438 replies to this topic

[Hyperspace21]

Would L-Glutamin work instead?

Maybe but you should try using glutamates.

[Hyperspace21]

Just got my lab test results, it seems that if you take huperzine A or other NMDA Antagonists; (ethanol too, which is used in alchoholic beverages and causes bad effects when taken in conjucnction with piracetam) it will inhibit glutamates from reaching the NMDA receptor thus not allowing piracetam to work to its full extent. (or even work at all.)

When trying the experiment, avoid taking alchohol, huperzine A, lead (i don't know why anyone would consume this) and Memantine. Overall just avoid using NMDA antagonists to let the glutamates reach your NMDA receptor allowing faster brain function.

Keep this in mind while doing the experiment.

[randomlex]

Thank you for your reply!I searched for any glutamate salt/pills, but there is none in my country, only L-Glutamine from bodybuilding stores.I did some research online, and it seems that Glutamine is used by our body to create glutamate, so taking a higher dosage of glutamine or taking it regularly for a prolonged period should work, at least a bit. I'll try it next week.Also, MSG is the stuff they use to make food taste better - didn't even realize that until just now :-)!

Would L-Glutamin work instead?

Maybe but you should try using glutamates.

[ScienceGuy]

it seems that if you take huperzine A or other NMDA Antagonists; (ethanol too, which is used in alchoholic beverages and causes bad effects when taken in conjucnction with piracetam) it will inhibit glutamates from reaching the NMDA receptor thus not allowing piracetam to work to its full extent. (or even work at all.)

When trying the experiment, avoid taking alchohol, huperzine A, lead (i don't know why anyone would consume this) and Memantine. Overall just avoid using NMDA antagonists to let the glutamates reach your NMDA receptor allowing faster brain function.

OK, whilst I applaud the effort being made to enable more people to reap the rewards of PIRACETAM usage, this is one of those instances wherein I feel the need to step in and 'set the train back on the tracks' so to speak due to matters having just ventured distinctly SIDEWAYS…

You are absolutely correct that PIRACETAM appears to function, at least to an extent, via the GLUTAMATE PATHWAY and via modulation of the NMDA RECEPTORS; however, we need to be careful not to 'throw the baby out with the bathwater' here so to speak.

PIRACETAM's mechanism of action is somewhat complex; it would be a mistake to oversimplify it and thereby eliminate utilization of compounds, which may in fact work hand in hand with PIRACETAM to improve COGNITION, such as NMDA RECEPTOR ANTAGONISTS.

Hyperspace21, with the utmost respect, please kindly note the following:

1) RE: "…NMDA Antagonists... will inhibit glutamates from reaching the NMDA receptor thus not allowing piracetam to work to its full extent. (or even work at all.)" - This statement, aside from being sheer academic conjecture, is in fact factually incorrect. You have no conclusive substantiated evidence (nor even substantial clinical practice) to support this statement. Your statement is akin to taking 1 plus 1 and making 12.

2) RE "...avoid taking alchohol, huperzine A, lead (i don't know why anyone would consume this) and Memantine. Overall just avoid using NMDA antagonists to let the glutamates reach your NMDA receptor allowing faster brain function." - With the utmost respect, it is wholly irresponsible to instruct others to takes actions for which you have no substantiated evidence whatsoever; and especially when there are severe implications regarding what you are instructing everyone to do.

I DO realise that you have prefaced this with "When trying the experiment..."; however, to the casual reader you are very much communicating the following message: "for PIRACETAM to work properly you must avoid taking all NMDA RECEPTOR ANTAGONISTS and take GLUTAMATE"

There is a common misconception within this forum that NMDA RECEPTOR ANTAGONISTS are wholly ANTI-NOOTROPIC.

With regards to the connection between NMDA RECEPTORS and COGNITION, it is vital to understand there is a U-SHAPED CURVE, in that both too little and too much activation of the NMDA RECEPTORS causes IMPAIRED COGNITION.

For example, see the following:

Neuropharmacology. 2007 Nov;53(6):699-723. Epub 2007 Aug 10.

Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system--too little activation is bad, too much is even worse.

Parsons CG, Stöffler A, Danysz W.
Source

Merz Pharmaceuticals, Eckenheimer Landstrasse 100, 60318 Frankfurt am Main, Germany.
Abstract

The neurotransmitter glutamate activates several classes of metabotropic receptor and three major types of ionotropic receptor--alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate and N-methyl-D-aspartate (NMDA). The involvement of glutamate mediated neurotoxicity in the pathogenesis of Alzheimer's disease (AD) is finding increasing scientific acceptance. Central to this hypothesis is the assumption that glutamate receptors, in particular of the NMDA type, are overactivated in a tonic rather than a phasic manner. Such continuous, mild, chronic activation ultimately leads to neuronal damage/death. Additionally, impairment of synaptic plasticity (learning) may result not only from neuronal damage per se but may also be a direct consequence of this continuous, non-contingent NMDA receptor activation. Complete NMDA receptor blockade has also been shown to impair neuronal plasticity, thus, both hypo- and hyperactivity of the glutamatergic system leads to dysfunction. Memantine received marketing authorization from the EMEA (European Medicines Agency) for the treatment of moderate to severe AD in Europe and was subsequently also approved by the FDA (Food and Drug Administration) for use in the same indication in the USA. Memantine is a moderate affinity, uncompetitive NMDA receptor antagonist with strong voltage-dependency and fast kinetics. This review summarizes existing hypotheses on the mechanism of action (MOA) of memantine in an attempt to understand how the accepted interaction with NMDA receptors could allow memantine to provide both neuroprotection and reverse deficits in learning/memory by the same MOA.

PMID: 17904591

--------------------------------------------------------------------------------------------------------------------------------------------------

Furthermore it is important to understand that appropriate administration of NMDA RECEPTOR ANTAGONISTS in fact produces long-term NOOTROPIC effects via UPREGULATION of the NMDA RECEPTORS and LONG-TERM POTENTIATION (LTP) OF SYNAPTIC STRENGTH.

