This is an excerpt of the explanation of Reverse T3:-
"What is reverse T3?
You might hear the term ‘reverse T3’ come up as you learn more about your thyroid health. Here’s what you should know:
First, it’s important to understand that the body can only use T3, which is the active form of thyroid hormone. T4 is basically inactive within the body, according to Yasmin Akhunji MD, a board-certified endocrinologist from Paloma Health. It’s really used to store and transport T3 around the body to where it’s needed.
Your thyroid gland makes about 80 percent T4 and only 20 percent T3. As a result, T4 is converted into T3 within your body by enzymes called deiodinases. This is why people with hypothyroidism are often treated with synthetic T4, which is then converted within your body.
According to Dr. Rose, “Reverse T3 (rT3) is the metabolically inactive form of T3. Reverse T3 contains the same number of iodine molecules [as T3] but attached to different areas.”
Reverse T3 is made from T4, Dr. Rose explains. “The normal process of thyroid hormone synthesis is the formation of T3 from T4. However, T4 can also form reverse T3.”
Why is this a potential problem? Reverse T3 can bind to a cell in the same way T3 does, except when reverse T3 binds to it, nothing happens. When this happens, Dr. Rose explains, “reverse T3 and T3 will then compete for receptors' at the cellular level. Your body can start showing symptoms of hypothyroidism when not enough T3 is binding to your cells.”
In cases of chronic disease such as HIV or kidney disease, starvation or extreme dieting, bone marrow transplantation, or kidney disease, reverse T3 can become elevated.
Why is this a potential problem? Reverse T3 can bind to a cell in the same way T3 does, except when reverse T3 binds to it, nothing happens. When this happens, Dr. Rose explains, “reverse T3 and T3 will then compete for receptors' at the cellular level. Your body can start showing symptoms of hypothyroidism when not enough T3 is binding to your cells.”
This is false. It's what used to be thought but now we know that rT3 has its own receptors. It does not block T3 receptors.
Reverse T3 is made from T4, Dr. Rose explains. “The normal process of thyroid hormone synthesis is the formation of T3 from T4. However, T4 can also form reverse T3.”
That isn't exactly correct, either. T4 is always converted to a certain amount of T3 and a certain amount of rT3. Always. It's just that when FT4 is too high, more is converted to rT3 and less to T3 as a safety valve to stop you becoming over-medicated.
There is no 'optimal' number for rT3, it's not something you need. It is inert and doesn't stay in the body for more than two hours, when it is converted to T2. It doesn't cause symptoms.
There are many, many causes of high/over-range rT3, and only one of them has anything to do with thyroid. And, that is when FT4 is too high.
That is a dreadful link, shaws. Think you ought to dump it.
There isn’t an optimal level for RT3 because its correct ratio within other thyroid hormone levels will alter from one individual to the next and because its causes are so multifactorial. Common causes on this forum are elevated FT4, low cortisol, iron deficiency, oestrogen dominance, inflammation, depression, other medications, etc, etc.
RT3 per se doesn’t cause our meds not to work effectively but the deiodinase enzyme (D3) that causes T4 to convert to excess RT3 levels does! ... by also causing T3 to convert to an inactive form of T2 called 3,3′-T2. D3 can not differentiate between T4 & T3 (ie when upregulated it converts both together) and it is this that results in cellular T3 loss that gives us hypothyroid symptoms.
Therefore, RT3 tests can be useful if results are understood, and it is better to aim for good RT3 levels (as in within a healthy ratio to other thyroid hormones), as this evidences the down-regulation of D3 enzyme and so less T3 conversion to inactive forms.
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