Fight post fin with fin?

[IHateFin]

Going back on finasteride has me feeling amazing for 10 days - testosterone boost?

im not encouraging this but would like the thoughts of those whom have either considered it or are smarter than I am and can give detail on the possibility of a good outcome on this. I'm especially looking at you, @gbolduev haha

I think it has been touched on before how it's possible, but if fin can cure PAS which is arguably a more severe PFS can the same be done for PFS?
There are those whom have cured PFS with dutasteride and there are instances where I read about fin making ppl feel better as they start to crash.

I'm thinking that the resurgence of dht is what killed our androgen sensativity when the hpg saw this as a means to alter hormones as a feedback loop.
If one can take a low enough dose (.125mg to .04mg) and taper off by gradually increasing spacing of doses could this help resensatize androgen receptors, increase brain 5AR to compentare for low 5AR outside of the CNS and increase 5beta reductase curing all the digestion problems too?

 

[IHateFin]

Do not stop finasteride cold turkey! A strong argument to taper to very low doses.

Taper info

 

[PFStinks]

Basically from what I've gathered, while on finasteride the body produces more androgen receptors (or possibly makes your receptors more sensitive) in order to get as much DHT as possible. Once you quit finasteride the influx in DHT puts your HPT axis into shock and your body doesnt know how to handle the new DHT in your system.

A new protocol I have been experimenting with, it can be used for both accutane and PFS sufferers

This person had a protocol where he brought his DHT down with high-doses of zinc in order to get a new baseline, it worked for him temporarily. It also worked for me when I tried it. Doing some research into zincs relationship with DHT I found that high-doses of zinc do indeed temporarily lower DHT, but over-time zinc use actually increases DHT.

So one person with temporary success from high-dose zinc, another with temporary success with finasteride and two cured from dutasteride. I'd say this is worth looking in to.

As for the person that had 10 days of success from finasteride, I'm guessing he went back on 1mg, and then shot his DHT way down again after 10 days. Perhaps if he were to go back on a quarter pill, 0.25mg every other day or every 3 days, and then super slowly decrease his dose his body may have had a better shot at adjusting to a higher baseline DHT level.


@gbolduev What do you think of all of this?

 

[Helen]

Going back on finasteride has me feeling amazing for 10 days - testosterone boost?

im not encouraging this but would like the thoughts of those whom have either considered it or are smarter than I am and can give detail on the possibility of a good outcome on this. I'm especially looking at you, @gbolduev haha

I think it has been touched on before how it's possible, but if fin can cure PAS which is arguably a more severe PFS can the same be done for PFS?
There are those whom have cured PFS with dutasteride and there are instances where I read about fin making ppl feel better as they start to crash.

I'm thinking that the resurgence of dht is what killed our androgen sensativity when the hpg saw this as a means to alter hormones as a feedback loop.
If one can take a low enough dose (.125mg to .04mg) and taper off by gradually increasing spacing of doses could this help resensatize androgen receptors, increase brain 5AR to compentare for low 5AR outside of the CNS and increase 5beta reductase curing all the digestion problems too?

I think it might be like this.
Fin binds NADPH. So 5 alpha reductase goes down. Body lowers DHT conversion to its metabolites. You go off fin, NADPH, does not go up. Since the body adjusted to live without NADPH and without 5 alpha reductase.


Without NADPH there is no 5 alpha reductase action even if the actual enzyme expression is high., there is high progesterone and low progesterone metabolites. And low axis since NADPH is what converts cholesterol into pregnenolone . And also there is a huge oxidative stress, since glutathione is not recycled. Thus scarring fibrosis etc. Also sugar metabolism is closed. since it would create oxidative stress. Since for that it needs thiamine. And thiamine is needed to start up NADPH production. This is body has to go and make NADPH using niacin and hydrogen and very little NADPH is made from NADH using malate. in the krebs cycle instead of making 12 NADPHs in pentose pathway using thiamine. This is why chronic fatigue takes place. Body pisses out thiamine and zinc. in order get rid of inflammation. Basically fin causes huge inflammation in the body which then downregulates all sugar metabolism and androgens.

This is basically why body does not start up NADPH huge. it simply cant use thiamine without glutathione protection. And chooses to live like it was.

To increase NADPH in this case, you need to covert DHT to its metabolites. Or block DHT receptors.( this is not good, since it will lower DHT conversion to its metabolites) and will lower 3 alpha and 3 beta hsd.

Fin makes no sense to me. It will just bind NADPH again.

It is better to take sulphoraphane or zinc , since 3 alpha hsd and 3 beta hsd break down DHT . 3 beta hsd work on zinc And take b50 vitamins. IF DHT is broken down, body will ask for NADPH to make DHT. And this will start cholesterol to androgens conversions, since they are all on NADPH








You basically forcefully lower DHT down to its metabolites. This asks the body to make more DHT. For that body need 5 alpha reductase and NADPH. So it will ask for niacin thiamin b2 and others Bs to make NADPH.

 

[PFStinks]

I think it might be like this.
Fin binds NADPH. So 5 alpha reductase goes down. Body lowers DHT conversion to its metabolites. You go off fin, NADPH, does not go up. Since the body adjusted to live without NADPH and without 5 alpha reductase.


