Choosing Wisely Canada, together with the Canadian Society for Endocrinology and Metabolism, have collaborated on a harmful toolkit to reduce Free T3 and Free T4 hormone testing in order to save money.
As you can see in their Table 2 from page 9 of their toolkit, they want to prevent T3 and T4 testing in almost all circumstances for hypothyroidism — all except rare cases like central hypothyroidism (hypothalamus & pituitary gland failure to secrete enough TSH) and suspected resistance to thyroid hormone.
Problems? You bet there are huge problems with this harmful policy.
1. BIAS IN THE GUIDELINES
They simply do not care about LOW T3. They do not care if the vast majority hypothyroid patients are left to languish for months, years or decades with a Free T3 level in the lower half of reference range or lower.
Their only concern for T4 and T3 is if it is too HIGH, not if it is too low. They fear T3 highs and dismiss its fluctuations on therapy, rather than respecting the fact that we need minimal levels of bloodstream Free T3 to maintain health and remove symptoms (Abdalla & Bianco, 2014; Hoermann et al, 2018).
Danger exists on both ends of the T3 spectrum, and their choice to fear only HIGH levels is a harmful bias against a fundamental hormone (deGroot, 1999; Rhee et al, 2015).
The second bias is pretty obvious — this toolkit is primarily money-driven, not health driven. Read the introductory material in their test kit. Keep in mind that in BC testing guidelines, they say the TSH test costs $9.90, the Free T3 costs just under $9.40 and the Free T4 costs just over $12. We’re not talking MRIs here.
The third bias is professional protectionism. They justify this draconian policy by citing the American Thyroid Association’s guidelines for testing in hypothyroidism.
Think about it. The ATA is strongly biased toward protecting its TSH testing regime (protecting its ego and its decision to test by TSH alone since the 1980s) and it wants to protect its T4-monotherapy monopoly. It would be more than an embarrassment to admit that choice was a mistake that resulted in the unnecessary suffering of patients.
Who benefits from cutting Free T3 and Free T4 testing? It is in the interests of endocrinologists to simplify medical workflow by giving one drug to all thyroid patients and having only one test, no matter whether patients pay the price in reduced health and quality of life.
2. TREATING US LIKE CHILDREN
For people taking T3 in their medication, they treat doctors and patients like children who don’t understand how T3 works and can’t manage their own therapy.
Yes, we know that our T3 levels fluctuate, but we also know how to read scientific articles on Free T3 fluctuations and how to read graphs.
We know from pharmacological studies that our Free T3 will peak 2.5 to 4 hours after a dose, and most of the peak will be gone by 8 hours, so we can to time our blood test around the fluctuations.
It is standard for us to test at 12 hours after a T3 medication dose so that we get the half-day mid-point of our T3 levels and know where we are just before taking our morning dose. The fluctuations in T3 and T4 are absolutely no reason NOT to test.
Do you want us to risk overdose or underdose? Then test Free T3 when medicating with any T3! It just makes logical sense.
3. TSH IS A LOCALIZED RESPONSE
The ATA guidelines do not take into account all the research proving that the TSH test is limited and can only tell you locally how the hypothalamus and pituitary gland obtain and metabolize T4 and T3.
The pituitary gland, which secretes TSH, is only one small organ in our body, and it can be biased by many health conditions and many medications, including thyroid hormone dosing.
The biological FACT is pituitary gland is not omniscient and it does not represent the rest of the body. Do they think that the pituitary gland sends tendrils or sensors out to your pinky finger? Come on. The pituitary cannot tell you about thyroid hormone supply to the heart, liver, lungs, kidney, skin, and brain. Each organ and tissue metabolizes thyroid hormone differently.
4. TSH IS NOT WIRED FOR THERAPY
The pituitary gland is “wired” to respond accurately only to endogenous (internal) hormone secretion and conversion, not to the artificial conditions of exogenous (external) oral thyroid hormone dosing that enters through the GI tract in daily constant doses.
They have known since 1987 (Liewendahl et al clinical study) that TSH responds differently in patients on T4 monotherapy. It’s been confirmed over and over. McAninch et al recently reported that T4 patients have a T3 deficit that is on average 15-20% lower (at the same TSH level) than people with healthy thyroids who are not on meds. That’s just an average, some of us have a larger deficit. The T4 will be higher and T3 lower than people not on meds. And this is a “sensitive” test? No. It’s insensitive.
In thyroid patients whose Free T3 drops low while T4 stays mid range or higher, the TSH could truly care less about their plight — it will calibrate to T4 alone and will not rise to flag our low T3. We can stay Low T3 for years or decades for all our doctors care, because our TSH can even be suppressed despite a chronic low T3 caused by poor T4-T3 conversion.
Therefore, the TSH is inaccurate. It does not reflect healthy T3 levels. It imprisons us in perpetual hypoT3-ism, which is a place of suffering and illness.
5. TSH IS OVERSENSITIVE TO T3 DOSING
Let’s talk about the opposite end of the spectrum. Why doesen’t the pituitary respond accurately to T3 dosing?
