88 replies to this topic

[Senka Lowris]

Thanks for the swift reply.

I don't eat much processed food at all.
Assuming i'm glutamate toxic like most people... Should i cut out dietary sources of glutamate?...or just MSG before starting my NMDA supplements? How long might it take to reduce glutamate toxicity? How would i know if its reduced?

Thanks again.

[Area-1255]

Thanks for the swift reply.

I don't eat much processed food at all.
Assuming i'm glutamate toxic like most people... Should i cut out dietary sources of glutamate?...or just MSG before starting my NMDA supplements? How long might it take to reduce glutamate toxicity? How would i know if its reduced?

Thanks again.

No don't cut out dietary glutamate completely, you need some glutamate , just avoid MSG and other neurotoxic foods...I would stay away from soy too. Also stay away from aspartame and try to avoid methyl paraben;s and also any estrogen like substances which all increase the risk of excitotoxicity.,

You would have an idea of reduced glutamate by the clarity of your thoughts and ability to relax, high glutamate feels like you have an electrical storm in your brain and can't relax - you might also have compulsions and a brain that doesn't easily switch off...

In contrast to high noradrenaline which is a feeling of paranoia, oncoming dread, lights being brighter, possible tinnitus and other strange symptoms. moderate noradrenaline can cause tremors, slightly elevated blood pressure, worrying and overthinking things etc

 

Glutamate is more like a dysphoric, almost emotionless worrying. But almost compulsive or totally. 

 

Edited by Area-1255, 09 October 2014 - 04:12 AM.

[Metagene]

MSG

As the gastrointestinal tract has a very high capacity for using GLU, dietary intake (free and bound GLU) has a minor impact on plasma levels. Only high concentrations (as bolus) (e.g. 550 mol/l) may lead to a transient increase of plasma level. Consequently food-derived GLU (including added GLU as food additive in normal amounts of <1 g/day) does not further increase the risk for toxic effects in cases of an impairment of BBB because plasma levels do not rise.

http://www.nature.co...526a.html#bib25

Edited by Metagene, 09 October 2014 - 03:37 PM.

[Area-1255]

MSG
 

As the gastrointestinal tract has a very high capacity for using GLU, dietary intake (free and bound GLU) has a minor impact on plasma levels. Only high concentrations (as bolus) (e.g. 550 mol/l) may lead to a transient increase of plasma level. Consequently food-derived GLU (including added GLU as food additive in normal amounts of <1 g/day) does not further increase the risk for toxic effects in cases of an impairment of BBB because plasma levels do not rise.

http://www.nature.co...526a.html#bib25

 

Idk, I've felt pretty overstimulated from products with MSG..and even pea protein isolate's which have tons of glutamic acid...

In fact, they generally all make my OCD worse. Whereas glutamate analogues that act on NMDA alleviate the symptoms...

I've found sarcosine to be relaxing and stimulating ...but stimulating in a good way not jittery way...

[Metagene]

MSG

As the gastrointestinal tract has a very high capacity for using GLU, dietary intake (free and bound GLU) has a minor impact on plasma levels. Only high concentrations (as bolus) (e.g. 550 mol/l) may lead to a transient increase of plasma level. Consequently food-derived GLU (including added GLU as food additive in normal amounts of <1 g/day) does not further increase the risk for toxic effects in cases of an impairment of BBB because plasma levels do not rise.

http://www.nature.co...526a.html#bib25

Idk, I've felt pretty overstimulated from products with MSG..and even pea protein isolate's which have tons of glutamic acid...
In fact, they generally all make my OCD worse. Whereas glutamate analogues that act on NMDA alleviate the symptoms...
I've found sarcosine to be relaxing and stimulating ...but stimulating in a good way not jittery way...

Interesting.

Isoforms of the neuronal glutamate transporter gene, SLC1A1/EAAC1, negatively modulate glutamate uptake: relevance to obsessive-compulsive disorder.

http://www.ncbi.nlm....ubmed/23695234/

http://en.m.wikipedia.org/wiki/SLC1A1

[Flex]

I get a worser performance when using fullspectrum Aminoacids, but perform better when taking a blend with something like:

L-Glutamine

Glutaminpeptide N-Acetyl-L-Glutamine

L-Glutamine Alpha-Ketoglutarate

Edited by Flex, 09 October 2014 - 05:20 PM.

[Area-1255]

I get a worser performance when using fullspectrum Aminoacids, but perform better when taking a blend with something like:

L-Glutamine

Glutaminpeptide N-Acetyl-L-Glutamine

L-Glutamine Alpha-Ketoglutarate

Wouldn't glutamine exert an inverted effect though, being that it is already converted from glutamate and thus it's uptake would be higher in the muscle and less in the central nervous system....?

My theory is it's effects would be more enzymatic even though you mention an acetylated form...I'm not so sure that effect would be the same as with glutamic acid.

Should also be known that msg is still very different than regular glutamate that the body uses, because it drives an unstable sodium molecule which causes rapid serotonin denervation and adrenergic activity to heighten as glutamate is delivered. This is basic chemistry.

[Metagene]

Should also be known that msg is still very different than regular glutamate that the body uses, because it drives an unstable sodium molecule which causes rapid serotonin denervation and adrenergic activity to heighten as glutamate is delivered. This is basic chemistry.

....In rats?

Edited by Metagene, 09 October 2014 - 08:34 PM.

[Area-1255]

 

Should also be known that msg is still very different than regular glutamate that the body uses, because it drives an unstable sodium molecule which causes rapid serotonin denervation and adrenergic activity to heighten as glutamate is delivered. This is basic chemistry.

....In rats?

 

General logic and basic chemistry my friend,

[Metagene]

Wait why would sodium ions pose a problem?

[Flex]

I´ve thought more in the direction that the other aminoacids alter the glutamate transmission.

E.g:

Proline-induced inhibition of glutamate release in hippocampal area CA1.

http://www.ncbi.nlm..../pubmed/9374203

 

But the BBB permeability of MSG still lacks of evidence.

Only 1 or 2 parts of the Brain arent protected by the BBB.

 

...Thus, the EAATs in the abluminal membrane shift glutamate from the ECF to the endothelial cell where glutamate is free to diffuse into blood on facilitative carriers. This organization does not allow net glutamate entry to the brain; rather, it promotes the removal of glutamate and the maintenance of low glutamate concentrations in the ECF. This explains studies that show that the BBB is impermeable to glutamate, even at high concentrations, except in a few small areas that have fenestrated capillaries (circumventricular organs). Recently, the question of whether the BBB becomes permeable in diabetes has arisen. This issue was tested in rats with diet-induced obesity and insulin resistance or with streptozotocin-induced diabetes. Neither condition produced any detectable effect on BBB glutamate transport.

