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Thyroid Science 3(3):E1-2, 2008
The Common Thread:
What the New Research Shows
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Jackie Yellin*
*Executive Editor, Thyroid Science
Education
Director, The Fibromyalgia Research Foundation
Contact:
Jackie@ThyroidScience.com
Th yroid Science began a little over a year ago, and
we were immediately accepted by the research community as a respected,
open-access online journal. My job as Executive Editor, in addition to
helping to prepare manuscripts, is to review and assess how we’ve done in
our first year. As I began to reflect upon the studies, letters, and
editorials we’ve published, I realized that they all seemed to point in
the same direction. The common thread, so to speak, is startling
considering the fact that we publish relevant submitted research without
prejudice or subject selection criteria. In other words, we did not
pre-decide what types of papers we would publish.
Because Thyroid Science was created simply to
foster truth in thyroid science and thyroid clinical practice, we’ve been fortunate to be able to publish papers
from around the world that clearly seem to contradict the conclusions of
the papers you’ll find in more "conventional" journals. What jumped out at
me—as I reviewed the new research papers as a body of evidence—is that the
current standard of practice in endocrinology with regard to
hypothyroidism is gravely deficient. More especially, using the TSH as a
universal and solitary gauge for both diagnosis and treatment should now
be seriously questioned.
Each of the studies we’ve published in this first year
(save Frank Thompson’s on depression that didn’t deal with actual
treatment technique) used a better and more direct assessment of patients’
thyroid status than the TSH test. And interestingly, the assessment method
was different in each study!
Dr. Bjørn Øverbye of Norway used the Van Vincent
Bio-Electrical-Terrain-Analysis, a system that evaluates the metabolic
status of structurally-supportive and essentially-producing tissues. In
his clinically hypometabolic patients, he found evidence of acidosis in
connective tissues and lymphatic and blood vessels. "The acidosis can be
explained by a lack of thyroid hormone effect at the cellular level." [1]
For almost all of his patients, the TSH was "in the normal range," whether
they had been treated (actually under-treated) or not.
In our most recently published paper, Dr. John Dommisse
of Arizona, USA describes what he believes to be a better assessment of
patients’ metabolic status than the TSH. [2]
He measures his clinically hypometabolic patients’ free T4 and free T3
levels by the tracer-dialysis method both for diagnosis and treatment. He
prescribes whatever type of thyroid hormone the patients need, including
T3, to "optimize" the free T4 and free T3 levels. Most importantly, he
doesn’t mind suppressing the TSH in the process.The group of studies from Sweden by Dr. Bo Wiklund and
Dr. P.O. Sanberg may be the most influential in persuading practitioners
that the sole use of the TSH and other blood tests is inadequate
for diagnosing autoimmune
hypothyroidism. [3][4][5] Many of Dr. Wiklund’s clinically
hypometabolic patients had normal range blood tests—TSH, thyroid hormone
levels, and antibody levels. But when Dr. Wiklund performed fine-needle
aspiration of the thyroid gland on these patients, cytologist Dr. P.O.
Sandberg found many samples to show lymphocytic infiltration. In other
words, these patients had evidence of autoimmune thyroid disease in the
tissues of the thyroid gland that did not show up in any blood test. Dr.
Wiklund believes that not only should a normal range TSH not be the
goal for these patients, but that the TSH should be suppressed because
"TSH signals trigger and maintain autoimmune activity.[3]
I want to briefly mention here that Frank Thompson’s
recommendation of T3 for depression implies that he, too, is
willing to ignore the "standard" approach to thyroid treatment. [6]
(Thompson is from California, USA.) Though he doesn’t say how he
assesses depressed patients’ thyroid status and whether or not he uses the
TSH in any way, the fact that "conventional" thyroid treatment allows only
T4 and Thompson recommends T3 tells us that he has
indeed found a better way to work with his depressed patients than the one
dictated by the endocrinology specialty.
Next, we come to the critiques of the flawed studies [10][11][12][13]
done on adding T3 to T4 in patient treatment.
Dr. John Dommisse’s letter[7]
about these studies and Dr. John
Lowe’s extensive examination of how they were flawed[8]
both
tell us that the conventional endocrinologists who performed the studies
were unwilling to give up their use of the TSH as the "gold standard." And
by using the TSH to decide how much thyroid hormone to give patients, the
results were pre-determined. It didn’t really matter whether they used T4
and T3 in combination, if the dosages merely normalized
patients’ TSH levels; the treatment was doomed to fail because these
symptomatic (clinically hypometabolic) patients already had normal range
TSH levels.
