T3 Treatment Dr. Lowe

[Guest guest]

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

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

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. 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 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, 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] 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 him—he was in

the ring with Frasier, a powerful slugger. But Ali’s overstimulating 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.

—Dr. 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., , 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. Méd. 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., son, 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.