Several fallacies in the TSH-T4 paradigm of thyroid therapy

Logical fallacies

When you are steeped in a medical paradigm, its fallacies can be as comfortable and taken for granted as an old pair of sneakers.

In this post, I’ll take apart several thyroid therapy fallacies, starting with the fallacy “description is not prescription.”

I will investigate many of the ways in which patients on T4 monotherapy are very different from the untreated healthy population.

There are too many aspects of inequity, illogic and apathy in standard hypothyroid therapy.

One of the most blatant inequities in this therapy is that normalizing TSH will forbid most T4-therapy patients’ access to the upper half of the Free T3 reference range.


The basic fault is allowing the descriptive data in health to become the guide for a thyroid hormone prescription’s dosing.

You shouldn’t do this without questioning what is different between the two populations.

If fundamental things have changed to a major degree, then applying the TSH of health to the TSH of thyroid therapy would be fallacious.

Many therapists believe that normalizing TSH will ensure both thyroid hormones will be in the range of health and therefore “adequate” for your body.

First of all, many don’t realize how much the TSH has become their medical slave.

In the context of thyroid therapy, the delicate HPT axis (hypothalamus-pituitary-thyroid axis) is subject to medical interference as well as the damage or loss of the crucial “T” (thyroid) that constitutes 1/3 of the HPT axis. TSH is no longer an unbiased _regulator_ of both T3 and T4 thyroid hormone supply to your entire body by means of the “feed-forward” function of thyroidal stimulation, nor is it an unbiased judge of hormone _supply_ to your entire body by means of the classic “feedback loop.” (Hoermann et al, 2013)

Let’s explore why that’s so.

In the state of therapy, thyroid hormone dosing controls the TSH like a driver controls a car. To the degree that TSH is no longer free to regulate living thyroid tissue but is rather the slave of dosing, this pituitary hormone no longer has free choice to rise and fall to adjust your metabolic rate up or down by shifting T4 and T3 supply to bloodstream. It is not an unbiased regulator or respondent to metabolic input like cold, illnesses, pregnancy, aging, exercise, diet or stress.


In thyroid health, as TSH freely rises or falls even within reference range, more TSH not only increases the quantity of T4 and T3 secreted by a thyroid gland, but also the ratio of T3 and T4 synthesized and secreted by it (Citterio et al, 2017).

TSH secretion rate also shifts the rate of T4 to T3 conversion that occurs as TSH-containing blood flows through thyroid gland tissues, which express both deiodinase type 1 and 2 (This process is called the “TSH-T3 shunt”; see Berberich et al, 2018; Dietrich et al, 2016).

In this way, the TSH and living thyroid tissue in a healthy, whole HPT axis partner to deliver a fine-tuned T3-T4 combination therapy that shifts T3 and T4 ratios and doses whenever your body requires them.


But in thyroid therapy, when TSH rises to request more thyroid hormone, it’s at the mercy of your doctor to fill that request.

In thyroid therapy, TSH might not rise high enough:

  • at the time of your blood draw (TSH is lowest in the afternoon), or
  • at a certain time of a female menstrual cycle (TSH is highest mid-cycle; Benvenga et al, 2017), or
  • at a certain time of year (TSH is higher in colder months; Gullo et al, 2017)

It has to be high enough to persuade your doctor to maintain or increase your dose for the entire year to come, despite these seasonal, monthly and daily fluctuations.

People who rely on a static dose of meds and less on the adaptibility of a real thyroid gland are more vulnerable to Free T3 and Free T4 levels not being enough when the internal or external environment requires it to shift.

In addition, during T4 monotherapy the TSH itself does not shift sensitively in response to FT3 levels, which can fall abnormally low. (Hoermann et al, 2013)

In T4 monotherapy, T4 hormone dominates the bloodstream, and the TSH is primarily driven by medical dosing — which drives the Free T4 level. (Werneck de Castro et al, 2015)

As artificial LT4 dosing and Free T4 rises in reference range during thyroid therapy, it rises significantly higher than the average for a healthy untreated person (Gullo et al, 2011).

Then a daily dose of T4 hormone makes sure Free T4 is relatively “pinned” at this unnaturally higher level. The FT4 does not have as much flexibility to adjust to a healthy level and meet the individual’s demands.

