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E TO A SCIENCE


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hey kids for all you wondering about what e really does to you- well here's what i figured out after all my years as a med student in the field of nueropharmacology...ill try to be as nonscientific as possible

first- when mdma is ingested into the blood stream, 1)broken down by the cyp-26b enzyme in your liver 2)broken down in your cerebral nuerons - when this happens, amino acids (the main ones being methionine and tryptophan) come to together to form your oh so favorite nuerostransmiiter, seratonin, when the concentration of seratonin builds up in the nuerons- it is released through protein channels down its concentration gradient, from there it travels through the plasma surrounding your nuerons and into other synaptic terminals (other nerve endings) in your brain from there it is picked up by transport protiens into the nueron whjere it is broken down to form a concentration gradient of (both chemical and electric- think back to your high school chemistry when molecules where broken down to form chanrged particals)- from there your nuerons fire sending siganls to your hypothalmus (nesr the middle-back of your brain0 the part responsible for emotion)making you feel oh so free

the recovery period- seratonin takes awhile to break down- like oh geez- four hours (any coinicidence- i think not)- and thats where your roll comes in- as long as relatively high levels of seratonin are running through your brain- yet it also takes even longer to build up- like up too a day-(to be able to feel a roll again)- but fully by 2-3 weeks (thats only for your veteran rollers- since your brain is getting used to the idea of being seratonin depleted- its stops producing as much - because- as to be explained later- its somewhat hazardous to your health)

ok- now here's why people are sayind e is bad- but first i have to explain the nuerotransmitter dopamine (the one responsible for your feelin on yabs- cocaine)- when you blow a line of coke same thing happens but dopamine is the nuerotransmitter - and its broken down in twenty minutes and rebuilt in about an hour or so-

both of these nuerotransmitters are running through your bain on a regular basis- both able to be picked up by the same transport proteins- BUT- when seratonin is picked up by by a nueron meant for dopamine- it will be broken down to form nydregen peroxide in your nueron- effectively killing it (think when you put that shit on an open cut)- and as you may know- nuerons are irreplacable-

ps to this- if high levels of both are in your brain (or when u do coke and e)- the seratonin has less of a chance to get where it needs to go- this is why coke stops your roll- and i know some of you may think that soem e pills have coke in the,- but just remeber how quickly dopamine is burned and rebuilt- even beofre you roll...

also- even from the first time you roll- your body builds up a life long tolerance to mdma- making it impossible to get that first roll back...ahh so sweet...and in terms of your mood- it actually helps- dec impulse urges- so people who roll seem to be just a lil more relaxed and laid back- so its not all a bad thing

other drugs: beware of dxm!!!- it acts on the same level as e- but causes the dissactioative effects seen with k- and is but it doesnt allow you sweat which i can't stress how hazardous that is to your health!!!- if u dont sweat your body heats up- your proteins denature- and u die!!-also it is broken down by the same cyp-26b enzyme in the liver- making combining the 2 a very deadly combo-

well thats all i think of for now- i think everyone should know what goin on in the body to make a concious shoice

luv ya all

jewelz

any q's please ask

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You are one smart cookie kid lol. No but seriously thank you for the information. I am just like you since i am a paramedic and

i like to read a lot of medical stuff.QUESTION????Do you know what happens if you roll and you are on Prozac and Wellbutrin. I read that it will not let you roll because of the MAO inhibitors.whats you view on this, what kind of info can you give me this. sou can email me at "NAMAX99@aol.com"

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to maxx 77:

shoot i just wrote the whole damn thing out and lost it- but here it goes again

seratonin (and dopamine) are condsidered amine nuerotransmitters- the level of amines in the brain can be altered by inhibiting the their re-uptake in the nerve endings (when nuerotransmitters are released-not all are takin up by the next cell over- instead some float back into the previous cell and are broken down- not allowing the full capacity to be recieved by the other nueron)-or by inhibiting the the activity of the enzymes which metabolize the amines- MAO (monoamineoxidases) are responsible for the reuptake and therefore dissolution of the amines- prozac, welbutrin, zoloft,etc...are exactly MAO inhibitors- they prevent the reuptake of the amines by the releasing cell-this is all good and dandy for depressed people- but when you roll- the same proteins that release the seratonin- also take it back up- so by blocking those channels- you wont roll when mdma is in your system- not all the seratonin can rush out at once instead it happens more slowly- so u may feel good- but not quite "oh - god damn this is good!!!" so my advice is stay away while rolling!!!!

