5 steps to individually-optimized thyroid therapy

Patients should not have to cross their fingers, wait, and hope for change.

The hopes of hypo- and hyperthyroid patients focus on attaining individually-optimized treatment.

Their hopes, wishes, and requests are not unreasonable. Effective treatment ought to alleviate symptoms and improve health outcomes. Relative changes in thyroid hormone doses have a measurable effect on certain symptoms and biomarkers.

However, standard thyroid treatment guidelines do not yet prioritize individually-optimized treatment. Instead, they consistently target “the clinical goal of normalization” of biochemistry (Ross et al, 2016, American Thyroid Association guidelines for the treatment of hyperthyroidism). Normalization means that a previously hypothyroid or hyperthyroid patient’s TSH, Free T4 (FT4), Free T3 (T3) and/or total T3 levels fall within the 95% reference interval of a healthy, untreated population.

Adjusting the treatment of thyroid diseases by the standard method of merely normalizing TSH, FT3, and/or FT4 will abandon an unknown percentage of thyroid-disabled individuals far from the optimal hormone levels and ratios that their bodies require. This results in diminished quality of life, broken families, reduced economic productivity, and poor health.

What happens when the patient’s body doesn’t respond to the treatment guidelines? Blame games.

Current guidelines defend their targets instead of questioning their legitimacy. They blame the patient’s other health conditions, blame the patient for imagining their symptoms, or blame the patient for making “inappropriate demands” (See the American Thyroid Association guidelines for the treatment of hypothyroidism, Jonklaas et al, 2014, section 9b, 5c, 11).

Thyroid therapy failure drives a growing alternative healthcare industry. This industry caters to many patients who are square pegs that don’t fit into conventional round holes.

However, some alternative medicine thyroid treatment protocols have also fallen into the error of failing to individualize therapy.

Instead of adopting the reference intervals as targets, some practitioners have declared narrow “optimal” ranges within the reference ranges of TSH, FT4 and FT3. Some even recommend a low-normal “optimal” Reverse T3 (RT3) range, which could be very hard to achieve in a patient with a severe chronic nonthyroidal illness.

Desperate, suffering patients whose standard therapy has failed will pay a lot of money to have their thyroid hormones optimized by a paint-by-number protocol. Their maladaptive treatment may make them too brain-fogged to think critically about the shortcomings of this protocol. It promises success, and the practitioner is offering to help them (for a fee), unlike the conventional physician. It appears that many patients have “gotten optimal” by this alternative method, because their testimonies are inspiring.

What is the basis of their claims that these are the “optimal” ranges for everyone, or even “most” people? Usually they claim the authority of collective patient experience or practitioners’ clinical wisdom. They offer no published trials with methods, data or percentages. It is very suspicious that these narrower, yet equally rigid, thyroid therapy targets fit neither the population medians of TSH, FT4 and FT3 in the untreated, healthy population, nor the FT3:FT4 ratios in many healthy, symptom-free patients on standard LT4 treatment.

But again, what happens to the patients who can’t place their hormone levels in all these narrow alternative “optimal” ranges? What happens to the patients whose stars are aligned but who fail to achieve symptom relief or improve overall health?

Alas, the same thing happens in both conventional and alternative medicine: Blame. The prescribers defend their protocol and pass the buck. Patients are told that their cortisol levels are off, or their iron is low, or that they have too much “stress” in their lives, or the patient didn’t follow the protocol correctly.

Such patients have been abandoned by both the conventional and alternative thyroid care systems.

Neither of these two systems attempt to discover and meet their physiological needs.

These one-size-fits-all biochemical targets of thyroid care have serious consequences not only for health, but also for health care expenditures.

I’ll begin with my own example to illustrate.

I’ll then summarize the scientific and ethical shortcomings of the “normalization paradigm.”

Finally, I’ll explain in more detail the 5-step path to optimize the treatment of thyroid dysfunction by adjusting the treatment to the patient.

Summary of the 5-step path:

  1. Prioritize the primary goals or “clinical endpoints” of therapy (symptom relief and health outcomes)
  2. Measure and analyze at least the three basic hormones (TSH, FT3, FT4)
  3. Engage in continuous professional development in thyroid disease and treatment.
  4. Engage in 2-way dialogue with thyroid patients.
  5. Encourage competent, highly-engaged patients to participate in their care between appointments.