As such, it has been demonstrated that MAGNESIUM, which is an NMDA-RECEPTOR ANTAGONIST, is in fact a NOOTROPIC; see attached published research paper: “Enhancement of Learning and Memory by Elevating Brain Magnesium”, which demonstrates this fact.

And there is no evidence whatsoever to indicate that administration of MAGNESIUM, which is an NMDA-RECEPTOR ANTAGONIST, interferes with PIRACETAM’s physiological NOOTROPIC effects, in any regard.

In fact, in my clinical practice I have often used MAGNESIUM in combination with PIRACETAM with fantastic results.

Furthermore, I like to practice what I preach, in that I myself take PIRACETAM in combination with high doses of MAGNESIUM, and I can personally vouch for the fact that the MAGNESIUM, which is an NMDA-RECEPTOR ANTAGONIST, has no effect whatsoever on the efficacy of PIRACETAM.

And finally, the fact that there is conclusive substantiated evidence that demonstrates that high dose PIRACETAM itself in fact proliferates NMDA RECEPTOR DENSITY, also warrants consideration.

Attached Files

•  Enhancement of Learning and Memory by Elevating Brain Magnesium.pdf   1.65MB   15 downloads

Edited by ScienceGuy, 12 February 2012 - 01:50 PM.

[Hyperspace21]

it seems that if you take huperzine A or other NMDA Antagonists; (ethanol too, which is used in alchoholic beverages and causes bad effects when taken in conjucnction with piracetam) it will inhibit glutamates from reaching the NMDA receptor thus not allowing piracetam to work to its full extent. (or even work at all.)

When trying the experiment, avoid taking alchohol, huperzine A, lead (i don't know why anyone would consume this) and Memantine. Overall just avoid using NMDA antagonists to let the glutamates reach your NMDA receptor allowing faster brain function.

OK, whilst I applaud the effort being made to enable more people to reap the rewards of PIRACETAM usage, this is one of those instances wherein I feel the need to step in and 'set the train back on the tracks' so to speak due to matters having just ventured distinctly SIDEWAYS…

You are absolutely correct that PIRACETAM appears to function, at least to an extent, via the GLUTAMATE PATHWAY and via modulation of the NMDA RECEPTORS; however, we need to be careful not to 'throw the baby out with the bathwater' here so to speak.

PIRACETAM's mechanism of action is somewhat complex; it would be a mistake to oversimplify it and thereby eliminate utilization of compounds, which may in fact work hand in hand with PIRACETAM to improve COGNITION, such as NMDA RECEPTOR ANTAGONISTS.

Hyperspace21, with the utmost respect, please kindly note the following:

1) RE: "…NMDA Antagonists... will inhibit glutamates from reaching the NMDA receptor thus not allowing piracetam to work to its full extent. (or even work at all.)" - This statement, aside from being sheer academic conjecture, is in fact factually incorrect. You have no conclusive substantiated evidence (nor even substantial clinical practice) to support this statement. Your statement is akin to taking 1 plus 1 and making 12.

2) RE "...avoid taking alchohol, huperzine A, lead (i don't know why anyone would consume this) and Memantine. Overall just avoid using NMDA antagonists to let the glutamates reach your NMDA receptor allowing faster brain function." - With the utmost respect, it is wholly irresponsible to instruct others to takes actions for which you have no substantiated evidence whatsoever; and especially when there are severe implications regarding what you are instructing everyone to do.

I DO realise that you have prefaced this with "When trying the experiment..."; however, to the casual reader you are very much communicating the following message: "for PIRACETAM to work properly you must avoid taking all NMDA RECEPTOR ANTAGONISTS and take GLUTAMATE"

There is a common misconception within this forum that NMDA RECEPTOR ANTAGONISTS are wholly ANTI-NOOTROPIC.

With regards to the connection between NMDA RECEPTORS and COGNITION, it is vital to understand there is a U-SHAPED CURVE, in that both too little and too much activation of the NMDA RECEPTORS causes IMPAIRED COGNITION.

For example, see the following:

Neuropharmacology. 2007 Nov;53(6):699-723. Epub 2007 Aug 10.

Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system--too little activation is bad, too much is even worse.

Parsons CG, Stöffler A, Danysz W.
Source

Merz Pharmaceuticals, Eckenheimer Landstrasse 100, 60318 Frankfurt am Main, Germany.
Abstract

The neurotransmitter glutamate activates several classes of metabotropic receptor and three major types of ionotropic receptor--alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate and N-methyl-D-aspartate (NMDA). The involvement of glutamate mediated neurotoxicity in the pathogenesis of Alzheimer's disease (AD) is finding increasing scientific acceptance. Central to this hypothesis is the assumption that glutamate receptors, in particular of the NMDA type, are overactivated in a tonic rather than a phasic manner. Such continuous, mild, chronic activation ultimately leads to neuronal damage/death. Additionally, impairment of synaptic plasticity (learning) may result not only from neuronal damage per se but may also be a direct consequence of this continuous, non-contingent NMDA receptor activation. Complete NMDA receptor blockade has also been shown to impair neuronal plasticity, thus, both hypo- and hyperactivity of the glutamatergic system leads to dysfunction. Memantine received marketing authorization from the EMEA (European Medicines Agency) for the treatment of moderate to severe AD in Europe and was subsequently also approved by the FDA (Food and Drug Administration) for use in the same indication in the USA. Memantine is a moderate affinity, uncompetitive NMDA receptor antagonist with strong voltage-dependency and fast kinetics. This review summarizes existing hypotheses on the mechanism of action (MOA) of memantine in an attempt to understand how the accepted interaction with NMDA receptors could allow memantine to provide both neuroprotection and reverse deficits in learning/memory by the same MOA.

PMID: 17904591

--------------------------------------------------------------------------------------------------------------------------------------------------

Furthermore it is important to understand that appropriate administration of NMDA RECEPTOR ANTAGONISTS in fact produces long-term NOOTROPIC effects via UPREGULATION of the NMDA RECEPTORS and LONG-TERM POTENTIATION (LTP) OF SYNAPTIC STRENGTH.

