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Brain Function Boosters 3.0
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Wise Guy
Level 4

Join date: Mar 2008
Location: Michigan, USA
Posts: 724

Thread One - http://tnation.tmuscle.com/...nction_boosters

Thread Two - http://tnation.tmuscle.com/...ion_boosters_20

I know its been covered before, but anyone here use adderall?

Scored some for finals couple weeks ago. Me likey very, very much.

Any opinions/experiences?

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sjodarski
Level 5

Join date: Sep 2007
Location: Wisconsin, USA
Posts: 14

Hey all

Just discovered and read through the first two threads. So much great information there! Right now I'm trying to finish up nursing school, and I've decided to try the stack of: Vinpocetine, DMAE, and Aniracetam. I'm also considering picking up some oxiracetam for sort of an "as needed" basis. I'd appreciate if anyone could PM me a good source to find these. Thanks for all the great info, keep it coming!

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Vegita
Level 3

Join date: Apr 2003
Location: New York, USA
Posts: 7516

Was going to update last week about my continuing "Dart" experience. My thursday league was off last week and will be this week do to the holidays. Anyways, Last wednesday was another successful night. 27.5 PPD. I think this is the third week in a row it has slipped but to be honest I forgot to even take my brain boosters before the match, so I was only running on the improved base state I have achieved so far.

Another variable I'd like to throw in, The bar decided to have thier christmas party that night and our matches start at 7:00. Well at 8:00 he started free beers and free food till midnight. So #1 it was packed, and #2 I might have imbibed in an extra beverage or two, seeing as they were free.

In any event, when I started taking the brain boosters. My season average was 23 I believe. I'll have to go back and look at the other thread to confirm. But one week in, I noticed very little. But after a couple weeks, my nights started going up fast. a 29 average, then a 32 average, then back to a 29 average and then finally a 27 average this past week.

But over the past 4 weeks my average is 29.25 versus my previous season average of 23 which was the first 7 or 8 weeks of the season. So I think it shows there is a very real improvement here. I will keep updating till I have equal samples of each, but halfway through the boosted period, I am very happy with the results, oh and so are my teamates.

And just one more side note, something unmeasurable. I have been involved in exactly 1 loss these past 4 weeks. I play 7 games per night out of the 13 my team plays. so I went 27-1 over the last 4 weeks. This is a really amazing stat line because everyone has a bad game here and there, and even if my partner has been struggling I have been able to play well enough to pick up thier slack and still overcome the other team.

And over this past 4 weeks I really have not had even 1 "bad" game, there were some average games in there, but nothing bad and a whole lot of really good ones.

V

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rehabman28
Level 4

Join date: Apr 2007
Location: North Carolina, USA
Posts: 133

Anyone have a good source of Aniracetam? I used RElentless improvement in the past, but they no longer carry it due to it being a poor seller.

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wfifer
Level 5

Join date: Jan 2006
Location: New York, USA
Posts: 1678

rehabman28 wrote:
Anyone have a good source of Aniracetam? I used RElentless improvement in the past, but they no longer carry it due to it being a poor seller.


I'm interested in this as well. In the past I bought Cognitive Nutrition's aniracetam powder, 100g for ~$30. Now they're selling 45g in caps for the same price. If that's the going rate, fine...but if anyone has a more reasonably priced source I'd be grateful.

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tolismann
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Join date: Apr 2009
Location: Greece
Posts: 467

Do any of the previously mentioned boosters have a positive effect on insulin sensitivity?

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Vegita
Level 3

Join date: Apr 2003
Location: New York, USA
Posts: 7516

Dart update. We played the #1 team last night, we are currently in second place. They have a 13 game lead on us. Niether of us has lost a match all season long, though the winner at the end of the year is soley decided on total wins or losses. So a 7-6 win is not as good as say a 11-2 win.

Anyways, I personally shot a 27.5 last night which is still a good deal above my old season average. I also had another really amazing game where I closed the game out in 4 rounds. I luckily left myself 150 with my third round and was able to hit the hat trick to win the game in 4 rounds. Also we managed to trounce the other team 10-3 on the night. It's really mind boggling how we were able to handle them like this.

