We asked Dr. DeSousa if any photos were available of the patient whose goiter he and his colleagues reported removing. He was kind enough to send the postoperation photo to the right below. We also posted below the photo of the patient from the authors' case report before they removed the goiter; it is the photo to the left.

Dr. De Sousa wrote to us that the photo to the right is the patient after two weeks of convalescence. The scar had been painted with mercurochrome. We are grateful to Dr. De Sousa for providing Thyroid Science with the photos, and I hope the postop photo is helpful to you, Dr. Roberts.

Tracy Majors
Assistant Editor

Click for Enlarged Photos

Letter to the Editor

Subject: Thanks to you!
From: Jacqueline Herrera
Date: Mon, December 8, 2008 9:32 pm

Dear Dr. Lowe: I'm so thankful I was told about I read the article on "Weight Gain and the TSH" and sent it to my three sisters who also suffer from hypothyroidism. I started the Armour Thyroid medication almost two weeks ago and feel so much better than the last 7 years of being on levothyroxine. I know this is a positive start in the right direction for me personally. I have 30 pounds to get rid of that I've gained in the last 7 years after two consecutive pregnancies in 2002 and 2003. Thank you for making this information available to the people (not just doctors) who are pro active about their health.

Jacqueline Herrera
Phoenix, Arizona

Editor’s Reply (December 25, 2008)

Jacqueline: Thanks so much for writing about feeling better on Armour Thyroid after gaining thirty pounds of weight while on levothyroxine. If you use a high enough dosage of Armour, I expect that you’ll lose the 30 lbs you gained over the seven years that you used levothyroxine. This is especially likely if you have a wholesome diet and regularly exercise to tolerance.

Armour Thyroid, like Nature-Throid and Westhroid, is more effective than levothyroxine at reducing body fat. The reason is that these products contain T3. Some researchers say that T3 has a “lipolytic”—that is, a fat-decomposing—action in fat cells.
[3] One way T3 reduces fat in the cells is by inhibiting an enzyme (cyclic-AMP phosphodiesterase) that slows down metabolism shortly after adrenaline and noradrenaline speeds it up.[1][3][8] By blocking this enzyme, T3 sustains the fat-decomposing effect of adrenaline and noradrenaline in fat cells.[1][2][8] Another way T3 reduces fat is by altering gene transcription for several compounds. When T3, acting through the relevant genes, increases fat cells’ production of these compounds, the compounds augment adrenaline’s and noradrenaline’s fat-lowering effect in the cells.[10]

In addition to weight loss, you may get another benefit from the T3 in Armour: that is, a reduction of fat that probably accumulated in your arteries[3] while you were on T4 replacement. As Duntas wrote,[11] As Duntas noted in 2002, the composition and transport of blood fats “are seriously disturbed in thyroid diseases.” Among patients with an high TSH and low thyroid hormone levels, cholesterol and LDL are typically high. Even when thyroid hormone levels are within the reference range but the TSH is high, patients on average have a slightly high total cholesterol, high LDL, and low HDL. These patients also have abnormalities of the linings of arteries, inflammation and fat accumulation in the aorta, and they are subject to have myocardial infarctions. They also have increased resistance to blood flow, weaker contractions of the heart muscle, and increase diastolic blood pressure. As Duntas pointed out, thyroid hormone therapy—especially with TSH-suppressive dosages—“usually leads to a considerable improvement in the lipid profile.”

T3 reduces fat in artery linings in part by increasing the activity of an enzyme called “lipoprotein lipase.”[4] Low activity of this enzyme leads to high blood fats, which is a risk factor for coronary heart disease.[7] Thyroid hormone increases the activity of the enzyme, and by doing so, it reduces blood fats.[4] Thyroid hormone also lowers LDL cholesterol by increasing the number of LDL receptors on liver cells.[11]

In my clinical experience, thyroid hormone therapy (with products that contain T3) is by far more effective than statin drugs in normalizing blood fats. I believe that if patients in general were allowed to use effective thyroid hormone therapy rather than T4 replacement, we could virtually eliminate the market for statin drugs. Then patients would be free from the potential adverse effects of statin drugs, such as chronic muscle pain and other pain syndromes, elevated liver enzymes, peripheral neuropathy, and muscle damage.[9]

Please let us know how you progress. I wish you the best for losing the weight you gained while on levothyroxine.


1. Bégin-Heick, N. and Heick, H.M.: Increased response of adipose tissue of the ob/ob mouse to the action of adrenaline after treatment with thyroxin. Can. J. Physiol. Pharmacol., 55(6):1320-1329, 1977.

2. Elks, M.L. and Manganiello, V.C.: Effects of thyroid hormone on regulation of lipolysis and adenosine 3',5'-monophosphate metabolism in 3T3-L1 adipocytes. Endocrinology, 117(3):947-953, 1985.

3. Mandel, L.R. and Kuehl, F.A., Jr.: Lipolytic action of 3,3'5-triiodo-L-thyronine, a cyclic AMP phosphodiesterase inhibitor. Biochem. Biophys. Res. Commun., 28(1):13-18, 1967.

