Discussion in 'Other Health News and Research' started by junkcrap50, Apr 16, 2019.
perhaps there might be viral-infected macrophages doing the same thing.
From the introduction of the paper:
Seems like sphingomyelin is important in exosome release.
Surely this could only ever be a holding action?
My, limited, understanding is that these things will keep being produced, that the only thing that stops that normally is death.
So all blocking them can achieve is buy time, sometimes that time might allow things to resolve but surely a lot of the time it's just prolonging things?
A bit like trying to stem someone bleeding out with a transfusion, unless the dirty great hole is fixed all you're doing is delaying things.
And in most cases they don't seem to have a clue what a metaphorical 'hole' is let alone how to fix it.
Unfortunately the data on sphingomyelin in ME/CFS is currently contradictory. One study found low levels, another high levels. This could be due to the technology still being unreliable or some other problem. So we don't know how sphingomyelin moves in this illness, or if it's even much different.
I'm not suggesting this will be a fix for ME/CFS disease. Maybe it could be. Perhaps it could "hold" long enough so that, if you believe in Ron Davis's or Nancy Klima's theory, our body can "reset" itself and get us out of some metabolic trap. Who knows.
Initially the paper looked interesting because it showed an exosome-driven mechanism of sepsis (which according to several researcher accounts ME/CFS resembles) and can control severity of sepsis. So it could possibly provide an explanation for ME/CFS.
But this research may also help in Ron Davis's testing of the nanochip. If this drug GW4869 blocks the "something in the blood" and can turn ME/CFS serum into "normal looking/working" serum on the different cells they test, then it would lend credence to the exosome theory. It would just be 1 more drug for them to test on the chip.
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