My own example

I believed I was a simple, easy case of severe primary autoimmune hypothyroidism, with a TSH over 150 mU/L at diagnosis. But 10 years after my hypothyroid diagnosis and treatment with LT4 began, my TSH-FT4 relationship went haywire. Normally, the TSH rises as the FT4 falls and vice versa, but mine did not do that, often fluctuating above range when FT4 was high-normal.

I also had an abnormally low FT3:FT4 ratio of 0.15 pmol/L repeatedly, test after test, while 0.31-0.33 is the mean in healthy populations. So, when my dose was reduced to re-normalize a mildly low TSH, my FT3 fell low, and it remained low.

Since I had never had a thyroid ultrasound, we did not know yet that my thyroid gland had completely atrophied (0.5 mL volume), which would have helped to explain my low FT3. In a study of 1,811 thyroidless individuals on standard LT4 therapy with a normalized TSH, 29.6% had FT3:FT4 ratios below reference range, and twice as many females than males had low FT3 (Gullo et al, 2011).

After three years of low FT3, when my FT4 was high-normal, a dose increase was given to address hypothyroid symptoms and my high TSH. My physician did not realize how bizarre my hormone profile was. The dose increase immediately induced random day and night chest pain which were followed by a numb arm or leg or lightheadedness. Despite reducing the dose, the body-jolting chest pains continued. Five days later, I visited hospital emergency. I visited emergency two more times in a period of three months. Many conventional tests were ordered and came back normal. I learned that my chest pain didn’t fit their cardiovascular paradigms, either. All the physicians were flummoxed, including an endocrinologist.

I did my own research in the scientific literature, which associated cardiovascular risk with low T3 levels like mine. I eventually found a physician willing to treat my T3 deficiency with LT3 (liothyronine) hormone, and my symptoms noticeably reduced after the first 5- microgram dose. As my T4 dose was reduced and my LT3 dose was increased, this disabling symptom faded and disappeared. My cholesterol levels, a well-known thyroid biomarker, fell from high to low, indicating reduced cardiovascular health risk. Since 2016 I remain healthy on LT3 therapy.

The standard thyroid treatment paradigm didn’t work for me. My treatment failure cost me and my healthcare system a lot of extra time and money.

How many physicians don’t know they are supervising a complex case because they don’t know how to interpret their treated thyroid patients’ abnormal TSH-FT3-FT4 relationships, or FT3 is never checked?

This was the unexpected treatment failure that drove me to study thyroid scientific literature to learn what most physicians don’t know. I learned how unusual I was in terms of my shriveled thyroid (completely atrophied by age 46). My condition, atrophic thyroiditis, is genetically different from Hashimoto’s, the most common autoimmune thyroid disease.

Motivated by my experience, my desire to help and educate others, and my enjoyment of biology, I have devoted a lot of my “free time” to studying thyroid scientific literature while working full-time as a university research professor in communications studies. To date, I have annotated more than 9,000 thyroid scientific journal articles (about 4 per day). I am also developing our thyroid patient-led nonprofit organization, which aims to educate patients and physicians and advocate for change using science, ethics and reason.

As a result, I have gained many insights into the barriers in the way of effective thyroid treatment, as well as the pathways by which patients, physicians and healthcare systems can overcome those barriers.

The scientific and ethical shortcomings of the normalization paradigm

The paradigm of normalization involves adjusting a disabled individual’s biochemistry so that it falls anywhere within the broad parameters of the healthy, non-disabled population. This biochemical state is then labeled “euthyroid.”

Physiology has far more precise and individualized targets than the population range. Outside the context of thyroid therapy, euthyroid status is not predetermined by 95% population intervals. Over many weeks and months, a healthy person’s TSH, Free T4 (FT3) and Free T4 (FT4) do not vary outside a narrow band of values 10-30% of the width of their population reference interval (Ankrah-Tetteh et al, 2008; Anderson et al, 2003, see review).

As a result of nature’s precise, individualized adjustment of hormones, the descriptive range of the population is a statistical composite image, like a group photograph. The features of the group photograph are not the same as the features of any individual within it. To fully describe the features of any individual, you require a series of portrait photographs of an individual over time to see how much they vary in response to changing environments.