The blood-brain barrier and glutamate

http://www.ncbi.nlm....les/PMC3136011/

[Area-1255]

Wait why would sodium ions pose a problem?

Causing dehydration of the cell, or the respective neuron to fire too rapidly. MonoSodium indicates a lone and often unstable sodium ion - in which can become quickly toxic, and cause overexcitation as glutamate is also simultaneously delivered.

[JellyRev]

Okay, so, for maybe 3-4 years now i have noticed a drastic decrease in anxiety, coupled with extreme clarity and hugely improved verbal articulation skills during extreme hangovers from alcohol. 
Of course, i don't feel fantastic physically at the time, but honestly i'd still rather be in that state all of the time due to the positive mental effects.

I have also found some other people online who experience the same thing... There is actually a thread about it on this forum here: http://www.longecity...ohol-hangovers/

Anyways...my current belief is that it has something to do with NMDA upregulation during the hangover phase... This theory was also postulated by the OP of that thread.. but it didn't seem to be his problem, although he didn't have anxiety...

 

 

I also have this feeling. It makes me very social and hilarious, the center of attention. This is very different from when I am drinking or drunk. These types of hangovers I only get a couple times a year.

Also to note that once I consume food(liquids are alright) within minutes by normal states comes rushing back. I honestly did not know how bad I had/have anxiety and other issues till I had these hangovers. In these minutes I can feel the muscle tension crawl back into every skeletal muscle, my stomach starts to churn with anxious pain, and my social ability completely shuts down.

I have not figured out what it is that is upregulating or downregulating due to this food intake. 

As the typical pathways have failed, the only pathway improved was acetylcholine using alpha GPC, but its gains were in cognition and memory.

NMDA receptors looks like the place to look now.

 

 

[Area-1255]

 

Okay, so, for maybe 3-4 years now i have noticed a drastic decrease in anxiety, coupled with extreme clarity and hugely improved verbal articulation skills during extreme hangovers from alcohol. 
Of course, i don't feel fantastic physically at the time, but honestly i'd still rather be in that state all of the time due to the positive mental effects.

I have also found some other people online who experience the same thing... There is actually a thread about it on this forum here: http://www.longecity...ohol-hangovers/

Anyways...my current belief is that it has something to do with NMDA upregulation during the hangover phase... This theory was also postulated by the OP of that thread.. but it didn't seem to be his problem, although he didn't have anxiety...

 

 

I also have this feeling. It makes me very social and hilarious, the center of attention. This is very different from when I am drinking or drunk. These types of hangovers I only get a couple times a year.

Also to note that once I consume food(liquids are alright) within minutes by normal states comes rushing back. I honestly did not know how bad I had/have anxiety and other issues till I had these hangovers. In these minutes I can feel the muscle tension crawl back into every skeletal muscle, my stomach starts to churn with anxious pain, and my social ability completely shuts down.

I have not figured out what it is that is upregulating or downregulating due to this food intake. 

As the typical pathways have failed, the only pathway improved was acetylcholine using alpha GPC, but its gains were in cognition and memory.

NMDA receptors looks like the place to look now.

 

Yeah, well alcohol itself acts as a benzo and yet also as an NMDA antagonist, though the secondary property can cause an issue itself, these side-effects are masked by the benzo-mimetic property of alcohol. In which case makes sense, NMDA activation itself without excitotoxicity by other means should have a calm-stimulant effect - it should raise GABA but also, NMDA activation would raise acetylcholine, glutamate, nitric oxide, and possibly dopamine as well. Though it would shift the effect of dopamine a bit as well.

I've always found having high androgen levels helps in averting alcohol cravings.

[Senka Lowris]

 

Okay, so, for maybe 3-4 years now i have noticed a drastic decrease in anxiety, coupled with extreme clarity and hugely improved verbal articulation skills during extreme hangovers from alcohol. 
Of course, i don't feel fantastic physically at the time, but honestly i'd still rather be in that state all of the time due to the positive mental effects.

I have also found some other people online who experience the same thing... There is actually a thread about it on this forum here: http://www.longecity...ohol-hangovers/

Anyways...my current belief is that it has something to do with NMDA upregulation during the hangover phase... This theory was also postulated by the OP of that thread.. but it didn't seem to be his problem, although he didn't have anxiety...

 

 

I also have this feeling. It makes me very social and hilarious, the center of attention. This is very different from when I am drinking or drunk. These types of hangovers I only get a couple times a year.

Also to note that once I consume food(liquids are alright) within minutes by normal states comes rushing back. I honestly did not know how bad I had/have anxiety and other issues till I had these hangovers. In these minutes I can feel the muscle tension crawl back into every skeletal muscle, my stomach starts to churn with anxious pain, and my social ability completely shuts down.

I have not figured out what it is that is upregulating or downregulating due to this food intake. 

As the typical pathways have failed, the only pathway improved was acetylcholine using alpha GPC, but its gains were in cognition and memory.

NMDA receptors looks like the place to look now.

 

 

Yep , exact same thing, very social, funny, quick witted even... Awesome word recall too, almost like some sort of filter has been removed.
I'm going to try an NMDA protocol and see what happens. It's interesting though, when i'm in that state it's almost like my nervous system has been turned down a few notches... Different energy altogether. Other things which can put me in this state: MDMA hangover, LSD hangover. Both of which have action on NMDA if i'm not mistaken. It's all very confusing :(.

Edit: Interestingly i also have muscle tension issues.

 

 

Okay, so, for maybe 3-4 years now i have noticed a drastic decrease in anxiety, coupled with extreme clarity and hugely improved verbal articulation skills during extreme hangovers from alcohol. 
Of course, i don't feel fantastic physically at the time, but honestly i'd still rather be in that state all of the time due to the positive mental effects.

I have also found some other people online who experience the same thing... There is actually a thread about it on this forum here: http://www.longecity...ohol-hangovers/

Anyways...my current belief is that it has something to do with NMDA upregulation during the hangover phase... This theory was also postulated by the OP of that thread.. but it didn't seem to be his problem, although he didn't have anxiety...

 

 

I also have this feeling. It makes me very social and hilarious, the center of attention. This is very different from when I am drinking or drunk. These types of hangovers I only get a couple times a year.

Also to note that once I consume food(liquids are alright) within minutes by normal states comes rushing back. I honestly did not know how bad I had/have anxiety and other issues till I had these hangovers. In these minutes I can feel the muscle tension crawl back into every skeletal muscle, my stomach starts to churn with anxious pain, and my social ability completely shuts down.

