DOCTOR SAYS NO PATIENT NEEDS T3, AND T3 CAN BE DANGEROUS

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Doctor Says No Patient Needs to Use T3, and T3

Can Be Dangerous

In the email

below, a physician wrote to a colleague of Dr. Lowe. In his email, the

physician argues that no patient needs to use T3. He also argues that T3

can be dangerous for patients. In the right column, Dr. Lowe replies to

the physician's arguments.

http://www.drlowe.com/jcl/comentry/t3dangerous.htm

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

Dangerous

In the email

below, a physician wrote to a colleague of Dr. Lowe. In his email, the

physician argues that no patient needs to use T3. He also argues that T3

can be dangerous for patients. In the right column, Dr. Lowe replies to

the physician's arguments.

Subj: T3 can

be dangerous

Date: Dec. 2, 2003

From: Dr. XXXXX

Dr. XXXXX

Dear Doctor Lowe,

I have enjoyed your emails and have read them with interest. Having done quite

a bit of Thyroid [sic] research, and having 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.

Dr.

Lowe's Reply

YOU MIGHT WANT

TO PRINT THIS OFF AND TAKE IT TO YOUR DOCTOR IF S/HE HOLDS A SIMILAR VIEW.

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 don’t validly follow from your evidence, and that your

conclusions are false.

I've had

decades of clinical experience with patients switching from T4 to T3. That

experience compels me to respectfully but adamantly content that you are

wrong as wrong can be about T3. Rather than T3 harming patients, for most of

those who switch from T4 to T3, the T3 is tantamount to life-giving sun arising

within them again—arising after years or even decades of darkness,

gloom, and suffering from clinicians such as you restricting them to T4.

It's T4, then, that's harmful to patients—not T3.

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,

we’re 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, don’t 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

didn’t have impaired T4-to-T3 conversion, and she didn’t have

mutated beta-thyroid hormone receptors. Despite this, extensive testing

showed that when she took this large amount of T3—and 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.

We’ve 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

mcg—although 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 Kaplan’s patient,

our patients overall have remained healthy for years on these

supra-physiologic 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. It’s noteworthy that

most of our patients who’ve 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 thyroid hormone to these patients and is

not recommended; this is especially true in chronic as opposed to acute

renal failure.[18] We agree with you about this, based on clinical trials. 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, you’d 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

Ali’s athletic performance. However, the Ali case doesn’t at

all logically lead to the conclusion that T3 is dangerous. I’ll

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] After studying

16,427 patients, Leese and Flynn recently found no increase in cardiac

effects, cardiovascular disease, dysrhythmias, or fractures among

patients whose TSH levels were " low. " The researchers defined

low as between (0.04–0.4 mU/L.[20] 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 over-stimulating dosage was indeed dangerous for

him—he was in the ring with Frasier, a powerful slugger. But

Ali’s over-stimulating dosage apparently didn’t endanger his

health in any other way. Consequently, the situational danger Ali faced

certainly doesn’t justify you inferring that using

T3—regardless of the dosage—is 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

Ali’s 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 Ali’s

impaired performance only to the T3?

I suspect

the answer to my question is that you hold a prejudice against T3—a

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

aren’t 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

shouldn’t be used because it’s 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 doesn’t treat patients with T4/T3 products or T3 alone. If

so, he’ll never learn how safe and effective these products are.

He’ll therefore remain miseducated about the products, and

he’ll lack clinical experience with them. Because of this, his

conclusion that T3 is dangerous will be nothing more than a statement of

prejudice that’s completely without merit.

As a

final note, I assume you’ve studied the book you mentioned, Ingbar

and Braverman’s The Thyroid. The book, which I’ve

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

that’s 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 Braverman’s

tutelage.

References

1.

Kaplan, M.M ., Swartz, S.L., and Larsen, P.R.: Partial peripheral

resistance to thyroid hormone. Am. J. Med., 70(5): 1115-1121,

1981.

