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SSRI's and Ecstasy: The Final Word (Hopefully)

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NYTFLY

Bluelighter
Joined
Apr 26, 2000
Messages
1,796
Location
Berkeley, CA, USA
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
 
Thats a incredible piece of information you just assembled.
In a depressive post roll state at a time when I was feeling miserable about life, and in the midst of a definite nervous breakdown.
After 12 hours or so of horrible depression. I took about 300 mg. of 5-htp. And two hours later, I was feeling I could at least cope again.
However, this will not be the case for everyone in all situations. But at the time it helped.
Of coarse 5-htp "theoretically" works by boosting the production of serotonin.(In a general description). And prozac works as you stated in your post. And people on on a SSRI for reasons stated in your post. The use of 5-htp may not be suitable for those on SSRI. And they definitly never should be combined, because in higher dosages that is dangerous.
But the 5-htp suppliments may help
applesbliss
------------------
***-apples-powered
 
Finally an informative and intelligent post that out-shines some of the crap I've seen lately. Thank you.
What's the bet that in a few days or a week someone posts a question asking about taking SSRI's and XTC?! Oh well, you can only try.
 
NYTFly--
*awesome*. Couldn't have said it better myself.
*bump*
------------------
be safe--
raverdoc
 
Question :
SSRI's (theoretically) prevent dopamine from being brokendown at the seritonin axom when post rolling and having depleted seratonin. From the info above I would assume that taking Prozac to prevent neurotox. would perhaps explain why "some" users experience more tolerance than others as "SSRI's 'downregulate' (inhibit the efficiency & the ability) of seratonin reuptake transporters". From what I have found out I'm unsure as to what is the best method if someone decides to take E; take an SSRI to prevent neurotox. and live with the other effects, or, just supplement before and after and moderate usage so that seratonin is never fully depleted. I would choose the latter but at what point does dopamine create neurotox.? 1 pill? 2 pills? 3? it's guesswork really. I guess what I'm trying to say is that if there is anyone in Medical Q&A looking for "THE POST" that says if you do these things then exstacy is perfectly safe you won't find it.
Good Post BTW
[This message has been edited by sanders (edited 25 July 2000).]
 
NYTFLY-
I'd like to talk to you personally (via e-mail) if you don't mind... I'm planning on going to the link you put in your posting but some of what you said (not that I don't believe it) upsets and disappoints me. Would you mind getting in touch with me when you have a chance? I'd really appreciate it... there are some things I just don't want to post in a public forum. Much obliged!
------------------
No matter who you are, no matter what you do, no matter how you spend your days... allow PLUR to be a part of your daily life, not just an attitude for parties or when you're rolling! You'd be surprised how it will open you up to wonderful things. My love to you all!
 
Once again, I'm splitting hairs...
>SSRI's work by stopping the seratonin reuptake in the brain.
SSRIs will prolong the effects of transmitter in synaptic cleft by interfering with
the transporter protein. They doesn't completely block reuptake.
>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.)
Antidepressants require on average couple of weeks to exert an effect, so the
increased synaptic serotonin can't explain solely their antidepressive effects.
It has been suggested that the antidepressive effects are due to decreased responsiveness
of somatodendritic 5-HT1A autoreceptors and decreased function of terminal 5-HT
autoreceptors. So, whatever it is, it's most likely due to adaptive changes.
>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.
You must remember that the biochemical interactions between the receptor and the
substrate(s) are concentration-dependent (in the case of competitive substrates).
In _In vitro_ test MDMA can displace paroxetine from its binding sites.
>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.
Please, give me some journal references about this serotonin draining in humans.
There is one new study about chronic MDMA use on striatal serotonin levels, but
I haven't been able to read that study yet, and I assume you neither have read it.
I'll include the abstarct here:
"The authors found that striatal levels of serotonin and those of its metabolite
5-hydroxyindoleacetic acid were severely depleted by 50 to 80% in brain of a chronic
user of methylenedioxymethamphetamine (MDMA) whereas concentrations of dopamine were
within the normal control range. Our data suggest that MDMA exposure in the human can
cause decreased tissue stores of serotonin and therefore some of the behavioral effects
of this drug of abuse could be caused by massive release and depletion of brain serotonin".
>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.
There is some evidence that serotonin transporter (SERT) binding is decreased
in some brain regions in animals treated continuously with SSRIs. I would like to see
some references about the long-term effects of SSRIs on SERT function. Do you have
them? It is interesting to notice, that according to one recent study, the SERT
and DAT binding is significantly increased in acutely absistent cocaine-dependent
patients, suggesting compensatory up-regulation of SERT and DAT (dopamine transporter).
You said, "the fact that your brain isn't using it [serotonin] as efficiently".
Can you clarify this comment?
And get the latest issue of Neuropsychobiology, it's dedicated to MDMA. It contains
lots of interesting topics.
BTW, good post NYTFLY.
 
