Dosing by the TSH can cause Low T3

Research has proven repeatedly that TSH is not the same to a thyroid patient as it is to a person who is not taking any thyroid hormone medication.

For example, on standard L-T4 monotherapy, at any given level of TSH, a thyroid patient will have a higher T4 and a lower T3.

If TSH is used as the only indicator (which is common) and interpreted poorly (also common), the TSH test will keep a significant number of thyroid patients T3-poor.

Here’s one example showing the significant shift in the TSH-T4 and TSH-T3 relationships even within the NORMAL TSH range.

TSH-FreeT3T4-GRAPHS-Hoermann-2017

Yes, this shift exists within the NORMAL TSH range.  Notice there’s a limited overlap between thyroid patients and NORMAL people in the NORMAL range.

These graphs, roughly based on the original scatterplots, cannot show the wide variation from patient to patient. A given patient may be low in both T4 and T3 but have a lower TSH. Another may be high in T4 and low in T3 and have an almost suppressed TSH.

A huge range of thyroid hormone imbalances and deficiencies are possible within thyroid therapy because all thyroid hormone therapy is artificial.

Some deviations from the norm, such as extremely low T3, are rarely seen in untreated healthy patients, only seen when a critically ill patient is hovering close to death (see Rationale: Low T3 Syndrome, part 1. Sadly, treated thyroid patients can be kept at “critical illness” levels of T3 for years, and the biological stress contributes to chronic illness and can lead to a serious health crisis.

Some unusual deviations of TSH and thyroid hormones can ONLY be created by oral thyroid hormone dosing and do not exist in nature, such as the phenomenon of a suppressed TSH coexisting with a T3 and T4 in the normal or low range.

Simply put, too many factors conspire against the thyroid patient’s health when “normal TSH” becomes the only index to judge thyroid hormone sufficiency. This blog post only lists some of them.

No metabolic flexibility

The statistical population-wide reference range is quite insensitive to thyroid patients whose TSH is less flexible. Only the doctor and medication, not the patient’s body, can adjust the TSH.

A normal human body can adjust its TSH and T4 across the entire reference range over time — every day there is a rise and fall. Menstruating women’s TSH rises when estrogen is high. In the winter, we need more thyroid hormone, so TSH turns up the thermostat. Fluctuations are normal. The reference range reflects normal human flexibility.

But in thyroid patients, their static dose of thyroid hormone regulates the TSH. It keeps the TSH on a tight leash. TSH is medically restricted from fluctuation.

If a thyroid patient’s TSH level is stressful to their body, it can’t change if the doctor won’t allow it.

TSH reference range controversy

Among endocrinologists and experts, significant controversy rages over the upper limit of the normal reference range.

There’s a good reason for that controversy.

The peak of the normal curve is narrowly focused on one half of the reference range. It is heavily “skewed” to the lower half of the range.

  • The vast majority of healthy people have a TSH below 2.5 mU/L.
  • Most laboratories have a reference range of approximately 0.4 – 4.0 mU/L.

The range above 2.5 takes into account the smaller percentage of occasions when the thyroid is being asked to produce more hormone.

For most people, 2.5 to 4.0 represents too little thyroid hormone for normal function, but their healthy thyroid gland may soon bring them back to a lower TSH.

Thyroid patients whose static dose limits their range of TSH fluctuation are less likely to be quite symptomatic with a higher level of TSH (and a lower level of thyroid hormone).

Some thyroid patients have languished for decades with a constantly high-normal pituitary output and insufficient hormone to meet their needs.

Physician bias toward high TSH

To add to the inherent bias in the reference range, doctors are currently trained to be more fearful of a low TSH than a high TSH.

The body has a safety mechanism to handle a short-term overdose of thyroid medication (see T3 depletion), but there is no safety mechanism to protect a thyroid patient from a deficiency.

Therefore, long-term thyroid insufficiency is far more harmful than short term overdose.

An overlooked T3 deficiency can lead to the very same chronic illnesses that doctors are taught to fear from low TSH. Osteoporosis and heart disease can be caused by low T3 even when TSH is normal. (See Fear of Low TSH causing osteoporosis ).

The pituitary gland can survive with low T3, but the rest of the body can’t.

