Comment · Thu, February 11, 2021 · ND Owner
N. DEPOP NEEDS to look into things that work on EAAT2 glutamate pump expression in central nervous system, therefore reducing glutamate toxicity.
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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
johnnycoconut · 1 points
Would you mind clarifying the last sentence? :)
u/MisterYouAreSoDumb · ND Owner
So your body has rate-limiting enzymes in place to control how much of various things get made, right? The two I talk about a lot are tryptophan hydroxylase (TPH) and aromatic L-amino acid decarboxylase (AAAD). TPH is what converts tryptophan into 5-HTP. AAAD is what converts 5-HTP into serotonin. If you supplement 5-HTP directly, you are bypassing TPH. This means you are going to saturate AAAD with more 5-HTP, which could have effects on dopamine later on; since L-DOPA shares the final rate-limiting enzyme of AAAD with 5-HTP. So supplementing tryptophan will create less serotonin than supplementing with 5-HTP. However, it will keep things more balanced.
With L-carnosine it is slightly different, as carnosinase is the rate-limiting enzyme that breaks down L-carnosine into beta-alanine and histidine. Carnosine synthase is the rate-limiting enzyme that controls the production of L-carnosine from beta-alanine and histidine. With TPH and AAAD, the direction is only one way. Tryptophan becomes 5-HTP and 5-HTP becomes serotonin. You don't have 5-HTP converting back into tryptophan. However, it's a two way street with carnosine and beta-alanine. Supplementing with beta-alanine will increase carnosine levels, but then serum carnosinase will bring them back down again. So to get enough L-carnosine to get the positive effects we are talking about, you need to saturate the carnosinase enzyme to give your body time with high enough levels of carnosine to act directly. Beta-alanine does a good job of increasing muscle carnosine, but we want it to reach the brain.
My last sentence specifically is saying that your body doesn't allow for rate-limiting enzymes to overwhelm subsequent ones, by design. TPH can't overwhelm AAAD, because that would completely negate their function. Carnosine synthase will not overwhelm serum carnosinase under normal conditions. The only caveat to this is in disease states, like carnosinemia. That is a rare disease where a person has too low of serum carnosinase. However, normal people will have enough serum carnosinase, so supplementing L-carnosine directly will lead to much higher plasma levels than supplementing beta-alanine, which is good if you want the central/anti-aging effects of carnosine.