They were a bit off, but to only win 3 games has to be demoralizing to them. Next week is the last week of the first half so we made a nice run at them and closed thier lead to 6 games. The boosters are still working good, I did lose one game last ngiht, but to be honest, the other team had a kid who just caught fire and had a 5 round out against us. Other than throwing another 4 rounder, I was not going to win that game.

There were several times my team was in a hole and several times where I was able to hit a really crucial round to give us the advantage at the end of a game. Sometimes that is more important than what your actual averages were. Being able to hit the clutch dart.

V

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bushidobadboy
Level 3

Join date: Nov 2004
Location: Wales
Posts: 15565

tolismann wrote:
Do any of the previously mentioned boosters have a positive effect on insulin sensitivity?

No, but more importantly, they do not have a negative effect in insulin sensitivity, unlike adderal, etc.

BBB

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toby_w
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Join date: Jun 2008
Location: England
Posts: 141

When talking about vinpocetine, is this periwinkle extract, or something synthetic?
Was thinking of DMAE, Vinpo and N-Acetyl Tyrosine for upcoming exams.
Also does anyone know a UK supplier of N-Acetyl Tyrosine?

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Rusty Barbell
Level 10

Join date: Aug 2005
Location:
Posts: 538

bushidobadboy wrote:
tolismann wrote:
Do any of the previously mentioned boosters have a positive effect on insulin sensitivity?

No, but more importantly, they do not have a negative effect in insulin sensitivity, unlike adderal, etc.

BBB


I started using piracetam and vinpocetine regularly over a year ago and my last A1C was 5.5 - which was a point (or maybe 1.5; previous record was 6.5 or 7.0) lower than it has ever been. Although I haven't been a good doctor-visiting diabetic lately and had it checked in about 8 months so I don't have any additional data points. But if anything they are supposed to improve your body's ability to utilize glucose, and I believe there is data floating around to show both of these compounds as capable of enhancing brain-glucose uptake (with possible other downstream effects on efficient glucose utilization and the insulin system).

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kakno
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Join date: Dec 2008
Location: Sweden
Posts: 2764

I have a question that is actually remotely relevant and I think you guys, if any, know the answer.

I take it Power Drive works in part because L-tyrosine turns into epinephrine (adrenaline), norepinephrine (noradrenaline) and dopamine, (some of which also turns into the aforementioned substances). But L-tyrosine is just and aminoacid, present in my protein shake and therefore in milk and probably meat and flour and whatever. What I wonder is:

Why don't I get any effect from tyrosine consumed with food, but when it's almost alone down there it gets me 11 deadlifts with my 5RM?

I have a theory, but it sounds like some kindergarten stuff, so could someone explain it to me? I know that it's probably a stupid question. I also read that Power Drive should be consumed on an empty stomach, 3 hours after and at least 45 minutes before anything else, I want to understand the mechanism.

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buffd_samurai
Level 100

Join date: Sep 2004
Location:
Posts: 1157

This is just a fantastic thread...all parts...1, 2, and now 3.

These are the type of discussions that bring me back to this site repeatedly. Thankyou to the posters who have resurrected it.

I, unfortunately, do not tolerate aniracetam very well. Seriously speaking, it puts me in a SERIOUSLY bad mood. It basically turns me into a "bad drunk", i.e. someone who is overly aggressive and "throws their weight around" when under its "influence". Why this is, I don't know. But it looks like fat soluable racetams are definitely not for me.

Anyone else like this? Anyone had a reasonable rationale mechanism that might explain such strange reactions for me?

Now, I did not consume the ani with DMAE, but I am taking a full dose of the liquid alpha-GPC in the evenings (for the growth hormone effect as well as the acetylcholine replenishment). I am considering redoing my experiment with DMAE with the ani while continuing to take the alph-GPC in the evening. OR, I am considering replacing my plan of using DMAE with just plain ol alpha-GPC.

With all the wonder talk of Ani on this thread, I am a little crushed that it didn't work for me. Piracetam will follow after another couple weeks of Ani.

