PFS BLOOD TESTS( and THEORY )

Helen

Well-Known Member
Staff member
Messages
5,415
here I collected the PFS bloods test. and as we can see from these tests. As i said tetrafolate is ZERO in PFS patients. Glutathione is zero also

Without folinic acid, you simply cant make DNA.


here are the tests

Person 1.

AminoAcids in Plasma
Glutathione (oxidised) 0.57 µmol/L Range (0.16 - 0.50)
Glutathione (reduced) 3.4 µmol/L (3.8 - 5.50)
Derivates
S-Adenosylmethionine (RBC) 219 µmol/dl (221 - 256)
S-Adenosylhomocysteine (RBC) 56.6 µmol/dl (38.0 - 48.0)

FOLIC ACID DERIVATES
5-CH3-THF 9.0 nmol/l (8.4 - 72.6)
10-Formyl-THF 5.4 nmol/l (1.5 -8.2)
5-Formyl-THF 4.9 nmol/l (1.20 - 11.70)
THF 0.60 nmol/l (0.6 - 6.80)
Folic Acid 10.7 nmol/l (8.9 - 24.6)

Folinic Acid (WB) 8.2 nmol/l (9.0 - 35.5)
Active Folate (RBC) 356 nmol/l (400 - 1500)

NUCLEOSIDE
Adenosine 25.5 10^-8 M (16.8 - 21.4 )



Person 2

GLUTATHIONE PANEL.png


person 3

AMINOACIDS IN PLASMA
Glutathione (oxidised) 0.55 µmol/L (0.16 - 0.50)
Glutathione (reduced) 3.0 µmol/L (3.8 - 5.5)

Derivates
S-Adenosylmethionine (RBC) 213 µmol/dl (221 - 256)
S-Adenosylhomocysteine (RBC) 53.4 µmol/dl (38.0 - 49.0)

FOLIC ACID DERIVATES
5-CH3-THF 11.4 nmol/l (8.4 - 72.6)
10-Formyl-THF 6.3 nmol/l (1.5 - 8.2)
5-Formyl-THF 1.20 nmol/l (1.20 - 11.70)
THF 0.51 nmol/l (0.6 - 6.80)
Folic Acid 12.5 nmol/l (8.9 - 24.6)
Folinic Acid (WB) 8.6 nmol/l (9.0 - 35.5)
Active folate (RBC) 322 nmol/l (400 - 1500)

NUCLEOSIDE
Adenosine 24.6 10^-8 M (16.8 - 21.4)




there are about 10-15 tests like that with IDENTICAL values in all tests.



As I said, NADPH is needed to make THF acid. without THF there is no histidine, and without folinic there is no BH4, there is also no glutathione and no nitric oxide.

Histone needs to be methylated, so without this stuff it will not happen.


What we see on hairtests are different oxidations, but all of them have this in common.


Androgen Receptor density is huge in PFS patients, and AR has no problems going from cytoplasm into nucleous at all. SO there is NOTHING wrong with the actual AR protein or its density, THIS IS 1000000% .



So now we have 2 possibilities here, either NADPH is shut down since receptor density is too much. and this is a feedback loop.


or second variant receptor density is high since the body is trying to compensate of the lack of signaling.

Lack of signaling is from histones or histone methylation. High DHT low DHT could be just your natural state, what you had before fin.


So the answer lays in

1) either this density is too big and this causes the shutdown of NADPH system which then leads to low folates.( which we see)
2) there is lack of signaling since glutathione and methylation block has happened and this is why receptor density is big and stays big trying to compensate for lack of signaling



Dont forget FIN binds NADPH and lowers it, so people who lived on fin for years like 5 -10 years, you will be living without Glutathione for years.

this means that you had the same disorder like autists have. You got so toxic in your brain with heavy metals that it is not even funny and liver.

SO for you to get back to pre FIN, it will be like fixing an autistic child.

This is what ELECTROLYTES protocol was aimed at. @bruschi11


this is why it is so hard to recover from PFS. or CSF. since as your nitric oxide production and antioxidant system never go back on line. the body simply cant signal steroids to do their job.



