must-be-a-way-to-heal

Has aneyone tried Coluracetam

102 posts in this topic

Hehe I'll be very trying it very soon :) It better be a panacea.. It's got "perfect" written all over it. Seriously.. If Colu doesn't work, I don't know if anything ever will.
The stuff is hard to get, and AFAIK there are only a handful of people who have tried it on this planet, none of which have HPPD.
Of note is that it has helped with Lyme Disease recovery and Benzo Withdrawal in anecdotes. I remember someone on this board with concurrent Lyme, and many of you also have issues with BZD WD, so thought it'd be worth mentioning. Damn I'm so excited about this stuff :)


In any case it should be available from 2 different suppliers (one UK based, the other US based) within days, weeks at most. And it comes with EMS shipping IIRC. So in all I speculate I'll have it within 2 weeks tops, preferably sooner of course. I've got this stuff on my radar like a hawk, so I'll inform you guys a.s.a.p. when it comes available. It should be quite affordable once it does.

Disclaimer: Coluracetam is a research chemical. It's metabolization is unknown (or undisclosed), and as such medication interactions are unpredictable aside from cholinergic speculations. Best would be to use it without anything concurrently. Remember: your life, your responsibility. Just use common sense and research the best you can when undertaking such radical approaches. Best you wait it out a little for me to try and report back though, yet if you're feeling assertive I'd say go for it. Seems pretty darn safe from what I've read. Just you know.. "It wasn't me".

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Coluracetam does indeed sound very exciting, I am almost tempted to push for that before my upcoming Keppra trial, but that's probably a bit risky. One question I have from your thread on racetams, which I can't find right now... if I remember correctly, Coluracetam seems to repair the visual cortex. Are there studies that conclude that psychedelic use damages the visual cortex? It might seem like a no-brainer ('of course our visual cortex is damaged, you idiot').. of course something(s) is/are damaged.. is there evidence that psychedelic use damages the visual cortex in particular (as opposed to other areas that might perceptually distort our vision, without the visual cortex being damaged itself). The bit about the Coluracetam's benefits for the visual cortex was one of the most exciting bits, but less so if there are not conclusive results of visual cortex damage in HPPD sufferers. Again, feels like I'm asking a silly question, but I don't recall reading anything about HPPD -- > visual cortex damage. Then again, my memory is very bad :)

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ok cool awesome, well that sound good.. fingers toes and everthing crossed lol   .... will definatley have a chat with my Doc about it once i get to see him next. I really pray that this works, good luck!

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Syntheso: No man not a stupid question. Actually your questions are pretty good!
Yes there is some evidence that psychedelics screw with the visual cortex... mate I just woke up so I'm not gonna go searching just yet. But it has been discussed on this forum, so I might add some links later after I've shaken off this oneirophrenic melatonin "hangover".

I wouldn't know if Coluracetam has benefits for the Visual Cortex. It would seem so, if you put together the pieces of the puzzle (see my 2 latest additions to Research Articles). But there's no evidence for that. Moreover it works throughout the entire CNS (or so I would presume.. no reason why it would be limited to one area as of yet). If you're concerned about losing the good side of your psych, then see if you can sneak around that and just go to your GP with this. No professional will actually prescribe the stuff, which is why all you ask for is for them to be informed and to monitor you.

Must-be: Yeah definitely check it out with your doctor. I'm also gonna discuss it with the specialist I'm seeing, but ultimately it's up to the individual of course. And the doctor might not know about it and advise against it (most likely that is). It's just the metabolization part that raises some questions really... Other safety issues might be allergies (if you're sensitive to those). To check for allergies just do a test with 1mg or so under the tongue and see if it burns, swells or w/e after having sat there for a while. Aside from that there's absolutely no need to worry about the stuff. If you still do, just make sure you're with someone who you trust and is informed for those few days you try it. Write down on a note what medicines you are taking and how much, and elaborate on the Coluracetam what it is (it won't mean shit to a medic unless you write down its mechanisms), and keep the note with your cards in your wallet (and see if you can have your doc punch it in to your medical file). Or so I've planned my precautions roughly.

But yeah: if only I had polydactyly so I could cross more fingers!

Seven-Fingers-in-one-hand-4d9a6501612cd.

