Shrooms + MDMA

[RedRainDrop]

first off, pure mdma is a fuckin safe drug, probly safer than eating mushrooms. so shut the hell up, because you obvously dont know shit.

Is That why you can OD, from MDMA, and noone has ever ODed on mushrooms?

[sanfrancyan]

Harvesthetic

you just made yourself the most ignorant jackass on this website.

first off, pure mdma is a fuckin safe drug, probly safer than eating mushrooms. so shut the hell up, because you obvously dont know shit.

Dude,

MDMA is noero-toxic, it can be VERY bad for you.. Shrooms are not, harmfull to the body nor do they pose a significant lasting effect on ones psyche if the user is of sound mind to begin with.

You should do some research before you jump all over someone for being ignorant. Because YOU obviously dont know much about the subject either.

http://www.erowid.org/chemicals/mdma/mdma_info7.shtml
MDMA Neuropharmacology

by Lamont Granquist



MDMA is primarily a seritonergic (5-HTergic) drug. Serotonin (5-hydroxytryptamine, 5-HT) is one of the major neurotransmitters in the brain, and is synthesized from tryptophan through the intermediate 5-hydroxytryptophan. It is synthesized in 5-HT neurons, and stored in synaptic vesicles. These vesicles release their 5-HT into the synaptic cleft in response to the firing of the 5-HT neurons. In the synaptic cleft the 5-HT neurotransmitter excerts its action on both pre- and post- synaptic receptor sites (sites on the 5-HT neuron itself, and on the neuron which it is communicating with.) 5-HT is then taken back into the 5-HT neuron via the synaptic membrane 5-HT transporter (aka "reuptake pump"), where it is again stored in the synaptic vesicles. 5-HT is metabolized primarily by monoamine oxidase (MAO) into 5-hydroxyindileacetic acid (5-HIAA).

Serotonin is thought to be responsible for many psychological (and physiological) states including mood and sleep. It has been particularly associated with major depression and obsessive compulsive disorder, and drugs to treat these disorders tend to effect 5-HT (although things are not quite clear-cut).

MDMA blocks the reuptake of 5-HT, similarly to SSRI (serotonin specific reuptake inhibiting) anti-depressants such as fluoxetine (Prozac), sertraline, and paroxetine. Unlike those drugs, however, MDMA appears to enter the neuron, either through passive diffusion or directly through the reuptake transporter, and causes the release of 5-HT. This release is calcium-independent (i.e. independent of the firing of the 5-HT neuron) and appears to come from cytoplasmic stores rather than from synaptic vesicles. The released 5-HT then enters the synaptic cleft through the 5-HT transporter. MDMA thus acts on 5-HT similarly to the way amphetamines act on dopamine.

It is thought that this efflux of 5-HT into the synaptic cleft, and the subsequent action of this 5-HT on pre- and post- synaptic binding sites is central to MDMA's neuropharmacology. MDMA, however, has micromolar potency for the serotonin 5-HT2, muscarinic M1, alpha-2 adrenergic and histamine H1 receptors. Agonist (stimulation rather than blocking) properties at the 5-HT2 receptor have been found to fairly universally be associated with "classical" psychedelic drugs such as LSD, psilocybin and mescaline. It is possible that some of MDMA's "psychedelic" effect occurs because of interactions with this receptor. The alpha-2 adrenergic receptor may be associated with some of the carciovascular effects of MDMA. MDMA also releases dopamine which may be central to both its psychological action and to its neurotoxicity in animal studies. Pre- treatment of an animal with a drug which blocks dopamine release will also block MDMA neurotoxicity. Also, serotonin specific releasing agents which are non-dopaminergic have been synthesized and been found to be devoid of MDMA's neurotoxicity in animals, they have also been found to be devoid of MDMA's psychological effects. MDMA tends to indirectly *inhibit* the firing and release of dopamine in nigrostriatal dopamine neurons (neurons projecting from the substantia nigra to the striatum) due to local 5-HT release.

