There are myths in medical practice, and misguided policies in health care systems, that prevent Free T3 (FT3) from being tested.
It could save a patient years or decades of suffering and illness to perform this cheap test to reveal problems that could otherwise go undiagnosed in a T3-blind medical system.
A fellow thyroid patient asked a question in our support group about why their FT3 was not being tested by their doctor. They wanted to know how they should approach the doctor to request that FT3 be tested.
It is not easy to make this request of a physician if you’re a thyroid patient and don’t know what the barriers are. It’s also not easy for a physician to respond. They may also face strict policies that prevent FT3 testing.
Many myths ingrained for decades are behind these policies.
From time to time, medicine has had to challenge beliefs that have become revealed as myths. For example, the Western Journal of Medicine went through this exercise:
“We aim to encourage readers to evaluate critically even the most standard and widespread practices, when they are based on tradition and the weight of authority, but in the absence of, or contrary to, available evidence.
… Myth does its work in the heart and can therefore be more powerful than the logic to which it has always been opposed.
… Medical myths based on authoritarian dictates, in the absence of or contrary to evidence, must also serve a similar [psychological] need.
… When myths convince us to act in ways that are contrary to our own interests, or (for healers) to the interests of patients, we must first recognize them for what they are, then critically challenge their assumptions, and finally, have the courage to abandon them.”(King & Hoffman, 2000)
In other words, when myths take root in medicine, it’s not a problem that can be easily solved with scientific education alone, although you always have to start there. Medical myths become a social-scientific problem, a medical culture problem, and they are ingrained in institutions, procedures, attitudes, and habits.
When mythical beliefs continue to endure despite the lack of science to demonstrate them, and despite the publication of contradictory scientific facts, you have a problem that is rooted in authority and emotion more than logic and evidence.
It takes intense critical thinking skills to dig down into cherished, deeply held assumptions. It takes medical “courage to abandon” the assumptions because it may cost the physician their career if they don’t have the tools to defend themselves by strategically myth-busting the myths of their peers.
In this post, I cover the types of myths that have resulted in physicians idolizing TSH, imagining this hormone’s concentration is far more omniscient, infallible, and omnipotent than it ever can be in reality.
The idolatry of TSH too often goes hand in hand with an illogical / unphysiological denigration of the body’s most powerful hormone concentration, FT3. Hyperbolic expressions of TSH’s exquisite sensitivity and authority provide excuses for ignoring FT3’s measurement.
Over time, myths have grown up around FT3 measurement itself to try to justify the continued refusal to test this level so vital for symptom relief and health outcomes. Inappropriately simplistic interpretations of this hormone level in isolation, only in relation to its population range, are part of its dismissal. Simplicity is attractive, but metabolic complexity and individual diversity is the reality in thyroid disorders.
Myths often arise from faulty reasoning that seems attractive.
Fallacies of logic and/or rhetoric are at the foundation of myths in thyroid therapy that dismiss FT3 testing and amplify the overreliance on TSH.
- Logical fallacies involve “reasoning that is logically incorrect, undermines the logical validity of an argument, or is recognized as unsound.” (Wikipedia: List of Fallacies)
- Rhetorical fallacies include not only logical fallacies but also inappropriate appeals to emotions or authority, such as “Claiming something is true because it’s commonly practiced.” (See Information is Beautiful: Rhetological fallacies)
When a myth has been firmly entrenched in medicine for decades, it is much harder to deconstruct the faulty reasoning that established the myth in the first place.
Over time, if enough people embrace the myth, it starts to feel not only natural and obvious, but also factual. Many people keep repeating the claim, and its logic stops being challenged. People who challenge the myth may be ridiculed or even attacked for undermining a foundational dogma.
A collection of beliefs or general principles, whether factual or mythical, supports a “paradigm” in medicine or science:
“In the philosophy of science, [a paradigm is] a general conception of the nature of scientific operation within which a particular scientific activity is undertaken.
