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Treating methamphetamine-induced anxiety with valproic acid

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For speed-induced anxiety, I use a beta blocker. 40 mg of Inderal (propranolol) pretty much eliminates all the somatic symptoms. No more tachycardia, efficient breathing rhythm...helps quite a bit. Nearly all the physical symptoms of my anxiety disappear. I never found benzos particularly effective for this. I've tried up to 40 mg Valium, 6 mg Klonopin, 4 mg Xanax...experimented with benzos with different half-lives all to no avail.

ETA: Although the propranolol seems to work nicely for me, I must admit I'm not that big on stimulants in general (heroin addict), so I'm sure I don't ever take anywhere near the levels that a true speed user probably does. Also, I usually tend to have a couple of drinks whenever I "crash" on any stimulant. Strange then that the benzos don't really seem to do much for me (since their action in the brain is very similar to that of ethanol). Oh well.

Try not to use beta blockers for psychostimulant-induced anxiety. In fact, I fully advise against it.
 
completely abolish the anxiety while not changing the euphoria.

Yeah, that is the trick, isn't it? But I've actually found the benzos to get the job done duty-free, so to speak. Amnesia, of course, and slight psychomotor impairment, but speed or no speed, the anxiety leaves and that's about it. Now, granted, I am a bit of an oddity with respect to the whole 'tweak freakout' thing, as I've never had a single issue in that regard.
 
Due to an extremely heavy workload (12-16 hours a day, for the past 2.5 weeks), I've been on meth everyday. I use benzodiazepines as anxiolytics PRN throughout the day. however, not wanting to withdrawal from both meth and benzos when I stop, I decided to try something non-habit forming and doesn't cause tolerance. I tried taking 300mg of valproic acid last night. Anyone have any thoughts?

To make suggestions and assistance easier (or better: more reliable) you should have mentioned your regimen of memantine, too.

If I counted right now, you are combining on a daily base methamphetamine, benzodiazepines (which exactly?), doxazosin, aspirin, and finally adding occasionally valproic acid.

My first and only recommendation: Taper down some components of this combo!!! This is far too much, too often. It would be totally over my head even to estime roughly the possible interactions, and I doubt anybody here could do so with certainty. But there's a good chance that there are actually interactions. Methamphetamine - in particular in the long term! - is a proven neurotoxin IIRC, so I'd definitely start there.

I absolutely understand your motivations ("...an extremely heavy workload (12-16 hours a day, for the past 2.5 weeks)..."), but in my experience is the supportive effect of any stimulant only viable during the first couple of days. After this, it will get compensated to a great extend by the lack of sleep (resp. quality of sleep, referring especially to meth and the benzos), nervousness and all the other side-effects. If your work requires you to be fully engaged for several weeks in a row, there's nothing better than a healthy portion of sleep, vitamins and at least one day per week off.


Peace! And take care!

- Murphy
 
I don't quite see the point of using valproic acid.

I've been on valproic acid for a few months after being hospitalized for seizures due to my 'brilliant' idea to cease my very very high clonazepam regimen cold turkey.

Valproic acid is hardly an axiolitic and is pointless especially when considering that you also take benzodiazepines along with them.
Benzos surely are no eau de vie for your body especially considering tollerance and potential addiction though they work great to tamper amphetamine negative side effects and to ease good sleep (always if following a responsigle regimen).
Meth per se is already pretty harsh on the liver and from what you have written so far my intuition tells me that you are being quite unconsiderate to your liver in general.
Valproic acid apart from its known hepatic pressure at medium-high therapeutic doses it works in a very similar way to benzodiazepines (one being an allosteric inhibitor the other being a GABA reuptake inhibitor) though having almost no anxiolitic potential ad is only good as an antiepileptic, a weak mood stabilizer and as mean to ease benzodiazepine withdrawal.
All it will do is increase the rate at which you will develop benzodiazepine tollerance, putting more load on your liver without hardly any advantages.

I deeply understand your motivation for this habit but try to formulate a more reasonaly and healthy-oriented solution. I know I can't really ask you with ease to switch to plain ol' d-amp instead of methamphetamine but there are a few things you could cut out.

1) Stop taking valproic acid, it's pretty much pointless and counterproductive considering your situation.
2) Try taking less aspirin or switch to ibuprofen or even better ketoprofen.
3) Use a high potency medium lasting benzo to be taken few hours before sleep and as you start wroking (assuming that u take meth before going to work)
4) Use and dose your memantine wisely since it helps relieve stress and counteracting amphetamine tollerance (not so sure about benzo tollerance though) also to be taken few hours before sleep.