By this mechanism of FT4 increase, TSH is also driven down, and actually pinned down, by T4 dosing, so that TSH is unable to rise as freely to signal an isolated lower Free T3 in blood.


In T4 monotherapy, your Free T4 is largely controlled by your absorption of your levothyroxine pill, the rate to which it becomes bound or free in your blood.

After Free T4 and Free T3 both enter the hypothalamus and pituitary, the TSH is controlled by the rate at which the hypothalamus and pituitary convert Free T4 into T3 locally, adding to the amount of FT3 that they also take in from blood. What you get is a net T3 supply to cells in the hypothalamus and pituitary.

The rate of T4-T3 conversion in the hypothalamus and pituitary can be significantly higher than the rate at which Free T4 is converted to T3 elsewhere in the body due to differences in central D2 enzyme expression (Hoermann et al, 2013).

This difference between local “pituitary-hypothalamus conversion efficiency” and the “global T4-T3 conversion efficiency” visible in blood levels can become more extreme as Free T4 climbs higher in reference range. (This is because Deiodinase type 2 is less sensitive to ubiquitination by T4 hormone within the hypothalamus than elsewhere; Gereben et al, 2015.)

At what point does the T4-T3 conversion in the hypothalamus so greatly outpace the rate of tissue conversion elsewhere in your body, and even the global Free T3 and Free T4 supply in your blood, that TSH becomes utterly deceptive regarding the “T3 sufficiency” status of your vital organs?


“Low T3 syndrome” during severe illness is another situation, like T4 monotherapy, in which TSH does not rise as T3 in blood falls.

It’s unfortunate that this syndrome is also misnamed “non-thyroidal illness” and “euthyroid sick syndrome” because these labels can be very misleading about the thyroid hormone status of tissues in the body.

Current theories do not account for what happens differently in this syndrome when it affects people with severely disabled or missing thyroid glands who are on thyroid therapy.

In people with healthy thyroids, a large percentage of patients in intensive care in hospital settings will go into a state of slow metabolism. Their body achieves this slower metabolic rate by depleting the most powerful thyroid hormone, T3. Meanwhile, they exhibit a normal TSH that will not flag their significantly lower Free T3.

The human body depletes T3 hormone by inducing a deiodinase enzyme imbalance.

“De-iodin-ases” metabolize thyroid hormones by removing iodine atoms from them.

In severe illness, the body gives more power to Deiodinase Type 3 and weakens the other two Deiodinases Types 1 and 2, effectively diverting thyroid hormone away from the normal pathway. Paradoxically, TSH generally remains in the normal range, and it occasionally drops.

During Low T3 syndrome, T3 levels in some vital organs, like heart muscle, can even fall below the levels found in blood.

In general, the global supply of T3 hormone can fall so low and stay low for so long that Low T3 supply in blood, by itself, is a statistic that can put vulnerable, sick people at significantly higher risk of death or long term morbidity. (See Rhee et al, 2015 for concise tables of many studies.)

In a low T3 state, having extra T4 hormone in blood is not helpful. It can’t make up for FT3 loss in a state when the deiodinases actively work against normal T4-T3 conversion.

Having an elevated FT4 at the same time as a low FT3 can even increase the rates of death in low T3 syndrome, especially in certain types of illness (Ataoglu et al, 2018).

Although the early phases of low T3 may be protective by lowering metabolic rate, the later phases are dangerous and the outcome is uncertain.

The TSH does not always “wake up” from its unnaturally normal state soon enough to enable recovery. Without recovery of FT3 levels, a patient can die or remain ill.

A significant rise in TSH is necessary to support recovery by overstimulating living thyroid gland tissue to vigorously resupply T3 without flooding the body with too much T4.

People without living thyroid glands would be continually oversupplied with T4 throughout their critical illness. Many thyroid patients do not have the biological equipment to recover T3 at a rate regulated by a freely-fluctuating TSH secretion.

What most people don’t realize is that an unknown percentage of treated thyroid patients are kept in a low(er) T3 state continually, with an overexpression of Deiodinase Type 3 that keeps their T3 level from rising.

During nonthryoidal illness, LT4 monotherapy by itself is incapable of raising low T3 (Soscia and Baglioni, 2010).

