Who needs “T3”?
We received a friendly and well-intended comment lately.
It illustrated that in today’s Global English, we sometimes have a hard time defining and understanding what “T3” means when a person is talking about T3.
Are they talking about T3 the hormone, or T3 the pharmaceutical?
“I like your content in general, but I’d like to see more articles that talk to things other than T3.
It’s a bit of a T3 focused blog.
While that is the answer for a portion of thyroid patients. It’s not always the case.
In fact, I’d guess only 30% or so of folks would need T3 in some way (just guessing no hard data on that).”– Commenter
I couldn’t help being a little bewildered by the context of the comment.
The article under which this comment was posted was about winter T3 loss, on average, found in a large cohort of thyroidless people on LT4 monotherapy compared to healthy people not dosing thyroid hormones.
Although “T3” was in the title, the article was certainly not focusing on the subset of people on LT4 therapy who may need to dose T3 from pharmaceuticals.
I even included two graphs showing small changes in FT3 levels in individuals who were not dosing any thyroid hormones, to show how narrow and individualized our healthy FT3 levels can be in people who still have thyroid function.
I mentioned in the article that the patients’ winter T3 loss could be resolved by adjusting their LT4 dose to cover the winter season demands, then talked about both pros and cons of T3 dosing as a solution.
No, T3 pharma is not always the answer to a T3 hormone problem.
So I responded, briefly,
“Hi, this article’s research sources mainly focused on LT4 therapy, meaning people dosing only T4.
Our concern is that all thyroid patients have enough to cover the T3 they lose in winter whether they are on LT4 therapy, combo, or desiccated thyroid.
T3 is the hormone that is active at most receptors where thyroid hormones have activity, no matter what you dose.”
I thought I’d also write a post on the topic to elaborate for others who might have difficulty with our society’s currently vague use of the word “T3.”
What do we at Thyroid Patients Canada usually mean when we talk about T3?
AND, why are we such a T3-hormone-focused blog?
How do we do our best to include not only readers and supporters who dose T4, T3, or desiccated thyroid, or anti-thyroid medication for hyperthyroidism, but also people with entirely healthy thyroids and pituitaries who are dosing no thyroid medications at all?
Two overlapping but different meanings of “T3”
The comments were negotiating between two meanings of “T3”:
- T3 is the vital hormone that does almost all the signaling in thyroid hormone receptors in cells, in every human being.
- T3 pharmaceuticals are an additional source of T3 beyond the thyroid gland and intracellular T4-T3 conversion.
When we talk about “T3” on this blog, we usually mean #1, the true queen of all thyroid hormones, either formed directly from raw ingredients in the thyroid gland, or the most potent daughter of circulating T4 hormone. It’s measured as Free T3 or Total T3 while it’s circulating in blood, but inside of cells, it’s just plain ol’ T3.
- Fully 100% of human beings, regardless of the health of their thyroid gland, need fine-tuned T3 signaling in all their bodily tissues.
T3 sufficiency in cells is supported by having enough Free T3 circulating in blood to supplement T4-T3 conversion rate in cells, since the conversion rate can vary from tissue to tissue, person to person, and in various health conditions. There is no tissue that is entirely dependent on local T4-T3 conversion — even the adult brain obtains 20% of its receptor occupancy using T3 that enters via the blood-brain barrier (Bianco et al, 2019).
Occasionally we talk about meaning #2, the pharmaceutical sources, but we usually refer to them as
- LT3 (liothyronine sodium) or
- desiccated thyroid (DTE / NDT)
- or we talk about “dosing/taking T3” or “T3-inclusive therapies” or T3/T4 combination therapy, generally using phrases that clarify we mean the pharmaceutical source of T3 hormone.
It is true, we don’t know how many people with thyroid function loss “need” to dose T3 or could benefit from it to obtain freedom from chronic symptoms and poor health.
But we will never know how many “need” LT3 or desiccated thyroid as long as patients are not routinely monitored for their FT3:FT4 ratios and FT3 levels in relationship to their symptoms and health outcomes.
What a society does not measure, it does not value.
Only one team of thyroid scientists has cared enough for the health and well being of total thyroidectomy patients to track their symptoms with TSH, FT3 and FT4 levels over many years of LT4 monotherapy adjustments, noticing that symptom presence and absence correlates most strongly with small relative changes in FT3 (Larisch et al, 2018; Hoermann et al, 2019). They do not study T3 pharmaceuticals but they are open to their being a valid solution for some people.