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bushidobadboy
Level 3

Join date: Nov 2004
Location: Wales
Posts: 15565

Rusty Barbell wrote:
bushidobadboy wrote:
tolismann wrote:
Do any of the previously mentioned boosters have a positive effect on insulin sensitivity?

No, but more importantly, they do not have a negative effect in insulin sensitivity, unlike adderal, etc.

BBB


I started using piracetam and vinpocetine regularly over a year ago and my last A1C was 5.5 - which was a point (or maybe 1.5; previous record was 6.5 or 7.0) lower than it has ever been. Although I haven't been a good doctor-visiting diabetic lately and had it checked in about 8 months so I don't have any additional data points. But if anything they are supposed to improve your body's ability to utilize glucose, and I believe there is data floating around to show both of these compounds as capable of enhancing brain-glucose uptake (with possible other downstream effects on efficient glucose utilization and the insulin system).


Ah yes! I didn't think about the increased ATP synthesis in neurones from the use of vinpo. Now whilst that is not a directly linked effect on muscle insulin sensitivity, it is, I suppose a good way to reduce blood glucose levels.

This has opened up a new train of thought for me, cheers!

BBB

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bushidobadboy
Level 3

Join date: Nov 2004
Location: Wales
Posts: 15565

kakno wrote:
I have a question that is actually remotely relevant and I think you guys, if any, know the answer.

I take it Power Drive works in part because L-tyrosine turns into epinephrine (adrenaline), norepinephrine (noradrenaline) and dopamine, (some of which also turns into the aforementioned substances). But L-tyrosine is just and aminoacid, present in my protein shake and therefore in milk and probably meat and flour and whatever. What I wonder is:

Why don't I get any effect from tyrosine consumed with food, but when it's almost alone down there it gets me 11 deadlifts with my 5RM?

I have a theory, but it sounds like some kindergarten stuff, so could someone explain it to me? I know that it's probably a stupid question. I also read that Power Drive should be consumed on an empty stomach, 3 hours after and at least 45 minutes before anything else, I want to understand the mechanism.


Firstly you need to consider the different total amounts of tyrosine in food, Vs a specific source of tyrosine. I have not experimented with the stuff, but some guys take 1000mg+. It's unlikely you will get that in a single intake from foostuffs.

Secondly you need to consider that a liquid (ior pure powder) for of tyrosine will be absorbed much faster (and probably more completely) than that found in foodstuffs.

BBB

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bushidobadboy
Level 3

Join date: Nov 2004
Location: Wales
Posts: 15565

On a related note:

Since tyrosince is converted into catecholamines, and since catecholamines are counterproductive to learning or at least memory, I suggest you do not use it as a nootropic.

I wrote an article about the effects of cortisol on memory for a friend actually, and whilst I'm not convinced it was that great, you can choose to read it if you so desire.

BBB

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bushidobadboy
Level 3

Join date: Nov 2004
Location: Wales
Posts: 15565

buffd_samurai wrote:
This is just a fantastic thread...all parts...1, 2, and now 3.

These are the type of discussions that bring me back to this site repeatedly. Thankyou to the posters who have resurrected it.

I, unfortunately, do not tolerate aniracetam very well. Seriously speaking, it puts me in a SERIOUSLY bad mood. It basically turns me into a "bad drunk", i.e. someone who is overly aggressive and "throws their weight around" when under its "influence". Why this is, I don't know. But it looks like fat soluable racetams are definitely not for me.

Anyone else like this? Anyone had a reasonable rationale mechanism that might explain such strange reactions for me?

Now, I did not consume the ani with DMAE, but I am taking a full dose of the liquid alpha-GPC in the evenings (for the growth hormone effect as well as the acetylcholine replenishment). I am considering redoing my experiment with DMAE with the ani while continuing to take the alph-GPC in the evening. OR, I am considering replacing my plan of using DMAE with just plain ol alpha-GPC.

With all the wonder talk of Ani on this thread, I am a little crushed that it didn't work for me. Piracetam will follow after another couple weeks of Ani.


That is valuable feedback and whilst I have no explanation, I do value your input as another 'point on the graph' of the vagaries of individual response.