Paradigms are, of their nature, persistent and hard to change.
Major advances in science–such, for instance, as the realization of the concept of the quantum or the significance of evolution in medicine–involve painful paradigmatic shifts which some people, notably the older scientists, find hard to make.(Paradigms; Collins Dictionary of Medicine (2004, 2005). )
Fallacies that inflate the power of TSH and T4 at the expense of T3 are at the core of what I call the “TSH-T4 paradigm” of thyroid therapy, which holds that TSH-normalized LT4 therapy works for everyone.
The opposite paradigm, which emphasizes the power of T3 hormone without dismissing TSH or T4, is what I call the “T3 paradigm” of thyroid therapy. (See “Infographic: T3 paradigm vs. TSH paradigm.”)
Purposes of FT3 testing
One myth is that FT3 is not a useful test in hypothyroidism. Period.
However, this myth arises because some people are not capable of distinguishing between what is NOT a very wise way to use the Free T3 test, and the many ways in which FT3 testing IS useful.
There is only one major limitation on FT3 use:
The FT3 and/or Total T3 test cannot be used as a screening test for hypothyroidism in isolation from FT4 and TSH.
A low FT3 is not independently diagnostic of untreated hypothyroidism for two reasons:
- In early thyroid failure, the FT4 usually falls below the normal range while FT3 remains within range, for reasons explained below.
- FT3 can be depleted by any severe, acute or chronic illness, not only by severe untreated hypothyroidism.
However, many important purposes remain for FT3 testing, such as:
- Optimizing FT3 during thyroid therapy to alleviate thyroid symptoms (Hoermann et al, 2019)
- Monitoring tablet potency, absorption, clearance, and TSH-FT3 relationships when dosing any medication including T3 hormone (Celi et al, 2010, 2011; Jonklaas et al, 2015)
- Diagnosing the development of an autonomously T3-secreting thyroid nodule during thyroid hormone treatment (See “In 1981, Canadian physicians argued T3 was the best test in thyroid therapy“)
- Screening for Graves’ hyperthyroidism and/or assessing the likelihood of remission in Graves’ disease (Khanna et al, 1996; Yong et al, 2001; Liu et al, 2016)
- Assessing the risk of mortality or morbidity in hospital emergency triage and a wide variety of nonthyroidal illnesses (Guo et al, 2020; Taroza et al; Bertoli et al, 2017; Bartalena et al, 1996; See also “Ataoglu: Low T3 in critical illness is deadly, and adding high T4 is worse.“)
- Calculating the unadjusted FT3:FT4 ratio to determine an approximate T4-T3 conversion rate to assess metabolism when not dosing T3 hormone (See below)
- To obtain a scientifically-adjusted Global Deiodinase efficiency (GD) score using SPINA-Thyr free endocrinology research software (See “Analyze thyroid lab results using SPINA-Thyr“)
Overgeneralizations that support anti-FT3-testing myths
Overgeneralization of two types is at the foundation of the TSH-T4 paradigm of thyroid therapy:
- From the part to the whole (from central to body-wide T4 metabolism) and
- From the whole to the part (from a mixed, untreated population to the thyroid-disabled, treated individual)
Part to whole: One hormone (TSH) to rule them all.
An overgeneralization from the part to the whole is the belief that one part of the body’s response to T4 (and T3) represents all we need to know about every other tissue’s response.
No matter how sensitive TSH is to T4-T3 conversion, this hormone does not speak for appropriate T4-T3 conversion in all tissues beyond the hypothalamus and pituitary.
This way of thinking can be traced back to major leaders in thyroid science history, such as Larsen in 1981 when he theorized that T4 metabolism was an “autoregulatory” system that took care of itself.
This dogma was promoted prematurely in scientific history. Scientists did not yet have enough understanding of the complexities and vulnerabilities of transport, metabolism or signaling. We now understand how localized and unique each tissue’s T4-T3 metabolism is.
