here’s an interesting theory, which comes from a facebook group about the syndrome and from a forum (whose name starts with h and ends in s, don’t know why but i cannot write it).
what i miss is the link between this theory and the solutions.
the solutions are fasting and tei (trace elements inc.).
1. the theory
"Good guys we advance!
I’m going to expose the only theory that seems to me reliable at present, it comes from an English forum and was published by a researcher.
Being suspicious, I asked the opinion of a researcher from the University of Strasbourg, lecturer in organic chemistry.
He confirms the theory. I first expose you first:
Finasteride is a drift of progesterone. (see synthesis of finasteride using progesterone as a precursor)
Unlike progesterone, finasteride can not convert to cortisol or progesterone metabolites.
Therefore, since it does not convert, it reduces the NADPH (see hormonal charts) which reduces the 5areductase (5AR)
Moreover, since it does not convert to cortisol, it artificially increases the “pressure” on cortisol, which reduces 5beta reductase (5BR)
This explains that the more Finasteride you take, the more you inhibit the 5BR plus cortisol increases.
5BR is one of the enzymes needed to make bile acids.
(Which may explain the biliary crises that some people undergo)
So you take finasteride, you inhibit NADPH and NADP, you inhibit 5AR and 5BR.
The majority of the symptoms come from the inhibition of the 5BR (I let you search on Google)
Now you stop finasteride, this will cause a big rise in NADPH, the 5AR works with NADPH and the product of 5BR is NADPH.
So by increasing, the NADPH will inhibit even more the 5BR
The bile acids will no longer be produced, the cortisol on the ceiling, the aldosterone on the ceiling, since the 5BR does not degrade them anymore.
You are in metabolic alkalosis.
In summary, you stop taking finasteride, 5AR is restarting, increasing the NADPH which further inhibits the 5BR.
The PFS could therefore be explained by an imbalance NADPH, NADP.
NADPH is the product of the 5AR, NADP of the 5BR. But NADPH inhibits the 5BR. If the NADPH increases the NADP decreases.
And here’s what the teacher told me:
The chemical structure of this compound has two amide groups totally foreign to conventional hormonal derivatives.
That this compound can modify the blood composition is not surprising, but, in my opinion, its danger comes from the oxidation of amides in vivo N-oxyamide, which will lead to the consumption of reducing agents such as NADPH or the cysteine.
So we have a track more than serious.
It is thus necessary to make refurb the 5BR, either by decreasing the NADPH or by increasing the NADP. Either by the way of the cysteine.
Hence the interest of testing progesterone, aldosterone, cortisol, potassium, sodium, and alkaline reserve.
Obviously, these are not treatment tips, do not try anything for now
2. questions: the missing link
2.1. if you go on that forum, you’ll find some protocols made by a user called helen, the one who made this theory.
one of these protocols is pretty easy and is the tei protocol: you take a bunch of hairs, you send it to a laboratory, they tell you which supplements to take, what to eat and what to avoid and this is it.
balancing minerals should rebalance our bodies.
and this is pretty clear.
2.2. but what is the link between this theory and fasting? why fasting seems to be so beneficial for some?