what is E?

[*STARFISH*]

ok so what exactally is E?
that sounds like the dumbest question ever
yes i know its MDMA
but what is MDMA?
(and please dont say C11H15NO2 because that means nothing to my nonscientifically educated brain)
just curious.

thanks!

edit: i cant spell

[candytabi]

hhmm.... u wanna know evrything? www.dancesafe.org
all i can say is that I'm too lazy to write all that shit down :c-tard:

[g l o w]

its a pill which doesn't taste like sushi, or smell like perfume.. LOL
m i right?! i can't be wrong!!! LOL... j/k

its a drug that brings u thru a wicked journey..
but on the other hand.. it kills u slowly.. and DOES ruin ur life...

at the time u r at ur peak having the most fun, thats the time when its hurting ur body the most..

but i would say this is a interesting drug...

[Veni*C]

teamhardcore has some good info on it.....
i did all my research on line on different websites so i could compare and see what was b.s.

ill be getting some good info soon...ill send it to ya when i get my hands on it... :kimmie:

[SEAN!]

its the meaning of life...


rave on

[*spacecase*]

^ ha ha

[Bevvy Swift]

go to erowid.org, they have everything you need to know about mdma and many other frugs.

[Iokua]

gotta love those frugs hey cheez?

[BenGiovanni]

methylene dioxy methyl AMPHETAMINE....

[MC Hammered]

Check the archives Christine.

I think someone else asked the same thing a while back and paragraphs were typed about it by myself and others.

[Goat]

eorwid is bullshit.

MDMA, MDE,MDA etc are all part of the Amphetamine family.
i'll post more later, i'm just finishing up a 10page report on it's origins, what it is, etc for a class.

in breif.

It's an Amphetamine, part of the speed family.
Medicinally, not usually recommended unless in extreme cases, it's been used as a dieting and attention focusing agent.

People with a.d.d. have used methamphetamines (of one sort or another) in miniscule amounts to help focus.

some side effects include: loss of appetite, nautiousness, anxiousness, paranoia and so forth.
it was first implamented (MDMA) to psychatry patients as a way to break down emotional walls --> extreme rush of euphoria overcoming emotional walls...in general....

blah, i'll post my report when early next week.

[BenGiovanni]

heheh
in other words
e is good HAHA

[BenGiovanni]

Mde; MDEA; Eve
Methylene-dioxy-Ethylampphetamine
In the chemist book "pihkal" Mde is like E but also renders your motor skills like a drunk feeling, meaning you get an intoxication feeling straight up instead of the akward high of e

[Mr.Wrong]

Originally posted by Iokua
gotta love those frugs hey cheez?

hahah
who doesnt

[Knigel]

"e" is no longer MDMA, "e" is generally a combination of many different substances passed off in a pill. "E" used to be MDMA but it has been degraded as it evolved in the party scene. To learn about MDMA you may want to check out the dance safe slide show http://www.dancesafe.org/slideshow/ or some of the links in my sig.

[PokemonMasta]

fuck noone does E anyone its all about doing jib

[decypher]

E lights ur brain's neurotransmitters up like a christmas tree

[pbreak]

Originally posted by Bozga
Mde; MDEA; Eve
Methylene-dioxy-Ethylampphetamine
In the chemist book "pihkal" Mde is like E but also renders your motor skills like a drunk feeling, meaning you get an intoxication feeling straight up instead of the akward high of e

it's the 5th letter of the english alphabet capitalized...

but as per the quote - a lot of times MDE is made by mistake since the only chemical difference between the two is an ethyl (CH2-CH3) group in place of a methyl group (CH3)

there is a LOT of info about all of this stuff, a lot of it is completely wrong or at least slightly wrong so be wary when doing research.

The following info is straight from a neuro-psycology researcher at UBC who did a rather informative lecture at my residence when i was living at UBC:

The shape of the MDMA molecule allows it to bond (permanently) with seratonin receptors in your brain. As many people know, seratonin is an important neuro-transmitter (signal transmitter) in your brain and the receptor is what recieves and relays the transmitted "signal" to other parts of your brain. Having numerous seratonin receptors continuously stimulated is what makes you feel high. Soon enough, your brain catches on that their is a foreign substance doing things it shouldn't and your brain starts to flush it out of your system. Unfortunately, as mentioned above, the MDMA is permantly bonded to the receptor so the only way to get rid of it is to flush out the receptor as well (i.e. killing brain cells). Your brain is able to recover from this damage, but only to a certain point - the toxicity limit, which is approxiamitely 1mg/kg of body weight, thereafter not all of the cells will be replenished. This is why for heavy users there is fear of long term damage to short term memory amongst othere things.

