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related to Dr. Lowe's rebuttal
to British Thyroid Association |
Readers responses to Dr. Najarian
and Dr. Rowsemitt's two papers
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
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
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.[1,p.109]
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
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.:
Protocol, Tablet Instability, and Absorption Effects on L-T4 Bioequivalence.
Thyroid, 19(2):103-110, 2009.
(This Q&A was published
simultaneously at drlowe.com)
Letter to the
Subject: Question about where to submit my paper
Date: June 12, 2010
From: Author prefers anonymity
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
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
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
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
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.”
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
search engines such as Google also index the papers that formerly were indexed
only in the traditional indexing systems. Plus, Internet search engines
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
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?
by Dr. John C.
Editor-in-Chief (November 24, 2009)
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
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
The Metabolic Treatment of Fibromyalgia
[available in the
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
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
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
Drs. De Sousa, Dilip, Mervyn
(March 2, 2009)
Dear Dr. Roberts:
We asked Dr. DeSousa if any photos were available of
the patient whose goiter
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.
Letter to the
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 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.
(December 25, 2008)
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
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.
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.
By blocking this enzyme, T3 sustains the fat-decomposing effect of
adrenaline and noradrenaline in fat cells.
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.
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 while you were on T4 replacement. As Duntas wrote, 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
reduces fat in artery linings in part by increasing the activity of an
enzyme called “lipoprotein lipase.”
Low activity of this enzyme leads to high blood fats, which is a risk
factor for coronary heart disease.
Thyroid hormone increases the activity of the enzyme, and by doing so,
it reduces blood fats.
Thyroid hormone also lowers LDL
cholesterol by increasing the number of LDL receptors on liver cells.
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.
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,
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.,
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.,
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.,
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
11. Duntas, L.H.: Thyroid
disease and lipids. Thyroid, 12(4):287-293, 2002.
Letter to the
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.
Med Vänlig hälsning
+46 40 137 765
Dear Mr. Németh: Thank you for your email and your thoughts. Yes,
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
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
We appreciate you expressing your opinion and prompting us to explain
why our reviewers and editors enthusiastically accepted Dr. Øverbye’s
paper for publication.
Dr. John C. Lowe
Thyroid Science (Editor@ThyroidScience.com)
Letter to the
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.
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
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
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
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.
Dr. John C. Lowe
Thyroid Science (Editor@ThyroidScience.com)
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.
Thyroid Science (www.ThyroidScience.com)
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.
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
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
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
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
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
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
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
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
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
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."
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
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
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
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
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
Dr. John C. Lowe
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
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'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
Dear Reader: Thyroid
Science is an open-access electronic journal started a couple
years ago by Dr. John C. Lowe's publisher, McDowell Publishing
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.
Thyroid Science (www.ThyroidScience.com)
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
resistance: A discussion based on mechanisms of reduced
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
(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
Subject: Re: Thyroid Science:
Jan. 18, 2008,
Date: Fri, January 18, 2008 4:53 pm
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 . . .
I hope you're doctor responded well to
Wikland’s paper. One of our purposes at
ThyroidScience.com 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?
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
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
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,
Thank you and best wishes,
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.
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.
Fortunately, in Sweden where I practice, some clinical pathologists
comment approvingly on a "suppressed" TSH that it is compatible with
I sincerely hope that you will be allowed the dose of
thyroid hormone you require.
1. Toft, A.: Thyroid, 15:124-126. 2005.
Bo Wikland, MD
SE-111 57 Stockholm, Sweden
Letters in Response to Dr. Lowe's Critique:
Replacement Therapies: Ineffective and Harmful for Many Hypothyroid
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
a popular telemedicine
He is a member of the Endocrine Society, which publishes
the Journal of Clinical Endocrinology and Metabolism (JCEM).
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!"
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.
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.
© 2012 Thyroid Science