4. Pykälistö, O., Goldberg, A.P., and Brunzell, J.D.: Reversal of decreased human adipose tissue lipoprotein lipase and hypertriglyceridemia after treatment of hypothyroidism. J. Clin. Endocrinol. Metab., 43(3):591-600, 1976.

5. Beisiegel, U.: Lipoprotein metabolism. Eur. Heart J., 19 Suppl A:A20-A23, 1998.

6. Otto, W., Taylor, T.G., and York, D.A.: Glycerol release in vitro from adipose tissue of obese (ob/ob) mice treated with thyroid hormones. J. Endocrinol., 71(1):143-155, 1976.

7. Salter, A.M. and Brindley, D.N.: The biochemistry of lipoproteins. J. Inherit. Metab. Dis., 11 Suppl 1:4-17, 1988.

8. Wahrenberg, H., Wennlund, A., and Arner P.: Adrenergic regulation of lipolysis in fat cells from hyperthyroid and hypothyroid patients. J. Clin. Endocrinol. Metab., 78(4):898-903, 1994.

9. Brown, W.V.: Safety of statins. Curr. Opin. Lipidol., 19(6):558-562. 2008.

10. Viguerie, N., Millet, L., Avizou, S., et al.: Regulation of human adipocyte gene expression by thyroid hormone. J. Clin. Endocrinol. Metab., 2002 Feb;87(2):630-634, 2002.

11. Duntas, L.H.: Thyroid disease and lipids. Thyroid, 12(4):287-293, 2002.

Letter to the Editor

From: “Lars” <>
Date: Sun, November 16, 2008 2:06 am

Has the paper below really been reviewed????

I do not question the Lowe thesis, but I believe that a poor paper to support it is in fact harming the cause—especially if the methods used are not backed up with known or accepted methods.

Kind regards
Lars Németh
Med Vänlig hälsning
+46 40 137 765

Editor’s Reply

Dear Mr. Németh:
Thank you for your email and your thoughts. Yes, indeed: Dr. Øverbye’s paper was reviewed. Several of our peer reviewers read the paper, and each strongly recommended that we publish it. As one of the reviewers commented after critiquing Dr. Øverbye’s manuscript, “This paper reports the type of cutting-edge, creative pilot research that we want to encourage.”

You suggest that Dr. Øverbye’s paper is "poor" because his methods were "not backed up with known or accepted methods." In conventional medicine, of course, creative research using innovative methods has traditionally been resoundingly discouraged. Recall the dictum, “Be not the first by whom the new is tried, nor the last to lay the old aside.” We at Thyroid Science reject this progress-stifling, herd-mentality orientation. Instead, we encourage originative and progressive clinical methods and research. That orientation is exemplified by Thyroid Science publishing Dr. Øverbye’s paper. As objectionable as this orientation may be to some people within conventional medicine, we steadfastly stand by it, as we believe this orientation is likely to bring help to millions of thyroid patients whom conventional medicine continues to fail.

Your assessment of Dr. Øverbye’s study and his paper brings to mind similar notable occurrences. They involved Professor Linus Pauling, a two-time Nobel Prize winner ranked among the ten most fruitful scientists in history. Pauling was also fruitful in his scientific investigations in the field of nutrition. But editors of medical journals often censored him by rejecting or delaying publication of his manuscripts because the contents challenged conventional medical prejudices. (To read his description of the censorship by editors—including the editor of the Journal of the American Medical Association—read his chapter titled “Organized Medicine and the Vitamins” in his book for the public titled How to Live Longer And Feel Better.)

By contrast, after some resistance early in his career, chemistry journals accepted Pauling’s thinking and methods that were clearly beyond the boundaries of “the box.” Some editors accepted his manuscripts containing extremely innovative material without sending them to peer reviewers. As one editor noted, peer reviews were impossible in that Pauling had no peers. The chemistry profession got the benefit of Pauling’s imaginative and innovative mind. But censorship of this scientific genius protected from refutation the presumptions and prejudices of the editors, commercial sponsors, and readers of some medical journals.

I’m not saying that Dr. Øverbye’s paper is certain to have the gargantuan scientific importance of many of Pauling’s papers (although I'm also not saying it won't). What I am saying is that Thyroid Science will not censor research simply because it involves thoughtful, fresh ideas, and innovative methods. As in Dr. Øverbye’s case, we encourage researchers to use well-established technologies from other fields to make scientific advancements in the field of medicine. He has done this, and admirably so.

We appreciate you expressing your opinion and prompting us to explain why our reviewers and editors enthusiastically accepted Dr. Øverbye’s paper for publication.

Best wishes,
Dr. John C. Lowe
Thyroid Science (  

Letter to the Editor

Subject: Thyroid Weight Gain
From: June Hyslop <Scotland, UK>
Date: Sun, November 16, 2008 6:34 am

Dear Dr. Lowe: I am printing off a copy of your article “Weight Gain and the TSH: Prevention Writer’s Good Deed.” I will take it to my next appointment with my endocrinologist in the hope that he’ll read it and adopt a less conservative approach to the management of my hypothyroidism. At my last visit he cut my thyroid medication because I was too near the top of the range for FT3 and FT4 (my TSH is suppressed already). It’s now two months later and I have gained five pounds. As I was already overweight and have extreme difficulty losing any, this is a big setback for me. I’m also fatigued and have seen the return of other hypothyroid symptoms since the reduction in dose.

