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​Following up on Naviaux’s excellent work around extracellular ATP (eATP) / “Cell Danger Response”, which can act as an “alarm signal” relay and/or loop that bridges nervous system cells and other tissues. This extracellular ATP signalling has been observed in ME/CFS, ASD, ADHD, PTSD and various other disorders / syndromes. https://t.co/KWvn7SzbBU The pathway also works in both directions, allowing a systemic cascade / loop to be created from any source, where sufficient eATP signalling exists to overcome CD39/73/ADA purine salvage metabolism, which also provides the corresponding “alarm dampening signal” - adenosine and inosine. Interestingly enough, the main de novo “dampening signal” synthesis pathway is inhibited by impaired glycolysis -> pentose phosphate pathway -> PRPP (and other) metabolism and the purine nucleotide cycle in muscles, post-exertion. These are known issues in ME/CFS, LC, PVS, etc In this manner, with the “dampening signal” inhibited, various accumulated “insults” could potentially lead to a form of dysautonomia, where the nervous system’s pattern recognition systems identify and amplify existing metabolic alarm signals, manifesting biochemically as a wide range of effectors - including hyperactive innate immune response and mast cell activation (see figure 19). Naviaux and others have been exploring suramin as an intervention to help shut down the P2X7 relay / loop with early success. I’m currently researching a different approach - restoring the problematic “dampening signal” metabolism, as part of a more comprehensive process. [Watch this space.]