So to me , 2 variants here are obvious.


1) overexpressed AR and cortisol GR for that reason. and may be gaba a which are stopping NADPH production, causing glutathione and folate deficiencies which total kill your nitric oxide bh4 levels etc and this is AR silencing mechanism not to cause hypokalemia.

2) glutathione depletion and brain toxicity is actually stopping AR receptor from working properly since methylation of histones is not working
and thus the body has to overexpress the AR to try to compensate.



@hairsuit
 
Last edited:

wuf

Well-Known Member
Messages
880
here I collected the PFS bloods test. and as we can see from these tests. As i said tetrafolate is ZERO in PFS patients. Glutathione is zero also

Without folinic acid, you simply cant make DNA.


here are the tests

Person 1.

AminoAcids in Plasma
Glutathione (oxidised) 0.57 µmol/L Range (0.16 - 0.50)
Glutathione (reduced) 3.4 µmol/L (3.8 - 5.50)
Derivates
S-Adenosylmethionine (RBC) 219 µmol/dl (221 - 256)
S-Adenosylhomocysteine (RBC) 56.6 µmol/dl (38.0 - 48.0)

FOLIC ACID DERIVATES
5-CH3-THF 9.0 nmol/l (8.4 - 72.6)
10-Formyl-THF 5.4 nmol/l (1.5 -8.2)
5-Formyl-THF 4.9 nmol/l (1.20 - 11.70)
THF 0.60 nmol/l (0.6 - 6.80)
Folic Acid 10.7 nmol/l (8.9 - 24.6)

Folinic Acid (WB) 8.2 nmol/l (9.0 - 35.5)
Active Folate (RBC) 356 nmol/l (400 - 1500)

NUCLEOSIDE
Adenosine 25.5 10^-8 M (16.8 - 21.4 )



Person 2

View attachment 1363


person 3

AMINOACIDS IN PLASMA
Glutathione (oxidised) 0.55 µmol/L (0.16 - 0.50)
Glutathione (reduced) 3.0 µmol/L (3.8 - 5.5)

Derivates
S-Adenosylmethionine (RBC) 213 µmol/dl (221 - 256)
S-Adenosylhomocysteine (RBC) 53.4 µmol/dl (38.0 - 49.0)

FOLIC ACID DERIVATES
5-CH3-THF 11.4 nmol/l (8.4 - 72.6)
10-Formyl-THF 6.3 nmol/l (1.5 - 8.2)
5-Formyl-THF 1.20 nmol/l (1.20 - 11.70)
THF 0.51 nmol/l (0.6 - 6.80)
Folic Acid 12.5 nmol/l (8.9 - 24.6)
Folinic Acid (WB) 8.6 nmol/l (9.0 - 35.5)
Active folate (RBC) 322 nmol/l (400 - 1500)

NUCLEOSIDE
Adenosine 24.6 10^-8 M (16.8 - 21.4)




there are about 10-15 tests like that with IDENTICAL values in all tests.



As I said, NADPH is needed to make THF acid. without THF there is no histidine, and without folinic there is no BH4, there is also no glutathione and no nitric oxide.

Histone needs to be methylated, so without this stuff it will not happen.


What we see on hairtests are different oxidations, but all of them have this in common.


Androgen Receptor density is huge in PFS patients, and AR has no problems going from cytoplasm into nucleous at all. SO there is NOTHING wrong with the actual AR protein or its density, THIS IS 1000000% .



So now we have 2 possibilities here, either NADPH is shut down since receptor density is too much. and this is a feedback loop.


or second variant receptor density is high since the body is trying to compensate of the lack of signaling.

Lack of signaling is from histones or histone methylation. High DHT low DHT could be just your natural state, what you had before fin.


