2014 ATA Therapy guidelines: 3. Desiccated thyroid

American Thyroid Association-desiccated

If we want to disagree with the American Thyroid Association’s prejudice against animal sources of thyroid hormone, we should to at least prove we’re trying to listen to them. Then we should fairly point out what they didn’t say, what truths they would rather not admit, and where they are being unfair or inconsistent.

This post continues my paraphrase of Jonklaas et al’s 2014 “Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement.”

THIS time, instead of letting this ATA group go on and on endlessly justifying their therapy choices by their beliefs and fears grounded in ignorance and selective evidence, I’ve inserted “P. S.” statements.

These “P. S.” statements are what I believe any reasonable, scientific and truly ethical ATA committee would be forced to admit, but perhaps only if they were being carefully cross-examined by a well-prepared lawyer and had time to examine their own research literature before replying.

Q12 What do we think of thyroid extracts? (desiccated thyroid)

ATA: Levothyroxine is routine care for all patients, and we prefer it over thyroid extracts. We know there is some recent clinical trial research on desiccated thyroid showing it to be safe and effective (an independent and objective 2013 trial by Hoang et al), but we don’t like it because it’s not a long-term controlled study.

ATA: We must require evidence that desiccated thyroid therapy has “superiority” over levothyroxine, our preferred therapy, before allowing anyone to deviate from today’s standard of care.

(P. S. We have decided that this question requires “superiority” clinical trials. This means it’s not enough for research to prove thyroid extracts to be “equally” safe or effective. We’re not interested in doing a “non-inferiority clinical trial,” even though that’s another valid type of clinical trial, because those trials are even more challenging to design and perform correctly.)

(P. S. We admit that a “superiority” drug trial is usually only required to test “new and experimental” pharmaceuticals, but that we want this kind of trial to be applied to re-validate a pharmaceutical that has long ago been approved by Health Canada and the FDA, and which, despite continuous clinical use, has raised no major red flags in the FDA’s side-effect reporting databases in comparison to the side effects noted for levothyroxine. We do not identify which superiority trials were successfully conducted in the 1960s and 1970s to validate levothyroxine monotherapy at the time when those who supported it were advocating for it to become the preferred mode of therapy.)

(P. S. Whenever we design any clinical trial involving levothyroxine, we will start with the presumption that levothyroxine is not only superior but the only safe therapy possible. Therefore, we’re not likely to use any clinical trial methods that might actually expose the aspects of levothyroxine therapy that can make it “inferior” for patients. Those rigorous methods could include linking treated patients’ T3:T4 ratios and dividing their Free T3 levels into quartiles tracked to long-term health outcomes. Therefore, because of a relative lack of levothyroxine insufficiency trials, our clinical trials will continue to reinforce our a priori assumptions of levothyroxine superiority.)

ATA:  We know that desiccated thyroid was “the primary therapy for hypothyroidism until the advent of synthetic T4 preparations in the 1960s.”

(P. S. We are reluctant to report this history more objectively and would prefer to make a statement that limits this therapy to the distant past. Our own reviews of our history have admitted that desiccated thyroid therapy did not end with the advent of synthetic T4, that levothyroxine only gradually achieved market dominance over desiccated thyroid during the 1970s. We are not willing to admit here that desiccated thyroid therapy has never been unapproved by the FDA or taken off the market due to safety concerns and it still enjoys effective use today.)

ATA: We acknowledge that desiccated thyroid contains T4 and T3 also found in synthetic preparations and that its “bioavailability” is the same as synthetic preparations.

P. S. We openly admit that nothing is intrinsically different between its T4 and T3 molecules and the T4 molecules in levothyroxine and T3 in liothyronine. Desiccated thyroid medication does not supply inferior quality thyroid hormone molecules. Therefore we must attack its T3:T4 ratio, which is our next point.

ATA: We have two main clinical concerns with desiccated thyroid medication:


ATA: We confidently assert desiccated thyroid pharmaceuticals will always lead to excessive T3 levels in blood: “The ratio of T4 to T3 in desiccated thyroid preparations is 4.2:1, which is significantly lower than the 14:1 ratio of secretion by the human thyroid gland. This relative excess of T3 leads to supraphysiologic levels of T3 (474–477).”