Thanks for the good wishes :)

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Hey guys,

 

I know of Coluracetam but could anyone explain to me why this should be helpful to us HPPD'ers? I have a good understanding of pharmacology/neurochemistry but Coluracetam isn't something I've looked into or been able to find much information on.

 

Cheers. :) 

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Hey Sam,
yeah here's what I threw together (mostly anecdotes of users though, many of which noticing moderate to extreme visual enhancement).
Check here and especially here for why Coluracetam is most likely very awesome for HPPD. Let me grab my pharmacology book...

In short:


Coluracetam is a High-Affinity Choline Uptake (HACU) enhancer.

 

The rate-limiting step of ACh synthesis is mediated not by choline acetyltransferase, but rather by the availability of the choline substrate, which depends on uptake of choline into the neuron. There are two processes responsible for choline transport. The first is low-affinity facilitated diffusion. This transport system is not sturable and is found in cells that synthesize choline containing phospholipids, such as the corneal epithelium. Far more important is the sodium-dependent, high-affinity transport system, specifically found in cholinergic nerve terminals. Because the high-affinity transporter is easily saturated, it sets an upper limit on the supply of choline for ACh synthesis. As the rate-limiting component, this transporter is a target for several (anti-cholinergic) drugs.

From "Principles of Pharmacology, 3rd Edition". I have no clue if this is copyright infringement or whatever, but I figured it'd be fine 'cause you can find the same text over at Google eBooks.

On a side note: Acetyl CoA synthesis occurs within the mitochondria, as such mitochondrial supporting supplements might synergize with Coluracetam.
 

So basically Coluracetam enhances the biosynthesis of ACh, causing an increase in ACh levels. As the above links will show you; ACh suppresses the spread of excitation in the visual cortex. 'Nuff said, right?

Ohh and apart from the visual benefits there's a number of other very interesting properties and effects, like excitotoxicity mitigation, anxiolysis, anti-depression, nootropic etc. that may be very beneficial to the common co-morbid symptoms of HPPD. You can read all about the experiences of people in the first link I provided.

Lastly (this is a rather crude theory), HPPD seems eerily similar to Acute Anti-Cholinergic Syndrome, but then in a chronic way. If anti-cholinergics can cause HPPD-like symptoms, then there's a good chance than pro-cholinergics will do the opposite.

Hmm I thought I had more to say about this, but my thoughts drifted. Anyway, there's sufficient information to indicate that Coluracetam has a very good chance at helping in HPPD.

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Hey Sam,

yeah here's what I threw together (mostly anecdotes of users though, many of which noticing moderate to extreme visual enhancement).

Check here and especially here for why Coluracetam is most likely very awesome for HPPD. Let me grab my pharmacology book...

In short:

Coluracetam is a High-Affinity Choline Uptake (HACU) enhancer.

 

From "Principles of Pharmacology, 3rd Edition". I have no clue if this is copyright infringement or whatever, but I figured it'd be fine 'cause you can find the same text over at Google eBooks.

On a side note: Acetyl CoA synthesis occurs within the mitochondria, as such mitochondrial supporting supplements might synergize with Coluracetam.

 

So basically Coluracetam enhances the biosynthesis of ACh, causing an increase in ACh levels. As the above links will show you; ACh suppresses the spread of excitation in the visual cortex. 'Nuff said, right?

Ohh and apart from the visual benefits there's a number of other very interesting properties and effects, like excitotoxicity mitigation, anxiolysis, anti-depression, nootropic etc. that may be very beneficial to the common co-morbid symptoms of HPPD. You can read all about the experiences of people in the first link I provided.

Lastly (this is a rather crude theory), HPPD seems eerily similar to Acute Anti-Cholinergic Syndrome, but then in a chronic way. If anti-cholinergics can cause HPPD-like symptoms, then there's a good chance than pro-cholinergics will do the opposite.

Hmm I thought I had more to say about this, but my thoughts drifted. Anyway, there's sufficient information to indicate that Coluracetam has a very good chance at helping in HPPD.

 

Hey,

 

That does sound extremely interesting. I'm curious to know, if Coluracetam inhibits excitation in the visual cortex then why should it be that some of the effects reported are colour enhancement, trails and tracers etc, which would suggest excitation rather than inhibition? Would this not be bad for us HPPDers and increase the severity of our trails etc? From the reports I've read it seems like a mild psychedelic on it's own.