Two additional problems get in the way of making a normalization protocol effective for all thyroid-disabled individuals.

  • Like a computer’s hardware, the underlying physiology or of a hypo- or hyperthyroid individual is characterized by a disability, a transformation or loss of a vital organ’s function, which will continue to distort the trio of TSH-FT3-FT4 hormone relationships in different ways even while undergoing therapy.
  • Like a software program, the pharmaceuticals used to treat thyroid diseases add another level of distortion. They can never perfectly replace the adjustable T4/T3 secretion ratios of a healthy TSH-stimulated thyroid gland. Depending on how the pharmaceuticals are used, they may be therapeutic or maladaptive.

As the two distortions combine in a treated thyroid patient, they are like two different stones being thrown into a pool. The ripples do not cancel each other out to restore normal TSH-FT3-FT4 interrelationships. Even if a physician normalizes all three of these hormones within their respective reference ranges, the hormone relationships and ratios can be extremely different from those of the healthy, untreated population (Gullo et al, 2011). As in the nursery rhyme, you can’t put Humpty Dumpty back together again.

Fortunately, if the abnormal hormone relationships are optimized to meet the disabled individual’s demands, an abnormality may be therapeutic for the patient.

Unfortunately, when the abnormal hormone relationships are maladaptive for the individual, the mere statistical normality of each hormone in isolation cannot induce or defend health.

The normalization paradigm’s errors results in distorted expectations during treatment. A biochemical description of a healthy population can’t function as a prescription for a disabled individual. This paradigm treats conformity to non-disabled statistical norms of biochemistry as if it had these powers over health:

  • a sufficient condition for health (“It’s statistically normal, so it will induce health”) and
  • a necessary prerequisite for health (“if you’re not in this range, you will never be healthy or safe”)

In contrast to the adherents of the normalization paradigm, those who promote individually optimized therapy believe in compensating for a disability to achieve optimal health outcomes for the individual. They understand that:

  • Statistical normality is a convenient starting place, but it is never precise enough to be a sufficient condition for health in any individual.
  • The borders of each isolated hormone’s 95% statistical reference range do not behave as physiologically meaningful risk thresholds for any individual in a healthy population, and they are even less applicable as risk thresholds for a disabled individual with distorted hormone relationships.

The final scientific flaw of the normalization paradigm one should consider is that biology permits at least four ways to define thyroid status, and hormone biochemistry is only one of them.

Now, let’s look at the problems with medical ethics that flow from scientific misunderstanding.

Just as sexism, ageism, and racism applies stereotypes and value to people by their sex, age, and ethnicity, forcing a disabled person to behave and look like a non-disabled person constitutes the prejudice we call “ableism.”

People who promote individualized optimization recognize and accommodate the biochemical abnormalities caused by a disability and its treatment. They are more ethical than people who refuse to acknowledge and accommodate disabilities.

Unfortunately, thyroid care has fallen into an unethical zone of adjusting treatment to avoid statistically calculated health risk based on population research. A healthcare provider does not play the role of a risk-averse health insurance provider. The healthcare provider must weigh benefit and risk for each individual case.

Imagine a health practitioner says this to a person with an injured or missing leg:

  • “To gain full access to health and safety, you must learn to use only two legs to walk, or one leg and one cane, instead of one leg and two crutches, and certainly do not ever use a wheelchair, because that’s statistically associated with significant health risk!”

How is that any less unethical or unreasonable than saying this to a person with a dysfunctional or missing thyroid? —

  • “To gain full access to health and safety, your TSH must fit within this statistical range. Therefore, you must submit to medically-induced TSH normalization, even though I can see that in your body, forcing your TSH to rise into the normal range forces your FT3 to fall low-normal, you become depressed, and your kidney function declines!”

People who understand a disability are not blind to the risks of treatment. They know that treatment-induced distortions away from thyroid-healthy normality may be either pathological or therapeutic to the disabled individual. But risk-benefit analyses must consider the individual’s actual response to treatment adjustments.

“Giving an individual improved function and quality of life and overall improved health today and for the forseeable future is far more important than preventing them from falling into a biochemical category that is statistically associated with a higher risk of osteoporosis and cardiovascular disease.”