but...after you roll it may be benficial to your emotional well-being and also to the health of your neurons- not only will it help u defeat the post-e blues by doing all that good stuff i said before (aka its job)- think back to when i was talking about hydrogen peroxide being produced from the uptake of seratonin to the wrong parts of cells- these protein channels are nonspecific to the amine they release or uptake- and therefore- niether is the medication- in effect, prozac, etc... may help prevent killing your nueron from the unwanted seratonin uptake by blocking those channels as well

i hope this helps

luv ya

jewelz

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the most successful people in life only look ahead to the great hpriszon of possibilities

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pre-loading-

one hour before- take 2 tablets of 5-htp tryptophan (this allows enough time for digestion and the building process for more seratonin - so close to your peak u have alot more of the good stuff to go)- watch it on the vitamins or anything with vitamins in it- most are coenzymes or antioxidants- that change the shape of the molecule either inc its productivity or tagging it aas a harmful chemical- mdma is considered the latter by your body- and thats why- even if u sit perfectly still during your roll- you may ache the next day (its your body's immune reponse to harmful chemicals- it swells- a histamine reponse to tell you not to do anything to drastic during its recovery to the chemical)- just drink a shit load of water before you have too- and the better mood your in- the more primed your body is to make seratonin- so be happy!!

post-loading

more tryptophan- prozac if u get it- if not st. john's wort!!- take as many vitamins if u can - and if you really feel like crap try a claratin or an antihistamine blocker

and dont roll for a few days too- this way u can give your body sufficient time to reapair itself as well as to build up seratonin levels- always remember- rolling straight for awhile will cause long term-depression- since your body will be used to the hight levels of seratonin in the brain itll think it needs to stop prducing more- 10 days is optimal b/w each roll for the heavy rollas out there- if not- 3-5 is ok

oh yeah make sure you got plenty of iron in your diet - esp girls- it helps with the post immune response- but u can od on it- so dont take more than recommended

hope its all helpful

luv ya lots

jewelz

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the most successful people in life only look ahead to the great hpriszon of possibilities

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Wow!!! Nice info.

Whats the difference beween maoi's & SSRI's?

because:.

One of the ways (if not THE way) MDMA enters the 5-HT

(serotonin) neuron is through the serotonin reuptake transporter. By

blocking 5-HT reuptake, you also seem to significantly block MDMA's

entry into the cell, thus probably reducing its effects. I haven't

seen any reports from humans about this, but I have seen microdilysis

data wherein an SSRI stopped the fenfluramine-caused increase in

extracellular 5-HT. On the other hand, Dave Nichols' group reported

that rats who were pretreated with an SSRI and then given MDMA still

responded as if they had been given MDMA. However, Nichols has more

recently concluded that the rats do not experience/respond to MDMA the

way humans do, since several substances which have no MDMA-like effect in

humans will substitute for MDMA in rats. Thus, I would not draw strong

conclusions from his SSRI+MDMA data.

Some people take SSRIs (selective serotonin reuptake inhibitors)

several hours after taking MDMA. Thus is not to prolong or potentiate

the MDMA trip but to prevent the possibility of a neurotoxin entering

the 5-HT cell and damaging the cell's axons. This has been shown to

happen in animals after relatively high or repeated doses.

Chronic use of SSRIs, as is done in the treatment of depression, seems to

reduce the effects of MDMA. That is, a higher dose of MDMA is required to

achieve the entactogenic effect.

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I want to go out blazing not fade away.

It's not just about the notes played, it's about the spaces in-between.

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Krakhed,bgirlxtce did a great job check this out for unreadable... which i think is what bgirlxtce was saying icon15.gif

MDMA is primarily a seritonergic (5-HTergic) drug. Serotonin

(5-hydroxytrytamine, 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.

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i'm very happy to see people doing their research. To be knowledgeable about what you put in your body is commendable. (i'm not alone in my novice study of drugs scientific effects and not the bullshit the media and other sources propagate, sorry off the subject, but) this weekend i rolled two days in a row, hard. i'm now experiencing a little post blues, this info helped me understand what is going on physiologically in my body. thanks for the help. these discussions reminded me of explaining the effects of ghb to young college kids at a house party.

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to jewelz: thank you, if your b-girlin, watch the headspins, not to hurt your critical knowledge, what is your area of study? is your research into these type of subjects personal interest or mainstream in your area of study?

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Awesome work, all of you! Nothing makes me more happy to be part of PLUR than to know that we understand what's happening to our bodies.