BBB

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middleageguy
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Join date: Aug 2004
Location: California, USA
Posts: 189

bushidobadboy wrote:
buffd_samurai wrote:
This is just a fantastic thread...all parts...1, 2, and now 3.

These are the type of discussions that bring me back to this site repeatedly. Thankyou to the posters who have resurrected it.

I, unfortunately, do not tolerate aniracetam very well. Seriously speaking, it puts me in a SERIOUSLY bad mood. It basically turns me into a "bad drunk", i.e. someone who is overly aggressive and "throws their weight around" when under its "influence". Why this is, I don't know. But it looks like fat soluable racetams are definitely not for me.

Anyone else like this? Anyone had a reasonable rationale mechanism that might explain such strange reactions for me?

Now, I did not consume the ani with DMAE, but I am taking a full dose of the liquid alpha-GPC in the evenings (for the growth hormone effect as well as the acetylcholine replenishment). I am considering redoing my experiment with DMAE with the ani while continuing to take the alph-GPC in the evening. OR, I am considering replacing my plan of using DMAE with just plain ol alpha-GPC.

With all the wonder talk of Ani on this thread, I am a little crushed that it didn't work for me. Piracetam will follow after another couple weeks of Ani.


That is valuable feedback and whilst I have no explanation, I do value your input as another 'point on the graph' of the vagaries of individual response.

BBB

The different amino acids (in foods) do compete with each other to cross the blood brain barrier, I think this is one reason...

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buffd_samurai
Level 100

Join date: Sep 2004
Location:
Posts: 1157

middleageguy wrote:
bushidobadboy wrote:
buffd_samurai wrote:
This is just a fantastic thread...all parts...1, 2, and now 3.

These are the type of discussions that bring me back to this site repeatedly. Thankyou to the posters who have resurrected it.

I, unfortunately, do not tolerate aniracetam very well. Seriously speaking, it puts me in a SERIOUSLY bad mood. It basically turns me into a "bad drunk", i.e. someone who is overly aggressive and "throws their weight around" when under its "influence". Why this is, I don't know. But it looks like fat soluable racetams are definitely not for me.

Anyone else like this? Anyone had a reasonable rationale mechanism that might explain such strange reactions for me?

Now, I did not consume the ani with DMAE, but I am taking a full dose of the liquid alpha-GPC in the evenings (for the growth hormone effect as well as the acetylcholine replenishment). I am considering redoing my experiment with DMAE with the ani while continuing to take the alph-GPC in the evening. OR, I am considering replacing my plan of using DMAE with just plain ol alpha-GPC.

With all the wonder talk of Ani on this thread, I am a little crushed that it didn't work for me. Piracetam will follow after another couple weeks of Ani.


That is valuable feedback and whilst I have no explanation, I do value your input as another 'point on the graph' of the vagaries of individual response.

BBB

The different amino acids (in foods) do compete with each other to cross the blood brain barrier, I think this is one reason...


Hmmm...I'm failing to understand the relationship of your answer to the issue I brought up...I didn't indicate eating anything (food) different with the Ani. Sorry...but thanks for thinking about it!

I'm wondering: when talking about brain function boosting, why do I not read anything about Spike? For me at least, Spike definitely belongs in this conversation. I find Spike to be VERY effective in helping with focus, with brain energy, and with motivation. I read alot of people's good words towards Moda and its effect on motivation...I'm just wondering if they had tried Spike for a decent comparison.

For that matter, I had also found Sclaremax to be quite "brain stimulating" as well.

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bushidobadboy
Level 3

Join date: Nov 2004
Location: Wales
Posts: 15565

middleageguy wrote:
bushidobadboy wrote:
buffd_samurai wrote:
This is just a fantastic thread...all parts...1, 2, and now 3.

These are the type of discussions that bring me back to this site repeatedly. Thankyou to the posters who have resurrected it.

I, unfortunately, do not tolerate aniracetam very well. Seriously speaking, it puts me in a SERIOUSLY bad mood. It basically turns me into a "bad drunk", i.e. someone who is overly aggressive and "throws their weight around" when under its "influence". Why this is, I don't know. But it looks like fat soluable racetams are definitely not for me.

