Caution: Doctors perform T3-ectomies without our consent

We all know a “thyroidectomy” is the surgical removal of a thyroid gland. Nobody removes a vital gland without a patient’s informed consent. If your medical system and doctor are ethical, you as a patient have the opportunity to weigh the risks and benefits of the procedure and give signed consent.

We need to consider requiring doctors to get our consent for a “T3-ectomy.”

What’s a T3-ectomy?

In metabolically vulnerable human beings, the standard “TSH-normalized T4 monotherapy” programme causes the removal of a significant portion of vital circulating T3 hormone supply from a person’s bloodstream. 

The idea of a T3-ectomy without consent points out that this T3 removal is a medically-authorized crime.

The crime is nothing less than the surreptitious theft of a significant portion of circulating T3, induced by forcing standard thyroid therapy on a body that can’t adapt to it. Standard thyroid therapy is usually forced upon us without information about its risks and often with no knowledge or offer of any alternatives.

The words are appropriately pointed language for the health crisis that can result from medication-induced T3 loss.

It’s a distressing experience to undergo T3 thyroid hormone depletion and subsequent illness within the context of standard thyroid therapy.  It’s an experience of unnecessary medical torture, utter helplessness, and dismissal of genuine health risk.

Currently the mere idea of a thyroid patient’s low(er) Free T3 elicits in most doctors a reaction of a mere shrug and an eyeroll, and a follow up question of “But look at your TSH.” — Exactly the response of an endocrinologist I saw.

The response reveals a naive belief that TSH gives the truest assessment of the body’s T3 supply in thyroid therapy. No, it can’t. Our HPT axis is unplugged by thyroid disease and therapy.  Hoermann et al’s 2016 graph shows we’re not at all like normal people in our TSH-T3 relationship.

Patients’ expression of righteous anger and pain play a key role in pointing out the cruelty of the theft. That’s what I have the right, the honor, and the duty to do here.

In this post, I’ll briefly describe the proof of harm of chronic low(ered) Free T3 levels.

I’ll talk about what it’s like to have a T3-ectomy, giving my own harrowing tale.

I’ll briefly discuss the paradigm shift in thyroid science that sees T3 loss as harmful — It shows there’s hope for change.

I’ll analyze the excuses people make for their medically-authorized T3 theft.

Then I’ll offer some potential solutions.

Recent research on T3 loss and harm in standard therapy

Two components in standard therapy cause T3 loss that can contribute to symptoms and illness. They work hand in hand:

1. The mode of therapy (T4 monotherapy) and
2. The mode of monitoring the therapy (TSH alone)

It’s quite logical, actually. When using a T3-blind TSH monotesting strategy to monitor, therapy is more likely to fail to achieve true T3-based euthyroidism, especially when you’re not replacing any T3.

Two pieces of recent research prove that the therapy mode and the lower Free T3 is associated with health risks. The second piece of research focuses more on the TSH versus FT3 monitoring policy in light of symptom scores.

First, in a study of diverse 469 patients on LT4 therapy participating in a US health survey 2001-2012, Peterson et al (2016) measured 52 clinical parameters and compared them with thousands of non-treated people in the same database.

What did they find?

• Participants using LT4 had higher serum total and free T4 and lower serum total and free T3 than healthy or matched controls. This translated to approximately 15–20% lower serum T3:T4 ratios in LT4 treatment, as has been shown in other cohorts.
• In comparison to matched controls, LT4-treated participants had higher body mass index despite report of consuming fewer calories/day/kg;
• were more likely to be taking beta-blockers,
  • statins, and
  • antidepressants;
• and reported lower total metabolic equivalents [less physical activity].
• A serum TSH level below the mean in LT4-treated participants was associated with a higher serum free T4 but similar free and total T3;
  • yet those with lower serum TSH levels exhibited higher serum high-density lipoprotein and lower serum low-density lipoprotein, triglycerides, and C-reactive protein.
• Age was negatively associated with serum free T3: free T4 ratio in all participants;
• caloric intake was positively associated [with FT3:FT4 ratio] in LT4-treated individuals.

