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Reply to Doctor who states that T3 is dangerous

Doctor Says No Patient Needs to Use T3, and T3 Can Be Dangerous

Reply by Dr. John C. Lowe
December 6, 2003

In the email below, a physician wrote to a colleague of Dr. Lowe, arguing that no patient needs to use T3 and that T3 can be dangerous. Below the physician’s email,
Dr. Lowe replies to his arguments.

Subj: T3 can be dangerous
Date: Dec. 2, 2003
From: Dr. XXXXX
To: Dr. XXXXX

Dear Doctor,

I have enjoyed your emails and have read them with interest. Having done quite a
bit of Thyroid [sic] research, spent three years in Dr.’s [sic] Sidney Ingbar and
Louis Braverman labs, the previous and most recent authors of the medical text
The Thyroid, I feel I can speak with a little bit of knowledge . . .

It is extremely unusual for patients not to be able to convert T4 to T3. The
common exception is when patients are deathly ill and they convert T4 to rT3
(reverse T3) which is inactive; this is referred to as euthyroid sick [syndrome].
Several ICU [intensive care unit] studies have not shown any better survival with
the addition of T3 to these patients and is not recommended.

Outpatient use of T3 with or without T4 can be dangerous. You may recall the
great rematch of Mohammed Ali with Joe Frasier. Mr. Ali needed to loose [sic]
weight to get in shape for the fight and took Thyrolar, a T4/T3 combination
medicine. He lost plenty of weight and the fight early in it’s course. I believe his
physician also lost his job. T3 is nothing to play around with. Moreover, I am
concerned with your recommendations [of T3] to the less knowledgeable.

Dear Doctor:
A colleague of mine, to whom you wrote the email above, asked me to reply to your
comments about T3. I’ve taken the liberty to do so because the replies to your
arguments can be extremely important to the health and well-being of many patients.
I hope that it’s acceptable to you that I’ve replied.

In your email, you reach two conclusions: (1) that no patient needs to use T3 alone,
and (2) that using T3 is dangerous for patients. Below, I address the implied or
explicit evidence you give for these two conclusions. My point is to show that your
conclusions dont validly follow from your evidence, and that your conclusions are
false.

Your First False Conclusion: You first imply that no patient needs to take T3. Your
reason is that except for those who are deathly ill, all patients effectively convert T4
to T3. That being the case, according to you, patients have nothing to gain by taking
T3.

Many doctors mistakenly believe that patients should use T3 because they have
impaired T4 to T3 conversion and, as a result, low T3 levels. But this has never been
the reason for our patients using T3. Unfortunately, were not certain why some
patients must use T3 to free themselves from hypothyroid-like symptoms.

Nonetheless, some patients must; T4 alone, and in some cases T4/T3 combination
medicines, dont relieve their symptoms and signs; only T3 in fairly high dosages
does.One such patient was reported by Kaplan and colleagues in 1981.[1] To be healthy, the
patient had to take 500 mcg of T3 per day. Testing showed that she didnt have
impaired T4-to-T3 conversion, and she didnt have mutated beta-thyroid hormone
receptors. Despite this, extensive testing showed that when she took this large
amount of T3and only then!her metabolism was normal and she was free of
symptoms. Importantly, she also had no tissue overstimulation.

We have studied and treated similar patients for the past seventeen years. Weve
reported our work with these patients as case reports and open systematic clinical
trials,[2][3][4][5] double-blind, placebo-controlled trials,[6][7][8] and a long-term
follow-up.[9] The patients T3 dosages ranged from 50 mcg to 500 mcgalthough I
hasten to add that most require dosages only between 100 and 150 mcg. None of
these patients had lab test results consistent with blocked T4-to-T3 conversion. Also,
among those whose T3-receptor genes we sequenced, none had mutations. As with
Kaplans patient, our patients overall have remained healthy for years on these
supraphysiologic dosages. None have experienced adverse health affects from their
continued use of T3, and none have had evidence of tissue overstimulation upon
serum and urine biochemical testing, electrocardiography, or bone densitometry. Its
noteworthy that most of our patients whove recovered with T3 therapy previously
failed to benefit from the use of T4 replacement.

I must comment parenthetically on one of your arguments for patients not needing to
use T3. You wrote, “Several ICU studies have not shown any better survival with the
addition of T3 to these patients and is not recommended.” Some thyroid researchers
agree with you about this,[18] including our research group. The low T3 levels of most
critically ill patients have a protective effect, aiding the patients in resting and
recovering from their illnesses.

