We hypothyroid patients on thyroid therapy have an argument to make about one of the secretions of the pituitary gland, the TSH.
But you won’t let us speak.
You have put the TSH in charge of monitoring our thyroid hormone medication dosage, and you won’t let any other measure, any other evidence, no matter how powerful it is, take the witness stand and speak against the TSH.
You continue to do this without looking at the research that proves the TSH responds with an unfair bias against high-normal Free T3 levels in thyroid patients. (refs 1, 2, 3)
You do not want to admit it, but thyroid therapy can medically induce an unacknowledged form of central hypothyroidism (lowered TSH in the presence of a lowered FT3).
What else can you call it when research proves that thyroid therapy biases the TSH lower than it would be in a normal person with the same level of Free T3 in their blood? (2)
You monitor thyroid therapy by TSH, but the TSH is being distorted by the therapy it is supposed to monitor.
That’s like asking a pharmaceutical company to set up a testing method to prove that a bestselling medication is effective and harmless to patients, and letting them disallow all other testing methods.
That’s like asking doctors to choose the test that justifies the therapy modality that they personally prefer to use for its simplicity and high status, and then letting them use this test result as an excuse to ignore all persisting clinical signs and symptoms of hypothyroidism.
You choose your biased witness in the human body and silence all other organs and tissues, and the patient himself or herself, from having a say.
Let’s take a vote
The pituitary only gets one vote in the matter. It’s only one gland that benefits from thyroid hormone supply in blood.
Free T3 is the most important witness against TSH. You cannot dismiss or avoid testing blood levels of Free T3 because the bloodstream provides an unbiased direct supply to all tissues and organs regardless of their ability to transport and convert T4. The healthy human body defends bloodstream T3 very carefully for a good reason. (4)
We know lowered Free T3 in bloodstream is associated with many pathologies, and the studies are too many to cite. (5, 6)
Besides, we have known for almost 15 years now that the bloodstream Free T3 is a good measure of the sum of all T4-T3 conversion that is happening beyond the bloodstream, (7) and this makes sense because thyroid hormone transport enables T3 to exit cells and re-enter the bloodstream. (11)
As the immediate beneficiaries of T3 in blood, you must give heart and cardiovascular system two votes — they alone should be able to veto the pituitary TSH if they are suffering from a low T3 situation. Ask a cardiologist who knows about low T3. (8)
You must hear the powerful voice of LDL cholesterol, which is usually high when T3 is low — unless other biological and medical factors interfere, such as lowering cholesterol with statins. (9)
Our tendons deserve a vote. Consider the testimony of the ankle reflex test, which used to be measured down to the millisecond by the technical devices you threw in the garbage. You historically dismissed the ankle reflex not because it was cheap and accorded with patient symptoms, but because it did not always vote with the TSH. (10)
And most of all, you must listen to thyroid patients. Give us the chance to speak on the witness stand, since we are the victims, not just the witnesses.
Generations of doctors have continually defended the role of TSH in thyroid therapy because it conveniently simplifies our therapy for you.
The normalized TSH helps you feel justified in continually dismissing our symptoms created by our T3 deficit and enables you to blame other diseases that you medicate us for instead.
By declaring that measuring Free T3 is unnecessary, (12) you imply that accessing Free T3 in the upper half of reference is unnecessary for anyone on thyroid therapy, which is a false and damaging belief.
How can it be possible that a T3 level at the bottom of reference is not harmful for a patient whose individual needs may require a T3 at the top of reference? Low T3 is only “too low” relative to biological need in the individual, and any given individual’s reference range for thyroid hormones in health is about 50% narrower than the reference range in the wider population. (13) This is why the individual thyroid patient’s experiential knowledge of hypothyroid symptoms is the most important witness.
By disallowing a $10 Free T3 test to take the witness stand along with patients’ own testimony, you take away the evidence that could teach a new generation of doctors and researchers the truth about the relationship between chronic lower Free T3 levels and chronic symptoms of hypothyroidism in thyroid therapy.
Admit it. True hypothyroidism is HypoT3ism as judged by the individual body, not judged by reference ranges and population statistics of people who are NOT on thyroid therapy.
All other organs and tissues as well as patients themselves deserve to have a voice in adjusting thyroid therapy modality and dose.
REFERENCES
1) 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
2) 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
3) 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
4) Abdalla, S. M., & Bianco, A. C. (2014). Defending plasma T3 is a biological priority. Clinical Endocrinology, 81(5), 633–641. https://doi.org/10.1111/cen.12538
5) 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. https://doi.org/10.3389/fendo.2017.00163
6) 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
7) Maia, A. L., Kim, B. W., Huang, S. A., Harney, J. W., & Larsen, P. R. (2005). Type 2 iodothyronine deiodinase is the major source of plasma T3 in euthyroid humans. Journal of Clinical Investigation, 115(9), 2524–2533. https://doi.org/10.1172/JCI25083
8) Fontana, M., Passino, C., Poletti, R., Zyw, L., Prontera, C., Scarlattini, M., … Iervasi, G. (2012). Low triiodothyronine and exercise capacity in heart failure. International Journal of Cardiology, 154(2), 153–157. https://doi.org/10.1016/j.ijcard.2010.09.002
9) Duntas, L. H., & Brenta, G. (2018). A Renewed Focus on the Association Between Thyroid Hormones and Lipid Metabolism. Frontiers in Endocrinology, 9. https://doi.org/10.3389/fendo.2018.00511
10) Shafer, B., & Nuttall, Q. (1972). Achilles reflex in thyroid disorders: a 10-year clinical evaluation. The American Journal of the Medical Sciences, 264(4), 313–317. https://doi.org/10.1097/00000441-197210000-00009
11) Bernal, J., Guadaño-Ferraz, A., & Morte, B. (2015). Thyroid hormone transporters—functions and clinical implications. Nature Reviews Endocrinology, 11(7), 406. https://doi.org/10.1038/nrendo.2015.66
12) Garber, J. R., Cobin, R. H., Gharib, H., Hennessey, J. V., Klein, I. L., Mechanick, J. I., … Woeber, K. A. (2012). Clinical practice guidelines for hypothyroidism in adults: Cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocrine Practice, 18(6), 988–1028. https://doi.org/10.4158/EP12280.GL
13) 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