CONCLUSIONS:: In a large population study, participants using LT4 exhibited lower serum T3:T4 ratios and differed in 12/52 objective and subjective measures.

Next study:

In 2019, Ito et al studied thyroidless patients and measured their hormones before and after thyroidectomy to see who returned to their former Free T3 levels and who experienced symptoms of hypothyroidism or thyrotoxicosis. They found this:

• “A mildly TSH-suppressive treatment (approximately 0.1 mU/L LT4) may not necessarily cause thyrotoxicosis. Rather, it may result in euthyroid status in patients who have undergone a total thyroidectomy for DTC [Differentiated Thyroid Cancer].”
• “On the other hand, in each case with mild TSH suppression, there were some who had an increase or decrease in FT3 levels and some who had drastic scale changes in their symptoms.”
• “In each case, it is considered necessary to adjust the LT4 dose comprehensively using not only serum TSH levels but also serum thyroid hormone levels [Free T3 and Free T4], physical symptoms, and metabolic markers.”

Research is showing that LT4 monotherapy is not working very well for many people’s Free T3 levels, symptoms and health, and it’s partly because TSH normalization is a misleading target in thyroid therapy.

Ito’s study shows that Free T3 response, even at low TSH, is highly variable among individuals, so you can’t predict how well someone will convert T4 to T3, and you definitely can’t judge them as thyrotoxic based on TSH.

Ito and team have been bold enough to suggest a radical policy change. Because of patients’ variable metabolic response to dosing at any level, you have to adjust therapy looking at Free T3 and Free T4 AND symptoms AND other metabolic markers, not just TSH.

Only this kind of change can help patients maintain the Free T3 levels that are right for their body.

Why have endocrinologists implemented a T3-blind testing system on a generally T3-depleting therapeutic system? It’s a recipe for disaster for some patients. 

What it’s like to have a T3-ectomy

The health effects of a T3 deficit can occur on different time scales. It can happen fairly suddenly after therapy, gradually over years, or you may have a health crisis that is delayed after years of low T3

• Sudden: Adverse health outcomes may occur within 1 year after thyroidectomy for thyroid cancer or multinodular goiter, or after radioiodine therapy for Graves disease.
• Gradual: In some with Hashimoto’s thyroiditis, suffering may gradually sneak up on them over the years as progressive thyroid function loss renders their T3 deficit deeper and deeper.
• Delayed: Most of the adverse health outcomes occur years after therapy commences, years after chronic Low T3 begins. When illness finally hits, it quickly worsens.

I am the third type of patient.

My T3-ectomy tale

I obtained records of 3 years thyroid lab results when I fell ill. They revealed I had had a T3-ectomy of significant proportions, occurring sometime around 2012, when I first began asking for T3 testing.

Lab tests revealed a pattern of a Free T4 near top of reference range and a Free T3 and/or Total T3 that was chronically just below reference range at 3.4 pmol/L (ref 3.5-6.5).

The Low T3 pattern was consistent over 9 lab tests in 3 years. My Free T4 fluctuated slightly with mild dose changes, but my Free T3 remained frozen, unable to rise.

Strangely enough, since 2012 my health was stronger than it had ever been in the past 15 years. I had made significant adjustment to my diet to adapt to my metabolic and autoimmune conditions, and I had experienced renewed vitality. My autoimmune arthritis and iritis were in full remission.

Clearly, my chronic T3 deficit was not caused by illness, as it is in standard “Low T3 Syndrome” or “nonthyrodial illness syndrome” (NTIS). I was not (yet) ill enough to trigger T3 depletion, and yet I had an extreme and continual T3 deficit.

Therefore, there was only one cause.

My T3-ectomy was caused by a thyroid therapy modality that worsened the impact of my unique undiagnosed thyroid disabilities, both autoimmune and genetic.

My health crisis was the delayed, inevitable effect of my T3 deficit.

I was 46 years old when the effects of my silent T3-ectomy hit, 13 years after my Synthroid monotherapy began. I was still young and healthy enough for my body to have overcompensated for this T3 loss for several years or more. I now understand that many bodily systems can become weakened from the stress of continually compensating for a significant T3 deficit. My body became more fragile than I realized. 

