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Amphetamine Neurotoxicity and Tolerance Reduction/Prevention III

tweex said:
There is nothing inherent in the "stimulant-ness" of a drug that causes a comedown, it is all a question of receptor up/downregulation, neurotoxicity, precursor and neurotransmitter depletion. There are no "comedown atoms" that are magically part of every stimulant molecule.
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Ou for real ? Thanks for enlightening me, Mr. White. Just because my English is not always on point does not mean I believe in fairies or "comedown atoms". ;) I may not have articulated my point in my last post. I say, if you dose 2-FMA that high, that the same quantities of monoamines are located in the presynaptic gap as while under the influence of an average dose of d-amphetamine, you will certainly experience a comedown. But it will be prolonged, because the still unknown metabolites of 2-FMA will float around in your organism for quite some time. That is my view, gathered from experience and speculation. If d-amphetamine is too jittery, one should take less instead of substituting with a rather unknown chemical, that provides a smoother stimulation (in my opinion it is just less potent and has some additional activity on other transporters, which makes it less predictable).

Moreover the metabolites of 2-FMA appear to be quite cardiotoxic, as the empirical evidence shows :

http://www.bluelight.org/vb/threads/648663-Best-stimulant-RC-Study-Aid/page2

See Post #30

So in my eyes it is underwhelming and pretty toxic. If you would make an A/B comparison by taking the substances (d-amph and 2-FMA) solo, I am sure you would confirm, that it has no advantages over amphetamine, despite maybe, that it is less addictive.

I see, you have quite some knowledge in pharmacology (more than myself at least). But with the hype of that particular substance you are most definitely on the wrong path.

So what about taking an NRE at a NDRA/NDRI comedown ? Should it not cause acute narcolepsy ?
 
tweex said:
One hypothesis I've had is lower VMAT binding, which seems to be a common thing with "comedown-free" stims.
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Paradoxically, though, high selectivity for activity at VMAT2 (no known ligands are particularly selective for this) is associated with "smoother highs".


So I'll turn that around then, why are the stimulants like (ar)modafinil that some people don't report any comedown from after protracted use?
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These are multi-mechanism stimulants that simply have effects differing from classical stimulants.


There are some newer compounds in the modafinil series out recently that display very potent and selective DRI properties, but I have yet to try.
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These compounds would provide good means to test your hypothesis.

Z said:
Would it be beneficial, if one takes a norepinephrine reuptake enhancer
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Theoretically, this should reduce the effects of the comedown, but do you know of any selective NREs?

But it will be prolonged, because the still unknown metabolites of 2-FMA will float around in your organism for quite some time.
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Most amphetamine by far is excreted unchanged renally. What metabolites should we expect to form from 2fma, and why would we expect to persist at duration? Why doesn't 2fa appear to share this issue? Honestly, just heavy use of other amphetamines would likely lead to similar complications.

ebola
 
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Right, which is nearly the opposite of a norepinephrine reuptake enhancer.

ebola
 
Didn't see you were speaking of NRE's, I absent mindedly mistook this to be about NRI's. Anyways, how is it that an NRE would reduce the comedown? If that's so, wouldn't a DRE reduce the comedown as well? Sulbutiamine comes to mind.

Also NRI's seem to reduce stimulant seeking behavior..
http://www.ncbi.nlm.nih.gov/pubmed/22089320
 
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exessive use of methylfenidate is not to be upp with exessive use of amfetaminsulfate. Its like compering cocain addiction with chewing cocaleaves. And I do not beleve that any serios resercher would simply asume that whats goes for meth goes for amfetaminsulfate. Maby not importent couse meth is here to stay but still. Sorry I do not have any scientific material to qoute I can only say as a living in the contry that has the most daily consumers of amfetaminsulfate in the world per capita the meth situation in the us is not to be recordnised here and I guess that befor the meth explotion in us people took just as much amfetaminsulfate there instead and there is simply not as severe impakt with good old speed. Would like to ad that the most imorten harmreduktion is not to stigmatise addicts se that averybodys basic needs is provided for and not being jailed upp all the time. Otherwise its very intresting with this resurch how to reduse side effekt and make drugjuse as safe as possible.

