NMDA receptor hypofunction?

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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So you are on the tianeptine and sarcosine and discontinuing the D-Serine?

I was unaware that D-Serine had safety concerns. I took D-Serine for 64 days straight recently. Next time I’ll know to be more careful with it

Apparently glycine modulates excitatory signals in the brain. I know you mentioned glycine in your opening post but did ever try glycine?

I think that if I had a classic case of hpa axis dysregulation I would see more evidence of it in my labs. I’m inclined to think silentpain89 is on the right path. But I’m only basing my opinion off my own experience

been taking magnesuim threnoate for only 5 days it makes sleep so much better and can feel some more energy.

but it also has dried out my skin and made it a weird soft feeling on face … almost like when you took ketamine in your first post it increased your skin numbness. it has a definite effect on something regarding skin .

will carry on for a full month as the best results were seen at 21+ days mark

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magnesuim has always been a game changer for my sleep along with glycine. The combo gives me dry eyes but I don’t care. I just use eye drops twice per day

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Any updates? @silentpain89

Still at 20%…Way better than before in all aspects, but still miles away from any recovery…

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That’s good that you kept some gains

Have you trialed the tianeptine and Sarcosine again since the last time you took it? How many “cycles” of tianeptine and sarcosine did you do?

I know you said the D-Serine is bad for the kidneys so you stopped so I’m assuming you have not taken this again…?

I was just reading about how the glutamate receptors require glycine as a co agonist for glutamate to even bind to the NMDA receptors. I read that glycine “opens” the NMDA receptors in order for glutamate to bind to them

I wonder how you would respond to glycine…

Also maybe a logical protocol for those us on this GABA/GLUTAMATE imbalance path would be to take tianeptine like you already seen benefits from for glutamate/NMDA receptor modulation and Bacopa for GABA receptor modulation per thisisarealbummer . Both at the same time in hopes that the NMDA and GABA receptors could “balance out” if this is our problem.

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You mentioned high kyurenic acid I have extremely low kyurenic acid and high allo in urine with low glutamate and gaba.

I have anhedonia
Bad tinnitus and hyperacusis
Depression
Feeling drugged and gassed in the morning
Head pressure
Etc etc…

Maybe my results may be of interest to you

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Interesting…

So your the 6th person with either higher reference range urine Allopregnanolone or flagged high Allopregnanolone. Out of the 6th tests I have organized you are the only one with low 3a-diol.

You are the 6th person with either low range glutamate or flagged low glutamate.

You are the 1st out of 6th people to not have flagged high testosterone. However you are the 6th to have flagged high DHT.

What’s most compelling about your results is that you have flagged high epi-testosterone just like the 6th other people. Your high epi testosterone is of the most interest out of the 6th tests we have so far because it’s high in spite of not having flagged high testosterone. This is a very interesting finding. Here is why:

Epi-testosterone is a 5AR inhibitor. It’s usually normally high when your testosterone is high. But your testosterone is not high while your Epi-testosterone is high. So your producing high amounts of epi-testosterone because if you were not you would not have high amounts of it in your urine. So let’s think about that for a second. You are producing high epi-testosterone the bodies natural 5AR inhibitor AND you are excreting high amounts of DHT

DHT rejection ? That’s what this suggests.

This site is the least expensive way to get the test for anyone who wants to participate. If you are interested order urine neurotransmitters with the add-on urine hormone metabolites.

If you are not in CA, NY or MD you can get it from this site for the least expansive price possible with no doctors order. Canada, Europe and most other countries can get tested as well from this site with no doctors order.

https://totalfunctionalhealthdiagnostics.com/

I think we are onto something

What are your symptoms ? Do you get the sexual sides, the sleep issues and the constipation? Any cognitive issues ?

What have you tried and how did you respond ? I want to analyze and think about it. Maybe your low 3a-diol makes your sides different than the others who got tested who have high 3a-diol. I want to try to connect specific results from these tests with specific sides

What other sites are you on ? Are you aware of anyone else who got tested? We need all this organized in one spot

Just so everyone is aware these urine neurotransmitter tests are the real deal. I cured my 7 years worth of constipation using the results. Increasing urine serotonin into the optimal range has me pooping every day almost like the good old days . All my stomach bloat is gone . And my constipation was so bad when it started seven years ago after my second saw P nightmare that the straining herniated my disk in my l4/l5 lumbar spine. I think this may be the way out of this nightmare for me

How did you manage to do this?

I just seen that amount of serotonin in my urine was not in the optimal range and increased it into the optimal range. Noticed that around the same I did this the constipation went away

Since that time I have ran multiple experiments with the things that increase serotonin to confirm the connection.

Also, when I initially took the things to increase serotonin I took other things with it to increase dopamine and glutamate which caused me to experience PFS level onset insomnia. The insomnia that I experienced was identical to the insomnia that I experienced when I took saw P for my second time 7 years ago. The only difference is that 7 years ago after Saw P mishap (2) I stayed up for 6 weeks straight compared to this time 8 days straight. The overly stimulated brain feeling in spite of my body physically wasting away due to exhaustion as I stayed up for 8 days was identical to what I experienced when I was 29 years old seven years ago from the Saw P nightmare number (2)

My body just handled it better when I was 29 compared to 36 although it was just as painful and horrible to experience at 29

What did you take to increase serotonin levels?

L-Tryptophan, 5-HTP and vitamin B6 as the co factor. B6 allows the L-Tryptophan and 5-HTP to convert to serotonin via the enzymes

Be advised others have gotten worse from 5-HTP

Also 80-90 percent of the bodies serotonin is produced in the gut. Serotonin in the gut stimulates Bowel movements

I think body Lowered serotonin in an attempt to find equilibrium and the result is constipation.

I also know that increasing serotonin does not cause me to fall in relapse Insomnia or make me worse in any other way. Because I have came off and went back on the l-tryptophan,
5-HTP and B6 several times. And all that happened’s is my constipation goes away a few days after I reintroduce.

So it had to be the dopamine or glutamate increase that caused the insomnia relapse in my case . This all suggests a neurotransmitter imbalance

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I did plasma tests for dopamine and melatonin levels. Dopamine was low, melatonin was high.But every time I try to boost dopamine with Buspirone , I lose sleep.

Plasma dopamin does not mirror brain/CNS levels, since it can’t cross the blood brain barrier.