I have not figured out what it is that is upregulating or downregulating due to this food intake. 

As the typical pathways have failed, the only pathway improved was acetylcholine using alpha GPC, but its gains were in cognition and memory.

NMDA receptors looks like the place to look now.

 

Yeah, well alcohol itself acts as a benzo and yet also as an NMDA antagonist, though the secondary property can cause an issue itself, these side-effects are masked by the benzo-mimetic property of alcohol. In which case makes sense, NMDA activation itself without excitotoxicity by other means should have a calm-stimulant effect - it should raise GABA but also, NMDA activation would raise acetylcholine, glutamate, nitric oxide, and possibly dopamine as well. Though it would shift the effect of dopamine a bit as well.

I've always found having high androgen levels helps in averting alcohol cravings.

 

 

Interesting, as usual. The feeling i'm seeking is kind of a feeling of my nervous system being turned down... hard to explain.  I suppose a calm-stimulant effect is kinda appropriate for what i'm experiencing.

Edited by Senka Lowris, 11 October 2014 - 03:29 PM.

[Area-1255]

 

 

Okay, so, for maybe 3-4 years now i have noticed a drastic decrease in anxiety, coupled with extreme clarity and hugely improved verbal articulation skills during extreme hangovers from alcohol. 
Of course, i don't feel fantastic physically at the time, but honestly i'd still rather be in that state all of the time due to the positive mental effects.

I have also found some other people online who experience the same thing... There is actually a thread about it on this forum here: http://www.longecity...ohol-hangovers/

Anyways...my current belief is that it has something to do with NMDA upregulation during the hangover phase... This theory was also postulated by the OP of that thread.. but it didn't seem to be his problem, although he didn't have anxiety...

 

 

I also have this feeling. It makes me very social and hilarious, the center of attention. This is very different from when I am drinking or drunk. These types of hangovers I only get a couple times a year.

Also to note that once I consume food(liquids are alright) within minutes by normal states comes rushing back. I honestly did not know how bad I had/have anxiety and other issues till I had these hangovers. In these minutes I can feel the muscle tension crawl back into every skeletal muscle, my stomach starts to churn with anxious pain, and my social ability completely shuts down.

I have not figured out what it is that is upregulating or downregulating due to this food intake. 

As the typical pathways have failed, the only pathway improved was acetylcholine using alpha GPC, but its gains were in cognition and memory.

NMDA receptors looks like the place to look now.

 

 

Yep , exact same thing, very social, funny, quick witted even... Awesome word recall too, almost like some sort of filter has been removed.
I'm going to try an NMDA protocol and see what happens. It's interesting though, when i'm in that state it's almost like my nervous system has been turned down a few notches... Different energy altogether. Other things which can put me in this state: MDMA hangover, LSD hangover. Both of which have action on NMDA if i'm not mistaken. It's all very confusing :(.

Edit: Interestingly i also have muscle tension issues.

 

 

Okay, so, for maybe 3-4 years now i have noticed a drastic decrease in anxiety, coupled with extreme clarity and hugely improved verbal articulation skills during extreme hangovers from alcohol. 
Of course, i don't feel fantastic physically at the time, but honestly i'd still rather be in that state all of the time due to the positive mental effects.

I have also found some other people online who experience the same thing... There is actually a thread about it on this forum here: http://www.longecity...ohol-hangovers/

Anyways...my current belief is that it has something to do with NMDA upregulation during the hangover phase... This theory was also postulated by the OP of that thread.. but it didn't seem to be his problem, although he didn't have anxiety...

 

 

I also have this feeling. It makes me very social and hilarious, the center of attention. This is very different from when I am drinking or drunk. These types of hangovers I only get a couple times a year.

Also to note that once I consume food(liquids are alright) within minutes by normal states comes rushing back. I honestly did not know how bad I had/have anxiety and other issues till I had these hangovers. In these minutes I can feel the muscle tension crawl back into every skeletal muscle, my stomach starts to churn with anxious pain, and my social ability completely shuts down.

I have not figured out what it is that is upregulating or downregulating due to this food intake. 

As the typical pathways have failed, the only pathway improved was acetylcholine using alpha GPC, but its gains were in cognition and memory.

NMDA receptors looks like the place to look now.

 

Yeah, well alcohol itself acts as a benzo and yet also as an NMDA antagonist, though the secondary property can cause an issue itself, these side-effects are masked by the benzo-mimetic property of alcohol. In which case makes sense, NMDA activation itself without excitotoxicity by other means should have a calm-stimulant effect - it should raise GABA but also, NMDA activation would raise acetylcholine, glutamate, nitric oxide, and possibly dopamine as well. Though it would shift the effect of dopamine a bit as well.

I've always found having high androgen levels helps in averting alcohol cravings.

 

 

Interesting, as usual. The feeling i'm seeking is kind of a feeling of my nervous system being turned down... hard to explain.  I suppose a calm-stimulant effect is kinda appropriate for what i'm experiencing.

 

NMDA itself is hard to find, you might have to custom synthesis or get from a bulk manufacturer...iforce nutrition sells intimidate which is pure NMDA but it also contains an anti-estrogen/aromatase inhibitor..,.other than that, sarcosine plus daa - d-aspartic acid is your best bet.

[Metagene]

 

Wait why would sodium ions pose a problem?

Causing dehydration of the cell, or the respective neuron to fire too rapidly. MonoSodium indicates a lone and often unstable sodium ion - in which can become quickly toxic, and cause overexcitation as glutamate is also simultaneously delivered.

 

 

Unless you are talking about knocking back a quart of soy sauce this is certainly not the case. There is no inherent difference in the way the body utilizes sodium ions be it from MSG or cheese.