In general amfataminsulfates (meth i dont know) has a recovery period of 3-day up to 3 weeks of cours induvidual circumstances could prolong this period. Within swedish helthcare thares a general assumpion that regular amp-use indicates that adhd/add and or autism. Couse even if its classifiade as addictiv narcotiks expirence with in the healthcare system and sientificly based treatment for addiction ( meening NOT the NA and such, thay can make a teenages thinking there addicts for life after a summer with drug experience) do not support the ide of patologic addiction to amfetamine, these patiant is usaly tranferd to a Neorpsykiatrist and given amfetaminebased medicins. It is intesting how less "addicted" the patiant becoms after hearing "its jus self medicationing going wrong". Maby the moodswings indicates something else? Personaly before chanching to the adhd-pills(have gone trhu 4 different types until staing on Dexadrin 40 mg) I used 1-3 grams amfetamin daily, took magnesium and B vitamins, began the morning with 2 liters lemonwater, stayd of coffie and tobacco and alcohol, eating well. If i could not sleep i always use the time to rest anyway (Its a wery easy to reach a meditatve state:). It went on for two years and knowone "could have guessed" untill I went to get diagnosed. It was not very hard to make the chance maby becuse I newer felt any guilt, do to my autism maby and was in god fysical shape. In my experience its the mixuses that get most problems, especially alcohol and opiats,. My dads girldfreind had a severe stroke and was in coma for many weeks, she had to learn to walk agian from scratsh, af ter two years she was not still not very funkional, for some reasen my dad started to us amfetamin at the age of 57 then she wanted to try of cours, in two month she vas fully recovered. true story! Rember Ive seen som japaneese stydy on dexadrin and stroke but dont remember were.

in my personal experiens with anti-psykotics inkl seroquel it will make you need more amp to get effect. Its also a drug with a lot of troubling side effect with high freaqvency. I would try an antiepileftic instead for reducing amp sideeffects and melatonin combiened with small dose benzo for a good night sleep. Long time use of ant psykotics will instead when you quit make the risk of psycotic tendensies higher and fuck up your meth use.
 
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Hi all, first I wanted to say thanks to the OP for putting this information on this thread. I am prescribed 20mg of adderall a day, and I have noticed an fairly large increase in my tolerance since I started. I am not a med student or anything and it is really hard for me to understand alot of what you guys are talking about. It's a little embarrassing for me to have to ask this but would it be possible for someone to put this in laymens terms for me. I'm sorry to ask but I really don't have a clue what most of u ate talking about lol. So of someone could please simplify this for the less educated people like myself, it would be very much appreciated. Thanks everyone!
 
So I just got prescribed Dexedrine and just took my antioxidants with the Dexedrine. Taking them with the Dexedrine isn't an issue is it? (By "with" I mean at the same time)
 
red22 said:
So I just got prescribed Dexedrine and just took my antioxidants with the Dexedrine. Taking them with the Dexedrine isn't an issue is it? (By "with" I mean at the same time)
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Unless you're taking a cocktail of only acidic or only alkaline antioxidant compounds in high doses, then no. The only thing that really matters with interacting drugs is an effect on central/peripheral monoamine activity. The only thing that matters with other substances, e.g., food, is the net/aggregate pH of your diet.
 
Thanks. I wouldn't think so, but there's no possibility that the antioxidants could neutralize the Dexedrine itself?
 
I think the best (only?) was to mitigate amphetamine tolerance is to not overuse adderall, methamphetamine or Mdx. Even then, you will slowly develop a tolerance: for MDMA, it can take several years, but once it happens, you rolling days are over. For amphetamine (adderall), after you've taken it every day for 12 years, you're tolerance is shot. Methamphetamine takes the longest to develop tolerance, but it will age you at a fast pace for years and years, and even meth develops tolerance eventually.

Save all these amphetamines for special occasions and don't overdo them! Moderation is key.
 
It seems that tolerance climbs more slowly just because people are able to push the dosages so high.

ebola
 
there's no possibility that the antioxidants could neutralize the Dexedrine itself?
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Dexedrine is not an oxidising agent: so no.
 
Would the beneficial effects of l-deprenyl on the brain outweigh the negative effects of its metabolites l-meth/l-amp on it?
 
The activity of L-methamphetamine is so low, I'd say yes.
 
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