Also listen to what the wise kraut wrote above:
Lots of vitamins with extra vitamin C and Bx, a good healthy sleep (some melatonin would be good too) and take a fucking break once a weak.

My 2 cents, take care!
Ciao!
 
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Valproic acid is hardly an axiolitic and is pointless

Stop taking valproic acid, it's pretty much pointless and counterproductive

http://www.ncbi.nlm.nih.gov/pubmed/12702897

http://www.biologicalpsychiatryjournal.com/article/0006-3223(93)90010-B/abstract

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VM1-4PYMWPK-1&_user=10&_coverDate=03/31/2008&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1556371399&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=9d109966f7f82f994fae78f0f5a7fa70&searchtype=a

http://journals.lww.com/psychopharmacology/Abstract/2000/02001/Comprehensive_Review_of_the_Psychiatric_Uses_of.1.aspx

GABA reuptake inhibitor

No. Valproate has no appreciable affinity for the GABA transporter.

All it will do is increase the rate at which you will develop benzodiazepine tollerance

Not if he cycles the two, as I recommended.

If I counted right now, you are combining on a daily base methamphetamine, benzodiazepines (which exactly?), doxazosin, aspirin, and finally adding occasionally valproic acid.

I count zero common interactions, aside from the slight risk of toxic potentiation of the benzos by valproic acid, which, again, would be nonexistent if the two were properly cycled.
 
1) Stop taking valproic acid, it's pretty much pointless and counterproductive considering your situation.
2) Try taking less aspirin or switch to ibuprofen or even better ketoprofen.
3) Use a high potency medium lasting benzo to be taken few hours before sleep and as you start wroking (assuming that u take meth before going to work)
4) Use and dose your memantine wisely since it helps relieve stress and counteracting amphetamine tollerance (not so sure about benzo tollerance though) also to be taken few hours before sleep.

1) I really appreciate your advice. To state the obvious (solely for the reason of being slightly facetious), I could just stop taking everything, and thus this thread would might very well be obsolete - for my own selfish intentions anyway. However, since that isn't the case, benzodiazepine tolerance & withdrawal is something I am trying to avoid by taking valproic acid (ie harm reduction). I have to say that the evidence a friend of mine posted earlier suggesting valproic acid's anxiolytic properties do appear to match the results of my own "empirical research" (please do not regard my flippant suggestion of trying out chemical combos on myself lightly, for I really do not, and am deeply torn)
2) I am not taking ASA for as an antipyretic or analgesic. I take only 100mg of long-acting ASA as an anticoagulant, which ibuprofen and (I believe) ketoprofen are not.
3) Refer to "1)". Additionally, why do you suggest to take a "high potency medium lasting benzo" before work & sleep? In terms of potency, assuming you aren't referring to their side effects, which benzo property are you referring to (hypnotic, sedative, muscle relaxant, anxiolytic, or anticonvulsant)? Are you saying to take one benzo as a hypnotic (to induce sleep "a few hours[???]" of sleep beforehand) AND the that very same one to relieve one's anxiety at work? If so, which benzodiazepine would you say does that, especially when one considers how the effects of benzos vary diversely from person to person, added to the pharmaceutical companies' "official" indications of their fancy benzo product, and the different mechanisms of action each one possesses, one would probably be at a lost for words as one tries to tidy up this lengthy sentence. Just for laughs, try to look for a benzo thread re: which is the best benzo in the world, or something along those lines. I don't mean to make fun of other green/bluelighters, but I humbly believe a sense of humour and humour when I find it are two very similar things that make some of the toughest moments in life just that much more bearable.
4) You're right with regards to using memantine wisely. I haven't come to any conclusive understanding about its pharmacodynamics.

Thank you everyone for giving your two cents. It's definitely given me much food for thought.
 
To make suggestions and assistance easier (or better: more reliable) you should have mentioned your regimen of memantine, too.

If I counted right now, you are combining on a daily base methamphetamine, benzodiazepines (which exactly?), doxazosin, aspirin, and finally adding occasionally valproic acid.