Thyroid patients can’t pull themselves out of the thyroid biochemistry found in nonthyroidal illness, and their L-T4 therapy can’t help them either. 

The outcome of this syndrome is not studied at all in people who are most at risk of failing to recover due to the failure of the thyroid gland itself.

In addition, nobody is studying how chronic, milder degrees of “low T3 syndrome” weakens thyroid patients’ bodies and contributes to other chronic diseases over months, years, or decades.


In any individual patient, how can you be so sure that TSH response is not being distorted by 1) the biases inherent in the T3:T4 ratio of the medication, 2) the patient’s specific thyroid disease status and 3) thyroid hormone metabolism disorders that make T4-T3 conversion lower than normal throughout the body?

If you want to hear the body’s response to T4 meds, you should not just “listen” to the testimony of the TSH. You should also “listen” to the significant FT3:FT4 ratio distortions commonly known to be induced by thyroid therapy itself.

Let’s see what the science says about the distortions shown by thyroid hormone measurements for FT3 and FT4 at a normalized TSH.


In fact, significant distortions exist between the two populations at a given TSH level.

Essentially, in the treated state, TSH does not represent natural, unmedicated T3 and T4 status.

The treated thyroid disease population’s TSH of 1.0 is achieved at a very different FT4 level and FT3 level than a healthy population’s TSH of 1.0.

Also, T4 monotherapy establishes new interrelationships between T3 and T4 that are not seen in untreated people in thyroid health. When you look at the ratio between T3 and T4, it has significantly shifted and altered in the medicated state. (Gullo, et al 2011; 2017)

Thirdly, even the “slope” of the FT4:TSH relationship differs — despite the belief that this is constant in all humans. As T4 lowers in the treated population, TSH does not respond with as much vigor by rising. TSH responsiveness in one population appears to be more sensitive than the other. (Gullo, et al 2017)


Another shock is simply what happens to FT3 alone on T4-monotherapy within normalized TSH.

Within the entire normalized TSH range, the guideline writers admit that treated patients’ FT3 will likely be in the LOWER HALF of its reference or even lower, below its reference. (Garber et al, 2012)

In contrast, at a normalized TSH, healthy untreated patients have access to the FULL range of FT3 normal values. 

Essentially, T4-dominant medication enforces a state of FT3 inequity.

It installs a glass ceiling by limiting the amount of FT3 the treated patient’s body has access to whenever TSH is within the reference range.

While TSH is “in range” the hormone concentration of FT3, which must be lower under a T4-dominant therapy regime, can be significantly oppressed, and the degree of T3-T4 split varies widely from patient to patient in the context of T4 monotherapy (Midgley et al, 2015).

Recent studies confirm what the ATA guideline writers complacently admit: On T4 monotherapy while FT4 is significantly higher in range and TSH normalized, the body is rarely able to raise FT3 higher than mid range.

It takes a TSH lower than reference to see more patients’ FT3 achieve and exceed the average. (Larisch et al, 2018)

In fact, even at a completely suppressed TSH level, the T4-treated thyroidless person’s Free T3 levels can vary extremely widely (Larisch et al, 2018)


(Figure 2 from Larisch et al, 2018; reproduced within the terms of fair use copyright, for the purposes of review and critique)

This is a problem because some organs cannot convert T4 as efficiently within their tissues and require more FT3 directly from bloodstream.

How could one fail to see the T3 inequity, both at a single TSH level and across the whole TSH range?

There is clearly a stark difference between the two populations’ thyroid hormone supply at normalized TSH.

Therefore, it is unfair to judge these two populations by the same TSH range as if any TSH number means the same thing to thyroid hormone status in both patients.

At a given TSH, one population is healthy. The other could be unhealthy in terms of their lack of T3 thyroid hormone binding with receptors in tissues.

TSH is not a health outcome in thyroid therapy.

In therapy, TSH is of extremely doubtful value as a “surrogate clinical endpoint” as defined today by the standard guidelines for pharmaceutical trials.


If you really want to evaluate any thyroid therapy honestly, you must tie a health outcome to a variable in the therapy that is actually likely to cause it.

