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.

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 Stevenson LW.: Thyroid hormone abnormalities in heart failure: possibilities for therapy. Thyroid, 6(5):527-529, 1996.

14. Hamilton, M.A., Stevenson, 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.