If a person imagines T4 metabolism can never be dysregulated while TSH is normal, then it means TSH could have more control over the whole system. The dogma is that T4 metabolism will just fall in line and obey.
This is wishful thinking. We love machines that let us push only one button to make everything work.
It makes us think that we’re actually helping people by pressing this TSH button during therapy, when we never check the results in FT3 and FT4 levels and symptoms.
If or when FT3 or FT4 is inconsistent with TSH, the dogma that “this part manages the whole system” gives false reassurance to the doctor that the TSH must be more trustworthy and powerful than it can be in reality. Therefore, they ignore the warning signs that the TSH may be lying about thyroid hormone status. They will keep pressing the TSH button.
Whole to part: The population’s description determines the individual’s prescription.
The opposite overgeneralization from the whole to the part is to claim that the TSH reference range’s boundaries for 95% of the human population represents the full range of healthy T4 (and T3) supply and metabolism in every thyroid-disabled individual on every type or combination of thyroid therapy.
Can we always reason from the population to the individual? No.
Scientists know that one must always ask “does this individual fit the most important parameters of the population”? What if most of the population have healthy thyroid function and are not being treated with any thyroid hormones?
Why should a thyroid-disabled individual under hormone treatment be judged by the statistical description of a very different population?
What is statistically significant (or insignificant) to a population as a whole is a mathematical construct, a concept. It is not necessarily revealing a direct cause-effect relationship in microbiology or physiology. Statistical significance, therefore, is not necessarily clinically significant (or insignificant) to a unique individual within a population.
Arising from this faulty logic is one of the most harmful myths in thyroid therapy. It is that the moment that TSH falls below the statistically-defined threshold between normal and low TSH, at that moment, and not before, your individual body has too much FT4 and/or FT3 in blood and too much T3 signaling in receptors.
Another myth that flows from the statistical inverse log-linear relationship between FT4 and TSH in large populations, is that the lower your TSH goes below the lower population boundary, the more thyrotoxic your tissues must become, everywhere in your body, even if your thyroid gland status, antibody status, concurrent FT4 and FT3 levels and/or thyroid treatment type are very different from the vast majority of people in population studies.
This overgeneralization reveals a fundamental misunderstanding of the function of TSH in a large population vs. its function in an individual.
Research shows that the thyroid-healthy human body’s thresholds for insufficient or excess thyroid hormone supply are not governed by the outer limits of the 95% population reference range for TSH. Instead, the thresholds for excess/deficiency sit at the boundary of a range that is far narrower, constituting 10-30% of the width of the population’s reference range. Moreover, the narrowest range of tolerance is not for TSH hormone supply, but for two very different hormones: FT3 and FT4 supply. (See “Individual thyroid ranges are far narrower than lab ranges“)
Keeping TSH within the outer limits of 95% of the population is not the body’s goal. It is an institutionalized goal constructed by statistics.
The individual’s threshold for excess FT3 and/or FT4 is unlikely to fall at the lower boundary for TSH.
The TSH statistical reference range’s outer boundaries are not clinically significant thresholds for the individual body.
Some of the leading scientists today (Antonio Bianco and colleagues; Rudolf Hoermann and colleagues) are trying very hard to communicate that TSH is a means to an end, not an end in itself. TSH is the main lever on the healthy thyroid gland. TSH will step outside the population range whenever it is trying to adjust thyroidal secretion rates and ratios to defend T3 levels in blood and T3 signaling in tissues. (See “The thyroid gland is a T3 shield. Defend the unshielded.” and “Relational Stability, part 3: Shifting TSH-T4-T3 relationships“)
As TSH adjusts, it is delivering a prescription to your thyroid gland, which functions as the T4 and T3 pharmacy in your neck.
