10 replies to this topic

[brain]

There was a night I combined alcohol (let's say, 4 - 9 beers [i can't remember] with lower tolerance,) large amounts of THC, dexmethylphenidate (focalin/ritalin), piracetam, Alpha-GPC, 100 mg caffeine pill (crushed, oral), and clorezepate (a benzodiazepine, later on and because of the crash.) Chain smoking, for what that's worth. I'm not going comment on what that combination felt like, but it was basically fine, until I crashed. I noticed some chest pains, had a pretty bad headache. I attributed it mainly to the ritalin being thrown in, as I've never had problems with anything else. 5mg ritalin, but with selegiline having been taken 15 - 20 days previously and on a regular basis. (It takes 40 days for MAO-B to fully regenerate.)


Similar combination on other nights, minus the benzo, mainly two other nights. No comments, please.

The only thing out of the norm around this time period is that I was taking ritalin (rather, dexmethylphenidate (focalin.) I think this may be a neurotoxic combination in conjunction with piracetam (or with selegiline, even if the ritalin is in low doses), but that's speculative on my part.

Basically, my divided attention seems damaged. If I don't fully pay attention to what I'm saying, my words will not come out correctly, or I will mix them up with other words. I cannot sense any differences in how I think, my reasoning ability, or my general intelligence. When writing, I often leave out words or groups of words or will mix them up with other words. This is strongly exacerbated when I'm tired, am generally not in a mentally active state of mind, or if I use alcohol or weed (which I've now totally stopped to try and aid my recovery.) Given the bad headache and chest pains, I think it's possible I had a minor stroke, but I have no idea. Prefrontal excitotoxicity maybe. Maybe something else. Maybe a combination of things.

Alpha-GPC, more piracetam, selegiline, ALCAR, abstaining from drugs, getting enough sleep, and eating enough and at the right times has helped me, but only when I'm in the temporarily heightened state of 'attentional awareness' they put me in. If i am at all tired or if I drink even small amounts of alcohol, it comes back. Anxiety also triggers it (and reduces pre-frontal lobe function in general, as has been studied). I have questioned if anxiety itself could be the culprit, but its much to cognitive, happens even in my own thought/writing, etc. Basically even when I'm completely calm. It's a divided attention/multitasking thing, or you could say that its likely something having to do with my 'lower level/background' forms of attention/processing.

Advice, interpretations, recommendations?

Edited by brain, 07 November 2010 - 04:40 AM.

[niner]

Advice, interpretations, recommendations?

Damn, brain, I wouldn't have said anything because it seems a little far fetched, but since you mention it, the mild aphasia made me think stroke. The good news is that you are young and healthy and will very probably get better. You need a dose of "tincture of time". That and clean livin'. You seem to already be on top of that, which is good. Good diet, exercise, and sleep are all your friends in this process. As for supplements, the basics are D3 and K2 in oil-based formulations, fish oil, and magnesium. I'd go higher than normal on the D3 for a while; maybe 5000 IU, shooting for a 25-OH-D3 level of ~70ng/ml. I like K2-MK7; I'd take 90mcg/d with that level of D. 2-3 grams fish oil and 400mg magnesium; glycinate is good. When you are feeling better, I would cut these doses approximately in half, and shoot for 50ng/ml on the D level.

I had to laugh at the "no comments please"... TBH, I don't see an obvious red flag in your polypharmacy, but it sounds like something didn't agree with you. Well, who hasn't been there, but I guess mama knows best after all. All this having been said, it wouldn't be crazy to talk to a neurologist. If you have decent health coverage, I would give that a shot. There's a lot of diagnostic work that could be brought to bear on it.