Anyone else like this? Anyone had a reasonable rationale mechanism that might explain such strange reactions for me?

Now, I did not consume the ani with DMAE, but I am taking a full dose of the liquid alpha-GPC in the evenings (for the growth hormone effect as well as the acetylcholine replenishment). I am considering redoing my experiment with DMAE with the ani while continuing to take the alph-GPC in the evening. OR, I am considering replacing my plan of using DMAE with just plain ol alpha-GPC.

With all the wonder talk of Ani on this thread, I am a little crushed that it didn't work for me. Piracetam will follow after another couple weeks of Ani.


That is valuable feedback and whilst I have no explanation, I do value your input as another 'point on the graph' of the vagaries of individual response.

BBB

The different amino acids (in foods) do compete with each other to cross the blood brain barrier, I think this is one reason...



You are right of course, but I meant that I have no explanation as to why aniracetam has such a paradoxical effect on this man.

BBB

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Alpha F
Level 4

Join date: Mar 2005
Location:
Posts: 3167

buffd_samurai wrote:

I, unfortunately, do not tolerate aniracetam very well. Seriously speaking, it puts me in a SERIOUSLY bad mood. It basically turns me into a "bad drunk", i.e. someone who is overly aggressive and "throws their weight around" when under its "influence". Why this is, I don't know. But it looks like fat soluable racetams are definitely not for me.

Anyone else like this?
Yes.

Anyone had a reasonable rationale mechanism that might explain such strange reactions for me?

You could be dopamine dominant in your genetic brain make up.
By taking a substance that might enhance dopamine levels in you pre frontal cortex you tip over an already high dopamine level. Two of the functions implicated on the pre frontal cortex are: personality expression and moderation of correct social behavior. If you are, by default, high dopamine, low serotonin and low norepinepherine, enhancing dopamine and serotonin might explain the neurological effect on your mood and behavioural changes.



"Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP

Shirane M, Nakamura K.

CNS Supporting Laboratory,
Nippon Roche Research Center,
200 Kajiwara, 247-8530, Kamakura, Japan
Brain Res 2001 Oct 19;916(1-2):211-21

Abstract

Aniracetam, a cognition enhancer, has been recently found to preferentially increase extracellular levels of dopamine (DA) and serotonin (5-HT) in the prefrontal cortex (PFC), basolateral amygdala and dorsal hippocampus of the mesocorticolimbic system in stroke-prone spontaneously hypertensive rats. In the present study, we aimed to identify actually active substances among aniracetam and its major metabolites and to clarify the mode of action in DA and 5-HT release in the PFC. Local perfusion of mecamylamine, a nicotinic acetylcholine (nACh) and N-methyl-D-aspartate (NMDA) receptor antagonist, into the ventral tegmental area (VTA) and dorsal raphe nucleus (DRN) completely blocked DA and 5-HT release, respectively, in the PFC elicited by orally administered aniracetam. The effects of aniracetam were mimicked by local perfusion of N-anisoyl--aminobutyric acid (N-anisoyl-GABA), one of the major metabolites of aniracetam, into the VTA and DRN. The cortical DA release induced by N-anisoyl-GABA applied to the VTA was also completely abolished by co-perfusion of mecamylamine. Additionally, when p-anisic acid, another metabolite of aniracetam, and N-anisoyl-GABA were locally perfused into the PFC, they induced DA and 5-HT release in the same region, respectively. These results indicate that aniracetam enhances DA and 5-HT release by mainly mediating the action of N-anisoyl-GABA that targets not only somatodendritic nACh and NMDA receptors but also presynaptic nACh receptors."

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bushidobadboy
Level 3

Join date: Nov 2004
Location: Wales
Posts: 15565

Useful info from Alpha F, thanks.

I guess that's why aniracetam is noted for its anxiolytic effects (at least in most people); by increasing DA and 5-HT slightly.


BBB

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buffd_samurai
Level 100

Join date: Sep 2004
Location:
Posts: 1157

Alpha F wrote:
buffd_samurai wrote:

I, unfortunately, do not tolerate aniracetam very well. Seriously speaking, it puts me in a SERIOUSLY bad mood. It basically turns me into a "bad drunk", i.e. someone who is overly aggressive and "throws their weight around" when under its "influence". Why this is, I don't know. But it looks like fat soluable racetams are definitely not for me.