So the answer lays in

1) either this density is too big and this causes the shutdown of NADPH system which then leads to low folates.( which we see)
2) there is lack of signaling since glutathione and methylation block has happened and this is why receptor density is big and stays big trying to compensate for lack of signaling



Dont forget FIN binds NADPH and lowers it, so people who lived on fin for years like 5 -10 years, you will be living without Glutathione for years.

this means that you had the same disorder like autists have. You got so toxic in your brain with heavy metals that it is not even funny and liver.

SO for you to get back to pre FIN, it will be like fixing an autistic child.

This is what ELECTROLYTES protocol was aimed at. @bruschi11


this is why it is so hard to recover from PFS. or CSF. since as your nitric oxide production and antioxidant system never go back on line. the body simply cant signal steroids to do their job.



So to me , 2 variants here are obvious.


1) overexpressed AR and cortisol GR for that reason. and may be gaba a which are stopping NADPH production, causing glutathione and folate deficiencies which total kill your nitric oxide bh4 levels etc and this is AR silencing mechanism not to cause hypokalemia.

2) glutathione depletion and brain toxicity is actually stopping AR receptor from working properly since methylation of histones is not working
and thus the body has to overexpress the AR to try to compensate.
SO, what to do to fix this shit?)))))
In my perosnal opinion, as I said years ago... you should take few voluntaries (with different or same carhacteristics) from here, ask the tests you need from them, ask their 100% responsability on themself about trying what you suggest to them and try to fix people.
I think this is the only way even for you to confirm all your theories, otherwise they will only be words basically useless, since people even do not know what you are talking about and do not know how to fix what you say we are missing.
This is my personal opinion, and I push for this, I mean you to try to fix someone as you did before with Scenes etc...doing so, at this time we would all be balanced and cured instead of keeping discussing theories till we will die.
Do not take it personally, it is just a way to see things and a way to get to another level for this forum...with concrete recoveries we would be on another level now cause we (YOU) would have understood much more with real facts.
But thank you anyway for the thoeries you are putting out!!
Love you man!!
 

RebelWithACause

Well-Known Member
Messages
2,703
I was thinking about this:

If Post Saw Palmetto and Post Finasteride both can get fixed by following the cdsnuts protocol (herbs, R-Andro) eventhough they do not have the same mechanics. Why does the cdsnuts protocol work for both? Why do both PFS and Post Saw Palmetto get better from it even though both drugs do different things in the body.

R-Andro lowers iron, potassium, copper, right? When you block estrogen your body gets rid of copper I am guessing.

R-Andro lowers estrogen like nothing else. People have bad joints, irritation, back pain. Similar to when you take AI or high amounts of zinc.

Which could mean R-Andro chelates toxic metals from the body (brain and liver) (toxic iron, copper).

This is why you get a snapback. You are on R-Andro -> lowers estrogen which will make you feel shitty: low energy, irritation, etc. - but also better from lower estrogen/crazy copper mind. But after stopping R-Andro you see the real benefits (snapback). Your hormones go back to normal but now you have less copper and other toxic metals. Which will make your steroids work better. Since you explained if the brain is copper toxic your body will lower estrogen in the rest of the body.

This could be why people who take zinc + vitamin C + other shit like that dude on PropeciaHelp forum got better. He chelated copper. Or the guy who used letrozole.

This is also why PFS guys seem to go up, down, up, down. Emotional rollercoaster. For me after the first cycle on TEI this was considerably less. My emotional stability increased and anxiety decreased.

If it is really as bad as it seems then taking a bit of zinc or lowering your estrogen for a short time will not help. You will need to do it for a longer time.

This just does not explain how some guys take finasteride once and crash. Since this would not built up toxic metals as much.
 
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Helen

Well-Known Member
Staff member
Messages
5,415
I was thinking about this:

If Post Saw Palmetto and Post Finasteride both can get fixed by following the cdsnuts protocol (herbs, R-Andro) eventhough they do not have the same mechanics. Why does the cdsnuts protocol work for both? Why do both PFS and Post Saw Palmetto get better from it even though both drugs do different things in the body.

R-Andro lowers iron, potassium, copper, right? When you block estrogen your body gets rid of copper I am guessing.