P. S. Don’t analyze these ratios too closely, because we don’t want you to ponder the fact that levothyroxine has a supraphysiological 100:0 ratio and SUB-physiological T3 ratio of 0:100. We also don’t want you to consider that when T4 is overdosed it will “lead to” supraphysiological T4 levels, which makes it equally dangerous to the human body. We would have to admit that T3 can reach supraphysiological in some patients whose TSH we therapeutically suppress with levothyroxine after undifferentiated thyroid cancer, and in documented cases of T4 overdose.  But we have developed a multitude of sophisticated ways of justifying our preferred medication’s imbalanced ratio, and we’ve mentioned them all elsewhere in our guidelines.

P. S. We don’t actually expect you to read items 474 through 477 that we cited as proof on this statement. If you do read them armed with enough scientific knowledge, you might see the major problems with the research methods and logic within those items. None of them actually proves our statement that desiccated thyroid always “leads to” or causes excess T3. It’s just that we prefer to believe that this pharmaceutical input “causes” this output just because some studies showed it “can” do that IF you dose it a certain way.

P. S. We admit that excess T3 is far more likely to happen while blindly refusing to titrate a desiccated thyroid dose to T3 and T4 levels, as was done in the studies we’ve cited. We will also admit that all standard laboratories today have the technology to test thyroid hormone levels and that these tests currently cost little more than the TSH test does. We would readily admit that the Free T3 test is very accurate at higher concentrations of T3, and that is why we measure T3 to diagnose true hyperthyroidism. Someday, perhaps, we will have to admit that our policy of declaring Free T3 testing unnecessary in hypothyroid therapy is illogical if we truly wanted to prevent supraphysiological T3 in all treated thyroid patients.

— P. S. We refuse to acknowledge something here what we will acknowledge later on in our section 14 about T3 monotherapy. There, we discuss the fact that a lower level of T4 will require a slightly higher-than-normal T3 in blood. This higher T3 in blood will not necessarily inevitably lead to excess T3 binding to receptors in cells throughout the human body IF you simultaneously have a way lower-than-normal T4. In other words, we won’t admit in this case that the lower T4 levels normally induced by desiccated thyroid therapy can be a safety feature because it means less T4 converts to T3 within tissues and cells beyond bloodstream.

P. S. Unfortunately, while we are vigorously attacking a competing medication, you can’t expect us to think logically about the body’s T3 supply in the context of T4 from which we derive the vast majority of our T3. We are incapable at this time of doing the simple endocrine math of T4 subtraction plus T3 addition. However, we will always overemphasize T4-T3 conversion when we’re justifying the opposite math of T4 addition and T3 subtraction. Doing endocrine math only in one direction enables us to dismiss all our concern for a patient who has chronic T3 levels below reference while on levothyroxine.

P. S. We will not re-examine the scientific basis of our dogma about “the 14:1 ratio of secretion by the human thyroid gland” in all healthy people even though it is based on a single study of 14 people (Pilo et al, 1990) who were being overdosed with 10 drops of Lugol’s iodine per day during the study.

P. S. We choose to ignore the scientifically proven fact that a healthy thyroid’s secretion ratio fluctuates and varies from person to person, and over time. We choose to ignore our past research that shows that the secretion ratio varies based on varying TSH stimulation, and that as TSH rises, even within reference range, T3 secretion ratio rises insofar as the gland is healthy enough to respond to TSH.

P. S. In spite of the naturally wide fluctuations of the healthy HPT axis, we will not question the logic of applying a statistically-derived average and eternally-static ratio to all thyroid medication we give to all our thyroidless and thyroid-damaged people.

P. S. We choose to ignore the fact that bloodstream T4:T3 ratios will always trump secretion/dose ratios when it comes to human health. We are not interested in the studies that associate lower Free T3 with various chronic diseases and all cause mortality because those studies usually exclude treated thyroid patients.

P. S. We know from research and clinical practice that we can’t predict a patient’s T4:T3 ratio in blood based on their T4:T3 input in medication. Nevertheless, we still claim that in the case of desiccated thyroid, its 4.2:1 ratio will “cause” a certain T4:T3 ratio in blood at any dose.