Q: Why does our blog focus so much on T3 (the hormone)?
A: T3 hormone is the most inclusive, relevant thyroid topic for all human beings.
If you look at all our posts in our site map, many of them do not talk about T3 pharmaceuticals at all. Some focus on LT4 monotherapy. Some of them focus on people not dosing any thyroid hormones at all.
However, it is true, many posts talk about T3 hormone — FT3 testing, low T3 syndrome, and FT3:FT4 ratios in health and illness.
Still other posts talk about topics that are indirectly related to this hormone, such as thyroid antibodies, Reverse T3, Triac, T2, TSH levels, thyroid hormone metabolism, and so on.
We align ourselves with the T3-centric paradigm, in contrast to the TSH-T4 paradigm. There is a very open and obvious paradigm battle in thyroid science literature. We agree with leading thyroid scientists Antonio Bianco and his coauthors, and Rudolf Hoermann and his coauthors, in claiming the HPT axis is designed to defend, prioritize and optimize circulating T3 hormone levels to individualized demands.
We also believe a T3-centric paradigm is the foundation of a more ethical and effective approach to thyroid therapy.
- The thyroid gland is a T3 shield. Defend the unshielded.
- Relational Stability, part 4: The new thyroid paradigm
- Thyroid therapy paradigm shift: T3 hormone testing is a battleground.
- Infographic: T3 paradigm vs. TSH paradigm
- Renew the paradigm of thyroid therapy
In people with healthy thyroids, T3 signaling is the goal of TSH-stimulated thyroid secretion of T4 and T3 hormones and the natural metabolic process of T4-T3 conversion in cells.
T3 hormone signaling, mostly via local T4-T3 conversion, regulates most of our TSH secretion rate. However, TSH is also hypersensitive to indicators of metabolic demand and is vulnerable to interferences. TSH is co-regulated by leptin, corticosteroids, retinoids, TSH-receptor antibodies, endocrine disrupting toxins, and inflammatory cytokines, and the list goes on and on.
T3 hormone remains at the core of thyroid hormone health in people with central hypothyroidism, and both FT4 and FT3 testing are necessary to evaluate the adequacy of LT4 therapy (Ferreti et al, 1999). In central hypothyroidism, people have TSH secretion disabilities. Many of them cannot secrete normal TSH levels, and some can’t secrete any TSH at all while they are rendered euthyroid by hormone therapy.
Despite all the “Low TSH risk” studies published to date (most of them T3-blind), people seldom ponder the fact that these central hypo humans’ inability to secrete TSH has not yet been proven to “cause” osteoporosis or heart problems when their FT4 and FT3 are optimized.
T3 hormone remains central to the healthy function of all organs and tissues in people who have no thyroid gland due to total thyroidectomy or no thyroid function due to complete autoimmune destruction of their thyroid tissue, or other causes that render a thyroid non-functional.
T3 matters to all thyroid-disabled people dosing T4 alone, who obtain all or some of their circulating T3 from their T4 pharmaceutical. It also matters to people dosing T4-T3 combos. In people dosing T3 hormone alone, T4 can be completely absent from blood and they can still be euthyroid and healthy if they titrate their T3 doses carefully.
T3, the hormone, matters to everyone’s health.
All human beings need optimized T3, which means avoiding both individually-insufficient and individually-excessive levels of T3 supply and T3 signaling.
- Ideally, a person will obtain T3 hormone naturally from their TSH-regulated healthy thyroid gland and from their cells’ internal T4-T3 conversion rates.
- But whenever necessary, people will need to have their T3 hormone levels adjusted by dose adjustments of their T4 pharmaceuticals, and/or their T3 pharmaceuticals, or their anti-thyroid medications to treat hyperthyroidism.
We defend individually-optimized T3 as we stand against “thyroid pharmaceutical prejudice.”
Thyroid pharmaceutical prejudice is an attitude that disparages or dismisses one type of thyroid hormone pharmaceutical as bad or unnecessary for all thyroid-disabled people.
Everyone on thyroid hormone therapy is dosing bioidentical hormones, not manufactured molecules foreign to the human body.
It’s hard for some people to understand who aren’t biochemists, but whether a hormone is made from vegetable matter or is borrowed from an animal, the human body recognizes it, metabolizes it and uses it as if it came from our own gland. FT3 and FT4 hormone tests can’t tell the difference, either.