Then my vulnerable state revealed itself in a progressive collapse of health.  A mild, unfamiliar illness struck, then another more debilitating illness began. As I and my doctors tried to treat the first two conditions and my increasing hypothyroid symptoms, a third form of illness struck. So it continued, as illness and new symptoms layered on worsening illness and worsening symptoms over weeks.

I had room within reference ranges to increase thyroid dose, which my doctors did to address my fatigue, brain fog, vertigo and balance problems when walking. It made things much worse within 48 hours, triggering unstable angina-like symptoms in my chest. I returned to the former dose, but the adverse vascular effects of the dose increase remained to haunt me for the next three months.

My T3 levels fell further due to increasing illness. T4 dose reductions gave about 10 days of mild relief from cardiovascular distress, but symptoms returned, and of course I was rendered more hypothyroid. But symptoms increased with a vengeance when I subsequently tried climbing back slowly toward my original pre-illness dose.

Eventually I was greatly disabled, in painful distress, symptomatically and biochemically very hypothyroid. I could hardly function normally in daily life. I had to endure day and night frequent body-jolting cardiovascular distress that drove me to Emergency three times in three months. I was sent to many specialists and had many costly tests paid for by the health care system, and some paid for by myself.

Nobody in my local medical system was capable of correctly diagnosing or resolving my shockingly sudden health crisis — despite the huge T3-shaped hole in the middle of my test results.  I also had an extremely unruly TSH nobody could explain, concurrent with high-normal Free T4.  (This paradox is a sign of my unique genetic profile, a likely SBP2 deficiency causing a core defect in all my deiodinases — see Dumitrescu et al, 2010 — or fluctuating TSHR blocking antibodies). But they just didn’t get it: no matter what my TSH was doing flying above range so crazily, it was not causing my hypothyroidism, the low T3 was.

I was clearly healthy on paper, other than these huge thyroid anomalies. However, I had the expected high total cholesterol, low heart rate, mixed plaque in carotid artery bulb, and borderline liver results that can go hand in hand with chronic low T3 from thyroid therapy failure. Nobody thought to do a test of endothelial dysfunction that could have caused microvascular angina.

I started to research my T3 deficit and its possible effects by reading scientific literature, starting with my known health conditions. I brought my questions and even some medical research articles with me to doctors and the hospital and tried to discuss them, with responses ranging from mild curiosity (to humor me) to the insulting statement that anyone can find their symptoms on Google.

I had many demeaning exchanges with medical people, including a clueless and arrogant young endocrinologist who wrongly assumed I was noncompliant with my thyroid therapy because both my Free T4 and TSH were often high at the same time. She foolishly boasted that she could control my TSH using T4, as if that’s not what my doctors had been trying to do for years while nobody had an eye on my dismal T3 levels.

My story ended well. I found a doctor willing to start me on T3 therapy, and eventually T3 monotherapy solved the problem. I tried going back to T4 therapy slowly, but it failed, bringing back the same distressing cardiovascular symptoms by the half-way point in the transition, so I returned to T3 alone, and back to health and safety.

Oh, the continual refusal to acknowledge my chronic Low T3 despite high-normal T4,  the unnecessary focus on an obviously errant TSH, and the condescending, dismissive way I was treated by medical people who listened more respectfully to my husband when I brought him with me — what ignorance and rudeness.

It doesn’t matter if you are a mature research professor with a rational mind. Once you’re a suffering thyroid patient in an emergency ward or doctor’s office, you are seen as just a TSH number with hypochondriac hysteria and imaginary symptoms you must be inventing as you read about your illness online. The memory of it still frustrates and aggravates me, and it motivates me to try to stop this cruel nightmare for other patients.

Few patients are as capable as I was of researching my own T3 loss, despite brain fog, and before my progressive illness completely incapacitated me.  I realized that if I was so necessary to (and eventually successful in) resolving my own T3 deficit despite such thyroid therapy ignorance in the medical system, I might just be one of the few people who can help others by learning and mediating thyroid science while agitating for therapy change. 

