For two related reasons:
- Because it is mistakenly believed that oral doses of thyroid hormone can sufficiently replace the natural secretion of living thyroid gland tissue.
- It is mistakenly believed that adjusting TSH secretion within the statistical “normal” range will create and/or signify thyroid hormone health in an individual treated thyroid patient.
The problem is…
For most thyroid patients, merely “normalizing the TSH” with a T4 hormone pill does not have the power to “create” nor accurately signify thyroid hormone balance.
It creates a laboratory test number for a pituitary hormone that has been incapacitated.
To the degree a person lacks responsive thyroid gland tissue, TSH cannot perform its normal physiological function by stimulating the thyroid.
Normal TSH signifies that your medicine has successfully manipulated your TSH secretion — without necessarily providing balance and sufficiency for both thyroid hormones, T4 and T3.
As summarized by Celi et al (2011),
“Therapy with L-T4 is the current standard of care, based on the assumption that conversion of inactive T4 into hormonally active T3 provides an adequate amount of [Thyroid Hormone] at the target end-organs.”
“Adequate replacement therapy is defined by a serum TSH within the normal range, indicating a state of euthyroidism at the hypothalamus-pituitary axis level.”
Thus, TSH testing, hand in hand with its counterpart of L-T4 therapy, are built on the assumption that pituitary-level euthyroidism will coexist with adequate thyroid hormone levels.
Answer this — Is correcting hypothyroidism about manipulating hypothalamus and pituitary gland secretions, or is it about verifying that one is truly optimizing thyroid hormone levels?
How can we be sure that “pituitary euthyroidism” equates with true euthyroidism?
Does it truly correlate with “sufficient” blood levels of T3 and signs of euthyroid status in organs and tissues?
TSH equity, yet T3 inequity
A TSH of 2.5 in a healthy person and a TSH of 2.5 in a thyroid patient actually gives the L-T4 monotherapy patient significantly less T3 on average and more T4.
We get less active hormone (T3), in exchange for more inactive hormone (T4).
The clinical studies show it is worst for patients without any thyroid gland tissue (athyreotic patients) —
Among the levothyroxine-treated patients
- 15.2% had lower serum FT3 and
- 7.2% had higher serum FT4
compared to euthyroid controls.
A wide range of FT3/FT4 ratios indicated a major heterogeneity in the peripheral T3 production capacity in different individuals.
The correlation between thyroid hormones and serum TSH levels indicated an abnormal feedback mechanism in levothyroxine-treated patients. (Gullo et al, 2011)
Unfortunately, pituitary TSH does not respond to thyroid hormones in the “normal” way in a treated thyroid patient as it does in an untreated person with a healthy thyroid gland.
Natural TSH vs. artificially-regulated TSH
Why are we trying to assess an artificial, medicated state by the same TSH yardstick as a natural, unmedicated state?
The control over pituitary TSH secretion gives the doctor and medical system a feeling of power, but it is a false sense of control over a patient’s health — too often, T3, the most important thyroid hormone for every organ in our body, is not sufficient for a thyroid patient’s individual health.
The thyroid hormone system in health is designed to be flexible within that individual healthy set point; it acts like a metabolic thermostat. When it’s cold outside, we turn up the heat. In a normal person, TSH and T4 flexibly rise and fall as the environment changes, as health status changes.
In a person with a living thyroid gland, TSH and T4 hold hands and cooperate in a lovely dance — actually, they dance in order to protect your precious Free T3 levels.
In biology, this dance is called “homeostasis.” (Hoermann et al, 2015)
This is what endocrinologists Abdalla and Bianco explain in “Defending Plasma T3 is a Biological Priority”
But when you’re a patient on T4-thyroid therapy, your T4 is not very flexible. T4 does not rise and fall in response to rising and falling TSH, but in response to your prescription. No, these two hormones don’t dance around T3 anymore. Instead, the T4 medication controls TSH.
To the degree that you depend on a pill more than a living thyorid gland, the hormone pill locks TSH in its grip with a static daily dose. You lose homeostatic control over your Free T3, and there will be a “TSH-T3 disjoint.” (Hoermann et al, 2015)
The TSH-T3 disjoint is seen in the relationship between the thyroid patient’s body and the medical system.
- In the thyroid patient’s body, T3 remains a core biological priority (your organs certainly care how much T3 they get!).
- But in the TSH-T4 therapy mindset, T3 is no longer a therapeutic priority. Your doctor and the medical system may not care to check how much T3 your organs are getting.
Let’s stop pretending that thyroid hormone therapy will instantly bring back the natural state of health in which TSH and T4 lived in perfect harmony with T3 as their precious ward. All thyroid hormone therapies can radically shift the body’s TSH-T4-T3 relationship, as I say another way in the counterpart to this post, “All thyroid therapy is artificial.” They can all trick the TSH. They all shift the hormone ratios.
That’s why we need to keep a watchful eye on thyroid hormone levels, not just TSH.
- See “Interpreting Free T3 and Free T4 in therapy“
- See the top 10 reasons why medicine needs to replace TSH with T3 as the target and indicator of thyroid therapy: Renew the paradigm of thyroid therapy.