Finasteride causes glutathione depletion and leads to CFS?

[Finatruth]

Monijitos with or without alcohol?

[mariovitali]

@Finatruth

Monijitos with or without alcohol?

Good Question. The positive effect was most of the times in cases where i had a Mojito without alcohol.

[bryce54]

i noticed some of you guys are jumping into supplementing your different mutations, but if you guys have CBS mutation (which I read something like 90% of people with these problems have), is you need to address the CBS mutation first or else others won’t work right. CBS mutation has a lot to do with what is going on with us IMO… FUCK PFS…

@droit, the supplement you posted from YASKO, the NHF multi vitamin contains milk thistle in it. i was about to buy it until i saw this. my thinking right now is that an optimized thyroid/adrenal function will allow us to handle these type of supplements that other people crashed on, but i really don’t want to risk it. i’m going to stick with a whole food multi right now.

Not sure if this has been posted here, but this is basically a cliff notes from YASKO’s book:

heartfixer.com/AMRI-Nutrigenomics.htm#CBS: Cystathionine Beta Synthase

Regarding CBS mutation…

My general treatment program for CBS (+) individuals and for BMHT (+) individuals who are overproducing ammonia and sulfite/sulfite will consist of:

1. Restrict animal protein (anything with eyes) from your diet and limit your exposure to sulfur group containing drugs and nutritionals.
2. To squelch ammonia, supplement with Yucca, ½ capsule twice a day (sprinkled on food containing protein), Ammonia Support RNA ½ dropper with meals, and a charcoal supplement at bedtime (away from other supplements; magnesium citrate may be used as needed to keep the GI tract moving as charcoal may lead to constipation).
3. Switch to a multi that does not contain B6 (B6 stimulate CBS; the P-5-P form of B6 is less of a problem – Dr. Yasko’s NHF multi is low in B6 - take two tablets three times a day). Additional mineral support will be needed and here we start with Trace Minerals Complex at 4 drops/day.
4. To stimulate SUOX begin Molybdenum 3 drops twice a day, Boron 3 mg/day, Vitamin E succinate 400 IU/day (contained in the NHF multi), and hydroxy-B12 2000 mcg/day.
5. Supplement with GABA 500 mg once or twice a day to blunt excitotoxicity; if you feel that GABA is helping you can increase the dose.
6. To increase energy production (this step is less critical and can be omitted for cost containment, especially in individuals not troubled with CV disease) supplement with NADH 5 mg, Co-Enzyme Q10 100 mg or Idebenone 100 mg, Carnitine 500-1000 mg daily, and Ribose 5 grams in water, two to three times a day. Co-Enzyme Q10, Carnitine, and Idebenone all provide Methyl groups, and are thus of additional value to COMT (-) and/or VDR Taq (+) individuals.
7. Additional measures designed to speed up the “back door” BHMT reaction will be discussed later.
8. Check and record your urine sulfate level every 7 days. Our goal is to reduce your reading to 400 mg/L (one yellow and three pink squares) or at least to 800 mg/L (two yellow and one pink), and then to keep it there for two months (at which time you will feel better). Measures that decrease your sulfate burden are beneficial. Conversely, any measure that increases your sulfate burden is either inappropriate or is being added to your program prematurely. A persistent reduction in your urine sulfate level will open the door to SAMe and/or BH4 supplementation and an eventual liberalization in your diet. Your urine sulfate score will thus be our primary measuring stick.
9. If not done already, we need to check your baseline blood homocysteine, ammonia, and Vitamin D levels, along with kidney and liver chemistries (if not done recently).
10. Consider wearing the Life Wave Glutathione patch 4-6 hours each day, removing the patch if you feel poorly (this would reflect a detoxification reaction - see our info sheet and lifewave.com/chc), the idea here being to use up free sulfur groups to generate Glutathione.
11. In 8-10 weeks we will likely wish to:
    a. Repeat some of the lab work.
    b. Carry out 24 hour urine studies for ammonia and amino acids, with a second study for toxic and nutritional minerals, and possible a SpectraCell intracellular nutritional assessment. We will use the results to modify our nutritional measures, specifically looking for nutrients that have been drawn in to your now open pathways, nutritionals that will now require more intensive supplementation. Favorable results will also allow us to back off on the dose of now less necessary supplements.

Really difficult part of optimizing CBS mutation is the diet… you can’t have animal protein. Found a post on phoniexrising where someone had success with this diet, a little less restrictive… but still really, really restrictive…
livingnetwork.co.za/chelatio … food-list/

[bryce54]

@mario, interesting on NAC. which SNP are you taking it for? have you handled CBS yet?

dr von K on NAC:

Hi, Dreambirdie.

As you probably know, NAC is N-acetylcysteine. It’s basically the amino acid cysteine with an acetyl group attached to it. It’s a chemically stable form of cysteine. Cysteine by itself becomes easily oxidized, and that’s why NAC is used to supplement cysteine.

Cysteine is one of the few amino acids that contains sulfur. In particular, the sulfur is in the form of a sulfhydryl or S-H group.

Several of the toxic metals, including mercury, readily bind to sulfhydryl groups.

I suggest that the benefit you are getting from NAC is that it is binding to the mercury that has been mobilized. This prevents the mercury from binding to sulfhydryl groups in your enzymes and other proteins, and interfering with their normal biochemistry, which is what causes mercury toxicity.

Apparently in your case the mercury is being bound by NAC and is being excreted. The kidneys will filter it out of the blood and excrete it in the urine. I don’t know why you are apparently not also experiencing transport of the mercury into your brain with this high dosage of NAC, which is the concern that caused Dr. Quig to set the dosage limit at 300 mg per day of NAC. It is known that cysteine bound to mercury can be transported by the LNAA (large neutral amino acid) transport system across the blood-brain barrier. This has been studied in rats. This can be blocked by leucine, another amino acid found in protein. So if you are on a high protein diet, or are supplementing branched-chain amino acids, this may be preventing the transport of mercury into the brain by the NAC.

Rich

forums.phoenixrising.me/index.ph … #post-3639

[mariovitali]

@bryce54

@mario, interesting on NAC. which SNP are you taking it for? have you handled CBS yet?

Hi bryce54,

I am really in the dark on this. What is SNP and CBS?

Unfortunately i cannot have any tests regarding specific gene mutations where i am located.

[bryce54]

@mariovitali

@bryce54

@mario, interesting on NAC. which SNP are you taking it for? have you handled CBS yet?

Hi bryce54,

I am really in the dark on this. What is SNP and CBS?

Unfortunately i cannot have any tests regarding specific gene mutations where i am located.

SNP is a DNA sequence. CBS is a SNP that 90% of individuals have a mutation on if they have methylation problems. I see… is it only 23andme you can’t take? There is another DNA test you can take besides 23andme… I foget the name of it though. Might be available in your area.

What is the reasoning behind your supplementing of NAC?

In other news, I have a theory for what is happening. I think our bodies cannot properly utilize sulfur due to PFS fucking up our methylation cycle. How it did it, I have no idea, but I see pretty clear patterns.

I think the main problem lies here… our bodies do not make this:

en.wikipedia.org/wiki/Hydrogen_sulfide

Hydrogen sulfide is produced in small amounts by some cells of the mammalian body and has a number of biological signaling functions. (Only two other such gases are currently known: nitric oxide (NO) and carbon monoxide (CO).)
The gas is produced from cysteine by the enzymes cystathionine beta-synthase and cystathionine gamma-lyase. It acts as a relaxant of smooth muscle and as a vasodilator[28] and is also active in the brain, where it increases the response of the NMDA receptor and facilitates long term potentiation,[29] which is involved in the formation of memory.
Eventually the gas is converted to sulfite in the mitochondria by thiosulfate reductase, and the sulfite is further oxidized to thiosulfate and sulfate by sulfite oxidase. The sulfates are excreted in the urine.[30]
Due to its effects similar to nitric oxide (without its potential to form peroxides by interacting with superoxide), hydrogen sulfide is now recognized as potentially protecting against cardiovascular disease.[28] The cardioprotective role effect of garlic is caused by catabolism of the polysulfide group in allicin to H2S, a reaction that could depend on reduction mediated by glutathione.[31]
Though both nitric oxide (NO) and hydrogen sulfide have been shown to relax blood vessels, their mechanisms of action are different: while NO activates the enzyme guanylyl cyclase, H2S activates ATP-sensitive potassium channels in smooth muscle cells. Researchers are not clear how the vessel-relaxing responsibilities are shared between nitric oxide and hydrogen sulfide. However there exists some evidence to suggest that nitric oxide does most of the vessel-relaxing work in large vessels and hydrogen sulfide is responsible for similar action in smaller blood vessels.[32]
Recent findings suggest strong cellular crosstalk of NO and H2S,[33] demonstrating that the vasodilatatory effects of these two gases are mutually dependent. Additionally, H2S reacts with intracellular S-nitrosothiols to form the smallest S-nitrosothiol (HSNO), and a role of hydrogen sulfide in controlling the intracellular S-nitrosothiol pool has been suggested.[34]
Like nitric oxide, hydrogen sulfide is involved in the relaxation of smooth muscle that causes erection of the penis, presenting possible new therapy opportunities for erectile dysfunction.[35][36]
In Alzheimer’s disease the brain’s hydrogen sulfide concentration is severely decreased.[37] In a certain rat model of Parkinson’s disease, the brain’s hydrogen sulfide concentration was found to be reduced, and administering hydrogen sulfide alleviated the condition.[38] In trisomy 21 (Down syndrome) the body produces an excess of hydrogen sulfide.[30] Hydrogen sulfide is also involved in the disease process of type 1 diabetes. The beta cells of the pancreas in type 1 diabetes produce an excess of the gas, leading to the death of these cells and to a reduced production of insulin by those that remain.[32]

If you notice, I underlined that gas is produced by the enzyme cystathionine beta-synthase… aka the CBS gene. 90% of people with methylation problems have the CBS mutation. This is a pretty direct correlation between CBS + something acting on erectile dysfunction.

[droit]

@mariovitali

@bryce54

@mario, interesting on NAC. which SNP are you taking it for? have you handled CBS yet?

Hi bryce54,

I am really in the dark on this. What is SNP and CBS?

Unfortunately i cannot have any tests regarding specific gene mutations where i am located.

@mariovitali

@bryce54

@mario, interesting on NAC. which SNP are you taking it for? have you handled CBS yet?

Hi bryce54,

I am really in the dark on this. What is SNP and CBS?

Unfortunately i cannot have any tests regarding specific gene mutations where i am located.

Mariovitali,

SNP is ‘single nucleotide polymorphism.’ It is just a site in a gene that may be mutated. For the enzymes in the methylation cycle, there are some well researched SNPs, so it is well documented whether they slow down or speed things up. Depending on how how many more mutations you have, you’re more predisposed to methylation cycle issues. Some are more severe than others.

The methylation cycle has two pathways.

co-cure.org/scan0003.bmp

In no particular order: 1) The methylation cycle has enzymes that shuttle raw materials around to eventually make SAMe. SAMe goes out and methylates something, and the byproduct; SAH, which is converted to homocystiene, is shuttled back around to make SAMe.

However, once SAMe donates its methyl group to something with biological meaning, SAH is converted to homocysteine, which can either go back around, or 2) it can go down the transulfuration pathway to glutathione. CBS is the enzyme that will send homocyteine down the transulfuration pathway.

Typically mutations in the enzymes in the methylation cycle will slow things down. For example, mutations in the MTHFR enzyme (the thing that converts folates into the active form), will weaken your ability to create methyl-folate by something like 60% if you have 2 mutations at a SNP.

However, mutations in CBS make it over efficient, thus draining things out of the methylation cycle. Which is bad because you want to perpetuate the methylation cycle and create glutathione in balance.

I’ve seen four 23andMe methylation outputs, and got a summary from a 5th. The results are in the format moonman1 posted here:

viewtopic.php?f=1&t=7293#p65035

I would really like more data so please send me a note if you’ve done 23andMe.

All five do have CBS mutations. 3 have homozygous mutations, but I’m the only one that is homozygous for the really bad one (C699T). The interesting thing I see in the other 4 is that they have lots BHMT mutations, but we don’t have enough data to say there is a statistical enrichment.

1 guy has homozygous mutations in all three snps
1 guy has homozygous mutations in two snps, and is heterozygous for the other one
1 guy has heterozygous mutations in all three snps
1 guy has one homozygous mutation, the rest are normal

I was a user for 7 years without problems. The other guys were very short term users. So if we can get more data a pattern with some statistical significance may emerge.

The BHMT mutations are not as well researched as CBS so I can’t really say what this would mean if there was a significant pattern. Most anecdotal forums say that BHMT has the same effect as CBS.

[bluejaysfan]

Glad you’re taking the test, Mario. I’m awaiting results, myself.

My erections are as hard as my cialis days. I am waking up after 6 hours sleep, practically, unable to sleep longer… But, I feel great, physically and mentally. Better than I would at 8 or 9 hrs sleep.

I’m hoping libido comes around next.

[Scotsman]

Hi there Mario

What are your IGF1 levels currently at?

[bryce54]

@mariovitali

@bryce54 / @Droit

I just had a look at the 23and me website and they ship the test to my country, So i will take the test. Is there any other test that you guys think i should take?

@Bryce54,

NAC is essentially what has cured me from all of my side effects and fixed my libido. I made the connection after analyzing my personal data and seeing that something was pointing to Glutathione production. Then i found that red peppers (which my analysis has shown to be very beneficial) are a precursor of cysteine.

With NAC all of my side effects ceased, i started sleeping better and my libido became great. Adding mint leaves to my regimen made me feel like a 25-year old (i am 44) - i have no idea why this happens. Even though i am cured, i want to get to the bottom of what is going on because this recovery could be temporary and i need to know what i am dealing with.

I will continue taking NAC, it may be that i am affected in a different way than other PFS sufferers. I also think that my attacks ( slight tinnitus which i hear in my ears bilateral - when they happen they signal problems such as low libido, low mood, insomnia) are actually over-excitation in the brain and Glutathione is a key modulator of Glutamate (which if not controlled leads to nerve apoptosis).

The activation of group I metabotropic glutamate receptor (group I mGlus) has been shown to produce neuroprotective or neurotoxic effects. In this study, we investigated the effects of N-acetylcysteine (NAC), a precursor of the antioxidant glutathione, on group I mGlus activation in apoptosis of glial C6 and MN9D cell lines, and a rat model of Parkinson’s disease (PD). We demonstrated that NAC protected against apoptosis through modulation of group I mGlus activity

See : plosone.org/article/info:doi … ne.0032503

I am also more than certain that some kind of neurodegeneration has occurred in my case but this could possibly be reversed with boosting my IGF-1 levels.

I am expecting results on TSH, Free T, E2 and Homocysteine on Tuesday, i will give an update then.

Thanks again for all the help and info

how long have you been taking NAC for? ineresting on those co factors you are doing… what worries me is i found out NAC contains high amounts of sulfur in it. it could be your other pathways are working because i saw you were supplementing witha few other things for methylation.

i would just get the test and then wait for the results and then go from there.

@bluejaysfan

Glad you’re taking the test, Mario. I’m awaiting results, myself.

My erections are as hard as my cialis days. I am waking up after 6 hours sleep, practically, unable to sleep longer… But, I feel great, physically and mentally. Better than I would at 8 or 9 hrs sleep.

I’m hoping libido comes around next.

that is awesome man.

[droit]

@mariovitali

@bryce54 / @Droit

I just had a look at the 23and me website and they ship the test to my country, So i will take the test. Is there any other test that you guys think i should take?

mariovitali,

Its great to hear we’ll get another data point. bluejaysfan will be number 6 and you will be 7. The 23andMe experience is great otherwise. I have learned a lot about myself.