 

Brain damage in neonatal mice following monosodium glutamate administration: Possible involvement of hypernatremia and hyperosmolality

 

The effects of glutamic acid hydrochloride, sodium chloride and sucrose administered orally to neonatal mice at levels equimolar and hyperosmolar to those used in obtaining brain damage with a monosodium glutamate (MSG) were examined. Hypernatremia is induced in neonatal mice at the highest dosage of MSG used to elicit neuropathologic changes. Glutamic acid hydrochloride was found to elicit the same pattern of brain lesions as does MSG. High sodium levels therefore, are not necessary to open the bloodbrain barrier for glutamate-induced neuronal lesions. Sodium chloride itself, although not causing lesions in arcuate nucleus, is capable of causing a wide spectrum of damage in neonatal mouse brain at lower levels (0.02–0.05 meq 1) than previously recognized. Glutamic acid and sodium caused brain lesions often in the same structures but their pattern of damage differed, probably as a result of different routes of entry into the brain. Glutamate, or more probably one of its metabolites, damaged cells close to circulating cerebrospinal fluid (CSF), while hypertonic saline apparently egressed into brain tissue from capillaries, arterioles and venules. Neuronal damage following MSG administration tends to radiate inward within structures in contact with circulating CSF. Lesions following sodium chloride ingestion present themselves as foci or bands occurring throughout a given structure. Sometimes neuronal necrosis accompanied hemorrhagic vessels within a structure, a phenomenon not seen following MSG administration. A high rate of animal mortality followed hyperosmolality induced by sucrose loads. Brain shrinkage and extensive vascular dilatation, unaccompanied by marked neuronal dehydration were the major neurological observations. Finally, while neither hyperosmolarity nor hypernatremia is capable of eliciting the patterns of lesions correlated with MSG ingestion, either condition can result in severe vascular changes in the neonatal mouse brain.

 

http://www.sciencedi...014488675901582

[Area-1255]

 

 

Wait why would sodium ions pose a problem?

Causing dehydration of the cell, or the respective neuron to fire too rapidly. MonoSodium indicates a lone and often unstable sodium ion - in which can become quickly toxic, and cause overexcitation as glutamate is also simultaneously delivered.

 

 

Unless you are talking about knocking back a quart of soy sauce this is certainly not the case. There is no inherent difference in the way the body utilizes sodium ions be it from MSG or cheese.

 

Brain damage in neonatal mice following monosodium glutamate administration: Possible involvement of hypernatremia and hyperosmolality

 

 

 

The effects of glutamic acid hydrochloride, sodium chloride and sucrose administered orally to neonatal mice at levels equimolar and hyperosmolar to those used in obtaining brain damage with a monosodium glutamate (MSG) were examined. Hypernatremia is induced in neonatal mice at the highest dosage of MSG used to elicit neuropathologic changes. Glutamic acid hydrochloride was found to elicit the same pattern of brain lesions as does MSG. High sodium levels therefore, are not necessary to open the bloodbrain barrier for glutamate-induced neuronal lesions. Sodium chloride itself, although not causing lesions in arcuate nucleus, is capable of causing a wide spectrum of damage in neonatal mouse brain at lower levels (0.02–0.05 meq 1) than previously recognized. Glutamic acid and sodium caused brain lesions often in the same structures but their pattern of damage differed, probably as a result of different routes of entry into the brain. Glutamate, or more probably one of its metabolites, damaged cells close to circulating cerebrospinal fluid (CSF), while hypertonic saline apparently egressed into brain tissue from capillaries, arterioles and venules. Neuronal damage following MSG administration tends to radiate inward within structures in contact with circulating CSF. Lesions following sodium chloride ingestion present themselves as foci or bands occurring throughout a given structure. Sometimes neuronal necrosis accompanied hemorrhagic vessels within a structure, a phenomenon not seen following MSG administration. A high rate of animal mortality followed hyperosmolality induced by sucrose loads. Brain shrinkage and extensive vascular dilatation, unaccompanied by marked neuronal dehydration were the major neurological observations. Finally, while neither hyperosmolarity nor hypernatremia is capable of eliciting the patterns of lesions correlated with MSG ingestion, either condition can result in severe vascular changes in the neonatal mouse brain.

 

http://www.sciencedi...014488675901582

 

Well either way it still contributes...and you certainly can't define everyone's genetic susceptibility based on a neonatal mouse study.

Edited by Area-1255, 11 October 2014 - 06:37 PM.

[Plasticperson]

whenever i take nmda antagonist i like everything neat and tidy

 

[JellyRev]

whenever i take nmda antagonist i like everything neat and tidy

 

which antagonist have you taken? 

[Metagene]

 

 

 

Wait why would sodium ions pose a problem?

Causing dehydration of the cell, or the respective neuron to fire too rapidly. MonoSodium indicates a lone and often unstable sodium ion - in which can become quickly toxic, and cause overexcitation as glutamate is also simultaneously delivered.

 

 

Unless you are talking about knocking back a quart of soy sauce this is certainly not the case. There is no inherent difference in the way the body utilizes sodium ions be it from MSG or cheese.

 

Brain damage in neonatal mice following monosodium glutamate administration: Possible involvement of hypernatremia and hyperosmolality

 

 

 

The effects of glutamic acid hydrochloride, sodium chloride and sucrose administered orally to neonatal mice at levels equimolar and hyperosmolar to those used in obtaining brain damage with a monosodium glutamate (MSG) were examined. Hypernatremia is induced in neonatal mice at the highest dosage of MSG used to elicit neuropathologic changes. Glutamic acid hydrochloride was found to elicit the same pattern of brain lesions as does MSG. High sodium levels therefore, are not necessary to open the bloodbrain barrier for glutamate-induced neuronal lesions. Sodium chloride itself, although not causing lesions in arcuate nucleus, is capable of causing a wide spectrum of damage in neonatal mouse brain at lower levels (0.02–0.05 meq 1) than previously recognized. Glutamic acid and sodium caused brain lesions often in the same structures but their pattern of damage differed, probably as a result of different routes of entry into the brain. Glutamate, or more probably one of its metabolites, damaged cells close to circulating cerebrospinal fluid (CSF), while hypertonic saline apparently egressed into brain tissue from capillaries, arterioles and venules. Neuronal damage following MSG administration tends to radiate inward within structures in contact with circulating CSF. Lesions following sodium chloride ingestion present themselves as foci or bands occurring throughout a given structure. Sometimes neuronal necrosis accompanied hemorrhagic vessels within a structure, a phenomenon not seen following MSG administration. A high rate of animal mortality followed hyperosmolality induced by sucrose loads. Brain shrinkage and extensive vascular dilatation, unaccompanied by marked neuronal dehydration were the major neurological observations. Finally, while neither hyperosmolarity nor hypernatremia is capable of eliciting the patterns of lesions correlated with MSG ingestion, either condition can result in severe vascular changes in the neonatal mouse brain.

 

http://www.sciencedi...014488675901582

 

Well either way it still contributes...and you certainly can't define everyone's genetic susceptibility based on a neonatal mouse study.

 

 

It still contributes to what exactly? I only intend to prove MSG is not neurotoxic when consumed in normal amounts nothing more.

[Area-1255]

 

 

 

 

Wait why would sodium ions pose a problem?