As such, it has been demonstrated that MAGNESIUM, which is an NMDA-RECEPTOR ANTAGONIST, is in fact a NOOTROPIC; see attached published research paper: “Enhancement of Learning and Memory by Elevating Brain Magnesium”, which demonstrates this fact.

And there is no evidence whatsoever to indicate that administration of MAGNESIUM, which is an NMDA-RECEPTOR ANTAGONIST, interferes with PIRACETAM’s physiological NOOTROPIC effects, in any regard.

In fact, in my clinical practice I have often used MAGNESIUM in combination with PIRACETAM with fantastic results.

Furthermore, I like to practice what I preach, in that I myself take PIRACETAM in combination with high doses of MAGNESIUM, and I can personally vouch for the fact that the MAGNESIUM, which is an NMDA-RECEPTOR ANTAGONIST, has no effect whatsoever on the efficacy of PIRACETAM.

And finally, the fact that there is conclusive substantiated evidence that demonstrates that high dose PIRACETAM itself in fact proliferates NMDA RECEPTOR DENSITY, also warrants consideration.

I really hope none of the casual readers take it that taking NMDA antagonists will completely inhibit piracetam's function, however, despite the statement not being entirely true, it was necessary to mention it, to rule out the possibilty of NMDA recptor blockage, so as to allow the experiment to determine the NMDA activity level with a correlation with piracetam's function.

Piracetam being a derivative of GABA, works in conjuction with glutamates and therefore those instructions were logical to provide. They were only for a short period of time (1 week), which would not affect a person's overall health unless the substances mentioned were prescribed to them.

Piracetam also works on the acetylcholine receptors, which means taking Huperzine A (which is an acetylcholine receptor inhibiter) would limit or restrict some functions. This a fact and has been clinically proven.

Although some substances might offer nootropic effects; it is safe to say that the substances taken along with a nootropic like piracetam may have contradictory effects.
it's like saying 3 - 2 = 5 (where 3 is a value of a particular substance and -2 is a value of a particular substance; together they cancel each other out but on their own they have a value which come in the same category (integers)).

I like your magnesium approach and am willing to research and do some lab tests on it, it seems that if you have too many NMDA recptors, magnesium can help regulate the amount to offer proper functioning.

Like many people have said, "too much of something is bad and too little of something is also bad" so I advise everyone to stay balanced and take logical decisions,

Results are crucial to experiments, (I will be receiving clinical trial results on the 22nd of Feb), so please post your experiences if you decide to try and experiment or wait till the 22nd of February.

I again warn you, if you are sensitive to glutamates especially MSG then Do Not Take It!!! If you feel unpleasant then Avoid MSG!

[ScienceGuy]

"too much of something is bad and too little of something is also bad" so I advise everyone to stay balanced and take logical decisions

Wise words... I think you've hit the nail on the head!

[Hyperspace21]

"too much of something is bad and too little of something is also bad" so I advise everyone to stay balanced and take logical decisions

Wise words... I think you've hit the nail on the head!

Glad to know I've cleared up some pending doubts, Thanks for pointing it out.

one of my group members had a problem where piracetam was causing his eyes to burn/ feel irritated. wonder if anyone has had this before,

he takes
piracetam
fish oil
Alpha Gpc

I think it was caused by sleep deprivation but not entirely sure, this is actually quite new stuff.
He claims that it happens about 1.5 -2 hours after he has taken piracetam. (along with the other supplements). We got an allergy test done but he didn't have any.
Your opinion could be of great help.

[Hyperspace21]

We got some tests done (I set up a camera in his room; with his permission of course), and saw that his eyes got the burning sensation because he took piracetam at night which kept him awake till 2:00 a.m. He did not have any mental fatigue but it looks like his eyes needed to be shut for at least a proper sleeping period ( 6 - 7 hours), so we concluded that although piracectam functions properly, sleep should not be neglected.

We tested different sleeping periods, 3-4 hours, 4-5 hours, 5-6 hours, 6-7 hours, 8-9 hours, 9-10 hours and 10-11 hours. ( he had this problem since last week, so we tested these over the period of 1 week and got the results today). We calculated the sleep times and symptoms, and the results came in, he needed to sleep for 9.51 hours ( roughly 9 and a half hours) to avoid the burning sensation.

The results also showed that after taking piracetam his oxygen intake increased by 1.5 times. His frontal and prefrontal cortex was lit up like a christmas tree. We also saw that his Alpha and Delta waves were abnormally high ranging from 10 -13 pulses per second and 2.7 - 4 cycles per second respectively. All this happened while he was dreaming. Which means he was in a deep sleep having some surreal dreams, this could open a new door to the way piracetam works.

I'll post more upcoming results and possibly a guide for beginners on piracetam if all results are desirable.

[ScienceGuy]

We got some tests done (I set up a camera in his room; with his permission of course), and saw that his eyes got the burning sensation because he took piracetam at night which kept him awake till 2:00 a.m. He did not have any mental fatigue but it looks like his eyes needed to be shut for at least a proper sleeping period ( 6 - 7 hours), so we concluded that although piracectam functions properly, sleep should not be neglected.

We tested different sleeping periods, 3-4 hours, 4-5 hours, 5-6 hours, 6-7 hours, 8-9 hours, 9-10 hours and 10-11 hours. ( he had this problem since last week, so we tested these over the period of 1 week and got the results today). We calculated the sleep times and symptoms, and the results came in, he needed to sleep for 9.51 hours ( roughly 9 and a half hours) to avoid the burning sensation.

The results also showed that after taking piracetam his oxygen intake increased by 1.5 times. His frontal and prefrontal cortex was lit up like a christmas tree. We also saw that his Alpha and Delta waves were abnormally high ranging from 10 -13 pulses per second and 2.7 - 4 cycles per second respectively. All this happened while he was dreaming. Which means he was in a deep sleep having some surreal dreams, this could open a new door to the way piracetam works.