 

It does seem that it could be quite helpful for DP/DR too. The Racetams are such fascinating compounds.

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Hmm the trails and tracers, as far as I've read, were only from one guy using it in combination with Amphetamines. Amphetamines are excitatory so that probably overloaded something. I have no clue really, I just know Amphetamines are bunk, and I'm not surprised this happened. Color enhancement needn't necessarily indicate excitation I would think? Rather the opposite I'd say: Improvement of signal-to-noise ratio by inhibition could be the cause for this. No clue.. but I know there are some studies on contrast perception etc. with visual cortex excitability correlations, if you feel like confirming it.

I'd say the Amphetamine combo was an isolated incident.. No one else reports visual distortions from Coluracetam. Actually, there's a guy who reports less visual distortions in combination with (what I later found out to be) 4-HO-MET, which I find pretty indicative of its therapeutic potential.

I think it's highly unlikely to increase severity of symptoms, all things considered. But even in the event that it does, we'll learn something new and valuable.

Ohh, and here's a wiki quote from Hemicholinium-3 (HACU blocker.. basically the opposite of Coluracetam):
 

Hemicholinium-3 has no clinical use, but is frequently used as a research tool in animal and in vitro experiments. The clinical use is limited since it prevents uptake (HACU) into the cell which is not a rate limiting factor under normal, physiological frequencies of activation. This type of inhibition only becomes apparent at excessively high firing rates, whereby the uptake of choline into the nerve terminal as a rate limiting factor becomes apparent.


Hmm, I'm not going to derive any conclusions out of that, but you can make of it what you will.

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I wouldn't know how relevant this is, but I thought I might add it anyway. Here's a quote from "EEG coherence in post-LSD visual hallucinations":
 

Coherence, a measure of spectral similarity over time, may estimate cortical coupling. In the eyes-open state in HPPD subjects, widespread reduction of coherence was noted. However, upon eye closure, the occipital region demonstrated augmented regional coherence over many frequencies but with reduced coherence of the occipital region to more distant regions.

...
 

Paradoxically, in HPPD, alpha peak frequency was increased and the latency of the P2 component of the visual evoked potential ŽVEP. was shortened.


Scopolamine, an anti-cholinergic alkaloid:

 

The present study of coherence analysis, in 16 healthy male volunteers, aged 24-31 years, showed that the administration of 0.25 mg of scopolamine significantly reduced interhemispheric coherence in the delta and beta-1 bands in the resting state.

http://www.ncbi.nlm.nih.gov/pubmed/10840634

 

Scopolamine in acute intramuscular doses of 0.25–0.75 mg reduced the P2-N3 flash-VEP amplitude and, in the quantitative EEG, the 8.5–12.0 Hz power and total power in 8 healthy young male volunteers.

http://www.sciencedirect.com/science/article/pii/0013469493901099

 

Yes, I know, amplitude and latency are two different things. But I thought it was interesting to note that... oh wait I found something!

 

The scopolamine produced a slowing of the flash P2 latency of approximately 6 ms (p < 0.05) two hours after drug administration. 

http://link.springer.com/article/10.1007/BF01203554

 

And here's my feeble attempt at understanding a VEP P2 Cholinergic Alzheimer's study.


How relevant this is, I leave up to you.

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Hmm the trails and tracers, as far as I've read, were only from one guy using it in combination with Amphetamines. Amphetamines are excitatory so that probably overloaded something. I have no clue really, I just know Amphetamines are bunk, and I'm not surprised this happened. Color enhancement needn't necessarily indicate excitation I would think? Rather the opposite I'd say: Improvement of signal-to-noise ratio by inhibition could be the cause for this. No clue.. but I know there are some studies on contrast perception etc. with visual cortex excitability correlations, if you feel like confirming it.

I'd say the Amphetamine combo was an isolated incident.. No one else reports visual distortions from Coluracetam. Actually, there's a guy who reports less visual distortions in combination with (what I later found out to be) 4-HO-MET, which I find pretty indicative of its therapeutic potential.