ATA: We know it’s more likely that on desiccated thyroid medication your peak T3 will fluctuate over the upper limit of the reference range for part of the day. We believe that this is likely what causes TSH suppression and hyperthyroid symptoms on desiccated thyroid. We believe that a lower TSH by itself makes the existence of thyrotoxicosis at the cellular level more likely, no matter what thyroid medication you are on. “Thus, there is concern for thyrotoxicosis if thyroid extract therapy is not adjusted according to the serum TSH.”

P. S. We have not done any research to confirm whether it is, in fact, having T3 above reference during part of the day that lowers the TSH during T3-based therapies.

P. S. We will not acknowledge our own research that shows that T3 dosing — whether desiccated thyroid or synthetic T3 — affects TSH differently than the same amount of T3 in bloodstream that is naturally secreted and converted in untreated patients. We will not take the time to examine our own studies on the classic “T3 suppression test” (which is misnamed) that involves using T3 dosing to suppress TSH, and therefore thyroid gland iodine uptake. We used to use this test routinely to identify cases of Graves’ disease before its antibodies were fully understood and tested, but now we’ve decided to bury that part of thyroid science in the untouched archives.

P. S. We will not ponder our own scientific research that has proven that using T3 in medication suppresses hypothalamic TRH secretion far more powerfully than naturally-produced T3. We will not ponder the puzzling results of our TRH stimulation tests during T3 monotherapy used in thyroid cancer therapy prior to remnant gland ablation. We will not even ponder the recent studies showing a clear TSH-T3 “disjoint” that occurs during thyroid therapy, which proves that treated thyroid patients’ HPT axis does not behave like that of an untreated person when it comes to T3. Theoretically, we do have the capability of understanding that T3 in medication, like other forms of medication, could induce a degree of “secondary” hypothyrodism in the pituitary or even “tertiary” central hypothyroidism in the hypothalamus. But that would force us to admit, based on such evidence, that the unique effects of T3 dosing makes adjusting T3-therapies based on TSH alone pointless and potentially harmful.

P. S. Someday in the far distant future, our next logical step–(after admitting that T3 dosing will progressively suppress hypothalamic TRH and therefore TSH more than endogenous T3)–would be to admit that by demanding TSH normalization in T3-based therapy, we have enforced a discriminatory testing policy that is designed to make T3-based therapies less effective. We would have to admit the fact that a patient on desiccated thyroid or T3-based therapy is more likely than a patient on levothyroxine to suffer chronic underdose (low or lower-normal Free T3 plus lower T4 levels) if their dose is blindly titrated only to their TSH. In the mean time, we secretly hope that all patients who are truly underdosed on desiccated thyroid therapy because of our TSH policy will beg to return to levothyroxine after failure to dose it effectively.

P. S. As for the dangers of fluctuating T3 levels over reference range, we don’t want to focus on the fact that “thyrotoxicosis” can only occur if cellular receptors are overstimulated by T3 hormone. Even within our current advanced understanding of thyroid hormone economy, we have to admit that thyrotoxicosis is not an absolutely necessary result when T4 is low or absent at the same time that T3 in bloodstream fluctuates higher in its range.

P. S. We will have to admit that no studies have ever proven any health risks of abnormally wide T3 fluctuations during T3-based thyroid therapies in which T4 is simultaneously low or absent. We admit we have neglected to do research on the patients who are currently maintained long-term on synthetic T3 therapy alone, even though their therapy involves much wider T3 fluctuation than desiccated thyroid therapy. Our lack of research on this topic proves that we are not interested in learning how a T3-fluctuating therapy within or beyond the confines of the reference range might actually affect a multitude of health factors in vivo (in living humans).