My first and only recommendation: Taper down some components of this combo!!! This is far too much, too often. It would be totally over my head even to estime roughly the possible interactions, and I doubt anybody here could do so with certainty. But there's a good chance that there are actually interactions. Methamphetamine - in particular in the long term! - is a proven neurotoxin IIRC, so I'd definitely start there.

I absolutely understand your motivations ("...an extremely heavy workload (12-16 hours a day, for the past 2.5 weeks)..."), but in my experience is the supportive effect of any stimulant only viable during the first couple of days. After this, it will get compensated to a great extend by the lack of sleep (resp. quality of sleep, referring especially to meth and the benzos), nervousness and all the other side-effects. If your work requires you to be fully engaged for several weeks in a row, there's nothing better than a healthy portion of sleep, vitamins and at least one day per week off.


Peace! And take care!

- Murphy

Murphy, thanks a lot. I do realise your good intentions. I do not take what I do lightly. In answer to your question earlier regarding which benzo(s) I take, I find that irrelevant because a) I don't take them in relatively large doses - I try to stick to a 10mg-diazepam-equivalent (if not that) and b) the effects of different benzos on different people are extremely diverse so c) let's just say I would rather prefer not to engage in a discussion or discourse over something along the lines of "which benzodiazepine is or isn't suitable..."

I will definitely keep in mind about the simple little routines, and their importance about which, amidst the utter chaos I seem to live, I have forgotten nearly. completely.
 
I totally disagree that Valproate is useless with Amphetamine.

A psychiatrist I used see for ADD used to put alot of his ADHD patients on both at the same time, including me. And they work really well together. The Valproate stops a lot of the Amphetamine side effects, and helps keep tolerance down.

They are still not sure how Valproate works, but it is a HDAC inhibitor for starters.
 
Dr Beat and /navarone/ summarized it indeed nicely: There are already several (!) biological activities known for valproate, but the deciding one seems to remain unknown yet. Which means that the following quotation is pretty pointless:
I count zero common interactions, aside from the slight risk of toxic potentiation of the benzos by valproic acid, which, again, would be nonexistent if the two were properly cycled.
Then count again!
And try to include the unknown activities that this compound possesses. And don't forget about the benzos, as well as the memantine... The calculation is simply too complex to be disregarded with one quick sentence.

A thinkable interaction is e.g. that memantine can increase the effects of dopaminergic substances (see e.g. Journal of Neural Transmission 1995, Supplement, 46, p.107), while (meth)amphetamine is a known dopamine-releaser. Still no sign of interaction? I'm really to lazy to search any further, but obviously - as suggested earlier - is the complex combo that vanboy5 is ingesting not free of risks...


- Murphy
 
but the deciding one seems to remain unknown yet

GABA transaminase inhibitor, a voltage gated sodium channel blocker and a T-type calcium channel blocker

You skillfully pilot my roflcopter. There is no "deciding one." Valproate's efficacy for a wider variety of neurologic indications than its anticonvulsant competitors is due its relative multitude of actions (none of which, by the way, are listed as having any dangerous interactions with the either meth or the other compounds in his regimen, aside from the negligible one I already mentioned). As an aside, its anxiolytic properties are predictably attributed to its GABA-T inhibition. Mystery solved.

try to include the unknown activities that this compound possesses. And don't forget about the benzos, as well as the memantine... The calculation is simply too complex to be disregarded with one quick sentence.

No one can (how clever), I didn't, and no it isn't.

A thinkable interaction is e.g. that memantine can increase the effects of dopaminergic substances (see e.g. Journal of Neural Transmission 1995, Supplement, 46, p.107), while (meth)amphetamine is a known dopamine-releaser. Still no sign of interaction?

Well sure, if you define the word 'drug interaction' in a rote, prosaic sense, as per the patrons of Wikipedia:

A drug interaction is a situation in which a substance affects the activity of a drug, i.e. the effects are increased or decreased, or they produce a new effect that neither produces on its own. Typically, interaction between drugs come to mind (drug-drug interaction)

However, since vanboy's inquiry was obviously inclined more toward practical concerns (and posted on a site dedicated to preventing users' suffering), I assumed the word 'interaction' when used in this context would refer to any untoward clinical event resulting directly from the combined actions of a set of repetitively administered psychoactive drugs in strategically applied dosages. This operational definition is generally more in accordance with the majority concerns regarding the potential adverse outcomes of drug combinations as they're discussed both on Bluelight and elsewhere. So excuse me for not mentioning that ultra-high doses of NMDA antagonists appear to have a behaviorally significant prodopaminergic effect via indirect disinhibition of midbrain catecholamine release within rats' brains. While I'm fully aware of that particular interaction and others, I'm not going to mention them here because I'm aware that the published (human) literature doesn't indicate that these isolated technical oddities result in a statistically significant likelihood of adverse interaction when these drugs are concomitantly administered in proper doses.