MDMA doses of 20mg/kg in animals can reduce levels of tryptophan hydroxylase, which is the rate-limiting enzyme in 5-HT synthesis. It is thought that this occurs because of oxidative stress which MDMA places on the neuron. This oxidative stress might occur through several possible channels (the metabolism of MDMA into a toxic Quinoid, 5-HT derived toxins, 5-HT mediated cellular events, or temporary inhibition of monoamine oxidase) and the exact mechanism is presently unknown. It is thought that this oxidative stress also leads to the neurodegenerative destruction of 5-HT axons which is observed to occur with large doses of MDMA in animals. Anti-oxidants, anti-dopaminergic agents, agents which block intracellular calcium increases and pre- or post- treatment (up to 6 hours) with fluoxetine all block MDMA's neurotoxicity. Research ontinues on the exact mechanism of MDMA-induced toxicity.

In summary, MDMA effects 5-HT similarly to the way that amphetamines effect dopamine, by inhibiting the reuptake and causing the release of 5-HT. This effect is somewhat similar to the effect that SSRI anti-depressant drugs have. It also effects the 5-HT2 (psychedelic) and alpha-2 adrenergic (cardiovascular) receptor sites. Also, its effects on dopamine appear, at this point, to be involved both with its neurotoxicity and psychological effects. For more information, see:

Rattray-M. "Ecstasy: towards an understanding of the biochemical basis of the actions of MDMA." Essays in Biochemistry. 26:77-87. 1991.

And for general info:

Synder, Solomon H. "Drugs and the Brain." Scientific American Books. 1986. (slightly out of date, but a good introduction).

Cooper-JR, Bloom-FE, Roth-RH. "The Biochemical Basis of Neuro- Pharmacology." Oxford Uniersity Press. 1991 (6th ed). (the bible for grad students)

[sanfrancyan]

pOwNeD :thumbsup:

[bedake]

actually the claims of adam's neurotoxcicity has been disputed as much as it has been claimed pwned cancled and you spelt it wrong, it isnt powned


sure that may be a scientific paper about how bad it is, theres many just like it which say it isnt toxic

[sanfrancyan]

actually the claims of adam's neurotoxcicity has been disputed as much as it has been claimed pwned cancled and you spelt it wrong, it isnt powned


sure that may be a scientific paper about how bad it is, theres many just like it which say it isnt toxic

then post one :dance: dont just say theres one. go find it and post a link. :thumbsup:

i love MDMA, but all the research i read points to neuro-toxic. Id love to see a papre saying otherwise.

and it can be spelled however you want you still knew what i meant. :stoned:

[yoda]

its called hippy flipping around where i am too, and i say go for it

[bedake]

ve heard E is "neurotoxic" - what does that mean?
'Neurotoxic' is applied to any substance which causes temporary or permanent changes in the brain. Animal tests have shown MDMA to be neurotoxic in large amounts. Nobody is sure at what level MDMA becomes neurotoxic in humans,

thats good enough for now, i got homework to do lol

but anyways i was reading awhile ago that the amount it takes for it to be a neurotoxin in animals is the equivalent of more than anyone will ever take, like absurdly more

http://www.erowid.org/chemicals/mdma...oxicity3.shtml

DMA Brain Scans Showing Neurotoxicity Discredited
Several Articles Highlight Questionable Science
by Erowid, April 2002


In another blow to the US Government's credibility as drug information provider, the Johns Hopkins brain scans which have been used to 'prove' MDMA causes brain damage have been called flawed by independent researchers and editors of the magazine New Scientist.

* New Scientist challenges the ethics and reliability of science-for-politics
* New Scientist documents errors and data obfuscation in compromised reasearch
* Toronto-based researcher Stephen Kish questions reliability of available PET scan data
* Other top PET scan experts criticize the PET scan data
* NIDA's credibility suffers once again

Under the cover story "E is for Evidence", the British science-oriented magazine "New Scientist" published a set of articles and editorials related to this topic in April 2002, denouncing the use of the questionable scientific data in the war on ecstasy consumption. There are several articles in the New Scientist, but most of them can be found following the links below.

The New Scientist article is a well-balanced, but critical, look at the issue of overstating the certainty of findings of brain damage in ecstasy users. "We are not saying that ecstasy is harmless to brain cells. It might not be. But the jury is still out. Which means scientists must resist the temptation to turn their always complex--and sometimes flawed--findings into simple scare stories in pursuit of grants and headlines."