R-Andro lowers estrogen like nothing else. People have bad joints, irritation, back pain. Similar to when you take AI or high amounts of zinc.

Which could mean R-Andro chelates toxic metals from the body (brain and liver) (toxic iron, copper).

This is why you get a snapback. You are on R-Andro -> lowers estrogen which will make you feel shitty: low energy, irritation, etc. - but also better from lower estrogen/crazy copper mind. But after stopping R-Andro you see the real benefits (snapback). Your hormones go back to normal but now you have less copper and other toxic metals. Which will make your steroids work better.

This could be why people who take zinc + vitamin C + other shit like that dude on PropeciaHelp forum got better. He chelated copper. Or the guy who used letrozole.

This is also why PFS guys seem to go up, down, up, down. Emotional rollercoaster. For me after the first cycle on TEI this was considerably less. My emotional stability increased and anxiety decreased.

If it is really as bad as it seems then taking a bit of zinc or lowering your estrogen for a short time will not help. You will need to do it for a longer time.

This just does not explain how some guys take finasteride once and crash. Since this would not built up toxic metals as much.





people who crash on fin right away, are g6pd deficient, they cant even make NADPH, their levels are low

you take fin, you kill little NADPH that you have and you get hemolytic ANEMIA. from low FOLATES


Saw palmetto has the same mechanics with fin.
 

RebelWithACause

Well-Known Member
Messages
2,703
people who crash on fin right away, are g6pd deficient, they cant even make NADPH, their levels are low

you take fin, you kill little NADPH that you have and you get hemolytic ANEMIA. from low FOLATES

So the people with g6pd deficiency are building up (a lot of) toxic metals even without the use of something like finasteride? Finasteride just pushes it over the edge and makes you completely crash.
 

Helen

Well-Known Member
Staff member
Messages
5,415
So the people with g6pd deficiency are building up (a lot of) toxic metals even without the use of something like finasteride? Finasteride just pushes it over the edge and makes you completely crash.

yes, this is what I said, people wiht low glutathione were losing hair because of low NADPH.

and then they take FIN)) they lose more hair)) and crash. with hemolytic anemia since FIN lowers NADPH

Steroids like testosterone also lower NADPH, thus those people CRASH on steroids. and g6pd deficient people cant take steroids))


Look at the tests above= all those people have hemolytic anemia)) and high bilirubin. since their red blood cells are not protected. they are all low on folate.

look at THF values and folinic acid))

they are done, they are in CRASH


SAME exactly how G6pd deficient people crash on FAVA BEANS. It is identical crash to PFS
 

Helen

Well-Known Member
Staff member
Messages
5,415
@RebelWithACause yes, most people were already sick pre FIN. and fin just caused the crash. accelerated the problem with folates
 

barbaar

Well-Known Member
Messages
807
So the people with g6pd deficiency are building up (a lot of) toxic metals even without the use of something like finasteride? Finasteride just pushes it over the edge and makes you completely crash.

People also get PSSD from taking SSRI just once. I'm pretty sure that happens when you're already fucked up in like 20 different ways, heavy metal toxicity, glutathione systems fucked etc. I remember taking the first damn pill of those things, it was like my brain instantly got wrapped in a thick heavy blanket. Looking back I had a looot of issues before PSSD already, brain fog, fatigue, all that fun stuff. PSSD just made everything worse and added sexual issues. (but hey at least depression and anxiety are gone lol)
 

Helen

Well-Known Member
Staff member
Messages
5,415
@RebelWithACause yes, if you are copper and iron toxic in the brain, then using zinc which against copper and manganese which is against iron lowers those

and you feel like shit, since you are copper deficient in the rest of the body, this is how TEI works.

and people are impatient.

this is why people who take testosterone just deliver copper to the rest of the body, and get more and more toxic in them.

thus they have to use THYROID with it.

and the minute they come off. boom, test just goes back into the garbage land))
 
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RebelWithACause

Well-Known Member
Messages
2,703
tonysoprano had a history with ADD drugs - he crashed fast on finasteride.