I think it's highly unlikely to increase severity of symptoms, all things considered. But even in the event that it does, we'll learn something new and valuable.

Ohh, and here's a wiki quote from Hemicholinium-3 (HACU blocker.. basically the opposite of Coluracetam):

 

Hmm, I'm not going to derive any conclusions out of that, but you can make of it what you will.

 

Ah yes, amphetamines are the devil so I guess we can write that experience off.

 

The only reason I mentioned the colour enhancement is that another racetam (Aniracetam) has similar visual effects from what I've read from reports (sharper edges, colour enhancement, the 'HD Vision' effect mentioned in Coluracetam reports.

 

A few quotes from Aniracetam reports:

 

'Aniracetam on its own causes a huge increase in visual accuracy, 3d and color perception, simultaneous geometric processing capabilities, auditive loudness and clarity

 

'With Aniracetam, many users experience extremely enhanced visual and hearing processing. 

 

The only reason I mention aniracetam is that it's effects seem remarkably similar to Coluracetam, with a noticable anxiolytic action, and after some reading I notice aniraceam has an antagonistic effect at D2, D3 and 5HT2a receptors. 5HT2a receptors could definitely cause colour enhancement and the dopamergenic antagonism could account for some of the visual sharpness etc, so I wonder if Coluracetam has any effect at these receptors also? Although they don't look too structurally similar.

 

Anyway, sorry to go off topic a bit! 

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Yep agreed with the devil bit.
Hmm as with most racetams, Aniracetam's MOA is really just a shot in the dark. From what I found, it modulates AMPA receptor, which in turn can modulate neuronal excitability. 5HT2a antagonism has been implicated to have beneficial effects for HPPD, IIRC. However, D2 and D3 antagonism don't seem like something favorable from an initial glance, but that's just speculation.

Coluracetam (sadly) has not been tested thoroughly enough to find other sites of activity. But then again, if you've done some reading on pharmacological research, 9 out of 10 times you'll read something like: Because introducing A showed B modulation, and introducing C cancelled out A, we conclude that D, E, and F are involved. Well that's a rather inadequate example, but what I meant to say was, is that pharmacology contains a fair bit of speculation and theories, and less so evidence. Thus, truly knowing the exact mechanisms of a substance, especially a new substance, is often quite difficult.

Haha maybe I just said that because of my personal troubles with comprehending such texts.

But with neurology there are so many parameters, that it's hard to pinpoint something unless you've actually started learning from scratch (as opposed to the 'community science' where you just kind of go "ohh that looks interesting, let me look into that" and then in that text you find 30 subjects you don't know shit about, then you have to learn about those to understand what you initially were trying to comprehend, and they all branch off as well until you get to own Chapter 1 of your first Biology class. I call it "backwards education"). Ohh I think I derailed and rambled a bit here.

Anyway, bottom line is that racetams are very interesting, and not much is known about them. All we can do is do our best to speculate what the outcome will be, but nothing can be certain until proven. Also, I haven't tried Aniracetam myself, only Piracetam and Levetiracetam.

However, it would seem that Coluracetam is both superior in its effects and in theory.

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Yep agreed with the devil bit.

Hmm as with most racetams, Aniracetam's MOA is really just a shot in the dark. From what I found, it modulates AMPA receptor, which in turn can modulate neuronal excitability. 5HT2a antagonism has been implicated to have beneficial effects for HPPD, IIRC. However, D2 and D3 antagonism don't seem like something favorable from an initial glance, but that's just speculation.

Coluracetam (sadly) has not been tested thoroughly enough to find other sites of activity. But then again, if you've done some reading on pharmacological research, 9 out of 10 times you'll read something like: Because introducing A showed B modulation, and introducing C cancelled out A, we conclude that D, E, and F are involved. Well that's a rather inadequate example, but what I meant to say was, is that pharmacology contains a fair bit of speculation and theories, and less so evidence. Thus, truly knowing the exact mechanisms of a substance, especially a new substance, is often quite difficult.

Haha maybe I just said that because of my personal troubles with comprehending such texts.

