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I hope after CSF studies people understand a possible mechanism of PFS more. I posted a possible explanation and the protocol to try , but no one is trying it.
People are on TEI which is good and will cure you , also I approved Cdnuts protocol ( after seeing the studies understanding the mechanism)
I want to try to outline 2 mechanisms here which are interrelated
1) Finasteride is a progestin, as any progestin it bind NADPH. but unlike progesterone it does not convert to allopregnenolone or cortisol using NADPH.
So finasteride lowers allopregnenolone, and also lowers DHT since it binds to NADPH
So now the body has low DHT. Now follow me carefully. since DHT levels go very low. The body overexpresses the ARs in all DHT sensitive tissues
It is mainly in prostate and the BRAIN. Also body acetylates the histone on the ARs proteins. by acetylating histones, the body increases the effect of DHT on gene expression.
This way even with very very little DHT levels in blood, it can act the same way as normal DHT.
Then after you come of the drug. your DHT goes up and you have insane DHT action in the brain , prostate and all DHT sensitive tissues. Since in those tissues DHT is 10 times the volume of testosterone. There is basically no testosterone there.
DHT is a stress hormone, it causes aldosterone secretion and adrenaline secretion beyond regular aldosterone regulation. this is why if a normal healthy person takes DHT bioidentical hormone, that person will lose libido and erections.
SO after you go off finasteride DHT goes back up and now the brain has to lower its action, but histones are already acetylated, and ARs are highly overexpressed in all DHT sensitive places.
So the only way for the body to stop DHT action is to bind it with proteins. and also to methylate DNA to silence the gene expression.
This is why we see extremely low DHT levels in CSF fluid of PFS people. and most people's SHBG goes up, since it is trying very hard to bind DHT.
Since the body turns on the methylation and methylates the DNA to silence DHT action. It does this methylation thing to ALL ARs, and no only in places where DHT is present.
It methylates the DNA in all places. And this way in all other places where testosterone is a major hormone , basically testosterone GETS totally shut down.
Since during PFS testosterone was not low, and ARs were not overexpressed in tissues where testosterone is ACTIVE.
And it is testosterone which is responsible for deep voice, and libido and erections. not DHT.
So basically all tissues which are DHT sensitive have highly overexpressed ARs and and all tissues where testosterone is dominant it has normal ARs. but body is trying to fight DHT and methylates all ARs, and this way DHT gets back to almost normal action in DHT sensitive tissues , but testosterone does not act at all in testosterone sensitive tissues.
This explains why Cdnuts and other proponents of r andro get cured. since they overwhelm the binding of DHT and force the numbers of ARs to die down in DHT sensitive tissues.
and upon withdrawal from DHT, the brain wants more DHT , and it demethylates globally by which it makes testosterone work again.
I think there is a much faster way to do it. You basically need to stop methylation and feed DHT in this moment which will downregulate receptor density .
This also explains why people feel cured while on Anavar or other weak dht derivates like proviron. Since those are weaker than DHT. and are anti dht.
This also explains why you feel better on thyroid. Since THYROID increases the need for estrogen, and basically turns more testosterone into estrogen and less into DHT , which balances the ratio of testosterone to DHT. Less DHT equals more working testosterone.
Basically the problem is in the ratio of action of testosterone and DHT in their sensitive tissues.
DHT got very strong in its tissues, and this basically switches off testosterone action globally.
This is why anyone who has PFS will feel totally recovered by taking testosterone plus thyroid as a stilt.. Since thyroid will lower DHT and increase estrogen, which will steer the ratio of DHT - Testosterone to the testosterone side.
2) second problem is that finasteride killed
both GABA regulators at the same time. allopregnenolone and 3 adiol.
I would assume it will upregulate gaba receptor big time, and later it could stop 3 alpha hsd from working after you come off the drug, which is basically making the DHT problem described above even worse, since 3 alpha hsd is needed to convert DHT into 3 adiol.
This explains why some people had success with GHB which overtime downregulated GABA A receptor, and allowed DHT levels to come down which basically helped the DHT receptor overexpression problem.
I would assume this route could help the situation to some extent.
This mechanism explains hormone levels in CSF.
You need to understand that only free forms of hormones act on the brain. and prostate. if you want to measure DHT, you need to measure free DHT, not total DHT .