The hypothalamus and pituitary are oversensitive to peak Free T3, because they assume the natural pathways of T3 production.
These glands are assuming that the T3 they sense has been secreted from a gland OR overconverted from T4, and that the peak T3 will stay at that peak level or go higher, when that is not the case at all, it is a transient peak originating from a pill.
Is the peak Free T3 on T3 meds dangerous? No, not if T4 is concurrently lower to the same degree T3 is higher. Do the math.
Also, our body is well equipped to handle any peak T3 by breaking it down via Deiodinase Type 3. Look it up. Science has proven that Deiodinase Type 3 is sensitive to T3 as its primary “substrate” and will break down T3 into T2 as soon as it goes over the body’s set point in any and every organ. We have a built-in failsafe to protect us from mild, transient T3 peaks.
Because of the way the pituitary is wired, if we are on desiccated thyroid or T4-T3 combination therapy, the pituitary TSH can be artificially low and falsely say “overdose” even if Free T3 is in fact still insufficient, in the lower half of reference range, and your dose is too low.
Implications? In persons taking T3 meds, the TSH can be a downright liar working against optimizing your T3 in the upper part of reference range.
What do you have to do? Test Free T3 and you will find the truth about your T3 level; don’t believe TSH.
CONCLUSIONS
We DO need direct T4 and T3 measures.
Endocrinologists and penny pinchers — If you believe T3 and T4 testing is unnecessary in hypothyroidism, you basically believe that it’s unnecessary to optimize our therapy for the rest of our lives! Why? Because you refuse to acknowledge what science says about the distorted TSH, T4 and T3 relationships in therapy. TSH numbers are biased toward one gland, and that gland is, in fact, proven to be biased against optimizing T3 in hypothyroid therapy.
No wonder doctors love the TSH. Dosing us by the TSH is one way to keep our T3 down; it keeps the majority of suffering thyroid patients too tired and depressed to become educated self-advocates and intelligent partners in their own therapy.
How’s that supposed to benefit our society, our economy, our health care system?
GRAPHIC SOURCE: See the Choosing Wisely Toolkit yourself, page 9
https://choosingwiselycanada.org/wp-content/uploads/2017/09/CWC_T3T4_Toolkit_V1.pdf
References
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
Cicatiello, A. G., Di Girolamo, D., & Dentice, M. (2018). Metabolic Effects of the Intracellular Regulation of Thyroid Hormone: Old Players, New Concepts. Frontiers in Endocrinology, 9. https://doi.org/10.3389/fendo.2018.00474
De Groot, L. J. (1999). Dangerous Dogmas in Medicine: The Nonthyroidal Illness Syndrome. The Journal of Clinical Endocrinology & Metabolism, 84(1), 151–164. https://doi.org/10.1210/jcem.84.1.5364
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
Hennessey, J. V. (2017). The emergence of levothyroxine as a treatment for hypothyroidism. Endocrine, 55(1), 6–18. https://doi.org/10.1007/s12020-016-1199-8 [NOTE: This article is strongly biased against T3 testing and therapy, but it reveals the history]
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. https://doi.org/10.3389/fendo.2017.00364
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, 3239197. https://doi.org/10.1155/2018/3239197
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- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3803574/
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(9), 546–552. https://doi.org/10.1055/s-0043-125064
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.
McAninch, E. A., & Bianco, A. C. (2016). The History and Future of Treatment of Hypothyroidism. Annals of Internal Medicine, 164(1), 50–56. https://doi.org/10.7326/M15-1799
McAninch, E. A., Rajan, K. B., Miller, C. H., & Bianco, A. C. (2018). Systemic Thyroid Hormone Status During Levothyroxine Therapy In Hypothyroidism: A Systematic Review and Meta-Analysis. The Journal of Clinical Endocrinology & Metabolism. https://doi.org/10.1210/jc.2018-01361
Mendoza, A., & Hollenberg, A. N. (2017). New insights into thyroid hormone action. Pharmacology & Therapeutics, 173, 135–145. https://doi.org/10.1016/j.pharmthera.2017.02.012
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/
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. https://doi.org/10.1089/thy.2017.0681
Rhee, C. M., Brent, G. A., Kovesdy, C. P., Soldin, O. P., Nguyen, D., Budoff, M. J., … Kalantar-Zadeh, K. (2015). Thyroid functional disease: an under-recognized cardiovascular risk factor in kidney disease patients. Nephrology Dialysis Transplantation, 30(5), 724–737. https://doi.org/10.1093/ndt/gfu024
Ruiz-Núñez, B., Tarasse, R., Vogelaar, E. F., Dijck-Brouwer, J., A, D., & Muskiet, F. A. J. (2018). Higher Prevalence of “Low T3 Syndrome” in Patients With Chronic Fatigue Syndrome: A Case–Control Study. Frontiers in Endocrinology, 9. https://doi.org/10.3389/fendo.2018.00097
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