- Thyroid pharma: Bioidentical yet harmful?
- All thyroid meds are bioidentical, but individual response varies widely
A prejudice against a thyroid pharmaceutical ends up being prejudiced against thyroid-disabled people who find the disparaged pharmaceutical, or a combination of pharmaceuticals, to be the most effective, or the only effective option for them.
- See “Thyroid pharmaceutical prejudice: How it works“
- See “Pharma prejudice refuses a paradigm shift in thyroid therapy“
- See “Pharmaceutical prejudice can lead to a thyroid therapy dystopia“
This means we encourage people to work with their physicians to discover their individually-optimal thyroid hormone levels on any pharmaceutical or any combination that works for them, whether it is:
- currently the most common and convenient (LT4 monotherapy), or
- the most rare and inconvenient last-resort therapy (LT3 monotherapy),
- or anything in between: any ratio of synthetic T4-T3 combination therapy, including even desiccated thyroid plus T4 and desiccated thyroid plus T3, which enables flexible adjustment of the ratio
- (or anti-thyroid medication to control hyperthyroidism, which of course don’t contain thyroid hormones, but significantly affects the levels and ratios of FT3 and FT4 in blood, and can lead to hypothyroidism if overdosed)
We defend individually-optimized T3 by clearing up misinformation and ignorance about T3 pharmaceuticals.
Why should we stop talking about T3 hormone dosing as an option, when healthy thyroids never stop secreting T3, and when healthy thyroids provide a larger TSH-stimulated T3 intravenous infusion while people are sleeping?
Essentially, all thyroid-healthy people get a daily dose of T3 from the pharmacy in their neck.
It’s a secret T3 dose. By the time they get to the laboratory to be tested, the FT3 peak has disappeared from blood.
- Circadian rhythms of TSH, Free T4 and Free T3 in thyroid health
- The significance of the TSH-FT3 circadian rhythm
Why should we stop talking about T3 pharmaceuticals, when historical record shows that “LT4 monotherapy for all” was a policy championed in the 1970s and 1980s partly on the basis of unduly strong faith in efficient peripheral metabolism, undue faith in TSH omniscience, and rabid anti-LT3 and anti-desiccated thyroid pharmaceutical prejudice?
It’s not a conspiracy, since conspiracies are secret. The scientific literature is an open record of the historical ignorance and bias.
The medical choice and preference for LT4 monotherapy on behalf of millions of patients worldwide was not made on the basis of objective double-blind comparative clinical trials of different thyroid hormone preparations on diverse patients with clinical outcomes as their endpoints.
Thankfully, the scientific record also contains the work of more objective, reasonable, and compassionate approaches to LT4 monotherapy that involved testing T3 and/or FT3. They aimed to educate doctors to defend their patients’ optimal circulating T3 levels as more physicians made the transition to treating with LT4:
- Ingbar and Braverman’s historic study of LT4 monotherapy
- In 1981, Canadians argued T3 was the best test in thyroid therapy
It is evidence of shameful scientific neglect and bias that the very first double-blind clinical trial of desiccated thyroid and LT4 monotherapy was conducted in 2013, with foolishly narrow TSH targets within the TSH range, an unscientific disregard for the very different FT3:FT4 ratios in blood due to differential absorption and metabolism, and like most T3-T4 combo trials, with no attempt to optimize either therapy to the individual’s response beyond their local pituitary-specific TSH response. But despite its methodological flaws, the study showed no danger and some benefit to NDT/DTE in some people.
No, without a study better than Hoang’s forty years prior, the medical shift in the 1970s and 80s was not a decision made on entirely objective and scientific grounds. Instead, some people conducted a few biased studies with mere biochemical ranges as their primary endpoints, using fear, ignorance, and ridicule as rhetorical tools of persuasion. A similar rhetorical bag of tricks are still used today to promote prejudice against T3-inclusive therapies and preference toward LT4 monotherapy.
- Biondi and Wartofsky’s 2014 dismissal of desiccated thyroid
- 2014 ATA Therapy guidelines: 3. Desiccated thyroid
We need more public voices explaining the unique pros and cons of T3 dosing in its many forms, by patients, scientists, and physicians who do not hold the opposite prejudice against LT4 monotherapy.
