Thanks for the feedback, everyone! : )
I did, and got no response.
And that is exactly what happens in the people who are mold-sensitive. They get better if they avoid it. Keep in mind that while mold and CCI were two factors that I was able to guess, there is probably many many more, some of which might be plain impossible to avoid. And most people probably have a combination of multiple factors, not just one. Hence not many full remissions after eliminating just mold (though there are some, I have personally talked to one or two).
Then you are a very, very far outlier.
Not quite. The NOX is not released into the cells. Or actually, it might be, but that's not the point. The point is that while the exosome travels in the blood, it by itself produces and releases ROS around it. So you would actually rather have an antioxidant free in the bloodstream rather than an infiltrating one. The lack of success with vitamins is because they are not nearly potent enough and they dont reach high concentrations in the blood. A mega dose of IV vitamin C might help a little bit, and I do hear some people felt a bit better from that. But the problem is that concentration will drop quickly. You would need to maintain super high concentration for days or even weeks for the body to have time to regenerate the broken ATPases, to actually get remission from it. And as soon as you stopped, the illness would come back right away. This is not a viable approach to treatment.
Good to know!
That is simply impossible. Unless you can break the rules of physics, your muscle will always require a lot of oxygen for activity. Anaerobic energy production is wildly inefficient.
The only actual good solutions to treat this, if this hypothesis is true, is to either block NOX or undo the IDO trap. But we need to test the hypothesis first. It might be very wrong.
https://www.ncbi.nlm.nih.gov/pubmed/30585477
It's this one, right? This is really interesting, thank you for telling me about it. This might add another feedback loop, where the IDO trap taking place further impairs NO clearance. But I don't know how significant of an impact it would have, there are certainly other mechanisms of NO clearance. Still, it's interesting to consider.
Small corrections:
The mechanism for PEM I propose does not involve immune activation, at least not in the classical sense. If that were the case we would be seeing a lot more cytokines. Instead, what I propose happens is that there is a constant ongoing NOX-exosome production by the immune system, which should normally be limited by IDO activity of some subtype of dendritic cells or T cells. And in ME/CFS this limiter is disabled because of the IDO trap. And PEM wroks by the means of NO (which we know for sure is abnormally high in exercise in patients) worsens the IDO trap.
Neither lactate, ATP nor NO can act systemically. They all act locally. NO slightly less locaclly, but still not systemically.
NOX exosomes are required to make this mechanism be systemic, as they can be carried by the blood while shedding ROS in their path, wherever they go.
Bigger correction:
The changes observed by Griffith are genetic. Meaning, you have them your whole life. Meaning, they cannot explain ME/CFS by itself, because patients would also have them before being sick with ME/CFS, and you would detect them in healthy people too. Both nanoneedle results as well as RBC deformability seem to be very specific to patients.
Furthermore, nanoneedle results reverse when you do a plasma switch. This means that something in the plasma is mediating the change. It cannot be mediated by a genetic mutation. This is the reason why a lot of genetic explanations for nanoneedle results simply don't work. Oxidative damage from outside the cell is the first thing I found which offers to explain both nanoneedle as well as RBC deformability data.
What I could see happening is that perhaps the TRPMs work in combination with cell surface Ca-ATPases to achieve some important functions in some immune cells, and hence having both fail results in some important change in ME/CFS. But I haven't really looked into this angle at all yet.
One other reason why I like this hypothesis is because rampant NOX exosomes and IDO trap might be a way to explain why we can see many immune alterations but they are all pretty weird and don't seem to involve much direct cell-to-cell communication (cytokines). Which has been a bit of a mystery.