Of course, it's taken for granted that any combination of drugs administered with the intent of altering such a sensitive, intricate network of interdependent chemical pathways as the human nervous system will have some interaction, whether readily discernible or not. But it's not the theoretical rodent-based disease models and in vitro studies that must taken into account before starting a harm-reducing regimen. I'm remain unconcerned in the wake of the study you alarmingly referenced, as should vanboy, because 1) I apparently do better research:

http://www.springerlink.com/content/l6991ql6lf7uq7xw/

and 2) while the array of poorly understood drug effects is astounding, and the apparent complexity of unknown facets daunting, I'm not about to fidget wondering how the psychoactive propionate food preservatives I just ingested in my toast might interact with the baclofen I just dropped, the biologically untested (or poorly tested) components of the aftershave I applied, the petrol fumes I inadvertently huffed at the gas station, the environmentally pervasive polyhalogenated biphenyl toxins that have accumulated in my hippocampal tissue over the course of their 2+ year half-lives, and fuck only knows what other shit happens to be floating around my lobes. And, presumably, neither do you, despite the convincing evidence that even considered alone, such things theoretically bear a great deal practical significance for both your brain and your life, not to mention their profusion of probable "interactions."

vanboy5's choice to continue chronically ingesting methamphetamine hydrochloride is his to make, and, as it appears to me, he has made it in no uncertain terms. Though he admits to being conflicted as to the advisability of perpetuating his 'habit,' he persists nonetheless. I can only hope to provide sensible input and help him make sound choices within the limits of his chosen behavior. No drug combination is "free of risk" (nor is the use of any single drug, at that), but that fact hasn't, and shouldn't, stop someone from responsibly using drugs, either for therapeutic reasons or otherwise, for the express purpose of improving their long-term outcome by including protective buffers and risk-minimizers to a feasible regimen; that is, so long as there's no damning evidence proscribing the habitual coadministration. Since you seem incapable of procuring any, and our research turned up none, I'm sure why you remain convinced that Van [I can only guess that's his name] is somehow in the wrong when it comes to strategically countering the long- and short-term hazards of his performance-related meth use.

To wit:

-Valproate significantly reduces (meth)amphetamine toxicity and limits behavioral stereotypy

-Benzodiazepines behave similarly to valproate, and are thus also desirable in their "interaction"

-VLP's neurogenic properties are also likely to be of benefit, but of this I can't be sure

-Any drowsiness incurred by the aforementioned drugs is eliminated by the meth

-Memantine (or another NMDA antagonist) further limits toxicity and likely tolerance as well

-The alpha-blockers reduce the meth's sympathomimetic load, preventing current and future cardiovascular complications if used judiciously

-Not one of these compounds has any known enzymatic/hepatic/renal, CNS, or sympathetic ADVERSE interactions, and are more likely to be benign when mixed appropriately than not
 
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Why do I get more and more the impression that I became your favourite target for ranting off? Care to elaborate?

P A said:
MurphyClox said:
try to include the unknown activities that this compound possesses. And don't forget about the benzos, as well as the memantine...
No one can (how clever), I didn't, and no it isn't.
For one thing, please stop commenting obvious rhetorical statements of mine. This is simply not helpful in any way. OF COURSE can no one consider any 'unknown activity'. I was simply trying to point out that there still remain several activities of valproate undiscovered yet, which adds some significant uncertainty to the whole calculation. Is this really so hard to agree to? (spare me either the obvious short "yes" or any lenghty answer to this question, because it was again only rhetorical)


P A said:
Well sure, if you define the word 'drug interaction' in a rote, prosaic sense, as per the patrons of Wikipedia...
Cynicism is as helpful as commenting rhetorical statements :| Furthermore, I'm neither into prose nor do I consider Wikipedia the No1 source for scientific definitions, although I check it regularly to get a quick idea of a topic. Why not using something more sophisticated, like "Principles of Clinical Pharmacology" by A. J. Atkins et al ... which coincidentally meet Wiki's definition quite well. But it's interesting that you dedicate so much time to educate me in your lenghty fashion, while occasionally interspersing your own definitions. Why not defining what we talk about beforehand?

