Giovanni
Greenlighter
Does anybody have an idea of how bad Mephedrone is for your body? Does anybody know about short and long term toxic effects? Thanks in advance.
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How toxic is Mephedrone?
Giovanni
Greenlighter
Does anybody have an idea of how bad Mephedrone is for your body? Does anybody know about short and long term toxic effects? Thanks in advance.
pofacedhoe
Bluelight Crew
clearly no-one knows, duh
its only been around for a couple of years (thank those sweet israeli gits) and it would be good if you use restraint as i dont want to have a source of cheap fun removed cos you experiment and it goes wrong.
here is my experience
-it can cause psychosis, when it wears off you feel great but have a decreased tolerance to irritaion and get in a rage easily.
-it can fuck with your heart like all stimulants and although unproven its highly likely that is causes 5ht2b stimulation and the problems associated with that (wiki). using it rarely, solves this danger as mdma also has affinity for that receptor (people just dont use mdma that often (if they have a brain)) and we havent seen a huge amount of pulmonary blah from all those ravers years ago.
-it can cause issues with blood clotting as it has a large effect on serotnin and said neurotransmitter has a very important role in blood clotting.
as for actual research you must be 'avin a jeer 'alf
so be wise and dont damage yourself
exactly. there has already been another thread in ADD about mephedrone toxicity in the last weeks iirc.
clearly no-one knows, duh
pulmonary blah
cardiac fibrosis (of the pulmonary valve) if i may help you
rangrz
Bluelighter
IIRC, it has limited MAOI properties and is probably more risky to mix then other similar subjective effect compounds.
thats just off my head tho.
ebola?
Bluelight Crew
While most-all 4-substituted AMPs and bk-AMPs have modest MAOI properties (Nuke 2009), it's 4-methoxy-methcathinone (aka methadrone) that is a strong MAOI and DARI in one. Don't let the silly names nab you.
ebola
pofacedhoe
Bluelight Crew
While most-all 4-substituted AMPs and bk-AMPs have modest MAOI properties (Nuke 2009), it's 4-methoxy-methcathinone (aka methadrone) that is a strong MAOI and DARI in one. Don't let the silly names nab you.
ebola
methedrone (which is mega dodge) or Mephedrone (less dodge, still dodge though).
i aint got no chemistry degree (purely psycho logic) but methoxy and methyl to me sound different, this would suggest they are in fact different compunds
methedrone (4-methoxy-methcathinone) was marketed with a nasty desire to sound similar to mephedrone (4-methyl-methcathinone) to catch the money of fools willing to buy something they overheard at a party ,yet 4-methoxy-methcathinone has some very toxic interactions within is effects. whereas with mephedrone its just bad in the short term like coke or speed and pulmonary blah( to explain it in one sentence is pointless as you should really read about it in detail if you plan on doing any mephedrone whatsoever) in the long term (read up on wiki for a bit of direction then do some reading of research articles-yes wiki is not to be relied upon but it can provide a usefull base for getting clues on what to look for in terms of acctual research, and diseases that exist).
always read up in detail and think before you jump or instead of tumbling off the garden wall you might end up diving down the angel falls
pofacedhoe
Bluelight Crew
Well, probably is a strong MAOI and DARI in one. There's no pharmacological data to support or deny this, but assuming it is, is a lot smarter than dying over it.
doesnt mean it is not the case just that it could and couln't be. maybe lean more towards could. this is logical given the possibly accuartely guessed risks.
why is thinking in grey so difficult. i find it essential to not go mental. everthing is a certain percent yes and a certain percent no. e.g 70/30 or 32/ 68 etc. life is a game of probability and so is everything ever... or maybe it isn't but i'd lean a little more to it is if you get my drift
the risk calculation is really easy.
what are the downside risks? --- we don't know
what are the worst possible downside risks, and of course we don't know if these are indeed the worst possible risks? --- death, heart valve fibrosis, brain damage, organ damage, clotting problems, death
what is the upside? getting somewhat high.
do you feel lucky???????
this rat will pass thankyou.
flacky
Bluelighter
Has this been proven to be a MAOI? If so, how long is the duration for MAO inhibition?
pofacedhoe
Bluelight Crew
the risk calculation is really easy.
what are the downside risks? --- we don't know
what are the worst possible downside risks, and of course we don't know if these are indeed the worst possible risks? --- death, heart valve fibrosis, brain damage, organ damage, clotting problems, death
what is the upside? getting somewhat high.
do you feel lucky???????
this rat will pass thankyou.
which rat?: Mephedrone (which seems to be gaining enough popularity to hit the mainstream
r Methedrone (which seems to have lost its shit atempt at gaining any vogue whatsoever):D
Coolio
Greenlighter
Since I seemed to have missed mephedrone's MAOI potential being discussed in any other threads, I'd like to ask someone here. What evidence or theory is there to support mephedrone being a strong MAOI? Is it MAO A or B selective? Irreversible of course?