Tania S. Smith, President, Thyroid Patients Canada

As a result, an ethical, scientific approach to thyroid treatment refuses to define euthyroidism (health) and risk narrowly, rigidly, or prejudicially, by isolated TSH, FT4 or FT3 levels that fall within the statistical norms of a non-thyroid-disabled population.

The five steps

Here are the five steps almost any physician can take to discover an individual’s optimal thyroid treatment.

If they seem too obvious or elementary, it is because they are consistent with “best practices” in medicine and the tenets of patient-centered care. Patients perceive that thyroid healthcare has fallen short of these best practices, but many practitioners are unaware that they have fallen short because they are conscious of following thyroid treatment guidelines.

How to apply them:

  • They are not a one-time procedure that is performed once and then you’re done. They are meant to be built into ongoing practice.
  • They are arranged in priority order. It is hard to imagine any practitioner performing steps 3, 4 and 5 without first re-orienting their priorities in step 1, and then gathering enough basic data to analyze in step 2.
  • Steps 3, 4, and 5 are long-term learning journeys. Those who already do steps 1 and 2 by habit will be continually challenged or inspired by the final three steps.
  • The final two steps involve a physician empowering their patients to assist themselves in providing effective thyroid care. If a physician cannot accommodate their competent patients’ involvement, the quality of care will suffer.

1. Prioritize the primary goals or “clinical endpoints” of therapy.

For the treatment of thyroid dysfunction, the primary clinical endpoints are symptom relief and improved health outcomes (Jonklaas et al, 2014, section 1b).

The term “clinical endpoints” is defined by many government agencies like the US FDA in contrast with “surrogate endpoints” like TSH normalization which stand in for, but cannot replace clinical endpoints. (Strimbu & Tavel, 2010). Clinical endpoints can be felt and perceived by the patient. Thyroid healthcare should prioritize the challenging clinical endpoints of thyroid treatment over the easier “surrogate endpoints” of mere biochemical normalization and risk-avoidance.

The dismissive medical attitude toward thyroid symptoms needs to change. No matter how “nonspecific” our thyroid symptoms are, they belong to our disease just as much as they belong to other more deadly, costly diseases. Let’s stop passing the buck. Poorly optimized thyroid therapy, even within the normal TSH range, is making other diseases worse — diabetes, cardiovascular disease, dementia, and so on.

These goals are not always perfectly achievable, but they ought to be a priority. Progress toward these goals should be more achievable when the remaining 4 steps are occurring.

2. Measure and analyze at least the three basic hormones.

The basic trio of tests is TSH, Free T3* (FT3) and Free T4 (FT4). Leading thyroid scientists now admit that “TSH should not be used as a single marker of thyroid function” (Sheikh et al, 2018), and that a large-scale review has found “Clinical parameters are more likely to be associated with thyroid hormone levels than with thyrotropin [TSH] levels” (Fitzgerald et al, 2020).

Barriers exist to prevent overtesting, but every healthcare system should permit physicians to order a basic set of thyroid tests in a treated thyroid patient, even when TSH is normal. Thyroid patients are a small minority of the population. These tests are cheap, easy, and should be available in every lab.

This trio enables a physician to assess not just whether each is low, normal, or high, but to assess the normality of their relationships and changes over time as doses are maintained or changed. You may wish to calculate the FT3:FT4 ratio to assess the presence of nonthyroidal illnesses and/or metabolic efficiency (Midgley et al, 2015, see our guide). Be vigilant about the health risks of low FT3 and low FT3:FT4 ratios (Hong et al, 2022; Lang et al, 2022). Look for unusually low or high TSH secretion in relation to thyroid hormones, which point to pituitary-level interference.

  • * Note: Some health care regions replace FT3 with total T3 (TT3), but there is no reason to avoid FT3 testing now that FT3 immunoassays are equal in precision to FT4 assays and just as cheap. Total T3 does not measure the free hormone available to enter cells. Many common health factors such as estrogen, albumin, and blood thinners can influence the percentage of T3 and T4 that is bound vs. free to enter cells. One cannot make a FT3:FT4 ratio if both free hormones are not measured. Nevertheless, if one suspects that abnormal binding proteins are influencing treatment, it is useful to gain insight into binding proteins by measuring both FT3 and TT3 at the same blood draw and noticing any distortions in their relative positions within or below the reference interval.