In therapy, a TSH is not in a position to “cause” thyroid gland secretion or regulate FT3 and FT4 levels, and so the TSH hormone does not have a direct cause-effect relationship with health outcomes.

TSH only has a general statistical association with health, and correlation is not causation.

In contrast, T3 supply is always essential to cells, and tissue T3 sufficiency alone defines whether any tissue is hypothyroid or hyperthyroid or in a healthy state.

Therefore, if you want to monitor a hormone that always regulates and “causes” health outcomes, both in therapy and beyond it, monitor the ability of the patient’s bloodstream to supply the entire body’s tissues with adequate T3 hormone.

That means that if you’re going to be fair to all tissues, one should consider not only TSH but also FT3 and FT4. These parameters will help you see

  • how much Free T3 is available to them in blood,

and to estimate

  • how much Free T4 is present AND likely to be converted to T3 within tissues given that patient’s global T4-T3 conversion rate found in blood (this can be assessed using free clinical research tools like SPINA-Thyr).


Some T4 will convert beyond bloodstream, but in health, daily T4 secretion averages approximately a 35% daily overall yield of T3 hormone, according to the kinetic studies of the 1970s through 1990s. (As old as this research is, it is the most up to date and recent study of its type — this research is still cited today.)

That’s just an average derived from Cavalieri et al, 1977.

Estimates also vary.


In Pilo et al’s study, 1990, the percentage of daily secreted T4 that converted to T3 peripherally was between 16.9% and 37.9%, averaging 27.3%.

What does this variable T4 conversion rate mean to a thyroid patient’s more active T3 thyroid hormone supply?

Because TSH is largely adjusting to the dominant FT4 in the T4-monotherapy model, TSH is calibrating to the hormone whose conversion rate to T3 within tissues cannot be predicted.

The data clearly show that T4-T3 conversion varies widely from person to person. Net T4 conversion to T3 is unpredictable, can be lower or higher even in “health,” and is generally limited to an average of 27% of the secreted T4 per day.

If T4-T3 conversion is reduced in the individual, the feedback to the thyroid gland of reduced FT3 in bloodstream will not sensitively adjust TSH, as explained above.

A more direct and accurate assessment of global thyroid hormone than TSH is Free T3 in the context of a given patient’s Free T4 level.

I challenge researchers to develop a clinical mathematical model that estimates this global T3 supply in blood. Take the Free T3 value and add to it an estimate of the T3 that would become converted from the FT4 supply every day. When estimating, realize that at a lower level of FT4 in serum, generally more of it converts to T3, and that you may need to measure Reverse T3 to understand where else the T4 is going when it’s not converting to T3. At a higher level of FT4 in serum, generally less of it converts to T3 (due to the ubiquitination of deiodinase type 2).


Are most thyroid therapy researchers interested in examining whether Free T3, either alone, or in ratio with Free T4, or in additive combination with Free T4, is a better surrogate endpoint for “health” than a normalized TSH?  No. 

Are most thyroid therapists and guideline writers concerned about optimizing our Free T3? No.

Instead, they institute a mid-reference limit on most thyroid patients’ Free T3 by making TSH-normalized L-T4 monotherapy the standard therapy. They even look with apathy on a FT3 that falls below reference.

Here’s proof of the institutionalized anti-T3 prejudice: The same therapy guidelines that admit to routinely suppressing and limiting thyroid patients’ Free T3 summarily discourage testing Free or Total T3 in hypothyroidism. (Garber et al, 2012)

They seem to be interested in normalizing and dismissing low T3 data.

In a paradigm and model of therapy that values the normalization of values within reference range, this apathy about a reference boundary ought to make anyone suspicious.

Why is FT3 being permitted to remain below the healthy mid-point of the FT3 referene range, and why is it permitted to fall below reference during therapy?

What are the long term health implications of a therapy that limits thyroid patients’ access to only the lower half of the range of FT3, or lower, given that we’re talking here about the most powerful, most essential thyroid hormone in human health?

No research has attempted to answer.

The silence attests to researchers’ apathy about the net T3 supply to tissues throughout the treated thyroid patient’s body.


The double standard is clear.

They play favorites with hormones. TSH is their favorite. FT3 is the ignored child.

