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NMDA antagonists and LDN

lenses

Bluelighter
Joined
Sep 27, 2006
Messages
726
Low dose naltrexone and NMDA antagonists taken together do something remarkable .

It's a way to increase baseline b-endorphin levels so high and in a safeish way ... it has profound effects and depression and well being ... if administered correctly .

Co-adminstration of MXE , K , 3-meo-PCP , 3-MEO-PCE ... etc , with 0.1 uq to 5 mgs sublingually or oral in a water solution ... did things that can not be said , only experienced . Kundalini .

Theoretically , naloxone causes the same effects .

Does anyone else have any experience with this ? This has remained the single most important pharmacological discovery I have ever made and it is time for this info to be published .

Please , let me know anything else you know about this . I will attach research as needed .

-lenses
 
It'd be worthwhile having 1. a measurable depression metric and 2. doing trials with placebo and both NMDA antagonist or ULD-Naltrexone alone as controls, to test that theory. NMDA antagonists alone can do the trick for depression, IME.

Naloxone is too short half life and lacks oral BA.
 
for the OP, what do you suggest thats more popular and available to combine with naltrexone versus all those obscure chemicals you just mentioned??
 
Trimethylglycine , sarcosine , taurine , magnesium and zinc are a good start . Stabilizes the NMDA co-receptors .

Memantine would be another interesting lead .

With the naloxone - yes oral will not work - nasal spray does , sublingual , IR , etc .

Naltrexone is where it's at !

Will write up and attach more studies when I have time .

I have diagnosed MDD , and my state of mind has moved from constant suicidal ideation to peace from low dose naltrexone .

- Lenses
 
why low dose naltrexone though? in studies of addictions, the dose are pretty high not sure how it really helps in low dose...

the only thinkg you mentioned i didnt try is sarcosine. trimethylglycine, i dont remember doing much and taurine, magnesium and zinc i have been taking forever with none of them helping with the disrupted NMDA system caused by excess alcohol.
only thing that might have helped is memantine in high dose as it causes this dissociation with memory impairment that helps prevent benzo and alcohol abuse and im curious to re-try it.
finding something that stabalizes NMDA is the key for benzo and alcohol use. if i find this gold, im rich! so far, only temporary optimism
 
naltrexone is very effective at sub miligram doses. I just took a regimen of 5 - 40mcg daily for several months tapering off opioids from an injury.
 
Samidorphan (3-carboxamido-4-hydroxynaltrexone) is currently in development in combination with olanzapine to reduce the incidence of weight gain associated with olanzapine monotherapy. Also being investigated in combination with buprenorphine as an adjunct to ADT for treatment-resistant depression. Funny because supposedly samidorphan really is just naltrexone with fewer side effects effectively rendering that combo nothing more than "new Suboxone". It seems like it MIGHT be more selective than naltrexone, but marginally at best. Pharma def knows the opioid system is a useful tool. As for the glutamate NMDA system, I've heard of pdocs using memantine like @asecin and @lenses mentioned as well as riluzole.
 
why low dose naltrexone though? in studies of addictions, the dose are pretty high not sure how it really helps in low dose...
Naltrexone seems to exert some regulatory effects on opioid receptors at very low doses. There may also be some aspect of Kappa Opioid Receptor blockade as well depending on the dosage in question, KOR activation tends to cause dysphoria so blocking it could be helpful for depression patients. There are also effects on Toll Like Receptors located on microglia, immune cells which can contribute to neuroinflammation. Neuroinflammation is seeing increasing attention as a cause of some mental illness like depression.

Blocking Toll Like Receptors seems to decrease microglial activation, and this seems separate of Naltrexone's effects on opioid receptors. Dextro-naltrexone has negligible affinity for opioid receptors but can still block Toll Like Receptors.
 
One thing ive always wondered : If Neuroinflammation causes depression shouldnt anti inflammatory drugs (aspirin, ibuprofen, etc.) be anti depressants ?
 
Not really, not unless the depression is caused by too much prostaglandin or whatever. Just because A causes B doesn't mean fixing B will fix A.
 
Doesn't ULD-naltrexone exert its effects partially through binding to a regulatory site on the protein filamin-A, and decreasing recruitment of beta-arrestin 2. As well, potentially as inhibition of a switch from MOR coupling from Gi/o to Gs and as such blocking a switch from the typical inhibitory effects of MOR stimulation to, with continued use of the opioid agonist, excitatory function after a corresponding switch in G-protein coupling.
 
^Correct, and I'd be curious if dextro-naltrexone still has affinity for filamin-A. In that case dextro-naltrexone could be helpful for the dependent/withdrawing opioid user, as well as the hedonists %)

Is normal naltrexone pretty 50/50 racemic? (chemistry illiterate here)
 
As far as the combination of NMDA antagonist/ULD-naltrexone, I've recently got my GP to agree to supporting getting me on memantine. After years of trying. Although we haven't finished. I intend to try and get an appointment with him tomorrow, in an effort to finalize it and get the script going.

He's aware of ULD naltrexone, which surprised me, usually I have to explain all that kind of thing to him, so I'm going to ask him for it.
 
Is normal naltrexone pretty 50/50 racemic? (chemistry illiterate here)

AFAIK it's exclusively levo because it's poppy-derived.
 
i tried to get naltrexone from my doctor today and he is like "i cant prescribe that, its an opiate" im like lol REALLY DUDE? it blocks opiates effect, idiot! welcome to USA!
 
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