A lot of other people had history with ADD drugs or even anti depressants. Me included for 6 month period (ADD drugs).

So for those people the possibility is that glutathione was already compromised. Probably even before the drugs. There is a reason why people have "ADD symptoms".

And in those time they already started "collecting" toxic metals in the brain and liver because of a glutathione deficiency caused by drugs and bad lifestyle.

Eventually this toxicity leads to hairloss. People take finasteride to combat this -> health goes down even more and potentially crash on (or off) the drug.

Then you have hairsuit who might have gp6d deficiency causing his sensitivity to finasteride. And maybe brix since he said finasteride did not work for him to stop hairloss. Which means even without a drugs history they are more suspendible to crashing on finasteride since they did not make NADPH in the first place.

The way out would be fixing the heavy metal toxicities by using R-Andro (lowering estrogen -> copper in the brain/liver), estrogen blocker and/or minerals, vitamins like (zinc, vitamin C, B6, etc.). This depends per person I am guessing.
 

wuf

Well-Known Member
Messages
880
here I collected the PFS bloods test. and as we can see from these tests. As i said tetrafolate is ZERO in PFS patients. Glutathione is zero also

Without folinic acid, you simply cant make DNA.


here are the tests

Person 1.

AminoAcids in Plasma
Glutathione (oxidised) 0.57 µmol/L Range (0.16 - 0.50)
Glutathione (reduced) 3.4 µmol/L (3.8 - 5.50)
Derivates
S-Adenosylmethionine (RBC) 219 µmol/dl (221 - 256)
S-Adenosylhomocysteine (RBC) 56.6 µmol/dl (38.0 - 48.0)

FOLIC ACID DERIVATES
5-CH3-THF 9.0 nmol/l (8.4 - 72.6)
10-Formyl-THF 5.4 nmol/l (1.5 -8.2)
5-Formyl-THF 4.9 nmol/l (1.20 - 11.70)
THF 0.60 nmol/l (0.6 - 6.80)
Folic Acid 10.7 nmol/l (8.9 - 24.6)

Folinic Acid (WB) 8.2 nmol/l (9.0 - 35.5)
Active Folate (RBC) 356 nmol/l (400 - 1500)

NUCLEOSIDE
Adenosine 25.5 10^-8 M (16.8 - 21.4 )



Person 2

View attachment 1363


person 3

AMINOACIDS IN PLASMA
Glutathione (oxidised) 0.55 µmol/L (0.16 - 0.50)
Glutathione (reduced) 3.0 µmol/L (3.8 - 5.5)

Derivates
S-Adenosylmethionine (RBC) 213 µmol/dl (221 - 256)
S-Adenosylhomocysteine (RBC) 53.4 µmol/dl (38.0 - 49.0)

FOLIC ACID DERIVATES
5-CH3-THF 11.4 nmol/l (8.4 - 72.6)
10-Formyl-THF 6.3 nmol/l (1.5 - 8.2)
5-Formyl-THF 1.20 nmol/l (1.20 - 11.70)
THF 0.51 nmol/l (0.6 - 6.80)
Folic Acid 12.5 nmol/l (8.9 - 24.6)
Folinic Acid (WB) 8.6 nmol/l (9.0 - 35.5)
Active folate (RBC) 322 nmol/l (400 - 1500)

NUCLEOSIDE
Adenosine 24.6 10^-8 M (16.8 - 21.4)




there are about 10-15 tests like that with IDENTICAL values in all tests.



As I said, NADPH is needed to make THF acid. without THF there is no histidine, and without folinic there is no BH4, there is also no glutathione and no nitric oxide.

Histone needs to be methylated, so without this stuff it will not happen.


What we see on hairtests are different oxidations, but all of them have this in common.


Androgen Receptor density is huge in PFS patients, and AR has no problems going from cytoplasm into nucleous at all. SO there is NOTHING wrong with the actual AR protein or its density, THIS IS 1000000% .