This research was performed on monkeys (don't worry, they were probably happy!) and she actually showed us MRI scans of their brains (namely the receptors) as the drug progressed and before and after pictures of the receptors as well.

As far as E not being MDMA... the vast majority of pills still have MDMA in them (believe me, i know the diffence), but obviously the amount varies greatly and I'm sure some pills don't have any at all.

good enough? anything to add/change there Goat?

[sidekick]

mmm i like christmas

[decypher]

^^ sounds about right... and MDMA and MDA are the common drugs used in pills.. obviously in varying amounts, and usually accompanied with K, caffeine, ephedrine, Jib, PCP, tylenol, filler etc etc etc

[Knigel]

Originally posted by pbreak


it's the 5th letter of the english alphabet capitalized...

but as per the quote - a lot of times MDE is made by mistake since the only chemical difference between the two is an ethyl (CH2-CH3) group in place of a methyl group (CH3)

there is a LOT of info about all of this stuff, a lot of it is completely wrong or at least slightly wrong so be wary when doing research.

The following info is straight from a neuro-psycology researcher at UBC who did a rather informative lecture at my residence when i was living at UBC:

The shape of the MDMA molecule allows it to bond (permanently) with seratonin receptors in your brain. As many people know, seratonin is an important neuro-transmitter (signal transmitter) in your brain and the receptor is what recieves and relays the transmitted "signal" to other parts of your brain. Having numerous seratonin receptors continuously stimulated is what makes you feel high. Soon enough, your brain catches on that their is a foreign substance doing things it shouldn't and your brain starts to flush it out of your system. Unfortunately, as mentioned above, the MDMA is permantly bonded to the receptor so the only way to get rid of it is to flush out the receptor as well (i.e. killing brain cells). Your brain is able to recover from this damage, but only to a certain point - the toxicity limit, which is approxiamitely 1mg/kg of body weight, thereafter not all of the cells will be replenished. This is why for heavy users there is fear of long term damage to short term memory amongst othere things.

This research was performed on monkeys (don't worry, they were probably happy!) and she actually showed us MRI scans of their brains (namely the receptors) as the drug progressed and before and after pictures of the receptors as well.

As far as E not being MDMA... the vast majority of pills still have MDMA in them (believe me, i know the diffence), but obviously the amount varies greatly and I'm sure some pills don't have any at all.

good enough? anything to add/change there Goat?

Actually can you post a study that proves this information?



One that wasn't retracted?

[pbreak]

Originally posted by Knigel



Actually can you post a study that proves this information?



One that wasn't retracted?

this isnt' her paper but it does a good job:

"NEUROBIOLOGY OF ECSTASY
The main neurological effects of Ecstasy are medical in increasing serotonin (5-HT) extra cellular level in the central nervous system, especially in striatum and hippocampus, as shown in rat brain homogenates (Doman et al, 1991). This extra cellular serotonin increase is due to presynaptic end nerves release of serotonin and its uptake blocked by MDMA. In addition, MDMA inhibits competitively serotonin catabolism by mono-oxydase A (MAO A) which is responsible of extra cellular degradation. (K = 22mM) Concentration response curves for MDMA inhibition of MAO show an IC50 44mM versus an IC50 of 370mM for MAO B. So MDMA is a preferential inhibitor of MAO A, (increasing extra cellular 5HT). Reciprocally fluoxetine (Prozac) inhibits MAO B (IC50 = 80mM) which increases the intra cellular content of serotonin (Leonardi, 1994)).

Ecstasy damage on brain sertonic neurones in humans have been recently studied (McCann, 1994): 30 MDMA users and 28 controls have been compared for the measurement of biological and behavioural indexes of central 5HT function. Measure obtained after two weeks of drug abstinence included monoamine metabolites in cerebral spinal fluid (CSF) and personality tests in which serotonin is implicated (ie. impulsiveness and agressivity) gave the following results: lower levels of 5 hydroxy indolacetique acid in MDMA users than in controls (p=0.01). Lower scores on personality measures of impulsiveness (p = 0.04) and indirect hostility (p=0.09) in users. These results mean that the serotonin brain system has a role in modulating aggressive personality traits and acting aggressively.