And when you measure all of the free forms, you will see that it should match the CSF study. Since only free hormones can enter CSF fluid.
People are on TEI which is good and will cure you , also I approved Cdnuts protocol ( after seeing the studies understanding the mechanism)
I want to try to outline 2 mechanisms here which are interrelated
1) Finasteride is a progestin, as any progestin it bind NADPH. but unlike progesterone it does not convert to allopregnenolone or cortisol using NADPH.
So finasteride lowers allopregnenolone, and also lowers DHT since it binds to NADPH
So now the body has low DHT. Now follow me carefully. since DHT levels go very low. The body overexpresses the ARs in all DHT sensitive tissues
It is mainly in prostate and the BRAIN. Also body acetylates the histone on the ARs proteins. by acetylating histones, the body increases the effect of DHT on gene expression.
This way even with very very little DHT levels in blood, it can act the same way as normal DHT.
Then after you come of the drug. your DHT goes up and you have insane DHT action in the brain , prostate and all DHT sensitive tissues. Since in those tissues DHT is 10 times the volume of testosterone. There is basically no testosterone there.
DHT is a stress hormone, it causes aldosterone secretion and adrenaline secretion beyond regular aldosterone regulation. this is why if a normal healthy person takes DHT bioidentical hormone, that person will lose libido and erections.
SO after you go off finasteride DHT goes back up and now the brain has to lower its action, but histones are already acetylated, and ARs are highly overexpressed in all DHT sensitive places.
So the only way for the body to stop DHT action is to bind it with proteins. and also to methylate DNA to silence the gene expression.
This is why we see extremely low DHT levels in CSF fluid of PFS people. and most people's SHBG goes up, since it is trying very hard to bind DHT.
Since the body turns on the methylation and methylates the DNA to silence DHT action. It does this methylation thing to ALL ARs, and no only in places where DHT is present.
It methylates the DNA in all places. And this way in all other places where testosterone is a major hormone , basically testosterone GETS totally shut down.
Since during PFS testosterone was not low, and ARs were not overexpressed in tissues where testosterone is ACTIVE.
And it is testosterone which is responsible for deep voice, and libido and erections. not DHT.
So basically all tissues which are DHT sensitive have highly overexpressed ARs and and all tissues where testosterone is dominant it has normal ARs. but body is trying to fight DHT and methylates all ARs, and this way DHT gets back to almost normal action in DHT sensitive tissues , but testosterone does not act at all in testosterone sensitive tissues.
This explains why Cdnuts and other proponents of r andro get cured. since they overwhelm the binding of DHT and force the numbers of ARs to die down in DHT sensitive tissues.
and upon withdrawal from DHT, the brain wants more DHT , and it demethylates globally by which it makes testosterone work again.
I think there is a much faster way to do it. You basically need to stop methylation and feed DHT in this moment which will downregulate receptor density .
This also explains why people feel cured while on Anavar or other weak dht derivates like proviron. Since those are weaker than DHT. and are anti dht.
This also explains why you feel better on thyroid. Since THYROID increases the need for estrogen, and basically turns more testosterone into estrogen and less into DHT , which balances the ratio of testosterone to DHT. Less DHT equals more working testosterone.
Basically the problem is in the ratio of action of testosterone and DHT in their sensitive tissues.
DHT got very strong in its tissues, and this basically switches off testosterone action globally.
This is why anyone who has PFS will feel totally recovered by taking testosterone plus thyroid as a stilt.. Since thyroid will lower DHT and increase estrogen, which will steer the ratio of DHT - Testosterone to the testosterone side.
2) second problem is that finasteride killed
both GABA regulators at the same time. allopregnenolone and 3 adiol.
I would assume it will upregulate gaba receptor big time, and later it could stop 3 alpha hsd from working after you come off the drug, which is basically making the DHT problem described above even worse, since 3 alpha hsd is needed to convert DHT into 3 adiol.
This explains why some people had success with GHB which overtime downregulated GABA A receptor, and allowed DHT levels to come down which basically helped the DHT receptor overexpression problem.
I would assume this route could help the situation to some extent.
This mechanism explains hormone levels in CSF.
You need to understand that only free forms of hormones act on the brain. and prostate. if you want to measure DHT, you need to measure free DHT, not total DHT .
And when you measure all of the free forms, you will see that it should match the CSF study. Since only free hormones can enter CSF fluid.
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