POTENTIAL explanation for PFS.

Walker

Well-Known Member
Oct 7, 2017
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Mountain Brook, AL
#63

Kjbigman

Well-Known Member
May 25, 2019
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#65
OK, So the reason why people got PFS in the first place is because they had problems with UDP gluconoryl transferase.

SO basically people had problems converting 3a- adiol into 3a- adiol G. before FIN. Since this conversion is done by UDP enzyme.

Same as people with Gilberts. This is why all Giberts people have POIS. and PFS.


Finasteride is metabolized by this enzyme UDP gluconoric transferase.

Some people still have finasteride in their body now since that enzyme was not working in the first place, this is why people got the hairloss.


The reason people have PFS and POIS is this. If you cant convert 3a- adiol into 3a- adiol G, then your 3 a- adiol accumulates. ( this was found in finasteride studies, that 3a - adiol was high in CFS.)

Body closes down 3 alpha hsd since 3 a-adiol is high. this increases DHT, this then closes down 5AR.


SO you end up with low 3alpha hsd and 5ar. Which then stops all conversion of progesterone and cortisol into its metabolites.

And you get low allopregnenolone and thdoc, and cortisol's thf and alpha thf metabolites.

This causes major problems with the immune system inflammation, anxiety and gaba regulations.



Since UDP enzyme is not working. body has higher DHT Test, progesterone and cortisol. And thus has to lose the zinc finger.

SO it dumps zinc into the urine constantly, to get rid of cortisol and DHT signaling






The fix is to increase UDP enzyme, which will convert 3 adiol into 3 adiol Gluc. This will lower 3 adiol, this will open up 3 alpha hsd and 5ar.

And this will lower cortisol and progesterone and DHT and 3 adiol and the body will actually ASK for the zinc finger.



UDP enzyme works on magnesium and glucoronic acid. ( UDP glucoronate)

Glucuronic acid is made out of glucose. in Uronic acid. pathway. How funny. but this is was first found in URINE))( may be this is how urine therapy works for so many diseases)


IN any case uronic pathway makes glucuronic acid. And in most species then vitamin C is made out of glucuronic acid.

They say in humans it does not happen, and vitamin C is not made out of glucuronic acid.

BUT and it is a huge but, when they give vitamin C , it increases UDP glucuronyl transferase activity 2 times, means that it is probably sparing the glucuronic acid. So may be we do make vitamin C out of glucurornic acid.

When glutathione recycling goes down, since FIN binds NADPH. And NADPH is needed for glutathione reductase. This basically oxidizes most of the vitamin C . and there is no ascrobate, but tons of DHA. Then may be the body starts using glucuronic acid to make extra vitamin C. And thus this enzyme UDP totally stops. And they call this Gilbert's syndrome.

Then when you stop finasteride , DHT goes back up, 3 a- adiol levels go sky high, but UDP is now totally FUCKED. and it is UDP which converts 3a adiol into 3a- adiol G. so the body first stops 3alpha and then 5ar, and and starts to lose zinc .. And CRASH. Look at the chart of hormones


This now makes sense for hairloss and PFS. Finasteride when you take it, kills 3 adiol, and DHT and basically stops the hairloss, which you had before FIn.

the hairloss was happening since your UDP enzyme was not working in the first place. and you had a type of gilbert syndrome.This is why after fin , you still lose hair, if you could metabolize it out. If you could not metabolize it out . you end up with low DHT.


So the fix for this situation, would be anything with glucuronic acid. May be ICELANDIC MOSS



And also you need to restore acrobate levels. with glutathione recylcing. And zinc manganese and b vitamins. vitamin C and E. Basically this is what TEI is trying to do .

And this is what @Orion is doing.





@tallglass13 Hairloss topic. Which brings hairloss basically to availability of ascorbate. which if not available since low glutathione recycling( magnesium b1 b2 etc) , probably causes too much pressure on glucuronic acid. And then your 3 -adiol goes up, 3 adiol G down, and DHT up.

And body loses zinc which is then called pyroluria.



@Orion UDP enzyme is what metabolizes retinoids.
Why can't you fix the problem by supplementing vitamin C while on finasteride so that your body doesn't need to use glucoronic acid to make it?

@Helen also, UDP is involved in retinoid acid metabolism as you said. I get really bad reactions from vitamin A it seems. Could it be that this is causing some kind of poisoning each time I consume vitamin A because the UDP is already very slow from finasteride+Gilberts? U know what's weird? My genetics said that I would be LOW in vitamin A. Probably they meant that my shitty enzymes/liver wouldn't be able to process it well. But that leads me to think that I have both toxicity and deficiency.

I was thinking that slow 3a-hsd could cause buildup of DHT as well (cuz my twin bro is on Paxil which speeds up 3a-hsd, so I was thinking maybe hair loss and depression is caused by slow 3a-hsd), but it makes more sense that people experience hair loss from something common like UGT1A1 deficiencies.
 

Minime

Well-Known Member
Oct 4, 2017
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#66
I must have overlooked this thread when it was first introduced. It is interesting...the part about Gilbert’s Syndrome. I have Gilbert’s and thus my bilirubin is always a bit high on my labs. Never really thought it may be a factor in PFS. But I do have both PFS and POIS symptoms.
 

Kjbigman

Well-Known Member
May 25, 2019
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USA
#67
Thinking about how to increase UGT activity, particularly UGT2B15 and 2B17, as those metabolize androgens most heavily.
So here is my guess at a protocol to increase UGT enzyme activity, by providing substrates:
Also, avoid this for more UGT activity:
Green and white teas suppress UDP-glucuronosyltransferase UGT2B17 mediated testosterone glucuronidation
calcium d-glucarate too