If a rising TSH prescription always says “increase both T4 and T3 secretion, and increase T3 preferentially,” why, in a thyroid-disabled person, must we always fill the prescription with only T4? (See “T3 is not always converted from T4: De novo T3 synthesis“)
Why should we trust that every human body will turn their prescribed T4 dosage into enough T3, when even in perfect thyroid health, metabolic dysfunctions can occur downstream of the thyroid gland to diminish T4 conversion to T3?
You can’t tell whether TSH’s prescription is being filled unless you measure the results: FT3 and FT4 and the individual’s symptoms and health outcomes.
An isolated TSH level gives no precise insight at an individual level if you know nothing about the individual’s FT4, FT3 and health status such as pregnancy or severe illness.
The omniscient, omnipotent TSH myth
Doctors have been taught the myth that TSH secretion, which is locally regulated by T4 and T3 being metabolized in pituitary and hypothalamus, is the most sensitive proxy for thyroid status even though it neither regulates nor monitors T4 and T3 supply and metabolism in tissues all over the body.
Physicians have been required to put blind faith in the theory that population statistics for this one hormone can speak for thyroid hormone metabolism and signaling in every bodily tissue and every individual.
To respond to that myth is like telling a flat-Earther that in fact, although it might seem like the earth is flat, the Earth is indeed round.
You might be able to convince a person who doesn’t fully identify with flat-earthism.
You might be able to convince a reasonable physician who has long ago understood that not everything taught in medical school is complete or unbiased.
A strategy: Should we ask questions?
Perhaps asking questions can help to get a doctor thinking about how they know what they think they know about the interpretation of TSH results.
We might know enough to ask them things like this:
- Whether the feedback loops in the diagrams in any of their medical textbooks ever showed the pituitary is capable of sensing the level of T3 signaling in heart tissue, kidney tissue, cerebral cortex tissue, or the T3 signaling in your big left toe? … (The answer is no. See “Visual bias: The pituitary gland in HPT axis diagrams.”)
- Or whether it is impossible for a nonthyroidal chronic illnesses such as heart failure, cancer, or kidney disease to prevent TSH from rising above normal? … (The answer is no. See “Ataoglu: Low T3 in critical illness is deadly, and adding high T4 is worse.)
- Or whether all the enzymes governing T4-T3 conversion and T3 clearance are regulated by TSH levels in blood? … (The answer is no. Beyond the thyroid gland, only D2 is co-regulated by TSH. See “Thyroid hormone journey: Metabolism.”)
- Or whether T3 and T4’s rate of transport into cells and T3’s rate of binding to receptors is regulated by TSH levels in blood? (The answer is no. See “How do we get enough T3 into thyroid hormone receptors?” and “What can prevent T3 from getting into thyroid receptors?“)
- Or whether any studies have shown that osteoporosis is caused by an isolated TSH deficiency, rather than being caused by dysregulated T4 and/or T3 supply or metabolism in bone tissues? … (The answer is no. See “As of 2019, still no proof that low TSH causes harm to bones“)
- Or whether science has proven that when TSH is suppressed, TSH receptors are always empty and do not send signals? (The answer is no. See “The TSAb stimulating antibody can lower TSH despite euthyroid status.”)
However, if you ask these questions, physicians committed to the TSH-T4 paradigm might not know how to answer, or may answer with myths. Your conversation would go nowhere in the doctor’s office. But you would understand your physician a little better.
Another likely possibility is that they might not understand the question if it is beyond their expertise. The average physician does not understand the mechanisms involved in T4 or T3 metabolism. Many do not realize that TSH concentrations in blood cannot govern tissue thyroid hormone status in the thyroid-disabled, treated individual.
Metabolic fiction vs. hard facts
It’s amazing how metabolic fiction can seem like hard facts.
A physician may be a very intelligent human being, but they are still human being.
Human beings can draw incorrect inferences about TSH’s supreme power — especially if they keep on hearing the mantra that TSH is the most sensitive and specific metric for thyroid status.
Why pick on FT3 testing alone?
Why is it so hard for medical people to believe that a Free T3 test really can tell them how much Free T3 is capable of being transported from blood into cells in a particular organ like the liver?