But with neurology there are so many parameters, that it's hard to pinpoint something unless you've actually started learning from scratch (as opposed to the 'community science' where you just kind of go "ohh that looks interesting, let me look into that" and then in that text you find 30 subjects you don't know shit about, then you have to learn about those to understand what you initially were trying to comprehend, and they all branch off as well until you get to own Chapter 1 of your first Biology class. I call it "backwards education"). Ohh I think I derailed and rambled a bit here.

Anyway, bottom line is that racetams are very interesting, and not much is known about them. All we can do is do our best to speculate what the outcome will be, but nothing can be certain until proven. Also, I haven't tried Aniracetam myself, only Piracetam and Levetiracetam.

However, it would seem that Coluracetam is both superior in its effects and in theory.

 

Hey,

 

Oh, I do apologise, I'm really not with it today. I meant that Aniracetam has been show to AGONISE not ANTAGONISE D2, D3 and 5HT2a receptors. My mistake! Also does something at the nACh receptors too from a glance at Wikipedia.

 

Quote:

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.

 

 

But yes, Coluracetam does sound very interesting, I'd love to get my hands on some if the pricing isn't too extreme.

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Ahh that changes things!

I don't think it'll be more than $100/g. With doses as low as 10mg TID being effective, that's $100 a month.
IMO that's a small price to pay.

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Indeed, Aniracetam does sound quite interesting too but I'm not willing to mess with my good ol' 5HT receptors any more haha.

 

Yeah I'd be more than happy to pay that, if there's a UK supplier as you say then I'll definitely give it a trial run.

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Vantage.cc is the UK supplier.

Cheers.

Ah cool, cheers for that.

It's tempting to give Aniracetam a trial run but the 5HT2a agonism might just worsen my HPPD...

Although a quote from a report 'it also becomes easier concentrate with improved mental energy and a feeling of awareness and wakefulness' seems like it could help DP/DR

Sunifiram looks interesting too, 'Sunifiram aids in the release of acetylcholine in the cerebral cortex'

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Sam93: Yeah.. that, along with the "deep feelings of peace" sounds pretty great, right?!

syntheso: It's not for sale yet. Else I would've had it by now of course! ;) But if you see his new Noopept page, there's something about Coluracetam arriving soon.
I had contact with him, and he confirmed that whilst he doesn't know exactly when, he's going to have it soon as well..

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Finally something new. Since i needed to make myself a Guine Pig for Keppra and Sinemet, I am glad that someone is taking over. I'll follow this with big interest. Hoping for something great improvments in meds. Current regime works but its sooo many pills to take each day.

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I'll try this med next week if my doc gives it to me. If I do I'll let you all know how it goes....

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1998: You're doctor can't prescribe this.. It's not a licensed medicine and all that stuff. The best he can do is monitor you and tell you not to eat an absurd amount of eggs while on this stuff.

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Actually can't wait to try this out, although I can't help but think while it could do wonders for the visuals it may not do much for DP/DR. I think reducing excitation in the temporal lobe and pre frontal cortex is the key to solving our DP/DR from what I've researched. Particularly the temporal lobe. Mild seizures in the temporal lobe cause extreme DP/DR.. Hmm.

 

Off topic - HPPD is making me want to pursue a career in Neuroscience, it's fascinating.

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Sam93: Why would you think that reducing excitation in the PFC would solve DP/DR? Sounds counter-intuitive to me.


From: EEG coherence in post-LSD visual hallucinations

We speculate from coherence and known clinical and psychophysical data that, in HPPD, there is widespread cortical inhibition in the eyes-opened state.


Sounds like there's enough inhibition going on as it is. Yes I know, there's some evidence that suggests that there's increased isolated activity of the DLPFC when DP/DR sufferers are exposed to emotional images or something like that. Ahh, here is one example. Seriously though, inhibiting your PFC is something you just never wanna do. Rather, stimulation of the areas that are not as active as they should be (in this case; limbic stimulation.. considering the hippocampus is pretty dependent on proper cholinergic function and is part of the limbic system, this, for example, may indicate that Coluracetam might have beneficial effects on DP in a crude theoretical way).

Just some random thoughts. From the user reports though, it sounds like it could be pretty darn awesome for DP/DR as well.
Yeah I've also considered studying neuroscience if my cognition returns to normal.. But I figure once I solve this, I really don't have any need to. I'll probably go back to sailing, haha!
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