Jhi-dou a dit:
Ahah...la blague.
Déjà qu'on ne connaît pas la neurotoxicité exacte des 2 premiers (qui sont des stimulants, donc neurotoxiques par nature), alors rajouter une 3ème molécule (4-HO-MET) pour laquelle on n'a pas d'infos précises ni de recul, pour soi-disant réduire la toxicité...c'est un peu nawak quand même.
Cobayes power !
MDMA seems to exert its primary neurotoxicity through a secondary metabolite, and if we can prevent its formation then it's likely that we can eliminate some or all of this toxicity. I won't go in depth into the mechanism here as
u/misteryouaresodumb has it covered, rather I will explain how I choose to avoid this risk.
Credit here belongs almost entirely to
/u/Cannibalsnail. Without him I would never have tried this combo, nor really even considered such an idea.
MDMA is a triple monoamine releaser whose precise releasing ratio and binding profile makes it the popular drug it is. Many RCs have tried to replicate this in the past but I think most people would agree that the attempts have only come quite close. The reason for the shortfall is usually clear upon examination - 6-APB lacks serotonin release, 5-MAPB has too little norepinephrine release.
Trying to balance with mixtures hasn't quite worked in the past either - a little bit of that special magic just seems to lack.
With a little informed experimentation it seems that it's necessary to balance both neurotransmitter release and receptor binding. Mixing a straight stimulant (non-neurotoxic please) with a selective serotonin releaser and a 5HT-1a agonist (most other phenethylamines lack this activity).
It's a year and a half down the line now. We've "tested" a few different mixtures and it seems that the ultimate mixture is 2-FMA, 5-MAPB and 4-HO-MET (5-MeO-MiPT is good too).
In tests MDMA veterans have proven unable to discern the two until the next day, when they are surprised at their near-total lack of comedown.
Both of the two major components are likely to have significantly less neurotoxic potential than their popular analogues because of the way their metabolic pathways are blocked.
- I prefer the effects of 2-FMA significantly but its duration makes redosing inconvenient. Do just bear that in mind.
- Most tryptamines are effective for 1a agonism and just a few mg are needed.
- MDAI is a good alternative to 5-MAPB but it may as well be gold dust at this stage; which means that 5-MAPB is the next most effective compound for inclusion in the mixture.
- I would still urge long breaks with a minimum of one month between uses. I stick to 2-3.
The doses are around 20mg 2-FMA, 50mg 5-MAPB and 3mg 5-MeO-MiPT. I actually use a formula to determine the precise dose depending on body weight and experience.
I hope this is useful to someone; it's saved me from the MDMA comedown since its discovery and think with careful use it could really be a boon to those who enjoy empathogens.
Edit: For those who are unclear, my intention is to specifically address chronic neurotoxicity. It is still possible to overdose from taking too much of this. The
therapeutic ratio may be worse for this combination than for MDMA.
Edit2: I think it is worth emphasising that 5-MAPB in particular can definitely cause problems if it is abused. This is less likely in this blend as the "completeness" prevents chasing a (dopamine) high one cannot capture, but on its own there are stories of people taking 2-300mg plus and then unsurprisingly suffering.
Edit3: Cannibalsnail has reminded me that 2-FA is unexpectedly lacklustre in this combination. Stick with 2-FMA.
Edit4: Some things to consider:
Can you explain to me then why 2-FMA would not be neurotoxic as amphetamine is?
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Borax[
S] 0 point1 point2 points il y a 1 an (14 enfants)Désole, l'élément a été archivé et n'est plus soumis aux votes.
Fluorine should deactivate the ring somewhat and will be a worse fit for the enzymes which metabolise phenethylamine in the brain. It may not be massively but any amount is useful.
I'm not claiming that no damage will be done, in fact I would be shocked if that was the case. The intention is to significantly reduce the damage by completely eliminating its primary cause.
That said:
- MDAI is non neurotoxic.
- The fluorine on 2-FMA will block enzyme binding which allows metabolism to a-methyldopamine.
- Metabolism of 5-MAPB to a-methyldopamine is blocked by the benzofuran moeity.
Edit: MDAI is non neurotoxic
in isolation it has not been studied in vivo in a system like this and it is likely that dopamine uptake into serotonin neurons would be facilitated here and cause some minor damage. This is one of the minor routes of MDMA toxicity too. TL;DR don't go thinking this is as safe as sugar and go sprinkling it on your breakfast.
Vrai ou faux je suis pas en connaissance d en juger mais c est interessant a lire.
Et de toute facon un tel combo approchera jamais ma bouche, ca me semble etre la gerbe assurée. Surtout que la mdma est pas si dure a trouver et que pris raisonnablement c'est pas dangereux. Ma lune de miel est deja passée depuis longtemps :mrgreen: