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All 7 posts Subject: Selegiline (MAOB inhibiton) and Tryptamines Please login to post Down

Psiloman
(Stranger)
10-15-04 23:37
No 536016
      Selegiline (MAOB inhibiton) and Tryptamines

Here is actually a question i always had but received no answer no matter how hard i looked.

It can be summarized in this two sentences

1)Would the coadministration of a MAOB inhibitor such as Selegiline (deprenyl) at low dose (5mg) qualitatively or quantitatively alter a tryptamine experience,and if so how?

2)Would the coadministation of the aforementioned inhibitor with an ayahuasca mixture qualitatively or quantitatively alter the experience and if so how? Notice that ayahuasca contains a MAOA inhibitor.

What follows is a post i made some time ago that got no answer and shows my train of though in a more detailed way.

I do not know if i got this right from my online reading but i have the impression that :When dopamine levels in the brain rise,serotonine levels in other areas in the brain are lowered.If my statement is not correct please elucidate!

So...whats my point? Ott said that high serotonine levels due to the use of a MAO-A inhibitor (propably prolonged use) can diminish tryptamines effects such as LSD even DMT>From y understanding this might happen because more 5HT receptors will be occupied by the abudant serotonine and less receptors will be free for those beloved molecules (Maybe serotonine has even a higher affinity for those receptors than psycedelics,i dont know...)

If the first "Statement" i made holds true then a MAO B inhibitor like the one discussed here would potentiate psychedelics by lowering serotonin levels in some parts of the brain and leaving more receptors for tryptamines.ALso that extra dopamine could be interesting.

What if one combines selegiline at low dosage (5mg) with an Ayahuasca brue (Which already contains a MAO inhibitor,MAO A inhibitor and DMT)?Many people say that harmine and harmaline "mellow" a bit the tryptamines making the ride more smooth although more intense at the peak and with a bigger duration.Harmaline inhibits MAOA in the gut but i think that some of it is reaching the brain as well and rises serotonin levels which could be responsible for this effect.Adding selegiline could counter this effect up to an extend,if all the above i stated is correct....

On the other hand harmaline is reputed to potentiate PEA's as well ,although i do not knwo the mechanism for that.Well,ecuse me if i am mistaken ,but isnt selegiline a phenethylamine as well? If that is so harmaline could potentiate it as well...Hmmm...That could be dangerous,any opinions on that? 5mg of selegiline in an ayahuasca brew could solve some of the questions at least bioassay-wise..

Also keep in mind that im talking still under the light of "TRYPTAMINES and Selegiline",i am pretty sure it will potentiate PEA's through straight MAOB inhibition...

and another post of mine which is along the same train of thought (please bear with me)

First of all sorry for "bringing from the dead" a conversation,but i had exactly the same question but with some extensions.

I have been studying Selegiline and its metabolites recently.The increase of dopamine in the brain due to its MAOI-B irreversible effects was of some interest to me.Why? Read on.

Putting it in simple laymans MAOI A "potentiate" (Mr Ott has a different opinion ) and alter tryptamine intensity and quality as far as the effects are concerned. A MAOI B could "potentiate" and alter the phenethylamine experience but selegiline is too risky for that.I bet that is due to its irreversible caracter and because also MAO B inhibition is generally "bad news" because of tyramine interactions. My first question is: could a reversible MAOI B be used instead of an irreversible and give the desired effect without nasty interactions? I think it can,although i do not recall hearing anything about reversible MAOI B.

That aspect though is not what trully concerns me .What is my true concern is the alteration that a MAOI B such as selegiline at the dose range of 5-10 mg could provide for a tryptamine experience.Sure,the interaction is not going to be direct ,since MAO B couldnt care less for a tryptamine substrate ,BUT...Here comes the "extra dopamine issue".Antagonism of 5HT-2a receptors plus extra dopamine.Could that account for a stronger experience? Maybe providing more "energy" to cope through the experience and combat some of the "sleepiness" felt on some tryptamines or concotions like ayahuasca? Would extra dopamine add some new features to the experience? Here are some interesting questions!

