Comment · Tue, November 24, 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
Do you think this would be of use for those that have gone through benzodiazepene withdrawal and are having persistent symptoms, even years out? Or is glutamate not the culprit there? There are plenty of folks who have withdrawn from benzodiazepenes and are seemingly left with (quasi?)permanent cognitive symptoms and generally dysfunctional brains.
u/MisterYouAreSoDumb · ND Owner
Glutamate is certainly PART of the culprit. I think there is a genetic portion of long-term tolerance as well that is much less understood. Look into IEG expression, or immediate early genes. This would explain the seemingly "permanent" tolerance that can happen. It's excess glutamate that leads to these expression changes, but the long-term nature of it is more to do with genes themselves. This is why it can be so difficult to get rid of tolerance sometimes. The genetic aspect of it is harder to reverse, and much less understood.