• MDMA &
    Empathogenic
    Drugs

    Welcome Guest!

deprenyl and mdma dose

I believe that some people have safely combined moclobemide with MDMA due to its reversibility. Whereas traditional MAO inhibitors bind irreversibly to the MAO molecules, moclobemide continuously jumps on and off the molecule; it can be displaced, for example, by tyramine. Thus 80% MAO-A inhibition caused by moclobemide is not the same as 80% MAO inhibition as caused by the traditional inhibitors.

Thus there does remain a mechanism for excess norepinephrine to build up.

Additionally, moclobemide's half life is only 1.5 hours. If a crisis situation does begin to eventuate, the reversibility of moclobemide combined with its short half-life will lead to a quick resolution.

NB: I am not suggesting you try this. If you push the boundary too far you will end up with serotonin syndrome or a hypertensive crisis or both. Moclobemide overdoeses have been noted and, more importantly, deaths have been reported involving a moclobemide/MDMA interaction:

Vuori E, Henry JA, Ojanpera I, Nieminen R, Savolainen T, Wahlsten P, Jantti M., "Death following ingestion of MDMA (ecstasy) and moclobemide." Addiction. 2003 Mar;98(3):365-8.

I'm really annoyed to see those statistics of 80% MAO-A inhibition and 30% MAO-B inhibition around the place, as I initially believed them too. They're wrong. :X Dumb websites just pass stuff on as facts with no sources. This is why we must try and stay academically rigorous!
 
Well adam X you really are shure of yourself aren't you?
Of course it is impossible to convince you but i assure that i have receaved my masters in psychology just about a half year ago, and in some months an article with me as the second author will be published in the Journal of Psychopharmacology about cocaine craving.
It is a bit sad that you continually come with these big statements instead of helping out and keeping a good and informative discussion going.
 
I'm not going to get into a pissing match here, I just find it exceedingly hard to believe that someone with so many basic spelling and grammatical errors has a Masters Degree in anything.


X
 
Call me a madman, but I have ordered Selegline over the internet, and if it gets through customs, and the post man dose not 'loose' it, I am going to take 5mg and then 30 minutes later take 1 medium strength mdma pill.

I will post the results hopefully in a few weeks.
 
VelocideX - thanks for the info on meclobemide. I wondered how that could be true (30% maoB inhibitor) because if it was, then people would have a lot of trouble eating Tyramine containing food, which is in large amounts in the modern western diet.

When I am on prozac (post loading a few hours after MDMA) i get pain in my temples if I eat lots of tyramine food (cheese, ect) as prozac inhibits mao B and A to a degree. That is why I do not want to post load with prozac anymore.
 
I think you'll find the MAO inhibitory properties of prozac are insignificant compared to moclobemide, hence the term "SELECTIVE serotonin reuptake inhibitor"
 
Eek. I withdraw that =\
From http://www.biopsychiatry.com/fluoxmaoa.htm

Mukherjee J, Yang ZY "Monoamine oxidase A inhibition by fluoxetine: an in vitro and in vivo study" Synapse 1999 Mar 15; 31(4):285-9

Monoamine oxidase A (MAO-A) inhibition was investigated both in vitro and in vivo in rat brains by using the radioligand, 18F-fluoroclorgyline (N-[3-(2',4'-dichlorophenoxy)-2-18F-fluoropropyl]-N-methylpropa rgylamine). In vitro binding affinities of six compounds, clorgyline, Ro 41-1049, deprenyl, fluoxetine, norfluoxetine and citalopram, were studied. Fluoxetine and norfluoxetine showed in vitro affinities of 36.5 and 68 microM for MAO-A, respectively. Fluoxetine and norfluoxetine also significantly inhibited (more than 20%) the binding of the radioligand in vivo while citalopram and deprenyl showed very poor affinities in vitro for MAO-A and had no effect in vivo. The in vivo effects of the various drugs were directly comparable to their in vitro affinities for binding to MAO-A as seen in the correlation plot of percent control in vivo binding of 18F-fluoroclorgyline and binding affinity, -log IC50 (R2 = 0.979). An acute dose of 20 mg/kg of fluoxetine inhibited binding of 18F-fluoroclorgyline by more than 20%, while lower doses had some significant effects. These results provide evidence on the in vitro and in vivo inhibition of monoamine oxidase A by fluoxetine.
 