Anyone else like this?
Yes.

Anyone had a reasonable rationale mechanism that might explain such strange reactions for me?

You could be dopamine dominant in your genetic brain make up.
By taking a substance that might enhance dopamine levels in you pre frontal cortex you tip over an already high dopamine level. Two of the functions implicated on the pre frontal cortex are: personality expression and moderation of correct social behavior. If you are, by default, high dopamine, low serotonin and low norepinepherine, enhancing dopamine and serotonin might explain the neurological effect on your mood and behavioural changes.



"Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP

Shirane M, Nakamura K.

CNS Supporting Laboratory,
Nippon Roche Research Center,
200 Kajiwara, 247-8530, Kamakura, Japan
Brain Res 2001 Oct 19;916(1-2):211-21

Abstract

Aniracetam, a cognition enhancer, has been recently found to preferentially increase extracellular levels of dopamine (DA) and serotonin (5-HT) in the prefrontal cortex (PFC), basolateral amygdala and dorsal hippocampus of the mesocorticolimbic system in stroke-prone spontaneously hypertensive rats. In the present study, we aimed to identify actually active substances among aniracetam and its major metabolites and to clarify the mode of action in DA and 5-HT release in the PFC. Local perfusion of mecamylamine, a nicotinic acetylcholine (nACh) and N-methyl-D-aspartate (NMDA) receptor antagonist, into the ventral tegmental area (VTA) and dorsal raphe nucleus (DRN) completely blocked DA and 5-HT release, respectively, in the PFC elicited by orally administered aniracetam. The effects of aniracetam were mimicked by local perfusion of N-anisoyl--aminobutyric acid (N-anisoyl-GABA), one of the major metabolites of aniracetam, into the VTA and DRN. The cortical DA release induced by N-anisoyl-GABA applied to the VTA was also completely abolished by co-perfusion of mecamylamine. Additionally, when p-anisic acid, another metabolite of aniracetam, and N-anisoyl-GABA were locally perfused into the PFC, they induced DA and 5-HT release in the same region, respectively. These results indicate that aniracetam enhances DA and 5-HT release by mainly mediating the action of N-anisoyl-GABA that targets not only somatodendritic nACh and NMDA receptors but also presynaptic nACh receptors."



What a wonderful rationale...thankyou so much for posting this!

Any information on whether other racetams could act in this manner? I am specifically interested in piracetam. My fear is that I won't be able to use any of them as I've read pira and ani have almost the same effects just that ani seems to be more powerful on a per unit dosage.

In the end though, the only way to really know is to try it as I plan to and report back here. I'm still going to continue my experiment with ani + DMAE to see if that possibly improves things....however the mechanism above would indicate things could get worse. I gotta try it though.

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bushidobadboy
Level 3

Join date: Nov 2004
Location: Wales
Posts: 15565

buffd_samurai wrote:
Alpha F wrote:
buffd_samurai wrote:

I, unfortunately, do not tolerate aniracetam very well. Seriously speaking, it puts me in a SERIOUSLY bad mood. It basically turns me into a "bad drunk", i.e. someone who is overly aggressive and "throws their weight around" when under its "influence". Why this is, I don't know. But it looks like fat soluable racetams are definitely not for me.

Anyone else like this?
Yes.

Anyone had a reasonable rationale mechanism that might explain such strange reactions for me?

You could be dopamine dominant in your genetic brain make up.
By taking a substance that might enhance dopamine levels in you pre frontal cortex you tip over an already high dopamine level. Two of the functions implicated on the pre frontal cortex are: personality expression and moderation of correct social behavior. If you are, by default, high dopamine, low serotonin and low norepinepherine, enhancing dopamine and serotonin might explain the neurological effect on your mood and behavioural changes.



"Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP

Shirane M, Nakamura K.

