Shame on the UK for torturing thyroid patients who need T3

The UK is torturing its most vulnerable hypothyroid patients who need T3 in therapy. The medical profession is throwing away more than a century of safe, effective clinical use of T3 all over the globe. Nobody is caring enough to take the time to read the recent scientific research on the importance of maintaining upper-mid range Free T3 levels. (See references below)

Forget the past 120 years of therapy

The T3 price hikes are creating roadblocks, medical mazes, reams of paperwork and specialist visits. After fighting tooth and nail, a fatigued hypo patient might, just might, be permitted to access T3 meds.


Regional Medicines Optimisation Committee. (2018, November). Guidance – Prescribing of Liothyronine. National Health Service, UK. Retrieved from


From November 2018 guidance document on prescribing T3 (Liothyronine): “Advise CCGs that prescribers in primary care should not initiate liothyronine [T3] for any new patient”

“Patients currently prescribed liothyronine, or levothyroxine and liothyronine combination therapy, for hypothyroidism should be reviewed to initiate switching to levothyroxine monotherapy where clinically appropriate.”

[Note the phrase “Where clinically appropriate” over & over — left undefined, left up to medical opinion & whim —]

“The consultant endocrinologist must specifically define the reason if any patient currently taking liothyronine should not undergo a trial titration to levothyroxine monotherapy, and this must be communicated to the General Practitioner.”

“In very rare situations where patients experience continuing symptoms with levothyroxine (that have a material impact upon normal day to day function), and other potential causes have been investigated and eliminated, a 3 month trial with additional liothyronine may occasionally be appropriate. This is only to be initiated by a consultant NHS endocrinologist. Following this trial the consultant NHS endocrinologist will advise on the need for
ongoing liothyronine.”

“All patients currently receiving liothyronine for a psychiatric indication should be reviewed by a consultant NHS psychiatrist, who should consider switching to an alternative treatment or levothyroxine monotherapy where clinically appropriate. Patients continuing to receive ongoing liothyronine in such circumstances should be overseen by a consultant NHS psychiatrist.”

“Use of unlicensed thyroid extracts (e.g. Armour thyroid, ERFA Thyroid), plus compounded thyroid hormones, iodine containing preparations, dietary supplementation: The prescribing of unlicensed liothyronine and thyroid extract products is not supported. ”


The saddest thing out of all this is that the Guidance document is in many ways a step forward from the chaos and disorder that caused a “postcode lottery” for T3 therapy in 2017 and 2018. However, sadly, many departments / units within the NHS are now refusing to follow this guidance, demanding first the money to pay for it.

As for the phrase “when clinically appropriate” —

It is difficult for medical opinion to be objectively based on careful T3-based scientific research on T3 therapy up to and including 2018 that provides the most convincing basis for T3 therapy. Are the specialists getting a stipend and 2 week holiday to read up on the research?

How are even endocrinologists open-minded enough to pursue a very thorough investigation of patient history and presentation — considering their profession’s history since the 1980s speaks of professional protectionism? Almost every endocrinologist appears to feel compelled to pay homage to the T4 monotherapy monopoly and prove that they engage in due TSH worship, and they may risk career shaming for saying that a patient with “normal” FT3 levels (but bottom of range) requires T3.

Plus, all the doctors are placed UNDER DURESS, pressured by penny-pinching administrators who are breathing down their necks to stop prescribing T3 for monetary reasons.

Essentially, nobody will want to go through this, the easiest route for the DOCTORS to avoid all the stress, letter-writing, careers at stake, and overall hassle — is simply to FORBID access to, and take T3 away from, as many patients as possible.

Taking T3 from patients with hypoT3ism is like stealing insulin from Type 1 diabetics.

I don’t think the vast majority of doctors, even endocrinologists, understand how to diagnose poor T4-T3 conversion and true T3 deficiency that can be debilitating even in the lower half of the Free T3 reference range. If you can’t convert T4 well enough to raise FT3 close to 5.0 pmol/L, you are still hypothyroid, even if all numbers are in reference range.