[NR2(x)]

Sounds rough,
I had a similar experience but it abated after 36 Hours, cause 7 bottles of wine over 12 hours and 300mg wellburton(drug navie) and Stim.
I imagine that the casual problem is dissassociative damage(maybe Anterior cingulate cortex
), coupled with reduce plasticity from down regulation of rate limiting enzymes Up the biological cascade from MAO-B, and potentially an amount excitoxicity.
Alcohol, THC ,MAO-b inhibition are dissoassociatives and Methylphenidate by a partial indirect route. Piracetam maybe not sure. Alot of these drugs also tend to lock in a neural pattern eg The benzos also faciliate Long Term Potentiation. Dissassociative damage isnt so much damage, just lack process or network, you need to think that patterns back into place.
Keeping of the dissassociatives must become a rule from now on, theres alot of material on this site that may help

[jadamgo]

Can you provide some sources for the assertion that THC, MAO-B inhibitors, and (indirectly) MPH are dissociatives? I'd love to look into that because it seems interesting.

No need to provide sources for the claim that alcohol is a dissociative, since it's an NMDAR antagonist at higher doses.

[Animal]

Can you provide some sources for the assertion that THC, MAO-B inhibitors, and (indirectly) MPH are dissociatives? I'd love to look into that because it seems interesting.

No need to provide sources for the claim that alcohol is a dissociative, since it's an NMDAR antagonist at higher doses.

I seriously doubt he can, NR2 has a tendency to spout 'personal insight' as fact, but typically it's just a load of semi-random nonsense.

Such as the claim that Modafinil and Buproprion have the same mechanism of action as Amphetamine.

MAO-B inhibitors, and MPH are not dissociatives, the opposite in fact. MPH wouldn't make a good ADD treatment if it was.

If anything I would expect the Deprenyl to reduce oxidative stress, since it not only reduces tyrosine hydroxylase activity but also reduces extracellular dopamine concentrations. So in theory there should be less excitotoxicity from the re-uptake inhibition effect of the MPH i.e. It reduces the 'peak' but increases the duration.

Brain, you've done this kind of shit multiple times before, taking stupid nootropic combinations with recreational drugs and then panicking about potential negative after-effects. Piracetam taken with a dopaminergic psychostimulant is a particularly bad combo as you well know...you're a moron.

[aLurker]

Can you provide some sources for the assertion that THC, MAO-B inhibitors, and (indirectly) MPH are dissociatives? I'd love to look into that because it seems interesting.

No need to provide sources for the claim that alcohol is a dissociative, since it's an NMDAR antagonist at higher doses.

I seriously doubt he can, NR2 has a tendency to spout 'personal insight' as fact, but typically it's just a load of semi-random nonsense.

Such as the claim that Modafinil and Buproprion have the same mechanism of action as Amphetamine.

MAO-B inhibitors, and MPH are not dissociatives, the opposite in fact. MPH wouldn't make a good ADD treatment if it was.

If anything I would expect the Deprenyl to reduce oxidative stress, since it not only reduces tyrosine hydroxylase activity but also reduces extracellular dopamine concentrations. So in theory there should be less excitotoxicity from the re-uptake inhibition effect of the MPH i.e. It reduces the 'peak' but increases the duration.

Brain, you've done this kind of shit multiple times before, taking stupid nootropic combinations with recreational drugs and then panicking about potential negative after-effects. Piracetam taken with a dopaminergic psychostimulant is a particularly bad combo as you well know...you're a moron.

I wholeheartedly agree with most of your post.

I was a bit taken aback by your statement that the deprenyl might have attenuated rather than caused some of the problems since deprenyl in combination with mph is explicitly contradicted. Your argument might have some merit because of the neuroprotective aspects of deprenyl yet I still wouldn't recommend the combination to anyone.

The real reason I posted is that I'd like you to elaborate and ideally also provide some citations on why Piracetam is a bad combination with methylphenidate. You may very well be right, brain seems to agree with you. Do you think this is the case for all racetams or would for instance aniracetam be better? Please enlighten me since I can't seem to find anything conclusive here despite doing some searches.