I feel there is a lack of understanding within the endocrinology community about how this affects patients physically and mentally, and I would like to see a more open-minded and individualized approach to patient management. Your efforts in this regard are greatly appreciated, and I look forward to receiving future issues of Thyroid Science.

June Hyslop
Scotland, UK

Editor’s Reply

Dear June:
Thank you for your email. Since we published the editorial on weight gain and the TSH, we’ve received many emails from hypothyroid patients expressing the same lament that you do. Over the years, I’ve heard so many patients express the same grief that I couldn’t begin to count them. Your complaint about weight gain and those of many others, and the studies I cited in the editorial, make one point clear: basing hypothyroid patients’ treatment on their TSH levels (or their thyroid hormone levels) is an egregious wrong imposed on the patients. Indeed, that approach is the very cause of many patients gaining weight that they can’t lose despite regular exercise and a wholesome, nonfattening diet.

One way to rectify this wrong in medical care is exactly what you’ve said you’ll do—put the evidence of its harm, shown in studies, before the eyes of endocrinologists and other practitioners. Patients must, of course, insist that the clinicians pay attention to the studies and rationally consider them. Of course, it’s now legend that many endocrinologists rudely dismiss patients who bring to their attention scientific evidence that contradicts their beliefs. The patient who accepts the dismissal and finds a more scientifically-thinking clinician is fortunate; he or she is far more likely to receive safe and effective care.

According to case law in the U.S., clinicians have a professional responsibility to stay abreast of scientific evidence that bears on the opinions they give their patients. So for an endocrinologist to deny to a patient that weight gain is associated with in-range rising TSH levels is—by virtue of the available scientific evidence—a breach of professional responsibility. But this is a breech that many endocrinologists sidestep. They do so by deferring to the practice guidelines written by committees within their specialty. The practice guidelines dictate standards for the diagnosis and treatment of hypothyroidism both within the endocrinology specialty and, by extension, in other medical specialties. Largely under the sway of corporations’ financial inducements, too many of the members of these committees ignore the scientific evidence that shows the potential harm from parts of their guidelines that favor corporate profits. (I heavily document these potential harms throughout The Metabolic Treatment of Fibromyalgia.) In essence, then, these committees nullify the practicing endocrinologists’ responsibility to listen and learn when patients troubled by weight gain give them the scientific evidence that the gain is associated with TSH levels within the reference range.

This harmful system within the endocrinology specialty has alienated countless hypothyroid patients who now hold the specialty in contempt. I believe this is a good dynamic because of a phenomenon in the 20th century history of medicine in the U.S. That phenomenon was that major changes in medicine came about because enough patients demanded them and made them profitable. The patients sought out and paid clinicians who provided services they wanted. Many of those patients wanted the services because they, unlike the clinicians, knew of scientific evidence that the services could benefit them. This market demand was a major influence on the emergence of sports medicine, nutritional medicine, integrative medicine, and manual manipulation by medical practitioners. Scientific evidence favoring these methods had long existed. It received little-to-no attention by physicians, however, until patients made it profitable for them to provide the services warranted by the evidence.

Will the endocrinology specialty overall yield to mass patient demand? Not until that huge barricade of corporate money is ceases to wall off the minds of most endocrinologists from the scientific evidence. Removing that barricade will be a difficult task indeed in this world where corporatism overwhelmingly prevails.

Over the last several years, however, I’ve seen signs that a minority of endocrinologists have come around. If patients like you seek out and patronize those endocrinologists, their numbers are likely to grow. I encourage you, then, to put the editorial on weight gain and the TSH before your endocrinologist’s eyes. (I recommend that you print the pdf version of the editorial, which you can download or print at no cost.) If you are rebuffed in your attempt to enlighten him, I hope you’ll move on and find one within that minority of endocrinologists who’ll give you better quality care by ignoring the levels of your TSH and thyroid hormones in deciding what dosage is best for you.

Yours sincerely,
Dr. John C. Lowe
Thyroid Science (

Subject: Re: Doing better on Armour
From: Anonymous patient in Australia
Date: Wed, August 27, 2008 6:11 pm

Dear Editors: I bow down to you as I read everything you publish on thyroid. Please keep it up.  After using thyroxine, I now use Armour and finally feel better.

Dear Reader: The next Q&A down from this one is a question from a physician and an answer to it by Dr. John C. Lowe, our Editor-in-Chief. As his answer indicates, we at Thyroid Science are aware of the superiority of desiccated thyroid products, such as  Armour, Nature-Thyroid, and Westhroid, over thyroxine (T4) alone. You may find very interesting an article we will soon publish. It is a rebuttal by Dr. Lowe to the British Thyroid Association's denouncement of desiccated thyroid products. We will send an email notice to our subscribers when we publish the rebuttal. We appreciate you letting us know that you are doing better on desiccated thyroid.

