Comment · Sun, November 29, 2020 · ND Owner
N. DEPOP NEEDS to look into things that work on EAAT2 glutamate pump expression in central nervous system, therefore reducing glutamate toxicity.
Original post in this thread
squirtking33 · 28 points
I suffer with some awful persistent infections that, when under stress, create an opportunistic environment for latent bacterial, viral and fungal infections to take a hold. Borreliosis has, however, been the worst infection I’ve had to fight. No, I’m not talking about Lyme Disease, which is a fraudulent case definition of a single bad knee, falsified by the likes of Wormser, Weinstein, Halaprin, Klmepner, Steere, Shapiro, etc., however, I won't get into that whole ordeal. In any case, neuroorreliosis is known to cause increased glutamate, Ammonia, in some cases; and especially Quinolinic Acid in the brain, a potent excitatory neurotoxin. Nothing had worked for me except one thing and that was the antibiotic ceftriaxone (Rocephin) even if it may not kill even half of viable spirochetes in vitro.
Ceftriaxone was amazing for my pain, brain sparks, probably due to QUIN; verbal fluidity, brain fog, headaches, anxiety and eradicated depression. No other nootropic or drug, had cleared my brain of noise and anxiety better than ceftriaxone, now I’m sure it was partly to do with it helping to clear out neuroborreliosis but its underlying mechanisms of actions are interesting. Plu,s I h…
What they were answering
chutney1 · 2 points
Interesting, digging into IEG expression now. Thank you for the pointer there, not sure I would have stumbled upon this otherwise.
Are there any stacks you would recommend to somebody dealing with the aforementioned situation? What pathways should one be trying to target via a supplement approach? The conventional stuff has all been tried. Even some more novel things like dihexa (two doses, spaced a week apart), NSI-189, various racetams, all of ND's mushroom extracts, MK-677, memantine and so forth. So far little relief has been found with this stuff, certainly nothing one would consider to be profound. Most of these things helped a little but not nearly to the degree one would hope and in many cases felt like a tolerance was quickly built, with the beneficial effects no longer being as pronounced.
Hoping something comes along which targets whatever mechanisms/pathways are broken. If extended neuronal insult via glutamate excitotoxicity can trigger changes in IEG expression, I wonder what hope there even is for us folks. Or ever will be. I am wondering how useful the b lactam antibiotics that OP mentioned would be for someone in this position, dealing with continuing brain dysfunction years after withdrawal. And what the risk/reward ratio there looks like. Always avoided antibiotics because I don't feel I ever have truly needed them and I have been keenly aware of the eme…
u/MisterYouAreSoDumb · ND Owner
I don't really have a proven answer, unfortunately. We are still learning about IEG expression. Perhaps this EAAT2 targeting will prove to be a workable strategy. We are certainly missing some big piece of the picture with long-term tolerance, based on reports from many people over the years. It's not limited to a single class of drug, either. I think glutamate and IEG expression plays a part in long-term tolerance to a lot of things, like benzos, opiates, MDMA, amphetamine, etc.