I admit, I was already aware before I placed my last post that memantine is rather helpful in combination with amphetamines like meth or MDMA than it is harmful, because it seems to reduce the neurotoxic load and cognitive impairment of these drugs. See e.g. Neuropharmacol 2008, 54, p.1254; NeuroToxicol 2008, 29, p.179; Eur J Pharmacol 2008, 589, p.132.
But that was not my point, because, as explained above, I followed the generally accepted definition of the term "interaction" when writing my last post. I don't see the reason why one should focus exclusively on adverse side-effects. After all is "adverse", at least to a certain degree, quite subjective.
Quoting now from the abstract of the paper to which you linked:
This study investigated the discriminative stimulus, subjective psychomotor performance, and cardiovascular effects of oral methamphetamine following acute oral memantine in humans.
[...]
Following memantine pretreatment, participants responded as if they had been given a novel compound, although memantine did not significantly alter most subjective-effects ratings following methamphetamine.
I read the above excerpt like memantine has indeed a significant influence on the outcome of the biological activity of methamphetamine. I do not necessarily claim that this effect is adverse in nature. But obviously does memantine (at the high doses used in that study, 40 mg) influence the effects of meth. As an example, the rating for the category "Social" was decreased upon coadministration of memantine. How do I know if vanboy5 cares if his social skills get impaired, at least potentially, or if this not relevant. How do YOU know?
Hence, I still consider it important to point out possible interactions of any kind! If these are received either positively or negatively depends entirely on vanboy5 and he may make up his own mind (which he surely did), but it is definitely not up to me to anticipate his decision in this respect. How come that you anticipate all this beforehand? Or do I miss something? (oh I'm sure I missed something and you will tell me in your next post)


P A said:
Since you seem incapable of procuring any, and our research turned up none, I'm sure why you remain convinced that Van [...] is somehow in the wrong when it comes to strategically countering the long- and short-term hazards of his performance-related meth use.
Then please tell what makes you so sure.


As final note let me thank you for the link to the Psychopharmacology-paper. That one was indeed new to me. Quite an interesting reading.


Peace! - Murphy
 
Why do I get more and more the impression that I became your favourite target for ranting off? Care to elaborate?


For one thing, please stop commenting obvious rhetorical statements of mine. This is simply not helpful in any way. OF COURSE can no one consider any 'unknown activity'. I was simply trying to point out that there still remain several activities of valproate undiscovered yet, which adds some significant uncertainty to the whole calculation. Is this really so hard to agree to? (spare me either the obvious short "yes" or any lenghty answer to this question, because it was again only rhetorical)



Cynicism is as helpful as commenting rhetorical statements :| Furthermore, I'm neither into prose nor do I consider Wikipedia the No1 source for scientific definitions, although I check it regularly to get a quick idea of a topic. Why not using something more sophisticated, like "Principles of Clinical Pharmacology" by A. J. Atkins et al ... which coincidentally meet Wiki's definition quite well. But it's interesting that you dedicate so much time to educate me in your lenghty fashion, while occasionally interspersing your own definitions. Why not defining what we talk about beforehand?

I admit, I was already aware before I placed my last post that memantine is rather helpful in combination with amphetamines like meth or MDMA than it is harmful, because it seems to reduce the neurotoxic load and cognitive impairment of these drugs. See e.g. Neuropharmacol 2008, 54, p.1254; NeuroToxicol 2008, 29, p.179; Eur J Pharmacol 2008, 589, p.132.
But that was not my point, because, as explained above, I followed the generally accepted definition of the term "interaction" when writing my last post. I don't see the reason why one should focus exclusively on adverse side-effects. After all is "adverse", at least to a certain degree, quite subjective.
Quoting now from the abstract of the paper to which you linked:

I read the above excerpt like memantine has indeed a significant influence on the outcome of the biological activity of methamphetamine. I do not necessarily claim that this effect is adverse in nature. But obviously does memantine (at the high doses used in that study, 40 mg) influence the effects of meth. As an example, the rating for the category "Social" was decreased upon coadministration of memantine. How do I know if vanboy5 cares if his social skills get impaired, at least potentially, or if this not relevant. How do YOU know?
Hence, I still consider it important to point out possible interactions of any kind! If these are received either positively or negatively depends entirely on vanboy5 and he may make up his own mind (which he surely did), but it is definitely not up to me to anticipate his decision in this respect. How come that you anticipate all this beforehand? Or do I miss something? (oh I'm sure I missed something and you will tell me in your next post)



Then please tell what makes you so sure.