Tracy Majors
Assistant Editor
Thyroid Science (

Subject: Safety Precautions for Thyroid Hormone Therapy
From: Anonymous physician
Date: Thu, August 24, 2008 12:29 pm

Dear Dr. Lowe: I am one of the many family physicians who has jumped off the ship of conventional medicine and onto that of natural medicine. I spent my first twenty years of practice disserving my thyroid patients by prescribing Synthroid only and changing their dosages by their TSH levels. It didn’t take much experience for me to see that products like Nature-Thyroid work better than Synthroid with most patients, especially when I ignore their TSH (as you give evidence for doing in your critique of T4 vs T4/T3 studies) and go by their symptoms, temperature, Achilles reflex, and physical appearance. I read in your book The Metabolic Treatment of Fibromyalgia about the change in some patients’ eyes and general appearance when they switch from T4 to desiccated thyroid or T3. When I use these meds correctly, they almost always seem to turn up the patient’s rheostat, whereas usually Synthroid just left it turned off. I feel bad that I spent so many years neglecting to treat patients better with thyroid hormone, but that is what I was taught in medical school. I know you’re big on treating underlying conditions that can interfere with thyroid patients responding well to thyroid therapy. Not wanting to harm my patients any more than I did over the last twenty years, can you brief me on the scope of underlying conditions I should look for. If you post my email, please do it anonymously. I have been cautioned that a low profile is best for keeping my license to practice medicine.

Dear Doctor: Welcome to the rational, scientific side of clinical thyroidology. I don’t know what caused you to jump ship from conventional (to me, commercial) medicine, but I’m pleased that you’re sailing with us now.

Precautions, of course, are steps we take to avert harming the patients we treat with thyroid hormone. We take most of the steps in advance of the patient beginning thyroid hormone therapy. But we must take some steps, as I explain below, after the patient has begun treatment.

The precautions I take involve the following steps: (1) ensuring the cardiac safety of the patient, (2) learning his or her cortisol status, (3) determining whether he or she has blood sugar dysregulation, (4) making sure he or she both exercises regularly and (5) takes a wide array of nutritional supplements.

A company (Erfa Canada, Inc.) that markets a brand of desiccated thyroid gives an   overview of prudent precautions with thyroid hormone therapy. The company’s precautions are important. I recommend additional ones, but their precautions are worth quoting.

Patient’ Cardiovascular Status: The company recommends: "Thyroid hormones should be used with great caution in a number of circumstances where the integrity of the cardiovascular system, particularly the coronary arteries, is suspect. These include patients with angina pectoris, hypertension, other cardiac conditions, or the elderly, in whom there is a greater likelihood of occult cardiac disease."

Some doctors unfortunately deny patients with delicate cardiovascular conditions any use of thyroid hormone. This is unfortunate because many of these patients can safely use and benefit from thyroid hormone; in fact, many cardiac patients must use thyroid hormone therapy to recover cardiac health.

Caution is the key to guiding these patients back to a healthy heart. The Erfa website describes a precautionary treatment approach: "In these patients, therapy should be initiated with low doses, i.e., 25 to 50 μg levothyroxine (T4) or its isocaloric equivalent (16 to 32 mg, or 0.25 to 0.5 grain of desiccated thyroid). When, in such patients, a euthyroid state can only be reached at the expense of an aggravation of the cardiovascular disease, thyroid hormone dosage should be reduced." (Italics mine.)

I agree with this cautious approach except for two things. First, the company mentioned the patient reaching a euthyroid state. This implies using a thyroid hormone dosage that keeps the TSH, free T4, and free T3 within their reference ranges. Bringing these hormones into their reference ranges, however, does not render most patients well. At its website, Erfa tells what does: "The principal pharmacologic effect of exogenous thyroid hormones is to increase the metabolic rate of body tissues." The safest and most efficient way to help patients get well is to free them from their symptoms by normalizing their metabolic rates. Hence, rather than a euthyroid state, we should instead strive for a eumetabolic state.

What I next disagree with is the company's advice that some cardiac patients start treatment with a T4 product. These products may not work at all for many cardiac patients, regardless of the dosages they use. If the patient is hypothyroid, I recommend a T4/T3 product with a T4 to T3 ratio of 4:1, or T3 alone. Some T4/T3 products with the proper ratio are Armour Thyroid, Nature-Thyroid, and Westhroid. I prefer the latter two products for two reasons. First, an occasional patient reports to me that when she takes  Armour, she develops itching, which I assume is an allergic reaction. Switching to Nature-Throid or Westhroid relieves the itching. Second, the manufacturer of Nature-Throid and Westhroid, RLC Labs, goes to great lengths to ensure the quality, safety, and evidential basis of their therapeutic products. This is obvious in their description of how they formulate a variety of therapeutic products.