I'm super busy right now...But I'll try to reply a bit. First off, Drug Dustbin, thanks for clarifying and correcting. I don't think my post was as accurate or as clear as it could be. So anyways, here goes...
>SSRIs will prolong the effects of transmitter in synaptic cleft by interfering with
>the transporter protein. They doesn't completely block reuptake.
You're absolutely right...My point was that overall reuptake is decreased, leading to an increase in saturation->More seratonin.
>Antidepressants require on average couple of weeks to exert an effect, so the
>increased synaptic serotonin can't explain solely their antidepressive effects.
>It has been suggested that the antidepressive effects are due to decreased responsiveness
>of somatodendritic 5-HT1A autoreceptors and decreased function of terminal 5-HT
>autoreceptors. So, whatever it is, it's most likely due to adaptive changes.
Exactly, and much better than I said it. My point was that there is an element of "mind over matter" in treating depression. The idea is (here's an exact quote from my local Berkeley psychiatrist and psychopharmacologist): "An increase in seratonin levels is believed to help sufferers of depression by giving them a seratogenic "boost" [Quotes are mine] that alleviates some of the physical neurochemical deficits associated with depression, enabling them to make the mental and physical changes in their methods of thought and actions needed to combat their depression." That's basically what I meant, just not in so many words.
>You must remember that the biochemical interactions between the receptor and the
>substrate(s) are concentration-dependent (in the case of competitive substrates).
>In _In vitro_ test MDMA can displace paroxetine from its binding sites.
Splitting hairs.. (My turn now) Are you sure it was _in vitro_ not _in vivo_? I don't have any reference to this. Do you have one? All I have is a reference to CPA in combination with MDMA inhibiting paroxetine binding. (See: Pharmacol Biochem Behav 2000 Feb;65(2):233-40)
>Please, give me some journal references about this serotonin draining in humans.
>There is one new study about chronic MDMA use on striatal serotonin levels, but
>I haven't been able to read that study yet, and I assume you neither have read it.
I'm a little confused...I'm talkin about temporarily low seratonin levels induced by MDMA causing heavy seratonin release...I thought this was common knowledge? Basically I'm talking about what Dancesafe has a set of pictures on (on the right side of the screen): http://www.dancesafe.org/edepress.html
And I don't have a journal reference. But isn't it obvious that MDMA induced seratonin release will drain seratonin stores until the brain has replenished it? Or maybe I'm missing your point entirely. Please comment.
>There is some evidence that serotonin transporter (SERT) binding is decreased
>in some brain regions in animals treated continuously with SSRIs. I would like to see
>some references about the long-term effects of SSRIs on SERT function. Do you have
>them?
The continous treatment study: (See: Journal of Neuroscience 1999 Dec 1;19(23):10494-501)
Here's a quote from the abstract: "Based on these results, it appears that the SERT is downregulated by chronic administration of SSRIs but not other types of antidepressants; furthermore, the downregulation is not caused by decreases in SERT gene expression."
As far as long-term effects, I was speaking in terms of months. I agree that there is no body of evidence that downregulation is permanent or has any sustained effect beyond several years, but that wasn't my point. My point was that chronic SSRI users who _go off their medication temporarily_ to do E, have a threshold of recovery of only several days to a few weeks (depending on the taper schedule of the patient.) I think you'd agree that this is simply not enough time for the brain to restore itself to equilibrium reuptake. Therefore, in the days-weeks-months after SSRI stoppage, there are still downregulated receptors. These receptors cannot reuptake, therefore there is less total reuptake ability, REGARDLESS of MDMA bioavailability, hence leading to a reduced roll. Thanks for clarifying by the way; my condensed version does seem to be a bit short of the mark.
>It is interesting to notice, that according to one recent study, the SERT
>and DAT binding is significantly increased in acutely absistent cocaine-dependent
>patients, suggesting compensatory up-regulation of SERT and DAT (dopamine transporter).
Splitting hairs (again), I think you mean abstinent, right? I looked it up just in case. Anyways this IS very interesting. The article is: Am J Psychiatry 2000 Jul;157(7):1134-40
I think this demonstrates that the more we learn about the brain, the more we realize how much the chemistry is interrelated.
>You said, "the fact that your brain isn't using it [serotonin] as efficiently".
>Can you clarify this comment?
Sorry, that was pretty unclear, and as it stands, incorrect. What I meant was that in the aggregate, with reduced SERT binding due to downregulation, the brain will not be able to absorb all the seratonin induced by MDMA usage (because of less binding sites available, regardless of bioavailability, like I said before), leading to a relatively "weaker" roll: Less seratonin saturation = weaker roll. You're right in that it has nothing to do with individual SERT efficiency, but rather as a semantic construction of mine: Brain less able use flood of seratonin = less "efficient" use of it. I'm using it kind of as a biased misnomer, but I think I got the point across.
BTW, excellent response. Please correct me if I'm wrong in any of the above. (I'm no doctor, just a chemistry student with a cushy UCSF research job that allows me great access to the LOANSOME system and all sorts of MD's.)
Peace.
-NYTFLY
------------------
*And to those from out of town...Welcome to the third world*
 