To my best understanding dopamine and serotonine systems are not unrelated,so my question is valid.Are there any further experience reports or other data on that? I think that since 2 years have passed from the last post on this topic some more knowledge could have been accumulated.

Thank you in advance

SpicyBrown
(Hive Bee)
10-16-04 01:25
No 536026
      Moclobemide != Deprenyl

1)Would the coadministration of a MAOB inhibitor such as Moclobemide (deprenyl) at low dose (5mg)

I don't have the exact answer you're looking for, however: Deprenyl is selegiline, not moclobemide. Brand-name moclobemide is Auroix. While selegiline may very well accomplish what you're looking for at doses as low as 5mg, I'm almost certain moclobemide requires doses more along the lines of ~75+mg. An acquaintence of mine has experimented with moclobemide and oral DMT - I'll have to try to get ahold of said individual and see what they recommend.

-SpicyBrown

Psiloman
(Stranger)
10-16-04 14:02
No 536084
      oooops my mistake!

Im sorry for the grave mistake ,i was thinking of SELEGILINE (Deprenyl) and wrote MOCLIBEMIDE (Aurorix).Excuse me for the mix up but it was a time of the night that my mind simply turned into porridge!

The question though still stands...MAOB Inhibition via Selegiline + Tryptamines = ?

(I have edited my post and made the appropriate corrections to it,thanks for pointing out)

Psiloman
(Stranger)
10-17-04 14:38
No 536186
      Hmmm,noone has a clue?

Is this "MAOB inhibition + tryptamine" a completely virgin area of experimentation?

Since selegiline is quite popular amongst "smart drug enthusiasts" and tryptamines is something well....widespread at least amongst knowledgable people i wonder why there are no data on their combination.

At best im looking for a theory behind this combination,that is "what could happen based on neurochemistry/pharmacology that we know".A firsthand or a SWIM experience would also suffice

nanobrain
(Stranger)
10-20-04 09:00
No 536764
      stand warned

in short, yes it would. selegeline (l-dep) is a tricky bastard and an irreversible and non-selective MAO inhibitor at higher doses. given individual metabolic differences, this may well hold true for lower doses, especially w/coadministration of strong cerebral activators.

you are on the money about the dopaminergic effects which manifest as a dirty body load in the best of cases, adding a whole new level of distortion to the experience.

anecdotal ADRs (over 50 collected) from intentional and accidental coingestion of l-deprenyl with tryptamines / 2C-X-X family include severe and unpredictable crosspotentiation, peripheral vascular events, hypertension, tachycardia and severe and persistent circadian headaches.

as well as acute, nasty, full blown psychedelic freakouts.

if you are chasing that elusive pharmahuasca revelation, stand warned.

DWTSBOL

scarmani
(Hive Bee)
10-29-04 08:49
No 538492
User Picture       One Datapoint

Swim has read several reports of adverse interactions between Selegiline and 2C-T-x's, but not tryptamines.

The following is not recommended; simply provided as a datapoint. At the time Swim had been taking Selegiline @ 15 mg daily for approximately 2 weeks and found it to be an effective pro-motivational antidepressant and nootropic.

Swim took 30 mg 4-HO-MiPT HCl orally. (This was a substance and a doseage level with which Swim was familiar, albeit not in combination with Selegiline. On a number of prior occasions, 30 mg 4-HO-MiPT had provided a gratifyingly involving "signature" tryptamine experience comparable for Swim to perhaps 5-7 grams dried psilocybe cubensis mushrooms. 4-HO-MiPT is Swim's favorite tryptamine, extremely vibrant and positive.)

In combination with the Selegiline, the 4-HO-MiPT was quite a bit stronger than it had been in previous excursions. The intensity of the experience significantly exceeded that described in the 20 mg report in TiHKAL, and could only be described as revelatory.

http://www.erowid.org/library/books_online/tihkal/tihkal22.shtml

For approximately 90 minutes, Swim had what could be described as massive ecstatic out-of-body ego dissolution. In contrast to Swim's previous psychedelic experiences, Swim was disinclined to move or communicate with others at all, though it was possible with great mental effort. Throughout the experience, Swim had a carcinoid flush and noticeable pressor symptoms. These physical effects were not present without Selegiline, and were unpleasant.