Paradigm shift: New science sees FT3 loss as harmful

The agent responsible for the T3-ectomy is not just a gullible and callous doctor, not just an individual, but a powerful group of endocrinologists that maintain a faulty medical paradigm:

The TSH-T4 paradigm of thyroid therapy.

This paradigm was not always dominant in thyroid therapy, but it came into dominance gradually through the 1970s and 1990s before we fully understood thyroid hormone conversion.

Recently we’ve been hearing increasing calls from scientists to shift the “paradigm” toward defending T3 levels in bloodstream. These calls for change are being made by leading thyroidologists with a long history of research in the field (Abdalla & Bianco, 2014; Bianco et al, 2019; Hoermann et al, 2013-2019; Midgley, 2019; Wiersinga, 2014)

Since 2014, one of our leading American Thyroid Association endocrinologist researchers, Antonio Bianco, has been trying to tell all his colleagues that the HPT axis and thyroid metabolism (the deiodinase system) have one aim and goal —

“The hypothalamus–pituitary–thyroid axis is wired to preserve serum T3.“

“the level of serum T3 is a main target around which serum T4 and TSH are adjusted”

(Abdalla & Bianco, 2014)

This message should echo in the minds of those who still think the ultimate goal of thyroid therapy is the defense of normalized TSH.

Only humans put TSH in that unphysiological position. The goal should still be T3.

Other endocrinologists agree heartily with Bianco’s point, proving it from the angle of clinical research studies on treated thyroid patients. (Ito et al, multiple years; Hoermann et al, multiple years)

The T3 paradigm is gradually proving how backwards and upside down the TSH-T4 paradigm is.

• See Infographic: T3 paradigm vs. TSH paradigm
• See Thyroid therapy paradigm shift: T3 hormone testing is a battleground.

In 2019, Bianco and many leading colleagues published a lengthy and comprehensive review on thyroid hormone transport, conversion, and signalling in cells.

They have made a very strong point that circulating T3 levels are foundational to tissue euthyroid status. We learn from his publication, and others, that

• Local variable T4-T3 conversion rates cannot compensate for the loss of too much circulating FT3. (Bianco et al, 2019)
• A healthy FT3 level is protected by a fully healthy thyroid gland that can secrete and convert hormone to raise our FT3 when it falls low. (Abdalla & Bianco, 2014; Bianco et al, 2019; Ito et al, multiple years; Hoermann et al, multiple years)

We have less or no thyroid gland tissue to protect our FT3, so it’s vulnerable to loss.

In thyroid therapy, our hormones are not regulated by the TSH to the degree that we don’t depend on thyroid tissue for our hormone. Instead, we are regulated by dosing and deiodinases.

The three deiodinases are powerful thyroid-hormone converting enzymes that rule over and regulate the success and failure of any form of thyroid therapy.

Euthyroidism is all about getting T3 into cell nuclei and binding a healthy percentage of receptors for a good duration of time with cofactors to support signaling.

Much of the T3 that is formed in cells is recycled into the bloodstream to enter other cells and do it all over again.

Therefore, our Free T3, in light of Free T4, is actually the closest indicator we have of the global activity of T4-T3 conversion in cells, in dynamic response to our dosing and any thyroidal secretion we might supply.

If the system is “wired to preserve serum T3” as Abdalla and Bianco say, the Low-T3 patient is clearly someone whose wiring is not working.

Who has the moral courage restore the T3 she has lost?  Shouldn’t a thyroid endocrinologist also be wired to support health by preserving our T3?

Listen to the excuses of T3 thieves!

Like an accused thief, the TSH-T4 paradigm endocrinologist’s rationale is

“we’re taking away ONLY 20% of your T3 supply on average by not resupplying to you what the average thyroid would secrete.”

Jaw-drop.

Why should we be left with ANY deficit if it is in your power to refund it?

This is our most vital and essential thyroid hormone, and you dare to justify its theft, loss or depletion by niggling over a statistical average of a percentage you refuse to give us?

ONLY 20% ?

In corporate theft, should a thief not to go to jail for stealing even 10% from his company’s operating budget?

Have you accounted for the further losses that your initial theft can trigger in some vulnerable people?

Let’s say we have 80% of our normal healthy T3 supply after a full thyroid loss and you refuse to grant us back our 20%.