I'll post more upcoming results and possibly a guide for beginners on piracetam if all results are desirable.

Very interesting!

[ScienceGuy]

See THIS THREAD for reasons why the DOSAGE will be some peoples' problem: PIRACETAM DOSAGE - Why you should be taking 4.8 grams / dose

Edited by ScienceGuy, 13 February 2012 - 12:06 PM.

[Hyperspace21]

See THIS THREAD for reasons why the DOSAGE will be some peoples' problem: PIRACETAM DOSAGE - Why you should be taking 4.8 grams / dose

Amzaing results, and I'm here to say that yes a dosage of 4.8g - 16.8g actually does show a large significance in piracetam's effect. I myself took 5 grams for 2 weeks when I started piracetam, after that; since piracetam 'builds up in your body', I only needed microdoses (800mg - 1600mg) to stimulate the same effect after 3 weeks.

The question that comes in now is choline. How much choline should you take (preferrably a ratio) to feel those synergetic effects, many people complain that piracetam on its own gives them headaches. While some people don't require choline because they get enough of it from their diet. So how many grams of choline citrate or Alpha GPC would it take to cause a syngergetic effect with piracetam?

This was a really helpful tip, Thanks for sharing it.

[ScienceGuy]

See THIS THREAD for reasons why the DOSAGE will be some peoples' problem: PIRACETAM DOSAGE - Why you should be taking 4.8 grams / dose

Amzaing results, and I'm here to say that yes a dosage of 4.8g - 16.8g actually does show a large significance in piracetam's effect. I myself took 5 grams for 2 weeks when I started piracetam, after that; since piracetam 'builds up in your body', I only needed microdoses (800mg - 1600mg) to stimulate the same effect after 3 weeks.

The question that comes in now is choline. How much choline should you take (preferrably a ratio) to feel those synergetic effects, many people complain that piracetam on its own gives them headaches. While some people don't require choline because they get enough of it from their diet. So how many grams of choline citrate or Alpha GPC would it take to cause a syngergetic effect with piracetam?

This was a really helpful tip, Thanks for sharing it.

I always recommend taking whatever is the minimum dosage of CHOLINE that 100% eliminates any PIRACETAM INDUCED CHOLINE DEFICIENCY SYMPTOMS (e.g. HEADACHE, BRAIN FOG); this will vary from individual to individual. I advise against taking any more CHOLINE than this due to surplus CHOLINE inducing undesirable SIDE EFFECTS, such as DEPRESSION.

Edited by ScienceGuy, 13 February 2012 - 04:17 PM.

[SuperjackDid_]

If get CHOLINE DEFICIENCY symptoms just before bed time ,should i take additional choline or leave them that headache symptom until subside ?

[ScienceGuy]

If get CHOLINE DEFICIENCY symptoms just before bed time ,should i take additional choline or leave them that headache symptom until subside ?

I would advise that you increase your CHOLINE DOSAGE starting with the next morning's dosage, since taking additional CHOLINE prior to bedtime will likely disrupt your sleep quality

[Hyperspace21]

I always recommend taking whatever is the minimum dosage of CHOLINE that 100% eliminates any PIRACETAM INDUCED CHOLINE DEFICIENCY symptoms; this will vary from individual to individual. I advise against taking any more CHOLINE than this due to surplus CHOLINE inducing undesirable SIDE EFFECTS, such as DEPRESSION.

the minimum ratio (from what I've heard) is 1:4 (4 parts piracetam per 1 part choline), a dosage of 4.8 grams would require 1.2 grams of choline, however some people require choline in a ratio of 1:2 (2 parts piracetam per 1 part choline), which could amount to 2.4 grams of choline for 4.8 grams of piracetam. It is true that you should never exceed choline intake, beacuse this will cause an imbalance in acetylcholine in the brain.

Also taking equal amounts of choline an piracetam is not a good move since you receive choline from your diet, (unless your diet consists of water only ).

so an amount of 1.2 grams - 2.4 grams or the minimum amount that satisfies your choline needs is enough for a dosage of 4.8 grams piracetam.

[Hyperspace21]

yeah choline does have a tendency to keep you awake in conjunction with piracetam, highly agree with ScienceGuy's statement.

[ScienceGuy]

I always recommend taking whatever is the minimum dosage of CHOLINE that 100% eliminates any PIRACETAM INDUCED CHOLINE DEFICIENCY symptoms; this will vary from individual to individual. I advise against taking any more CHOLINE than this due to surplus CHOLINE inducing undesirable SIDE EFFECTS, such as DEPRESSION.

the minimum ratio (from what I've heard) is 1:4 (4 parts piracetam per 1 part choline), a dosage of 4.8 grams would require 1.2 grams of choline, however some people require choline in a ratio of 1:2 (2 parts piracetam per 1 part choline), which could amount to 2.4 grams of choline for 4.8 grams of piracetam. It is true that you should never exceed choline intake, beacuse this will cause an imbalance in acetylcholine in the brain.

Also taking equal amounts of choline an piracetam is not a good move since you receive choline from your diet, (unless your diet consists of water only ).

so an amount of 1.2 grams - 2.4 grams or the minimum amount that satisfies your choline needs is enough for a dosage of 4.8 grams piracetam.

Do you have any scientific substantiation for recommending a 1:4 and/or 1:2 ratio of CHOLINE: PIRACETAM?

[Hyperspace21]

I always recommend taking whatever is the minimum dosage of CHOLINE that 100% eliminates any PIRACETAM INDUCED CHOLINE DEFICIENCY symptoms; this will vary from individual to individual. I advise against taking any more CHOLINE than this due to surplus CHOLINE inducing undesirable SIDE EFFECTS, such as DEPRESSION.

the minimum ratio (from what I've heard) is 1:4 (4 parts piracetam per 1 part choline), a dosage of 4.8 grams would require 1.2 grams of choline, however some people require choline in a ratio of 1:2 (2 parts piracetam per 1 part choline), which could amount to 2.4 grams of choline for 4.8 grams of piracetam. It is true that you should never exceed choline intake, beacuse this will cause an imbalance in acetylcholine in the brain.

