Not everything needs to be backed by some “research” paper on pubmed to be true, credentialism and this mindset are exactly the reason tons of people struggle to get better.
See these articles/websites for the relationship between high cortisol and rt3:
To be clear, supplementing with thyroid hormone (T4) in the presence of high reverse t3 and/or cortisol levels is not going to be beneficial (if not worse). So bringing rt3 down first then re-introducing NDT/Armour is more than likely the best route. HC may also be required at low dosages to support the adrenals and delivery of thyroid hormones.
Cortisol enhances T4 to T3 conversion. There is no evidence available that suggests high cortisol is responsible for increased T4 to rT3 conversion - association is not causality.
There is no rational in ‚correcting‘ rT3 first.
rT3 signals that the body is in a ‚bad‘ status eg systemic inflammation, starvation etc. rT3 is a symptom and does not need treatment, treating the underlying cause will correct rT3 automatically.
Any form of cortisol treatment is something one should avoid unless absolutely necessary because it can lead to adrenal insufficiency.
Anyway I think I won’t be able to convince you and it’s fair enough that you are following your own path and thoughts. Hope you are doing better soon whatever the cause and the solution is/will be.
Personally, i disagree with all of @johann77 takes when it comes to t3 and rt3. I believe his thoughts on these are most likely antiquated at best.
T3 and rT3 are indeed important but you should be searching for an underlying cause for this issue instead of throwing a bunch of hormones into your body and hoping something sticks.
Do you have your latest thyroid and adrenal bloodwork at least?
As a scientist i analyze the available data and come to a conclusion.
I am perfectly fine with changing my point of view if convincing evidence is provided. STDM doesnt count as a scientific reference, by no means.
Binding of rT3 to the thyroid receptor hasnt changed since the 1980s where it was on several occassions demonstrated to be of significantly lower affinity than T3.
And regarding T3; only in the last 5 years we have discovered the significantly elevated risks for cardiac events in subjects with fully surpressed TSH as it is encountered in eg T3 only treatment of hypothyroidism.