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. Apparently patients are erecting barriers to their own therapy when they refuse to believe it when the TSH alone declares them biochemically euthyroid.

A good sign: Thyroid patient self-advocacy

Dear Esfandiari and colleagues,

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. You prove that we’re making some headway in the right direction by showing physicians the power of reason, evidence and compassion over the dogma of the 2014 ATA guidelines (Jonklaas et al, 2014):

  • 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 alas, I know why we could not have done this long ago.

Ineffective thyroid therapy leads to brain fog and fatigue, which makes it hard to self-educate and self-advocate. 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.

Now we have social media platforms like Facebook that have enabled patients to share their lab results, symptoms, articles, and tips with each other. We have created a “para-clinical” space where we can talk about our FT3 and FT4 levels in a way that we can’t talk about them with our ignorant physicians. We know those hormone levels correlate with our symptoms more than our TSH concentrations do. That para-clinical peer support has made it easier for us to build the supportive community we often lack. We can now see that our problems with the TSH-obsessed, T3-blind 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.

A long-awaited paradigm shift has been happening within thyroid science: It’s 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 that makes a positive difference for our therapy.

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 tradition and prejudice rather than evidence and science.

Your inevitable backlash against patients

Our self-advocacy isn’t going over well with some of you.

You, dear Esfandiari and colleagues, are noticing the trend of increasing patient requests as we become more educated in thyroid science and thyroid therapy.

We’re inspiring the inevitable resistance from those of you who strongly adhere to a rigid, outdated and narrow TSH-obsessed paradigm.

We’re a source of workplace stress for doctors like you who are used to more patient compliance when treating other medical conditions.

It would not be so stressful to “manage” us if the simplistic TSH target actually made physiological sense.

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 your own patients. First you lash out in the privacy of your office where nobody can witness your hateful behavior except the victim. Next, if you receive encouragement from peers at the water cooler when you roll your eyes at your naive thyroid patients, you then feel safe to take your anger into the public forum.

You are now doing everything you can to diminish your patients’ experiential knowledge, scientific insight, rational intelligence and self-defensive motives so that you can boost and defend your own professional status.

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.

In the leaves of a scientific journal, this attack was veiled in scientific garb. You can now add a loathsome diatribe against your suffering patients to your academic curriculum vitae.

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 your medical indoctrination. You think they should swallow it just as willingly as you have.

We are not uninformed people. We understand the basic TSH-based definitions of euthyroidism, hypothyroidism and hyperthyroidism. We know why they apply outside of therapy, when people are being screened for a thyroid disease.

We are not gullible people who think that TSH-centric definitions of untreated naturally-achieved euthyroidism still apply in the context of thyroid therapy.

Treating a disease is not as simple as adjusting a single hormone to pass a screening test.

Are you reading thyroid science carefully?

You can’t see the scientific basis of our requests because you haven’t been keeping up with your own science.

You’re not reading the thyroid science articles we are reading, such as articles by your own ATA president 2015-2016, Antonio Bianco, and his coauthors, which reveal the complexity of thyroid hormone metabolism and signaling beyond the pituitary (Bianco et al, 2019).

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.

You should be ashamed of yourselves.

Thyroid patients who know the science can tell when you cite articles you don’t read past the title and a glimpse at the abstract.

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 give the citation you used.

Levothyroxine monotherapy maintains an adequate level of serum T4, and the iodothyronine deiodinases provide physiologic regulation of T3 availability.(Gereben et al, 2015)

You reason that a normal TSH clearly proves that their levothyroxine (LT4) medication is working because levothyroxine monotherapy maintains an adequate level of serum T4, and the iodothyronine deiodinases provide physiologic regulation of T3 availability.

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.”

(Gereben et al, 2015)

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.

(Gereben et al, 2015)

Even in the 1990s rat studies of LT4 therapy vs. T3-T4 combination therapy, TSH-normalized LT4 monotherapy was incapable of achieving normal T3:

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

(Gereben et al, 2015)

Therefore, in those rats, a lower TSH can be a side effect of effective thyroid therapy. We allow this in rats, but not in humans.

It should be embarrassing when a cited article directly contradicts the statements you think you’re making by wielding it.

These things should be caught during the peer-review process in the journal, so it reflects badly on your journal editors as well.

Where does harm really exist?

Esfandiari and colleagues, you believe that two patient requests in particular are noxious. You think that these requests

could potentially cause patient harm (e.g., maintaining TSH below reference range and adjusting thyroid hormone dose to symptoms or to serum T3 levels).”

(Esfandiari et al, 2019)

But all you have to do to see lack of patient harm from lowering TSH to relieve thyroid symptoms is to read some recent articles by Larisch et al, 2018; Hoermann et al, 2019; and Ito et al, 2012 – 2019.

You, Esfandiari and colleagues, are clearly oblivious to the individual variation in human response to LT4 monotherapy that is revealed in FT3:FT4 ratios (Midgley et al, 2015).

