My magnesium L Threonate is coming in today :)…
While Magnesium blocks the NMDA receptor in its resting state, it cant block it while the cell is depolarized. I have read 2 studies that say that Magnesium raises the NMDA receptor transmission through blocking it in resting state (where the cell would produce more of it), and when the time comes that it should fire the magnesium would dislodge from the receptor and as we have more receptors it will fire more aggressively…Its one of the main mechanism that scientists think the MAgnesium L threonate helps with cognition (I know there is a lot of debate about that)…But hey what do i have to lose 
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Ah this is a certain kind of magnesium ? Is it to specifically help with brain fog etc ?
Interestingly I improved in all areas for a few hours for no reason until I reviewed what id recently eaten. A single stem of uncooked asparagus which is high in magnesium and vit k. Repeating brought nothing as is often the case. I only get uplifts from new one off foods which is very strange but not uncommon.
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Its one of the most effective ways to raise magnesium levels in the brain…Magnesium can in the fact cross the blood brain barrier but in a very ineffective way (As mg plays a big role in multiple brain processes, the body has found a way to limit its ability to wander in the brain wheneverit wants 
)…
But not with Magneisum l THreonate…With this formulation, magnesium gets to the brain without any problem, and this raises its levels significantly. If that would help, i will tell you in a couple of days or rather weeks ;D
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Good look. I was looking into trying it, sparingly as half of one capsule of a magnesium supp brought me trouble. Akin to tremor seizure like symptoms.
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That would be interesting to find out - let us know and good luck !!
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I remember you saying that happened - may be worth giving it a try if @silentpain89 try works ? Or stick with the asparagus !!
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I’m going to give it a few more days before having another stem. What a life where harmless normally very healthy foods can cause problems. No wonder some think we’re loons! I’ll follow silentpain and this thread with interest. Cheers @Forwardsnotbackwards
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I have found some interesting studies on the how DHT actually enhances NMDA function and synaptogenesis by raising calcium levels In cells while this effect can be blocked by blocking NMDA…according to the study of Meclnagi we are highly deficient in DHT in the cereospinal fluid, which I’m assuming can be assumed as well on cellular level (interesting enough, DHT level in serum was normal)…The other study of Meclangi proving a increased methylation of the 5a-reductase II and consequently decreased DHT at cellular level might explain why increasing NMDA might help a bit but still isn’t enough to bring the system back at work…(I don’t think supplementing with DHT would be the answer, since to bring enough of it at cellular level would be taking much more than one might be comfortable with…
I wonder if there is a compund that can raise the activity of 5a reductase through positively modulating the enzyme 
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aspartic acid is nmda agonist, but i think many tried
We are not diagnosed with shizophrenia, but with PSSD/PFS.
Look up negative symptoms of schizophrenia…
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That’s correct. That’s what I’m reading as well
Glycine is an inhibitory neurotransmitter in the central nervous system especially in the spinal cord, brainstem and retina. When glycine receptors are activated chloride enters the neuron via ionotropic receptors causing an inhibitory postsynaptic potential.
Glycine is also a required co-agonist along with glutamate for the NMDA receptors.
There is some key language here that suggests glycine still needs glutamate and works as a co agonist to agonize the NMDA receptors which yes obviously would be an excitatory reaction.
I pee out low amounts of glutamate and low amounts of glycine even when I supplement glycine. So my glycine is being used one way or the other which tells me it’s needed. Also after I recently agonized the NMDA with extra glutamate by taking enough L-Glutamine to ensure L-Glutamine’s conversion to L-Glutamate I crashed. When I say I crashed the exact same thing that happened to me when I took saw P seven years ago happened. Note that I was also taking SAMe which is a co factor involved in excitatory neurotransmitter synthesis.
So I don’t necessarily think that increasing inhibitory neurotransmitter synthesis is the answer either. In fact I’m taking 3500-5000 MG’s per day of glycine to help me sleep which it does a really good job at by the way and it’s not helping my sexual sides. So if a neurotransmitter imbalance of some kind is responsible for my sexual sides then I suspect it’s an imbalance involving both the GABA and GLUTAMATE receptors.
I have been mentioning this in other threads but I am low in saliva pregnenolone sulfate which is a neurosteriod that acts as a potent negative allosteric modulator of the GABA receptors.
This is my current line of thinking:
So if I don’t have enough negative modulation of the GABA receptors maybe the GABA binding to my GABA receptors would result in too strong of an inhibitory reaction. So to prevent this the glutamate receptors now need to become more sensitive “to match” the “overly agonized” GABA receptors. I read that the GABA and GLUTAMATE receptors need to stay balanced and because they are the bodies main inhibitory and excitatory neurotransmitter. And now maybe my body may lower L-Glutamine to L-Glutamate conversion because the glutamate receptors are overly sensitive in order to avoid too much glutamate binding to and agonizing the overly sensitive glutamate receptors.
