Psychedelia.dk

Ved ikke om denne har været posted før, men super fed info...

I'd like to clarify this whole mess on SSRI's and Ecstasy.
First the mumbo-jumbo. But it's important mumbo-jumbo, so please read it (or at least skim it.)
First of all, both SSRI's (Selective Seratonin Reuptake Inhibitors )(This includes Prozac, Zoloft, Paxil, and the like, and no, there really isn't any difference between them for our purposes here) and Ecstasy both have affinity (Meaning they will interact with and affect) the brain's seratonin reuptake transporters. Seratonin has an extremely important role in brain chemistry, as we all know, and regulates all sorts of things. SSRI's work by stopping the seratonin reuptake in the brain. The idea is for those that are depressed is that by reducing the amount of seratonin reabsorbed back into one's neurochemical system (and thereby increasing the amount of seratonin present), an increased amount of seratonin will help people feel better (With the help of therapy, of course. Very rarely will SSRI's work without the will and help of both the user and his/her doctor.)
Okay, now for the role of Ecstasy. Ecstasy works by flooding the synapse in the brain with seratonin. (again, as we all know.) Because Ecstasy uses the actual reuptake transporter mechanism to cause seratonin release, obviously any sort of chemical (Like an SSRI) blocking that mechanism (Which SSRI's do,) with a higher affinity for it (Like Ecstasy) will severely reduce or completely eliminate the affects of the Ecstasy. Ecstasy (beyond the threshold dose of ~40-60mg) without the presence of SSRI's generally drains a large amount of the brain's seratonin for 12-24 hours, and the brain has generally not reached full seratonin levels for up to a week afterwards.
SSRI's "downregulate" (inhibit the efficiency & the ability) of seratonin reuptake transporters. This means SSRI's affect your brain's seratonin system in a negative way as well as a positive way; the idea is that the positive effects outweigh the negative i.e. higher seratonin levels outweight the fact that your brain isn't using it as efficiently. Basically this means that even for MONTHS after one quits taking an SSRI, the brain is less efficient at using seratonin. Those who go off SSRI's and take E, even MONTHS later, will most likely have a REDUCED roll, regardless of the amount of E you take. Essentially, your brain's maximum of seratonin concentration (what makes rolling feel good) goes DOWN. So taking more only excacerbates the OTHER affects, like the dopaminergic (feeling speedy)and side-effects (like jaw-clenching).
END MUMBO-JUMBO
Okay, if you're still with me, that's the end of the medical crap. Most eveyone knows this, but a zillion people keep asking about trying E on SSRI's or tapering their meds and are missing the main point. So here goes.
Because SSRI's (prescribed for depression, as opposed to premature ejaculation, for example, because, yes, SSRI's almost always reduce ability to reach orgasm) are prescribed to help people assumed to have seratonin imbalances, most people on SSRI's (prescribed for depression) DO HAVE some sort of seratonin imbalance, tapering one's SSRI's (regardless of the time period, from cold turkey to a month or so) to do Ecstasy is A VERY DANGEROUS THING. It will often lead to an incredible low of depression. I'm talking absolute hell. I'm NOT trying to be anti at all, but I am speaking from my experience and the experience of many people I've talked with. It's just so dangerous for those predisposed to clinical depression (I'm not talking about being sad because your dog got hit by a car, I'm talking diagnosed by a doctor), and those predisposed or suffering clinical depression are often on SSRI's.
Please see my posting thread from my E-experience BEFORE you taper off your meds to do a serious and possibly dangerous drug. I'm not saying E will give you brain cancer or drain your spinal fluid or make your brain bleed or any other rumor garbage, I'm saying your emotions/feelings/mental stability has the severe possibility of getting MAJORLY FUCKED for days, or even a week. Trust me, it sucks.
Please see: http://www.bluelight.ru/ubb/Forum15/HTML/000228.html
Sorry for the huge post, but I just wanted to clarify things.
Quick Summary:
1. SSRI's (all of 'em) inhibit or prevent rolling
2. Those taking SSRI's for depression generally have seratonin imbalance issues
3. Taking E really fucks up your seratonin for a while.
4. For many, this isn't a problem
5. BUT, for those on SSRI's, it may very well be a VERY serious problem.
6. Rolling after being on SSRI's for any significant amount of time will most likely be reduced.
7. Think AT LEAST twice about it
Some warning signs you may be more likely to have a problem when you take E after being on SSRI's (collected from experience)
1. After missing doses (1 day-several days-week-whenever) you go through a withdrawal (i.e. nauseau, "brain bounce"->electro-shock sensations in your head when you move suddenly, or vertigo->feeling like you don't have balance or are "falling up" or sideways.
2. You were/are on a relatively high dose of your med
3. You were/are prone to anxiety attacks associated with your depression
This doesn't cover them all, and even if you fit the bill, you may not have a problem taking E.
BOTTOM LINE: Be very very very careful. Knowledge is everything. This post doesn't apply to everyone; some people can stop their meds and roll and be fine. Some can't. That's just the way it is. I'm not telling you not to. Just please be careful. The last thing I want is for the uninformed to go through the hell I and many others have gone through. Have fun, but most of all, be safe.
Peace
-NYTFLY

