The blindness of TSH to the most powerful thyroid hormone.

tsh-cant-detectStandard therapy for hypothyroidism today is built on a myth of TSH omniscience.

“Thyroid stimulating hormone (TSH) is the most sensitive and specific test for the
investigation and management of primary thyroid dysfunction” (1)

If TSH is so “sensitive,” then why is TSH completely blind to blood levels of the most powerful thyroid hormone, T3, during thyroid therapy?

Why is the TSH-T3 relationship so distorted during “management” of primary thyroid dysfunction?

Did you know that in any patient on thyroid therapy, if the TSH is below reference, the Free T3 level, the most powerful thyroid hormone, could actually be anywhere?  It could be below reference range or above reference. The TSH would give you no clue.

Let me prove it to you with this simple graph from a research study.

As permitted under copyright fair dealing, (2) I’m reproducing here Larisch et al’s (2018) Figure 2 from their study of 319 thyroidectomized patients on T4 monotherapy, some of whom were maintained at a “normal” TSH and some of whose TSH was suppressed. (3)

In this clinical study, the reference ranges were

  • 0.4 to 4.0 mIU/l for TSH
  • 3.1 to 6.8 pmol/l for FT3.


The black dots represent the 319 thyroid patients’ Free T3 levels at various levels of TSH along the horizontal axis.

Notice the X axis where the TSH is at 0.50. The normal reference range starts at 0.4, so at around 0.50 is where the light-colored dots of 271 UNtreated healthy people’s Free T3 begins and moves into the right-hand side of the chart in a much narrower band.

The wide _vertical_ scatter you see in the black dots of treated thyroid patients is completely different from the small cluster of light-colored dots representing the Free T3 levels of healthy control subjects.

This chart clearly proves that a healthy thyroid gland, in the absence of thyroid medication, is capable of maintaining a narrower band of FT3 levels hovering around 5.1.

It also shows that in a healthy control subject, Free T3 rarely goes lower than 4.2 (within a reference range of 3.1 to 6.8 pmol/l).

Below 4.2 is where many people without functioning thyroid glands are forced to eke out the rest of their lives, with a level of T3 hormone that normal people rarely experience except in states of caloric deprivation, depression, exhausting exercise, and critical illness.

Even life below the  midpoint of 5.1 could be a life of suffering for many patients, since some healthy people maintain an FT3 higher than that. It all depends on where an individual’s healthy set point resides–it’s different for each person.

However, this study found that the lower half of the FT3 reference range is where chronic hypothyroid symptoms occur. In this study, unsurprisingly, the authors found that “Hypothyroid symptom relief was associated with . . . FT3 elevated further into the upper half of its reference range.”


See the researcher’s trendline tilting slightly vertically in the graph.  It is a tilted trendline because of what happens at the extreme edges of the graph.

Meanwhile, the dots across most of the middle of the graph tell a different story than the trendline, a story of not much trend — rather, randomness.

But on the far right, notice how the Free T3 levels shift lower in patients whose TSH is higher than 2.0 (near mid-reference = 0.4 to 4.0 mIU/l).  This is what happens when the T4 dose is too low — there’s not enough T4 to bring down the TSH to where it is in 80% of healthy people (under 2.5) (4), and there’s not enough T4 for the body to convert into T3.

On the left, almost suddenly, between a miniscule TSH concentration between 0.02 and 0.01, the pattern of treated patients’ FT3 levels became MORE diverse. I have to assume that this 0.01 includes all the patients whose TSH was 0.01 and lower (undetectable).

One would expect the region of suppressed TSH to be where more patients have a FT3 above 7.0, but here’s the paradox. The vast majority have a normal Free T3 level, and most shockingly — there were still patients with Free T3 below reference range.

How do you explain that? The pituitary gland has one eye on the high T4, and… that’s all it has its eye on.

Another important question — if the normal range applies to treated thryoid patients, why didn’t any shift to higher T3 levels happen at 0.40 where the lower edge of the reference range is located?

Nobody asks these questions because they are uncomfortable to ask.

They are paradigm-shifting questions. They might make people start to mistrust the sacred TSH.


Today, thyroid patients “thyroid hormone levels” are being misjudged by a healthy person’s “right-shifted” TSH reference range.

It is unbelievable that doctors still classify a patient with a completely suppressed TSH as “subclinically hyperthyroid” when their Free T3 is suppressed, remaining in the HYPOthyroid range.

TSH is incredibly blind and insensitive to the plight of treated thyroid patients.

The truth is, there is a stark T3 inequity between treated patients and healthy controls.

Our medication has NOT normalized our thyroid hormones if it can’t normalize the most powerful and essential thyroid hormone. Thyroid therapy itself has distorted the T3-TSH hormone relationship.  It’s abnormal.

Doctors, why are you trusting the report of an abnormal, biased, skewed TSH secretion?

Could you honestly look at this graph and tell a judge in court that the TSH is “the most sensitive and specific test,” the most accurate (indirect) measure of thyroid hormone levels in the “management of primary thyroid dysfunction”?


  1. Toward Optimized Practice. (2014, April). Investigation and Management of Primary Thyroid Dysfunction: Summary of the Clinical Practice Guideline. Retrieved from
  2. See Section 29.1, Canada Copyright Act,
  3.  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.
  4. Hamilton, T. E., Davis, S., Onstad, L., & Kopecky, K. J. (2008). Thyrotropin Levels in a Population with No Clinical, Autoantibody, or Ultrasonographic Evidence of Thyroid Disease: Implications for the Diagnosis of Subclinical Hypothyroidism. The Journal of Clinical Endocrinology and Metabolism, 93(4), 1224–1230.

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