What happens next?

It can get worse. Your favorite therapy can trigger a domino effect of imbalances.

In LT4 monotherapy, average Free T4 is significantly higher than it is in the average healthy person. So, what happens when dosing of T4 medication slows down our rate of conversion below normal due to the way D2 enzyme is progressively inactivated as FT4 rises in reference?  

After lowering our D2 conversion rate by raising T4, some of us may be left with 70% of our healthy FT3 or less, for all you know or care.  

Next, in LT4 monotherapy, Free T3 is significantly lower than it is in the average healthy person. Science teaches that D1 conversion is upregulated by T3, and it converts less efficiently as FT3 lowers in reference range. What happens when the lower T3 supply downregulates D1 enzyme more severely ?

After lowering both our D2 and D1 by shifting our T3:T4 ratio in blood, some of us may be left with 60% of our necessary FT3, give or take, for all you know or care.

In all humans, D3 enzyme increases as we raise FT3 and/or FT4, and you’ve raised our FT4. We know D3’s role is to protect tissues from mildly elevated thyroid hormones, but it doesn’t pick and choose only the more abundant hormone, T4 to inactivate. D3 will not only progressively inactivate T4 by conversion to RT3, but will also inactivate our precious T3 by conversion to T2, even if T3 is already low. 

After you have initiated a full cascade of D2, D1, and D3 imbalances by only dosing us with the T4, let’s say some of us are left with only 50% of our healthy T3 supply, give or take, for all you know or care.  

Now what?

We are stuck with lower T3 without a paddle.

Now what happens when people don’t have enough thyroid tissue to resupply the T3 depleted by deiodinases?

We’re stuck in the deficit you have worsened and which you refuse save us from.

Chronic low FT3.

Now what happens when this person with 50% Free T3 develops a condition like heart failure, kidney failure, or liver cirrhosis?

Chronic illness depletes FT3 even further.

What happens if we have a heart attack or end up in a car accident that damages our vital organs?

Acute illness depletes FT3 even further and puts life at more risk. 

The real risk is the failure to restore enough T3 at the right time for recovery.

We know in 2019 that an already low Free T3 is a severe liability when entering critical illness.

Something important hasn’t yet dawned on the people recommending TRH-TSH stimulation as a therapy for nonthyroidal illness.  What if you have no thyroid gland tissue to stimulate with TSH to bring back some lost T3? 

Passing the buck to other doctors

Endocrinologists, you don’t want to admit that we’re far more vulnerable when our FT3 is lowered.

And moreover, you don’t care, because the blame will always be placed on the nonthyroidal illnesses that our low FT3 worsens, not on the endocrinologist T3-thief.

This system is entirely self-protective. We and other doctors bear the risk instead of you.

• If we’re well at the moment, our low T3 must not be a problem! (until we get sick).
• If we’re sick, the other -ologist, not you, will be responsible what T3 does to us.
• Our normalized TSH makes you immune to the health risk we bear from lower T3.

Nobody will tell the truth on our death certificate:

• “Died from Illness X after years of Lower T3 while on Thyroid Therapy.
• “During Illness X, her already Lower T3 fell lower and could not rise enough to help her recover.”

Admit this is the self-protective reason why you haven’t studied nonthyroidal illness in your chronically low-T3 thyroidless patients on LT4 until recently.

When people finally discover the degree to which your favorite thyroid therapy jeopardizes our recovery from a complicated and expensive coronary bypass surgery, our illness or death will come back to knock on your door, and you might be held to account, finally.

Stop being ethically noncompliant. Get consent.

You occasionally suggest that a T3 combination therapy trial could be attempted in a suffering TSH-normalized T4 patient if all the risks were explained to us up front!

Turn the tables on yourselves!

Why do you think only T3 combination therapy needs all the cautions and consent when your favorite medication already comes attached to so many health risks?

Nobody should have the moral or medical right to impose this potentially T3-depleting, illness-associated therapy without our consent and alternatives on the table.

It should no longer be a medically authorized crime, but simply a crime, to do nothing to monitor or fix an obvious T3 deficit during thyroid therapy.

