116 replies to this topic

[Endymion]

It might be worth taking it just for its neuroprotective effects, regardless of its nootropic value (in some sense this is a long-term nootropic benefit). Of course if it makes you depressed and/or unable to think clearly then by all means ditch it.

Finally, I'm not sure if anyone else noticed this recent article (May, 2013) indicating it may be effective in promoting cardiovascular health:

Vinpocetine attenuates lipid accumulation and atherosclerosis formation.
Abstract

Atherosclerosis, the major cause of myocardial infarction and stroke, is a chronic arterial disease characterized by lipid deposition and inflammation in the vessel wall. Cholesterol, in low-density lipoprotein (LDL), plays a critical role in the pathogenesis of atherosclerosis. Vinpocetine, a derivative of the alkaloid vincamine, has long been used as a cerebral blood flow enhancer for treating cognitive impairment. A recent study indicated that vinpocetine is a potent anti-inflammatory agent. However, its role in the pathogenesis of atherosclerosis remains unexplored. In the present study, we show that vinpocetine significantly reduced atherosclerotic lesion formation in ApoE knockout mice fed with a high-fat diet. In cultured murine macrophage RAW264.7 cells, vinpocetine markedly attenuated oxidized LDL (ox-LDL) uptake and foam cell formation. Moreover, vinpocetine greatly blocked the induction of ox-LDL receptor 1 (LOX-1) in cultured macrophages as well as in the LOX-1 level in atherosclerotic lesions. Taken together, our data reveal a novel role of vinpocetine in reduction of pathogenesis of atherosclerosis, at least partially through suppressing LOX-1 signaling pathway. Given the excellent safety profile of vinpocetine, this study suggests vinpocetine may be a therapeutic candidate for treating atherosclerosis.

This excites me.
A huge amount of variability in responses to vinpocetine, it seems, but I am going to start taking it regularly. I noticed no negative effects when taking it by itself or as part of Alpha Brain.
I will keep you posted.

[Climactic]

I am going to start taking it regularly.

Great study. As I recall, anything less than a 10mg dose 3-times daily is not considered therapeutic. I wish an extended release pill for vinpocetine was available. Given its short half-life of 2.5 hours, using a single 30mg dose won't be perfectly efficacious either.

Anyhow, there is a possible side effect of agranulocytosis (very low infection-fighting WBCs) that may be of concern. Getting the dose just right (not high or too low) should serve useful.

Edited by Climactic, 19 July 2013 - 12:24 PM.

[Endymion]

I am going to start taking it regularly.

Great study. As I recall, anything less than a 10mg dose 3-times daily is not considered therapeutic. I wish an extended release pill for vinpocetine was available. Given its short half-life of 2.5 hours, using a single 30mg dose won't be perfectly efficacious either.

Anyhow, there is a possible side effect of agranulocytosis (very low infection-fighting WBCs) that may be of concern. Getting the dose just right (not high or too low) should serve useful.

Thanks for your post. Converting the doses used in the above study to humans it does indeed equate to 30mg for a 70kg human. They gave it once every other day in mice (i.p). Maybe there is still benefit with more sporadic dosing. I am not familiar with its metabolism, but maybe some of vinpocetine's metabolites are active and protective.

I am under the impression that agranulocytosis is not a dose-related response but rather a rare side-effect. Nevertheless, you're right that the immune suppression is of concern, although it could be part of the reason why atherosclerosis is diminished. Double-edged sword, just like omega-3, it seems.

[CLR]

As an anti-epileptic and voltage-sensitive Na+ channel inhibitor, couldn't vinpocetine demonstrate some efficacy for bipolar disorder? Lamictal (lamotrigine) is an anticonvulsant given to epileptics and bipolar patients with the same Na+ channel inhibiting properties. The two also seem to increase intracellular Ca2+ concentrations.

Edited by CLR, 19 July 2013 - 04:50 PM.

[rautavaara]

The article only refers to in-vitro studies. I don't see how this warrants taking it daily in the hope of preventing atherosclerosis in the long term -- or do you plan to some lab tests that could show a positive effect in a short timeframe?

It might be worth taking it just for its neuroprotective effects, regardless of its nootropic value (in some sense this is a long-term nootropic benefit). Of course if it makes you depressed and/or unable to think clearly then by all means ditch it.