AND it is absolutely shocking that cheaper, safe & effective desiccated thyroid meds are forbidden to prescribe!

UK thyroid patients, maybe you need to make a secret deal with pork, sheep or beef industry to get the thyroid glands from the slaughterhouse and fry up a slice for breakfast — just like the doctors ordered in the 1890s.

Or is that forbidden too? You can eat liver and heart and kidney but no, never pig thyroid bits?

Selected bibliography

Diagnostic tools for thyroid therapy

Dietrich, J. W., Landgrafe-Mende, G., Wiora, E., Chatzitomaris, A., Klein, H. H., Midgley, J. E. M., & Hoermann, R. (2016). Calculated Parameters of Thyroid Homeostasis: Emerging Tools for Differential Diagnosis and Clinical Research. Frontiers in Endocrinology, 7.

Dietrich, J. W. (2015). SPINA: Structure parameter inference approach for endocrine feedback control (Version 4.0). Free computer software. Retrieved from

Biological Importance of T3, health effects of suboptimal FT3

Abdalla, S. M., & Bianco, A. C. (2014). Defending plasma T3 is a biological priority. Clinical Endocrinology, 81(5), 633–641.

Mancini, A., Di Segni, C., Raimondo, S., Olivieri, G., Silvestrini, A., Meucci, E., & Currò, D. (2016). Thyroid Hormones, Oxidative Stress, and Inflammation. Mediators of Inflammation, 2016.

Dietrich, J. W., Midgley, J. E. M., & Hoermann, R. (2018). Editorial: “Homeostasis and Allostasis of Thyroid Function.” Frontiers in Endocrinology, 9.

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, 126(09), 546–552.

Weaknesses of T4 monotherapy

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.

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).

Verburg, F. A., Smit, J. W. A., Grelle, I., Visser, T. J., Peeters, R. P., & Reiners, C. (2012). Changes within the thyroid axis after long-term TSH-suppressive levothyroxine therapy. Clinical Endocrinology, 76, 577–581.

Liewendahl, K., Helenius, T., Lamberg, B. A., Mähönen, H., & Wägar, G. (1987). Free thyroxine, free triiodothyronine, and thyrotropin concentrations in hypothyroid and thyroid carcinoma patients receiving thyroxine therapy. Acta Endocrinologica, 116(3), 418–424.

Sjoberg, S., Eriksson, M., Werner, S., & Bjellerup, P. (2011). L-thyroxine treatment in primary hypothyroidism does not increase the content of free triiodothyronine in cerebrospinal fluid: A pilot study. Scandinavian Journal of Clinical and Laboratory Investigation, 71(1), 63.

Mallipedhi, A., Vali, H., & Okosieme, O. (2011). Myxedema coma in a [L-T4-treated] patient with subclinical hypothyroidism. Thyroid: Official Journal of the American Thyroid Association, 21(1), 87–89.

Biases and weaknesses in T4-T3 clinical trials

Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2018). Lessons from Randomised Clinical Trials for Triiodothyronine Treatment of Hypothyroidism: Have They Achieved Their Objectives? Journal of Thyroid Research, Article ID 3239197.

Recent positive T4-T3 clinical trials

Carlé, A., Faber, J., Steffensen, R., Laurberg, P., & Nygaard, B. (2017). Hypothyroid Patients Encoding Combined MCT10 and DIO2 Gene Polymorphisms May Prefer L-T3 + L-T4 Combination Treatment – Data Using a Blind, Randomized, Clinical Study. European Thyroid Journal, 6(3), 143–151.

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.

HPT axis shifts in disease and thyroid therapy, TSH not indicative

Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2017). Recent advances in thyroid hormone regulation: Toward a new paradigm for optimal diagnosis and treatment. Frontiers in Endocrinology, 8.

Hoermann, R., Midgley, J. E. M., Dietrich, J. W., & Larisch, R. (2017). Dual control of pituitary thyroid stimulating hormone secretion by thyroxine and triiodothyronine in athyreotic patients. Therapeutic Advances in Endocrinology and Metabolism, 8(6), 83–95.

