Warmingham’s TSH Hypothesis – TSH is not useful

[DrMariano2]

Here is an interesting article:

Effect of Exogenous Thyroid Hormone Intake on the Interpretation of Serum TSH TEst Results http://www.thyroidscience.com/hypotheses/warmingham.2010/warmingham.intro.7.2010.htm

Here is the free PDF: http://www.thyroidscience.com/hypotheses/warmingham.2010/warmingham.7.18.10.pdf

I prefer monitoring actual thyroid hormone levels in addition to TSH (Thyroid Stimulating Hormone) to determine treatment, rather than relying on TSH alone.

One major factor is that there are two separate compartments for thyroid hormone: The brain compartment and the body compartment. These are separated by the blood brain barrier. Thyroid hormone cannot pass through the blood brain barrier without active transport. This is controlled by astroglial metabolism and signaling.

The astroglia are non-electrical signaling, mobile brain cells which, among their numerous functions, maintain the integrity of the blood brain barrier, maintain brain metabolic activity, control neuron growth, control synaptic connections and signaling activity, network neurons and other glial cells, and participate in information processing. They are the most numerous cells in the brain. They also are the brain cells that convert T4 to T3. A large number of astroglial cells are also the stem cells of the brain (approximately 55 billion of them). The number of neuroglial cells determines one’s intelligence. Einstein’s cerebral cortex, for example, had twice as many neuroglial cells than normal. He had about the same number of neurons as a normal person.

TSH is a brain signal to the pituitary gland that more thyroid hormone needs to be produced. Given that TSH is made by the brain, TSH actually represents the brain’s need for thyroid hormone since the brain is in a different compartment than the body.

TSH production depends significantly on brain health / mental health. If one has metabolic problems, for example (and mental illnesses often have metabolic problems as part of their pathophysiology), then the brain may not be capable of either measuring thyroid hormone signaling adequately or may not be capable of producing adequate TSH. Thus, TSH may be low relative to the actual blood levels of Thyroid Hormone (T4, T3, Free T4, and Free T3). In this case, TSH can be low and blood thyroid levels can be low. Such a person will be physiologically hypothyroid yet TSH falsely indicates adequate or high thyroid levels.

Given the two thyroid compartments, another problem may arise: If the body’s activation of thyroid hormone (T4 to T3 conversion) is greater than the brain’s activation of thyroid hormone or if active transport of thyroid hormone across the blood brain barrier is impaired (such as in conditions where ATP production is slowed), then one can have high Free T3 (representing active thyroid hormone) yet also high TSH. The body may be in a state of hyperthyroidism (there are only T3 receptors and no T4 receptors) yet the brain is hypothyroid.

The above are examples of non-thyroid illnesses – where the may be nothing wrong with the thyroid gland yet thyroid signaling is affected.

Thyroid hormone levels in the brain and in the body can be very different. This has been shown in studies measuring blood thyroid hormone levels and Cerebrospinal Fluid thyroid levels. This can lead to misinterpretations of thyroid function – particularly when it comes to brain and body function. This is why I prefer to monitor actual thyroid hormone levels (Total T4, Free T3 at least, and Total T3, Free T4) and TSH to help get the bigger picture of thyroid signaling activity and thus function. Since thyroid signaling is also affected by other factors (e.g. nervous system, endocrine system, immune system function, metabolism and nutritional status), these other factors may be also highly important to assess how a certain thyroid signaling state was created.

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