Jeg har ikke set den før.

- Men IMO er det en alt for lang og alt for skabsvidenskabelig tekst, til et meget kortfattet budskab...

LAD NU VÆR MED AT TAGE STOFFER NÅR I HAR EN DEPRESSION!!!!! - især ecstasy og psychedelika.

Synes den er udmærket.. Mener den er fra http://thedea.org ? (NEJ det er ikke DEA's hjemmeside..)
Sagen bliver ihvertfald nævnt, forklaret og diskuteret derpå under Neurotoxicity.

The Prozac Misunderstanding

There are also some 'exotic' neuroprotective regimens using prescription drugs. SSRIs such as Prozac or Paxil can protect against neurotoxicity by preventing access to the inside of the axon. However, these drugs also partially block MDMA's effects. There has been a popular belief that taking an SSRI like Prozac up to six hours after taking MDMA can prevent any neurotoxicity from occurring. This is untrue. Here's a graph from the research that inspired this idea:


[32]

The height of the bars indicates how much serotonin each test group's brains had one week after the experiment. Lower levels of serotonin indicate neurotoxicity has occurred (since serotonin is made by and stored in the serotonin axons.)

Although giving the rats Prozac (fluoxetine) up to six hours after the MDMA prevented some of the damage, it was only a partial solution. Even at three hours, significant damage appears to have occurred. If there were reason to believe that somebody was beginning to suffer neurotoxic damage (high dose, heatstroke) an SSRI might be an effective 'rescue' medication to limit the extent of the damage. However, because 'post-loading' with an SSRI is only partially effective, I am of the opinion that the first line of defense against neurotoxicity should be to prevent the 'neurotoxic scenario' from happening in the first place through moderation and preventing overheating. Antioxidants are more practical then SSRIs since they can be taken in advance (providing some protection from the start) without interfering with the desired MDMA high (as an SSRI would.)

A more radical approach is the use of the MAOI L-Deprenyl (Selegiline), which has proven to be extremely effective in preventing MDMA neurotoxicity in lab animals and does not interfere with MDMA's desired activity. In theory, Deprenyl is arguably the most potentially effective neuroprotective regimen, but more work needs to be done before any substantive statement on safety can be made. Several users have reported taking Deprenyl before MDMA with little or no effect (one user reported that Deprenyl made the MDMA dose uncomfortably 'speedy'.) In order to use Deprenyl as a neuroprotectant, a moderate dose (perhaps 5 mg) should be taken before the MDMA. This combination may prove to be quite dangerous! People experimenting with it should be medically knowledgeable and have a support system in place to provide immediate emergency medical attention if a problem arises.

[32] Schmidt CJ "Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine" J Pharmacol Exp Ther, 1987; 240(1):1-7 (Abstract: http://www.erowid.org/references/refs_view.php?ID=931)

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