Metabolism and Analysis of MDMA
In microsomal preparations, MDMA has shown to be dementhylated by the enzyme debrisoquine hydroxylase in dihydroxymethyl amphetamine (DHMA) this enzyme belongs to the cyt.p450 system. Incubation of MDMA isomers with human microcosms has demonstrated that their demethylation is deficient in some poor metablizer phenotypes. This may induce genetically determined difference in toxicity (Tucker, 1994)

Amphetamine derivated molecules are relatively stable in blood and urine so they can be detected in non-degraded form by gas on H.P.L chromatography and by mass spectrography (Rudler, 1988). The immuno-enzymatic method in urine provided by Roche Laboratories permits a group molecule detection. The delay for detection in urine is about 24-48 hours.

TOXICITY OF ECSTASY
The direct toxicity of MDMA in several animal species is now well established; human toxicity is still being investigated. In rodents, myelinic degeneration of the central nervous system, in 5HT1 terminal nerves, has been demonstrated. (Dornan et al, 1991) In dogs, overdosage resulted in death from hypothermia, hyperbactacidemia, candia hypertension and tachycardia (Dawis, 1994).

In male rats, the repeated septemic administration of MDMA produced a rapid, transient outburst of copulary behaviour, also ejaculation latency and the post-ejaculatory interval were lengthened (Darnan et al, 1991)

In humans, MDMA toxicity could be distinguished in immediate or in short-term actions and delayed actions, concerning mainly mental disorders. In fact, effects could be intricated so that unexpected pathologic disorders emerged.

Descriptions of systemic toxicity induced by MDMA are now widely available. Classical symptoms are: dilated pupils, agitation, excitement, delusions, incontinence, tachycardy, depression and death by heart failure or arythimiae breathing problems (Cregg, 1994).

Some particular cases have also been described:

one case of a patient with intra-cranial haemorrhage was associated with MDMA ingestion (Hughes, 1993)
two cases of aplastic anaemia following exposure to Ecstasy have been reported. Anaemia regressed spontaneously 7-9 weeks after presentation. These results, after studies on bone marrow culture, suggest that drug toxicity is transient or affects a mature cell progenitor as its target . (Marsch et al, 1994)
another case concerned a man who was admitted with hypothermia, rhabdomyolysis disseminated intravascular coagulation (Tehan et al, 1993).
Another effect of MDMA neurotoxicity could be sleep disturbance. All night polysomnograms of MDMA users compared to those of controls have shown a decrease of some 19 minutes total sleep in users; stage 2 sleep was principally affected. This neurotoxicity is thought to involve serotonin neurones (Allen et al, 1993). "

or read it here:

http://casr.adelaide.edu.au/T95/paper/s16p4.html

[Knigel]

Ok Pbreak lets turn this around instead of playing the usual back and forth game. Lets have some actual fun! Of course if you want to play?

Since you seem curious and like information as it's indicated by your posts in this thread I'm sure you'd want to pass around correct information...

So this is where it gets fun...

Take the article you've posted and become a devils advocate, try to debunk as much information as possible and find the correct info to replace it. Find as many flaws as you can. Start by asking yourself different questions. "Is there any other reports that contradict this one?" "Can I find other articles that back this up?" "What is the authors reputation and what do they have to gain by writing this article?" "Where is she getting her information and what can I find out about these authors?" "How much evidence can I find either way to confirm or question actual neurotoxicity of MDMA and how much is theory?" "Is there any words that could be misleading such as using the term ecstasy instead of MDMA?" "Where can I find any case reports, what was the full story behind them?"

There are alot of questions that you can ask yourself, be creative.

So lets play and if anyone wants to join in all the better!

[aurora]

Originally posted by pbreak
but as per the quote - a lot of times MDE is made by mistake since the only chemical difference between the two is an ethyl (CH2-CH3) group in place of a methyl group (CH3)

This could only happen if the chemist couldn't distinguish between methylamine and ethylamine - which are used to aminate the 3,4-MDP2P into MDMA and MDE, respectively. They are two different chemicals, and there is no way a chemist could 'accidentally' make MDE instead of MDMA.

there is a LOT of info about all of this stuff, a lot of it is completely wrong or at least slightly wrong so be wary when doing research.
The following info is straight from a neuro-psycology researcher at UBC who did a rather informative lecture at my residence when i was living at UBC:

Be careful trusting someone's opinion just because they have papers. Just because someone with credentials tells you something doesn't make it true. I had a debate with someone who was getting his doctorate about MDMA's effect on dopamine. He maintained that MDMA was toxic to dopamine neurons, and I suggested that he was basing this on the Ricaurte study which was later retracted due to the fact that Ricaurte gave the monkeys METH and not MDMA. But he was convinced, that because he learned this at school, that he was right... until a psychedelic expert came up and said the exact same thing I was saying.