Odds ratios for risk below the TSH reference range have not divided patients into cohorts by their FT3:FT4 ratios but have presumed the TSH reference cutoff is physiologically significant, using it to define a statistical cohort.

They represent the efforts of scientists to reaffirm treatment guidelines — to make the abnormal TSH level appear to be the primary indicator of risk. Physicians soon forget that these statistics do not represent the risk of every patient in a TSH category, but rather the average between those who are truly thyrotoxic and those who are truly euthyroid with a low TSH.

Patient diversity means that some hypothyroid patients require TSH-lowering or even 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 within reference range to relieve symptoms. This FT3 level becomes their “glass ceiling” that they’re not permitted to rise above due to the nature of their LT4 monotherapy.

Somehow, certain physicians can’t fathom that the benefit from T3-inclusive thyroid therapy is that it gives access to the widest range of FT3 and FT4 values and ratios. Somewhere in that wide range one is bound to find levels and ratios that are the most conducive to health.

The safest hormone levels are those that suit the disabled individual’s body, rather than conform to a statistical normality defined by a huge healthy-thyroid population.

Fearing low TSH more than inadequate FT3

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 in some tissues if they have a FT3 below reference, so claiming a person is thyrotoxic based on a low TSH alone is erroneous dogma.

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

You are imagining, against the teachings of thyroid science, that a TSH concentration in blood is a proxy for T3 hormone signaling in tissues all over the human body.

No, the TSH hormone is neither infallible nor omniscient during thyroid therapy. You prefer to think it is, because you misuse TSH to validate your dogma and your medical decisions. You also use a normalized TSH to dismiss patient symptoms to defend your feeling of professional accomplishment.

Just because TSH secretion responds so easily to your LT4 prescription, you presume that you have successfully normalized T3 signaling in the patient’s brain, liver, or heart. You prefer to believe this pleasant fiction that the deiodinases are serving enough T3 to these organs. But you can’t measure that directly. You take it on faith.

You are medically interfering with the broken feed-forward loop of TSH stimulation of a thyroid gland, and yet you think that TSH’s voice is speaking freely when you force it to say “good job, Dr. Esfandiari, you’ve normalized me, and I’ll do the rest for you”?

Of course the pituitary can’t sense that. When drugged by levothyroxine, pituitary TSH focuses mainly on the T3 it converts locally from higher-than-average FT4 levels, and to a much lesser extent the circulating FT3:

FT3 levels were significantly lower in L-T4-treated vs untreated nonhypothyroid autoimmune thyroiditis (median 4·6 vs 4·9 pm, P < 0·001), despite lower TSH (1·49 vs 2·93 mU/l, P < 0·001) and higher FT4 levels (16·8 vs 13·8 pm, P < 0·001) in the treated group.”

(Hoermann et al, 2014)

Why would you think pituitary cells can sense the patient’s FT3:FT4 ratio in blood and see how low the FT3 level is, when TSH lowers significantly at the command of higher FT4 alone, while ignoring the lower FT3?

The TSH is a localized tissue response. You can see in data provided by Hoermann et al, that TSH is relatively apathetic to the circulating FT3 level that may be low in reference range. Hoermann and team found that

“In LT4-treated patients, FT4 and FT3 contributed on average 52% versus 38%, and by interaction 10% towards TSH suppression.”

(Hoermann et al, 2017)

Their analysis only considered relative contributions of FT3, FT4, excluding other influential factors like TRH, leptin, ghrelin, and so on.

The hypothalamus and pituitary can’t sense the degree to which insufficient FT3 is harming other organs that depend on T3 to contribute to their nuclear receptors.

A normal TSH of 1.5 mIU/L would never prescribe a hormone dose ratio of 1:0 T4 to T3 that you are providing to your patient. Do you think you succeed by tricking the pituitary?

You misuse scientific citations like bullets in a drive-by shooting to blame patients and shame doctors for “harm” from T3 dosing that has never been demonstrated, only insinuated.

You attack your patients’ integrity, embodied knowledge and intelligence in the name of protecting them from harm.

Your bullets are as ineffectual as styrofoam pellets in a child’s toy gun if you don’t read or understand what you cite.

I advise you to read more widely in your own thyroid science literature before assuming that all published research supports the narrow restrictions you place on thyroid therapy.

  • 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


Click to view reference list

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., Dietrich, J. W., & Larisch, R. (2017). Dual control of pituitary thyroid stimulating hormone secretion by thyroxine and triiodothyronine in athyreotic patients. Therapeutic Advances in Endocrinology and Metabolism, 8(6), 83–95.

Hoermann, R., Midgley, J. E. M., Giacobino, A., Eckl, W. A., Wahl, H. G., Dietrich, J. W., & Larisch, R. (2014). Homeostatic equilibria between free thyroid hormones and pituitary thyrotropin are modulated by various influences including age, body mass index and treatment. Clinical Endocrinology, 81(6), 907–915.

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.

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