Finally, I'm not sure if anyone else noticed this recent article (May, 2013) indicating it may be effective in promoting cardiovascular health:

Vinpocetine attenuates lipid accumulation and atherosclerosis formation.
Abstract

Atherosclerosis, the major cause of myocardial infarction and stroke, is a chronic arterial disease characterized by lipid deposition and inflammation in the vessel wall. Cholesterol, in low-density lipoprotein (LDL), plays a critical role in the pathogenesis of atherosclerosis. Vinpocetine, a derivative of the alkaloid vincamine, has long been used as a cerebral blood flow enhancer for treating cognitive impairment. A recent study indicated that vinpocetine is a potent anti-inflammatory agent. However, its role in the pathogenesis of atherosclerosis remains unexplored. In the present study, we show that vinpocetine significantly reduced atherosclerotic lesion formation in ApoE knockout mice fed with a high-fat diet. In cultured murine macrophage RAW264.7 cells, vinpocetine markedly attenuated oxidized LDL (ox-LDL) uptake and foam cell formation. Moreover, vinpocetine greatly blocked the induction of ox-LDL receptor 1 (LOX-1) in cultured macrophages as well as in the LOX-1 level in atherosclerotic lesions. Taken together, our data reveal a novel role of vinpocetine in reduction of pathogenesis of atherosclerosis, at least partially through suppressing LOX-1 signaling pathway. Given the excellent safety profile of vinpocetine, this study suggests vinpocetine may be a therapeutic candidate for treating atherosclerosis.

This excites me.
A huge amount of variability in responses to vinpocetine, it seems, but I am going to start taking it regularly. I noticed no negative effects when taking it by itself or as part of Alpha Brain.
I will keep you posted.

[Climactic]

I don't see how this warrants taking it daily in the hope of preventing atherosclerosis in the long term -- or do you plan to some lab tests that could show a positive effect in a short timeframe?

Prevention, if it is aided by vinpocetine, will only happen if vinpocetine is taken regularly due to its limited half life. It will also not permanently adjust your body as far as I can tell. I don't know how you could expect effects in a short timeframe. You would have to get the internal flow thickness of your blood vessels measured over time against controls to know if it's working.

Edited by Climactic, 20 July 2013 - 01:20 PM.

[Endymion]

As an anti-epileptic and voltage-sensitive Na+ channel inhibitor, couldn't vinpocetine demonstrate some efficacy for bipolar disorder? Lamictal (lamotrigine) is an anticonvulsant given to epileptics and bipolar patients with the same Na+ channel inhibiting properties. The two also seem to increase intracellular Ca2+ concentrations.

I reckon you could be right. Although perhaps if it causes depression in some people then it might exacerbate that aspect of BD. Certainly seems sound though.

The article only refers to in-vitro studies. I don't see how this warrants taking it daily in the hope of preventing atherosclerosis in the long term -- or do you plan to some lab tests that could show a positive effect in a short timeframe?

It was in vivo as well, rautavaara.

"In the present study, we show that vinpocetine significantly reduced atherosclerotic lesion formation in ApoE knockout mice fed with a high-fat diet."

The in vitro part was performed to elucidate the mechanism, but in the full text they measured the formation of plaque in major vessels on these mice and showed it was greatly reduced with vinpocetine.

[Climactic]

I don't know if the following article delving into the dopamine connection has been posted here.

Vinpocetine and α-tocopherol prevent the increase in DA and oxidative stress induced by 3-NPA in striatum isolated nerve endings (2013)
Vinpocetine is a neuroprotective drug that exerts beneficial effects on neurological symptoms and cerebrovascular disease.3-nitropropionic acid (3-NPA) is a toxin that irreversibly inhibits succinate dehydrogenase, the mitochondrial enzyme that acts in the electron transport chain at complex II. In previous studies in striatum-isolated nerve endings (synaptosomes), we found that vinpocetine decreased dopamine (DA) at expense of its main metabolite 3,4-dihydroxyphenylacetic acid (DOPAC), and that 3-NPA increased DA, reactive oxygen species (ROS), DA-quinone products formation, and decreased DOPAC. Therefore, in this study, the possible effect of vinpocetine on 3-NPA-induced increase in DA, ROS, lipid peroxidation, and DA-quinone products formation in striatum synaptosomes were investigated, and compared with the effects of the antioxidant α-tocopherol. Results show that the increase in DA induced by 3-NPA was inhibited by both 25 μM vinpocetine and 50 μM α-tocopherol. Vinpocetine, as α-tocopherol, also inhibited 3-NPA-induced increase in ROS (as judged by DCF fluorescence), lipid peroxidation (as judged by TBA-RS formation), and DA-quinone products formation (as judged by the nitroblue tetrazolium reduction method). As in addition to the inhibition of complex II exerted by 3-NPA, 3-NPA increases DA-oxidation products that in turn can inhibit other sites of the respiratory chain, the drop in DA produced by vinpocetine and α-tocopherol may importantly contribute to their protective action from oxidative damage, particularly in DA-rich structures.

