A Thyroid Patients Manifesto

Thyroid-patients-manifestoManifesto: “a written statement declaring publicly the intentions, motives, or views of its issuer” (Merriam-Webster)

I humbly offer the following manifesto for us as thyroid patients.

WE, as citizens maintained by thyroid hormone therapy,

declare our equal rights to health and well being as other citizens with complex chronic health conditions like diabetes, cancers, and heart disease.

We have the right to agency and choice within our thyroid therapy. We are not just patients to be passively managed according to physician choices.

We ought to have access to patient-centered, collaborative care in partnership with doctors who truly respect all the evidence that can guide our thyroid therapy.

Respect for evidence

Respect for evidence in our therapy must go beyond our blind obedience of consensus opinions expressed in standard thyroid treatment guidelines.

Many types of evidence ought to carry influence, including our first-hand testimony of our symptoms, our thyroid laboratory test history, and scientific research not cited by guidelines.

No patient should be ridiculed or bullied for researching their own health condition and for bringing what they learn to an appointment. “Informed consent” implies we as patients have the right to obtain enough information from authoritative sources beyond our physicians in order to respectfully agree or disagree, and intelligently consent or refuse consent.

We as patients have the right to learn enough thyroid science to participate in the interpretation of our laboratory results and decision-making about treatment options.

We have a right to bring to our doctors any evidence we find in medical journals that could inform our treatment, and our doctors should show due respect for science.

Patients’ knowledge of scientific evidence may not yet be complete or accurate, and it may conflict with physicians’ medical training. But physicians’ knowledge is not always complete or accurate, and what is taught in medical school may conflict with thyroid science.

Physicians and patients ought to be in a collaborative search for truth and better health.

Pharmaceutical choice, not prejudice

We have the right to informed consent for our pharmaceutical therapy, which means being informed of both the benefits and the risks of standard T4 monotherapy.

We are the ones who must live with our body’s response to thyroid pharmaceuticals every day for the rest of our lives.

We ought to be informed that despite its convenience and success in treating many patients, T4 monotherapy may result in a significantly reduced FT3 per unit of TSH and incomplete resolution of tissue hypothyroidism in some individuals.

There is no ethical or scientific basis for thyroid hormone pharmaceutical prejudice.

All thyroid hormone preparations are capable of achieving euthyroid status, whether synthetic T4, desiccated thyroid, or any dose ratio of T4 and T3 whatsoever. (7, 8, 9)

Once our thyroid hormones reach our bloodstream, our cells cannot distinguish between thyroid hormones from a pig, a cow, a human, or hormones synthesized in a laboratory. Any thyroid pharmaceutical may all be dosed alone or in combination.

No single thyroid pharmaceutical or T4:T3 dose ratio should be expected to work well for all individuals, and some may be harmful to some patients. Each of us responds differently to thyroid therapy modalities and ratios. (5, 6)

Our doctors should not have the right to declare off-limits any pharmaceutical source of thyroid hormones in favor of their preferred therapy modality.

National thyroid associations should not have the right to imbalance the pharmaceutical marketplace by evidence-selective consensus, drive up prices for orphaned drugs, influence shortages and cut off our options. (10, 11, 12)

We ought to be free to choose among all thyroid hormone pharmaceuticals on the market when we and our insurance companies share the cost, as we often do in Canada.

There is no such thing as a thyroid pharmaceutical that is intrinsically dangerous, since T3 and T4 are naturally occurring hormones. Any thyroid medication can be underdosed or overdosed. Any thyroid pharmaceutical can have an adverse effect on an individual.

The superior thyroid pharmaceutical is the one that achieves the best health outcomes in an individual.

Respect for evidence includes respect for experience with thyroid hormone pharmaceuticals across thyroid therapy history. Human bodies have not changed, and hormone preparations have not changed very much. Short-term clinical trials of T3-T4 combination therapy since 1995 are not more authoritative than the long-term clinical track record of safe and effective treatment with desiccated thyroid. Treatment with synthetic T3 began in 1952, only three years after T4 became a thyroid pharmaceutical in 1949. Clinical knowledge and experience of effective thyroid therapy using both T3 and T4, or only T3, are articulated in older thyroid science publications.