There is, however, a notable exception that the other researchers and you neglect to
consider: critically ill cardiac patients who benefit from T3 treatment. Studies show
that T3 improves these patients heart function in a variety of ways. It also decreases
the severity and incidence of their cardiac abnormalities, and increases their survival
rate.[10][11][12][13][14][15][16] Endocrinologists might not recommend T3 for these heart
patients, but some cardiologists and cardiac surgeons definitely do. Rather than
doctors such as you roundly denouncing T3 therapy, youd better serve patients
welfare by reading the relevant studies and then rectifying your judgment of T3 to
reflect its safety and the potential benefits for select patients.

Your Second False Conclusion: Your second conclusion is that T3 can be
dangerous. Your evidence is that Thyrolar, which contains T4 and T3, impaired
Mohammed Alis athletic performance. However, the Ali case doesnt at all logically
lead to the conclusion that T3 is dangerous. Ill explain why.

Both Thyrolar and Armour Thyroid contain 38 mcg of T4 and 9 mcg of T3 per grain
(60 mg). Many millions of patients have used and continue to use these products with
no harm to themselves. Moreover, before the advent of the TSH test in the early
1970s, patients used these products in much higher dosages than nowadays. Yet the
record does not show that patients were harmed by the higher dosages.[17] Most of
our hypothyroid patients recover within the higher dosage range used before the early
1970s. Our meticulous safety monitoring for many years has revealed no adverse
effects whatever; instead, the patients in general remain extraordinarily healthy.

However, some patients clearly do occasionally use dosages of the products that are
too high for them individually. Ali was one such patient; an excessively high dosage
left him weak, fatigued, and a poor match for Joe Frasier. The overstimulating dosage
was indeed dangerous for himhe was in the ring with Frasier, a powerful slugger.
But Alis overstimulating dosage apparently didnt endanger his health in any other
way. Consequently, the situational danger Ali faced certainly doesnt justify you
inferring that using T3regardless of the dosageis dangerous in general.

Prejudice Against T3: Your conclusion that T3 is dangerous is unsound in another
way. You imply that it was the T3 in the Thyrolar that impaired Alis boxing
performance. Indeed, too much T3 can impair athletic performance and can have
other adverse affects. But so can too much T4. In fact, for patients whose cells
effectively convert T4 to T3, too much T4 causes exactly the same adverse effects as
too much T3. In that Thyrolar contains both T4 and T3, why did you attribute Alis
impaired performance only to the T3?
I suspect the answer to my question is that you hold a prejudice against T3a
prejudice you inculcated into your belief system while studying with Ingbar and
Braverman. Working under the supervision of prominent conventional thyroid
specialists such as Ingbar and Braverman carries a risk: The student doctor may
unquestioningly accept prejudicial pronouncements by the prominent specialists
pronouncements that arent based on research findings but instead on financial
incentives from corporations. One such pronouncement is that the only thyroid
hormone any patient ever needs to use is T4. Another is that T3 shouldnt be used
because its dangerous.

The student doctor, enchanted by his teachers seeming authority, may believe the
pronouncements throughout his medical career, and he may reflexly defend them
without open-mindedly considering evidence that contradicts them. His reflex defense
of the pronouncements may ensure that he doesnt treat patients with T4/T3 products
or T3 alone. If so, hell never learn how safe and effective these products are. Hell
therefore remain miseducated about the products, and hell lack clinical experience
with them. Because of this, his conclusion that T3 is dangerous will be nothing more
than a statement of prejudice thats completely without merit.

As a final note, I assume youve studied the book you mentioned, Ingbar and
Bravermans The Thyroid. The book, which Ive scrupulously studied, contains much
good academic and some practical information. But the only method of thyroid
hormone therapy the authors advocate and describe in the book (except in the thyroid
hormone resistance chapter) is T4 replacement. So the book contains paltry little
thats useful about thyroid hormone therapy. For the most comprehensive coverage of
T4, T4/T3, and T3 therapies ever published, I strongly recommend my book The
Metabolic Treatment of Fibromyalgia.[19] I suggest that you read the exhaustive
information in the book on all forms of thyroid hormone therapy. Doing so is the
single best way to fill the gaps and inaccuracies in your knowledge left by Ingbar and
Bravermans tutelage.
Dr. John C. Lowe (December 5, 2003)