So now we have 2 possibilities here, either NADPH is shut down since receptor density is too much. and this is a feedback loop.


or second variant receptor density is high since the body is trying to compensate of the lack of signaling.

Lack of signaling is from histones or histone methylation. High DHT low DHT could be just your natural state, what you had before fin.


So the answer lays in

1) either this density is too big and this causes the shutdown of NADPH system which then leads to low folates.( which we see)
2) there is lack of signaling since glutathione and methylation block has happened and this is why receptor density is big and stays big trying to compensate for lack of signaling



Dont forget FIN binds NADPH and lowers it, so people who lived on fin for years like 5 -10 years, you will be living without Glutathione for years.

this means that you had the same disorder like autists have. You got so toxic in your brain with heavy metals that it is not even funny and liver.

SO for you to get back to pre FIN, it will be like fixing an autistic child.

This is what ELECTROLYTES protocol was aimed at. @bruschi11


this is why it is so hard to recover from PFS. or CSF. since as your nitric oxide production and antioxidant system never go back on line. the body simply cant signal steroids to do their job.



So to me , 2 variants here are obvious.


1) overexpressed AR and cortisol GR for that reason. and may be gaba a which are stopping NADPH production, causing glutathione and folate deficiencies which total kill your nitric oxide bh4 levels etc and this is AR silencing mechanism not to cause hypokalemia.

2) glutathione depletion and brain toxicity is actually stopping AR receptor from working properly since methylation of histones is not working
and thus the body has to overexpress the AR to try to compensate.



@hairsuit
I will report these questions to Melcangi.
 

barbaar

Well-Known Member
Messages
807
tonysoprano had a history with ADD drugs - he crashed fast on finasteride.

A lot of other people had history with ADD drugs or even anti depressants. Me included for 6 month period (ADD drugs).

So for those people the possibility is that glutathione was already compromised. Probably even before the drugs. There is a reason why people have "ADD symptoms".

And in those time they already started "collecting" toxic metals in the brain and liver because of a glutathione deficiency caused by drugs and bad lifestyle.

Eventually this toxicity leads to hairloss. People take finasteride to combat this -> health goes down even more and potentially crash on (or off) the drug.

Then you have hairsuit who might have gp6d deficiency causing his sensitivity to finasteride. And maybe brix since he said finasteride did not work for him to stop hairloss. Which means even without a drugs history they are more suspendible to crashing on finasteride since they did not make NADPH in the first place.

The way out would be fixing the heavy metal toxicities by using R-Andro (lowering estrogen -> copper in the brain/liver), estrogen blocker and/or minerals, vitamins like (zinc, vitamin C, B6, etc.). This depends per person I am guessing.

Can confirm, I was on ritalin for a while too before going on SSRI. I had super bad reactions to it but I pushed through because I needed it to not be basically retarded at university. Man how I wish I could've just gone on TEI instead.
 

Helen

Well-Known Member
Staff member
Messages
5,415
tonysoprano had a history with ADD drugs - he crashed fast on finasteride.

A lot of other people had history with ADD drugs or even anti depressants. Me included for 6 month period (ADD drugs).

So for those people the possibility is that glutathione was already compromised. Probably even before the drugs. There is a reason why people have "ADD symptoms".

And in those time they already started "collecting" toxic metals in the brain and liver because of a glutathione deficiency caused by drugs and bad lifestyle.

Eventually this toxicity leads to hairloss. People take finasteride to combat this -> health goes down even more and potentially crash on (or off) the drug.

Then you have hairsuit who might have gp6d deficiency causing his sensitivity to finasteride. And maybe brix since he said finasteride did not work for him to stop hairloss. Which means even without a drugs history they are more suspendible to crashing on finasteride since they did not make NADPH in the first place.

The way out would be fixing the heavy metal toxicities by using R-Andro (lowering estrogen -> copper in the brain/liver), estrogen blocker and/or minerals, vitamins like (zinc, vitamin C, B6, etc.). This depends per person I am guessing.



yes this is definitely the case. This is why I posted the electrolytes protocol which is in Boris's signature on hackstasis wiki. It was all explained there.