Researchers ignore studying the potential health risks associated with thyroid patients’ significantly lower FT3 levels and below reference.

But they have been very enthusiastic about researching the health risks associated with TSH below reference!

Playing favorites, they do all they can to make the TSH reference range seem meaningful for health because it justifies the therapy model of TSH-normalization in millions. It keeps in place the obsession over the lower boundary of the TSH reference range.

The emphasis on low TSH risk has itself become an epidemic.

Is a low TSH by itself really dangerous if FT3 and FT4 are not both in the upper half of reference or higher? How do we know?

There is now so much research into the question low TSH and its suppression that it is commonly assumed that a low TSH independently “causes” increased health risk.

Just talking about it more, and researching it over and over, is enough to raise fear and emphasize the estimates of the risk.

However, the number of studies that try to assess risk never make low TSH risk an inevitable outcome. The TSH hormone’s role in causality at the molecular level is never accurately modeled and rarely addressed in regard to the thyroidless population. 

Even if you say, hypothetically, that 50% get a sick and 50% don’t when going below a given hormone’s reference, if you are a good researcher, you ought to be interested in explaining why 50% remained healthy.

Healthy results within the data should speak just as loudly regardless of the percentage and demand an effort at cause-effect explanation. 

Some people with suppressed TSH on thyroid therapy do NOT have osteoporosis or heart disease. That’s clear in the data.

What is protecting these people’s health at a low TSH? Why is no one asking that question?

Therefore, TSH alone cannot directly cause disease, or there would be higher rates of disease AND there would be an explanation for its function at a molecular level. 

The underlying presumption, of course, is that a low TSH means thyrotoxicosis. That is an assumption based on biased definitions of thyroid hormone syndromes according to TSH, rather than based on thyroid hormones themselves. 

We know that thyrotoxicosis, if you define it as net elevated thyroid hormone supply, can increase risk of another disease.

Can a low TSH coexist with a hypothyroid net hormone supply?

Yes, it certainly can! — in the sub-population on thyroid therapy whose FT3 is oppressed, not elevated, at the same TSH as the untreated person (Hoermann et al, 2016). 

In all persons with suppressed TSH, are their thyroid hormones always elevated to the same degree? No.

How many of these people with suppressed TSH also have elevated net T4 and T3 supply in blood at the same time? Not very many. See the figure by Larisch et al, 2018 above.

Look at the articles that supply detailed enough data and you will see wide individual variability between thyroidless people and untreated people, and added to this, wide individual variability among the treated thyroidless.

Studies that average these factors will hide variability and turn it into meaningless statistical mud.

Therefore, a low TSH alone does not determine the state of thyrotoxicosis.

Why aren’t people thinking clearly? Something else must be causing disease in some but not in others at the same TSH. Look at the FT3 in the context of FT4.


Do research studies of TSH and health risk measure both Free T3 and Free T4? In my experience of reading this research, in 99% of studies, the answer is no.

Do any of these risk studies consider both thyroid hormones together as a net supply to tissues? No. They considered them as if they were separate hormones, which is a fallacy, since thyroid hormone conversion is crucial.

Did any risk studies attempt to even estimate the net percentage of T4 conversion rate to T3 beyond tissues by assessing the ratio of the two main conversion products, Reverse T3 and T3 in these patients? No.

Therefore, does any risk study come close to assessing net thyroid hormone supply to tissues when associating disease risk with TSH instead? No.

The vast majority of risk studies, if not all, were incapable of accurately discerning the differences in thyroid hormone supply in one person with a suppressed TSH compared to another.


How do practitioners know they have achieved our health when they have induced our normalized TSH? … Because they have normalized our TSH!

This is a false circular argument, known as a tautology!

A tautology is a fallacy because it is true only because it is a restatement using other language.

It is circular to say “We know they are healthy with a normalized TSH because their TSH is kept within reference range like that of health people.”

Cheating on their own self-evaluation, they declare that medically manipulating TSH to the range of healthy people is the only valid criterion for evaluation because it is associated with health outcomes in an entirely different population of healthy people. 

Ignoring even the fact that TSH reduces FT3 in the treated people, which they readily admit, they still believe that a normalized TSH validates their choice of T4-monotherapy as the best and only therapy. (Garber et al, 2012; Jonklaas et al, 2014)

Therefore, the testimony of TSH during thyroid therapy is not a testimony of health or of T3 sufficiency throughout the body.