I always do an electrocardiogram (ECG) when I see patients personally. If I consult with a patient long distance, I also ask that he or she get an ECG from a local clinician and fax a copy of the tracing to me. I have two purposes for obtaining the ECG. First is to study the tracing for any evidence that aggressive thyroid hormone therapy is contraindicated. For example, my 12-lead electrocardiograph occasionally shows evidence of right heart damage and pulmonary hypertension in a patient who has used various weight-loss  drugs. Second is to see whether the voltage of the patient’s R wave is low. If it is, increasing voltage may serve as a useful physiologic barometer of metabolic improvement.

Erfa, in a statement I quoted above, suggests that thyroid hormone therapy may reveal "occult cardiac disease." This is true and important. Rarely, thyroid hormone therapy does unveil a cardiac problem that has been obscured over time by inadequate thyroid hormone regulation of the cardiovascular system. You mentioned that you have a copy of The Metabolic Treatment of Fibromyalgia. I recommend that you read the section on the heart (pages 875-888), especially the subsection titled "Worsening of the Manifestations of Coronary Heart Disease" on page 877. The entire chapter is about the safe use of thyroid hormone, but it’s the heart that most practitioners are concerned about. I address those concerns and explain how to avoid adverse cardiac effects in patients using thyroid hormone. Except in the rarest cases, patients with fragile heart conditions can use thyroid hormone. But, again, caution is the key.

Erfa also mentions other precautions I strongly agree with: "Thyroid hormone therapy in patients with concomitant diabetes mellitus or insipidus or adrenal cortical insufficiency aggravates the intensity of their symptoms. Appropriate adjustments of the various therapeutic measures directed at these concomitant endocrine diseases are required."

Diabetes: I ask my patients to check their blood sugar regulation in two ways: (1) by taking several random measurements of their fasting blood sugar levels, and (2) by doing a 6-hour home glucose tolerance test (hGTT). These tests often show that a patient has glucose dysregulation. Some have fasting or reactive hypoglycemia, but most, in my clinical experience, have glucose intolerance.

In either case, too little glucose reaching a patient’s cells can cause what I view as an energy crisis. This occurs when thyroid hormone therapy accelerates intracellular energy metabolism by increasing a wide range of enzymes, but the increased energy demand conflicts with too little energy substrate in the form of glucose. Clinicians and patients often misinterpret the resulting symptoms as thyrotoxicosis. In fact, glucose dysregulation is the primary source of the symptoms. And the symptoms block the patient from using a fully therapeutic dosage of thyroid hormone.

Cortisol Deficiency: I recommend salivary testing for ruling out a cortisol deficiency. Bear in mind, though, that if a patient’s liver is underregulated by thyroid hormone, it may not clear cortisol from the body at a normal rate. The person’s adrenal cortices are producing too little cortisol, but the slowed liver clearance leaves the body fluids with a reference range concentration of cortisol. But as thyroid hormone increases the patient’s liver clearance of cortisol to a normal rate, the patient begins to develop cortisol deficiency symptoms. In this case, thyroid hormone therapy has unveiled an adrenocortical insufficiency. This phenomenon is similar to thyroid hormone therapy unveiling an occult cardiac disorder, which I mentioned above.

The precautions Erfa recommends are indeed important ones. However, in addition to those precautions, I also ask my patients to take two other precautions; that is, to  exercise and take nutritional supplements.

Exercise: I ask my patients to regularly engage in stretching, resistance, and cardiovascular exercise to tolerance. Some patients have especially low cardiovascular and muscular fitness. Despite their low muscle fitness, their muscles tend to be chronically too tight. Most of these patients must begin exercise with baby steps, increasing the intensity of their workouts only after light exercise and thyroid hormone therapy increase their tolerance for the three types of exercise.

Stretching is helpful in temporarily reducing the excess muscle tightness caused by low muscle energy from too little thyroid hormone regulation. Muscle bulking exercise is important because lean body mass is the only factor that increases the resting metabolic rate more than does thyroid hormone. And aerobic exercise gradually increases the patient's level of cardiovascular fitness. This makes the heart more resistant to adverse effects from a dosage of thyroid hormone high enough to enable the patient to get well.

Nutritional Supplements: Next, I ask each patient to take a wide array of nutritional supplements, especially B complex vitamins. The importance of this can hardly be overemphasized.

If a patient hasn’t been taking supplements, he or she may have borderline nutritional deficiencies. Many micronutrients function in cells as coenzymes. Thyroid hormone increases the production of many enzymes, causing a faster expenditure of their micronutrient coenzymes. When a patient doesn’t take nutritional supplements, as thyroid hormone accelerates his or her metabolic rate, borderline nutritional inadequacies may become severe deficiencies. A deficiency of some B complex vitamins, calcium, or magnesium can cause nervous system and muscle hyperirritability. Clinicians and patients may mistakenly believe that too much thyroid hormone is at fault. In fact, the patient isn’t even taking a fully therapeutic dosage of thyroid hormone.

A particularly harmful nutritional deficiency involves depletion of vitamin B1 from accelerated energy metabolism caused by thyroid hormone. The patient must regularly take in enough vitamin B1 to compensate for its increased intracellular expenditure. If he or she doesn't, a resulting B1 deficiency can cause beriberi-type cardiomyopathy—even though he or she is still taking too little thyroid hormone to recover from the hypothyroid symptoms.