Causing dehydration of the cell, or the respective neuron to fire too rapidly. MonoSodium indicates a lone and often unstable sodium ion - in which can become quickly toxic, and cause overexcitation as glutamate is also simultaneously delivered.

 

 

Unless you are talking about knocking back a quart of soy sauce this is certainly not the case. There is no inherent difference in the way the body utilizes sodium ions be it from MSG or cheese.

 

Brain damage in neonatal mice following monosodium glutamate administration: Possible involvement of hypernatremia and hyperosmolality

 

 

 

The effects of glutamic acid hydrochloride, sodium chloride and sucrose administered orally to neonatal mice at levels equimolar and hyperosmolar to those used in obtaining brain damage with a monosodium glutamate (MSG) were examined. Hypernatremia is induced in neonatal mice at the highest dosage of MSG used to elicit neuropathologic changes. Glutamic acid hydrochloride was found to elicit the same pattern of brain lesions as does MSG. High sodium levels therefore, are not necessary to open the bloodbrain barrier for glutamate-induced neuronal lesions. Sodium chloride itself, although not causing lesions in arcuate nucleus, is capable of causing a wide spectrum of damage in neonatal mouse brain at lower levels (0.02–0.05 meq 1) than previously recognized. Glutamic acid and sodium caused brain lesions often in the same structures but their pattern of damage differed, probably as a result of different routes of entry into the brain. Glutamate, or more probably one of its metabolites, damaged cells close to circulating cerebrospinal fluid (CSF), while hypertonic saline apparently egressed into brain tissue from capillaries, arterioles and venules. Neuronal damage following MSG administration tends to radiate inward within structures in contact with circulating CSF. Lesions following sodium chloride ingestion present themselves as foci or bands occurring throughout a given structure. Sometimes neuronal necrosis accompanied hemorrhagic vessels within a structure, a phenomenon not seen following MSG administration. A high rate of animal mortality followed hyperosmolality induced by sucrose loads. Brain shrinkage and extensive vascular dilatation, unaccompanied by marked neuronal dehydration were the major neurological observations. Finally, while neither hyperosmolarity nor hypernatremia is capable of eliciting the patterns of lesions correlated with MSG ingestion, either condition can result in severe vascular changes in the neonatal mouse brain.

 

http://www.sciencedi...014488675901582

 

Well either way it still contributes...and you certainly can't define everyone's genetic susceptibility based on a neonatal mouse study.

 

 

It still contributes to what exactly? I only intend to prove MSG is not neurotoxic when consumed in normal amounts nothing more.

 

Contributes to a neurotoxic / anxiogenic state...keep in mind there are many biochemical factors and in those pre-disposed especially, this can become an issue. As was mentioned earlier....gene mutations of glutamate activity do play a role in the pathophysiology / etiology of neurological disorders and anxiety disorders....

[Metagene]

 

 

 

 

 

Wait why would sodium ions pose a problem?

Causing dehydration of the cell, or the respective neuron to fire too rapidly. MonoSodium indicates a lone and often unstable sodium ion - in which can become quickly toxic, and cause overexcitation as glutamate is also simultaneously delivered.

 

 

Unless you are talking about knocking back a quart of soy sauce this is certainly not the case. There is no inherent difference in the way the body utilizes sodium ions be it from MSG or cheese.

 

Brain damage in neonatal mice following monosodium glutamate administration: Possible involvement of hypernatremia and hyperosmolality

 

 

 

The effects of glutamic acid hydrochloride, sodium chloride and sucrose administered orally to neonatal mice at levels equimolar and hyperosmolar to those used in obtaining brain damage with a monosodium glutamate (MSG) were examined. Hypernatremia is induced in neonatal mice at the highest dosage of MSG used to elicit neuropathologic changes. Glutamic acid hydrochloride was found to elicit the same pattern of brain lesions as does MSG. High sodium levels therefore, are not necessary to open the bloodbrain barrier for glutamate-induced neuronal lesions. Sodium chloride itself, although not causing lesions in arcuate nucleus, is capable of causing a wide spectrum of damage in neonatal mouse brain at lower levels (0.02–0.05 meq 1) than previously recognized. Glutamic acid and sodium caused brain lesions often in the same structures but their pattern of damage differed, probably as a result of different routes of entry into the brain. Glutamate, or more probably one of its metabolites, damaged cells close to circulating cerebrospinal fluid (CSF), while hypertonic saline apparently egressed into brain tissue from capillaries, arterioles and venules. Neuronal damage following MSG administration tends to radiate inward within structures in contact with circulating CSF. Lesions following sodium chloride ingestion present themselves as foci or bands occurring throughout a given structure. Sometimes neuronal necrosis accompanied hemorrhagic vessels within a structure, a phenomenon not seen following MSG administration. A high rate of animal mortality followed hyperosmolality induced by sucrose loads. Brain shrinkage and extensive vascular dilatation, unaccompanied by marked neuronal dehydration were the major neurological observations. Finally, while neither hyperosmolarity nor hypernatremia is capable of eliciting the patterns of lesions correlated with MSG ingestion, either condition can result in severe vascular changes in the neonatal mouse brain.

 

http://www.sciencedi...014488675901582

 

Well either way it still contributes...and you certainly can't define everyone's genetic susceptibility based on a neonatal mouse study.

 

 

It still contributes to what exactly? I only intend to prove MSG is not neurotoxic when consumed in normal amounts nothing more.

 

Contributes to a neurotoxic / anxiogenic state...keep in mind there are many biochemical factors and in those pre-disposed especially, this can become an issue. As was mentioned earlier....gene mutations of glutamate activity do play a role in the pathophysiology / etiology of neurological disorders and anxiety disorders....

 

 

Yet you have not provided a single shred of evidence that supports the notion MSG given at non-pharmaceutical dosse contributes to a  neurotoxicity / anxiogenic state in the presence of the blood brain barrier. 

[Flex]

 

 

 

 

 

 

Wait why would sodium ions pose a problem?

Causing dehydration of the cell, or the respective neuron to fire too rapidly. MonoSodium indicates a lone and often unstable sodium ion - in which can become quickly toxic, and cause overexcitation as glutamate is also simultaneously delivered.

 

 

Unless you are talking about knocking back a quart of soy sauce this is certainly not the case. There is no inherent difference in the way the body utilizes sodium ions be it from MSG or cheese.