But still we need to keep in mind 2 possibilities which I outlined in the first post. since we have fast and slow oxidizers.
 
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Helen

Well-Known Member
Staff member
Messages
5,415
@RebelWithACause this is why it is so important for people to do hairtest properly, since if they do some stupid test( pubic) or do hair while taking hormones or some other procedures it can impair the hairtest and give wrong results.

TEI can give them simply wrong shit and they will get even worse.
 

bruschi11

Administrator
Staff member
Messages
2,971
Autism link is just so real. Especially those suffering from major mental side who are flooded with pathogens, toxins ruining their system.

It’s funny- since 2011 I’ve had CFS/Lyme. my healthiest was actually during pfs after I treated Lyme and pretty much beat it to good degree in late ‘17 early ‘18.

But Lyme with PFS before treatment and when it recurred (this past summer till now) is so much worse than pre pfs.

Pre-pfs Lyme just did not annihilate my gut, my brain the way this has. My body had hard time with stress, but I would normally come back to feeling normal-ish if I took a day or two of rest.

PFS Lyme is just another ball game and the system needs a lot more help at feeling stable on your average day. I think body just has such harder time detoxing ammonia with the low glutathione.

I did get better from it though before. I’m actually planning on running pretty exact regiment beginning next week. Will be on antidepressant (mirtazapine- hopefully will help gaba-a restoration while I know will control cortisol which I need most) and beginning a month long antibiotic regiment followed by LLLT/Rife, herbal treatment as I plan to run more fasting/electrolytes/ herbs/ urine/ norvaline afterward.

As I did in late 2017 and early 2018 which essentially cured me to good degree.

I think a lot of us are in similar ballpark to I was in. Just a diagnosis (Lyme) gave me the opportunity to get on my feet. So thankful I fixed it first time to good degree as I got sexuality back say 60-70% at this point in time lol I’ve been horny lately.

I think our PFS community would do so much better if we went to doctor and were all told we were “autistic” and to follow Klindhardt type model.

Instead we are told it’s all hormonal and people just experiment and experiment and with little success.
 

hairsuit

Well-Known Member
Messages
460
here I collected the PFS bloods test. and as we can see from these tests. As i said tetrafolate is ZERO in PFS patients. Glutathione is zero also

Without folinic acid, you simply cant make DNA.


here are the tests

Person 1.

AminoAcids in Plasma
Glutathione (oxidised) 0.57 µmol/L Range (0.16 - 0.50)
Glutathione (reduced) 3.4 µmol/L (3.8 - 5.50)
Derivates
S-Adenosylmethionine (RBC) 219 µmol/dl (221 - 256)
S-Adenosylhomocysteine (RBC) 56.6 µmol/dl (38.0 - 48.0)

FOLIC ACID DERIVATES
5-CH3-THF 9.0 nmol/l (8.4 - 72.6)
10-Formyl-THF 5.4 nmol/l (1.5 -8.2)
5-Formyl-THF 4.9 nmol/l (1.20 - 11.70)
THF 0.60 nmol/l (0.6 - 6.80)
Folic Acid 10.7 nmol/l (8.9 - 24.6)

Folinic Acid (WB) 8.2 nmol/l (9.0 - 35.5)
Active Folate (RBC) 356 nmol/l (400 - 1500)

NUCLEOSIDE
Adenosine 25.5 10^-8 M (16.8 - 21.4 )



Person 2

View attachment 1363


person 3

AMINOACIDS IN PLASMA
Glutathione (oxidised) 0.55 µmol/L (0.16 - 0.50)
Glutathione (reduced) 3.0 µmol/L (3.8 - 5.5)

Derivates
S-Adenosylmethionine (RBC) 213 µmol/dl (221 - 256)
S-Adenosylhomocysteine (RBC) 53.4 µmol/dl (38.0 - 49.0)