Optimization of hormone levels

Respect for evidence includes respect for thyroid hormone data, not just TSH data. Our health care system should not overrule the mutual discernment of doctors and patients by cancelling the Free T3 and Free T4 hormone tests they wisely order. Mechanistic flowcharts and penny-pinching policies do not have the right to declare these tests “unnecessary” in all but rare cases, when many scientists have found them quite relevant to optimizing thyroid therapy. (1, 2)

We have the right to seek and achieve true euthyroid status, which ought to be defined accurately as individually-optimized Free T3 (FT3) and Free T4 (FT4) hormone levels that meet our whole body’s needs, not just normalize our TSH. (3, 4)

Our TSH does not stimulate a healthy thyroid gland, so we need manual fine tuning of doses to meet individual needs.

If our medical systems are truly evidence-based, they must acknowledge that our TSH, FT3 and FT4 behave differently in each thyroid-disabled body.

There is no TSH, FT3 or FT4 range, level or hormone ratio that is capable of rendering every treated patient optimal or euthyroid, but we ought to be able to search for our individually optimal levels.

All we seek is individual freedom from both hypothyroid and hyperthyroid symptoms, a state that our fellow citizens can achieve naturally by means of a TSH-stimulated healthy thyroid gland.

Take any 100 patients with autoimmune hypothyroidism and you will find some people who have concurrent health conditions that impair T4-T3 metabolism, some who take medications that interfere with thyroid hormone transport, metabolism or signaling, some with thyroid nodules that secrete T3 hormone and destabilize thyroid therapy, some with kidney disorders who lose T3 and T4 in urine at variable rates, and some with Graves’ disease antibodies that cause sporadic TSH suppression despite normal FT3 and FT4.

Take any 100 people with total thyroidectomies dosed with LT4 alone, and you will find that each person will have a different TSH, FT3 and FT4 configuration and a different symptomatic response to underdose or overdose.

Some people need more FT3 in blood to compensate for poor T4-T3 metabolism and no thyroidal T3 secretion, while others may not require more than low-normal FT3 because their bodies do not metabolize or clear T3 hormone very quickly.

Respect that our disability makes us different

Our biochemistry ought to be compared to the norms of our thyroid disability cohort and treatment cohort, not just by the norms and statistics of thyroid-healthy untreated populations.

Thyroid status cannot be adequately judged by healthy population statistics for TSH, FT3 or FT4 because a thyroid-disabled, hormone-dosed body supplies and metabolizes hormones differently.

Dosing is not a true thyroid gland replacement. Thyroids don’t just create new hormones, they are also metabolic engines that transform hormones. Try to find a tablet that metabolizes itself. They can’t, but a thyroid can metabolize its own hormones.

Blood carries both TSH and T4 into the thyroid, and human thyroid tissue has the highest density of D1 and D2 enzymes that convert T4 to T3 (Human Protein Atlas). Healthy thyroids metabolize hormones at a rate largely determined by TSH stimulation.

People with no thyroid function do not benefit as much from TSH in blood because very few TSH receptors are expressed on cells beyond the thyroid. TSH may influence D2 enzymes outside the thyroid, but TSH is incapable of upregulating D1 or D3 outside the thyroid gland.

Our oral absorption of T3 and/or T4 is not the same as secreting hormones from a thyroid gland, even if we’re on a T3-T4 combo that supposedly mimics a thyroid’s average secretion ratio.

We are not like you, the majority with a healthy thyroid.

Your healthy thyroid continually secretes T4 and T3 directly into blood every minute of the day, but our oral hormones arrive in daily pulses. Our oral LT4 may be poorly absorbed if we have gastrointestinal health problems. Our oral LT3 is very quickly absorbed, and then more quickly metabolized and cleared during its peak post-dose levels.

Your nightly TSH-driven circadian rise in FT3 supports many other hormones that peak at night. On T4 monotherapy without a thyroid, our FT3 is flatlined, which is just as abnormal as T3 dosing which induces large post-dose FT3 peaks and valleys.

