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Thanks for the explanation. Sorry, I misunderstood what “Anti-Peat” means.
I dont know what reverse T3 is. Ive only tested free T3.
I followed the Peat diet for 6 months.
Cool, thank you, and thanks for clarifying
Reverse T3 has 1% metabolic activity of T3, and it binds to the T3 receptor, preventing T3 from binding to it, so it’s essentially a metabolic blocker.
Could be a detox event. Each detox event brings a level up where you are stronger and more resilient on the other side.
Case closed. Don't blame liver for your problems.
What is the larger puzzle regarding accutane, if not liver & A accumulation?
I think you meant an accutard. (This is just for the joke Daniel, I don't want to insult you).
thought that at first too , but following is convincing rt3 doesnt block t3
Nobody uses Reverse T3 to suppress T3 in Graves’ disease. We don’t see RT3 pills sold on the market. This is because Graves’ disease will naturally have RT3 concentrations that far exceed the reference range to the degree that their FT4 is above reference. They become thyrotoxic anyway.
The highest RT3 levels are found in untreated hyperthyroidism.
- When D3 is working properly, it defends us from hyperthyroidism. It’s an intracellular defense mechanism.
- When D3 is temporarily upregulated in acute illnesses, it temporarily gives us extra intracellular and circulating iodine by removing iodine atoms from T4 and T3 molecules.
- But when D3 enzyme becomes chronically upregulated and the D1 and D2 enzymes become downregulated, it can cause a chronic problem of metabolic imbalance that steals intracellular T3.
While this happens, the imbalanced enzyme activity in cells causes RT3 to build up in blood, as RT3 is created at a faster rate than it is converted to inactive T2.
Essentially, hypothyroid symptoms and higher mortality rates are not caused by RT3 gain, but by chronic intracellular T3 losses.
There is evidence that points to high RT3 as a bad sign.
However, it’s a common logical fallacy to mistake correlation for causation.
These beliefs were proven false long ago in an experiment by Shulkin & Utiger in 1984, titled “Reverse triiodothyronine does not alter pituitary-thyroid function in normal subjects.”
They overdosed people with Reverse T3 until they had not just “high-normal” RT3, but 10-fold the amount of normal RT3 in blood.
What were the results? The healthy people did not become hypothyroid or unhealthy. Even their pituitary gland continued to perform T4-T3 conversion and T3 transport and signaling, because TSH did not rise.
The key was that these were healthy people with healthy thyroids dosed with RT3 whose FT3:FT4 ratios were not abnormal when the experiment started. They were not producing their own endogenous excess RT3 per unit of FT4 due to “nonthyroidal illness syndrome” (NTIS) that dysregulated their metabolism. Their metabolism was not taking apart their T3 at a high rate. Their bodies were capable of continuing to convert T4 to T3 despite excess RT3.
In these visuals, you will see that the net effect of Deiodinase Type 3 is to deplete T3 within the intracellular space, not to “block” the receptors with RT3.
You don’t need an RT3 plug to block the receptor in this scenario.
Neither Reverse T2 nor RT3 have enough affinity to the thyroid hormone receptors in the nucleus to bind with it.
Long ago, research proved that RT3 lacks an iodine atom at a key position on the molecule. It is handicapped and can’t bind to the nuclear receptors.
As a result, only T3 has the iodine “key” to enter the receptor’s “lock.”
However, RT3 is not entirely inactive as a hormone. This missing key doesn’t inactivate RT3 from binding to an entirely different receptor for thyroid hormones. We now know that T4 and RT3 bind to receptors on the cell membrane, called “integrin” receptors, where they don’t compete with T3 and sometimes don’t do friendly things. But that’s the subject of an entirely different post, the one on Cancer, T4, and RT3.