Despite the vast and unexpected strength of the mental effects, and the appearance of unwanted physical side effects, for Swim the experience was extremely positive overall.

With a different set /or setting, or a different individual, the results could have easily been doubleplus ungood.

A last note; the length of the 4-HO-MiPT experience was substantially unchanged by Selegiline; that is to say the plateau lasted about 4 hours with a 2-4 hour afterglow.

boot from the shadow of a broken mirror

Psiloman
(Stranger)
10-29-04 14:10
No 538536
      Very Nice!

Very Nice information guys!

Yes,with phenethylamines bad reactions can be explainable...

So as i see there was some interaction between the tryptamine and selegiline! What i can comment on was that you were on a high dose regimen of selegiline,so you could possibly have had full MAOB inhibition.

Maybe the experience profile would differ if it was a one time administration or if harmine/harmaline was addes as in an ayahuasca!

Thank you very much for the information if someone has mor feedback i would appreciate it!

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	All 7 posts		Subject: Selegiline (MAOB inhibiton) and Tryptamines		Please login to post		Down


		Psiloman (Stranger) 10-15-04 23:37 No 536016				Selegiline (MAOB inhibiton) and Tryptamines
						Here is actually a question i always had but received no answer no matter how hard i looked. It can be summarized in this two sentences 1)Would the coadministration of a MAOB inhibitor such as Selegiline (deprenyl) at low dose (5mg) qualitatively or quantitatively alter a tryptamine experience,and if so how? 2)Would the coadministation of the aforementioned inhibitor with an ayahuasca mixture qualitatively or quantitatively alter the experience and if so how? Notice that ayahuasca contains a MAOA inhibitor. What follows is a post i made some time ago that got no answer and shows my train of though in a more detailed way. I do not know if i got this right from my online reading but i have the impression that :When dopamine levels in the brain rise,serotonine levels in other areas in the brain are lowered.If my statement is not correct please elucidate! So...whats my point? Ott said that high serotonine levels due to the use of a MAO-A inhibitor (propably prolonged use) can diminish tryptamines effects such as LSD even DMT>From y understanding this might happen because more 5HT receptors will be occupied by the abudant serotonine and less receptors will be free for those beloved molecules (Maybe serotonine has even a higher affinity for those receptors than psycedelics,i dont know...) If the first "Statement" i made holds true then a MAO B inhibitor like the one discussed here would potentiate psychedelics by lowering serotonin levels in some parts of the brain and leaving more receptors for tryptamines.ALso that extra dopamine could be interesting. What if one combines selegiline at low dosage (5mg) with an Ayahuasca brue (Which already contains a MAO inhibitor,MAO A inhibitor and DMT)?Many people say that harmine and harmaline "mellow" a bit the tryptamines making the ride more smooth although more intense at the peak and with a bigger duration.Harmaline inhibits MAOA in the gut but i think that some of it is reaching the brain as well and rises serotonin levels which could be responsible for this effect.Adding selegiline could counter this effect up to an extend,if all the above i stated is correct.... On the other hand harmaline is reputed to potentiate PEA's as well ,although i do not knwo the mechanism for that.Well,ecuse me if i am mistaken ,but isnt selegiline a phenethylamine as well? If that is so harmaline could potentiate it as well...Hmmm...That could be dangerous,any opinions on that? 5mg of selegiline in an ayahuasca brew could solve some of the questions at least bioassay-wise.. Also keep in mind that im talking still under the light of "TRYPTAMINES and Selegiline",i am pretty sure it will potentiate PEA's through straight MAOB inhibition... and another post of mine which is along the same train of thought (please bear with me) First of all sorry for "bringing from the dead" a conversation,but i had exactly the same question but with some extensions. I have been studying Selegiline and its metabolites recently.The increase of dopamine in the brain due to its MAOI-B irreversible effects was of some interest to me.Why? Read on. Putting it in simple laymans MAOI A "potentiate" (Mr Ott has a different opinion ) and alter tryptamine intensity and quality as far as the effects are concerned. A MAOI B could "potentiate" and alter the phenethylamine experience but selegiline is too risky for that.I bet that is due to its irreversible caracter and because also MAO B inhibition is generally "bad news" because of tyramine interactions. My first question is: could a reversible MAOI B be used instead of an irreversible and give the desired effect without nasty interactions? I think it can,although i do not recall hearing anything about reversible MAOI B. That aspect though is not what trully concerns me .What is my true concern is the alteration that a MAOI B such as selegiline at the dose range of 5-10 mg could provide for a tryptamine experience.Sure,the interaction is not going to be direct ,since MAO B couldnt care less for a tryptamine substrate ,BUT...Here comes the "extra dopamine issue".Antagonism of 5HT-2a receptors plus extra dopamine.Could that account for a stronger experience? Maybe providing more "energy" to cope through the experience and combat some of the "sleepiness" felt on some tryptamines or concotions like ayahuasca? Would extra dopamine add some new features to the experience? Here are some interesting questions! To my best understanding dopamine and serotonine systems are not unrelated,so my question is valid.Are there any further experience reports or other data on that? I think that since 2 years have passed from the last post on this topic some more knowledge could have been accumulated. Thank you in advance