3. Engage in continuous professional development in thyroid disease and treatment.

This will make you a better physician to all your patients. Discover how T3 and T4 thyroid hormone levels interact with common non-thyroidal disorders including gastrointestinal disorders, cancers, kidney diseases, and so on. Find out how thyroid disorders and circulating T3 levels correlate with complete blood counts, electrolytes, cholesterol, and nutritional deficiencies.

Here are a few tips for as-needed, self-directed learning by searching online:

  1. In Google, add “ncbi” as a keyword to prioritize search results from the PubMed database and those that cite articles from that database.
  2. Narrow down searches and find authoritative sources by using technical keywords for things of interest, like “FT3” or “triiodothyronine” instead of just “T3.”
  3. Interpret a study’s results and clinical relevance by its methods, i.e. “Did this study exclude anyone with a thyroid disorder and anyone on thyroid treatment?” It may still be very informative, but be cautious.
  4. Search for the product monograph or drug information required by your regulatory body to understand a thyroid pharmaceutical’s basic, well-known properties and interactions. For example, in Canada, I would search for Cytomel product monograph to find the PDF and then search within it (Ctrl+F) by keywords like “niacin,” “aspirin,” “statins,” “corticosteroids,” or “insulin.”

For advanced thyroid practitioners only: Learn how the three deiodinase enzymes (D1, D2, D3) work in complex synergy to metabolize thyroid hormones. Each enzyme in each tissue type responds differently to changes in FT3 and FT4 hormone levels and ratios within, and slightly outside of, the reference ranges. A growing understanding will assist in interpreting the relationships between thyroid hormone levels, a patient’s symptoms, and health outcomes.

4. Engage in 2-way dialogue with thyroid patients.

Physicians should be humble and willing to learn from patients and from trial and error and feedback. In response to dose changes, each patient has a different threshold for thyroid symptoms and tissue-specific signs. During long-term treatment, patients become experts at observing their body’s unique responses to treatment adjustments. Small-scale treatment mistakes and adjustments are opportunities to learn.

Relative changes in symptoms are not strongly correlated with changes in TSH, but with changes in thyroid hormones (Meier et al, 2003; Hoermann et al, 2019). Symptoms respond to thyroid hormone levels and ratios because cells and tissues respond to a given FT3 level in the context of the concurrent FT4 supply and intracellular T4-T3 and T3-T2 conversion rates. Symptoms can sometimes behave paradoxically (hypothyroid symptoms after increasing a dose) because of cellular-level and tissue-specific positive and negative feedback on metabolism.

5. Encourage competent, highly-engaged patients to participate in their care between appointments.

Some patients may be willing to track thyroid-relevant signs (temperature, heart rate, blood pressure, sleep, activity), use wearable monitoring devices, and bring their data to appointments. Some may wish to safely perform small experiments with dose timing or nutritional support and report their findings. Valuing and discussing patient-collected data builds mutual trust and cooperation. Troublesome symptoms can be decoded by data that may point to their causes.

Optimization of thyroid therapy is a process of discovery.
Which thyroid pharmaceuticals at which ratios and doses will achieve the FT3 and FT4 levels and FT3:FT4 ratios in blood that meet the individual body’s demands?

Clinical outcomes should be at the heart of any treatment. Optimal treatment minimizes thyroid symptoms and achieves the best health outcomes and the best quality of life possible.”

– Tania S. Smith, President, Thyroid Patients Canada

Contrast these five steps with the approach recommended by thyroid treatment guidelines:

Treatment guidelines tend to pay lip service to clinical endpoints and then promptly replace them with idolizing TSH normalization by means of the recommended pharmaceutical agent(s), and preventing health risk.

Guidelines will minimize step 2 not only to cut lab testing costs, but because most physicians lack the knowledge and skill to interpret the clinical significance of TSH, FT3, and FT4 relationships.

Guidelines tend to expect little to nothing at all from a physician’s practice of steps 3, 4, or 5 because they have such confidence that their instructions and normalization targets will make them unnecessary. They know physicians are pleased with quick and easy success.