 

Brain damage in neonatal mice following monosodium glutamate administration: Possible involvement of hypernatremia and hyperosmolality

 

 

 

The effects of glutamic acid hydrochloride, sodium chloride and sucrose administered orally to neonatal mice at levels equimolar and hyperosmolar to those used in obtaining brain damage with a monosodium glutamate (MSG) were examined. Hypernatremia is induced in neonatal mice at the highest dosage of MSG used to elicit neuropathologic changes. Glutamic acid hydrochloride was found to elicit the same pattern of brain lesions as does MSG. High sodium levels therefore, are not necessary to open the bloodbrain barrier for glutamate-induced neuronal lesions. Sodium chloride itself, although not causing lesions in arcuate nucleus, is capable of causing a wide spectrum of damage in neonatal mouse brain at lower levels (0.02–0.05 meq 1) than previously recognized. Glutamic acid and sodium caused brain lesions often in the same structures but their pattern of damage differed, probably as a result of different routes of entry into the brain. Glutamate, or more probably one of its metabolites, damaged cells close to circulating cerebrospinal fluid (CSF), while hypertonic saline apparently egressed into brain tissue from capillaries, arterioles and venules. Neuronal damage following MSG administration tends to radiate inward within structures in contact with circulating CSF. Lesions following sodium chloride ingestion present themselves as foci or bands occurring throughout a given structure. Sometimes neuronal necrosis accompanied hemorrhagic vessels within a structure, a phenomenon not seen following MSG administration. A high rate of animal mortality followed hyperosmolality induced by sucrose loads. Brain shrinkage and extensive vascular dilatation, unaccompanied by marked neuronal dehydration were the major neurological observations. Finally, while neither hyperosmolarity nor hypernatremia is capable of eliciting the patterns of lesions correlated with MSG ingestion, either condition can result in severe vascular changes in the neonatal mouse brain.

 

http://www.sciencedi...014488675901582

 

Well either way it still contributes...and you certainly can't define everyone's genetic susceptibility based on a neonatal mouse study.

 

 

It still contributes to what exactly? I only intend to prove MSG is not neurotoxic when consumed in normal amounts nothing more.

 

Contributes to a neurotoxic / anxiogenic state...keep in mind there are many biochemical factors and in those pre-disposed especially, this can become an issue. As was mentioned earlier....gene mutations of glutamate activity do play a role in the pathophysiology / etiology of neurological disorders and anxiety disorders....

 

 

Yet you have not provided a single shred of evidence that supports the notion MSG given at non-pharmaceutical dosse contributes to a  neurotoxicity / anxiogenic state in the presence of the blood brain barrier. 

 

 

True and IIRC You´ve advised to everyone to stay away from MSG.

This genetic disposition isnt at least common.

Ergo, You adviced to the Healthy ones, so the vast majority, to stay away from everyday food..

 

If Your assumption isnt correct, is the assumption of the non-toxicity of NMDA still correct ?

 

Overactivation of NMDA receptors is a known cause of nerve-cell toxicity.

http://www.scienceda...40122134242.htm

 

Our results are consistent with the idea that NMDA-mediated toxicity is caused by activation of NR2B- but not NR2A-containing NMDA receptors leading to calpain activation and that developmental changes in NMDA toxicity reflect developmental changes in NMDA receptor subunit composition.

http://www.ncbi.nlm....pubmed/16540573
 

With utter respect, but this is basic recherche !

It took me 2 minutes to find it, and Nitric oxide is never mentioned in the both above.

Could it be that this just Your own thesis ?

Since Nit.Oxi. wasnt able to prevent the toxicity !

 

Suggesting someone that NMDA is completly harmless leads to consequences of someones Health !

Ask Your self, have You done allready harm ?

 

If yes, could You turn back the time ?

Edited by Flex, 11 October 2014 - 10:04 PM.

[Area-1255]

 

 

 

 

 

 

 

Wait why would sodium ions pose a problem?

Causing dehydration of the cell, or the respective neuron to fire too rapidly. MonoSodium indicates a lone and often unstable sodium ion - in which can become quickly toxic, and cause overexcitation as glutamate is also simultaneously delivered.

 

 

Unless you are talking about knocking back a quart of soy sauce this is certainly not the case. There is no inherent difference in the way the body utilizes sodium ions be it from MSG or cheese.

 

Brain damage in neonatal mice following monosodium glutamate administration: Possible involvement of hypernatremia and hyperosmolality

 

 

 

The effects of glutamic acid hydrochloride, sodium chloride and sucrose administered orally to neonatal mice at levels equimolar and hyperosmolar to those used in obtaining brain damage with a monosodium glutamate (MSG) were examined. Hypernatremia is induced in neonatal mice at the highest dosage of MSG used to elicit neuropathologic changes. Glutamic acid hydrochloride was found to elicit the same pattern of brain lesions as does MSG. High sodium levels therefore, are not necessary to open the bloodbrain barrier for glutamate-induced neuronal lesions. Sodium chloride itself, although not causing lesions in arcuate nucleus, is capable of causing a wide spectrum of damage in neonatal mouse brain at lower levels (0.02–0.05 meq 1) than previously recognized. Glutamic acid and sodium caused brain lesions often in the same structures but their pattern of damage differed, probably as a result of different routes of entry into the brain. Glutamate, or more probably one of its metabolites, damaged cells close to circulating cerebrospinal fluid (CSF), while hypertonic saline apparently egressed into brain tissue from capillaries, arterioles and venules. Neuronal damage following MSG administration tends to radiate inward within structures in contact with circulating CSF. Lesions following sodium chloride ingestion present themselves as foci or bands occurring throughout a given structure. Sometimes neuronal necrosis accompanied hemorrhagic vessels within a structure, a phenomenon not seen following MSG administration. A high rate of animal mortality followed hyperosmolality induced by sucrose loads. Brain shrinkage and extensive vascular dilatation, unaccompanied by marked neuronal dehydration were the major neurological observations. Finally, while neither hyperosmolarity nor hypernatremia is capable of eliciting the patterns of lesions correlated with MSG ingestion, either condition can result in severe vascular changes in the neonatal mouse brain.

 

http://www.sciencedi...014488675901582

 

Well either way it still contributes...and you certainly can't define everyone's genetic susceptibility based on a neonatal mouse study.

 

 

It still contributes to what exactly? I only intend to prove MSG is not neurotoxic when consumed in normal amounts nothing more.

 

Contributes to a neurotoxic / anxiogenic state...keep in mind there are many biochemical factors and in those pre-disposed especially, this can become an issue. As was mentioned earlier....gene mutations of glutamate activity do play a role in the pathophysiology / etiology of neurological disorders and anxiety disorders....

 

 

Yet you have not provided a single shred of evidence that supports the notion MSG given at non-pharmaceutical dosse contributes to a  neurotoxicity / anxiogenic state in the presence of the blood brain barrier. 