Your healthy thyroids predictably induce a FT3:FT4 ratio of 0.32 mol/mol. Oral hormone treatment induces unnaturally low or high FT3:FT4 ratios that the TSH is not used to responding to.

As your TSH rises in normal range, it drives up thyroidal T3 secretion as T4 falls. If we lack thyroid function, our TSH in the upper part of reference range does not maintain our FT3. Our FT3 falls along with FT4, which is abnormal.

Unlike most citizens, some of us have great difficulty accessing the upper half of the Free T3 reference range while TSH is normal. (15, 16) T4 monotherapy with poor thyroid function installs a FT3 glass ceiling, which is abnormal.

Unlike most citizens, some of us can have low-normal FT3 even if our TSH is fully suppressed by standard LT4 thyroid medication. (15, 19) In what unmedicated human being can this extreme TSH-FT3 paradox and disjoint occur? It is very abnormal.

Unlike most citizens who are not dependent on thyroid hormone therapy, we can suffer chronic T3 insufficiency even while TSH is normal, without suffering a severe nonthyroidal illness. (5, 15) This is abnormal.

Unlike most citizens, we may not easily recover from nonthyroidal illness (Low T3 syndrome), a metabolic imbalance that occurs during a severe chronic or critical illness. When you raise your TSH as you recover from illness, your thyroid helps replenish your T3 levels and helps to metabolize T4 to T3, but our thyroid may not. (17, 18) We suffer an abnormal metabolic disability on top of our severe illness if we have little to no thyroid gland function.

Even when our TSH is normal, we are abnormal. We are different from you. Our thyroid disability must be accommodated by individualized therapy or we will suffer unfair health limitations. (13, 14)


Our expectations are reasonable. We expect no less than that our thyroid hormone therapy be set free from the narrow TSH-centric paradigm and pharmaceutical prejudice reflected in current guidelines.

We are disabled people whose health outcomes, symptoms, agency, intelligence, and diversity deserve respect.

We deserve to have affordable access to our body’s preferred thyroid hormone pharmaceuticals at our body’s preferred dose ratio.

We are not just like thyroid-healthy, untreated populations. Normalizing our hormone levels won’t make us all healthy, and some of us don’t have to be forced to conform to normal biochemistry in order to be healthy.

We deserve to have our doses adjusted on the basis of rich evidence: FT3 and FT4 levels, symptoms and T3-sensitive tissue biomarkers, not just TSH tests.

Some scientists join us in stating that thyroid therapy ought not to be monitored by TSH testing alone. The TSH reference interval is not the ultimate judge of adequate dosing. (24-28)

The TSH is a local tissue response. It is not omniscient and cannot speak for the entire body. It will not tell the physician when the individual’s optimal FT3 and FT4 in blood has been achieved for the liver, heart, or brain.

This TSH-centric and T4-dominant treatment paradigm has resulted in symptom-denigration, FT3-blindness, thyroid hormone pharmaceutical prejudice, and oversimplified one-size-fits-all treatment guidelines that do not fit all diversely disabled individuals.

Thyroid therapy should be based on more appropriate evidence and respect for human diversity, and focused on individual health outcomes.