CNS Supporting Laboratory,
Nippon Roche Research Center,
200 Kajiwara, 247-8530, Kamakura, Japan
Brain Res 2001 Oct 19;916(1-2):211-21

Abstract

Aniracetam, a cognition enhancer, has been recently found to preferentially increase extracellular levels of dopamine (DA) and serotonin (5-HT) in the prefrontal cortex (PFC), basolateral amygdala and dorsal hippocampus of the mesocorticolimbic system in stroke-prone spontaneously hypertensive rats. In the present study, we aimed to identify actually active substances among aniracetam and its major metabolites and to clarify the mode of action in DA and 5-HT release in the PFC. Local perfusion of mecamylamine, a nicotinic acetylcholine (nACh) and N-methyl-D-aspartate (NMDA) receptor antagonist, into the ventral tegmental area (VTA) and dorsal raphe nucleus (DRN) completely blocked DA and 5-HT release, respectively, in the PFC elicited by orally administered aniracetam. The effects of aniracetam were mimicked by local perfusion of N-anisoyl--aminobutyric acid (N-anisoyl-GABA), one of the major metabolites of aniracetam, into the VTA and DRN. The cortical DA release induced by N-anisoyl-GABA applied to the VTA was also completely abolished by co-perfusion of mecamylamine. Additionally, when p-anisic acid, another metabolite of aniracetam, and N-anisoyl-GABA were locally perfused into the PFC, they induced DA and 5-HT release in the same region, respectively. These results indicate that aniracetam enhances DA and 5-HT release by mainly mediating the action of N-anisoyl-GABA that targets not only somatodendritic nACh and NMDA receptors but also presynaptic nACh receptors."



What a wonderful rationale...thankyou so much for posting this!

Any information on whether other racetams could act in this manner? I am specifically interested in piracetam. My fear is that I won't be able to use any of them as I've read pira and ani have almost the same effects just that ani seems to be more powerful on a per unit dosage.

In the end though, the only way to really know is to try it as I plan to and report back here. I'm still going to continue my experiment with ani + DMAE to see if that possibly improves things....however the mechanism above would indicate things could get worse. I gotta try it though.


Well it is ani that is noted for its anxiolytic effects. Nothing I have read on pira, mentions this.

I would suggest you try bacopa, for a different type of anxiolytic effect.

BBB

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Alpha F
Level 4

Join date: Mar 2005
Location:
Posts: 3167

buffd_samurai wrote:
What a wonderful rationale...thankyou so much for posting this!

Any information on whether other racetams could act in this manner? I am specifically interested in piracetam.


You are welcome.
I have an interest in neurology as a hobby and it is only from that position that I speak.
I have read papers indicating piracetam has adverse side effects; increased aggression, agitation and irritability and sexual arousal.
My observation is that whilst a substance may not increase dopamine levels it can enhance it by inhibiting the enzyme that breaks down dopamine.
I also invite you to think about piracetam's role in the catecholamine system.
As suggested with antipshycotic drugs, piracetam might accelerate brain catecholamine turnover by blocking its receptors.

Other research papers suggest Piracetam increases the brain's turnover of Adenosine Triphosphate (ATP) within the Cerebral Cortex which is associated with increased Energy production within the brain ( think of the effects of enhanced protein synthesis and energy output in a brain wired this way: high dopamine, low serotonin, low norepinephrine ).

Also consider that where nootropics are being compared to MAOI such as Prozac, the rise in dopamine levels may not be significant. However, in a brain which is high in dopamine, low in serotonin and low in norepinephrine, this insignificant enhancement becomes significant enough to cause adverse effects. Coincidently, Prozac was notorious for causing aggressive and violent behavior in certain individuals in spite of being labelled "The Happy Pill" ( I read three books on it in the 90's ). These individuals literally 'lost their minds' and acted on their base impulses without inhibition.

Another paper also suggested piracetam also increased prolactin concentrations in serum. I don't know what that would mean for you - if you are not on steroids that may be significant and add to your adverse effect in ways only you can discern as you must consider your individual endocrine and neurological make up.