Without NADPH there is no 5 alpha reductase action even if the actual enzyme expression is high., there is high progesterone and low progesterone metabolites. And low axis since NADPH is what converts cholesterol into pregnenolone . And also there is a huge oxidative stress, since glutathione is not recycled. Thus scarring fibrosis etc. Also sugar metabolism is closed. since it would create oxidative stress. Since for that it needs thiamine. And thiamine is needed to start up NADPH production. This is body has to go and make NADPH using niacin and hydrogen and very little NADPH is made from NADH using malate. in the krebs cycle instead of making 12 NADPHs in pentose pathway using thiamine. This is why chronic fatigue takes place. Body pisses out thiamine and zinc. in order get rid of inflammation. Basically fin causes huge inflammation in the body which then downregulates all sugar metabolism and androgens.

This is basically why body does not start up NADPH huge. it simply cant use thiamine without glutathione protection. And chooses to live like it was.

To increase NADPH in this case, you need to covert DHT to its metabolites. Or block DHT receptors.( this is not good, since it will lower DHT conversion to its metabolites) and will lower 3 alpha and 3 beta hsd.

Fin makes no sense to me. It will just bind NADPH again.

It is better to take sulphoraphane or zinc , since 3 alpha hsd and 3 beta hsd break down DHT . 3 beta hsd work on zinc And take b50 vitamins. IF DHT is broken down, body will ask for NADPH to make DHT. And this will start cholesterol to androgens conversions, since they are all on NADPH








You basically forcefully lower DHT down to its metabolites. This asks the body to make more DHT. For that body need 5 alpha reductase and NADPH. So it will ask for niacin thiamin b2 and others Bs to make NADPH.

What is the explanation for the people cured from dutasteride, or the person who had 10 good days on finasteride?

 

[Helen]

lets also think if the body could not handle DHT after quitting fin . The body will lower axis and not make DHT, and it will convert DHT into it metabolites rapidly

I thought post finasteride has low DHT metabolites. ( may be I am wrong.) can some one clarify this? Did anyone test their DHT metabolites?

 

[PFStinks]

lets also think if the body could not handle DHT after quitting fin . The body will lower axis and not make DHT, and it will convert DHT into it metabolites rapidly

I thought post finasteride has low DHT metabolites. ( may be I am wrong.) can some one clarify this? Did anyone test their DHT metabolites?

I'm not sure how accurate this is, but this person theorized that there's two types of PFS.

A new protocol I have been experimenting with, it can be used for both accutane and PFS sufferers

"
PFS type 1: 5AR/DHT levels are impaired but androgen receptors are still somewhat functional. (They are still abnormal though) People with PFS type 1 respond best to things like creatine, sorghum, weightlifting, etc. Basically anything that boosts 5AR/DHT.

PFS type 2: 5AR/DHT levels are too high relative to the sensitivity levels of the androgen receptors. People with PFS type 2 respond best to things that lower 5AR/DHT levels, such as zinc, marijuana or even things like saw palmetto and microdoses of propecia. (wouldnt recommend the last one though)"

 

[Helen]

I wrote extensively that there are 2 types of PFS

 

[PFStinks]

I wrote extensively that there are 2 types of PFS

Ah okay, sorry. Perhaps one of the types has high DHT metabolites... I wonder if it would be a bad thing to block only SOME 5ar, with low-dose finasteride, trying to do a balancing act so more NADPH is made than destroyed. I think high dose zinc is a temporary solution and sulforaphane is hard to get a hold of in reliable quantities.

 

[PFStinks]

Thyroxine Upregulates 3a-HSD (which converts DHT to 3-Adiol G) : Other Studies

This thread about Thyroxine upregulating 3a-HSD is interesting, apparently it cured somebody.

 

[Helen]

Ah okay, sorry. Perhaps one of the types has high DHT metabolites... I wonder if it would be a bad thing to block only SOME 5ar, with low-dose finasteride, trying to do a balancing act so more NADPH is made than destroyed. I think high dose zinc is a temporary solution and sulforaphane is hard to get a hold of in reliable quantities.

sulforaphane is sold everywhere. Jarrow Formulas, BroccoMax, Myrosinase Activated, 120 Veggie Caps

Sulforapahne is what upregulates 3 alpha hsd. And thought about as a cure for hairloss.

 

[Helen]

This is why for PFS it is all about starting up sugar metabolism. In both cases sugar metabolism is closed. In one case there is a high reverse t3 hormone , which tells you that the body is missing glutathione recycling, basically glutathione plus b vitamins.

And in another case. body is missing SOds and selenocysteine. and b vitamins

 

[PFStinks]

sulforaphane is sold everywhere. Jarrow Formulas, BroccoMax, Myrosinase Activated, 120 Veggie Caps

Sulforapahne is what upregulates 3 alpha hsd. And thought about as a cure for hairloss.

Yes but the bio-availability of sulforaphane in supplement form is really bad.

Growing them yourself is much better, but more of a hassle.