For example: Some patient groups are quite adamant that LT4 monotherapy yields suboptimal levels of FT3 and “too much” FT4.
It certainly can lead to suboptimal FT3 if a physician is using the standard TSH-normalization target rather than individualized FT3 optimization and symptom relief targets and has no clue that some people are “poor converters” while on LT4, and that high-normal FT4 can pose a health risk for some people.
- See “Are you a poor T4 converter? How low is your Free T3?
- See “Caution: Doctors perform T3-ectomies without our consent“
- See “Cancer scientists point finger at T4 & RT3 hormones“
- See “Ataoglu: Low T3 in critical illness is deadly, and adding high T4 is worse.“
However, the medical misuse of LT4 monotherapy that harms poor T4-T3 converters is a problem one should blame on prejudiced policies and FT3-ignorance, not the LT4 pharmaceutical itself. In wiser hands, it may serve a lot of people a lot better.
Many people on LT4 have partly functioning thyroids, but some people are both severely thyroid-disabled and metabolically disabled at the same time. LT4 monotherapy cannot serve everyone.
Having all forms of thyroid pharmaceuticals available on the market serves a diverse population of thyroid-disabled people with variable handicaps in thyroid function, pituitary TSH secretion, oral absorption, bloodstream binding proteins, intracellular transport, and metabolism and signaling.
One does not need to know all the complex causes of thyroid therapy problems to know by clinical experience that different people respond to different thyroid pharmaceuticals and sometimes respond well to unique combinations and dose ratios.
For example: Many people are unaware that LT3 behaves a little differently from desiccated thyroid’s T3 content at the point of absorption. Some patients find the T3 obtained from desiccated thyroid to be more gentle and more slowly absorbed, perhaps because it comes bound to thyroglobulin protein. Desiccated thyroid appears to help some people tolerate T3 dosing who have symptoms in the first hour of dosing synthetic LT3. This is something that patient communities know by comparing patient experiences, but no pharmacokinetic study has yet explored because of scientific prejudice against studying desiccated thyroid.
For people who do not tolerate synthetic T3 but only require a little direct T3 dosing, combining desiccated thyroid with synthetic T4 permits the alteration of the dose ratio with a T3-containing preparation that behaves more gently at the point of absorption. For people who require a higher T3:T4 dose ratio than desiccated thyroid provides, and who also readily tolerate synthetic dosing, synthetic T3 may be added to desiccated thyroid.
One of the major misunderstandings we try to remove is the prejudice regarding dose ratios of T3-T4 combination therapy, which is largely based on misunderstanding of the difference between naturally appearing T3 hormone and pharmaceutically-dosed T3 hormone.
- See “Free T3 peaks and valleys in T3 and NDT therapy“
- See “No, 25 mcg of L-T3 Liothyronine isn’t equivalent to 100 mcg L-T4“
- See “Q&A. Dosing T3 in light of circadian rhythm“
- See “LT3 monotherapy withdrawal: Clearance and effects“
In brief summary, science shows that when a person doses T3, it is more quickly absorbed than oral T4, but also more quickly metabolized to T2 and other metabolites and/or is cleared to urine during its post-dose peak. Adding oral T3 shifts FT3:FT4 ratios in blood and also changes T3 responses within cells, including TSH-secreting cells. If you add 5 micrograms of T3 to 100 micrograms T4, the metabolic dynamics are very different from adding 50 micrograms of T3 to 50 micrograms of T4, because the T3 dose will not be 10x as potent and the T4 dose will not be half as potent! Dosing T3 once a day is very different from dosing it 5 times a day, and dosing T3 at bedtime is very different from dosing at noon. Testing FT3 12+ hours post-dose is necessary for stable results that can be compared over months and years.
All these facts are based on scientific studies of T3 pharmacodynamics and our current state of understanding the three deiodinase enzymes, thyroid hormone transport and signaling, and they are not just guesses based on patients’ experience-based lore.
One of the most unreasonable and utterly unphysiological ideas that has arisen is that pharmaceutical T4-T3 combinations ought to mimic an average thyroidal secretion T3:T4 ratio.
Everything else in thyroid is judged by falling within a wide range, so why cherry-pick a precise ratio found only in a small minority of people?