2. Lowe, J.C.: Improvement in euthyroid fibromyalgia

patients treated with T3 (tri-iodothyronine). J. Myofascial Ther.,

1(2):16-29, 1994.

3. Lowe, J.C.: T3-induced recovery from fibromyalgia

by a hypothyroid patient resistant to T4 and desiccated thyroid. J.

Myofascial Ther, 1(4):21-30, 1995.

4. Honeyman, G.: Metabolic therapy for hypothyroid and

euthyroid fibromyalgia: two case reports. Clin. Bull. Myofasc. Ther.,

2(4):19-49, 1997.

5. 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.

6. Lowe, J.C., Reichman, A.J., and Yellin, J.: The

process of change during T3 treatment for euthyroid fibromyalgia: a

double-blind placebo-controlled crossover study. Clin. Bull.

Myofascial Ther., 2(2/3): 91-124, 1997.

7. Lowe, J.C., Garrison, R.L., Reichman, A.J., and Yellin,

J.: Triiodothyronine (T3) treatment of euthyroid fibromyalgia: a small-N

replication of a double-blind placebo-controlled crossover study

(abstract). Clin. Bull. Myofascial Ther., 3(14):23-24, 1997.

8. Lowe, J.C., Garrison, R.L., Reichman, A.J., Yellin,

J., , M., and Kaufman, D.: Effectiveness and safety of T3

(triiodothyronine) therapy for euthyroid fibromyalgia: a double-blind

placebo-controlled response-driven crossover study. Clin. Bull.

Myofascial Ther., 2:(2/3):31-58, 1997.

9. Lowe, J.C.: A case-control study of metabolic therapy for

fibromyalgia:

long-term (1-to-5 year) follow-up comparison of treated and

untreated patients. Clin. Bull. Myofascial Ther.,

2(2/3):91-124, 1997.

10. 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,

1994.

11. Klemperer, J.D., Zelano, J., Helm, R.E., et al.:

Carediopulmonary bypass, myocardial management, and support techniques. J.

Thorac. Cardiovasc. Surg., 109:457-465, 1995.

12. Hamilton, M.A., et al.: Altered thyroid hormone

metabolism in advanced heart failure. J Am Coll Cardiol.,

16(1):91-95, 1990.

13. Hamilton, M.A. aned son LW.: Thyroid hormone

abnormalities in heart failure: possibilities for therapy. Thyroid,

6(5):527-529, 1996.

14. Hamilton, M.A., son, L.W., Fonarow, G.C., et al.:

Safety and hemodynamic effects of intravenous triiodothyronine in

advanced congestive heart failure. Am. J. Cardiol., 81(4):443-447,

1998.

15. Ascheim, D.D. and Hryniewicz, K.: Thyroid hormone

metabolism in patients with congestive heart failure: the low

triiodothyronine state. Thyroid, 12(6):511-515, 2002.

16. Bettendorf, M., Schmidt, K.G., Grulich-Henn, J., et al.:

Tri-iodothyronine treatment in children after cardiac surgery: a

double-blind, randomized, placebo-controlled study. Lancet,

356:529–534, 2000.

17. PEARCE, C. and HIMSWORTH, R.L.: Total and free

thyroid hormone concentrations in patients receiving maintenance

replacement treatment with thyroxine. Brit. Med. J., 288:693-695,

1984.

18. Acker, C.G., Singh, A.R., and Flick, R.P., et al.: A

trial of thyroxine in acute renal failure. Clin. Nephrol., Kidney

International, 57:293-298, 2000.

19. Lowe, J.C,: The Metabolic Treatment of

Fibromyalgia. Boulder, McDowell Publishing Co., 2000.

20. Leese, G. and Flynn,, R.: Is it safe for patients taking

thyroxine to have a low but not suppressed serum TSH concentration. Endocrine

Abstracts, 21 OC5.6, 2010.