The above abstract essentially suggests that the drop in DA can be perceived as a good thing. The full PDF is available for free.

Edited by Climactic, 24 July 2013 - 01:05 PM.

[CLR]

I would also like to say that there is a possibility that vinpocetine could have a negative interaction with the popular supplement phenibut, because phenibut has been shown to modulate the function of some epilepsy medications such as anticonvulsants like carbamezepine. Vinpocetine exhibits some anticonvulsant mechanics.

http://www.ncbi.nlm.nih.gov/pubmed/2431377

[overfocused]

Has anyone taken Vinpocetine with Tianeptine ? - is it a bad combination, given how Vinpocetine lowers dopamine and Tianeptine increases it ?

Also has anyone else noticed a tendency to wake up early next morning if they take Vinpocetine in the evening ?. For me this is very pronounced effect as I have had a tendency to over-sleep my entire life. Therefor this sudden ability to wake up an hour earlier than my alarm clock with high energy, is actually a very pleasant surprise and not likely to be a placebo given my persistent lifelong sleep problems.

Edited by overfocused, 24 July 2013 - 06:14 PM.

[Endymion]

I don't know if the following article delving into the dopamine connection has been posted here.

Vinpocetine and α-tocopherol prevent the increase in DA and oxidative stress induced by 3-NPA in striatum isolated nerve endings (2013)
As in addition to the inhibition of complex II exerted by 3-NPA, 3-NPA increases DA-oxidation products that in turn can inhibit other sites of the respiratory chain, the drop in DA produced by vinpocetine and α-tocopherol may importantly contribute to their protective action from oxidative damage, particularly in DA-rich structures.

The above abstract essentially suggests that the drop in DA can be perceived as a good thing. The full PDF is available for free.

An interesting find. It lends further credibility to the original post that vinpocetine lowers DA to a level that actually has appreciable effects. Interesting to see it repainted in a positive light though.

I've never noticed a tendency for early waking with vinpocetine, unfortunately (I would also find that positive).
I'm unsure how it would interact with the effects of tianeptine. If I were you, overfocused, maybe I'd keep taking it if you feel alright, but just remain alert to any potential cancellation of tianeptine's antidepressant activity?

[alecnevsky]

I kind of scanned this thread since my last comment and, just as outside observer, it sounds ridiculous to dose something that may impair your visuo-spacial faculty to avoid atherosclerosis. I mean, there are countless dietary/lifestyle measures you can take to avoid atherosclerosis and taking a research chemical with a warning for that reason is something that I must condemn as unfounded if not irrational.

Granted, since I discontinued Vinpo I've been giving it a shot every 3-5 days just to finish the damn bottle and isolate the effects. I do have to say, taken at like 6pm affords some clarity of thought fatigue notwithstanding. Otherwise, I am still just as concerned about the warning posted.

[empedocles]

I had nothing but headaches when using Vinpo, as such i stopped using it and advising others to not use it years ago.

[Climactic]

may impair your visuo-spacial faculty to avoid atherosclerosis.

Where did you get this part about vinpocetine impairing spatial vision? Also, it's not just for preventing atherosclerosis, if that's what you think.

Edited by Climactic, 25 July 2013 - 02:44 PM.

[alecnevsky]

may impair your visuo-spacial faculty to avoid atherosclerosis.

Where did you get this part about vinpocetine impairing spatial vision? Also, it's not just for preventing atherosclerosis, if that's what you think.

I said nothing about vision. Visuo-spacial processing/ thinking is a metric of cognitive performance involved in maths and possibly other abstract subjects. See cambridgebrainsciences.com

[Climactic]

Visuo-spacial processing/ thinking is a metric of cognitive performance involved in maths and possibly other abstract subjects.

How exactly are you connecting vinpocetine to visuospatial issues?

Edited by Climactic, 25 July 2013 - 04:42 PM.

