Technically, the term “hibernation hormone” is inappropriate to describe reverse T3. Reverse T3 can be elevated in conditions associated with a reduction in the metabolic rate, notably starvation, extreme carbohydrate restriction, chronic heart failure, and the non-thyroidal illness syndrome (also called “euthyroid sick syndrome” or “low T3 syndrome”) seen in critical illness, very elderly patients, chronic stress, myocardial infarction, and chronic inflammatory states. In these cases, the rise in rT3 is a consequence, not a cause, of the alterations in intracellular thyroid hormone metabolism directed by the deiodinase enzymes, the relative activities of which are affected by the condition itself.
Some observed elevations in serum rT3 in the presence of exogenous thyroxine treatment are difficult to interpret, and can depend on the assay used. T4 can cross-react in immunoassays for rT3, resulting in a false increase in rT3 when T4 is high; more reliable tests for rT3 are performed using liquid chromatography/tandem mass spectrometry (LC-MS/MS). A study in euthyroid subjects receiving thyroxine suggested that the observed rise in rT3 was a result of increased substrate availability for the peripheral inactivation of T4 [10]. And elderly patients may either have an adaptive response to reduce thyroid hyperactivity at the tissue level, or have some type of non-thyroidal illness with consequent reactivation of D3, in both cases resulting in increased T4 inactivation via conversion to rT3; it has therefore been suggested that older patients with hypothyroidism may require lower replacement doses of T4 [11].
Goosey gives good advice when she tells people to not go on severe dietary restrictions. Seems it causes reverseT3 production.
There are quite a number of other interesting blog posts on this laboratory's website.
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gabkad
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Good article showing the immensely complicated psychology of a very small part of the endocrine system. I guess the term "hibernation hormone" refers to (extremely lucky) healthy individuals unlikely to experience the RT3 imbalances or dominance that accompanies thyroid issues.
At least the agreement seems to be that RT3 is a symptom rather than a cause and elevated levels are bad news. Also in order to overcome the generated high D3 enzyme activity, the underlying cause must be corrected such as high/low cortisol, low iron, insufficient nutrients, inflammation - these all applicable to Hashi sufferers and relatively easy to correct .... . BUT perhaps it depends on the severity and longevity of the said RT3 and then ... of course there are numerous others causes too ! ! ...
As we know reading RT3 test results is immensely difficult as so multi-multi-multi-multi-factorial and do most endos even know what a deiodinase is ? ? ...
The second article has the blood measurement ranges for fT3 and rT3. There's a lot more rT3 in the circulation by orders of magnitude than fT3 in healthy individuals. rT3 is measured in nanograms per and fT3 in picograms per.
I'm in Ontario and rT3 stopped being a lab test here in 2009.
There's a lot more rT3 in the circulation by orders of magnitude than fT3 in healthy individuals. rT3 is measured in nanograms per and fT3 in picograms per.
And despite this there are people on thyroid forums who claim that a high Free T3 must be "mostly Reverse T3". To me this is like saying a pint pot of Free T3 contains a few gallons of reverse T3. It's total nonsense.
Yes HB ... and how would they know ? ? .. as a high RT3 in one won't always equate to being higher than proportionate in anothers own thyroid psychology and whole general wellbeing.
... and why are they always in different measures ? ?
There is an equation for conversion but it is a bit beyond "necessary" work//maths. Education is good to have the ability to rectify so a basic understanding of thyroid function is excellent, but we should go on how we feel.
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