 

[HerrFisch]

Just use the supplement with the myrosinase with eating a lot of raw broccoli

 

[hairsuit]

This is why for PFS it is all about starting up sugar metabolism. In both cases sugar metabolism is closed. In one case there is a high reverse t3 hormone , which tells you that the body is missing glutathione recycling, basically glutathione plus b vitamins.

And in another case. body is missing SOds and selenocysteine. and b vitamins

So, if I have been taking a liposomal glutathione supplement and a heavy super B vitamin, would that rule out those things as an issue for me since it has done nothing? Or is the problem that the body cannot assimilate what I am putting in?

 

[IHateFin]

I think it might be like this.
Fin binds NADPH. So 5 alpha reductase goes down. Body lowers DHT conversion to its metabolites. You go off fin, NADPH, does not go up. Since the body adjusted to live without NADPH and without 5 alpha reductase.


Without NADPH there is no 5 alpha reductase action even if the actual enzyme expression is high., there is high progesterone and low progesterone metabolites. And low axis since NADPH is what converts cholesterol into pregnenolone . And also there is a huge oxidative stress, since glutathione is not recycled. Thus scarring fibrosis etc. Also sugar metabolism is closed. since it would create oxidative stress. Since for that it needs thiamine. And thiamine is needed to start up NADPH production. This is body has to go and make NADPH using niacin and hydrogen and very little NADPH is made from NADH using malate. in the krebs cycle instead of making 12 NADPHs in pentose pathway using thiamine. This is why chronic fatigue takes place. Body pisses out thiamine and zinc. in order get rid of inflammation. Basically fin causes huge inflammation in the body which then downregulates all sugar metabolism and androgens.

This is basically why body does not start up NADPH huge. it simply cant use thiamine without glutathione protection. And chooses to live like it was.

To increase NADPH in this case, you need to covert DHT to its metabolites. Or block DHT receptors.( this is not good, since it will lower DHT conversion to its metabolites) and will lower 3 alpha and 3 beta hsd.

Fin makes no sense to me. It will just bind NADPH again.

It is better to take sulphoraphane or zinc , since 3 alpha hsd and 3 beta hsd break down DHT . 3 beta hsd work on zinc And take b50 vitamins. IF DHT is broken down, body will ask for NADPH to make DHT. And this will start cholesterol to androgens conversions, since they are all on NADPH








You basically forcefully lower DHT down to its metabolites. This asks the body to make more DHT. For that body need 5 alpha reductase and NADPH. So it will ask for niacin thiamin b2 and others Bs to make NADPH.

I can't say this doesn't make sense haha and I always appreciate the level of detail you put into your posts, but what about the down regulated androgen receptor angle?

If someone's PFS is solely due to androgen resistance like those who feel nothing or worse from normal or Supra physiological doses of androgens then would this be the reason it could have merit or why dut works?

I feel dutasteride works due to the long half life basically causes a suuuuuper slow taper depending on how the liver is able to metabolize the drug

 

[MNK99]

Brother used fin no major problem (he has some add himself) but always forgot to take it.
Has dermatology friends that take Duta like once every 4-8 weeks maybe it was 6 weeks.
Not sure how someone is supposed to remember to take a pill every 42 days or a fraction every 14 or so.
People taking it intermittently and getting results is in line with that slow taper, I thought about this. But obviously I get deadly rxns and wouldn't risk it. Esp after the hell of last yr.

 

[Jaxx]

Interestingly there is someone that got cured from pssd with a low, on/off dose of ssri. Doubt it is the same mechanism though...

 

[Jaxx]

Basically from what I've gathered, while on finasteride the body produces more androgen receptors (or possibly makes your receptors more sensitive) in order to get as much DHT as possible. Once you quit finasteride the influx in DHT puts your HPT axis into shock and your body doesnt know how to handle the new DHT in your system.

A new protocol I have been experimenting with, it can be used for both accutane and PFS sufferers

This person had a protocol where he brought his DHT down with high-doses of zinc in order to get a new baseline, it worked for him temporarily. It also worked for me when I tried it. Doing some research into zincs relationship with DHT I found that high-doses of zinc do indeed temporarily lower DHT, but over-time zinc use actually increases DHT.

So one person with temporary success from high-dose zinc, another with temporary success with finasteride and two cured from dutasteride. I'd say this is worth looking in to.

As for the person that had 10 days of success from finasteride, I'm guessing he went back on 1mg, and then shot his DHT way down again after 10 days. Perhaps if he were to go back on a quarter pill, 0.25mg every other day or every 3 days, and then super slowly decrease his dose his body may have had a better shot at adjusting to a higher baseline DHT level.


@gbolduev What do you think of all of this?

That protocol is actually outdated, check this site for more details Cure PFS and Accutane Side Effects

 

[PFStinks]

That protocol is actually outdated, check this site for more details Cure PFS and Accutane Side Effects

I wouldn't say its outdated, he appears to have changed his protocol quite a bit now.
His older protocol was more about directly getting DHT into a certain range, and now it's turned into a whole thing with demethalyzation.
The guy was clearly getting results from zinc but they didn't stick because zinc was a temporary solution.
I'm very tempted to try the low-dose finasteride every 3 days and see how I feel.