PFS BLOOD TESTS( and THEORY )

[hairsuit]

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.

Duh, of course it is...... that’s not normal for you?

 

[bruschi11]

Duh, of course it is...... that’s not normal for you?

For like 16 of last 18 months of my life.... yup. Very normal.

All my roommates, friiends, friends gf’s, my parents, yup everyone knows it. Coffee enemas have been a big part of my life. I talk about them quite openly! ))))))

 

[TubZy]

For like 16 of last 18 months of my life.... yup. Very normal.

All my roommates, friiends, friends gf’s, my parents, yup everyone knows it. Coffee enemas have been a big part of my life. I talk about them quite openly! ))))))

I do not think I could allow myself to ever stick anything up my ass let alone a tube with coffee in it lol, I give you props my friend

 

[Helen]

I do not think I could allow myself to ever stick anything up my ass let alone a tube with coffee in it lol, I give you props my friend

Haha, scared you might like it? LOL

 

[mbax44]

I always have high bilirubin. They test for direct , indirect etc and each one is high everytime I test. Sam-e the supplemen always made me feel much more normal. Nadh and nad which I guess have things to do with b4h? Recycling also help at times. Just another person/example of what you’re describing.

 

[Admiral]

Appreciate all the effort. The fact that we all have something in common is comforting, somewhat. Hopefully we can come up with protocols out of this.

The autistic part freaked me out, though. If my succes rate is as high as that I am making an appointment with my endocrinologists right now and try to live my life on thyroid + test.

 

[mbax44]

Gilbert’s Syndrome, UGT1A1: More Than Meets The Eye

Found this. may be relevant

 

[RebelWithACause]

Appreciate all the effort. The fact that we all have something in common is comforting, somewhat. Hopefully we can come up with protocols out of this.

The autistic part freaked me out, though. If my succes rate is as high as that I am making an appointment with my endocrinologists right now and try to live my life on thyroid + test.

The protocol right now is: GET A HAIRTEST FROM HEAD HAIR. No fucking around with random supplements in between the tests or right before the test.

No pubic hair, no armpit hair.

Then you run the supplements for 2 months - you re-evaluate: did you improve, did you experience a snapback, etc. Just like Goose wrote down. Keep a log for yourself.

Otherwise do cdsnuts protocol and try that. But your hormones are low so first you will be herb cycling for a while.

You need to make a choice and commit to it. And make sure you lower the chance of failure by doing all the things right. The pubic hair is a new revelation but slowly everything will be more streamlined as these mistakes are being made.

 

[hairsuit]

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

@Helen im confused on the Folinic Acid. Since I have the MTHFR mutation, shouldn’t I have to use methylated B?

 

[tanedout]

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

This is VERY interesting! What is noticeable here, other than the low Glutathione, is the ratio of SAM to SAH.

In all cases there is low SAM (S-Adenosylmethionine), and high SAH (S-Adenosylhomocysteine).

This totally ties in with the following study which looks into SAMe as a therapy for mitigating side effects from retinoid treatment (including isotretinoin/accutane). One of the key findings of the study is that SAM:SAH ratio is messed up by retinoid therapy. The studies actually reckon that taking SAMe alongside isotretinoin would mitigate getting side effects based on rat studies

With the crossover with PFS, and the fact these bloods are from PFS people suggests it might be the same for both groups. What are your thoughts on this @Helen ?

https://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=4063&context=etd

From my basic understanding it seems people are left with high GNMT, SAM gets depleted, SAM:SAH ratio is messed up and methylation issues cause a cascade of issues as a result.

A few points to take away from this..

Given the essentiality of SAM, the primary methyl group donor, it is imperative that these methyltransferase reactions be regulated. To that end, the ratio of SAM to its post-reaction metabolite, SAH, can inhibit SAM-dependent reactions. Glycine N-methyltransferase is an enzyme primarily expressed in the liver, kidney, and pancreas that can help maintain the SAM:SAH ratio6,7. It functions by converting glycine to sarcosine, thus forming SAH from SAM. The SAM:SAH ratio therefore serves as an gauge of transmethylation potential.

Retinoic acid has been shown to disturb methyl group metabolism by activating and inducing glycine N- methyltransferase (GNMT)16,18. GNMT acts to optimize the intracellular ratio of S-adenosyl methionine (SAM) to its metabolite, S-adenosyl homocysteine (SAH), a primary indicator of transmethylation potential

Overall, our study showed numerous undesirable effects of retinoic acid therapy, including depleted hepatic SAM, development of fatty liver, and some modulation of serotonin, norepinephrine, and dopamine. Supplemental SAM appeared to be an excellent conjunctive therapy, preventing or partially preventing nearly all negative effects of retinoic acid.

Anyone else have bloods for SAM and SAH?

 

[Helen]

This is VERY interesting! What is noticeable here, other than the low Glutathione, is the ratio of SAM to SAH.

In all cases there is low SAM, and high SAH.