- Does this test tell you nothing about how much circulating Free T3 is ready to be transported across the blood-brain barrier into the brain? Of course it does!
- Does this test not at least partly reflect the amount of T4 hormone molecules being converted to T3 in cells, and subsequently exiting from those cells to rejoin any other sources of T3 in blood? Of course it does!
Why does anyone trust a FT4 test? It is undoubtedly necessary to test FT4 in addition to TSH when diagnosing untreated subclinical hypo, or untreated subclinical hyper, or suspected central hypo.
Now here’s the thing. They say T3 is an intracellular hormone, but T4 is also an intracellular hormone. The main purpose of T4 is to enter cells where it is metabolized into other thyroid hormones. A certain percentage of FT4 is always hiding from the blood test. Some T4 is inevitably in transit through cells or in the act of being transformed in a cell. We cannot predict from a FT4 test what percentage of intracellular T4 will be changed into a non-T3 metabolite, like T4 sulfate or RT3. So does this hidden T4 make the FT4 test invalid? No it doesn’t. The hidden T3 won’t make the FT3 test invalid, either.
Fortunately, we do not need to guess about how much T4 converts to T3 when we can measure FT3. We can use medical inductive reasoning to learn a lot from the results:
- Measuring FT3 will give us a general sense of how much T4 has recently converted to T3 and then rejoined the pool of T3 that is also coming into blood from a thyroid gland and/or any T3 dosing.
- The FT3 you have measured in blood will have also already been diminished by the recent clearance rate of T3.
- Now you know how much FT3 is poised ready to re-enter many cells all over the body.
The main things you can’t see with a FT3 test (nor a TSH or FT4 test either) include the diverse tissue-specific T4-T3 metabolic rates, the diverse, tissue-specific T3 clearance rates, and the T3 receptor occupancy rates inside cells in particular organs and tissues that you’re interested in, such as heart, brain, liver, muscles, GI tract, and so on. But you can also induce some of that from additional data such as FT4, TSH, biomarkers of T3 signaling like total / non-HDL cholesterol, and clinical presentation.
FT3 lab test precision and reliability vs. harmonization
If anyone is deeply aware of the controversies regarding harmonizing thyroid hormone reference ranges to an international standard, they should know that this is not a major barrier to interpretation of FT3 test results for most clinical purposes.
Despite problems with standardizing results among FT3 and FT4 manufacturers, both tests have approximately the same degree of precision and reliability from test to test using the same assay manufacturer (Thienpont et al, 2010).
FT3 and FT4 tests are based on similar methodologies and technologies. If you can trust a FT4 assay today, you can trust a FT3 assay today, with one exception: Precision at the lower end of the FT3 reference is a challenge, with borderline low FT3 on a common ELISA assay often yielding much lower results using the generally more precise mass spectrometry method (Jonklaas et al, 2014).
For this reason and due to the increased probability of hypothyroid symptoms (Hoermann et al, 2019), it is best to avoid FT3 in the lower end of reference or lower during LT4 thyroid treatment, because it could be lower than the standard assay will reveal.
Assay quality control and poorly constructed reference ranges are a problem for many lab tests, not just FT3 and FT4. Let’s continue to improve the quality of TSH, FT4, and FT3 assays while we continue to rely on the tests.
Why “Free T3” not just Total T3?
Another myth is that total and free T3 are interchangeable as hormone tests.
The free fraction is more closely aligned with tissue effects of T3 hormone.
Total T4 (TT4) measurements have largely been left behind because they can be inflated and deflated too easily by changing levels of binding proteins.
For the same reason, Total T3 (TT3) should be considered a rather outdated test in most circumstances.
Measuring TT3 is better than not measuring T3 at all, but Free T3 is usually more clinically relevant.
FT3 and/or the FT3/FT4 ratio is often more statistically significant than FT4 or TSH in scientific studies that correlate thyroid hormone levels with symptoms and health outcomes (Hoermann et al, 2019).