P. S. We refuse to ponder in this case what we have already learned about the three deiodinases that convert thyroid hormones. We know that during peaks in T3, the body’s tissues are being protected by an upregulation of deiodinase type 3 (D3), the “safety-net” enzyme that is actually expressed in all bodily tissues. We know that D3 is highly sensitive and when activated can increase T3 conversion to T2 within hours. When deiodinase type 3 is active, it also simultaneously converts T4 into Reverse T3, further limiting T3 occupancy of cellular receptors. We admit that we often apply this science to explain how thyroid hormones are inactivated during non-thyroidal illness, but we won’t apply this science when it inconveniently defends desiccated thyroid therapy.


ATA: We truly don’t care if you feel better on desiccated thyroid. Patient satisfaction and quality of life, especially if measured without a “validated questionnaire.”

P. S. See our responses to questions 1c-1d to understand that we only validate symptoms by their correlation to “hypothyroid-specific” measures, namely TSH. Symptoms cannot be an independently valid health outcome even if the questionnaire is validated in other ways. Only a high TSH can validate symptoms as genuine hypothyroid symptoms, so disappearance of symptoms on desiccated thyroid proves nothing but the placebo effect.

ATA: Our literature review shows that our own thyroid researchers haven’t studied desiccated thyroid therapy enough to learn about its benefits or harms, and we’re extremely horrified and fearful by our lack of research.

P. S. We admit that we are collectively to blame for our own ignorance that is the root of our fear. Any reasonable person will understand that our medical fear and loathing of this source of thyroid hormone will likely ensure that we will fear and loathe researching it, which will continue to promote this fear and loathing based on lack of research. It’s a self-perpetuating cycle.

ATA: Some people claim that desiccated thyroid is better because it contains other metabolites like T2 and calcitonin. You have to understand what science has discovered about these metabolites before you claim that ingesting them is necessary or beneficial. There’s not enough known about their benefits, so you can’t claim that you need them.

P. S. We have not conducted any studies that compare metabolites of T2 within levothyroxine monotherapy versus safely-dosed desiccated thyroid therapy or T3 therapy. We are only beginning to understand the different genomic and nongenomic effects of the two different T2 metabolites formed by inner ring vs. outer ring deiodination of T3 and Reverse T3. We have not yet understood all that a lack of calcitonin can do to the treated thyroid patient, so we can’t yet claim that its lack is inconsequential.

ATA: Finally, don’t even think about using desiccated thyroid in pregnancy. There are some theories out there, largely based on tests conducted on cells on a laboratory bench and patients with iodine deficiency, that suggest that lower T4 levels common in this form of therapy, regardless of your T3 levels, just might be harmful to your fetus!

P. S. We’re actually not sure what the risk level for this is within well-managed desiccated thyroid therapy because we ethically can’t enroll desiccated thyroid patients in such studies due to unknown risk to the fetus. However, we’d have to admit that historical evidence on a mass scale doesn’t point to harm: We haven’t seen historical evidence of a higher incidence of brain-damaged children among the large number of pregnant mothers who were dosed on desiccated thyroid in the many decades prior to the pharmaceutical dominance of levothyroxine. But still, we can’t let you harm your baby if there is the least chance that your lower T4 levels might do so.

P. S. We realize that risk to babies always has instant pathos appeal. Fear of causing unborn babies harm always trumps the fear of causing their mothers lifelong harm while they are not pregnant. That’s why we end this section by voicing this fear that you might just get pregnant while on desiccated thyroid.


… No, it won’t be as long as this post, because the ATA are much more kind and reasonable toward synthetic sources of thyroid hormones.


Jonklaas, J., Bianco, A. C., Bauer, A. J., Burman, K. D., Cappola, A. R., Celi, F. S., … Sawka, A. M. (2014). Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid, 24(12), 1670–1751. https://doi.org/10.1089/thy.2014.0028

Notice I haven’t cited anything else … Why?

This series of posts is meant to be a conversational dialogue that inspires the ATA and thyroid experts to do further research within their own literature. I’d like to encourage the ATA and those who know their thyroid science to dig it out and read it carefully, just like I have. If you are a doctor and you question where the basis is of my statements, you can do your own lit review on the key words I’ve raised in the P.S. Statements — I should not have to always do all the work for you.

If you don’t know where to start with your research, consult our Campaign Statement References. It includes about 200 items, many of which are selectively ignored by the huge reference lists at the ends of ATA guidelines documents.

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