Also taking equal amounts of choline an piracetam is not a good move since you receive choline from your diet, (unless your diet consists of water only ).

so an amount of 1.2 grams - 2.4 grams or the minimum amount that satisfies your choline needs is enough for a dosage of 4.8 grams piracetam.

Do you have any scientific substantiation for recommending a 1:4 and/or 1:2 ratio of CHOLINE: PIRACETAM?

I don't, which is why I said that I heard it from somewhere and had included this in brackets, I also did not recommend anything, I just stated that the minimum amount of choline that satisfies piracetam's choline needs should be used. (like you said). The ratios, I think were a result of a poll on a thread/may have been published in an article somewhere or maybe I heard it in a discussion on piracetam , i frankly I don't remember the source of this information.

However, as long as the choline intake is below the actual piracetam intake and is also on par with daily choline requirements, it is safe to say that these ratios, could give a good numerical starting point.

choline uptake related resaearch evidences : PMID:3149192 PMID:1494300 PMID:4294142

[ScienceGuy]

The ratios, I think were a result of a poll on a thread/may have been published in an article somewhere or maybe I heard it in a discussion on piracetam , i frankly I don't remember the source of this information.

However, as long as the choline intake is below the actual piracetam intake and is also on par with daily choline requirements, it is safe to say that these ratios, could give a good numerical starting point.

OK, that's what I thought

For the record I strongly disagree with the whole 'CHOLINE RATIO' mumbo-jumbo; the basis of which is fundamentally flawed

The 1:4 rato is something anecdotally invented by users, and is in no way scientifically substantiated. Also, bear in mind that data taken from any such poll will in fact be contaminated by users who's dosage of PIRACETAM is less than 9.6 grams, and as a result is unfortunately useless

It should be borne in mind that surplus CHOLINE induces undesirable SIDE EFFECTS, including (but not limited to) DEPRESSION, IRRITABILITY and NAUSEA. 1.2 grams CHOLINE is excessive and will induce SIDE EFFECTS in most people

I personally recommend starting with CHOLINE at a dosage of 100 mg (N.B. that's 100mg of actual CHOLINE, not the raw material); and ONLY increase dosage above this in the instance of manifestation of PIRACETAM INDUCED CHOLINE DEFICIENCY symptoms (e.g. HEADACHE, BRAIN FOG), in which case the CHOLINE dosage should be increased in 100 mg increments until the minimum dosage that eliminates the PIRACETAM INDUCED CHOLINE DEFICIENCY symptoms is ascertained

Edited by ScienceGuy, 13 February 2012 - 07:27 PM.

[Hyperspace21]

OK, that's what I thought

For the record I strongly disagree with the whole 'CHOLINE RATIO' mumbo-jumbo; the basis of which is fundamentally flawed

The 1:4 rato is something anecdotally invented by users, and is in no way scientifically substantiated. Also, bear in mind that data taken from any such poll will in fact be contaminated by users who's dosage of PIRACETAM is less than 9.6 grams, and as a result is unfortunately useless

It should be borne in mind that surplus CHOLINE induces undesirable SIDE EFFECTS, including (but not limited to) DEPRESSION, IRRITABILITY and NAUSEA. 1.2 grams CHOLINE is excessive and will induce SIDE EFFECTS in most people

I personally recommend starting with CHOLINE at a dosage of 100 mg (N.B. that's 100mg of actual CHOLINE, not the raw material); and ONLY increase dosage above this in the instance of manifestation of PIRACETAM INDUCED CHOLINE DEFICIENCY symptoms (e.g. HEADACHE, BRAIN FOG), in which case the CHOLINE dosage should be increased in 100 mg increments until the minimum dosage that eliminates the PIRACETAM INDUCED CHOLINE DEFICIENCY symptoms is ascertained

come to think of it, that actually is a better way of measuring the right amount of choline , the adequate intake for adult men and male teens is 550mg/ per day, but that's only the amount that should be consumed by males.. The maximum allowed choline intake before choline becomes toxic is 3.5 grams per day.

So your approach seems far more better and logical too for choline consumption. Keep in mind that we get choline from the foods that we eat too; especially if you are non-vegetarian or consume soy, average humans tend to consume about 100 - 500 mg of choline everyday, the ratios are not backed up by scientific research nor do they have any evidence that these ratios work, so they should not be taken in to consideration.

Although finding the right amount of choline is crucial, it is also time consuming not to mention the fact that you'd have to bear headaches if choline amounts are too low or too high,
but, I think its worth the time to experiment and find the right amount of choline.

[ScienceGuy]

come to think of it, that actually is a better way of measuring the right amount of choline , the adequate intake for adult men and male teens is 550mg/ per day, but that's only the amount that should be consumed by males.. The maximum allowed choline intake before choline becomes toxic is 3.5 grams per day.

So your approach seems far more better and logical too for choline consumption. Keep in mind that we get choline from the foods that we eat too; especially if you are non-vegetarian or consume soy, average humans tend to consume about 100 - 500 mg of choline everyday, the ratios are not backed up by scientific research nor do they have any evidence that these ratios work, so they should not be taken in to consideration.

Wholeheartedly agreed on all points

Although finding the right amount of choline is crucial, it is also time consuming not to mention the fact that you'd have to bear headaches if choline amounts are too low or too high,
but, I think its worth the time to experiment and find the right amount of choline.

Wise words indeed

I completely agree that everyone is different, both in CHOLINE UTILIZATION as well as their respective intake of choline through DIETARY SOURCES, and as such you should ascertain what is the right CHOLINE dosage for you

[brokenportal]

http://www.longecity.org/forum/donate/goal-8-cryopreservation-research/ ' class='bbc_url' title='External link' rel='nofollow external'>

[Hyperspace21]

We got a few results today on the effects of piracetam and vision.