My friends call me Obi when we roll. They say that I've rolled enough to be the Obi Wan Kenobi of roll parties. I take what I've experienced over the time that I've done it, and just help them thru it.

Sometimes, the best thing that you can do for a friend doesn't come from a book. Sometimes the best thing you can do is just be there. If they're having a funky roll, or going too hard, you just being there and walking them thru it is the best med's of all.

Ok, that was -way- too Kodak moment...

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~~~~~~~~~~~~~~~~~~~~~~~

We are the music makers,

and we are the dreamers of dreams.

~~~~~~~~~~~~~~~~~~~~~~~

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to dede:

you hit the nail on the head- the seratonin depletion is exactly what causes the post-e blues- and taking 5-htp tryptophan (for all those worried about the 5-htp in front- there was a bad batch of real tryptophan made- so this is the new fda approved stuff) will definately help - especially if u don't eat alot of turkey or drink alot of milk (your two main natural sources of it)- if u don't have the tryptophan in your system you can't make the seratonin- its like trying to build a lego castle without legos-

ps. to this- if u ever here of people going cold turkey to quick smoking- which all of you should do now! (trust me it hits home when you see someone die infront of you of it and then u have to tell there family)- the nicotine in smoking actually causes something comparable to a five second roll- it tell your nuerons to release it for a brief period of time- and to get back to that feeling you take puff after puff of a cigarette- (ya ever smoke to calm your nerves- strange coincidence huh?)- but when people who quit cold turkey- they supply there body with the essential building blocks- to keep there seratonin levels stable- so they don't have to reach for that cigarette (oh yeah anyone here of ziaban- has anyone taken it and it kinda felt like u were rollin)- also- for all u trying to lose weight out there... it turns out that when your body senses food and glucose levels rise- a seratonin release is triggered- this is responsible for the nice tired, full feeling u get when u eat (not when u binge though- pure stomach sstretching pain takes over)- so if you wanna lose weight try taking- sam-e or st. johns wort to help ya out!- also- if you can invest in some maoi's (mono-amine-oxidase inhibitors)(aka prozac)- it helps keep the seratonin in your sytem longer- but dont take it while u roll- read the next post!!

luv ya

jewelz

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the most successful people in life only look ahead to the great hpriszon of possibilities

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  • 3 weeks later...
Guest clubkid77

Couple of mistakes i saw in some of the info.

1. Seratonin is not broken down into Hydrogen Peroxide. You have the right ida but its reversed. Its Dopamine is taken up the seratonin uptake, and attacked my MAO and broken down into Hydrogen Peroxide "burning the axon" This is because the 1/2 life of 5HT is shorter than that of dopamine. So basicaly AFTER you roll you have leftover dopamine in the synapses...

2. Prozac, Paxil, etc.. are NOT MAOI's this is VERY IMPORTANT they are SSRI's they work by blocking the uptake transporter. If your on SSRI's rolling is gona be tough if ir works at all cuz the SSRI has a high affinity to the transporter and MDMA aint gona work well.

3.On the abome mention of MAOI's these are EXTREMLY DANGEROUSE TO MIX WITH MDMA!!!!! Most people are NOT ON MAOI's they are older antidepressants. They work by inhibiting Monoamineoxidaise hence making you happier by slowing the breakdown of seratonin. This is DANGEROUSE to mix with mdma cuz your releaseing tons of seratonin and have little MAO to break it down, you get searonin syndrom and this can be fatal.

4. Taking an SSRI on the comedown helps if not completely prevents neurotoxicity by blocking the Uptake transporters. SSRI's are generaly active for 24 hours or so, so the uptakes for your seratonin axons are plugged and no free dopamine can get sucked up. Therefore the dopamine is brokendown normally and you dont fry yer 5HT Axons.

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Nice to see smart people on the boards! Ya see, the government doesn't need to protect us from whatever is out there, its the responsibility of everyone out there to educate themselves and ultimately decide for themselves!!! Party safe everybody!!!

<<<PEACE>>>

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"...I'm going to show them a world, without you. A world without rules and

controls, without borders or boundaries. A world where anything is possible.

Where we go from there is the choice I leave to you." -THE MATRIX

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just to back up clubkid77:

there was one very significant mistake:

Prozac, Welbutrin etc. are NOT MAOI's, they are SSRI's.

Some names of the more popular MAOI's are Nardil(phenelzine), Parmate and Marplan(isocarboxazid). For more information about MAOI's and thier interactions with MDMA see: www.erowid.org/chemicals/maois

Taking MAOI's with E is can be very dangerous.

For all of you out there that choose to...

Be Safe!

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