Thyroid Science 3(3):E1-2, 2008 www.ThyroidScience.com Editorial

The Common Thread:

What the New Research Shows

Jackie Yellin*

*Executive Editor, Thyroid Science and Education Director, The Fibromyalgia Research Foundation

Contact: Jackie@ThyroidScience.com

Keywords: hypothyroidism • TSH • clinically hypometabolic • indirect calorimeter

Thyroid Science began a little over a year ago, and we were immediately accepted by the research community as a respected, open-access online jour
nal. My job as Executive Editor, in addition to help
ing to prepare manuscripts, is to review and assess how we've done in our first year. As I began to re
flect 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 rele
vant submitted research without prejudice or subject selection criteria. In other words, we did not pre-de
cide what types of papers we would publish.

Because Thyroid Science was created simply to foster truth in science, 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' thy
roid 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 lev
el."[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 be
lieves to be a better assessment of patients' metabol
ic 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 "opti
mize" the free T4 and free T3 levels. Most impor
tantly, 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 pa
tients 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 tis
sues 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 be
cause "TSH signals trigger and maintain autoim
mune 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 "stan
dard" 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 de
pressed patients than the one dictated by the endo
crinology 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 con
ventional endocrinologists who performed the stud
ies were unwilling to give up their use of the TSH as the "gold standard." And by using the TSH to de
cide 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 symp
tomatic (clinically hypometabolic) patients already had normal range TSH levels.

Finally, what we consider to be the most im
portant study published in the last 10 years for fi
bromyalgia patients is our paper "Lower Resting Metabolic Rate and Basal Body Temperature of Fi
bromyalgia 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—inclu
ding lack of exercise—our results showed that indeed, fibromyalgia patients have lower resting metabolic rates and basal temperatures than con
trols. 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 meta
bolic rates, so we cannot rule out inadequate thyroid hormone regulation as the mechanism of the fibro
myalgia patients' low metabolic rates. Once again, then, we have evidence that the TSH is not the prop
er gauge for judging whether or not a patient is hy
pometabolic.

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 con
clusions, is simply that research done openly, with
out prejudice or politics playing a role, will always come closer to the truth.

References

1.	Øverbye, B.J.: Metabolic failure as the cause of fibromyal
gia 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 compre
hensive 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 autoimmu
nity. Thyroid Science, 3(2):CLS1-2, 2008.

6.	Thompson, F.K.: Is there a thyroid-cortisol-depression ax
is? 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 replace
ment 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'-triiodo
thyronine improve depressive symptoms better than T4 alone in patients with hypothyroidism? Results of a doub
le-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 com
pared 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.