 

 

True and IIRC You´ve advised to everyone to stay away from MSG.

This genetic disposition isnt at least common.

Ergo, You adviced to the Healthy ones, so the vast majority, to stay away from everyday food..

 

If Your assumption isnt correct, is the assumption of the non-toxicity of NMDA still correct ?

 

Overactivation of NMDA receptors is a known cause of nerve-cell toxicity.

http://www.scienceda...40122134242.htm

 

Our results are consistent with the idea that NMDA-mediated toxicity is caused by activation of NR2B- but not NR2A-containing NMDA receptors leading to calpain activation and that developmental changes in NMDA toxicity reflect developmental changes in NMDA receptor subunit composition.

http://www.ncbi.nlm....pubmed/16540573
 

With utter respect, but this is basic recherche !

It took me 2 minutes to find it, and Nitric oxide is never mentioned in the both above.

Could it be that this just Your own thesis ?

Since Nit.Oxi. wasnt able to prevent the toxicity !

 

Suggesting someone that NMDA is completly harmless leads to consequences of someones Health !

Ask Your self, have You done allready harm ?

 

If yes, could You turn back the time ?

 

 

 

 

 

                 And so begins my evidence....look and behold

 

 

 

 

 

 

http://www.ncbi.nlm..../pubmed/9795199

 

 

Gonadotropin-releasing hormone (GnRH) gene regulation by N-methyl-D-aspartic acid in GT1-1 neuronal cells: differential involvement of c-fos and c-jun protooncogenes.

Jung N1, Sun W, Lee H, Cho S, Shim C, Kim K.

Author information

 

Abstract

The present study examined the regulatory mechanisms of GnRH gene expression by N-methyl-d-aspartic acid (NMDA) in immortalized hypothalamic GnRH neurons (GT1-1 cells). NMDA (100 microM) stimulated GnRH mRNA levels transiently at 2 h after treatment. Dose-response experiment showed that there was a biphasic action of NMDA on GnRH mRNA levels: GnRH mRNA levels were increased by NMDA at lower concentrations (10 and 100 microM), but not at higher concentrations (1 and 10 mM). NMDA (100 microM)-induced GnRH mRNA levels were efficiently blocked by pre-treatment with NMDA receptor antagonists, MK-801 and AP-5. We next examined the signal transduction pathways involved in NMDA-induced GnRH gene expression based on previous findings that NMDA signal propagates into the cell through Ca2+ and nitric oxide (NO) pathways in many neurons. While ionomycin, a Ca2+ ionopore, application failed to alter GnRH gene expression, treatment of GT1-1 cells with sodium nitroprusside (SNP), an NO donor, increased GnRH gene expression with a similar time course to NMDA treatment. Moreover, application of GT1-1 cells with nitric oxide synthase (NOS) inhibitors (l-NAME, d-NAME, and NA) prior to NMDA treatment, inhibited NMDA-induced GnRH gene expression. These results indicate that the effect of NMDA is mediated by the NO signalling cascade. The mouse GnRH promoter activity was also increased by NMDA at low concentration (100 microM), but not at high concentration (1 microM), confirming the biphasic action of NMDA on GnRH mRNA levels. Since NMDA (100 microM) and SNP (1 microM) markedly induced c-jun expression, but not c-fos expression, we hypothesized that Jun activation is responsible for the transcriptional activation of GnRH gene expression. To examine this, we performed two different experiments. Treatment of NMDA greatly increased the activity of heterologous promoter of Fos/Jun responsive sequence (-187/-69) from the mouse GnRH promoter fused to hsv-tk minimal promoter. Moreover, overexpression of c-jun induced GnRH promoter activity, while c-fos overexpression decreased GnRH promoter activity. Taken together, this study indicates that NMDA regulates GnRH gene expression in GT1-1 cells through the NO-Jun signal transduction pathway.

 

 

Stimulation of NMDA receptors activates neuronal nitric oxide synthase (nNOS) and the production of nitric oxide (NO). Dephosphorylation of nNOS increases nNOS enzymatic activity. We have examined the regulation of nNOS phosphorylation in rat cortical neurons following NMDA receptor activation. We show that nNOS is constitutively phosphorylated and that NMDA receptor activation decreases the level of nNOS phosphorylation by a mechanism that is blocked specifically by NMDA receptor antagonists and inhibitors of the Ca²⁺-regulated phosphatases calcineurin and PP1/PP2A. Using quantitative digital microscopy, we show that NMDA receptor activation induces the accumulation of nitrotyrosine, a measure of nNOS activity, and TdT-mediated fluorescein-dUTP nick end labeling (TUNEL) positivity, a measure of cell death. A calcineurin inhibitor blocked the increase in both TUNEL and nitrotyrosine positivity.

http://www.sciencedi...197458003001799

 

 

http://www.ncbi.nlm....pubmed/21471392

 

 

J Neurophysiol. 2011 Jun;105(6):2897-906. doi: 10.1152/jn.00287.2010. Epub 2011 Apr 6.

NMDA receptor activation enhances inhibitory GABAergic transmission onto hippocampal pyramidal neurons via presynaptic and postsynaptic mechanisms.

Xue JG1, Masuoka T, Gong XD, Chen KS, Yanagawa Y, Law SK, Konishi S.

Author information

 

Abstract

N-methyl-D-aspartate (NMDA) receptors (NMDARs) are implicated in synaptic plasticity and modulation of glutamatergic excitatory transmission. Effect of NMDAR activation on inhibitory GABAergic transmission remains largely unknown. Here, we report that a brief application of NMDA could induce two distinct actions in CA1 pyramidal neurons in mouse hippocampal slices: 1) an inward current attributed to activation of postsynaptic NMDARs; and 2) fast phasic synaptic currents, namely spontaneous inhibitory postsynaptic currents (sIPSCs), mediated by GABA(A) receptors in pyramidal neurons. The mean amplitude of sIPSCs was also increased by NMDA. This profound increase in the sIPSC frequency and amplitude was markedly suppressed by the sodium channel blocker TTX, whereas the frequency and mean amplitude of miniature IPSCs were not significantly affected by NMDA, suggesting that NMDA elicits repetitive firing in GABAergic interneurons, thereby leading to GABA release from multiple synaptic sites of single GABAergic axons. We found that the NMDAR open-channel blocker MK-801 injected into recorded pyramidal neurons suppressed the NMDA-induced increase of sIPSCs, which raises the possibility that the firing of interneurons may not be the sole factor and certain retrograde messengers may also be involved in the NMDA-mediated enhancement of GABAergic transmission. Our results from pharmacological tests suggest that the nitric oxide signaling pathway is mobilized by NMDAR activation in CA1 pyramidal neurons, which in turn retrogradely facilitates GABA release from the presynaptic terminals. Thus NMDARs at glutamatergic synapses on both CA1 pyramidal neurons and interneurons appear to exert feedback and feedforward inhibition for determining the spike timing of the hippocampal microcircuit.