The pituitary gland is equipped to survive a quite extreme T3 deficit.  This is a protective mechanism for times of extreme illness when the metabolic rate drops dangerously low.

When T3 levels in blood are low but T4 is sufficient, the pituitary gland can convert T4 into T3 within its own tissues at a higher rate than many other bodily organs and systems. (This is due to its higher expression of Deiodinase Type 2. See How the three deiodinases regulate T3.)

This unique trait of the pituitary gland makes it blind to lower T3 thyroid levels beyond its own tissues.

While the pituitary has enough T3 within itself, other parts of the body that depend more heavily on T3 levels in the circulation, such as the cardiovascular system, kidneys, and liver, may be very hypothyroid. To most organs in the body, Low T3 is hypothyroidism.

TSH will not always indicate a T3 deficit

Research shows that the standard L-T4 monotherapy — induces higher T4 and lower T3 at any given level of TSH.  In this situation, the TSH level will calibrate only the dominant thyroid hormone.

Some patients’ bodies convert T4 into T3 significantly better than others.

In patients who are “poor converters” of T4 hormone, the gap between their low T3 and a significantly higher T4 leaves them in a T3 deficit.

Benign TSH suppression due to T3 oral dosing

Thyroid patients who are poor converters of T4 hormone may require T3 hormone in their medication. T3-based therapies, when used optimally, will result in a healthy T3 level that is higher than the T4 level, due to the body’s need for more T3 to compensate for for the lower level of T4.

The hypothalamus and pituitary glands are so hypersensitive to T3 dosing that they can be suppressed by even a moderate, harmless dosage. TSH will be naturally suppressed to the degree that T3 rises above the patient’s T3 baseline level, even if the peak T3 level is not dangerously high.  This is because the glands are designed to respond to T3 that is gradually secreted and converted, not orally dosed.  (See T3 dosing effects.)

When orally dosing T3 hormone, T3 levels in blood rise 2-3 hours after a dose. By 5 hours after a dose, this peak T3 has passed. Thereafter, the patient’s T3 levels decrease at a much slower rate until they are back at baseline. After a single dose that is above the body’s set point, TSH can remain fully suppressed for up to 3 days. In order to avoid T3 peaks and valleys that are extreme, T3-dominant therapies usually divide the daily dose into at least 2 doses taken at least 6 hours apart.

Depending on the timing of the lab test after the patient’s dose, TSH may be an indicator of the peak T3, average T3, or lowest T3.

Sadly, a doctor who is trained to prevent low TSH regardless of T4 and T3 levels will often restrict T3 dosing too far for an individual patient. The patient may have very insufficient T3 and T4 hormone levels while the TSH is suppressed merely by transient T3 oral dosing effects.

In some patients, T4 may drop below reference and TSH may be entirely suppressed.  Yet research shows that a low TSH is not harmful unless it exists alongside excess T3.  (See Rationale: Low TSH vs. true hyperthyroidism

Unlike the opposite imbalance (high T4, low T3) having a low T4 is not as harmful to the body as long as the active form of thyroid hormone, T3, can meet all the body’s needs (See Rationale: L-T3 monotherapies )

Trusting the TSH alone in this case biases the doctor toward the hypersensitive hypothalamus and pituitary gland and against the rest of the patient’s body.

How to test and dose more wisely

Test both Free T3 and Free T4 so that you can understand what is going on underneath the too-broad TSH normal reference range.

If you really can only afford ONE test, Free T3 is actually the most clinically significant test. (See Rationale: Free T3 testing )

6 thoughts on “Dosing by the TSH can cause Low T3

  1. Pingback: Why T4 monotherapy has dominated over T3 therapies – Canadian Thyroid Patients Campaign

  2. Pingback: Why T4 monotherapy has dominated over T3 therapies – Canadian Thyroid Patients Campaign

  3. Pingback: Why T4 monotherapy has dominated – Canadian Thyroid Patients Campaign

  4. Pingback: Low T3 effects on the cardiovascular system – Canadian Thyroid Patients Campaign

  5. Pingback: Infographic: The dangers of Low T3 Syndrome – Canadian Thyroid Patients Campaign

  6. Pingback: Thyroid patients call the bluff – Canadian Thyroid Patients Campaign

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