What does TSH tell you, then, in therapy?

In the context of T4 monotherapy, a normalized TSH is a strong testimony to the power of T4 medication to keep TSH secretion artificially normalized by significantly higher Free T4 levels than the normal average.

Thyroid therapy creates a situation in which TSH is blind to your T3 supply in blood and your T3 sufficiency in tissues throughout your body underneath. It hides under the TSH-T4 relationship.

Too many scientific studies of thyroid hormone effects on other parts of the body focus only on TSH and T4, or they treat T3 as if it were a separate hormone and independent variable from T4. They also routinely exclude treated thyroid patients from study. They have reached superficial conclusions about thyroid hormone’s influence on health on the basis of superficial, oversimplified data (TSH-T4 relationship data only) and flawed theoretical and mathematical modelling.


If you wish to investigate the scientific literature carefully, it will be easy to see that in the context of thyroid therapy, the bloodstream thyroid hormones have more power to induce disease or health than the TSH.

In the context of thyroid therapy, the TSH can often give inaccurate or unreliable information about the T3 sufficiency in tissues beyond the hypothalamus and pituitary.

Fear of low TSH and ignorance of FT3 supply is bred by incomplete and biased research methods, and fear drives a draconian, prejudicial policy. Guidelines say FT3 must not be tested in hypothyroid therapy unless TSH is low and therefore they fear FT3 will be high.

The policy is that our medical system decides to forbid a suppressed TSH and therefore measurement of thyroid hormones to all but a small subset of thyroid cancer patients.

Most patients on TSH-normalized T4 monotherapy are continually subjected to FT3-oppression. They are limited to the lower half of the FT3 reference range or lower for the rest of their lifetime. This is a glass ceiling.

Millions of people, mostly women over 40, who are hypothyroid but do not have permission to access FT3 and FT4 optimization, are being treated with health discrimination.

This anti-FT3 testing policy functions to cover up the many weaknesses of this fallacious and potentially harmful medical paradigm.

  • Tania S. Smith, Ph.D.


Click to reveal reference list

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Benvenga, S., Di Bari, F., Granese, R., & Antonelli, A. (2017). Serum Thyrotropin and Phase of the Menstrual Cycle. Frontiers in Endocrinology, 8.

Berberich, J., Dietrich, J. W., Hoermann, R., & Müller, M. A. (2018). Mathematical Modeling of the Pituitary–Thyroid Feedback Loop: Role of a TSH-T3-Shunt and Sensitivity Analysis. Frontiers in Endocrinology, 9.

Cavalieri, R. R., & Rapoport, B. (1977). Impaired peripheral conversion of thyroxine to triiodothyronine,. Annual Review of Medicine, 28, 57–65.

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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.

Gullo, D., Latina, A., Frasca, F., Le Moli, R., Pellegriti, G., & Vigneri, R. (2011). Levothyroxine Monotherapy Cannot Guarantee Euthyroidism in All Athyreotic Patients. PLoS ONE, 6(8).

Gullo, D., Latina, A., Frasca, F., Squatrito, S., Belfiore, A., & Vigneri, R. (2017). Seasonal variations in TSH serum levels in athyreotic patients under L-thyroxine replacement monotherapy. Clinical Endocrinology, 87(2), 207–215.

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.

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.

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.

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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Scoscia, E., & Baglioni, S. (2010). Hypothyroidism complicated by low T3 state: An issue in intensive care unit. Respiratory Medicine CME, 3(2), 106–108.

Werneck de Castro, J. P., Fonseca, T. L., Ueta, C. B., & McAninch, E. A. (2015). Differences in hypothalamic type 2 deiodinase ubiquitination explain localized sensitivity to thyroxine. Journal of Clinical Investigation, 125(2), 769–781.

Wiersinga, W. M. (1979). The peripheral conversion of thyroxine into triiodothyronine (T3) and reverse triiodothyronine (rT3) (PhD, University of Amsterdam). Retrieved from

Categories: T4-monotherapy, Testing policy, Therapy guidelines, Therapy paradigms, TSH test

5 replies


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