Thyroid patient blaming and shaming, part 3: Advocacy and Science


In this Part 3, I continue my rebuttal of a research article that blames thyroid patients for causing harm to themselves by making requests of doctors for tests and therapies.

In this post, I explain the good signs that thyroid patients’ self-advocacy is sometimes effective and is making a difference.

We are standing on the firm ground of thyroid science, and there’s a lot of support building to defend our cause.

I address the common charge that thyroid patients who make such requests are naive and uneducated Googlers who don’t know thyroid science.

I prove that it’s actually the writers of the article that don’t know enough about thyroid science, and they reveal their ignorance quite clearly.

The paper I’m responding to is titled “Patient Requests for Tests and Treatments Impact Physician Management of Hypothyroidism.

According to this article, patients erect “barriers” to their own appropriate care when they request ways of relieving their suffering while the standard thyroid therapy programme set forth in ATA guidelines declares them biochemically euthyroid.

A good sign: Thyroid patient self-advocacy

Based on the way you’ve portrayed our requests as patients, it seems that more and more thyroid patients are becoming educated about the ways their thyroid therapy can be improved, and they are becoming self-advocates.

I think it’s wonderful to see evidence that we are doing this as patients.

Thanks for encouraging us by your article that we’re making a little headway:

  • 21% of physicians would adjust thyroid hormone dose based on symptoms when biochemically euthyroid (among 52% of physicians who reported patient requests),
  • 12% of physicians would prescribe preparations other than synthetic thyroxine (among 52% who reported patient requests),
  • 15% would maintain TSH level below reference range (among 32% who reported patient requests) and
  • 8% would adjust thyroid hormone dose according to serum T3 levels (among 21% who reported patient requests).

So let’s keep it up, patients!

I wish we could have made more requests like this long ago, like 15 years ago.

But I know why we could not have done this long ago.

It’s not just because ineffective thyroid therapy leads to brain fog and fatigue, which makes it hard to self-educate and self-advocate. Yes, that’s a major hindrance to evidence-based thyroid patient advocacy at all times, but something more recently has allowed us to overcome this handicap.

It’s not just because we didn’t have social media platforms like Facebook that have enabled patients to share their lab results, symptoms, articles, and tips with each other. Yes, that has certainly made it easier for us to build the supportive community we often lack and need. Yes, we can now see that our problems with the thyroid therapy system are not just isolated to our individual case.

But something beyond a patient support community is necessary, otherwise they would just be places where we moan about our doctors and symptoms and share band-aid coping strategies that don’t fix the core problems.

A major reason why we’re requesting intelligent and reasonable things like “adjusting thyroid hormone dose according to serum T3 level” is this:

More and more published thyroid science since 2011 has proven just how blind, harmful, and narrow your guidelines truly are. The long-awaited paradigm shift has been happening within thyroid science, the shift from the TSH-T4 paradigm to the T3 paradigm, and it’s enabling a revolution in thyroid patient advocacy.

Science-enlightened thyroid patients like me, and many science-enlightened thyroid doctors, are publicly disseminating thyroid science by publishing books and blogs and videos and images. The newer publications are giving me clearer lenses that I can use to re-read scientific publications going back to the 1950s.

As a result, even many patients who don’t directly read the scientific journal articles are starting to understand the approaches to testing and treatment that form the basis of more effective thyroid care.

It’s about time that we patients became aware of the ways your thyroid therapy guidelines have become derailed from thyroid science and are rooted in prejudice rather than proof.

Your inevitable backlash against patients

You, dear doctors, are noticing the trend of increasing requests as we become more educated in thyroid science and thyroid therapy. Even our most reasonable, scientific and respectful self-advocacy isn’t going over well with some of you.

We’re inspiring the inevitable resistance from those of you who strongly adhere to a rigid, outdated and narrower paradigm.

It’s causing stress on doctors like you who are used to more patient compliance when treating other medical conditions.

Your first reaction is to adhere even more religiously to the guidelines, resorting to reactionary and self-defensive positions.

Your next reaction, if you feel very threatened, annoyed and angry, is to lash out against us, first in the privacy of your office, and eventually, in the public forum, doing everything you can to diminish our knowledge, intelligence and motives in relation to yourselves.

You’ll say we’re gullible Googlers swayed by snake-oil salesmen touting the benefits of desiccated thyroid for weight loss purposes rather than health benefits, or that we just got this crazy idea because a friend on Facebook is taking T3 hormone.

We’re not just uneducated, gullible patients.