The results, showed that the glutamate increase in the synapses; (released in controlled amounts); showed that people experienced a higher perception of colour and detail who had normal and slightly higher glutamate levels in the brain. The calcium ion channels (Ca^₊ ions) were responsible for the release of the glutamate neurotransmitter. The study showed that people with TOO MUCH Calcium in their neurons and post-synaptic space, experienced dulled/ normal perception of colour an detail; the same goes for the people who had TOO LITTLE Calcium in their brain. It is like the 'U' shaped curve with experienced with Piracetam dosage.

Piracetam controls the release of Ca+ ions and glutamates in the brain, like previous studies have concluded, a dosage of 4.8 grams secretes the right amount of glutamate in the brain and regulates the Calcium ion channels. However, it was noticed that people who previously took Piracetam for more than 3 weeks required less dosage amounts of Piracetam (between 1000mg and 2800mg; some people exhibited the same effects when they took 4800mg) as compared to the new consumers.

The private clinical trials proceeded as so:
The test was conducted between the period of Jan 15 and Feb 15. It consisted of 100 people, 50 of whom were regular piracetam consumers and had consumed it for over the 3 weeks while the other 50 were new consumers. The tests were carried out over the period of 4 weeks in a double-blind placebo controlled study. The first set of 25 people (consisting of previous piracetam consumers and new piracetam consumers) were given 4.8 grams of Piracetam with 300mg - 700mg of choline supplementation.

The second set of 25 people (also consisting of previous piracetam consumers and new piracetam consumers) were given 4.8 grams of Piracetam with 300mg - 700mg of Choline supplementation and 10mg - 100mg L-Glutamate supplementation.

The third set of 25 people (consisting of previous piracetam consumers and new piracetam consumers) were given Piracetam with 300mg - 700mg of Choline supplementation and 500mg L-Glutamate supplementation.

The Fourth set of 25 people (consisting of previous piracetam consumers and new piracetam consumers) were given placebo.

The results were recorded as so:
11 Previous Piracetam consumers and New Piracetam consumers in the first set experienced the 'enhanced vision' effect without glutamate supplementation. The other 14 people experienced no such effect ,however, they did feel the other effects that Piracetam provides (enhanced speech,cognitive function and music). The responders had regular a amount of glutamate in their brain (due to their diet). The non-responders lacked the glutamate levels and some lacked calcium ion levels.

21 Previous Piracetam consumers and New Piracetam consumers in the second set reported the 'enhanced vision' effect. The other 4 did not respond. The responders showed slightly elevated glutamate levels in the brain, with a regular amount of calcium ions between post-synaptic spaces and neurons. The non - responders did not react due to insufficient amount of calcium ions in their brain.

7 Previous Piracetam consumers and New Piracetam consumers reported the 'enhanced vision' effect.11 Previous Piracetam consumers and New Piracetam consumers did not report the 'enhanced vision' effect or any effect at all, 7 people reported the other benefits that Piracetam provides. The responders had a high amounts of glutamates in their brain but they also had a lower calcium ion concentration. The complete non-responders had too much glutamate in their brain with a regular concentration of calcium ions. the non-responders to the 'enhanced vision' but responders to the other effects had too much glutamate in their brain but the also had a slightly low concentration of calcium ions.

All 25 Previous Piracetam consumers and New Piracetam consumers in the fourth set did not report anything (they were given a placebo).

The conclusions made, were based on this report.

In other news our research team has cracked some small pieces for the 'Ultimate Nootropic' , the composition of which is highly classified, but don't get your hopes up though, they are still a long way from cracking the components of the other 70% of the Nootropic. We are trying to get some of our results published in a few science magazines and also trying to catalog this information on a well known database. Wish us luck.

There is also an article that exhibits the effect of glutamates on the eyes.

http://www.ncbi.nlm....les/PMC2474471/

Edited by Hyperspace21, 15 February 2012 - 04:31 PM.

[ScienceGuy]

We got a few results today on the effects of piracetam and vision.

The results, showed that the glutamate increase in the synapses; (released in controlled amounts); showed that people experienced a higher perception of colour and detail who had normal and slightly higher glutamate levels in the brain. The calcium ion channels (Ca^₊ ions) were responsible for the release of the glutamate neurotransmitter. The study showed that people with TOO MUCH Calcium in their neurons and post-synaptic space, experienced dulled/ normal perception of colour an detail; the same goes for the people who had TOO LITTLE Calcium in their brain. It is like the 'U' shaped curve with experienced with Piracetam dosage.

Piracetam controls the release of Ca+ ions and glutamates in the brain, like previous studies have concluded, a dosage of 4.8 grams secretes the right amount of glutamate in the brain and regulates the Calcium ion channels. However, it was noticed that people who previously took Piracetam for more than 3 weeks required less dosage amounts of Piracetam (between 1000mg and 2800mg; some people exhibited the same effects when they took 4800mg) as compared to the new consumers.

The private clinical trials proceeded as so:
The test was conducted between the period of Jan 15 and Feb 15. It consisted of 100 people, 50 of whom were regular piracetam consumers and had consumed it for over the 3 weeks while the other 50 were new consumers. The tests were carried out over the period of 4 weeks in a double-blind placebo controlled study. The first set of 25 people (consisting of previous piracetam consumers and new piracetam consumers) were given 4.8 grams of Piracetam with 300mg - 700mg of choline supplementation.

The second set of 25 people (also consisting of previous piracetam consumers and new piracetam consumers) were given 4.8 grams of Piracetam with 300mg - 700mg of Choline supplementation and 10mg - 100mg L-Glutamate supplementation.

The third set of 25 people (consisting of previous piracetam consumers and new piracetam consumers) were given Piracetam with 300mg - 700mg of Choline supplementation and 500mg L-Glutamate supplementation.

The Fourth set of 25 people (consisting of previous piracetam consumers and new piracetam consumers) were given placebo.

The results were recorded as so:
11 Previous Piracetam consumers and New Piracetam consumers in the first set experienced the 'enhanced vision' effect without glutamate supplementation. The other 14 people experienced no such effect ,however, they did feel the other effects that Piracetam provides (enhanced speech,cognitive function and music). The responders had regular a amount of glutamate in their brain (due to their diet). The non-responders lacked the glutamate levels and some lacked calcium ion levels.