This set of precautions and recommendations are the base from which I operate to ensure my patients' safety during thyroid hormone therapy. Keeping the precautions and recommendations in mind can make thyroid hormone therapy with a T4/T3 product or T3 alone truly effective. It can also provide your patients with the safety you’re admirably concerned about. If you learn of other precautions that clinicians should be aware of, we’ll be happy if you’ll share them with the readers and staff of Thyroid Science. I wish you the most rewarding and prosperous sailing with natural medicine.

Dr. John C. Lowe
Thyroid Science

August 4, 2008

From the Editors:

We have just received notice that Thyroid UK, the thyroid patient advocacy organization in the United Kingdom, has officially received charity status. Thyroid UK has been working towards registered charity status for some time and after a lot of work, they have now achieved this.

Thyroid UK’s objects are the relief of sickness of people suffering from thyroid disease and related illnesses, for the benefit of the public. To this end, those who work through Thyroid UK provide a number of humanitarian services. These include disseminating information and support to sufferers of thyroid disease; promoting public awareness of thyroid disorders; acting as a informational resource center; encouraging scientific research for the education, alleviation, care, treatment and cure of thyroid disease; and raising funds needed to achieve their objectives.

Lyn Mynott is Chief Executive of the organization. “Achieving registered charity status," she said, "will mean that we will be seen as a more professional organization and also that more funds will become available to us to achieve our objects.”

Thyroid UK was recently been chosen by the Department of Health from over 120 applications to participate in the testing phase of a new scheme to ensure good quality information across the health and social care sector. Thyroid UK is the second largest thyroid charity in the UK and is an independent organization. It is run by patients for patients.

Dr. John C. Lowe, Editor-in-Chief of Thyroid Science, is proud to be a member of the Board of Medical Advisors of Thyroid UK. "Part of pride in being involved with Thyroid UK is the affiliation with Lyn Mynott. After being ill for 15 years and without knowing what was wrong, she had a thyroidectomy and treatment with thyroxine. This enabled her to regain her health. Lyn then began to campaign for better treatment, and she started a small support group that met in her living room. After appearing on BBC Watchdog Healthcheck in 1999, she was inundated with emails and phone calls. This spurred her on to set up Thyroid UK.

Thyroid UK's Contact Information:Tel: 01255 821733Fax: 01255 820407

Subject: About Thyroid Science
From: Anonymous Reader
Date: Thu, June 19, 2008 10:21 am

Dear Editor: I have been taking Eltroxin then later Synthroid since 1974. I discovered Thyroid Science just today. It is apparently a new publication? I would like information regarding the journal. Thank you

Dear Reader: Thyroid Science is an open-access electronic journal started a couple of
years ago by Dr. John C. Lowe's publisher, McDowell Publishing Company,
LLC. It is committed to providing a publishing outlet for scientifically-oriented patients, clinicians, and researchers whose writings are usually censored by conventional endocrinology journals. The latter journals usually publish only papers that, as Dr. Lowe says, favor the financial interests of the drug companies that advertise in the journals. For all practical purposes, he says, those journals are ruled by advertising drug companies with the complicity of the endocrinology specialty. In contrast to those journals, Thyroid Science is dedicated to publishing papers without censoring their content to facilitate commercial interests. You are welcome to read anything published in Thyroid Science, and, if you wish, to contribute to the journal. I hope this answers your question.

Tracy Majors
Assistant Editor
Thyroid Science (

Subject: Fine-needle aspiration and thyroid hormone resistance
Date: February 23, 2008

Dear Dr. Lowe: Are you aware of the paper by E Tjørve, KMC Tjørve, JO Olsen, R
Senum, H Oftebro titled "On commmonness and rarity of thyroid hormone
resistance: A discussion based on mechanisms of reduced sensitivity in
peripheral tissues" (Medical Hypotheses, (2007) 69, 913-921)? In it the
authors call for a test for peripheral resistance. Since the standard thyroid function blood tests don't serve this purpose. which of course the standard thyroid function blood tests don't. Maybe the fine-needle aspiration (FNA) technique used by Dr Bo Wikland and his colleagues would fit the bill? 

Peter Warmingham, Thyroid UK Committee

Dear Peter: I have read the E Tjørve paper. I was pleased that Dr. Tjørve and his coauthors mentioned measuring the basal metabolic rate as a method for testing for resistance. I have used the test in my clinical practice for several years and published two studies so far using the method:

Report at Medical Science Monitor:

(When you reach the page at Medical Science Monitor, scroll down to the second paper under "Clinical Research".)

Report at Thyroid Science:

Along with Tjorve et al, I believe that the basal or resting metabolic rate measurement is most useful clinically for identifying resistance patients, at least those with peripheral resistance. (Having peripheral resistance, of course, means that a patient's pituitary gland is normally or almost normally responsive to thyroid hormone, but most tissues peripheral to the pituitary are partially resistant.) Dr. Wikland’s FNA identifies patients who have autoimmune thyroiditis despite reference range antithyroid antibody levels. Most of the patients are hypothyroid, which is the reason he and his colleagues term the disorder “subchemical hypothyroidism.”