A firm foundation in endocrinology is the “free hormone hypothesis.” Why are so many reluctant to apply this hypothesis to FT3, when they long ago applied it to measuring FT4 instead of TT4?
According to this hypothesis, only the free concentration of T3 and T4 can be carried into cells.
More than 99% of our thyroid hormones are bound to carrier proteins while they circulate in blood. Binding proteins help the vast majority of thyroid hormone supply to pass through liver unmetabolized. Although the liver (and thyroid, and kidney) plays a major role in T4-T3 metabolism via D1 enzyme, T3 and T4 are unlike most other drugs, substances and hormones that are metabolized primarily by liver enzymes. Instead, thyroid hormone must be distributed to all tissues where both T3 and T4 are metabolized locally at the rates required by that specific tissue or organ.
- Once Free T3 gets inside cells, the T3 hormone can perform intracellular signaling or become metabolized to another hormone such as T2, Tetrac, or T3 sulfate.
- Also, once Free T4 gets inside cells, the T4 hormone can be converted to T3 or RT3 or other metabolites such as Tetrac or T4 sulfate.
Free T4 is measured because it is the 0.02-0.04% fraction of total T3 that is capable of entering the pituitary and hypothalamus cells and converting to T3. The new-born T3 hormone then signals in receptors to adjust the TSH secretion rate. As a result, a key feature of the HPT axis is the log-linear inverse relationship between Free T4 and TSH concentrations.
For the same reason, Free T3 ought to be measured if you want to correlate symptoms and health effects with T3 concentrations.
Only 0.3% of the Total T3 concentration is Free and capable of being carried into cells. Free T3 will be transported along with Free T4. Some of that Free T3 is likely to bind to nuclear receptors and mitochondria before it is converted to another hormone. (See “How do we get enough T3 into thyroid hormone receptors?“)
Another purpose of binding proteins is retention of hormone in blood. Bound hormone is less vulnerable to being lost in urine too quickly (unless you have proteinuria and are losing T3 bound to albumin).
Approximately 75% of T4 and T3 is bound to thyroxine binding globulin (TBG). High estrogen levels can increase TBG levels and increase the portion of T4 and T3 that is bound. Women on both thyroid hormone replacement and estrogen replacement need to be aware of this, and it is a factor in pregnancy and during menopause.
The rest of T3 is largely bound to Albumin more than Transthyretin, and the rest of T4 is the opposite — largely bound to Transthyretin more than Albumin. Therefore, T3 is more vulnerable when albumin levels or kidney problems occur.
- In a person with a healthy thyroid gland, if more T4 and T3 are bound and less is free, they just create more T4 and T3 so that their Free fractions remain constant.
- In a person without thyroid function, if more hormone becomes bound, you have to increase the dose, or the person may become hypothyroid from lower levels of free hormone.
It is a good idea to run a Total T3 test occasionally, in addition to Free T3, if you really need to know the entire concentration, both bound and free. Perhaps the patient is on heparin (which uniquely distorts free thyroid hormone tests), or another blood thinner, or has severe illness, or albuminuria, or has low albumin levels that could inflate Free in relation to Total.
Testing both FT3 and TT3 can reveal a large disjoint between the two that can be a clue to a problem with T3 urinary loss or low albumin in blood.
What FT3:FT4 ratios can reveal
Now consider hormone ratios. Isolated FT3 hormone levels can’t tell you how efficiently FT4 is being metabolized. But the FT3:FT4 ratio can give you insight.
Our cells interpret FT3 in the context of concurrent FT4 as both are simultaneously transported into cells.
Of course, the same ratio can exist with a FT4 low in range and FT4 high in range and will result in different clinical manifestations. But when the FT3:FT4 ratio is anchored in a FT4 level and clinical context and history, it helps to answer vital metabolic questions:
- “In this individual and her context, how much T4 is likely converting to T3 in cells and then exiting the cells as T3, and how much additional FT3 is coming from a thyroid and/or a pill?”