I'd like to know if mephedrone could be used to orally activate DMT and DPT.
flacky
Bluelighter
And if I could quickly tag on to Coolio's question: How long are its effects as a MAOI present for?
mephedrone:
Since I seemed to have missed mephedrone's MAOI potential being discussed in any other threads, I'd like to ask someone here. What evidence or theory is there to support mephedrone being a strong MAOI? Is it MAO A or B selective? Irreversible of course?
I'd like to know if mephedrone could be used to orally activate DMT and DPT.
it is likely just to be a substrate inhibitor like most amphetamine type compounds, a competitive inhibitor and probably a weak one at that, however the stuff is being taken at stupid doses so who knows.
I have seen no solid data, so all is speculation.
the metabolites, which are guaranteed to include beta hydroxy compounds would seem more interesting with respect to toxic potential.
vortex30
Bluelighter
MMCAT toxicity/neurotoxicity
It isn't too bad at all.
Methamphetamine is fucking toxic, it is an effective dual DA/SE cascader aswell as a slight reuptake inhibitor, Methcathinone and mephedrone are the other way around, they are decent reuptake inhibitors, with less of a cascading effect, particularly on dopamine as the ketone on the beta carbon is electronegative and won't fit through SER correcctly, despite the methyl being partially SE mimicking the cascade is still small, and the reuptake inhibition fairly abysmal for the same reason.
Thus the SE release is far less for both chemicals, meaning that : -
A) The cathinone is not take up into the presynaptic neuron (despite the methyl being a hydroxyl mimicker) where due to the methyl on the amine and alpha carbon, it inhibits MAO to a large degree, creating an MAOI effect.
B) The dual release, and consequent DA "hoover" effect is significantly lessened, again resulting in less breakdown product damage in the neuron.
For the dopamine side of things, the molecules double bonded carbon makes it a far more effective DARI as opposed to releaser, again product breakdown inside the neuron is far less and the overall subsequent monoamine depletion is less, leading to far lower depletion. Again as the molecular is primarily a reuptake inhibitor as opposed to a cascader MAO inhibition is not seen to anywhere near the same degree as amphetamines/methamphetamines, however you do notice a definate adrenaline increase after the drug has worn off, as the DARI action lessens and the amount of DA and consequently NA/A in the presynaptic neuron shoots up causing a cascade.
Evidence to support these claims.
Cathinones cause a fairly hefty DA mediated rise in body temperature, and the high is far more of a sustained one than the initial rush (cascade) of amphetamines. Cascaders are fucking evil in principle, I really can't understand why people have used and DA mimicked for so fucking long .
MBDB is primarily serotonergenic with little to no DA effects, yet as soon as you put a double bonded oxygen on it, you get a much higher affinity for the NE and DA transporters and considerably lessened to almost nill reuptake into the SE neuron.
Dimethylamphetamine is nearly inactive, because the molecule is a shit DARI, and causes it's effects through cascading, whereas Dimethylmethcathinone is only 1.6x less active than methcathinone (with the extra steric bulk on the amine compensating for the lowered charge and bining) proving that the primary mechanism of the cathinones is reuptake inhibition as opposed to cascading.
The above information showing cathinones lesser affinity for the SE transporter also means that compounds such as 4 methoxy amphetamine, and 4 methyl amphetamine are rendered harmless as MAOI's as they do not get transported into the presynaptic SE neuron, hence no massive overheating.
Furthermore, the 4 fluorinated and 4 methylated versions of both methcathinone and cathinone will have barely any 5HT2b agonism, as SE, being a mood regulator amongst other things, will have evolved to not accept electronegative groups there, otherwise NE/E would have a far larger effect, causing heart issues in humans.
Can someone explain how the reasoning here is wrong/right for each point and how likely any of this is going to wind up being correct. I won't name who wrote this, but some people on here will know right away.
Its something to read, at least speculation over Mephedrone that takes a bigger leap than it possibly being an MAOI and DARI therefore bad. I'd like to have this refuted/confirmed for this forum, and another forum, so thanks to the ADD people who take the time to go over the thought process and offer up a counter-argument, or a confirmation of sound logic, etc.
Thanks!
lineartransform
Bluelighter
I would argue that it is very much worth discussing, if only to discredit these claims in a coherent manner.
Information is valuable, and vetted information even more so. Leaving a comment like that to stand on its own when toxicity could be a very significant risk could expose many to unnecessary harm.
I would argue that it is very much worth discussing, if only to discredit these claims in a coherent manner.
Information is valuable, and vetted information even more so. Leaving a comment like that to stand on its own when toxicity could be a very significant risk could expose many to unnecessary harm.
