The plausibility of NAC inducing b12 deficiency or 'methyl-trap'

Gondwanaland

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NAC does chelate zinc and other essential minerals out
https://pubmed.ncbi.nlm.nih.gov/1529808/
I saw my own zinc going down in blood plasma after about 3 months taking 150 mg NAC daily (one hundred fifty MILIgrams)
Perhaps it does the same to cobalt? I don't test B12 very often.
As mentioned in the paper you cite:
"NAC exerts no detectable influence on the metabolism of essential trace metals when used in the above context (i.e. at doses near 600 mg per day)."
I was taking a tiny dose and it tanked my zinc. My nutritionist said she has seen it happening frequently before
 
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Hey guys,

What do you think... I was having a good time in the past weeks and months. Last Thursday, I started to carsh, and I have felt not so good since then (it is not a severe crash, but I feel sick and lack energy).

30 days ago, I started a course of Q10 and glutathione, and I felt great. I also take 6 pills of Oxymatrine (Alternative Medicine Solutions) and have done so for 8,5 months (7 months with a dosage of 6 pills a day). A week ago, I reduced my dosage of oxymatrine to 4 pills a day.

What do you think? Could my symptoms bue due to the decrase in dosage of Oxymatrine? For some reason, my CRP-level was slightly increased yesterday, today it is normal again.

I would be interested in your thoughts. Many thanks!!

Best wishes

Johnny Minnesota :-/
 
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Last Thursday, I started to carsh, and I have felt not so good since then (it is not a severe crash, but I feel sick and lack energy).
30 days ago, I started a course of Q10 and glutathione, and I felt great.
A week ago, I reduced my dosage of oxymatrine to 4 pills a day.
Yes, it does sound like it's related to the reduction in Oxymatrine dose.
Doesn't seem related to glutathione at all.
 
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Thank you, @Pyrrhus, very kind of you!

Do you think my crash symptoms could be due to the vaccination I had 24 days ago? I got my AstraZeneca shot, developed a strong headache and some limb pain, but two days after the vaccination everything was fine again.

I don't know... how long does the body produce antibodies after a vaccination?
 
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I don't know... how long does the body produce antibodies after a vaccination?
The standard answer to that question is that the body needs 2 weeks after a vaccination to produce the desired antibodies. This is consistent with the fact that most vaccine-related seizures occur two weeks after receiving a vaccine.

But the reality is that everyone's immune system is different, every vaccine is different, and the amount of time needed to produce antibodies may vary from the "standard" 2 weeks.

Hope this helps.
 
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I just read that the body's immune system (through its b-cells) starts its immune processes right after the vaccination. The production of antibodies, however, sarts two weeks after the vaccination. Maybe my problems are signs of my immune system producing Covid-19 antibodies...

It's really hard to tell... :-/
 

bread.

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Glutathione can attach to B12 when B12 enters the cell and it appears to be necessary for B12 to be optimally utilized inside the cell.[1] This glutathionyl-cobalamin appears to be converted to methyl-cobalamin (or adenosyl-cobalamin) during the actual enzymatic use of B12.[2][3] (I'm skipping a lot of details.)

A problem with people who have low glutathione is that blood tests can theoretically show normal, or even excessive B12 levels despite the presence of symptoms of B12 deficiency. This is because the B12 in the blood can not be fully utilized by the cells lacking glutathione. There is also the possibility of B12 deficiency in the brain, but with normal B12 levels in the blood.[4] (This has been mostly talked about in autism, but may apply equally to ME patients.)

Long story short: It is perfectly natural for an ME patient to have dramatic, sometimes intolerable, start-up effects when starting NAC. Rest assured that these are start-up effects, not permanent side effects. As with many supplements that turn out to be helpful, you can "start low and go slow". For me personally, I could only tolerate a single 500mg dose of NAC the first week I took it. The second week I took a single 500mg dose on Monday and another one on Friday. The third week I took a single 500mg dose on Monday, Wednesday, and Friday. After 2-3 months, I was able to take 500mg every day without any effects whatsoever.

Hope this helps.

EDIT: clarifications and references

REFERENCES:
[1] https://www.ncbi.nlm.nih.gov/pubmed/2357215
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5312744/pdf/42-49.pdf
[3] https://ghr.nlm.nih.gov/gene/MMACHC
[4] https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0146797&type=printable
Hi,

I have idiopathic raised B12, I am very severe, so have to keep it short: is there a paper that strikes the connection between low glut and highb12?
 