My reference for MDMA and paroxetine interaction is Battaglia G et al.
"Pharmacologic profile of MDMA (3,4-methylenedioxymethamphetamine)
at various brain recognition sites". Eur J Pharmacol, 149 (1988) 159-163
It must be noticed that concentrations used in this study are not necessarily
reached _in vivo_ in humans.
I recommend the following article:
Liechti ME, Baumann C, Gamma A, Vollenweider FX.
Acute psychological effects of 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy")
are attenuated by the serotonin uptake inhibitor citalopram.
Neuropsychopharmacology. 2000 22(5):513-2
I'll check that Pharmacology Biochemistry and Behavior article at monday.
>I'm a little confused...I'm talkin about temporarily low seratonin levels induced
>by MDMA causing heavy seratonin release...I thought this was common knowledge?
>Basically I'm talking about what Dancesafe has a set of pictures on
>(on the right side of the screen): http://www.dancesafe.org/edepress.html
Yeah, you're right. Actually I ment how do you know that over 60 mgs is enough
to drain brain serotonin stores in humans. In other words, 60 mgs of MDMA will
release 5-HT, but how do you know how much it will drain your serotonin.
>The continous treatment study: (See: Journal of Neuroscience 1999 Dec 1;19(23):10494-501
Actually I have that study right here front of me.
smile.gif
It would be
nice to see some PET or SPECT studies about the effects of SSRIs on human
SERT density.
There is also couple of other interesting studies:
Hébert C, Habimana A, Élie R, Reader TA.
Effects of chronic antidepressant treatments on 5-HT and NA transporters in
rat brain: an autoradiographic study. Neurochemistry International 308 (2001) 63-74
And about the regulation mechanisms:
Ramamoorthy S, Giovanetti E, Qian Y, Blakely RD.
Phosphorylation and Regulation of Antidepressant-sensitive Serotonin
Transporters. Journal of Biological Chemistry 273(4):2458-2466, 1998.
Ramamoorthy S, Blakely RD.
Phosphorylation of Serotonin Transporters Differentially Modulated by
Psychostimulants. Science 285:763-766, 1999.
Blakely RD, Bauman AL. Biogenic amine transporters: regulation in flux.
Current Opinion in Neurobiology 2000, 10:328-336.
>Splitting hairs (again), I think you mean abstinent, right? I looked it up just
>in case. Anyways this IS very interesting. The article is: Am J Psychiatry 2000
>Jul;157(7):1134-40 I think this demonstrates that the more we learn about the brain,
>the more we realize how much the chemistry is interrelated.
Yeah, abstinent, my spelling is pretty lousy. English is not my native tongue,
as you might notice.
smile.gif

Here's a little quote from that study:
"Our failure to observe a relationship between depressive symptoms during
acute cocaine withdrawal abd serotonin transporter or dopamine transporter
binding availability likely reflects the very low rates of depressive
symptoms reported by this group. This is consistent wit previous
observations that depressive symptoms experienced by patients withdrawing
from chronic cocaine use in the inpatient setting are mild".
>Sorry, that was pretty unclear, and as it stands, incorrect. What I meant was that in
>the aggregate, with reduced SERT binding due to downregulation, the brain will not be
>able to absorb all the seratonin induced by MDMA usage (because of less binding sites
>available, regardless of bioavailability, like I said before), leading to a relatively
>"weaker" roll: Less seratonin saturation = weaker roll.
There is most likely also some adaptive changes in postsynaptic receptors, like
desensitization 5-HT2 receptors, which has an important role in the actions of psychedelics.
 