I'm interested to hearing what you have to say now....with the evidence and all.   

Edited by Area-1255, 11 October 2014 - 10:25 PM.

[Metagene]

Forgive my ingorance but would bioavalility be an issue with oral NMDA supplementation? The animal studies used i.v or i.p administration.

Heavy Resistance Training and Supplementation With the Alleged Testosterone Booster Nmda has No Effect on Body Composition, Muscle Performance, and Serum Hormones Associated With the Hypothalamo-Pituitary-Gonadal Axis in Resistance-Trained Males

http://www.ncbi.nlm....les/PMC3918557/

[Area-1255]

Forgive my ingorance but would bioavalility be an issue with oral NMDA supplementation? The animal studies used i.v or i.p administration.

Heavy Resistance Training and Supplementation With the Alleged Testosterone Booster Nmda has No Effect on Body Composition, Muscle Performance, and Serum Hormones Associated With the Hypothalamo-Pituitary-Gonadal Axis in Resistance-Trained Males

http://www.ncbi.nlm....les/PMC3918557/

Well d-aspartic acid certainly has strong bioavailability, or bb'ers and enthusiasts wouldn't be using it...NMDA always helped me sleep and gave me focus for the next day.Plus strong pumps...read my review

http://area1255.blog...srt-review.html

[Metagene]

N-methyl-D-aspartic acid does not readily cross the BBB. Oral administration would be subject to I pass metabolism so I'd hesitate to attribute positive or negative effects from 30mg of NMDA.

[Area-1255]

N-methyl-D-aspartic acid does not readily cross the BBB. Oral administration would be subject to I pass metabolism so I'd hesitate to attribute positive or negative effects from 30mg of NMDA.

Ehh, well I always felt something from it personally.,

[totflare]

 

Hello area. Thank you for all your great work.

 

I'm currently attempting to treat my long term anxiety and have a few questions pertaining to NMDA.

Okay, so, for maybe 3-4 years now i have noticed a drastic decrease in anxiety, coupled with extreme clarity and hugely improved verbal articulation skills during extreme hangovers from alcohol. 
Of course, i don't feel fantastic physically at the time, but honestly i'd still rather be in that state all of the time due to the positive mental effects.

I have also found some other people online who experience the same thing... There is actually a thread about it on this forum here: http://www.longecity...ohol-hangovers/

Anyways...my current belief is that it has something to do with NMDA upregulation during the hangover phase... This theory was also postulated by the OP of that thread.. but it didn't seem to be his problem, although he didn't have anxiety...

 

One thing that intrigues me is that normally i have horrible anxiety/psychotic behaviour when smoking marijuana. I always used to joke to myself that smoking marijuana is the ultimate test to see if my deep anxiety is gone. This anxiety is eliminated 100% during an acute hangover.

 

Interestingly, marijuana has some kind of interaction with NMDA and glutamate too. On a side note I always suspected id be very prone to going schizophrenic if i kept smoking that stuff over a long period in high amounts.

I also learned that hypo function of NMDA is involved with schizophrenia too.....Actually you mentioned it int he first lien of this thread :p

This all has to be linked somehow, i dunno if you have any input regarding this, but i'm thinking of buying sarcosine etc to test on myself, but i don't have much spare funds so i'd really like to hear if you have any opinions on this before i do, whether it's worth a try.

Again, thanks for your help regardless of whether you respond or not, you're a good guy.

 

.

Yes, cannabinoid receptors interact with glutamate channeling.

CB active substances, such as forms of THC have differential effects on glutamate. 

Delta9-thc tends to decrease excitory currents.  http://www.ncbi.nlm..../pubmed/9882692

 

However , in one study, extracellular glutamate had increased and GABA had decreased, selective for the prefrontal cortex. http://www.ncbi.nlm....pubmed/12383968

Considering cannabinoids generally increase philosophical thinking, and this is evident when I have smoked it as well - and also in eating aka "munchies" this is all more connected with increased glutamate imHo. However, they also increase dopamine and have a number of other effects.

 

http://www.ncbi.nlm....les/PMC1575338/

 

It seems though that decreases in serotonin in the VTA may also occur due to THC's ability to inhibit zone specific GABA and glutamate interneurons...it's all very interesting.

 

In regards to sarcosine...yes I've always had positive effects from sarcosine plus d-aspartic acid...and I am probably one of the few who isn't going crazy with the concept of NMDA blockade; in fact , I take a far different view in this regard.

 

I believe that blocking NMDA's is generally counter-effective and not a good idea in the long-run, even though short-term it might have some benefits by positively affecting dopamine reuptake transporters and endorphin release....

In the long-run, NMDA blockade leads to several unfavorable effects, including decreased testosterone, neurosteroids, GABA and cholinergic activity, and messed up opioid receptors. It also produces a notable transient but possibly controlled, psychotic / psychotomimetic effect.

 

Now let's be clear, I've had chronic OCD, anxiety and tourette's as a child...as well as a long list of experimentation in substances and chemicals....

 

I can tell you that all in all...NMDA agonism has an excellent effect; including with sarcosine plus d-aspartic acid....and it actually decreases incidences of intrusive thoughts and gives a general sense of mental clarity and even restores excitement and counteracts anhedonia.

 

 

However, I should also mention that although NMDA agonism has favorable effects, this is probably not the case if you are consuming MSG and / or are already glutamate toxic; in this case, the benefits are probably over ridden by kainate / AMPA / metabatropic glutamate receptor overactivation.

 

Hence why I see the best effects (different as well, not exclusive to the diet, tested separately and together) when on a clean diet and avoid MSG containing foods.

 

Yes, from my own experience also it is very clear that we don't want our NMDA receptors to be antagonized and instead we want them to be activated and functional. It seems to be a key switch in the brain that turns everything else on.

 

My quest is to find a sustainable way to upregulate and stimulate those receptors. You say antagonism is bad but my idea has always been that using an NMDA antagonist might lead to upregulation in the long run. You yourself mentioned that we should try to predict the homeostatic response of the body. Wouldn't agonizing with sarcosine or anything else lead to downregulation in the long term?