[alecnevsky]

Visuo-spacial processing/ thinking is a metric of cognitive performance involved in maths and possibly other abstract subjects.

How exactly are you connecting vinpocetine to visuospatial issues?

Did you make it to page 2 of this thread? It acts like reserpine.

[Endymion]

Visuo-spacial processing/ thinking is a metric of cognitive performance involved in maths and possibly other abstract subjects.

How exactly are you connecting vinpocetine to visuospatial issues?

Did you make it to page 2 of this thread? It acts like reserpine.

One of its multiple mechanisms of action appears to be similar to reserpine, yes, in that it inhibits vesicular uptake of catecholamines.
However, as Climactic says, it also has many other activities such as PDE inhibition leading to increased cerebral blood flow, inhibition of inflammatory mediators, etc.

To date, the few studies examining the effects of vinpocetine on cognition have been a little inconsistent, but there is a suggestion it improves memory - it has not been reported to impair cognitive function as far as I am aware. I appreciate people drawing these links in comparing reserpine and vinpocetine, it is very interesting and I'm sure more will be known in time. However, the studies have not borne out the theory of a proposed negative impact on performance.

On the other hand, there is some actual evidence, albeit preliminary, that vinpocetine might prevent atherosclerosis and other damage associated with inflammation and ageing. This is an evidential step above the conjecture from comparison to another compound's mechanism. You say that my stance on this is irrational and unfounded - I would argue that at this point in time your position is less rational and less evidence-based.

I won't get onto the topic of approaches to modifying heart disease risk at this point, other than to say there seems to be a lack of consensus on many of the diet-related strategies.

Edited by Endymion, 26 July 2013 - 02:51 AM.

[overfocused]

The reserpine connection of vinpocetine is of cause potentially alarming if it was finally proven which I am not sure it is (note that even reserpine is not as undisputedly bad as some here claim it to be). For me vinpocetine definitely does something positive, if not improving my memory then at least it clears my head and gets me going in the morning (and apparently it does this for rats as well) which is a welcome change for a person like me suffering from excessive sleep induced by atypical depression.

Edited by overfocused, 26 July 2013 - 03:12 PM.

[alecnevsky]

Visuo-spacial processing/ thinking is a metric of cognitive performance involved in maths and possibly other abstract subjects.

How exactly are you connecting vinpocetine to visuospatial issues?

Did you make it to page 2 of this thread? It acts like reserpine.

One of its multiple mechanisms of action appears to be similar to reserpine, yes, in that it inhibits vesicular uptake of catecholamines.
However, as Climactic says, it also has many other activities such as PDE inhibition leading to increased cerebral blood flow, inhibition of inflammatory mediators, etc.

To date, the few studies examining the effects of vinpocetine on cognition have been a little inconsistent, but there is a suggestion it improves memory - it has not been reported to impair cognitive function as far as I am aware. I appreciate people drawing these links in comparing reserpine and vinpocetine, it is very interesting and I'm sure more will be known in time. However, the studies have not borne out the theory of a proposed negative impact on performance.

On the other hand, there is some actual evidence, albeit preliminary, that vinpocetine might prevent atherosclerosis and other damage associated with inflammation and ageing. This is an evidential step above the conjecture from comparison to another compound's mechanism. You say that my stance on this is irrational and unfounded - I would argue that at this point in time your position is less rational and less evidence-based.

I won't get onto the topic of approaches to modifying heart disease risk at this point, other than to say there seems to be a lack of consensus on many of the diet-related strategies.

I do hope you keep up with the research on this subject and trust that you will update us on the developments. Although, this is a brain health thread and should come with no surprise that negative "conjectures" are more heavily weighed as they should. Instead of posting something about an unrelated subject, I would have much rather appreciated you refuting the connection to reserpine or otherwise clarifying the relationship. But, really I don't care either way. I am not invested in this research chemical gamble, you are.

[Climactic]

I am not invested in this research chemical gamble

I don't believe it's fair to label vinpocetine as a research chemical. Such a label would more aptly apply to substances that have not been tested much or at all in humans. I'll go so far as to say that the safety of vinpocetine (in most people) is established.

I agree that users have a responsibility to keep up to date with research, and also to discuss findings of concern. The simplest way to the track the research this may be to follow this PubMed RSS feed on vinpocetine. The associated PubMed search query is "(vinpocetine[Title]) OR Cavinton[Title]". Note that the default sort order is by Recently Added, which is fine.