This totally ties in with the following study which looks into SAMe as a therapy for mitigating side effects from retinoid treatment (including isotretinoin/accutane). One of the key findings of the study is that SAM:SAH ratio is messed up by retinoid therapy. The studies actually reckon that taking SAMe alongside isotretinoin would mitigate getting side effects based on rat studies

With the crossover with PFS, and the fact these bloods are from PFS people suggests it might be the same for both groups. What are your thoughts on this @Helen ?

https://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=4063&context=etd

From my basic understanding it seems people are left with high GNMT, SAM gets depleted, SAM:SAH ratio is messed up and methylation issues cause a cascade of issues as a result.

A few points to take away from this..

I wrote about GNMT for accutane people. And suggested things for Orion you can read it. I think we tried Same , and sarcosine


But to turn homocysteine back to the methionine cycle you need folate. of course high homocysteine will lower Same. I dont think that is the problem.

I think original problem is with NADPH system, which makes NADPH.

and then you run low on folate.

and then homocysteine gets high


If NADPH system is not restored then you cant get to methylfolate. and you need FAD and NADPH for that. and tetrafolate

that is why B2 is used to lower homocysteine. folate is used to lower homocysteine, zinc, b1.

If Homocysteine is high , GNMT probably will be induced and you can also run low on glycine.

 

[Helen]

@tanedout with low Same, you will have low adrenaline.

without folates all neurotrasmitters should be screwed since you cant make Bh4 without folate.

and without bh4 you have no nitric oxide. low neurotrasmitters. etc.


this is why Finasteride by binding NADPH basically lowers active folate. and then histidine goes away.

and people get a crash in form of hemolytic anemia.

since you create methylation block you can never restore it.

Or androgen or cortisol or gaba receptor is stopping NADPH system from restoring. since all those hormones are made with NADPH and may be in some cases the body stops NADPH production (which we observe with very very low insulin levels in some people)

and this keeps this perpetual cycle.

 

[JasonSky]

Super interesting stuff, I also had a long history with using ADD medication (ritalin) throughout part of my childhood (ages 9-15).

So really our only sustainable solution for now is just to support our overall health by balancing the body holistically(such as TEI), and then hoping NADPH goes back online to signal glutathione and NO etc.

 

[MNK99]

I speculated maybe, increased blood brain permeability from amphetamines (possible according to primate studies, in europe), caused me to be more likely to crash from finasteride. I don't want to put that out there as "a truth". But who knows. I crashed fast and hard, extremely hard. If I recovered A LOT over a year, I suffered a ton the year before that. AND realistically my ADD MEDICINE was spaced out like 3-4months, because I had just finished final courses and (petitions/arguments against administration) as well as just began titrating an AED. --so I wanted to see if AED would "work". --but definitely I crashed hard and fast. ---Possibly amps are not prescribed in certain parts of Europe due to the studies there showing BBB permeability increase and changes seen whenever tolerance is rapidly increased (which is FAST for a lot of people).

-While I like one such stimulant, I strongly believe as per it being a reuptake inhibitor rather than a dopamine agonist (that can cause damage neurologically at least on some level), I strongly believe (high quality) cocaine is actually "safer" in a way. However, MPH Methylphenidate is more chemically similar as well in action to cocaine , than say it is to Adderall or Dexedrine. The agonistic stimulants like Methamphetamine (especially at high doses, when used as a substance of abuse) are quite damaging.

(NOTE: Cocaine can be pretty harsh too, and addictive. And it's illegal. And it has killed people. Not everything is so amazing when it comes to ANY drug).

 

[TubZy]

funny alcohol depletes glut but a lot of feel better whether it be during or after drinking Lol. Maybe it also stimulates the liver to produce glut during the withdrawal like a rebound effect as well compared to just the GABA mechanism?

 

[wuf]

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.

Do you think hydrogenperoxide can make NADPH, higher?
I have some bottles with me, Worth to try it?

 

[Jack17]

These findings are important. The SAM e and accutane study is interesting. Since I am restarting low dose 1/4 tab weekly of Propecia, I think I might start SAM e. I have already added folic acid and glutathione. Interestingly, some say when they restart Fin, they might feel a little better initially but then worse. Maybe this is from further depleting the above. I will post more in my log.

 

[JasonSky]

funny alcohol depletes glut but a lot of feel better whether it be during or after drinking Lol. Maybe it also stimulates the liver to produce glut during the withdrawal like a rebound effect as well compared to just the GABA mechanism?

For me the day after drinking, I notice my voice sounds deeper and fuller again and I feel more relaxed. What does this indicate if anything?

 

[TubZy]

For me the day after drinking, I notice my voice sounds deeper and fuller again and I feel more relaxed. What does this indicate if anything?

Same, also my appetite comes back in full force like my metabolism and digestion is back online again. We don't really know exactly what it's doing in the case of PFS but it does reverse many of the symptoms if not all. We do know alcohol increases GABA and allopreg specifically the GABA-A receptor which fin inhibits. Other GABA type supplements I tried like phenibut work while I use it (for some symptoms) but when I stop it I feel horrible like worse than baseline since phenibut acts on GABA-B.

It's the day or two after I feel the best not actually while drinking (although I do get the drunk feeling).

 

[Jack17]

I've never noticed a benefit post alcohol. I have higher T and DHT. Wonder if that it related???