L Pathomechanisms and possible interventions in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) latest paper from fluge and mella
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It's on my list. But the 0.4% spray
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I only know that Goldstein used 0.04 sublingual... And it only helps a few hours... But better than Ativan
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This seems similar to the latest writings on the health rising website, they were apparently coming at it from the 'long covid' angle though. I thought it was a very good theory about the Ang II. I still think persistent viruses could be relevant and interlinked somehow. Would be nice to hear from Stanford about what they think about all this stuff. I'm skeptical that the metabolic trap is the genesis.
https://www.healthrising.org/blog/2021/07/29/long-covid-chronic-fatigue-syndrome-hypothesis-merging/ Angiotensin II level is elevated in ME/CFS and POTS. What these guys have newly hypothesised is that a dysfunctional RAS can trigger barrier disruption, dysbiosis and amino acid malabsorption, and can be associated with both aberrant immune responses and dysfunctional intestinal permeability.
Apparently, high ANG II levels could knock out the mitochondria in endothelial cells lining the blood vessels – reducing nitric oxide (N0) levels and inhibiting the blood vessels from dilating properly.
This may contribute to an imbalance in the response between vasodilation and vasoconstriction at the microvascular level, and a nitrate (or just boosting nitric oxide) may be able to smooth this response out somewhat.
Thread discussing nitrate use and Fluge and Mella's initial patent application
https://forums.phoenixrising.me/thr...ith-or-without-b-cell-depletion-in-cfs.36592/
Another thread on boosting nitric oxide
https://forums.phoenixrising.me/thr...since-starting-nitric-oxide-supplement.43761/
Apparently, high ANG II levels could knock out the mitochondria in endothelial cells lining the blood vessels – reducing nitric oxide (N0) levels and inhibiting the blood vessels from dilating properly.
This may contribute to an imbalance in the response between vasodilation and vasoconstriction at the microvascular level, and a nitrate (or just boosting nitric oxide) may be able to smooth this response out somewhat.
Thread discussing nitrate use and Fluge and Mella's initial patent application
https://forums.phoenixrising.me/thr...ith-or-without-b-cell-depletion-in-cfs.36592/
Another thread on boosting nitric oxide
https://forums.phoenixrising.me/thr...since-starting-nitric-oxide-supplement.43761/
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Thought to try drinking red wine to experiment with this theory, turns out i'm not very alcohol intolerant as some people describe here, I was able to drink a whole bottle and 2 beer bottles in about 6 hours. I had quite bad aches all over yesterday and quite low energy, it seemed to largely fix that.
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"where the autoantibodies are produced"
... it's more a matter of "why" or "how".... and more about "autoreactivity" rather than "autoantibodies"
I guess the answer is infection. Rather, persistent infection. But the pathogen doesn't make the autoantibodies.
The persistent infection keeps the immune system evolving. Trying to attack the infection from more and more angles. Like diversification of the immune system's arsenal. This amplifies the autoimmune potential.
Basically, the infection leads to retarded B cells and/or T cells. So, lowered self-tolerance (recognizing who's a good guy and who's a bad guy), and increased immune response (hyperactive).
At that point, there's prob going to be autoantibodies, as there's just a bunch of autoreactivity. Subtle differences in each of us can result in an autoantibody to something antinuclear (ANA), or to a neurotransmitter receptor, etc. I think that's why all of us seem to display such a unique set of autoantibodies w/ a lot of diverse autoimmune conditions.
The likely cause of specific autoantibodies that end up forming from all this... well, a lot of it appears to be viral proteins that look very similar to our own proteins. Like, maybe they share extremely similar amino acid sequences.
And then there's an issue like TS-HDS antibodies, which a few of us have. It's basically a carbohydrate on a cell's surface, and a virus like Coxsackie can bind to and infect a cell w/ TS-HDS (Trisulfated heparin disaccharide IdoA-2S GlcN-S-6S). Our body recognizes this and the retarded immune cells are like "I'm gonna kill everything w/ IdoA-2S GlcN-S-6S".
Then you got destroyed peripheral nerve cells that have IdoA-2S GlcN-S-6S. Small Fiber Neuropathy
They talk about the potential B cell involvement in the autoimmunity in the article.
btw, these 2 "theoretical" types of autoimmunity are molecular mimicry and epitope spreading. This is a good article that covers some interesting stuff on the topic. Oldie but goodie - https://pubmed.ncbi.nlm.nih.gov/11130456/
... it's more a matter of "why" or "how".... and more about "autoreactivity" rather than "autoantibodies"
I guess the answer is infection. Rather, persistent infection. But the pathogen doesn't make the autoantibodies.
The persistent infection keeps the immune system evolving. Trying to attack the infection from more and more angles. Like diversification of the immune system's arsenal. This amplifies the autoimmune potential.
Basically, the infection leads to retarded B cells and/or T cells. So, lowered self-tolerance (recognizing who's a good guy and who's a bad guy), and increased immune response (hyperactive).
At that point, there's prob going to be autoantibodies, as there's just a bunch of autoreactivity. Subtle differences in each of us can result in an autoantibody to something antinuclear (ANA), or to a neurotransmitter receptor, etc. I think that's why all of us seem to display such a unique set of autoantibodies w/ a lot of diverse autoimmune conditions.
The likely cause of specific autoantibodies that end up forming from all this... well, a lot of it appears to be viral proteins that look very similar to our own proteins. Like, maybe they share extremely similar amino acid sequences.
And then there's an issue like TS-HDS antibodies, which a few of us have. It's basically a carbohydrate on a cell's surface, and a virus like Coxsackie can bind to and infect a cell w/ TS-HDS (Trisulfated heparin disaccharide IdoA-2S GlcN-S-6S). Our body recognizes this and the retarded immune cells are like "I'm gonna kill everything w/ IdoA-2S GlcN-S-6S".
Then you got destroyed peripheral nerve cells that have IdoA-2S GlcN-S-6S. Small Fiber Neuropathy
They talk about the potential B cell involvement in the autoimmunity in the article.
btw, these 2 "theoretical" types of autoimmunity are molecular mimicry and epitope spreading. This is a good article that covers some interesting stuff on the topic. Oldie but goodie - https://pubmed.ncbi.nlm.nih.gov/11130456/