There is not sufficient information with respect to mephedrone and its ilk upon which to base a properly informed judgement either way, it is all speculation and extrapolation, but at least those who speculate should get basic chemistry right.
As for people being exposed to unecessary harm, well there is no necessity to consume mephedrone.
Until there is solid data available the default position should be to leave the stuff alone.
lineartransform
Bluelighter
Sorry vecktor, what I meant was - to those who are not intimately familiar with the chemistry, the above quoted post seems credible. Combine that with the fact that mephedrone is somewhat addictive, there exists the possibility of people rationalizing their use by referencing that post.
A quick explanation of what chemistry is in error would help to drastically reduce the credibility of that post. If this has been explained in another thread I apologize, and would like to request the link to it.
my comments in red, in short the whole treatise is a festering pile of contradictory self serving rubbish
I can't believe I wasted 20minutes of my finite existance on this planet bothering to comment on this piece of crap.
MMCAT toxicity/neurotoxicity
It isn't too bad at all.
Methamphetamine is fucking toxic, it is an effective dual DA/SE cascader
there is no scientific term cascader what is a cascader (a transport reverser, a vmat inhibitor what?????
aswell as a slight reuptake inhibitor, Methcathinone and mephedrone are the other way around, they are decent reuptake inhibitors,
there is no evidence whatsoever for this [/COLOR]
with less of a cascading effect, particularly on dopamine as the ketone on the beta carbon is electronegative and won't fit through SER correcctly,
It doesn't have to be taken up by SERT, however the assertion that a ketone alpha to the phenyl prevents uptake is fanciful
despite the methyl being partially SE mimicking the cascade is still small, and the reuptake inhibition fairly abysmal for the same reason.
Thus the SE release is far less for both chemicals, meaning that : -
A) The cathinone is not take up into the presynaptic neuron (despite the methyl being a hydroxyl mimicker)
bullshit, the cathinone can diffuse into the neuron it is a weak base
where due to the methyl on the amine and alpha carbon, it inhibits MAO to a large degree, creating an MAOI effect.
there is little or no evidence that these cathinones are MOAI's other than being substrates like amphetamine
B) The dual release, and consequent DA "hoover" effect is significantly lessened, again resulting in less breakdown product damage in the neuron.
For the dopamine side of things, the molecules double bonded carbon makes it a far more effective DARI as opposed to releaser,
no evidence, those cathinone derivatives which are effective DAT inhibitors generally have more complex substitution on the nitrogen and a longer or more complex side chain
again product breakdown inside the neuron is far less and the overall subsequent monoamine depletion is less, leading to far lower depletion. Again as the molecular is primarily a reuptake inhibitor as opposed to a cascader MAO inhibition is not seen to anywhere near the same degree as amphetamines/methamphetamines, however you do notice a definate adrenaline increase after the drug has worn off,
Earlier the author said it was a strong MAOI - MAKE YOUR MIND UP MAN FWIW amphetamine is only a weak MAOI at normal doses
as the DARI action lessens and the amount of DA and consequently NA/A in the presynaptic neuron shoots up causing a cascade.
Evidence to support these claims.
Cathinones cause a fairly hefty DA mediated rise in body temperature, and the high is far more of a sustained one than the initial rush (cascade) of amphetamines. Cascaders are fucking evil in principle, I really can't understand why people have used and DA mimicked for so fucking long .
body temperature increases are also associated with serotonin release, so this is a baseless conclusion
MBDB is primarily serotonergenic with little to no DA effects, yet as soon as you put a double bonded oxygen on it, you get a much higher affinity for the NE and DA transporters and considerably lessened to almost nill reuptake into the SE neuron.
Dimethylamphetamine is nearly inactive, because the molecule is a shit DARI, and causes it's effects through cascading, whereas Dimethylmethcathinone is only 1.6x less active than methcathinone (with the extra steric bulk on the amine compensating for the lowered charge and bining) proving that the primary mechanism of the cathinones is reuptake inhibition as opposed to cascading.
a conclusion way beyond the evidence there is only limited data wrt to dimethylamphetamine primarily from the DEA who found it in some clandestine labs
The above information showing cathinones lesser affinity for the SE transporter also means that compounds such as 4 methoxy amphetamine, and 4 methyl amphetamine are rendered harmless as MAOI's as they do not get transported into the presynaptic SE neuron, hence no massive overheating.
wrong
Furthermore, the 4 fluorinated and 4 methylated versions of both methcathinone and cathinone will have barely any 5HT2b agonism, as SE, being a mood regulator amongst other things,
irrellevent
will have evolved to not accept electronegative groups there,
methyl is not electronegative so this is bullshit
otherwise NE/E would have a far larger effect, causing heart issues in humans.
bullshit again
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