In Chatizomaris et al’s (2017) article, Table 2 illustrates the many health conditions — beyond thyroid gland failure — in which a TSH test result is NOT indicative of the patient’s true thyroid hormone status. The table shows what usually happens to thyroid hormones and TSH in a patient who is NOT taking any thyroid hormones.
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. Link: https://www.frontiersin.org/articles/10.3389/fendo.2017.00163/full
As you see in the table above, the column that is most consistently blue (low) or red (high) is Free T3.
T3 is the most powerful and active thyroid hormone. It determines the body’s thyroid hormone status more than TSH or T4 does.
In these states, the hypothalamus and/or pituitary gland are influenced by health factors other than their thyroid hormone levels, so the TSH cannot be trusted as an indicator of thyroid status.
The hypothalamus and pituitary gland respond to T4 and T3 in a different way than the rest of the body. Each organ has its own rate of T4 to T3 conversion, and as a result, the pituitary may have a good T3 supply within its tissues while the rest of the body lacks T3.
In addition, some health conditions may cause temporary hypothalamus and pituitary gland dysfunction (central hypothyroidism).
In the few cases that Free T3 does not provide the correct indication, a full thyroid panel plus Total T3 or Reverse T3 provides an aid to confirming the patient’s thyroid hormone status.
The dangers of Low T3
Research cautions that Low T3 syndrome (the blue squares under FT3) can itself pose a health risk in illness if it remains below reference range for too long.
“Low” is relative to the body’s needs, and in our Campaign Statement pages, we cite and discuss research that proves even slight T3 depletion within the reference range has physiological effects.
When T3 is low in bloodstream, it’s likely that peripheral tissues are also T3-deficient because every organ depends to some degree on T3 from bloodstream, and Free T3 is the fraction that can be transported into cells.
Peripheral organs like the brain and bones supplement T3 from bloodstream with local T4-T3 conversion, but their T4 conversion is hindered under these health conditions, partly because the TSH is not high enough to stimulate further conversion and partly because the thyroid hormone metabolism is converting T4 into more RT3.
The lower the T3 is, and the longer the person remains in a low T3 state, the less chance they will be able to recover, and they may die. Sufficient T3 is absolutely essential for life and health.
Therefore, the low T3 is not just an effect of these altered physiological states, but continued low T3 levels can prevent recovery from them.
This is why some researchers have studied T3 therapy in non-thyroidal illness. T3 therapy has helped even healthy-thyroid patients to recover from heart failure or low-T3 after cardiac surgery.
Relevance to thyroid patients
All of these hypo and hyper states can occur in persons who have a healthy thyroid gland, AND in persons whose thyroid gland is damaged or missing.
In the thyroid patient, TSH-only testing will make it very difficult or impossible to diagnose early autoimmune thyroid disease or to discern a problem with a patient’s thyroid medication type or dosage.
For example, in the early stages of Hashimoto’s thyroiditis, an “abnormally-normal” TSH despite lower T4 and T3 can prevent accurate diagnosis — because in contemporary medicine, primary hypothyroidism is only officially diagnosed when TSH is above reference range.
A patient with a damaged thyroid gland may temporarily have a high or high-normal T3 due to the altered thyroid hormone metabolism in obesity, pregnancy, or PTSD.
In thyroid therapy, T4 medication itself can be a cause of T3 depletion, since excess T4 above the individual’s set point (even within reference range) can stimulate the metabolism to inactivate T4 into RT3 and T3 into T2.
Therefore, in hypothyroid patients treated with T4 hormone, the FT4 level may be inflated and maintained by daily doses of T4 medication, and the TSH can be manipulated by T4 medication alone. No matter what the T4 and TSH levels are, the patient’s T3 could be too low, and T3 deficiency alone can create or worsen hypothyroid symptoms and prevent recovery from illness.
Can thyroid patients recover?
In order to initiate recovery in a patient with a healthy thyroid, the TSH must rise to stimulate the thyroid gland to increase T3 production. This happens even before the thyroid hormone metabolism recovers.
However, in a thyroid patient on therapy, the TSH will not rise if it is being suppressed by T4 therapy, and the gland will not be able to produce more T3 if it is damaged or missing.
In a thyroid patient on therapy, if excess T4 dosage is the main cause of Low T3 or preventing T3 recovery, a doctor can fix it simply by reducing T4 medication dose while adding T3 medication to prevent the patient’s body from suffering hypothyroidism. Switching from T4 monotherapy to desiccated thyroid (which contains approximately 80% T4 and 20% T3) can have the same effect and may resolve the Low T3 if the T3 dosage it contains is sufficient to remedy the patient’s deficit.
Unfortunately, it is NOT known whether thyroid patients on thyroid therapy can recover from a chronic or acute Low T3 state without the assistance of T3 hormone therapy.
Why don’t we know? Because no one has yet conducted a study of Low T3 syndrome in patients who do not have a functional thyroid gland. Yes, this is surprising, but true.
See our blog post “Thyroid patients excluded from research.”