Peripheral Thyroid Conversion And Its Impact On TSH And Metabolic Activity

[Dotdash]

This is one of the best explanations I've come across as to why and how T3 in the blood is not equivalent to that amount in the tissue, and why the current thyroid lab tests continue to be a source of confusion rather than revelation. It lists a number of other blood markers that are more relevant at tissue diagnosis of T3 that could be investigated if one chooses to do so. From personal experience and what I read on this forum the question of "why do I feel so bad when my thyroid blood work is great" continues to be one that is unsolved.

Some of the most helpful information I've gleaned from this forum is what blood tests can be done to reveal a situation. An example is the marker for prolactin indicating high estrogen activity because estrogen in the blood is not the same as estrogen in the tissue.

Perhaps everyone already know this information but from the Idealabs threads on Tyromix, Tyronene, and Tyromax it seems the focus is still on the TSH and T4 blood markers in determining if a product is working or not. I recognize every one is different which is what makes this article interesting to me. The variables are acknowledged, examined, and possible tests provided to help sort out the complexities.

 

[Tristan Loscha]

Bump for visibility, very high importance for members.What i get from it is that labs cant be trusted in the presence of disorder because of the defective sensoring of the body,that the estimation of the body in regards to distribution and amount of needed Thyroid itself is faulty,and as a reading worthless,basically we just see what the system misrepresents to itself internally.




ABSTRACT
There have been recent advances in understanding of the local control of thyroid
activity and metabolism, including deiodinase activity and thyroid hormone
membrane transport. The goal of this review is to increase the understanding of
the clinical relevance of cellular deiodinase activity. The physiologic significance
of types 1, 2 and 3 deiodinase (D1, D2 and D3, respectively) on the intracellular
production of T3 are discussed along with the importance and significance of the
production of reverse T3. The difference in the pituitary and peripheral activity of
these deidoidinases under a wide range of common physiologic conditions results
in different intracellular T3 levels in the pituitary and peripheral tissues, resulting
in the inability to detect low tissue levels of thyroid hormone in peripheral tissues
with TSH testing. This review demonstrates that extreme caution should be used in
relying on TSH or serum thyroid levels to rule out hypothyroidism in the presence of
a wide range of conditions, including physiologic and emotional stress, depression,
dieting, obesity, leptin insulin resistance, diabetes, chronic fatigue syndrome,
fibromyalgia, inflammation, autoimmune disease, or systemic illness, as TSH levels
will often be normal despite the presence of significant hypothyroidism. The review
discusses the significant clinical benefits of thyroid replacement in such conditions
despite having normal TSH levels and the superiority of T3 replacement instead of
standard T4 therapy.
Keywords:
Deiodinase; T3; Reverse T3 (RT3); D1; D2; D3