As final note let me thank you for the link to the Psychopharmacology-paper. That one was indeed new to me. Quite an interesting reading.


Peace! - Murphy

Murphy, I need to run a new hotel that my family's built so I'll write what I'd like to express in numerical, point-form fashion.

1) You've completely missed P A's point because you were thrown off by his writing style (I think "cynicism" was the word you used to describe it)
2) Why wouldn't you assume that I cared about my own well-being? Consider the fact that I came to a site dedicated toward harm-reduction to post a thread concerning the usage of non-benzo anxiolytics as prophylactic for benzodiazepines' dangerous withdrawal effects? (This question IS rhetorical)
3) I think "commenting rhetorical statements" is just as effective in making one's point as asking a rhetorical question.
4) Why do you think P A anticipated any decision of mine? (This too, is rhetorical, because I am shocked at how oblivious you were to the fact that he didn't anticipate any of my decisions)
5) Just because someone disagrees with you doesn't necessarily mean he has picked on you as a favourite target. I believe you are exhibiting a common, mildly histrionic reaction as a psychological, defensive mechanism.
6) I would like to go back to the reason why I started this thread. Thank you again Murphy for your time and your sound advice with regards to sleep, vitamins and hydration.

Torabora, thanks for your suggestion!!!!!! Will definitely look into pregabalin as another alternative... it never even crossed my mind...

Cheers,
Van
 
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I would like to add that the fact that memantine blocks amphetamine/MDMA induced neurotoxiticy is because of the initial A7 antagonism wich blocks monoamine release induced by those drugs, basicly it initially interferes with their action leading to less monoamine release and less oxidative stress occurding.

Most ppl initiating memanintine notice that the first week it inhibits amphetamine from working untill A7 upregulates.
In synaptosomes, MDMA decreased 5-HT uptake by about 40%. This decrease was prevented by MEM and by MLA but enhanced by PNU 282987. A similar pattern was observed when we measured the dopamine transport inhibited by METH.
PMID: 18455739
 
Uh

Why do I get more and more the impression that I became your favourite target for ranting off? Care to elaborate?

Sure [unless the question was, ah, rhetorical]. If you disagree with me without presenting a convincing enough counterargument to persuade me otherwise, I'll promptly disagree back. If you disagree with me vehemently, I'll respond similarly.

For one thing, please stop commenting obvious rhetorical statements of mine.

Welcome to sensible argument in the English language. Addressing others' points by responding to the content of their rhetoric, while certainly not doing justice to their statement as a whole, provides a convenient substrate upon which you can mount your own rhetorical devices and from which any central counterarguments can be conveniently segued. As in the case the response you criticized, I was just adamantly restating our central points of disagreement, both for clarity and for teh lulz. I then went on to qualify and support my claims in exhaustive detail over the course of the rest of the post (much of which you apparently neither read, nor seriously considered).

[Though I'm sure all that sounded unbelievably pompous and unnecessarily high-winded, I really don't how else to respond to something as silly as "ignore all of my rhetorical devices." If responding to your artful punctuation of argumentative dialogue truly offends you, I'll certainly stop, but that would definitely hamper the effective construction of a clear, effective response, or at least one that sounds casual and human]

Cynicism is as helpful as commenting rhetorical statements

More rhetoric? In what way was my post cynical? I was expressing a small degree of annoyance at the realization that we had effectively been talking past one another, with a disparity in operational definition to blame...which I subsequently acknowledged and admitted to be the result of presumptuous oversight and undue elaborative restriction on my part (and rote dictionary sticklerism on yours). Or was that too negative for you? [oh look, a rhetorical question! feel free to respond]

I'm neither into prose

:|:|:|:|:|:|:|

http://dictionary.reference.com/browse/prosaic

interspersing your own definitions

I think I adequately explained my rationale for assuming a nontechnical, typically implied definition for a word that, when used in the context of explicit risk minimization, obviously isn't intended as broadly as it would if employed under more technical circumstances (published literature, conversation between professionals, etc.). Yes, you're absolutely right, I should have clarified. Kaykay?