Also, make sure to report your Homocysteine levels.

To test whether or not you have a methylation block, the hallmark test is the ‘Methylation Pathways Panel’ from Vitamin Diagnostics.

This test is done in the US and in Europe.

hdri-usa.com/tests/methylation/
europeanlaboratory.nl/

You’ve previously said that your country doesn’t have access to this test, so the next best thing would be an oxidative stress stress. One example is the 8-Hydroxy-2-deoxyguanosine test in the Organix test by Metametrix.

You’ve been going pretty hard on the methylation protocol, so if you were able to get either test, I don’t think it would be as severe as from before you started. It still may be helpful to see where you’re at.

[mariovitali]

@Scotsman

Hi there Mario

What are your IGF1 levels currently at?

Hi Scotsman,

I have no idea, i will try to find out if such a test exists. I will add Creatine to my regimen which boosts IGF-1 and see what happens.

[Scotsman]

Thanks for replying Mario. The reason I was asking was that my own IGF1 levels were tested when I was referred to an endo regarding my own concerns. Although I was told that everything was fine I still feel that an IGF1 level of 135 ug/L (65-350) is low and I’ve noted others on propeciahelp with low IGF1.

[droit]

@mariovitali

@Scotsman

Hi there Mario

What are your IGF1 levels currently at?

Hi Scotsman,

I have no idea, i will try to find out if such a test exists. I will add Creatine to my regimen which boosts IGF-1 and see what happens.

IGF-1 is one of, at least, two androgen receptor gene targets (PSA is another) reported on this forum as low.

mariovitali, what did make you think you have low levels?

[Cap]

I think you guys mentioned folate as part of the things you are discussing? I just got my bloodwork back and my folate was REALLY low. The doctor said that folate was very important for DNA repair or function or whatever. Just thought I’d mention it.

[droit]

@Cap

I think you guys mentioned folate as part of the things you are discussing? I just got my bloodwork back and my folate was REALLY low. The doctor said that folate was very important for DNA repair or function or whatever. Just thought I’d mention it.

Cap,

Thank you so much for the post.

A year ago, before I heard the Chris Kresser podcast posted in the beginning of this thread, I took a SpectraCell vitamin test. SpectraCell is more functional in that they look at how your cells do in the absence of each vitamin they are testing for, instead of measuring blood concentrations.

I was also severely low on Folate (low on all the B-vitamins). And I didn’t know what that meant until I heard Chris Kresser’s podcast.

For those of you who have had normal folate or B12 on a typical serum test, that doesn’t necessarily mean you’re not in the state we’re talking about here. As Chris Kresser says in that podcast, serum tests are usually for the inactive forms.

If you decide to supplement folate, take a look at active folate in the form we discuss here. The school of though we are investigating in this thread is that ‘folic acid,’ which is typically found in supplements, is not nearly as good as methyl-folate. In fact some say ‘folic acid’ is bad. You can see the MTHFR lecture I posted earlier (viewtopic.php?f=27&t=7178&start=80#p71743).

If you get interested in full protocol or testing in this area, please let me know if you have any questions.

[mariovitali]

Here are my blood results. Really happy with Free T as i haven’t had an HCG shot for over 25 days :

TSH 2.986 μIU/ml (0.3 - 5.0)
Homocysteine 13.4 μMol/l (5 - 20)
E2 15 pg/ml (11-44)
Free T 14 pg/ml (13-41)

Homocysteine within normal levels although somewhat on the upper scale. Unfortunately i did not have homocysteine levels tested prior starting NAC + Methylation cycle supplements.