  1. British Columbia Ministry of Health, & Guidelines and Protocols Advisory Committee. (2018, October 24). BCGuidelines.ca: Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder. [Flowchart p. 12.] Retrieved from https://www2.gov.bc.ca/assets/gov/health/practitioner-pro/bc-guidelines/thyroid-function-testing.pdf
  2. Choosing Wisely Canada, Gilmour, J., & Mukerji, G. (2017, August). Less is more with T3 & T4: A toolkit for reducing free thyroid hormone testing. Version 1.0. Retrieved from https://choosingwiselycanada.org/wp-content/uploads/2017/09/CWC_T3T4_Toolkit_V1.pdf
  3. 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
  4. 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
  5. 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
  6. Sawin, C. T., Hershman, J. M., & Chopra, I. J. (1977). The comparative effect of T4 and T3 on the TSH response to TRH in young adult men. The Journal of Clinical Endocrinology and Metabolism, 44(2), 273–278. https://doi.org/10.1210/jcem-44-2-273
  7. Tariq, A., Wert, Y., Cheriyath, P., & Joshi, R. (2018). Effects of Long-Term Combination LT4 and LT3 Therapy for Improving Hypothyroidism and Overall Quality of Life. Southern Medical Journal, 111(6), 363–369. https://doi.org/10.14423/SMJ.0000000000000823
  8. Kearns, J. E. (1957). Liothyronine (l -triiodothyronine) as a substitute for desiccated thyroid. Quarterly Bulletin of Northwestern University Medical School, 31(2), 97–98. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3803574/
  9. Newman, S., & Escamilla, R. F. (1958). TRIIODOTHYRONINE—Clinical Effects in Patients with Suboptimal Response to Other Thyroid Preparations. California Medicine, 88(3), 206–210. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1512399/
  10. Jackson, I. M., & Cobb, W. E. (1978). Why does anyone still use desiccated thyroid USP? The American Journal of Medicine, 64(2), 284–288. [Anti-desiccated diatribe.]
  11. McMillan, H. J., & Campbell, C. (2017). We need a “made in Canada” orphan drug framework. CMAJ, 189(41), E1274–E1275. https://doi.org/10.1503/cmaj.170195
  12. America’s Health Insurance Plans. (2016, October). Orphan Drug Utilization and Pricing Patterns (2012 – 2014). Retrieved from https://www.ahip.org/wp-content/uploads/2016/10/OrphanDrug_DataBrief_10.21.16.pdf
  13. Nexo, M. A., Watt, T., Pedersen, J., Bonnema, S. J., Hegedüs, L., Rasmussen, A. K., … Bjorner, J. B. (2014). Increased risk of long-term sickness absence, lower rate of return to work, and higher risk of unemployment and disability pensioning for thyroid patients: a Danish register-based cohort study. The Journal of Clinical Endocrinology and Metabolism, 99(9), 3184–3192. https://doi.org/10.1210/jc.2013-4468
  14. Bertoli, A., Valentini, A., Cianfarani, M. A., Gasbarra, E., Tarantino, U., & Federici, M. (2017). Low FT3: a possible marker of frailty in the elderly. Clinical Interventions in Aging, 12, 335–341. https://doi.org/10.2147/CIA.S125934
  15. 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
  16. Woeber, K. A. (2002). Levothyroxine therapy and serum free thyroxine and free triiodothyronine concentrations. Journal of Endocrinological Investigation, 25(2), 106–109. https://doi.org/10.1007/BF03343972
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  18. Feelders, R. A., Swaak, A. J. G., Romijn, J. A., Eggermont, A. M. M., Tielens, E. T., Vreugdenhill, G., … Berghout, A. (1999). Characteristics of recovery from the euthyroid sick syndrome induced by tumor necrosis factor alpha in cancer patients. Metabolism – Clinical and Experimental, 48(3), 324–329. https://doi.org/10.1016/S0026-0495(99)90080-X
  19. 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
  20. Biondi, B., & Wartofsky, L. (2014). Treatment with thyroid hormone. Endocrine Reviews, 35(3), 433. https://doi.org/doi: 10.1210/er.2013-1083
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  24. Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2013). Is pituitary TSH an adequate measure of thyroid hormone-controlled homoeostasis during thyroxine treatment? European Journal of Endocrinology, 168(2), 271–280. https://doi.org/10.1530/EJE-12-0819
  25. Wiersinga, W. M. (2014). Paradigm shifts in thyroid hormone replacement therapies for hypothyroidism. Nature Reviews Endocrinology, 10(3), 164–174. https://doi.org/10.1038/nrendo.2013.258
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  27. Toft, A. D. (2017). Thyroid hormone replacement – a counterblast to guidelines. Journal of the Royal College of Physicians of Edinburgh, 47(4), 307–309. Retrieved from http://www.rcpe.ac.uk/sites/default/files/jrcpe_47_4_toft.pdf
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