These cytokines can severely impact mitochondrial and brain function, which leads me to believe they might be causes of symptoms. But if cytokines decrease in long term patients (as Hornig's study indicates) while symptoms still persist, then perhaps not
This question has haunted me for a long time now!
It's very clear to me that LPS from my gut are causing symptom flares, I'm assuming from cytokine up-regulation. I took a course of Rifaximin a couple of months ago, after struggling with extreme die off from antibiotic herbs.
I tried to get to a therapeutic dose of herbs over 4 months, but I could not even get close to a reasonable dose because of the die off. After I took the Rifaximin, I was able to increase my dose of antibacterial herbs dramatically faster, without the profound die off. Since Rifaximin only works in the small intestine, not the large intestine and is not absorbed into the bloodstream.
It just makes sense, that the reason my die off, after the Rifaximin was so much less was because of the lowered bacteria count in the small intestine. My health has also improved overall greatly, do to the gut treatments I have been doing for the last 4-5 months.
So I really don't understand why they can't find the cytokines that the LPS activate, that are causing, at least in my view, some of the symptoms directly in cfs and maybe all the the symptoms, either directly or indirectly. Color me -
. LOL