also splitting hairs...
for the purposes of this discussion i think it would be beneficial to take into account the different half lives of the ssri's in question. e.g. prozac has a very loooooong half life and is hard to get out of the system quickly, while serzone can be taken in the am, and be out of the body by the pm ready for rollin.
i don't know the exact numbers, but they're all out there, and unfortunately they're all averages/estimates.
-fag
 
Once again, I'm splitting hairs...
>SSRI's work by stopping the seratonin reuptake in the brain.
SSRIs will prolong the effects of transmitter in synaptic cleft by interfering with
the transporter protein. They doesn't completely block reuptake.
Paxil is the most potent SSRI, prozac, the least......If anyone cares
>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.)
Antidepressants require on average couple of weeks to exert an effect, so the
increased synaptic serotonin can't explain solely their antidepressive effects.
It has been suggested that the antidepressive effects are due to decreased responsiveness
of somatodendritic 5-HT1A autoreceptors and decreased function of terminal 5-HT
autoreceptors. So, whatever it is, it's most likely due to adaptive changes.
true..downregulation plays an important role...remember, "biological depression" is based on the theory that the 5HT system is not functioning correctly...downregulation allows for the existing serotonin to "connect" to receptors on the post synaptic cleft...
>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.
You must remember that the biochemical interactions between the receptor and the
substrate(s) are concentration-dependent (in the case of competitive substrates).
In _In vitro_ test MDMA can displace paroxetine from its binding sites.
interesting, I have read numerous studies saying that Prozac displaces MDMA...it is this higher affinity that attenuates neurotoxicity (by "kicking out" MDMA from the reuptake site, thus preventing dopamine intrusion, etc)...This theory is also supported by the *fact* that SSRI users don't feel the empathetic qualities of the roll...yet feel the amphetamine qualities)
>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.
Please, give me some journal references about this serotonin draining in humans.
There is one new study about chronic MDMA use on striatal serotonin levels, but
I haven't been able to read that study yet, and I assume you neither have read it.
I'll include the abstarct here:
Recently...a postmortum study of a brain of am MDMA user showed 50%-80% decrease in 5HT markers....but "he" was a polydrug user....
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10908909&dopt=Abstract
"The authors found that striatal levels of serotonin and those of its metabolite
5-hydroxyindoleacetic acid were severely depleted by 50 to 80% in brain of a chronic
user of methylenedioxymethamphetamine (MDMA) whereas concentrations of dopamine were
within the normal control range. Our data suggest that MDMA exposure in the human can
cause decreased tissue stores of serotonin and therefore some of the behavioral effects
of this drug of abuse could be caused by massive release and depletion of brain serotonin".
>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.
There is some evidence that serotonin transporter (SERT) binding is decreased
in some brain regions in animals treated continuously with SSRIs. I would like to see
some references about the long-term effects of SSRIs on SERT function. Do you have
them? It is interesting to notice, that according to one recent study, the SERT
and DAT binding is significantly increased in acutely absistent cocaine-dependent
patients, suggesting compensatory up-regulation of SERT and DAT (dopamine transporter).
You said, "the fact that your brain isn't using it [serotonin] as efficiently".
Can you clarify this comment?
Lots of interesting news about SSRI's comming out....including morphological changes in the axon (high dose of SSRI...but could this happening to CHRONIC SSRI users...of which myself is included???) I stoped taking my SSRI because of some of the new info that is comming out...I use a MAOI now..and YES I have used MDMA while on an MAOI...but thats another story...
djmm (former Bluelighter...from the "old" page)
And get the latest issue of Neuropsychobiology, it's dedicated to MDMA. It contains
lots of interesting topics.
BTW, good post NYTFLY.
 