Guideline writers might laugh derisively at steps 4 or 5 since they portray the patient as either happily ignorant and as compliant as a lab rat, or as demanding, naive, somatizing misinterpreters of their own symptoms. For instance, they make claims that undermine patient discernment, like “patients are unable to detect differences in the symptoms associated with hypothyroidism,” which was not in fact proven by the single source they cited to support their claim (Jonklaas et al, 2014, section 1a). Section 11 of the 2014 treatment guidelines for hypothyroidism contains a rationalization for divesting patients of agency through a paternalistic medical model.

Applying these 5 steps will improve thyroid healthcare.

Patients should not have to cross their fingers, wait, and hope for change.

Individualized treatment is needed for all patients, and especially for people like me, who are not just a simple, easy case to treat.

For physicians, discovering that the “evidence-based guidelines” that promise success are flawed can be disillusioning. Finding a better way forward can be inspiring and empowering. Consider how many abandoned patients will flock to your care and finally achieve relief and improvements to their health!

The five steps are feasible and flexible. They can accommodate beginners and advanced-level clinicians. As a practitioner attempts them repeatedly, they build their thyroid treatment skills and knowledge. They can become healthy, efficient habits. They can also accommodate all types of thyroid patients, no matter what their condition is.

Neglecting the five steps perpetuates a medical status quo that is harmful to vulnerable thyroid patients, but which keeps physicians and healthcare systems blind to the harms they may inflict.

The current system is not truly simple or cheap, it’s dysfunctional. The mismatch between this approach and the patient’s disability results in hidden expenditures. The large-scale indirect healthcare costs of thyroid therapy failures, and the numbers of frustrated patients who seek alternative thyroid care, will be unknown until researchers conduct longitudinal studies that reveal them.

The normalization paradigm is unscientific, unreasonable, and unethical in the demands it places on disabled, dosing individuals to achieve health anywhere within, and only within, the statistical norms of the non-disabled population.

Few people are aware of the scientific and ethical weaknesses of the biochemical normalization paradigm. Most people take it for granted. It’s useful to interrogate the normalization paradigm to reveal its shortcomings:

  • Why should everyone expect quick and easy success by the protocol of biochemical normalization?
  • Why should a physician expect every thyroid-disabled and treated human body to respond to treatments according to the “average” results in research studies?
  • Why should anyone expect physicians and guideline-writers to know in advance exactly what hormone levels and ratios a disabled individual needs?
  • Why should we expect that normalizing isolated hormone levels will induce health or prevent risk when disease and dosing transform the hormone ratios and relationships of thyroid biochemistry?

When reading thyroid treatment guidelines, keep these questions in the back of your mind.

And finally, a physician can’t succeed without observing the health outcomes of their own dose adjustments. Individually-optimized thyroid treatment enables patients and physicians to work together. Let us help our physicians succeed by trial and error. Let’s all be forgiving of well-intended treatment adjustment errors and learn from them. Let us help our physicians alleviate our symptoms. Give us a role in making our treatment effective.


Click to view reference list.

Andersen, S., Bruun, N. H., Pedersen, K. M., & Laurberg, P. (2003). Biologic Variation is Important for Interpretation of Thyroid Function Tests. Thyroid, 13(11), 1069–1078. https://doi.org/10.1089/105072503770867237

Ankrah-Tetteh, T., Wijeratne, S., & Swaminathan, R. (2008). Intraindividual variation in serum thyroid hormones, parathyroid hormone and insulin-like growth factor-1. Annals of Clinical Biochemistry, 45(Pt 2), 167–169. https://doi.org/10.1258/acb.2007.007103

Fitzgerald, S. P., Bean, N. G., Falhammar, H., & Tuke, J. (2020). Clinical Parameters Are More Likely to Be Associated with Thyroid Hormone Levels than with Thyrotropin Levels: A Systematic Review and Meta-Analysis. Thyroid: Official Journal of the American Thyroid Association, 30(12), 1695–1709. https://doi.org/10.1089/thy.2019.0535

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). https://doi.org/10.1371/journal.pone.0022552