Some of these patients may also have peripheral resistance. But if they improve or recover with doses of thyroid hormone that are lower than supraphysiologic amounts, that would indicate that they are only hypothyroid and not resistant.

Most thyroid hormone resistance patients have to use supraphysiologic dosages of T3 to get well. Even T4/T3 products such as Armour usually don't work for them, not unless they use huge dosages, such as 12 grains or more. I have a book published in 1962 written by an endocrinologist—an endocrinologist from the time when many of them practiced clinical medicine rather than the extremist technocratic medicine of most endocrinologists today. In the book, the endocrinologist wrote that some of his “hypothyroid” patients didn't recover until they took as much as 60 grains of desiccated thyroid per day. I assume those patients really had peripheral resistance, as that amount would contain roughly 540 mcg of T3. That's truly a supraphysiologic daily dosage!

As I have, Dr. Wikland has found that most hypothyroid patients must suppress their  TSH levels before they recover. I don't know the dosages his patients typically use, but if some of them use dosages that are well into the supraphysiologic range, the patients are probably partially resistant to thyroid hormone.

I use the following criteria to diagnose peripheral resistance: the patient has before treatment (1) hypothyroid-like symptoms before treatment, (2) reference range TSH and thyroid hormone levels, and (3) an abnormally low resting metabolic rate; and after treatment, he or she (4) recovers from his or her symptoms with a supraphysiologic  dosage of plain T3 (5) with no evidence of thyrotoxicosis.

There are laboratory methods for testing for resistance. For example, we can use fibroblasts from a patient’s skin. If a supraphysiologic amount of T3 is needed to inhibit the fibroblasts' synthesis and secretion of connective tissue constituents such as fibronectin, then the patient's cells (at least his or her fibroblasts) are resistant to thyroid hormone. I don’t use this particular test for two reasons: first, it isn't available commercially; and second, even if it was, it requires a painful punch biopsy of the skin that I would prefer not to subject patients to.

To sum up, Dr. Wikland's FNA can certainly identify patients who are hypothyroid due to autoimmune thyroiditis. However, the procedure would not identify or rule out peripheral resistance to thyroid hormone.

Dr. John C. Lowe
Thyroid Science

Subject: Re: Thyroid Science: Jan. 18, 2008, New Publications
Date: Fri, January 18, 2008 4:53 pm

Dear Dr. Lowe:  Dr. Bo Wikland's paper (regarding treating euthyroid Hashimoto's patients with thyroxine) is unbelievably timely. I am seeing my doctor for the first time in over a month. I will be getting the results from my last full thyroid panel and hope to see a lowered antibody count.

I recently dosed up to 120mg of Armour and remained on the dose for three weeks prior to testing. At this point I need to bring my doctor up to date on what I've been trying to accomplish. I'm now up to 150mg of Armour and with the addition of Cortef to my program believe I may be beginning to get the improvement that I hoped for.

As my doctor views me as a "euthyroid Hashimoto's patient," it will be helpful to come armed with research as I try to get him onboard with my current strategy. My doctor and I have a good working relationship, and we go back many years. He's a long standing alternative doc and a good listener—so I am cautiously optimistic that all will go well. Thank you again for all that you, Tammy, and your staff do. Regards . . .

Dear Chris: I hope you're doctor responded well to Dr. Wikland’s paper. One of our purposes at is to provide patients like you with publications by experts in the thyroid field whose publications are often truncated and placed in inconspicuous places in endocrinology journals, or rejected for publication altogether to avoid offending the journals' advertisers—usually ones that profit from T4-replacement therapy. I appreciate you writing. Your email lets us know that we're on the right track in publishing

Dr. John C. Lowe

Patient Asking Weather Thyroiditis Can Be Detected by Needle Aspiration in a Treated Patient? Response to editorial on Dr. Bo Wikland's Research on Autoimmune Thyroiditis

December 7, 2007

Dear Dr. Wikland: I was very interested to read Dr. Lowe’s editorial in Thyroid Science about "subchemical hypothyroidism," which you discovered and named. I am one of Dr Gordon Skinner's patients, and likely to get hung out to dry if the General Medical Council does its worst. I hope you can answer this for me, if you don't mind.

I was wondering whether the needle biopsy would still show anything useful in a clinically hypothyroid, but biochemically euthyroid, patient who has received treatment. I take 3.5 grains of Armour Thyroid.

Untreated, I had a TSH of 4.0 (reference range was 0.4-4.0) and a basal temp of 35 C-36.2 C (95 F-97.16 F). I was chronically fatigue for 28 years with other signs and symptoms (except I had normal reflexes for some reason). I had 'normal' levels of thyroid antibodies.

I cannot get treatment under our UK National Health System, as I can from Dr Skinner, because my TSH is now undetectable and my original need for thyroid replacement denied. So if this method would still show anything now (without my having to come off the Armour to satisfy anyone's curiosity now as to my untreated status), I would be very grateful to know. Dr Skinner is a bit busy just now, poor man.