- Meet a person with the perfect T3:T4 thyroid secretion ratio
- The foundations of synthetic T3-T4 therapy in the 1990s
- Mimicry: The idol of T3-T4 combo therapy 2004-2014
How do we know how much T3 and T4 are secreted by thyroids? It’s not an easy question to answer, because a thyroid gland cut out of a body may “contain” less T3 than it actively secretes under TSH stimulation as blood flows through it, as Laurberg’s review cautioned in 1984. Most kinetic studies in living people performed between the 1970s and 1990s used imprecise methods and theoretical models, radioactive iodine-tagged hormones, iodine overdoses, and a lot of fancy math. The most recent study in 1990 showed that human thyroid glands secrete a wide range of T3:T4 ratios from 6:1 to 71:1, not a narrow 14:1 or 16:1 ratio. Averages are not representative of their wide 14-person data set, and we must take the whole study with a grain of heavily iodized salt.
- Question Pilo’s study: The wide range of thyroid hormone adaptation
- Question Pilo’s 1990 study. It can be misused to limit your T3 supply.
It is also strange that most scientific pundits who require T4-T3 combinations to conform to a narrow dose ratio fail to admit that T4 monotherapy contains an unphysiological ratio of 100% T4 to 0% T3.
The ratios and levels of hormones in blood are far more significant to an individual’s health than the ratio of hormones in two tablets. Bloodstream ratios and levels are never predetermined by the ratio in the dose. Instead, hormone levels are determined by one’s absorption and metabolism, which vary significantly from person to person.
We defend individually-optimized T3 as we stand against “biochemical bigotry.”
Many people find the word “bigotry” offensive, but this is a simple dictionary definition that explains what we mean:
“obstinate or intolerant devotion to one’s own opinions and prejudices.”(Merriam-Webster)
In thyroid therapy, biochemical bigotry is the dogmatic belief that a thyroid-disabled person’s health only exists within the healthy population’s reference ranges for TSH, FT3 and FT4, and that a risk of illness only exists outside those statistical ranges.
This belief is false even in people who are not being treated with a thyroid disorder.
High-normal FT4 and high-normal TSH (within reference range) raises cardiovascular health risk, while mildly elevated FT3 is less risky than the worst of all, an isolated low FT3.
Secondly, statistical description of a population is a very poor basis for an individual prescription, especially when talking about thyroid hormones.
In thyroid hormones, the 95% range of the population is far too wide to fit any single healthy individual within it. Most individuals do not stray from a narrow band 10-30% of the width of the reference range.
In thyroid hormones, variation between two individuals is so extreme that one person with a healthy thyroid gland will find health only with FT3 near top of range, while another will find it only with FT3 near the bottom of range.
However, in people without thyroid function, FT3 is rarely symptom-free in the lower half of reference range, according to the best longitudinal research study of symptoms and hormone levels ever performed. Some people have extremely narrow therapeutic windows for optimal FT3 within range while on LT4 therapy (See Hoermann et al, 2019).
Mid-range FT3 is a good starting place for therapy dose adjustments given that it’s the statistical average … but that’s the average when the hormones are adjusted by a TSH-regulated thyroid gland, and when the FT3:FT4 ratio is also average for adults, at 0.32 pmol/L.
Despite the usefulness of health-thyroid biochemistry as a context and comparison, mimicry is not a valid therapeutic target in a person who can’t mimic “normal” healthy thyroid physiology, can’t mimic the “normal” absence of TSH-receptor antibodies, or can’t mimic “normal” intracellular thyroid hormone dynamics.
Forcing a thyroid-disabled person’s biochemistry to conform to the ranges for non-disabled people can be unhealthy and discriminatory.
Canada, like many democratic western societies, has laws regarding discrimination against people who are disabled. We do not expect people with wheelchairs to fit through narrow doors, nor do we expect people with walkers to run to catch a bus. We accommodate and respect people’s disabilities.
Dosing thyroid hormone through the GI tract is very unlike secreting hormone gradually from a thyroid and converting T4 and T3 within cells every minute of every day.
A prosthetic (fake) leg is different from a real leg. Oral thyroid hormone dosing is a thyroid prosthesis, not a true thyroid gland replacement.
Accommodations must be made for pharmaceutically-induced biochemistry in a metabolically-handicapped individual. The abnormalities of LT4 dosing will differ from LT3 dosing.