21 Previous Piracetam consumers and New Piracetam consumers in the second set reported the 'enhanced vision' effect. The other 4 did not respond. The responders showed slightly elevated glutamate levels in the brain, with a regular amount of calcium ions between post-synaptic spaces and neurons. The non - responders did not react due to insufficient amount of calcium ions in their brain.

7 Previous Piracetam consumers and New Piracetam consumers reported the 'enhanced vision' effect.11 Previous Piracetam consumers and New Piracetam consumers did not report the 'enhanced vision' effect or any effect at all, 7 people reported the other benefits that Piracetam provides. The responders had a high amounts of glutamates in their brain but they also had a lower calcium ion concentration. The complete non-responders had too much glutamate in their brain with a regular concentration of calcium ions. the non-responders to the 'enhanced vision' but responders to the other effects had too much glutamate in their brain but the also had a slightly low concentration of calcium ions.

All 25 Previous Piracetam consumers and New Piracetam consumers in the fourth set did not report anything (they were given a placebo).

The conclusions made, were based on this report.

In other news our research team has cracked some small pieces for the 'Ultimate Nootropic' , the composition of which is highly classified, but don't get your hopes up though, they are still a long way from cracking the components of the other 70% of the Nootropic. We are trying to get some of our results published in a few science magazines and also trying to catalog this information on a well known database. Wish us luck.

There is also an article that exhibits the effect of glutamates on the eyes.

http://www.ncbi.nlm....les/PMC2474471/

Hey Hyperspace21,

Let me be the first to APPLAUD and CONGRATULATE you on this excellent report; and THANK you and your team for conducting such ground-breaking and incredibly important research into the NOOTROPIC effects and usage of PIRACETAM. Brilliant! Well done!

Your results appear to conclusively demonstrate that accompanying PIRACETAM with supplemental L-GLUTAMATE at a dosage of 10-100mg to be significantly beneficial regards improving consitency of efficacy regards PIRACETAM'S NOOTROPIC therapeutic effects.

It is VERY interesting to note that the U-Shaped Curve that relates to dosages for both PIRACETAM and CHOLINE, in that "too much of something is bad and too little of something is also bad" (as you so excellently phrased it) clearly also relates to the L-GLUTAMATE dosage; and it seems that, for each individual, ascertaining what is their particular optimum dosage for the L-GLUTAMATE is just as important as ascertaining what is their particular optimum dosage for the CHOLINE.

Incidentally with regards to the 10 - 100mg dosage range for the L-GLUTAMATE, how exactly did the dosages vary? i.e. did everyone take differing dosage ranging from 10 - 100mg or was it weight dependant or what? Should the supplemental L-GLUTAMATE dosage be towards the 10mg end or 100mg of spectrum?

Given this considerable value of this information, it seems practically a crime to have it buried away within this particular thread. Might I suggest that you consider starting a NEW TOPIC, with title along the lines "PIRACETAM should be taken with both L-GLUTAMATE and CHOLINE" and post your report within it?

Edited by ScienceGuy, 15 February 2012 - 05:59 PM.

[Hyperspace21]

We got a few results today on the effects of piracetam and vision.

The results, showed that the glutamate increase in the synapses; (released in controlled amounts); showed that people experienced a higher perception of colour and detail who had normal and slightly higher glutamate levels in the brain. The calcium ion channels (Ca^₊ ions) were responsible for the release of the glutamate neurotransmitter. The study showed that people with TOO MUCH Calcium in their neurons and post-synaptic space, experienced dulled/ normal perception of colour an detail; the same goes for the people who had TOO LITTLE Calcium in their brain. It is like the 'U' shaped curve with experienced with Piracetam dosage.

Piracetam controls the release of Ca+ ions and glutamates in the brain, like previous studies have concluded, a dosage of 4.8 grams secretes the right amount of glutamate in the brain and regulates the Calcium ion channels. However, it was noticed that people who previously took Piracetam for more than 3 weeks required less dosage amounts of Piracetam (between 1000mg and 2800mg; some people exhibited the same effects when they took 4800mg) as compared to the new consumers.

The private clinical trials proceeded as so:
The test was conducted between the period of Jan 15 and Feb 15. It consisted of 100 people, 50 of whom were regular piracetam consumers and had consumed it for over the 3 weeks while the other 50 were new consumers. The tests were carried out over the period of 4 weeks in a double-blind placebo controlled study. The first set of 25 people (consisting of previous piracetam consumers and new piracetam consumers) were given 4.8 grams of Piracetam with 300mg - 700mg of choline supplementation.

The second set of 25 people (also consisting of previous piracetam consumers and new piracetam consumers) were given 4.8 grams of Piracetam with 300mg - 700mg of Choline supplementation and 10mg - 100mg L-Glutamate supplementation.

The third set of 25 people (consisting of previous piracetam consumers and new piracetam consumers) were given Piracetam with 300mg - 700mg of Choline supplementation and 500mg L-Glutamate supplementation.

The Fourth set of 25 people (consisting of previous piracetam consumers and new piracetam consumers) were given placebo.

The results were recorded as so:
11 Previous Piracetam consumers and New Piracetam consumers in the first set experienced the 'enhanced vision' effect without glutamate supplementation. The other 14 people experienced no such effect ,however, they did feel the other effects that Piracetam provides (enhanced speech,cognitive function and music). The responders had regular a amount of glutamate in their brain (due to their diet). The non-responders lacked the glutamate levels and some lacked calcium ion levels.

21 Previous Piracetam consumers and New Piracetam consumers in the second set reported the 'enhanced vision' effect. The other 4 did not respond. The responders showed slightly elevated glutamate levels in the brain, with a regular amount of calcium ions between post-synaptic spaces and neurons. The non - responders did not react due to insufficient amount of calcium ions in their brain.