Thank you and best wishes,
UK patient

Dear Belinda: Thank for your inquiry. I understand that you have achieved wellness on Armour Thyroid, but fear that you might be denied continued treatment in the UK because your TSH level is undetectable.

Having a desirable TSH level when on supplementary treatment with thyroid hormone is a hot potato. Mainstream opinion advocates "restoring TSH levels to normal," irrespective of patients' response to the treatment needed to achieve this. This is a theoretical point of view, which, when confronted with the patient’s unsatisfactory response, very often proves to be wrong.

Our rationale for thyroid hormone replacement in autoimmune thyroid disease when the patient has symptoms of hypothyroidism is not to correct the hormone deficiency—the levels of circulating hormone, free T4 and free T3 are, usually appear normal. Rather, our intention with hormone supplementation is to mitigate autoimmune activity. Our hypothesis is that the TSH in this context is detrimental in promoting autoimmune activity. Therefore many (but not all) patients require a low level of TSH.

It is very unfortunate that patients requiring "suppressive" doses of thyroid hormone are denied adequate treatment. Patients are the best judges of their own health.

In the UK, there is one highly respected specialist, Dr. Anthony Toft, who advocates a flexible approach in managing treatment with thyroid hormone.[1] Fortunately, in Sweden where I practice, some clinical pathologists comment approvingly on a "suppressed" TSH that it is compatible with adequate supplementation.

I sincerely hope that you will be allowed the dose of thyroid hormone you require.


1. Toft, A.: Thyroid, 15:124-126. 2005.

Best wishes,
Bo Wikland, MD
torget Medical Center
ägen 13
SE-111 57 Stockholm, Sweden

Letters in Response to Dr. Lowe's Critique: Thyroid Hormone Replacement Therapies: Ineffective and Harmful for Many Hypothyroid Patients

On June 19, 2004, Dr. John Dommisse sent an email to Dr. Lowe in response to his critique of the replacement studies. Dr. Dommisse is a physician who practices nutritional, metabolic, and psychiatric medicine, and who hosts a popular telemedicine website. He is a member of the Endocrine Society, which publishes the Journal of Clinical Endocrinology and Metabolism (JCEM). JCEM published two of the replacement studies in 2003, and an editorial in which the authors reiterated the invalid conclusion of the endocrinologists who conducted the studies.

Dr. Dommisse's email included a copy of a letter he'd written to the Editor of JCEM. He wrote the letter in response to the reports of the replacement studies. JCEM declined to publish his letter, so he gave Dr. Lowe permission to publish it here as support for Dr. Lowe's critique.

In his email to Dr. Lowe, Dr. Dommisse wrote, "JCEM would not even publish a (longish, admittedly) LETTER that I wrote to the editor in response to that spate of bogus articles!"[1]

Dr. Lowe replied:

I am not surprised that JCEM didn't publish your letter. I'm not surprised despite your letter's precise relevancy to the articles about the replacement studies, despite the excellent points you raised about treatment and avoiding adverse effects, and despite your clear prose. We became convinced long ago that, regarding the diagnosis and treatment of hypothyroidism, most major medical journals are not published in the pursuit of truth. If they were, they would provide for debate of dissenting views—as is traditional in real sciences. Instead, in our view, the purpose of the journals, in regard to the diagnosis and treatment of hypothyroidism, is to perpetuate medical acceptance of financially profitable beliefs and to censor dissenting views that might threaten financial markets nourished by those beliefs. What bothers me most is that, in my opinion, to serve those two purposes, those who decide what will and won't be published in those journals must carry on with cavalier disregard for the pernicious impact of those beliefs on humanity.[2]

Dr. Dommisse's full letter to the Editor of the Journal of Clinical Endocrinology and Metabolism

1. Dommisse, J.: Personal written communication with Dr. John C. Lowe. June 19, 2004.
2. Lowe, J.C.: Personal written communication with Dr. John Dommisse. June 19, 2004.  

Subj: Brief Comment on Critique of Thyroid Hormone Replacement Studies
Date: 6/8/2004 4:47 PM Mountain Daylight Time
Sent from the Internet

Dear Editor: The original Bunevicius research found benefits for T3/T4 over T4 and was followed up by a further analysis (Int. J. Neuropsycopharmacology, 2000, 3:167-174) which demonstrated that these benefits applied only to those on TSH-suppressive doses of thyroid hormones, particularly for thyroid cancer. Each of the four replacement studies tested patients on lower doses.

However, "Combined Thyroxine/Liothyronine [T4/T3] Treatment Does Not Improve Well-Being, Quality of Life, or Cognitive Function Compared to Thyroxine Alone: A Randomized Controlled Trial in Patients with Primary Hypothyroidism" (Walsh et al. JCEM 88(10):4543-4550) is a classic. ". . . subjects attended after an overnight fast and before taking T4 or study medication (i.e. 24 h after the previous dose)." Their data shows that the T3/T4 group had lower T3 levels than the T4 group and in the Discussion section they acknowledge the 24-hour half life of T3! Duh!!!  Jim Harwood.

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