- “And in this context, how much FT3 available to enter cells is likely to bind with receptors in the nucleus and mitochondria? What other enzymes are likely to be upregulated in cells that could convert T3 to other metabolites before it can reach receptors?”
Answering these questions begins with a FT3:FT4 ratio. Although the investigation does not end there, the ratio is vital data that can begin to address the issue of abnormal thyroid hormone metabolism.
In many recent studies, the FT3:FT4 ratio has become a useful indicator of intracellular thyroid hormone conversion rates that influence health outcomes. It gives you information that TSH alone, and TSH plus FT4, cannot provide.
Anderson’s recent study offered a data set that showed that in large untreated populations, cohorts with low FT3:FT4 ratio averages had higher rates of various chronic disease diagnoses. (See “Prevalence rates for 10 chronic disorders at various FT4, TSH and FT3 levels“)
Not every low-TSH state carries the same level of health risk. If you look at the FT3:FT4 ratios in Anderson and team’s large study, you will see that the hormone levels AND the ratio between the two hormones combine to affect risks associated with thyrotoxicosis. (See “Anderson, 2020: Thyroid hormones and atrial fibrillation“)
However, comparing across diverse thyroid-hormone treated and untreated populations is a challenge. Ratios during thyroid disease and its treatment will be influenced by the degree of thyroid function loss, the presence of TSH receptor antibodies, thyroid medication types, and dosing ratios of T3 and T4. It’s best to compare the ratio of an individual dosing LT4 alone with other patients dosing LT4 alone.
One can always gain the most insight by comparing an individual’s values over time to detect changes in absorption or metabolism.
FT4 and FT3 in blood can reveal an individual body’s unique response to thyroid medication. The diversity from patient to patient is significant. (See “Are you a poor T4 converter? How low is your Free T3?” and “Gullo: LT4 monotherapy and thyroid loss invert FT3 and FT4 per unit of TSH“)
The ratio between these two hormone levels is the closest a clinician today can ever get to judging the amount of Free T4 being converted to T3 hormone in cells, minus the clearance rate of Free T3 hormone, in cells all over our body.
The FT3 fluctuation myth
Another myth is that T3 fluctuates too much from hour to hour so it’s not worth testing.
If you hear that as a patient, it’s because the research on circadian rhythms for TSH and thyroid hormones hasn’t yet reached medical textbooks and policies.
It’s like telling someone that something was discovered by scientists in 2008 and 2011, but the news has not informed medical education or thyroid treatment guidelines yet.
Physicians will find it hard to believe that the leading experts in their field could be so collectively ignorant.
Yet what else but collective medical ignorance, driven by the social-psychological phenomenon of confirmation bias, could explain the selective trickle of scientific knowledge about FT3 testing flowing from the literature into medical textbooks and thyroid guidelines?
Evidence is the only cure for ignorance. Let’s briefly learn how these hormones really fluctuate in health, and during thyroid therapy.
The first thing to understand is that FT3 “fluctuations” differ between people who aren’t on any thyroid therapy, and people who are.
In healthy, undosed individuals, TSH fluctuates much more every day from hour to hour than FT4, and their FT3 fluctuates even less than FT4. The FT3 circadian rhythm is deeply connected to TSH rhythm because of the way TSH preferentially enhances T3 in the thyroidal T3/T4 secretion ratio. (See “Circadian rhythms of TSH, Free T4 and Free T3 in thyroid health.”)
However, you will lose the natural circadian rhythm if you are dosing T3 and/or T4 while you have very little thyroid function.
- Research shows that in populations dosing T4 alone, there is a flat line of FT3. There is NO circadian or dose-dependent rhythm. No fluctuation. This is abnormal. Normally FT3 rises highest while we are sleeping at night, and nature likely does this for a good reason, to synergize with other hormones that peak while we sleep.