7 Previous Piracetam consumers and New Piracetam consumers reported the 'enhanced vision' effect.11 Previous Piracetam consumers and New Piracetam consumers did not report the 'enhanced vision' effect or any effect at all, 7 people reported the other benefits that Piracetam provides. The responders had a high amounts of glutamates in their brain but they also had a lower calcium ion concentration. The complete non-responders had too much glutamate in their brain with a regular concentration of calcium ions. the non-responders to the 'enhanced vision' but responders to the other effects had too much glutamate in their brain but the also had a slightly low concentration of calcium ions.

All 25 Previous Piracetam consumers and New Piracetam consumers in the fourth set did not report anything (they were given a placebo).

The conclusions made, were based on this report.

In other news our research team has cracked some small pieces for the 'Ultimate Nootropic' , the composition of which is highly classified, but don't get your hopes up though, they are still a long way from cracking the components of the other 70% of the Nootropic. We are trying to get some of our results published in a few science magazines and also trying to catalog this information on a well known database. Wish us luck.

There is also an article that exhibits the effect of glutamates on the eyes.

http://www.ncbi.nlm....les/PMC2474471/

Hey Hyperspace21,

Let me be the first to APPLAUD and CONGRATULATE you on this excellent report; and THANK you and your team for conducting such ground-breaking and incredibly important research into the NOOTROPIC effects and usage of PIRACETAM. Brilliant! Well done!

Your results appear to conclusively demonstrate that accompanying PIRACETAM with supplemental L-GLUTAMATE at a dosage of 10-100mg to be significantly beneficial regards improving consitency of efficacy regards PIRACETAM'S NOOTROPIC therapeutic effects.

It is VERY interesting to note that the U-Shaped Curve that relates to dosages for both PIRACETAM and CHOLINE, in that "too much of something is bad and too little of something is also bad" (as you so excellently phrased it) clearly also relates to the L-GLUTAMATE dosage; and it seems that, for each individual, ascertaining what is their particular optimum dosage for the L-GLUTAMATE is just as important as ascertaining what is their particular optimum dosage for the CHOLINE.

Incidentally with regards to the 10 - 100mg dosage range for the L-GLUTAMATE, how exactly did the dosages vary? i.e. did everyone take differing dosage ranging from 10 - 100mg or was it weight dependant or what? Should the supplemental L-GLUTAMATE dosage be towards the 10mg end or 100mg of spectrum?

Given this considerable value of this information, it seems practically a crime to have it buried away within this particular thread. Might I suggest that you consider starting a NEW TOPIC, with title along the lines "PIRACETAM should be taken with both L-GLUTAMATE and CHOLINE" and post your report within it?

Thanks for the support!

Here is how we determined the L-glutamate amounts:
Each person was first tested for glutamate sensitivity. When a person consumes too much glutamate they become restless and show signs of dehydration. Their blood pressure drops too. Too little glutamate causes glucose levels to drop. A good balanced amount of glutamate keeps the blood sugar stable.

To test the right amount of L-glutamate that should be given to each person, we started off with a preliminary test by giving everyone in the second set 10mg of L-Glutamate, (secretly)
The people who responded well were given 10mg of L-Glutamate, the ones who did not respond and showed signs of lack of glutamate (no one exhibited hyper-sensitivity), were given 20mg,
using this incremental and elimination process we gave everyone the right amount of glutamate until we reached 100mg.(beyond this everyone exhibited signs of too much glutamate or hyper-sensitivity).

[ScienceGuy]

Thanks for the support!

Here is how we determined the L-glutamate amounts:
Each person was first tested for glutamate sensitivity. When a person consumes too much glutamate they become restless and show signs of dehydration. Their blood pressure drops too. Too little glutamate causes glucose levels to drop. A good balanced amount of glutamate keeps the blood sugar stable.

To test the right amount of L-glutamate that should be given to each person, we started off with a preliminary test by giving everyone in the second set 10mg of L-Glutamate, (secretly)
The people who responded well were given 10mg of L-Glutamate, the ones who did not respond and showed signs of lack of glutamate (no one exhibited hyper-sensitivity), were given 20mg,
using this incremental and elimination process we gave everyone the right amount of glutamate until we reached 100mg.(beyond this everyone exhibited signs of too much glutamate or hyper-sensitivity).

Brilliant! Thank you for the GLUTAMATE dosing details!

[Hyperspace21]

Brilliant! Thank you for the GLUTAMATE dosing details!

You are welcome!!!

[SuperjackDid_]

Is one cup of Whey Protein morning enough for GLUTAMATE synthesis or need to take individual (Free-Form)?

One more thing ,body can synthesis if they need more GLUTAMATE ,why need supplement.

Edited by Nootropix, 16 February 2012 - 03:04 PM.

[ScienceGuy]

Is one cup of Whey Protein morning enough for GLUTAMATE synthesis or need to take individual (Free-Form)?

One more thing ,body can synthesis if they need more GLUTAMATE ,why need supplement.

FREE FORM AMINO ACIDS, including L-GLUTAMATE have very different physiological effects as the COMPLEX CHAIN AMINO ACIDS that comprise PROTEIN

As such, supplementing with 10 - 100mg of L-GLUTAMATE cannot be replaced by PROTEIN consumption

It is akin to the fact that HYDROGEN GAS + OXYGEN GAS mixed together is not the same as WATER (H2O)

Edited by ScienceGuy, 16 February 2012 - 03:20 PM.

[Hyperspace21]

Is one cup of Whey Protein morning enough for GLUTAMATE synthesis or need to take individual (Free-Form)?

One more thing ,body can synthesis if they need more GLUTAMATE ,why need supplement.

FREE FORM AMINO ACIDS, including L-GLUTAMATE have very different physiological effects as the COMPLEX CHAIN AMINO ACIDS that comprise PROTEIN

As such, supplementing with 10 - 100mg of L-GLUTAMATE cannot be replaced by PROTEIN consumption

It is akin to the fact that HYDROGEN GAS + OXYGEN GAS mixed together is not the same as WATER (H2O)

Perfectly explained!