In this set of four social media memes, I chose the theme of the iceberg and glacier as a metaphor because Low T3 generally causes low body temperature.
This article does not cite references, since we have already provided enough in our Campaign Statement Rationale pages:
Meme 1: The exclusion of thyroid patients with Low T3
Only the tip of the iceberg of Low T3 has been explored in thyroid research.
This is because those who are most at risk of chronic low T3 levels (thyroid patients on L-T4 monotherapy) are not being studied.
Typically the “methods” section of these articles explain that the study has excluded anyone with a diagnosis of thyroid dysfunction (whether determined by TSH levels or as part of their medical history) and anyone taking thyroid hormone medication.
This exclusion exists because of the way the pheonomenon of Low T3 Syndrome is conceived through linguistic and medical categories.
The syndrome typically goes by the alternative name “non-thyroidal illness,” and at its root it is conceptualized as a syndrome that is not caused by dysfunction of the thyroid gland itself.
The interest in Low T3 Syndrome is, at its root, an interest in a paradox: “How can a person without any sign of thyroid gland dysfunction experience a life-threatening state of hypothyroidism due to an isolated deficiency in T3 hormone?”
Therefore, if one were to study Low T3 in patients who have been diagnosed with hypothyroidism, the study would not be very interesting, the reasoning goes, because their Low T3 is assumed to be caused by either
- UNtreated hypothyroidism caused by thyroid gland dysfunction
- UNDERtreated hypothyroidism caused by insufficient dose of thyroid medication
However, because of the unfortunate exclusion of thyroid patients, the most interesting hypotheses regarding Low T3 syndrome have not been explored, namely, that chronic Low T3 can coexist with treated hypothyroidism because of
- MIStreated hypothyroidism by emphasis on replacement of T4 hormone alone, the choice to exclude T3 hormone from patients’ medication. In such patients, higher levels of T4 can paradoxically result in reduced levels of T3 hormone.
- A patient’s genetically reduced ability to convert T4 to T3 hormone, often seen in DIO1, DIO2 polymorphisms and the “partial SPB2 deficiency”
- A patient’s genetic “resistance to thyroid hormone” (RTH) which requires a higher level of T3 to activate thyroid hormone receptors either in the nucleus or at the cell wall.
Meme 2: The causes of Low T3 and the harms of Low T3
The cause-effect relationship between Low T3 Syndrome and Illness has always been assumed as Illness CAUSES Low T3. That’s because in people with thyroid glands, the main occasion for T3 loss is the body’s decision to lower their metabolism to protect itself during illness.
However, in thyroid patients on L-T4 monotherapy, the CAUSE of Low T3 is not necessarily the body’s choice to lower metabolism in illness.
The choice of L-T4 monotherapy itself can also be a cause of Low T3. By giving a supraphysiological dose of T4 without any T3 to support it, this therapy distorts the T4-T3 ratio so that T4 dominates and T3 is suppressed.
In treated thyroid patients, Low T3 is often a natural result of medically-induced thyroid hormone imbalance.
- As T4 dominates over T3 in bloodstream and tissues, the “Deiodinase Type 2,” responsible for the majority of T4-T3 conversion in the body, is downregulated.
- In addition, as T4 levels breach the boundary from physiologically adequate to “supraphysiological” or excess, “Deiodinase type 3,” which inactivates both T4 and T3 hormones, is upregulated.
Because Low T3 is caused by illness in persons with normal thyroid glands, medicine has overlooked the potential of Low T3 to induce illness in treated thyroid patients.
Low T3, from the perspective of the body’s organs and tissues, is a pathological state. Organs require T3 sufficiency to operate at their best.
If Low T3 does not cause illness immediately, it is because the effects of hypothyroidism take more time to manifest than the effects of hyperthyroidism. Hypothyroidism is like a glacier slowly advancing down a mountain. Conversely, hypERthyroidism is like a raging fire that quickly consumes by means of energy overexpenditure.
Meme 3: The myth that Low T3 is not only benign but always temporary
One thing that studies of Low T3 syndrome have taught us is that once you are very ill, Low T3 can prevent recovery.
In patients with normal thyroid glands, Low T3 may indeed be a temporary state — that is, if Low T3 does not kill them first!
What makes Low T3 temporary? The presence of a healthy thyroid gland.
In people with normal thyroid glands, the body can very quickly “turn up the heat” during recovery by raising TSH. Under high TSH stimulation, the thyroid gland produces not only T4, but a higher percentage of T3.
The patients whose thyroid gland responds with sufficient T3 supply are the ones who recover. Conversely, those whose T3 remains too low for too long during a fragile state of critical illness are the ones who die.
Therefore, the resolution of low T3 is needed for recovery from illness. What if you can’t make your own T3 hormone? You can’t recover easily, and Low T3 may not be temporary, but chronic.
In thyroid patients treated with L-T4 monotherapy, Low T3 status can persist for years or decades.
If Low T3 can be deadly to fragile, critically ill patients, why would it be benign to people who are not yet critically ill? This continuous Low T3 state is unnatural and one should assume it is unhealthy for the body unless there is evidence to the contrary. Yet nobody has bothered to study the harm of chronic Low T3 in L-T4 monotherapy.
Meme 4: The clinical relevance of Reverse T3 testing
If a patient continues to secrete T4 or take T4 medication during Low T3 Syndrome, they will build up a “mountain” of Reverse T3.
Therefore, a common feature of the “early phase” of Low T3 syndrome is high Reverse T3 levels. High reverse T3 does not persist in later phases, after the lower TSH has resulted in less thyroidal secretion of T4, and this depletes the only source of Reverse T3.
However, in the L-T4 treated patient with Low T3 syndrome, a daily resupply of T4 hormone diverts conversion to T3 and continually emphasizes conversion to Reverse T3 instead.
There are no “natural phases” of Low T3 syndrome in LT4 treated thyroid patients, only a continual depletion of T4 and T3 that is medically induced by their T4 dosage. Their rate of Reverse T3 buildup and T3 loss speeds up when there is more T4 dosage added and slows down when T4 intake is reduced.
The most worrisome result of this process is the depletion of T3 levels, which induses hypothyroidism. This happens because of the overactivity of Deiodinase Type 3.
Deiodinase Type 3 is the enzyme is responsible for THREE simultaneous hormone conversions that remove an iodine atom from the “inner ring” of a thyroid hormone molecule:
- D3 converts T4 to Reverse T3
- D3 converts T3 to 3,3′ T2, which can be considered “Reverse T2,” and
- D3 converts RT3 to 3′,5′ T2 which can be considered a “Reverse T3 byproduct”
We do not yet have a standard lab assay kit available for T2 testing, and therefore Reverse T3 testing provides a metric for the degree of thyroid hormone inactivation occurring in bloodstream.
When D3 is overactive in bloodstream, it may be assumed to be overactive in peripheral tissues and organs if they experience excess T4 levels.
Reverse T3 itself also has some harmful side-effects.
RT3 is not merely “inert” — science has shown that both T4 and RT3 can activate receptors on the plasma membrane of endothelial cells and cancer cells. When these hormones are present in excess quantity, their role is biologically harmful. In endothelium (the lining of blood vessels, heart tissue, and lymphatic vessels), RT3 activates cell wall receptors that cause endothelial dysfunction and worsen diseases of the heart and vascular system. In cancer cells, both T4 and RT3 can trigger the proliferation of cancer.
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