Yohimbe Bark, as piracetam, is also suggested as a dopamine re uptake inhibitor. Interestingly enough I cannot tolerate yohimbine very well. HOT-ROX is overkill for me and Spike pill with yohimbine only when my progesterone levels are high ( luteal fase ).
I need to be severely sleep deprived not to become volcanic on HOT-ROX. Seriously.

Interesting you mentioned Spike, because Caffeine-Free Spike was the best for brain alertness for me. When sleep deprived a pill of Caffeine-Free Spike and a can of Spike Shooter was perfect. I once took this concoction rested and my brain did not stop for 48 continuous hours, no sleep at all and relentless.
Real shame I cannot find Caffeine-Free Spike any more.


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buffd_samurai
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Join date: Sep 2004
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Posts: 1157

bushidobadboy wrote:
buffd_samurai wrote:
Alpha F wrote:
buffd_samurai wrote:

I, unfortunately, do not tolerate aniracetam very well. Seriously speaking, it puts me in a SERIOUSLY bad mood. It basically turns me into a "bad drunk", i.e. someone who is overly aggressive and "throws their weight around" when under its "influence". Why this is, I don't know. But it looks like fat soluable racetams are definitely not for me.

Anyone else like this?
Yes.

Anyone had a reasonable rationale mechanism that might explain such strange reactions for me?

You could be dopamine dominant in your genetic brain make up.
By taking a substance that might enhance dopamine levels in you pre frontal cortex you tip over an already high dopamine level. Two of the functions implicated on the pre frontal cortex are: personality expression and moderation of correct social behavior. If you are, by default, high dopamine, low serotonin and low norepinepherine, enhancing dopamine and serotonin might explain the neurological effect on your mood and behavioural changes.



"Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP

Shirane M, Nakamura K.

CNS Supporting Laboratory,
Nippon Roche Research Center,
200 Kajiwara, 247-8530, Kamakura, Japan
Brain Res 2001 Oct 19;916(1-2):211-21

Abstract

Aniracetam, a cognition enhancer, has been recently found to preferentially increase extracellular levels of dopamine (DA) and serotonin (5-HT) in the prefrontal cortex (PFC), basolateral amygdala and dorsal hippocampus of the mesocorticolimbic system in stroke-prone spontaneously hypertensive rats. In the present study, we aimed to identify actually active substances among aniracetam and its major metabolites and to clarify the mode of action in DA and 5-HT release in the PFC. Local perfusion of mecamylamine, a nicotinic acetylcholine (nACh) and N-methyl-D-aspartate (NMDA) receptor antagonist, into the ventral tegmental area (VTA) and dorsal raphe nucleus (DRN) completely blocked DA and 5-HT release, respectively, in the PFC elicited by orally administered aniracetam. The effects of aniracetam were mimicked by local perfusion of N-anisoyl--aminobutyric acid (N-anisoyl-GABA), one of the major metabolites of aniracetam, into the VTA and DRN. The cortical DA release induced by N-anisoyl-GABA applied to the VTA was also completely abolished by co-perfusion of mecamylamine. Additionally, when p-anisic acid, another metabolite of aniracetam, and N-anisoyl-GABA were locally perfused into the PFC, they induced DA and 5-HT release in the same region, respectively. These results indicate that aniracetam enhances DA and 5-HT release by mainly mediating the action of N-anisoyl-GABA that targets not only somatodendritic nACh and NMDA receptors but also presynaptic nACh receptors."



What a wonderful rationale...thankyou so much for posting this!

Any information on whether other racetams could act in this manner? I am specifically interested in piracetam. My fear is that I won't be able to use any of them as I've read pira and ani have almost the same effects just that ani seems to be more powerful on a per unit dosage.

In the end though, the only way to really know is to try it as I plan to and report back here. I'm still going to continue my experiment with ani + DMAE to see if that possibly improves things....however the mechanism above would indicate things could get worse. I gotta try it though.


Well it is ani that is noted for its anxiolytic effects. Nothing I have read on pira, mentions this.

I would suggest you try bacopa, for a different type of anxiolytic effect.

BBB


Thankyou for the suggestion my good friend. I will indeed get some for further experimentation. Currently, I have some L-Theanine that I wanted to try later on....and I did read your earlier posts where you suggested the use of Bacopa.

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