I will re-test in 30 days for Free T and Homocysteine

[bryce54]

im sure droit can chime in to some of your other quesitons as i’m not 100% sure. but regarding your first quesiton on NAC, i was actually just reading this…

The most important patch is the Y-Age Glutathione patch. This patch directs your body to manufacture more glutathione, using raw materials already present and your body’s own enzyme systems. Glutathione is the key antioxidant/detoxification molecule in your body. Conversely, glutathione depletion occurs in response to chronic oxidative stress and toxicity (as in the average American). IV administration of glutathione increases excretion of toxic substances. Oral glutathione is not absorbed; instead we give your its precursor substance N-Acetyl Cysteine (used in Medicine to prevent kidney failure during angiographic procedures, tolerance to long-acting nitrates, or liver failure in Tylenol overdose situations). Those of you with the Methyl Cycle Cystathionine Beta Synthase (CBS) up regulation will not tolerate N-Acetyl Cysteine (due to its Sulfur content), but you should have no trouble with the patch. The patch does not provide you with Sulfur-containing molecules; rather it directs you to assemble these molecules into glutathione, a molecule that you can put to good use and a molecule that you likely need.

Regarding the CBS upregulation…

CBS initiates the trans-sulfuration pathway, converting homocysteine in to cystathionine and its downstream metabolites. This is the most important Methyl Cycle defect and is present in 90% of the patients who we have tested. The CBS defect is an up regulation. CBS is operating at up to ten times its normal rate.

heartfixer.com/AMRI-Nutrigenomics.htm#CBS: Cystathionine Beta Synthase

Basically, if you have these problems, there’s a 90% chance you have the CBS mutation. If that is the case, NAC will do more harm than good because of the high sulfur content found in it. CBS means we can’t utilize sulfur properly, thus glutathione is not being made properly and too much sulfur circulating in blood, leading to many issues…

regarding you feeling crappy… iv’e read through taht site above many times… and it’s pretty clear you need to treat the high sulfur issues first if you have that mutation (which 90% of people have if they have methylation issues), so i would start there… but check what your results are.

[gefinauser]

yo, getting interested in this (newbie in this) but i think i shouldn’t go about without any prior knowledge on what mutations I have. do you know if there is any comprehensive test for all possible mutations there are? who does this, any links to it etc?

i’m hesitating as well cos jarrow’s formula was changed and i still don’t know which are the best brands to use for methyl and adenocob…

EDIT dunno why but serum B12-vitamin is way over upper limit despite not supplementing so if i’m any judge, all kinds of (probably inactive) b12 is pooling up in my blood for some reason…

[droit]

I am always hesitant to strongly advocate for someone supplement in a certain way because it is like playing with fire. We’ve seen different flavors of this plan work for different people. And that is consistent with the diversity in other communities. So I’ll just comment based on what I’ve read and my interpretations. Please consider your personal history and what has worked for you.

1. Is it ok if i use methylation boosting supplements and NAC which increases Glutathione? Is there a possibility that by taking also NAC i will suppress any possible restart of the methylation cycle?

It is possible to back up chemical reactions with too much end product, depending on how the enzymes are regulated.

But from what you describe, I don’t know if that’s your situation. If you had a lot of glutathione, that would be good and it would be more persistent that the quick ups and downs you’ve had. Unless you have some form of oxidative stress in your life.

If you were backing up the transulfuration pathway (the direction toward glutathione) with NAC, I would expect methylation to keep cycling. If don’t have the CBS mutations that would draing your methylation cycle into the transulfuration pathway, you may have to take the CBS cofactors (B6) to push the metabolites of the methylation cycle into the transulfuration pathway toward glutathione. But we would need genetic data and the methyaltion pathway panel to see where things are at.

2. I assume that if i have an MTHFR mutation then the methylation cycle restart does not apply and i should receive methylation supplements for life. Is this assumption correct?

I have an MTHFR mutation and will happily drop a little methyl-folate once a week or so after I get out of this.

If you do find that you do have MTHFR mutations, you have to ask yourself if you liked how you felt before all this. If do have a methylation block now, and are able to get out of it, its completely possible that without a stab of oxidative stress, you’d be fine without it.

In the Dr. Van Konynenburg lecture he said that the patients that responded, got off the supplements and just took antioxidants from time to time.