Edited by Climactic, 28 July 2013 - 02:03 AM.

[noot_in_the_sky]

Funny I stumble upon this post, as I was just beginning to consider vinpocetine. I shall definitely give this one a little more consideration.

I wish an extended release pill for vinpocetine was available. Given its short half-life of 2.5 hours, using a single 30mg dose won't be perfectly efficacious either.

Climactic have you try the techniques suggested in this thread?: http://www.longecity...-release-pills/

Also has anyone else noticed a tendency to wake up early next morning if they take Vinpocetine in the evening ?. For me this is very pronounced effect as I have had a tendency to over-sleep my entire life. Therefor this sudden ability to wake up an hour earlier than my alarm clock with high energy, is actually a very pleasant surprise and not likely to be a placebo given my persistent lifelong sleep problems.

Do you guys think that maybe the reason overfocused had a better quality of sleep was because it cause a drop of dopamine, which in turn drop norepinephrin? Consequentially, after the effects of vinpocetine stop he could had experience a rebound of his DA and NE levels making him wake up a little earlier then usual?

Edited by noot_in_the_sky, 29 July 2013 - 03:22 AM.

[overfocused]

Do you guys think that maybe the reason overfocused had a better quality of sleep was because it cause a drop of dopamine, which in turn drop norepinephrin? Consequentially, after the effects of vinpocetine stop he could had experience a rebound of his DA and NE levels making him wake up a little earlier then usual?

Interesting theory, its such a pronounced effect that I am completely baffled by it. As I said I have battled excessive sleep for years, most likely due to undiagnosed atypical depression, while I am now under treatment for this using tianeptine and CBT, neither of these has affected my sleep in any positive way (except for more vivid dreams caused by the tianeptine). However if I take a pill of vinpocetine around 8-9pm and go to bed at 11pm then I wake up at refreshed around 6am. If I skip a pill then I oversleep and wake up groggy as always around 7-8am. So taken in the evening It somehow seams to shorten my need for sleep.

SAM-e taken in the evening used to do the same thing for me when I was on it, but it also affected my memory and ability to concentrate negatively the next day (likely due to changes in sleep architecture) so I switched to taking it in the morning. So far I have seen no such bad side effect from the vinpocetine.

Edited by overfocused, 29 July 2013 - 04:21 PM.

[george362a]

It may be that this is a case of Vinpocetine not being very useful as part of a nootropic stack, but rather as specific therapy for a particular condition. Let's face it, none of these drugs were specifically designed to be "stacked" and used for aggressive neural enhancement.

 

Some work together well, but as far as I am concerned that's the result of chance, rather than any of them being engineered to work synergistically.

 

When stacking nootropics, it might be better to think about what each drug does and see how you can blend them to support each other.

 

Look up Dr. Stephen Sinatra's "metabolic cardiology" protocol. This is 4 nutrients:

 

coenzyme q10

ribose

carnitine

magnesium

 

He specifically researched these and found they all were important in the production of ATP in mitochondria, thus they all work synergistically.

 

This stack might (and I say might) provide a base for other nootropics because they serve to boost ATP production, which is going to make other nootropics work better.

 

I DO know that both piracetam AND idebenone increase info transfer across the corpus callosum, so they work together.

 

Adding a "phenyl" group as in phenylpiracetam seems to increase dopamine and have a stimulant effect in the brain.

 

Also I have used lecithin (granules) as a source of choline (phosphadtidyl choline) which seemed very effective for some reason, and also a product called "Homozone" which is powdered magnesium oxide. When you boost oxygen to the brain and you are using piracetam, it heightens the effect of Piracetam. I believe this is because Piracetam ramps up ATP production, and oxygen is a key factor in the phosphorylation cycle that makes ATP.

 

[Climactic]

It may be that this is a case of Vinpocetine not being very useful as part of a nootropic stack

I disagree with this assertion completely. Yes, vinpocetine is a drug, but I find vinpocetine all too useful not just as a nootropic but also as an overall health assistor, by virtue of its antiinflammatory effect. One can even practically feel it working in the brain, although it has a short half-life. I would've liked an extended-release product.

coenzyme q10
ribose
carnitine
magnesium

A superior list is:
Ubiquinol, i.e. the reduced form of CoQ10
D-ribose, not to be substituted with DL-ribose
Acetyl-L-carnitine - more available to the brain than L-carnitine
Magnesium as citrate or glycinate or other high-bioavailability form

I have used lecithin (granules) as a source of choline

Even if useful, lecithin is a rather crude source of choline. For the brain, it doesn't compare with citicoline or alpha GPC, both of which are specifically for the brain. Natural sources of choline such are lecithin are more likely to be metabolized by bad gut bacteria leading to byproducts that cause heart disease.[1]

Thank you for reminding me to not overlook piracetam!