- On the other hand, in people who dose even 10 mcg of T3 once a day, the FT3 peak is predictable by the number of hours after a T3 dose (Saravanan et al, 2007; see “T3 peaks” article again). It makes sense to test 12+ hours post dose after the volatile peak has ended and you’ve landed gently on your baseline FT3.
Clearly, the interpretation of FT3 thyroid lab tests has to occur in the context of thyroid gland health and thyroid therapy type.
TSH, the false idol of medical religion
TSH has unfortunately become a false idol of medical religion, an omniscient and omnipotent god over all things thyroid. TSH is being expected to prophesy what it cannot foretell. It is as if all prescriptions must be issued from the sacred gland dangling from one’s brain, and it’s as if none of nature’s prescriptions will ever ask for T3 hormone to be secreted from a thyroid or provided by a pill.
There’s an inappropriate exaltation of TSH at the expense of FT3.
Myth after myth about FT3 testing diminishes scientists’ and clinicians’ ability to get closer to assessing T4 and T3 metabolism and T3 hormone signaling in cells.
Part of the problem is that T4 and T3 thyroid hormone activity in cells, including the activity that co-regulates TSH secretion, is invisible to the naked eye — they seem like powerful, yet invisible, gods.
Thyroid hormones are not like a broken arm with bones clearly misaligned. Therapy would be much simpler if our thyroid hormone dysfunctions were as visible as a broken arm, but we rely on laboratory tests and contextualized, scientifically-informed interpretation of those tests.
Without enough scientific insight into TSH, FT3 and FT4’s cellular behavior (beyond population statistics), a lot of guesswork and theory grows up around the interrelationships between these hormone-gods, until beliefs about their behavior and interaction becomes like a religion.
When invisible causes have huge effects on health outcomes and symptoms, people naturally want to believe that the hormone variable that changed the most (TSH) is the variable that we should focus on. It makes it appear, superficially, as if TSH is still the puppet master in control of it all, even after TSH’s main role of thyroid stimulation is diminished or taken away by thyroid function loss.
But the hormone the body protects and defends the most (FT3) is the hormone that changes the least in relationship to the population’s reference range, during health.
The thyroid-healthy, untreated body’s use of TSH and FT4 to adjust and defend FT3 hormone levels sends a signal about FT3’s biological priority in thyroid disorders, thyroid therapy, and severe illnesses.
When our TSH and FT4 are failing to protect our FT3, we need physicians to help us by defending FT3 levels that yield euthyroid clinical status.
How can we fight these myths?
You, the suffering patient, may be arriving at a medical appointment with brain fog and no medical degree, and with no knowledge-making authority but only common sense reasoning within the doctors office.
Somehow it is now your job to inform the person sitting in the expert’s chair what scientific research says?
Fortunately, not all physicians lack critical thinking and reasoning skills.
However, we know how some physicians can respond with arrogance, or worse.
In fact, some physicians have publicly revealed their backwards logic in presuming that we are the ones who have been duped by myths, and that we erect barriers to our own thyroid treatment when we ask for FT3 tests and/or T3 treatment.
- 2019 ATA article engages in patient-blaming and doctor-shaming
- Thyroid patient blaming and shaming, part 2: True barriers
- Thyroid patient blaming and shaming, part 3: Advocacy and Science
Medical myths are the barrier, reinforced by the need for every physician to defend their own authority, expertise, and career by conforming to the TSH-T4 paradigm.
Because of our powerlessness in the physician’s office, I’m not sure that many of these myths can be countered in that setting.
Yet we must try to persuade and inform our physicians or find better ones if we can, because our well being depends on it.
The endless labor of myth busting is the main reason why Thyroid Patients Canada has to be a public-facing, science-educating campaign.
Help us keep busting myths.
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Tania S. Smith, PhD.
President, thyroid patient, and thyroid science analyst,
Thyroid Patients Canada