But what dose that mean in English?

If I take 40mg of prozac, which has about a 9 day half life (nor-fluxotine inhibits MaoB more than fluxotine) how much MAO inhibiting am I getting for the next few weeks ???

Because everytime I post load with prozac, I have to keep away from foods with Tyramine in them or I get a headache. (MAO A and B normally break down tryamine, so that is why you should only inhibit A OR B, not both). And if I eat lots of tuna, which I have read is an MAO inhibitor (myth or fact?) I get a pounding heart.

Anyway, fuck prozac off. Selegiline to the rescue.
Emotional rescue...
 
If you take 40mg of prozac, assuming you weigh about 65kg then you're getting about 0.6 mg/kg
That study investigated 20mg/kg, which would be about 1300mg of prozac.

This produces about 20% MAO-A inhibition (or so it seems)... which still leaves plenty to deal with tyramine.
You may be interested in Bowsher DJ, Rowe H, Farid NA, Tenbarge JB, Lemberger L. "Pressor responses to tyramine and norepinephrine after subchronic administration of fluoxetine to man." Life Sci. 1988;42(25):2569-75., which says that at 60mg/day for 45 days, no increase in the tyramine pressor response was found.

I'd suggest perhaps it's a psychosomatic effect? Or there may be something else at work?
 
Dr Beat, keep us posted on your experiences with combining deprenyl and mdma. I was going to do it this weekend but i got sick, so no data here yet.
 
Adam X: perhaps you should apologise? After all, smartshop is Dutch so his typos are understandable.:\

Anyhow, unless I was either a neurologist, neuropsychiatrist or senior pharmacologist I wouldn't even consider weighing into this discussion both because of the conflicting information that is around, plus the potential for serious adverse consequences yada yada yada.

What I will do is give you a link from the Dancesafe discussion board


:)
 
superbabydoc said:
Anyhow, unless I was either a neurologist, neuropsychiatrist or senior pharmacologist I wouldn't even consider weighing into this discussion both because of the conflicting information that is around, plus the potential for serious adverse consequences yada yada yada.
Click to expand...

Agreed. The potential for MAOA inhibition is just too great IMO.

Just an idea, but why not just do 3 months on Deprenyl, without the MDMA? If the drug is effective at what it's said to do, it may even alter the urge to do a potentially neurotoxic drug like MDMA.
 
My experience : mixing Selegiline (l-Deprenyl) with MDMA <-- right here


--
I've had much of a think about things, and I've decided there MUST be a significant difference between the reversible and irreversible MAO inhibitors. I have successfully combined moclobemide and MDMA, though I was rather careful about doing it -- slowly working up doses etc. In all honestly <150mg of moclobemide helped a bit, but any more and I started to feel a little too warm, and so stopped there... don't particularly want to die from a hypertensive crisis.

Think about it -- the moclobemide-MAOA interaction is an equilibrium. Though a certain percentage of MAO inhibition is achieved, in reality the moclobemide molecule is hopping on and off the molecule all the time. There's no reason it shouldn't be metabolising serotonin in that interim period. I agree it reduces the total effective amount of MAO, but even "100%" MAO inhibition does not correspond to no MAO enzyme present because of the equilibrium nature of the reaction.

Moreover, moclobemide has a really short half life.
 
Binding kinetics is a crazy business, which isn't really studied at all, and somethings, which you would assume are real basics, aren't even known.

reversible vs irreversible is an interesting problem. 99% of the time it doesn't make a difference. In a solution of a reversable ligand (the MAOI say) and a receptor(MAO), when the concentration of the ligand is 9 times is Kd (bassically a measure of affinity, i.e. the concentration where 50% of the ligand is bound), then at any one point in time 90% of the ligand will be on the receptor, effectivley equivalent to removing 90% of the receptor/enzyme by irreversable/suicide inhibition. i.e. when there there is no competion irreversable and reversable inhibitors do the same stuff

In this case here however, its not just the receptor/enzyme and the ligand, there's also the natural substrate i.e. serotonin/dopamine.