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Hi,

I have idiopathic raised B12, I am very severe, so have to keep it short: is there a paper that strikes the connection between low glut and highb12?
There are indeed many possible reasons why one can have high B12 in the blood, but still have a functional B12 deficiency. With regard to intracellular oxidative stress (which implies low glutathione), here's one paper:

Supraphysiological vitamin B12 serum concentrations without supplementation: the pitfalls of interpretation (Vollbracht et al., 2020)
https://academic.oup.com/qjmed/article/113/9/619/5524896
Excerpt:
Vollbracht et al 2020 said:
Elevated serum B12 levels may also be associated with a functional deficiency of the vitamin. Functional deficiency has been described despite high B12 concentrations and is due to a failure of cellular uptake or intracellular processing, trafficking or utilization.
[...]
Recent findings in diseases associated with oxidative stress have revealed that intracellular oxidative stress results in local functional B12 deficiency.8 Insufficient intracellular processing of B12 due to oxidative stress has been reported in diabetes mellitus or in Alzheimer’s disease,9,10 where it has been postulated to be a significant pathophysiological factor.9 Intracellular reduction of the central cobalt atom is essential for the formation of the metabolically active forms of B12. This process requires reduced glutathione and the hydroquinone form of flavin adenine dinucleotide (FADH2), it is therefore compromised by oxidative stress.9 In such conditions treatment with glutathione and/or vitamin C, a key physiological regenerator of intracellular glutathione, may provide therapeutic benefit. This warrants further investigation.
Hope this helps.
 

bread.

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There are indeed many possible reasons why one can have high B12 in the blood, but still have a functional B12 deficiency. With regard to intracellular oxidative stress (which implies low glutathione), here's one paper:

Supraphysiological vitamin B12 serum concentrations without supplementation: the pitfalls of interpretation (Vollbracht et al., 2020)
https://academic.oup.com/qjmed/article/113/9/619/5524896
Excerpt:


Hope this helps.

https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004039


I know you are well versed in Enterovirus and NAC. I had an Enterovirusinfection when I was moderate/severe and NAC is something that made me acutely worse in that time.
 

Busson

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The genetic defect that @richvank described is called "methylmalonic aciduria and homocystinuria, CblC type". It does not result in B12 deficiency, it just means that the cell has problems converting B12 from one form to another.
@Pyrrhus The defects in CblC (MMACHC) occur early enough along the pathway to cause both methylmalonic aciduria and homocystinuria, though not necessarily equally. I haven't heard CblC affects the conversion between adenoB12 and methylB12. I believe it is the most common of the cobalamin defects.

Methylmalonic aciduria is quite rare but nevertheless I think it is under-discussed (if that's a word) on this forum. But I'm biassed as that's my primary complaint along with propionic aciduria!
 
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bread.

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Thanks for sharing that paper. The paper you cite only describes how some enteroviruses use glutathione to assemble capsids. Capsids are important in the acute phase of the infection, when the virus spreads as virions, but they are less relevant in the persistent phase of the infection, where the virus appears to spread via other methods.
Is it unlikely that they could switch from persistent to acute again after years?
 

Busson

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What are the implications of depleted glutathione from taking frequent acetaminophen (UK: paracetamol) painkillers?

Glutathione binds to toxic by-products of acetaminophen and neutralises them. When there is no more glutathione then acetaminophen's toxic by-products will cause damage.

Would regular acetaminophen cause problems with methylB12 absorption (as described here) well before glutathione was completely depleted?

Is there a case for taking NAC to maximise methylB12 absorption even when not taking acetaminophen?
 
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Glutathione binds to toxic by-products of acetaminophen and neutralises them. When there is no more glutathione then acetaminophen's toxic by-products will cause damage.
This occurs in the liver, which uses glutathione in its detoxification and excretion functions.

So excessive use of acetaminophen/paracetamol can deplete glutathione in the liver, causing liver damage:
https://en.m.wikipedia.org/wiki/Paracetamol_poisoning#Pathophysiology

Is there a case for taking NAC to maximise methylB12 absorption even when not taking acetaminophen?
Interesting question. Maybe...

Is it unlikely that they could switch from persistent to acute again after years?
My guess is that it's unlikely, but a whole lot more research would be needed in order to know for sure.
 

Judee

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Do you think the sore feeling in lungs could be the result of the intake of glutathione?
Could also be a sulfur/thiol sensitivity. I can eat them but if I eat them too consistently I start getting pain in my lungs and migraine headaches. I do have some gene issues with stage 1 and stage 2 liver detoxing as well as CBS mutation so I don't think my system can process an overload of sulfur/thiols.