TSH-normalized LT4 monotherapy carries risks we now understand much better than the risks of the combination therapies many still fear.

This standard therapy requires informed consent for its KNOWN risks, as well as the currently unknown risks that good researchers will discover next year. 

Endocrinologists’ collective behavior as a profession has divested them of their right to thyroid patients’ trust to defend their T3 levels. Such monopolizing behavior should have lost many ethical medical professionals’ trust long ago.

To earn back our trust,

• You must ask for our informed consent before you put us on a trial of your favorite therapy. You clearly can’t be trusted to institute such a consent system yourselves, so you will need to be forced by health ethics watchdogs or your more ethically-minded peers in other medical fields.
• You must give us a full list of all the health problems that could occur in various parts of our bodies as a result of us losing Free T3 during your favorite therapy.
• You must do all you can to minimize the incidence rate of low(er) Free T3 and T3:T4 ratio in any therapy modality by actually testing thyroid hormones in addition to TSH, since we are more vulnerable to T3 loss the less living thyroid tissue we have.
• You must listen to our symptoms as an indication of being close or far from optimal Free T3 even within the reference range, as Ito and team and Larisch and team’s research show that symptoms are clinically significant.
• You must put all competing T3 therapy options on the table no matter how much you personally dislike giving patients any freedom to choose a different pharmaceutical. This will help enhance mutual respect and cooperation.
• You must stop tyrannizing over the pharmaceutical marketplace by using guidelines to tell doctors what bioidentical thyroid hormones they must not prescribe to us. Nobody has ever proven T4 monotherapy’s intrinsic superiority over all other T3-based therapies or combinations thereof. Historically ingrained fear and hatred of the former gold standard therapy, desiccated thyroid, is an institutional blindness that renders many endocrinologists unable to exercise scientific objectivity about the true risk/benefit ratio when larger amounts of T3 are dosed to euthyroid levels.

Tania S. Smith

REFERENCES

Abdalla, S. M., & Bianco, A. C. (2014). Defending plasma T3 is a biological priority. Clinical Endocrinology, 81(5), 633–641. https://doi.org/10.1111/cen.12538

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. https://doi.org/10.1210/er.2018-00275

Dumitrescu, A. M., Di Cosmo, C., Liao, X.-H., Weiss, R. E., & Refetoff, S. (2010). The syndrome of inherited partial SBP2 deficiency in humans. Antioxidants & Redox Signaling, 12(7), 905–920. https://doi.org/10.1089/ars.2009.2892

Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2013). Is pituitary TSH an adequate measure of thyroid hormone-controlled homoeostasis during thyroxine treatment? European Journal of Endocrinology, 168(2), 271–280. https://doi.org/10.1530/EJE-12-0819

Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2016). Relational Stability in the Expression of Normality, Variation, and Control of Thyroid Function. Frontiers in Endocrinology, 7. https://doi.org/10.3389/fendo.2016.00142

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Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2019a). Functional and Symptomatic Individuality in the Response to Levothyroxine Treatment. Frontiers in Endocrinology, 10. https://doi.org/10.3389/fendo.2019.00664

Ito, M., Miyauchi, A., Hisakado, M., Yoshioka, W., Ide, A., Kudo, T., … Amino, N. (2017). Biochemical Markers Reflecting Thyroid Function in Athyreotic Patients on Levothyroxine Monotherapy. Thyroid, 27(4), 484–490. https://doi.org/10.1089/thy.2016.0426

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. https://doi.org/10.1507/endocrj.EJ19-0094

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. https://doi.org/10.1055/s-0043-125064

Midgley, J. E. M., Toft, A. D., Larisch, R., Dietrich, J. W., & Hoermann, R. (2019). Time for a reassessment of the treatment of hypothyroidism. BMC Endocrine Disorders, 19(1), 37. https://doi.org/10.1186/s12902-019-0365-4

Peterson, S. J., McAninch, E. A., & Bianco, A. C. (2016). Is a Normal TSH Synonymous With “Euthyroidism” in Levothyroxine Monotherapy? The Journal of Clinical Endocrinology & Metabolism, 101(12), 4964–4973. https://doi.org/10.1210/jc.2016-2660