Doctor Says No Patient Needs to Use T3, and T3 Can Be Dangerous
Doctor Says No Patient Needs to Use T3, and T3 Can Be Dangerous
If your GP/Endocrinologist tells you a similar story, or even if you suspect that s/he might, then copy out http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1341585/”
Dr John Lowes response and take it to your doctor and insist that they read it there and then while you are sat there. Alternatively, if any of you have already been denied a trial of any form of T3 and you have been left on T4-only and still suffering symptoms, then copy this off and send it to them, and ask for a written response and for the letter to be placed into your medical notes and for them to acknowledge that this has been done in writing.
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. John Lowe’s Reply
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.
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 againarising 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 patientsnot 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, 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. 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, double-blind, placebo-controlled trials, and a long-term follow-up. 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 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. 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 thyroid hormone to these patients and is not recommended; this is especially true in chronic as opposed to acute renal failure. 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. 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. 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 (0.040.4 mU/L. 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 himhe was in the ring with Frasier, a powerful slugger. But Alis over-stimulating 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 specialistspronouncements 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. 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.