|
Letters to Editors
& Authors |
|
Want to be notified about new publications in Thyroid Science? |
|
|
|
To submit a letter to an editor
or author through Thyroid Science, please read our
guidelines
for submitting letters. Submit your letter to
Editor@thyroidscience.com.
Letters may be edited and shortened. Thank you.
Subject: About Thyroid Science
From: Anonymous Reader
Date: Thu, June 19, 2008 10:21 am
To: Editor@thyroidscience.com
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
Reply
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 adverting 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.
Sincerely,
Tracy Majors
Assistant Editor
Thyroid Science (www.ThyroidScience.com)
Subject: Fine-needle aspiration
and thyroid hormone resistance
Date: February 23, 2008
To:
Editor@ThyroidScience.com
From:
peter.warmingham@whsmithnet.co.uk
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
Reply
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:
http://www.medscimonit.com/abstracted.php?level=4&id_issue=40182
(When you reach the page at Medical Science Monitor, scroll down
to the second paper under "Clinical Research".)
Report at Thyroid Science:
http://www.thyroidscience.com/studies/lowe.2006/lowe.2nd.rmr.fms.htm
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
Editor-in-Chief
Subject: Re: Thyroid Science:
Jan. 18, 2008,
New Publications
Date: Fri, January 18, 2008 4:53 pm
To:
Editor@ThyroidScience.com
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 . . .
Reply
Dear Chris:
I hope you're doctor responded well to
Dr.
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 ThyroidScience.com.
Dr. John C. Lowe
Editor-in-Chief
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
Reply
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.
Reference
1. Toft, A.: Thyroid, 15:124-126. 2005.
Best wishes,
Bo Wikland, MD
Hötorget
Medical Center
Sveavägen
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
References
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
From: piek@waitrose.com
To: drlowe@drlowe.com
Sent from the Internet
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.
piek@waitrose.com
© 2008 Thyroid Science
|
