

That makes sense, but unfortunately in a frustratingly unhelpful way. NF-kB is the central mediator of cellular immunity. What that means is that everything that needs an immune response triggers NF-kB and everything immunity-related gets activated due to NF-kB. Likewise, TNFa is the prototypical pro-inflammatory cytokine. It’s remarkably good at triggering immune responses in a wide variety of cells, and every immune response that I know involves TNFa in some way.
In other words, having inflammatory symptoms be caused by NF-kB>TNFa is less of a “that’s an interesting pathway” and more of a “yeah, of course NF-kB and TNFa would be involved, what’s new?”
The concern is that we don’t really know what’s activating NF-kB in the first place, and so as a result you can’t really fix the core problem. And because NF-kB and TNFa are involved in basically every immune process, it’s hard to tell if these proteins are the ones actually responsible for causing your symptoms. You’d be operating on a hunch, essentially. Though I will say that your unusually nondescript and broad symptoms do seem roughly in line with what I would expect from TNFa signaling.
All that to say, I’m not a doctor and I have no experience with translating knowledge into practicable therapies, so definitely talk to a doctor about it. But TNFa is very easy to detect in your blood, and if TNFa is causing your symptoms, then it’s really easy to just check to see if you’ve got high TNFa in your blood when you’re taking the antibiotics vs. when you’re not. If you had the money, you could even buy a test kit yourself and get an answer in a single day, assuming you know how to use the kit






Thanks, we had that issue but I think we just solved it by downclocking