Edited by Climactic, 12 January 2014 - 06:27 AM.

[george362a]

As far as Vinpocetine, I think it depends on the individual. I don't take it because I get really constipated when I do, but it may not affect others that way.

I agree with you on the ALCAR, and I will even go you one better, I like using arginate although it's kind of pricy. I too think Ubiquinol is better than q10, especially for those who have methylation issues. Sinatra actually uses a full spectrum magnesium in his formula, as well as several forms of carnitine.

I like Alpha GPC as a choline supplement while on nootropics BUT, lecithin seems to have a beneficial effect even though as you say it's a cruder form of choline. It's a phospolipid and may be beneficial for that reason.

Poracetam seems to be hit or miss with me. I need high doses or I don't feel it. I may try phenlypiracetam next round, although I have heard it's very potent. All in all, nootropics seems a very individual thing, as far as what works and for whom.

[Climactic]

Thank you for your feedback!

I don't take it because I get really constipated when I do

I use organic psyllium husk powder and it helps me avoid constipation. Oat fiber works very well for me too in this regard. Fortunately I have never been constipated by vinpocetine.

lecithin seems to have a beneficial effect even though as you say it's a cruder form of choline. It's a phospolipid and may be beneficial for that reason.

You are right - one shouldn't overlook phospholipids.

I may try phenlypiracetam next round, although I have heard it's very potent.

I like phenylpiracetam but it's something that can't be used regularly due to its moderately fast tolerance. It's good at 50-500 mg doses, increased gradually. Typically I just use 100 mg Phenotropil pills that I ordered from nootropic.ru.com, generally no more than two days a week.

Edited by Climactic, 12 January 2014 - 07:35 AM.

[Climactic]

http://www.mskcc.org/cancer-care/herb/vinpocetine

Vinpocetine: Mechanism of Action
Vinpocetine has been shown to possess antioxidant and hydroxyl radical scavenging properties in vitro ⁽⁸⁾⁽⁹⁾. It inhibits phosphodiesterase 1 (PDE1) activity and improves cerebral blood flow by elevating cGMP and cAMP, by increasing mitochondrial function and also by improving glucose and oxygen utilization by the brain. Vinpocetine helps improve spatial memory in rats through its ability to prevent neuronal damage and to favorably modulate cholinergic function ⁽⁸⁾. In an animal study, it increased cerebral microcirculation and blood flow by inhibiting platelet aggregation. Administration of vinpocetine to chronic stroke patients increased glucose uptake and release in unaffected areas of the brain ⁽⁶⁾. Vinpocetine does not possess systemic circulatory effects or any effects on heart rate or blood pressure ⁽¹⁰⁾. It demonstrated antiepileptic effects by suppressing the abnormal neuronal excitability through the regulation of sodium channels and release of dopamine in the striatal nerve endings ^(11)(12)(13). Vinpocetine can increase the effects of radiation by increasing tumor oxygenation ⁽⁷⁾. It also shows anti-inflammatory effects by inhibiting TNF-alpha-induced NF-kappaB activities ⁽¹⁴⁾.

Edited by Climactic, 12 January 2014 - 07:29 AM.

[george362a]

I use psyllium as well to prevent constipation, and eat whole cooked oats pretty much every day. For me though, the Holy Grail of cognition is to find a way to increase info transfer massively across the corpus callosum. I think that is the key to big increases in creativity, and I am searching for a way to do this.

There was a guy years ago named Robert Monroe who founded the famous "Monroe Insitute." It is alledged that he was consulted at one point by the CIA for his insights into enhanced cognative abilities and extra sensory abilities. He was the inventor of the patented "Hemi-Sync" sound technology.

Monroe believed that certain frequencies of sound could unlock specific brainwave states and allow us to use far more of our brain's potential. If we ever do figure this out, I think we can approach the potential that was demonstrated in the ficticious movie "Limitless."

[basicdude]

Would this be useful to take on amphetamine/stimulant break days?