FOLIC ACID DERIVATES
5-CH3-THF 11.4 nmol/l (8.4 - 72.6)
10-Formyl-THF 6.3 nmol/l (1.5 - 8.2)
5-Formyl-THF 1.20 nmol/l (1.20 - 11.70)
THF 0.51 nmol/l (0.6 - 6.80)
Folic Acid 12.5 nmol/l (8.9 - 24.6)
Folinic Acid (WB) 8.6 nmol/l (9.0 - 35.5)
Active folate (RBC) 322 nmol/l (400 - 1500)

NUCLEOSIDE
Adenosine 24.6 10^-8 M (16.8 - 21.4)




there are about 10-15 tests like that with IDENTICAL values in all tests.



As I said, NADPH is needed to make THF acid. without THF there is no histidine, and without folinic there is no BH4, there is also no glutathione and no nitric oxide.

Histone needs to be methylated, so without this stuff it will not happen.


What we see on hairtests are different oxidations, but all of them have this in common.


Androgen Receptor density is huge in PFS patients, and AR has no problems going from cytoplasm into nucleous at all. SO there is NOTHING wrong with the actual AR protein or its density, THIS IS 1000000% .



So now we have 2 possibilities here, either NADPH is shut down since receptor density is too much. and this is a feedback loop.


or second variant receptor density is high since the body is trying to compensate of the lack of signaling.

Lack of signaling is from histones or histone methylation. High DHT low DHT could be just your natural state, what you had before fin.


So the answer lays in

1) either this density is too big and this causes the shutdown of NADPH system which then leads to low folates.( which we see)
2) there is lack of signaling since glutathione and methylation block has happened and this is why receptor density is big and stays big trying to compensate for lack of signaling



Dont forget FIN binds NADPH and lowers it, so people who lived on fin for years like 5 -10 years, you will be living without Glutathione for years.

this means that you had the same disorder like autists have. You got so toxic in your brain with heavy metals that it is not even funny and liver.

SO for you to get back to pre FIN, it will be like fixing an autistic child.

This is what ELECTROLYTES protocol was aimed at. @bruschi11


this is why it is so hard to recover from PFS. or CSF. since as your nitric oxide production and antioxidant system never go back on line. the body simply cant signal steroids to do their job.



So to me , 2 variants here are obvious.


1) overexpressed AR and cortisol GR for that reason. and may be gaba a which are stopping NADPH production, causing glutathione and folate deficiencies which total kill your nitric oxide bh4 levels etc and this is AR silencing mechanism not to cause hypokalemia.

2) glutathione depletion and brain toxicity is actually stopping AR receptor from working properly since methylation of histones is not working
and thus the body has to overexpress the AR to try to compensate.



@hairsuit
Love this. Have been using the Folinic Acid for 4 days now? Haven’t felt any difference as of yet. Also, I have liposomal glutathione here, but I guess my question is, do we want to be supplementing glut, or will that just kill what little production we have?
 

bruschi11

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Love this. Have been using the Folinic Acid for 4 days now? Haven’t felt any difference as of yet. Also, I have liposomal glutathione here, but I guess my question is, do we want to be supplementing glut, or will that just kill what little production we have?

That’s what I worry about too.

On that point... this time I’m going enema-less against Lyme (anal fissure- it healed but I don’t want to disrupt haha).

So no major glutathione spikes from coffee enemas this time around.
 

hairsuit

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That’s what I worry about too.

On that point... this time I’m going enema-less against Lyme (anal fissure- it healed but I don’t want to disrupt haha).

So no major glutathione spikes from coffee enemas this time around.
See, I would think that coffee enemas, if you were going to do anything, would be the way to go. You are naturally spiking your glut, vs adding a supplement.
 

bruschi11

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See, I would think that coffee enemas, if you were going to do anything, would be the way to go. You are naturally spiking your glut, vs adding a supplement.

Well, is sticking a tube and flowing coffee up your ass actually natural?

Too many can deplete b2- which is part of the equation for glutathione production.

I think they are best for occasional and/or necessary use. Once a week wouldn’t be bad idea IMO.