In brief summary: In LT4 monotherapy, FT4 may be higher than normal, and in LT3 monotherapy, FT3 may be higher than normal 12-hours post dose, but in both cases patients may be euthyroid with no signs of thyrotoxicosis when the other hormone is significantly lower in blood. Euthyroid dosing of T3 and combination T4-T3 therapy may induce TSH suppression as a medication side-effect, but effect is localized to the hypothalamus and pituitary, and again, no signs of thyrotoxicosis may exist.
We should all defend each human being’s optimal T3 supply.
- The thyroid gland is a T3 shield. Defend the unshielded.
- Defend our plasma T3. Today.
- Thyroid warriors: We speak of years lost
We exist as a thyroid patient’s organization because we know, by our collective experience, that a normalized TSH does not always defend optimal T3, and T4-T3 conversion does not always happen at a rate that provides T3 sufficiency in all tissues. Our thyroid disability makes it hard to compensate for metabolic handicaps.
We give voice to that reality of suffering either T3 excess or T3 deficiency, and we point toward scientific understanding and potential ways out of it.
- Evidence-based thyroid advocacy
- Evidence-based thyroid therapy
- Thyroid science naivety and quackery: Definitions
It is an unfortunate, institutionalized lie that every person with a normal TSH (due to normal levels of local T3 signaling in the pituitary) has truly “euthyroid” T3 hormone status beyond the pituitary.
We fight for the statistical outliers, the misdiagnosed, and the symptom-plagued patient who is being told it’s all in their head, because we know it is very likely, given medical T3 ignorance, that their T3 might not be optimized to their body’s needs.
We praise and support good thyroid doctors. Fortunately, the 2012 ATA guidelines come with a disclaimer they can use in case they are threatened disciplinary action for nonconformity:
Nothing in ATA guidelines ever forbade testing FT3 or even RT3. They only strongly recommended against misusing a certain FT3 level or range as a therapy target for large categories of patients in isolation from other hormone levels and clinical signs. They should have recommended the same for the misuse of TSH in isolation, but that was their blind spot and bias.
When physicians test FT3 and develop the skill to assess it in the evidence-rich context of thyroid hormone dosing, FT4, TSH, and other signs and symptoms, physicians can free many patients from their suffering and either prevent or alleviate many other chronic diseases like heart disease, diabetes, or mental health problems.
T3 pharma is certainly not a cure-all, just as T4 pharma is not a cure-all. No thyroid therapy is perfect.
Patients do have to adjust ratios and doses if or when our hormone metabolism and thyroid gland health change. Rising estrogen levels bind more of our T4 and T3 to TBG proteins, menopause and pregnancy pose complex challenges, health problems and seasonal change can cause metabolic T3 losses. Aging, female sex, and illness can make T4-T3 conversion less efficient.
Moreover, most hypothyroid patients have an autoimmune etiology. If you’re fine on LT4 therapy today, you might not be fine 10 years from today. Autoimmune thyroid disease is progressive or fluctuating in most cases. The nastiest sort of thyroid antibodies, TSH-receptor antibodies (TRAb: blocking TBAb, and/or stimulating TSAb), can (re)emerge in response to iodine deficiency or excess and/or thyroid hormone underdose or overdose. There is no such thing as an antibody-ectomy. Antibodies do not always disappear when a thyroid is dead or gone.
- Remissions and fluctuations in autoimmune thyroid disease: TRAb
- The Spectrum of Thyroid Autoimmunity
- Research: TSAb antibody and TSH
In our thyroid patient support community, we will not blame any thyroid patient for “not trying hard enough” if they find their body can’t become optimal at a recommended FT3 and FT4 level on a recommended thyroid hormone pharmaceutical. One of our mantras is that “optimal is individual.”
All we ask is that patients, doctors, and scientists respect human diversity, diverse thyroid disabilities, diverse pharmaceutical responses, and stop being blind to FT3 levels in the context of FT4.
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
Ferretti, E., Persani, L., Jaffrain-Rea, M. L., Giambona, S., Tamburrano, G., & Beck-Peccoz, P. (1999). Evaluation of the adequacy of levothyroxine replacement therapy in patients with central hypothyroidism. The Journal of Clinical Endocrinology and Metabolism, 84(3), 924–929. https://doi.org/10.1210/jcem.84.3.5553
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
Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2019). Functional and Symptomatic Individuality in the Response to Levothyroxine Treatment. Frontiers in Endocrinology, 10. https://doi.org/10.3389/fendo.2019.00664
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., 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. https://doi.org/10.1530/EC-15-0056