The shape of the MDMA molecule allows it to bond (permanently) with seratonin receptors in your brain. As many people know, seratonin is an important neuro-transmitter (signal transmitter) in your brain and the receptor is what recieves and relays the transmitted "signal" to other parts of your brain. Having numerous seratonin receptors continuously stimulated is what makes you feel high.

First of all, MDMA's action is not permanent, it is metabolized out of the system rapidly. MDMA is metabolized in the body within a few hours.

Furthermore, MDMA may have some affinity for 5-HT receptors (1 and 2 being the subtypes), but it has been shown that R-MDMA has higher affinity for these receptors than S-MDMA, which is thought to be the more active of the stereoisomers. Since most MDMA is racemic, the less active R-MDMA would have preference for the 5-HT receptors over the S-MDMA, meaning that 5-HT receptor agonism likely plays little part in the MDMA experience (if MDMA was a potent agonist of 5-HT2 receptors, it would likely exhibit more hallucinogenic effects)

MDMA is thought to bind to the serotonin uptake transporters - temporarily - and cause the release of serotonin into the synapse. The serotonin is what interacts with the 5-HT receptors, and this overstimulation causes the MDMA feelings of euphoria, empathy and warmth.

Soon enough, your brain catches on that their is a foreign substance doing things it shouldn't and your brain starts to flush it out of your system.

MDMA is primarily metabolized in the liver. This is a natural course of any chemical that enters the body, be it psychoactive or whatnot. The brain does not 'flush it out', the liver just does its job, which takes a certain period of time, and as the levels in the bloodstream drop one feels a comedown.

Unfortunately, as mentioned above, the MDMA is permantly bonded to the receptor so the only way to get rid of it is to flush out the receptor as well (i.e. killing brain cells).

MDMA has not been show to 'kill brain cells'. If MDMA over 1mg/kg was doing this sort of damage to people's brains, we would be dead. Honestly. MDMA is not destroying serotonin receptors.

Your brain is able to recover from this damage, but only to a certain point - the toxicity limit, which is approxiamitely 1mg/kg of body weight, thereafter not all of the cells will be replenished. This is why for heavy users there is fear of long term damage to short term memory amongst othere things.

1mg/kg of body weight is a very, very small dose of MDMA. It is not far above threshold. Heavy users.... you mean people who drop ONLY half-caps? 1mg/kg is not likely to be approaching any level of neurotoxicity, if that even does exist.

The actual extent of damage caused by MDMA is still inconclusive. It is true that MDMA does reduce brain serotonin levels after the experience, which will climb to normal within a period of 1-4 weeks. This depletion has been shown to be completely eliminated in rats when MDMA was administered concurrently with antioxidants, suggesting oxidative stress to be a mechanism of MDMA neurotoxicity.

One study, involving former heavy users with an average lifetime use of *799 DOSES*, tested their serotonin levels 18 months after their last dose of MDMA. Interestingly enough, these people had serotonin levels comparable to non-users.

This is not to suggest that MDMA may not be doing damage, but there is no brain cell erosion going on. With moderate use, the risk of major damage is not as high as many would like you to believe.

One must also remember that when taking "E" they are risking other sorts of damage due to the adulterants that may be present. "E" is a lot riskier than pure source MDMA.

This research was performed on monkeys (don't worry, they were probably happy!) and she actually showed us MRI scans of their brains (namely the receptors) as the drug progressed and before and after pictures of the receptors as well.

And... there was a lot of receptor activity? Of course brain scans are going to be different during drug activity and afterwards. Many people 'colour' scans in a certain way too, to make damage seem more prevalent. A lot of people have a lot of money and life invested in making MDMA sound dangerous, and they will go to great and misleading lengths to do so. Read about Ricaurte's mislabed MDMA-methamphetamine study on dopamine, if you want to know what I mean.

[Knigel]

Wicked reply Aurora if anyone is interested in the Ricaurte controversy with the MDMA/METH mix up and alot more you might be interested in this link: http://www.maps.org/mdma/studyresponse.html#foia012804