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Enhancing neuroprotection while combining E and meth

Prestacy972

Greenlighter
Joined
Mar 27, 2011
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I know the ins-n-outs of preloading with rolls (though you don't always get clean pills), but I wonder, are there any methods of lessening neurotoxicity of meth (smoked or capsule ingestion)? I mean I know they're inhibitors to different receptors so as to quote "comparing apples to oranges" from another thread.

Even so, I've discovered upon reading about the existence of glial cell-derived neurotrophic factors (GDNF). I'm curious if I could find an external GDNF supplement being that it promotes dopamine uptake and neuron survivability. If possible, where or how would you obtain a GDNF?

So mixing meth and rolls leads me to conclude the increase in dopamine presence from the meth poses a higher oxidation threat considering there's more of it. The oxidation resulting from the rolls of course. Checks out theoretically right?
 
Keep well hydrated, well fed, and avoid becoming over-heated.

Don't combine it with an MAOI, don't redose methamphetamine too often, don't become physically or psychologically dependent on methamphetamine.

I would not combine methamphetamine and MDMA together.
 
I say the absolute best bet is only use minimal ammounts, and possibly half of that since they are combined.

Once had a really good experience to having one pill(actually didnt like the experience all that much, I suspect it was mde or very low amounts of mda, because of the low key feeling and trippy thoughts) and then like >10 mg of crystal shards, orally 5 or 6 hours later.
I was SO FUCKING Up feeling even like 18 hours after I had the pill.
The wisdom is dont dose both at the same time perhapse?

This isnt ADD material and I do not have time to go into whats good antioxidants, trace minerals, and smart drugs to dose.

One of the worst experiences Ive had is on an adderall binge of a sort, crashing taking a mda pill and then more adderall. I wouldnt wish that shit on my worst enemies.

I just say atleast as efficent as possible dosing, as an after thought to the captins thoughts.
 
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I'm not exactly sure why this was moved to ADD.
Nonetheless, the best thing that you can do is avoid this combination, as methamphetamine has been demonstrated neurotoxic on its own, and the addition of more release of 5ht should exacerbate this toxicity. Nonetheless, you can:

Minimize the size of attack doses and frequency of redosing of each.*
Stay hydrated and avoid over-heating
Maintain an adequate intake of reasonable nutrition, particularly a spectrum of amino-acids including ample tryptophan and tyrosine.
Supplement with long-acting anti-oxidants that cross the BBB well (these tend to be fat soluble)

ebola
*note: users of methamphetamine tend not to do this. :P
 
It's interesting that both MDMA and meth have similar mechanisms of neurotoxicity. I think SSRIs could be helpful for MDMA-induced neurotoxicity, but might be toxic when combined with the meth/mdma combo. I've taken Selenium, NAC, CoQ10, and R-ALA before for the little neuroprotection they provide.
 
SSRI's aprevent MDMA induced neurotoxicity by blocking most of the serotonin-releasing effects. Strong monoamine releasing agents are generally neurotoxic (read: methamphetamine).

I agree that this thread really isn't "advanced drug discussion". This thread is kind of like asking "how do I reduce brain damage from pounding my head on a wall." Don't do that then?
 
SSRI's aprevent MDMA induced neurotoxicity by blocking most of the serotonin-releasing effects. Strong monoamine releasing agents are generally neurotoxic (read: methamphetamine).

I agree that this thread really isn't "advanced drug discussion". This thread is kind of like asking "how do I reduce brain damage from pounding my head on a wall." Don't do that then?

It's a question of how "fast" the drug releases the agent as well, correct? Cocaine is neurotoxic because it releases dopamine to the point where the brain's receptors can't cope with it and there's a significant loss of DAT density. Combining meth and mdma will probably lead to severe damage of serotonergic axons too.
 
Cocaine isn't a releasing agent, it's just a reuptake inhibitor.

Elevated levels of dopamine are neurotoxic on their own (due to redox cycling) but toxicity is much less of an issue with reuptake inhibitors as compared to releasers. The logical end point of this are drugs like p-chloroamphetamine.
 
Cocaine isn't a releasing agent, it's just a reuptake inhibitor.

Elevated levels of dopamine are neurotoxic on their own (due to redox cycling) but toxicity is much less of an issue with reuptake inhibitors as compared to releasers. The logical end point of this are drugs like p-chloroamphetamine.

I didn't mean to say it was a releasing agent, just that it caused more dopamine to become present than what is normal. The mechanisms are different but the result is the same: a severe excess of dopamine is present than what the brain is used to and the receptors down-regulate as a response, continued abuse would lead to some destruction of actual receptors and loss of dopamine transporter density.
 
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Cocaine is neurotoxic because it releases dopamine to the point where the brain's receptors can't cope with it and there's a significant loss of DAT density.

Cocaine tends not to be neurotoxic, except with severe overuse, when chronic vasoconstriction fosters cranial hypoxia and increased stroke-risk sufficient to exacerbate cocaine's effects on dopaminergic circuits.

ebola
 
Cocaine tends not to be neurotoxic, except with severe overuse, when chronic vasoconstriction fosters cranial hypoxia and increased stroke-risk sufficient to exacerbate cocaine's effects on dopaminergic circuits.

ebola

ebola how come d-amp / meth-amp are considered neurotoxic then? Is the difference caused by the fact that they reverse the dopamine transporters, leading to other effects? Everyone has their own perspective on the relative neurotoxicity of these agents it seems. By the same token I guess "Ritalin" would not be neurotoxic?
 
Releasers far more effectively increase intercellular dopamine (estimates indicate by three-fold, at saturation levels), and then more readily deplete vesicular stores of dopamine, since releasers induce additional release of neurotransmitter, irrespective of the presence of prior signaling. This leads to the types of neurotransmitter depletion that allow reversed transporters to take up toxic compounds.

ebola
 
Releasers far more effectively increase intercellular dopamine (estimates indicate by three-fold, at saturation levels), and then more readily deplete vesicular stores of dopamine, since releasers induce additional release of neurotransmitter, irrespective of the presence of prior signaling. This leads to the types of neurotransmitter depletion that allow reversed transporters to take up toxic compounds.

ebola

Cocaine is probably neurotoxic by other mechanisms even though it may not cause dopamine release-induced oxidative stress

http://www.ncbi.nlm.nih.gov/pubmed/16733807
http://www.ncbi.nlm.nih.gov/pubmed/17093073
 
"Cocaine-induced [Ca(2+)](i) increases are likely to accentuate the neurotoxic effects from cocaine-induced vasoconstriction and to facilitate the occurrence of seizures from the catecholaminergic effects of cocaine."

*BOOM*, head shot.

ebola
 
"Cocaine-induced [Ca(2+)](i) increases are likely to accentuate the neurotoxic effects from cocaine-induced vasoconstriction and to facilitate the occurrence of seizures from the catecholaminergic effects of cocaine."

*BOOM*, head shot.

ebola

Are you agreeing or disagreeing with that study?
 
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