You incorrectly think that we’re uneducated about our TSH test results and our T4 monotherapy. What you’re calling lack of patient education is actually patients’ ability to see through mere medical indoctrination that you think they should swallow.

We are not uninformed people. We understand the basic TSH-based definitions of euthyroidism and we know why they apply outside of therapy.

We are also not gullible people who think that TSH-centric definitions of euthyroidism are scientifically accurate in the context of thyroid therapy, and science can prove it.

You can’t see the scientific basis of our requests because you haven’t been keeping up with your own science. You’re probably not reading the thyroid science articles we are reading, such as articles by your own ATA president 2015-2016, Antonio Bianco, and his coauthors. Perhaps some of you read thyroid science only through the filter of TSH-T4 paradigm lenses, or choose the simplified formats of guidelines, flowcharts, or maybe your medical school textbooks.

Are you reading thyroid science carefully?

You should be ashamed of yourselves. Thyroid patients who know the science can easily catch you with your pants down when you cite things you really don’t read.

It should be embarrassing when a citation directly contradicts the statements you think you’re making. These things should be caught during the peer-review process in the journal, so it reflects badly on your journal editors as well.

First of all, you’ve misread a key thyroid science article co-authored by Antonio Bianco (Gereben et al, 2015)

In the dialogue above, your words are in italics and I gave the citation you used.

A normal TSH clearly proves that their medication is working, because levothyroxine monotherapy maintains an adequate level of serum T4, and the iodothyronine deiodinases provide physiologic regulation of T3 availability. I think the recent article by Gereben et al, 2015 probably confirms that further, but I haven’t read it carefully yet, to be honest.

It is painfully obvious you have not read the article you cited after your claim. The citation proves the exact opposite.

Gereben’s article showed why levothyroxine monotherapy may not maintain T3 availability in tissues and blood despite a normalized TSH:

The latest studies indicate that unique biochemical aspects of the iodothyronine deiodinases in the hypothalamus prevent normalization of serum levels of T3 in patients treated with levothyroxine monotherapy.”

This article pointed out that a paradigm shift is occurring with regard to the role of TSH and T3 in thyroid therapy.

The new thyroid science explains why patients still have hypothyroid symptoms at a normal TSH:

Once heralded as the ultimate regulators of thyroid-hormone availability and the key to levothyroxine treatment efficacy, iodothyronine deiodinases might actually underpin the inability to normalize serum levels of TSH and T3 in patients receiving levothyroxine monotherapy and the insufficient symptomatic response experienced by an appreciable proportion of patients with hypothyroidism.

Even in the rat studies of T4 therapy vs. T3-T4 combination therapy, the monotherapy was incapable of achieving normal T3 at a normal TSH,

the dose of levothyroxine required to normalize serum concentrations of TSH is lower than the dose that normalizes serum levels of T3.

Therefore, TSH can be suppressed by a higher dose that is necessary to normalize bloodstream levels of T3, and the suppression of TSH can be a side effect of effective thyroid therapy.

As for your belief that two patient requests in particular “could potentially cause patient harm (e.g., maintaining TSH below reference range and adjusting thyroid hormone dose to symptoms or to serum T3 levels),” all you have to do to see lack of patient harm from lowering TSH, dosing to symptoms and FT3 is to read some recent articles by Larisch et al, 2018; Hoermann et al, 2019; and Ito et al, 2012 – 2019.

You are clearly oblivious to the individual variation in human response to LT4 monotherapy (Midgley et al, 2015). You either don’t test or don’t have the skill or knowledge to interpret FT3 levels, because you don’t yet realize that some thyroidless people require TSH-suppressive doses to achieve normalized FT3, while others will become thyrotoxic with an elevated T3 if they suppress the TSH too far (Larisch et al, 2018). Still others can’t raise their FT3 high enough no matter how low their TSH falls, and if they remain symptomatic, they would likely benefit from some other form of therapy.

As for your many citations on the dangers of overtreatment causing atrial fibrillation, osteoporosis, and multiple horrible causes of death that you use to fearmonger, it is too easy to point out again what I’ve just said above. Some people with a suppressed TSH can still be hypothyroid if they have a FT3 below reference, or euthyroid if their FT3 is not elevated, so claiming a person is thyrotoxic based on TSH alone is erroneous dogma within thyroid therapy.

Don’t you know that even outside of thyroid therapy the core definition of thyrotoxicosis is not dependent on TSH at all, and for good reasons?