This is all based on the assumption that you’re currently in a methylation block, and before fin you were not. And that a methylation block is the source of all of your problems. But only testing would tell us there.

3. Is there the possibility of over-methylating? If yes, How can one treat this condition? Unfortunately MTHFR.net doesn’t answer this adequately.

There is a such thing as over driving the methylation cycle. I know I’m certainly not in that position.

But its been suggested that Niacin is a good treatment for over methylators, since niacin will eat up methyl groups during its metabolism.

mthfr.net/methylfolate-side-effects/2012/03/01/
mthfr.net/forums/topic/question- … acinamide/

Now, niacin is needed as co factor for a lot of things so I take a normal dose of niacin in my B-complex.

But in my case I don’t take too much because it will ‘mop up’ methyl groups and I know from testing that my SAMe is low.

Remember that there are two paths in the methylation cycle, around the circle, and down toward glutathione. One of the interpretations from Dr. Van Konynenburg is that if you stimulate the circle too aggressively then little will be able to go down the transulfuration pathway toward glutathione.

forums.phoenixrising.me/index.ph … lts.19348/

In my case, I have the CBS mutation that up regulates the drain to the transulfuration pathway. So I probably would have a hard time beating transulfuration pathway.

4. Do you take MethylCobalamin - B12 and Active Folate at the same time or you are taking B12 first and then Folate? (say after 6 hrs)

I take hydroxocobalamin. I have found first hand and from my genomics that I don’t do good with excessive methyl groups. I feel best on hydroxocobalamin.

But that is not everyone’s experience. Some start on hydroxo-B12, and don’t notice a change until they get on methyl-B12.

Dr. Van Konynenburg actually suggested that hydroxo-B12 might not be enough, and was switching over to methyl-B12 for his ‘simple methylation protocol.’

forums.phoenixrising.me/index.ph … nce.11729/

In the end the constant message is to titrate up with your protocol.

It seems that my health has deteriorated since i minimized NAC intake and started the methylation protocol.

Is this true? It seems like you have been doing great. And you’ve been on the methylation protocol for a long time now.

The thing we need to understand is why is NAC making you feel so good and why so quickly. Going off of my tests, glutathione shouldn’t be generating at that rate and to the magnitude that you feel recovered.

I made a very small improvement in my glutathione in four months, and the biochemist at the last that was great.

Once you generate glutathione, its a little more persistent than the effect you’re describing of a quick downturn. All the lectures on this subject say when you have healthily glutathione, the cellular environment is ripe to perpetuate the methylation cycle and continue generating glutathione as needed. Assuming you don’t have a stress that overcomes your capacity to generate glutathione.

I wonder if you’re just getting the direct antioxidant effect from NAC. You could test this by taking another antioxidant like some Vitamin E or C to see if you feel better.

To further complicate things: the people on phoenixrising has said that glutathione precursors (like NAC) make them feel worst. The theory (this is unsubstantiated by any publication) is that the NAC is conjugating the B12 and removing it from the system.

For completeness, one possibility is that you are an over methylator and the NAC is tuning it down. But again, without testing, no one can be sure and the above is just a theory. Trying to supplement to bring down methylation would be an aggressive change and you should really think before doing something like that.

But make sure any changes you make you feel comfortable with.

Until i get my 23andme results i will stop all supplements supporting the methylation cycle and just receive NAC 600mg daily and ALA which helps in Glutathione recycling.

I would say that to you any one reading. You really want to get tested for the methylation parameters (SAMe and reduced glutathione). That methylation panel I described is of course the most reportable.

The 2 real Methylation Panels, the 2 other high oxidative stress results and the 5 genetic data points all suggest we would be in a methylation block, low glutathione stage, but without testing you’re just in the dark which will lead to haphazard supplementing.

I understand its quicker and cheaper to just try the supplements. But as a community we should be aggregating tests and finding patterns.

There’s been one or two people who have posted that didn’t like the way they felt when trying this protocol. If they were able to get some testing, then they could verify what state they were in and dedicate the time to getting out of it.