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

Hong, J., Liu, W.-Y., Hu, X., Chen, W.-W., Jiang, F.-F., Xu, Z.-R., Shen, F.-X., & Zhu, H. (2022). Free Triiodothyronine and Free Triiodothyronine to Free Thyroxine Ratio Predict All-Cause Mortality in Patients with Diabetic Foot Ulcers. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 15, 467–476. https://doi.org/10.2147/DMSO.S354754

Jonklaas, J., Bianco, A. C., Bauer, A. J., Burman, K. D., Cappola, A. R., Celi, F. S., Cooper, D. S., Kim, B. W., Peeters, R. P., Rosenthal, M. 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. https://doi.org/10.1089/thy.2014.0028

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

Lang, X., Li, Y., Zhang, D., Zhang, Y., Wu, N., & Zhang, Y. (2022). FT3/FT4 ratio is correlated with all-cause mortality, cardiovascular mortality, and cardiovascular disease risk: NHANES 2007-2012. Frontiers in Endocrinology, 13. https://www.frontiersin.org/articles/10.3389/fendo.2022.964822

Meier, C., Trittibach, P., Guglielmetti, M., Staub, J.-J., & Müller, B. (2003). Serum thyroid stimulating hormone in assessment of severity of tissue hypothyroidism in patients with overt primary thyroid failure: Cross sectional survey. BMJ, 326(7384), 311–312. https://doi.org/10.1136/bmj.326.7384.311

Sheikh, S. I., Parikh, T. P., Kushchayeva, Y., Stolze, B., Masika, L. S., Ozarda, Y., Jonklaas, J., Nigussie, G., Remaley, A. T., Sampson, M., Sun, Q., Ling, C., & Soldin, S. (2018). TSH Should not be used as a Single Marker of Thyroid Function. Annals of Thyroid Research, 4. https://doi.org/10.26420/annalsthyroidres.2018.1038

Strimbu, K., & Tavel, J. A. (2010). What are Biomarkers? Current Opinion in HIV and AIDS, 5(6), 463–466. https://doi.org/10.1097/COH.0b013e32833ed177

5 thoughts on “5 steps to individually-optimized thyroid therapy

  1. Hi Tania , I totally agree about the massive waste of healthcare resources as a direct result of lack of GP knowledge. (not to mention the loss of patient earnings/ taxes)
    I’m in UK . To investigate my symptoms 2 doctors and a nurse referred me to secondary care (hospital consultant) for:
    1) a kidney Ultrasound.
    2) an Endoscopy, and Colonoscopy.
    3) a CT scan with contrast. (all were fine)
    The actual problem was spotted by an elderly semi-retired GP who in a 10 minute appointment:
    1) examined me properly.
    2) listened to what i said in answer to her questions,.
    3) asked me to hold my hands out.
    Slight overmedication with Levo was her very experienced guess… reduction of 25mcg …. ‘et viola’ …… multiple problems with overactive bladder / nasty kidney area pain / massive startle reflex / clumsyness./ exhausution / unexplained weight loss/, and generally feeling awful ….. all went away.
    Cost of 1) 2) and 3) ?? …. i dread to think .
    Fortunately for me the NHS paid for them all … unfortunately for the country, the NHS is currently falling to bits….. anybody see a connection ?

    1. Thanks for sharing that story, imbogle! That reduction of 25 mcg levothyroxine made a huge difference!! Thyroid hormones can affect so many organs and tissues.

      1. Hi Tania
        I feel there s a strong link to autoimmune with Thyroid and endocrine thoughts? And two my organs are being affected now been on thyroid meds for 42 yrs has there been studies on long term effects ? Very good article by the way !!

  2. Hi
    I would like to have a thorough blood test to find out if I have a thyroid problem.
    It’s 23 in my home and I feel cold My fingers and feet feel cold. I have to add an extra sweater and when I’m sitting down I wrap myself in a blanket. This is not normal. I don’t have a GP. I heard that tests to detect if a person has a thyroid problem are not good. Often it will show normal but it’s not. Thank you

    1. Hi Suzanne, sorry to hear about your cold temp. It sounds like you may need to go to a walk in clinic and bring a list of symptoms you’re concerned about, if you don’t have a GP. At this time, our group only offers 1-1 peer-based patient support in our private Facebook group; click on “Groups” in our main menu.

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