Bits from the article:
The “hibernation hormone” that isn’t
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 . 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 .
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.