It is refreshing to see a mainstream technical magazine publishing critiques of the science-for-politics which has compromised the credibility of government-sponsored science in the eyes of many. Historically, it has been left to fringe groups to criticize the fundamental system of peer-reviewed "science" and the often unscientific politics and economics which govern publication. The New Scientist describes how journal editors have joined in the War on Drugs by turning down articles which do not support the "anti-drug" view, including papers which report "no-effect" results.

It's an open secret that some teams have failed to find deficits in ecstasy users and had trouble publishing the findings. "The journals are very conservative," says Parrott. "It's a source of bias." Parrott himself has had two papers of this sort turned down. -- New Scientist, April 2002.

What is most troubling, perhaps, is how often "Science" has been misappopriated for the moral crusade against recreational psychoactive use. The now debunked moral panics surrounding LSD and chromosome damage, 'reefer madness', cannabis and brain damage, "crack babies", and most recently the ecstasy 'holes in your head' campaign, have all come from premature, controversial, or invalid science foisted onto the public by overeager, overfunded Drug Warriors.

Two years ago, then NIDA director Alan Leshner launched an anti-ecstasy campaign based on images from flawed PET-scan research conducted at Johns Hopkins. The campaign's trademark was a stylized image of two brain halves, side by side, with the darkened hemisphere marked "brain after ecstasy". Unfortunately for the public, NIDA has once again allowed politics and morality to trump their science. The US has spent millions of dollars pressing its "brain after ecstasy" images in widely-distributed postcards and online. Even months after NIDA learned of the data problems, and weeks after the Ricaurte and McCann PET scan studies were publicly discredited, NIDA is still pushing them as unadulterated 'fact' on their web sites (nida.nih.gov and clubdrugs.org).




The centerpiece of NIDA's Anti-Ecstasy Campaign, now widely considered invalid.

Stephen Kish's article in "Pharmacology, Biochemistry, and Behaviour" published in April, 2002 investigates the reliability of the PET brain scanning showing damage. He concludes that the studies completed to date include serious methodological flaws, huge variations between individuals tested, use of non-serotonin specific tests, lack of test-retest reliability data, and other invalidating assumptions about the types of tests used. He says that, based on the brain scan research to date, "it cannot be assumed that ecstasy exposure [causes] a chronic serotonin deficiency condition."

"Because of the serious methodological concerns in the PET measurement related to the high scatter of the values for the control and drug groups and lack of testâ??retest results, the data derived from the McCann investigation can only be considered, at most, â??â??semiquantitive.â??â??" -- Kish SJ, April 2002

Another paper currently in the process of publication also examines the PET scans, showing that the serotonin binding levels recorded for even extremely heavy ecstasy users (estimated 500mg average dose between 70 and 400 times) in the 1998 McCann & Ricaurte study were typical for controls in other studies using the same chemicals (ligands) and scanning techniques. As one PET researcher described to us, the Ricaurte team didn't have the necessary skills required to competently analyse the data. They were undertrained in the technically demanding field of PET Scanning and their results reflect both a lack of ability and a failure to notice when their results were coming back wrong.

"There are no holes in the brains of ecstasy users," says Stephen Kish, a neuropathologist at the Center for Addiction and Health in Toronto. "And if anyone wants a straightforward answer to whether ecstasy causes any brain damage, it's impossible to get one from these papers." Marc Laruelle, a Columbia University expert on brain scanning probes, agrees: "All the papers have very significant scientific limitations that make me uneasy."

According to both experts, the key flaw in the 1998 study is the sheer variability of the measurements. Some control brains performed up to 40 times better than others, and even some of the ecstasy brains outshone control brains by factors of 10 or more -- a level of scatter that both experts say is unprecedented in this type of study. -- New Scientist, April 2002

The New Scientist and Pharmacology, Biochemistry, and Behaviour investigations of flawed research practices offer a breath of fresh air in the ongoing debate about ecstasy's effects on the brain. Perhaps better reporting and editorial leadership will emerge over time, in spite of the political pressures faced by peer-reviewed journals.

[sanfrancyan]

i read about that. neuro toxicity in animals happens at what would be human recreational doses.

its mentioned in the article i posted.

[bedake]

double post i know but i wanted to make sure this was seen:

http://www.guardian.co.uk/drugs/Stor...686283,00.html

http://www.mapinc.org/drugnews/v02/n753/a12.html


3 articles huh huh huh dawg

[sanfrancyan]

hmmm.......


thats interesting.......