Finally, what we consider to be the most important
study published in the last 10 years for fibromyalgia patients is our
paper "Lower Resting Metabolic Rate and Basal Body Temperature of
Fibromyalgia Patients Compared to Matched Healthy Controls." [9]
Dr. Lowe used the indirect calorimeter to measure resting metabolic rates
in fibromyalgia patients. After controlling for almost all the factors
that could influence resting metabolic rate—including lack of exercise—our
results showed that indeed, fibromyalgia patients have lower resting
metabolic rates and basal temperatures than controls. By definition, then,
fibromyalgia patients can be said to be clinically hypometabolic. In
addition, the patients’ TSH levels failed to correlate with their resting
metabolic rates. In other studies, the TSH has not been shown to reliably
predict resting metabolic rates, so we cannot rule out inadequate thyroid
hormone regulation as the mechanism of the fibromyalgia patients’ low
metabolic rates. Once again, then, we have evidence that the TSH is not
the proper gauge for judging whether or not a patient is hypometabolic.
The publications in Thyroid Science, as a body
of evidence, all relate to clinically hypometabolic patients who were
failed by the use of the TSH to diagnose and treat them. And, most of the
studies offer better ways to assess and treat patients than the TSH test.
Remember that we did not set up criteria for publication in Thyroid
Science that would lead to the above "common thread." But when a group
of unrelated and unselected papers all show the same thing, honest
scientists and clinicians must consider that the conclusions of these
publications come much closer to the truth than what was previously
believed. The reason why we have the compilation of international studies
in Thyroid Science that we now have, and the reason they come to
similar conclusions, is simply that research done openly, without
prejudice or politics playing a role, will always come closer to the
truth.
References
1. Øverbye,
B.J.:
Metabolic failure as the cause of fibromyalgia syndrome: exploring
the John C. Lowe thesis. Thyroid Science, 11(1):CLS1-18, 2007.
2. Dommisse, J.V.:
Hypothyroidism: Sensitive diagnosis and optimal
treatment of all types and grades—a comprehensive hypothesis based on a
review of the standard and "alternative" literature and extensive clinical
experience. Thyroid Science, 3(2):H1-14, 2008.
3. Wikland, B.:
What is optimal treatment of hypothyroidism? A matter
of clinical common sense. Thyroid Science, 3(1): H1, 2008.
4. Wikland, B.:
Redefining hypothyroidism—a paradigm shift. (Invited
Editorial) Thyroid Science, 3(1):E1, 2008.
5. Sandberg, P.O.:
Fine-needle aspiration of the thyroid gland—its role
in the investigation of thyroid autoimmunity. Thyroid Science,
3(2):CLS1-2, 2008.
6. Thompson, F.K.:
Is there a thyroid-cortisol-depression axis? Thyroid
Science, 2(10):1, 2007.
7. Dommisse, J.V.:
Rejected letter by John Dommisse, MD to the editor
of "The Journal of Clinical Endocrinology and Metabolism." Thyroid
Science, 1(12):C1-2, 2006.
8. Lowe, J.C.:
Four 2003 studies of thyroid hormone replacement
therapies: logical analysis and ethical implications. Thyroid Science,
1:C1-C21, 2006.
9. Lowe, J.C,, et al.:
Lower resting metabolic rate and basal body
temperature of fibromyalgia patients compared to matched healthy controls.
Thyroid Science, 1:CLS1-24, 2006.
10. Walsh, J.P., Shiels, L., Mun Lim, E.E., et al.: Combined thyroxine/liothyronine
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. J. Clin. Endocrinol. Metab.,
88(10):4543-4550, 2003.
11. Sawka, A.M., Gerstein, H.C., Marriott, M.J., et al.: Does a
combination regimen of thyroxine (T4) and 3,5,3'-triiodothyronine improve
depressive symptoms better than T4 alone in patients with hypothyroidism?
Results of a double-blind, randomized, controlled trial. J. Clin. Endocrinol. Metab., 88(10):4551-4555, 2003.
12. Clyde, P.W., Harari, A.E., Getka, E.J., and Shakir, K.M.M.:
Combined levothyroxine plus liothyronine compared with levothyroxine alone
in primary hypothyroidism: a randomized controlled trial. J.A.M.A.,
290:2952-2958, 2003.
13. Cassio, A., Cacciari, E., Cicgnani, A., et al.: Treatment of
congenital hypothyroidism: thyroxine alone or thyroxine plus
triiodothyronine? Pediatrics, 111(5):1055-1060, 2003.
Yellin, J.: The Common Thread: What the New Research
Shows.
Thyroid Science, 3(3):E1-2, 2008.
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