June 12, 2010
Question: 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
To: editor@thyroidscience.com

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
To: editor@thyroidscience.com

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
To: editor@thyroidscience.com

Dear Dr. Lowe: I'm so thankful I was told about ThyroidScience.com. 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)

Dear 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.

References

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.

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
Editor-in-Chief
Thyroid Science (Editor@ThyroidScience.com)  

Letter to the Editor

Subject: Thyroid Weight Gain
From: June Hyslop <Scotland, UK>
Date: Sun, November 16, 2008 6:34 am
To: editor@thyroidscience.com

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,
Sincerely,
Dr. John C. Lowe
Editor-in-Chief
Thyroid Science (Editor@ThyroidScience.com)

Subject: Re: Doing better on Armour
From: Anonymous patient in Australia
Date: Wed, August 27, 2008 6:11 pm
To: editor@thyroidscience.com

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.

Sincerely,
Tracy Majors
Assistant Editor
Thyroid Science (www.ThyroidScience.com)

Subject: Safety Precautions for Thyroid Hormone Therapy
From: Anonymous physician
Date: Thu, August 24, 2008 12:29 pm
To: Editor@thyroidscience.com

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.