Illness as trigger of T3 depletion
Science understands this process of T3 depletion as “non-thyroidal illness.” It has been called “non-thyroidal” because paradoxically, people with normal thyroid glands experience this deep, yet temporary hypothyroidism when they become very ill.
It is believed that during illness, the body protects itself by lowering its metabolic set-point. The most efficient way of doing this is to reduce the supply of the active thyroid hormone, T3, that is essential to raising metabolic rate.
The danger of Low T3
Research has proven, over and over, that if a person experiences “non-thyroidal illness,” they are at very high risk.
- The lower T3 drops, the higher the risk of DEATH and continued illness.
- Low T3 is a powerful predictor of poor outcome than any other indicator.
Therefore, researchers are now starting to consider Low T3 pathological, so much so that they are performing studies of therapeutic approaches to help patients with low T3 during various stages of the illness and recovery process.
Read more about the research on “Non-thyroidal illness” here
L-T4 monotherapy as trigger
Illness is not a prerequisite for Low-T3 syndrome.
According to the well-established theory of what triggers it, the body’s set-point does not have to lowered, T4 just has to be higher than the set-point.
Everyone has a DIO3 gene that makes D3 enzyme. Everyone’s DIO3 gene is sensitive to T4 levels above the body’s individual set-point.
The thyroid hormone set-point is different for each individual. Science has long ago proven that each healthy individual has a set-point for thyroid hormone levels that is 50% narrower than the statistical population reference range. One’s internal set-point for thyroid hormone cannot be predetermined by an external “reference range.”
L-T4 monotherapy causes a T3:T4 ratio that is significantly lower than healthy people. Because of this, a patient may require more T4 in bloodstream in order to have sufficient T3 hormone for normal physiological function. We already know that patients with the highest T4 levels often have extremely low T3 levels (very low T3:T4 ratios).
Therefore, some patients may be maintained at a L-T4 dosage that continually triggers T3 depletion.
Every day, their thyroid pill adds more T4, and every day, their body removes the slight “excess” T4 at the price of a T3 deficit.
If a thyroid patient gets sick, they can’t just turn down their natural thyroid production to prevent T4 “excess.” They depend on a static dosage of L-T4 medication. Their dosage can easily exceed a “set point” that becomes lower due to an illness.
But nobody is watching out for Low-T3 hypothyroidism in thyroid patients.
Why?
No Free T3 testing for you!
It’s not standard practice to measure thyroid patients’ Free T3 levels.
Current guidelines say to test only TSH, once a year, for the rest of your life on thyroid therapy.
The problem is — T3 depletion happens while TSH is maintained.
Yes, that is correct. TSH will not rise if only the active hormone, T3, drops.
Why?
If you are replacing a thyroid gland with a T4 pill every day, your dosage rigidly maintains T4. This maintains a TSH within the target range for L-T4 therapy — even if T3 drops. Hiding underneath that normal or suppressed TSH and a normal or high-normal T4 may be a T3 deficiency.
Only Free T3 testing can reveal Low T3 and low T3:T4 ratios in treated thyroid patients.
Recovery?
For a discussion of what we know about patients’ recovery from T3 depletion, see part 2:
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