You prove that you don’t understand enough about thyroid hormone metabolism and signalling within diverse forms of thyroid therapy. By saying that it could be harmful to dose to T3 levels or symptoms, you are implying that you can judge someone to be thyrotoxic from overtreatment based on an elevated FT3 and suppressed TSH without looking at their concurrent FT4. It would be utterly false to jump to this conclusion if their FT3 is elevated but FT4 is concurrently low or completely absent from blood, since FT3 must rise about twofold to compensate metabolically for absent FT4. (Busnardo et al, 1983)

Overall, you use scientific citations like bullets in a drive-by shooting to blame patients and shame doctors for “harm.”

Your bullets are as ineffectual as styrofoam pellets if you don’t read or understand what you cite. You show what you don’t know.

I advise you to read more widely in your own thyroid science literature before assuming that all published research supports the narrow restrictions and fearmongering found in your sacred ATA guidelines.

  • Tania S. Smith


Links to all 3 parts of my rebuttal:

  1. 2019 ATA article engages in patient-blaming and doctor-shaming
  2. Thyroid patient blaming and shaming, part 2: True barriers
  3. Thyroid patient blaming & shaming, part 3: Advocacy and Science


Bianco, A. C., Dumitrescu, A., Gereben, B., Ribeiro, M. O., Fonseca, T. L., Fernandes, G. W., & Bocco, B. M. L. C. (2019). Paradigms of Dynamic Control of Thyroid Hormone Signaling. Endocrine Reviews, 40(4), 1000–1047.

Esfandiari, N. H., Reyes-Gastelum, D., Hawley, S. T., Haymart, M. R., & Papaleontiou, M. (2019). Patient Requests for Tests and Treatments Impact Physician Management of Hypothyroidism. Thyroid: Official Journal of the American Thyroid Association, 29(11), 1536–1544.

Garber, J. R., Cobin, R. H., Gharib, H., Hennessey, J. V., Klein, I. L., Mechanick, J. I., … Woeber, K. A. (2012). Clinical practice guidelines for hypothyroidism in adults: Cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocrine Practice, 18(6), 988–1028.

Gereben, B., McAninch, E. A., Ribeiro, M. O., & Bianco, A. C. (2015). Scope and limitations of iodothyronine deiodinases in hypothyroidism. Nature Reviews. Endocrinology, 11(11), 642–652.

Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2019). Individualised requirements for optimum treatment of hypothyroidism: Complex needs, limited options. Drugs in Context, 8, 212597.

Ito, M., Miyauchi, A., Hisakado, M., Yoshioka, W., Kudo, T., Nishihara, E., … Nakamura, H. (2019). Thyroid function related symptoms during levothyroxine monotherapy in athyreotic patients. Endocrine Journal.

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.

Jonklaas, J., Tefera, E., & Shara, N. (2018). Physician Choice of Hypothyroidism Therapy: Influence of Patient Characteristics. Thyroid, 28(11), 1416–1424.

Jonklaas, J., Tefera, E., & Shara, N. (2019a). Prescribing Therapy for Hypothyroidism: Influence of Physician Characteristics. Thyroid: Official Journal of the American Thyroid Association, 29(1), 44–52.

Jonklaas, J., Tefera, E., & Shara, N. (2019b). Short-Term Time Trends in Prescribing Therapy for Hypothyroidism: Results of a Survey of American Thyroid Association Members. Frontiers in Endocrinology, 10, 31.

Larisch, R., Midgley, J. E. M., Dietrich, J. W., & Hoermann, R. (2018). Symptomatic Relief is Related to Serum Free Triiodothyronine Concentrations during Follow-up in Levothyroxine-Treated Patients with Differentiated Thyroid Cancer. Experimental and Clinical Endocrinology & Diabetes: Official Journal, German Society of Endocrinology [and] German Diabetes Association, 126(9), 546–552.

Midgley, J. E. M., Larisch, R., Dietrich, J. W., & Hoermann, R. (2015). Variation in the biochemical response to l-thyroxine therapy and relationship with peripheral thyroid hormone conversion efficiency. Endocrine Connections, 4(4), 196–205.

Categories: American Thyroid Association, Doctors, Endocrinologists / CSEM, Research Reviews, T4-monotherapy, Therapy guidelines, Therapy paradigms, Thyroid pharma

4 replies


  1. Thyroid patient blaming and shaming, part 2: True barriers – Thyroid Patients Canada
  2. 2019 ATA article engages in patient-blaming and doctor-shaming – Thyroid Patients Canada
  3. What if some thyroid endocrinologists are like programmers? – Thyroid Patients Canada
  4. The myths that idolize TSH and denigrate FT3 – Thyroid Patients Canada

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