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.

Chatzitomaris, A., Hoermann, R., Midgley, J. E., Hering, S., Urban, A., Dietrich, B., … Dietrich, J. W. (2017). Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming. Frontiers in Endocrinology, 8.

Strich, D., Karavani, G., Edri, S., & Gillis, D. (2016). TSH enhancement of FT4 to FT3 conversion is age dependent. European Journal of Endocrinology, 175(1), 49–54.

Ito, M., Miyauchi, A., Morita, S., Kudo, T., Nishihara, E., Kihara, M., … Amino, N. (2012). TSH-suppressive doses of levothyroxine are required to achieve preoperative native serum triiodothyronine levels in patients who have undergone total thyroidectomy. European Journal of Endocrinology, 167, 373–378. 10.1530/EJE-11-1029

Sesmilo, G., Simó, O., Choque, L., & Casamitjana, R. (2011). Serum free triiodothyronine (T3) to free thyroxine (T4) ratio in treated central hypothyroidism compared with primary hypothyroidism and euthyroidism. Endocrinología y Nutrición (English Edition), 58(1), 9–15.

Peripheral thyroid hormone conversion: Deiodinases

Little, A. G. (2016). A review of the peripheral levels of regulation by thyroid hormone. Journal of Comparative Physiology B, 186(6), 677–688.

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

Patient experience and symptoms
Peterson, S. J., Cappola, A. R., Castro, M. R., Dayan, C. M., Farwell, A. P., Hennessey, J. V., … Bianco, A. C. (2018). An Online Survey of Hypothyroid Patients Demonstrates Prominent Dissatisfaction. Thyroid, 28(6), 707–721.
Resistance to thyroid hormone (RTH)
Dumitrescu, A. M., & Refetoff, S. (2015, August 20). Impaired Sensitivity to Thyroid Hormone: Defects of Transport, Metabolism and Action. Retrieved January 4, 2018, from

Genetic defects in Deiodinases
Taylor, P. N., Peeters, R., & Dayan, C. M. (2015). Genetic abnormalities in thyroid hormone deiodinases: Current Opinion in Endocrinology & Diabetes and Obesity, 22(5), 402–406.

Medici, M., Chaker, L., & Peeters, R. P. (2017). A Step Forward in Understanding the Relevance of Genetic Variation in Type 2 Deiodinase. The Journal of Clinical Endocrinology & Metabolism, 102(5), 1775–1778.

Bianco, A. C., & Kim, B. S. (2018). Pathophysiological relevance of deiodinase polymorphism. Current Opinion in Endocrinology, Diabetes, and Obesity, 25(5), 341–346.

Park, E., Jung, J., Araki, O., Tsunekawa, K., Park, S. Y., Kim, J., … Lee, S. (2018). Concurrent TSHR mutations and DIO2 T92A polymorphism result in abnormal thyroid hormone metabolism. Scientific Reports, 8.

Nishimura, K., Takeda, M., Yamashita, J., Shiojima, I., & Toyoda, N. (2018). Type 3 iodothyronine deiodinase is expressed in human induced pluripotent stem cell derived cardiomyocytes. Life Sciences, 203, 276.

McAninch, E. A., Rajan, K. B., Evans, D. A., Jo, S., Chaker, L., Peeters, R. P., … Bianco, A. C. (2018). A Common DIO2 Polymorphism and Alzheimer Disease Dementia in African and European Americans. The Journal of Clinical Endocrinology and Metabolism, 103(5), 1818–1826.

Jo, S., Fonseca, T. L., Bocco, B. M. L. C., Fernandes, G. W., McAninch, E. A., Bolin, A. P., … Bianco, A. C. (2018). Type 2 deiodinase polymorphism causes ER stress and hypothyroidism in the brain. The Journal of Clinical Investigation.

Salvatore, D. (2018). Deiodinases and stem cells: an intimate relationship. Journal of Endocrinological Investigation, 41(1), 59–66.


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

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

Beadles, C. (1893). Thyroid extract and its effects. The Lancet, 142(3657), 839–839.

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