[brain]

Animal, there really wasn't and still isn't much theoretical concern for piracetam being dangerous when combined with dopaminergic agents in general. Its amphetamine which is a problem, which releases glutamate and dopamine. MPH isn't a releasing agent, it's only a DNRI. On paper, there shouldn't be an interaction. I threw alcohol and some pot on top of my daily stack, that's it. There are people who claim to have safely combined ritalin + piracetam for extended periods, plus, there is little to no evidence it releases glutamate (leading to excitotoxicity.) The only reason I have to believe its dangerous is my own experience, which could well be off the mark. I don't know what happened. It's possible all of this is unrelated. Its also possible its more so the residual selegiline and ritalin that caused a mini stroke or some sort of damage. I raised the dosage slowly and noticed no adverse effects at first. Believe it or not, when I said "no comments, please" I specifically had you in mind, recalling your responses to other posters, which I found off-putting even when I wasn't involved. I already feel bad enough as it is, I really don't think the "you're a moron and deserve what you get" mentality is helpful here.

Edited by brain, 08 November 2010 - 12:42 AM.

[brain]

I think it may actually just be an unrelated choline deficiency. It all goes away when I take 600mg alpha-gpc. Around this time, I also got off of piracetam and started smoking a lot of weed. I began noticing problems around then. I think it's possible that getting of of the piracetam and also using other stuff with anticholinergic properties (alcohol, thc) resulted in a sort of chronic choline deficiency.

[jadamgo]

Well, anticholinergics would cause similar symptoms to choline deficiency, but presumably the cholinergic system is actually up-regulating to compensate for the effects of an anticholinergic. So if you discontinued the anticholinergics, especially if you were taking choline supplementation, would you not experience an improvement in cholinergic function?

Smoking large amounts of weed, of course, has problems of its own. Depending on the absolute and relative amounts of THC and CBD (and other actives) that you were consuming, you might expect significant cognitive dysfunction.

Or, for different proportions and amounts, you might not experience any cognitive dysfunction at all. So perhaps it IS due to cholinergic problems.

[Animal]

Believe it or not, when I said "no comments, please" I specifically had you in mind, recalling your responses to other posters, which I found off-putting even when I wasn't involved.

Ha ha ha, I'm touched, but I'm afraid I'm going to continue to express how I feel about the stupidity I see so often on display here, whether you like it or not. I don't censor my opinions for anyone, online or off.

As for the rest of you post, well it's an excellent contradiction of what you've previously posted. Don't try and defend your behaviour to me, I really don't care. I'm sure you'll continue to take stupid combinations in the future regardless of what anyone says, because you seem to have a fantastic capacity for self-delusion. It's all about the buzz right!?

aLurker, I have no interest in providing evidence for my claim that Piracetam and a psychostimulant are a bad combination; aside from the numerous anecdotal reports of such on this forum and from my friends. There is little research on Piracetam in combination with anything, so you'll have to come to your own conclusions. Deprenyl is not explicitly contraindicated with a dopamine re-uptake inhibitor, MAO-AB inhibitors are. This is of course based upon the assumption that Brain was only taking selective doses of Deprenyl for it's neuroprotective/life extensionist properties. I think we can safely conclude that after 20 days, the degree of MAOB inhibition would be minimal. I'm not saying the combination is recommended, but unless significant amounts of both Deprenyl and a SDRI were combined then there should be no problem.

[NR2(x)]

Deprenyl is not explicitly contraindicated with a dopamine re-uptake inhibitor, MAO-AB inhibitors are. This is of course based upon the assumption that Brain was only taking selective doses of Deprenyl for it's neuroprotective/life extensionist properties. I think we can safely conclude that after 20 days, the degree of MAOB inhibition would be minimal. I'm not saying the combination is recommended, but unless significant amounts of both Deprenyl and a SDRI were combined then there should be no problem.

To make a declaration on the pharamacology/Safety of a substance where one knows nothing of the relevent Bindings and Metabolites, is dangerous and foolhardy. So I challenge you to show me 5 neuroactive endogenous ligands that are formed from phenylethylamine, there are thousands.