So if I’m right this would make sense why when I took a substantially amount of
L-Glutamine for 64 days straight in order “to force” the production of L-Glutamate and succeeded that I crashed. Like you said issues with the glutamate receptor can cause these symptoms.
if I’m right the solution could possibly be to correct what’s wrong starting with the GABA receptors which in my case may require an increase in pregnenolone sulfate
Would you be interested in getting a Saliva pregnenolone sulfate test done as well as a urine Allopregnanolone and urine 3a-diol test done ? I want to see if my results can be replicated in someone else who gets worse when agonizing the glutamate receptors.
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I don’t think enzymes can be positively modulated. They can be inhibited or increased.
I wonder if the PFS group in Meclangi’s study that showed low DHT and Allopregnanolone in the CNS of the PFS group accurately represents most PFS people’s CNS levels. Thisisarealbummer reported high amounts of Allopregnanolone in his CNS if I remember correctly. He also had high Allopregnanolone in urine as do I.
So just to recap:
You used Ketamin which is a NMDA receptor antagonist nasally and ten min later you got worse.
You took tinaeptine which is a glutamate receptor modulator and got better but went back to baseline in 4-5 days.
You took Sarcosine 8 months ago which is a co-agonist of the NMDA receptor and glycine receptor agonist and got better
Most recently you took tianeptine, Sarcosine and D-Serine which is also a co-agonist of the NMDA and got better.
Is this summary accurate ?
Are you still on the tianeptine, sarcosine and D-Serine?
Too bad we don’t have a urine neurotransmitter test for you so we could compare it to mine. Your experience thus far, my experience and possible findings thus far and thisisarealbummers experience we may be onto something
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That summarizes everything i did pretty much…
To be honest i have never been the same since i started this regimen (In a good way), but im only stuck at 20% pre pfs now…Im not getting any better, but for that matter not worse…
Please note that before this, i was literally at -100% pre pfs, and i was contemplating suicide every little minute of the day, so somehow im doing fine now.
I will be stopping D-serine in the next few days, since it has some safety issues when taken for long periods of time…Im hoping this wont change much…In the mean time, im still searching for things that might effect the glutamergic system and bring me back my sensitivity.
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did the magnesuim help in any way ? i have been using mag citrate for sleep but thinking about changing too mag threonate after reading this thread
Sadly i got very lazy with. My intake of Magnesium, and that’s becuz im working 60 hours weekly, so i only focused on the Tinapetine+Sarcosine+D-Serine…
I took Magensium threonate only for 5 days, and thats not enough time to evaluate anything…
I didnt really feel different in those 5 days…
You can look up reddit (Am i allowed to mention that here?), and see what ppl are talking about it…There are postitive as well as negative reviews.
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Hmmm…
So you are currently at a 20 percent improvement from your regular PFS baseline ?
Ok so when you agonize the glutamate receptors you get an improvement. Thisisarealbummer based off his CNS testing concluded that his GABA receptors were down regulated. This is what he said:
“Upon disinhibition, ALLO levels rise acutely and stay elevated (at least seemingly elevated to my body’s new set point after finasteride treatment) and fomented a quick and substantial downregulation of the receptors most responsive to ALLO positive allosteric modulation”
So maybe in theory in this scenario if this is also your scenario the Glutamate receptors adjust to match the GABA receptors. Because if you read about it it’s straight forward that the GABA receptors which are the bodies main inhibitory neurotransmitter need to match the Glutamate receptors which are the bodies main excitatory neurotransmitter. Maybe this is why you get a 20 percent improvement when agonizing possibly insensitive glutamate receptors and worse when you antagonize the insensitive glutamate receptors. If this theory is correct it would probable mean like you are saying that improper functioning of excitatory neurotransmitters could be responsible for the sexual sides. But I’m taking it a step further and theorizing that that proper functioning of excitatory neurotransmitters cannot be achieved without proper functioning of inhibitory neurotransmitters. Just a theory…
We could also spin this and try to say ok if you have insensitive glutamate receptors and you then antagonize the insensitive glutamate receptors with ketamine in theory would the insensitive glutamate receptors now become “more sensitive” in response to being antagonized by the ketamine? This theory leads me to ask this question:
When you got worse from the Ketamin and then came off of the Ketamin what did you experience specifically in the immediate period of time upon discontinuation of the ketamine ? Did you feel better compared to regular baseline or worse compared to regular baseline?
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My take is that we have hpa axis dysregulation, so we are stuck in flight or fight mode with adrenaline. When you took tianeptine you reduced your stress level on your hpa axis lowering corticosterne levels briefly and probably fell out of tge flight or fight mode.
Look up tianeptine and hpa axis.
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