References

[1] Kaplan, M.M., Swartz, S.L., and Larsen, P.R.: Partial peripheral resistance to thyroid hormones. Am. J. Med., 70:
1115-1121, 1981.
[2] Lowe, J.C.: Improvement in euthyroid fibromyalgia patients treated with T3 (tri-iodothyronine). Journal of Myofascial
Therapy, 1(2):16-29, 1994.
[3] Lowe, J.C.: T3-induced recovery from fibromyalgia by a hypothyroid patient resistant to T4 and desiccated thyroid.
Journal of Myofascial Therapy, 1(4):21-30, 1995.
[4] Lowe, J.C.: Results of an open trial of T3
therapy with 77 euthyroid female fibromyalgia patients. Clin. Bull. Myofascial
Ther., 2 (1):35-37, 1997.
[5] Honeyman, G.S.: Metabolic therapy for hypothyroid and euthyroid fibromyalgia: two case reports. Clin. Bull. Myofascial
Ther., 2(4):19-49, 1997.
[6] Lowe, J.C., Garrison, R., Reichman, A., Yellin, J., Thompson, M., and Kaufman, D.: Effectiveness and safety of T3
therapy for euthyroid fibromyalgia: a double-blind, placebo-controlled response-driven crossover study, Clin. Bull.
Myofascial Ther., 2(2/3):31-57, 1997.
[7] Lowe, J.C., Garrison, R., Reichman, A., Yellin, J.: Triiodothyronine (T3
) treatment of euthyroid fibromyalgia: a small-n
replication of a double-blind placebo-controlled crossover study. Clin. Bull. Myofascial Ther., 2(4):71-88, 1997.
[8] Lowe, J.C., Reichman, A., Yellin, J.: The process of change with T3
therapy for euthyroid fibromyalgia: a double-blind
placebo-controlled crossover study, Clin. Bull. Myofascial Ther., 2(2/3):91-124, 1997.
[9] Lowe, J.C., Reichman, A., Yellin, J.: A case-control study of metabolic therapy for fibromyalgia: long-term follow-up
comparison of treated and untreated patients (abstract). Clin. Bull. Myofascial Ther., 3(1):23-24, 1998.
[10] Goichot, B. and Schlienger, J.L.: Les indications extrathyroVdiennes des traitements par hormones thyroVdiennes.
Rev. Md. Interne, 19:720-725, 1998.
[11] Dyke, C.M., Yeh, T., Jr., Lehman, J.D., et al.: Triiodothyronine-enhanced left ventricular function after ischemic injury.
Ann. Thorac. Surg., 52:14-19, 1991.[12] Klemperer, J.D., Zelano, J., and Helm, R.E.: Triiodothyronine improves left ventricular function without oxygen
wasting effects after global hypothermic ischemia. J. Thorac. Cardiovasc. Surg., 109:457-465, 1995.
[13] Vavouranakis, I., Sanoudos, G., Manios, A., et al: Triiodothyronine administration in coronary artery bypass surgery:
effect on hemodynamics. J. Cardiovasc. Surg. (Torino), 35(5):383-389, Oct., 1994.
[14] Wechsler, A.S., Kadletz, M., Ding, M., et al.: Effects of triiodothyronine on stunned myocardium. J. Card. Surg.,
8(Suppl.2):338-341, Mar., 1993.
[15] Salter, D.R.: Acute severe post-ischemic myocardial depression reversed by triiodothyronine. Ann. Thorac. Surg.,
54(2):301-305, Aug., 1992.
[16] Hamilton, M.A., Stevenson, L.W., Fonarow, G.C., et al.: Safety and hemodynamic effects of intravenous
triiodothyronine in advanced congestive heart failure. J. Cardiol., 81(4):443-447, 1998.
[17] Pearch, C.J. and Himsworth, R.L.: Total and free thyroid hormone concentration in patients receiving maintenance
replacement treatment with thyroxine. Brit. Med. J., 288: 693-695, 1984.
[18] Burman, K.D. and Wartofsky, L.: Thyroid function in the intensive care unit setting. Crit. Care Clin., Jan;17(1):43-57,
2001.
[19] Lowe, J.C.: The Metabolic Treatment of Fibromyalgia. Boulder, McDowell Publishing Co., 2000.

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