SSRI's definately *DO* prevent and stop you from rolling.
I took 5htp 200mg/day for 3 days before the Saturday night, and an hour after taking a Gold CK, I was peaking as hard as I ever have before.
3 Hours later, another CK, and an SSRI ("Fluvox" for anyone who's interested).
The rest of the night I was sitting on my arse. Didn't want to dance (although I was earlier in the night), didn't want to talk to anybody.
I have no doubt in my mind that the SSRI totally reversed the effects of MDMA, almost to the extent that I felt as if I hadn't had any. (though, I did feel VERY spaced out)
So yeah, I'm never taking anything with XTC again.... oh, except maybe 5Htp, which I've found definately does help before, and after.
Greedy!
smile.gif
 
djmm, wrote:
>interesting, I have read numerous studies saying that Prozac displaces MDMA...
>it is this higher affinity that attenuates neurotoxicity (by "kicking out" MDMA
>from the reuptake site, thus preventing dopamine intrusion, etc)...This theory is
>also supported by the *fact* that SSRI users don't feel the empathetic qualities of the
>roll...yet feel the amphetamine qualities)
Yes, this is most likely true _in vivo_ in normal concentrations. But with
higher concentrations it seems to be possible to get more effects with MDMA+SSRI
combination. Check out McCann et al. "Reinforcing Subjective Effects of
(+/-) 3,4-methylenedioxymethamphetamine ("Ecstasy") May Be Separable from its
Neurotoxic Actions: Clinical Evidence. J Clin Psychopharmacol 1993; 13(3):214-217.
It gives some evidence that high doses of MDMA with small doses of fluoxetine will
still give some effects.
 
true...but fluoxetine is a comparitively weak antidepressant...as far as potency is concerned...something like paxil (which is significantly more potent) will block the serotonin effect of MDMA at any level that a human would consume...FYI, paxil is about 20 times as potent as prozac...potency being calculated:
10^27 3 1/Ki....where Ki is equal to inhibitor consistant in molarity
 
Hmmm, I think it's better to compare serotonin uptake blockers
in this case with this table:
Paroxetine 3.0 +/- 1
Fluoxetine 40 +/- 10
Imipramine 140 +/- 20
Amitriptyline 200 +/- 50
Desipramine 800 +/- 100
Numbers are EC50 (nM) for inhibition of MDMA-induced [3H]5-HT release.
This table was taken from Hekmatpanah CR, Peroutka SJ. 5-Hydroxytryptamine
uptake blockers attenuate the 5-hydroxytryptamine-releasing effect of
3,4-methylenedioxymethamphetamine and related agents. Eur J Pharmacol, 177 (1990):95-98
Citalopram, fluvoxamine, and sertraline are most likely somewhere between paroxetine
and fluoxetine.
 
I just wanted to throw in some over-the-counter advice...
(In my own experience)
I have found that the following have similar effects as the ssri's in relation to mdma:
St. John's Wort
Kava Kava
Gotu Kola
Passion Flower
Have any of you seen any official reports that support this?
 
Saint Johns Wart acts as a mild SSRI and has some MAOI activity
Kava Kave may or may not effect GABA, but does act as a very mild norepinephrine reuptake inhibitor.
Gotu Kola is a natural source of theobromine, which is an adenoside antagonist (indirectly increases dopamine, very similar to caffeine)
Passion flower contains flavonoids (chemo protective compounds) which are responsible for its anti-anxiety effects.
 
Just reading over this again and am curious if the info below can be translated into something even I could understand.
Drug Dustbin
Bluelighter posted 23 August 2000 01:22 PM
--------------------------------------------------------------------------------
Hmmm, I think it's better to compare serotonin uptake blockers
in this case with this table:
Paroxetine 3.0 +/- 1
Fluoxetine 40 +/- 10
Imipramine 140 +/- 20
Amitriptyline 200 +/- 50
Desipramine 800 +/- 100
Numbers are EC50 (nM) for inhibition of MDMA-induced [3H]5-HT release.
This table was taken from Hekmatpanah CR, Peroutka SJ. 5-Hydroxytryptamine
uptake blockers attenuate the 5-hydroxytryptamine-releasing effect of
3,4-methylenedioxymethamphetamine and related agents. Eur J Pharmacol, 177 (1990):95-98
Citalopram, fluvoxamine, and sertraline are most likely somewhere between paroxetine
and fluoxetine.
 
well....
we were discusing how potent the SSRIs (class of antidepressants) are...
currently, the most potent is:
1. celexa
2. paxil
3. zoloft
4. luvox
5. prozac
6. desyrel (mainly effects 5-ht2 sites)
the most selective..meaning, it doesn't effect other neurotransmitter systems (they all do, but, some do more than others):
1. celexa
2. paxil
3. zoloft
4. luvox
5. prozac
 
thanks- i actually did know what ssri's where. hehe. i dont know why i am suprised to find out that celexa is the most potent and that prozac is the least - maybe i should add celexa to my wellbutrin since wellbutrin gets me going but is doing a minimal job with the depression. ill be sure to talk to my doc about it!
 
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