I don't see the reason why one should focus exclusively on adverse side-effects. After all is "adverse", at least to a certain degree, quite subjective.

Really? How so? Can you provide a nontrivial example of a drug interaction that is commonly accepted as universally "adverse" within the medical and public spectra that could be conceived as plausibly "beneficial?" Vice versa? And by nontrivial, I mean something more substantive than "the highest recommended dose of memantine happened to slightly alter a subjective component of amphetamine." By the way, I only cited that study as evidence that, no, I'm not a fucking idiot, and, no, I'm not throwing out amateur internet psychoactive drug prescriptions with blind enthusiasm unrequited by concerns of adverse interaction. That study was just proof of concept that in real world circumstances, the test-tube/rodent-based data usually isn't directly applicable to practical concerns, and posted in direct response to your rat study. It wasn't meant to demonstrate tolerability (there's already ample clinical proof of that), just that no particularly marked deterioration in biological or psychoscial functioning occurred that was egregious enough to warrant serious concern. So yeah Murph, a small sample size of polysubstance users/abusers reported one anomalous adverse effect in a high dose study. I would hardly call that significant. Any doctor would consent to coprescribing the drugs based upon those data and the rest of the clinical research (all of which indicates a high degree of safety and efficacy, or at the very least, a lack of severe adverse effect in combination with a wide variety of drugs). Furthermore, if you had taken a small amount of time to actually read some of Van's posts, you would have understood that the dose he considered was much more conservative than that used in the study, and more than likely free of adverse event. Am I absolutely positive? No. Can he and I be reasonably sure? Yes. Does all this warrant his ingesting the drugs on a regular basis for obvious additive benefit? I think so, but that's ultimately up to him.

"Social" was decreased upon coadministration of memantine

OH NOES he might be severely socially crippled for lief!!!1!!11one11eleven and all because of a few drug users said they felt slightly less outgoing and personable on a questionnaire

Hence, I still consider it important to point out possible interactions of any kind! If these are received either positively or negatively depends entirely on vanboy5 and he may make up his own mind (which he surely did), but it is definitely not up to me to anticipate his decision in this respect.

Oh please, give me a fucking break. So basically, in order to fulfill your straw standard of absolution and 100% certainty, before conferring my solicited opinion that a proposed polypharmacy aggregate is likely to be essentially benign and/or helpful, I must present full peer-reviewed toxicity data in PDF format to be critically reviewed by your pharmacologic lordship? What of the hundreds of other members of this site who make similar, and often far less well-substantiated adages? Do they also receive your swift intellectual retribution? Do you balk at and proceed to rebuke the proposed regimens of anyone else with whom you come into contact on this site?

And nice misrepresentation of my clearly stated intent. NO, I'm obviously not making decisions on Van's behalf. Rather, as explicitly stated (which I shouldn't have even had to do in the first place), I'm simply providing requested input based upon what I understand to be his current goals. Again, fucking excuse me for not including within the lines of my posts every inane tidbit of trivia that can be scrounged from high-dose intracerebral rodent studies; but while you're busy providing what ultimately amounts to redundant, unhelpful critique based upon dreary, pessimistic nihilism (you'll just never know all those little interactions mannn) and alarmist references to what are (more than likely) practically inconsequential technical findings in non-human studies and inventories posed to polydrug-using volunteers, I'll be busy offering constructive advice and feedback tailored toward actually helping the guy out and minimizing harm within the context of his already clearly-dictated decisions. Why is this so difficult for you comprehend? Your advice is just about comparable to telling a psychologically dependent heroin addict to 'just stop' or 'get help.' While Van doesn't appear to be functionally disturbed nor addicted in any way, he is, as stated in his posts, taking meth in a sustained, controlled manner for a short period in his life for purposes of performance enhancement - and sorry for the wild extrapolation, but I just kind of assumed by default that he will, you know, continue to do so. Evidently, minimizing harm and risk within those relatively facile parameters seems like too difficult a concept for you to comprehend, so I guess this remains something of an impasse. Oh well.

Also, what in fuck's name do you mean by "anticipating his decision?" Are you implying that the Bluelight member in question is illiterate or in some way intellectually inferior to you or I? Perhaps you're assuming he's incapable of using Google Scholar or Medline? Aside from being base and insulting, it's pretty presumptuous of you to imply that the guy is fully ignorant of the subject matter and dismissively refer to him as though he's the equivalent of a scientific prole. Why not ask Van what he thinks before criticizing what you assume I've decided for him? I provided links to studies for support. I try explain my ideas in detail. This is as transparent as it can possibly get. What am I missing, Murphy?

(oh I'm sure I missed something and you will tell me in your next post

Again, how clever. And as you put it, very "helpful." Jackass.

In summary, you didn't even attempt to respond to any of the primary points made in my previous post (like, for instance, my extended analogy regarding what, by your own ridiculous standards, appear to be hopelessly complex toxic interactions with both your environment and the drugs I assume you semiregularly take), but resorted to restating a the same tired tautology (that no one can ever combine two psychoactive drugs without incurring some kind "interaction," no matter how small, irrelevant, or clinically insignificant), and dictated a rather bizarre standard by which all recommendations regarding polypharmacy should be evaluated. You misrepresented my intent (helpin a brutha out by providing a combination of personal theory and currently accepted clinical consensus) and substituted it with an aggressive straw version (that I'm making potentially risky decisions on Van's behalf based upon some kind of esoteric information to which only you and I, and not Van, have access). The latter is something to which I can't help but take mild personal offense. To question my rationale is fully acceptable, but to try to take the moral high ground by questioning my intent or concern? Ignominious at best. In the end, it's up to the OP to do whatever he likes, based upon whatever view to which he chooses to subscribe. Obviously, as I assume any OP is aware, the studies we cite in support for our educated opinions are equally free to be read and independently evaluated by him/her. This fact is implicit and reasonably taken for granted, but I'm compelled to mention the fact, just to be absolutely clear what my stance is here. Though with all this said, I'm still not so sure what exactly it is that you're trying to say, in more specific terms than "taper some of that down." That he shouldn't use any drugs? That he shouldn't use anxiolytic medicines for anxiety? That he shouldn't alternate those with a neuroprotective, additively anxiolytic compound to minimize concerns regarding addiction? That he shouldn't try to reduce tolerance to any or all of the above with a low dose of a reasonably well-tested, frequently used, largely benign low-affinity NMDA antagonist? Do you even know?
 
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^I agree with cycling of the two.
From my experience in this situation, beta blockers won't do much at all. I personally find them semi-useful for sleep and that's about it. My physical tolerance to most of them raises quicker than benzodiazepines.
 
^^ Ow no he di-in't!!

LOL, P A you seriously went too deep with your fangs. Your extended and critical knowledge simply do not justify such extents of arrogant-'mother in law like'-comebacks and Youtubish-bitchfit derisions.
Murph's rensponser are indeed crude and got me a bit uncomfy more than once in the past but they keep themselves into the realms of diligence and correctness considering some modesty in giving you credit for the paper you linked and the rightfull statement of yours, still it seems that it quasi-personal on your side (IMO) as soon as you read the following:

Originally Posted by P A:
I count zero common interactions, aside from the slight risk of toxic potentiation of the benzos by valproic acid, which, again, would be nonexistent if the two were properly cycled.

Then count again!
And try to include the unknown activities that this compound possesses. And don't forget about the benzos, as well as the memantine... The calculation is simply too complex to be disregarded with one quick sentence.

That seemed to have started the quite a 'Who do you think you are?' reaction by your side you.

I strongly suggest you take some time to refomulate your tone before Murphy chews you up with the poise and zeal of a French sommelier. Something you are probably incapable of considering your taunting reaction.
 
^^And you're a too-ool!

still it seems that it quasi-personal on your side (IMO) as soon as you read the following:

So someone posted an unnecessarily inflammatory comment, and I responded accordingly? This is personal? Since you can't point to anything 'personal' in my posts in specific, I'm guessing you have nothing other than your moronic little opinion for validation. Thank you for your constructive post.

Murph's rensponser keep themselves into the realms of diligence and correctness

No. Up until the last line, the content was pretty vapid, redundant, and at one point, just offensive.

before Murphy chews you up with the poise and zeal of a French sommelier

What's that about Murphy's Bluelight level? It's over 9000? Lawlzees, it's not like this is some formal dialectic debate in which two argumentative connoiseurs artfully duke it out. This is just a bland disagreement due largely to what should have been a small issue of semantic clarity, one with which I'm becoming increasingly bored.

I strongly suggest you take some time to refomulate your tone

I strongly suggest you go fuck yourself.

While your at it, kindly take your crass, petulant attitude and shove it back up the fetid ass from which it came.
 
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