Now normally, the amount of serotonin is very low, so it is just like the situation above. But things seperate when the concentration of the natural substance gets high, i.e. when you might be suffering from serotonin syndrome. Now here, if the concentration of serotonin gets up to around its Kd for the enzyme, it will start kicking off the ligand.

Indeed, if you put 100x the Kd of serotonin and 100x the Kd of your reversable ligand, you would find about 50% of the serotonin bound, and 50% of the ligand bound.

But the irreversable inhibitor has blocked the enzyme no matter what. Even it there was a massive amount of serotonin, there would be increase in serotonin turnover.

And thats why reversable inhibitors aren't as dangerous, because they effectively inhibit less, when the concentration of the natural ligand gets high.

You can learn quite a lot about that kinda stuff, as well as how you actaully do binding experiments here
 
^^ Cheers for the info. I know that tyramine successfully competes with moclobemide for MAO-A...

I've also seen around somewhere that deprenyl reversibly inhibits MAO-A, but I'm not so inclined to believe that straight up. I'll look for references in a bit
 
I think I've read that people have wondered about that too, but deprenyls affinity for MAO-B is more than 10,000 times higher than its affinity for MAO-A... so that will just be of scientific interest.
 
Hey i just got an e-mail that this thread had some action again. I got a message from doctor beat a while ago. I'll post it here because it adresses the deprenyl mdma combo from the practical side of things. I think the comments about feeling serotonin, dopamine etc should not be taken literally, but it is a great report. Of course it still dousn't tell us about neurotoxicity. Also i believe that if deprenyl has any neuroprotective effects against mdma it would probably be because of the induction of SOD enzyme. In animals higher sod animals do not seem to have neurotoxicity from mdma.
*snip*
edit - I don't really see the point in reposting what is in this thread, which I linked too a few posts above :) -V
*snip*

Deprenyl is great stuff !
 
Last edited by a moderator:
Ok i am copy and pasting this from another thread. But some more from doctor beat(positive. And from velocidex (negative).
I had no comedown at all, which I was very happy about, because a few years ago (2000) I used to get very bad comedowns because I did not take any suppliments with mdma.

I did take 5htp 2 days after the rave so that may have masked any comedown.

Even when I take prozac (40mg) after pills, I still get a little dip 3 days later, but far less less comedown than pills with no prozac.

I must admit though, I did have a slight pressure on my temples for about 3-4 days after the rave, and my body felt a little bit strange, but I was happy and high so I did not care much about that. I did have high dopamine all week after the rave, but by now (12 days after the rave) my dopamine has gone back down to normal levels.

And this was the first time I have tried ALA with MDMA. Usually I would have grape seed extract, vit E and other anti-oxidents, but this time I added ALA and I think it works REALLY WELL. And a mate who tried it said it made his comedown really small.

ALA for the ignorant is ALpha - Liopic Acid, a super strong anti-oxident that protects your brain big time.

And you are right - taking deprenyl alot makes you feel a bit strange - I felt scattered on the high dopamine - mind racing - a bit of mania (good mania) and lots of mind energy and a desire to do things. Normally I am pretty relaxed and am in no rush to do anything, but on deprenyl I felt like doing a lot more (not that i DID much more). I also talked alot more than normal and had many a good rave(rant) at people.

Good stuff, but not something I am going to take often. I am mostly going to use it for raves.

The 5mg dose effects lastet about a week.
The 10mg dose effects lasted about 1.5 weeks.

Anyway, I think it is 100 times better than taking prozac. Post loading with Prozac was really annoying me last year and I was really keen to replace it with something else, and I think deprenyl 'fits the bill' perfectly.

Then the negative:

I recently tried a pill I know to be fairly decent the day after taking 5mg selegiline.

I found the experience to be, on the whole, disappointing.

I certainly felt hotter than usual, but felt much more clearheaded. I did not feel "trashy", nor did I ever really peak.... Similarly the visual effects of the pill seemed much less pronounced.

It's hard to know what to attribute this to, but the conclusion is that pills taken during or immediately after a course of selegiline will be far less rewarding
 
You must log in or register to reply here.
Top