		SpicyBrown (Hive Bee) 10-16-04 01:25 No 536026				Moclobemide != Deprenyl
						1)Would the coadministration of a MAOB inhibitor such as Moclobemide (deprenyl) at low dose (5mg) I don't have the exact answer you're looking for, however: Deprenyl is selegiline, not moclobemide. Brand-name moclobemide is Auroix. While selegiline may very well accomplish what you're looking for at doses as low as 5mg, I'm almost certain moclobemide requires doses more along the lines of ~75+mg. An acquaintence of mine has experimented with moclobemide and oral DMT - I'll have to try to get ahold of said individual and see what they recommend. -SpicyBrown



		Psiloman (Stranger) 10-16-04 14:02 No 536084				oooops my mistake!
						Im sorry for the grave mistake ,i was thinking of SELEGILINE (Deprenyl) and wrote MOCLIBEMIDE (Aurorix).Excuse me for the mix up but it was a time of the night that my mind simply turned into porridge! The question though still stands...MAOB Inhibition via Selegiline + Tryptamines = ? (I have edited my post and made the appropriate corrections to it,thanks for pointing out)



		Psiloman (Stranger) 10-17-04 14:38 No 536186				Hmmm,noone has a clue?
						Is this "MAOB inhibition + tryptamine" a completely virgin area of experimentation? Since selegiline is quite popular amongst "smart drug enthusiasts" and tryptamines is something well....widespread at least amongst knowledgable people i wonder why there are no data on their combination. At best im looking for a theory behind this combination,that is "what could happen based on neurochemistry/pharmacology that we know".A firsthand or a SWIM experience would also suffice



		nanobrain (Stranger) 10-20-04 09:00 No 536764				stand warned
						in short, yes it would. selegeline (l-dep) is a tricky bastard and an irreversible and non-selective MAO inhibitor at higher doses. given individual metabolic differences, this may well hold true for lower doses, especially w/coadministration of strong cerebral activators. you are on the money about the dopaminergic effects which manifest as a dirty body load in the best of cases, adding a whole new level of distortion to the experience. anecdotal ADRs (over 50 collected) from intentional and accidental coingestion of l-deprenyl with tryptamines / 2C-X-X family include severe and unpredictable crosspotentiation, peripheral vascular events, hypertension, tachycardia and severe and persistent circadian headaches. as well as acute, nasty, full blown psychedelic freakouts. if you are chasing that elusive pharmahuasca revelation, stand warned. DWTSBOL



		scarmani (Hive Bee) 10-29-04 08:49 No 538492				One Datapoint
						Swim has read several reports of adverse interactions between Selegiline and 2C-T-x's, but not tryptamines. The following is not recommended; simply provided as a datapoint. At the time Swim had been taking Selegiline @ 15 mg daily for approximately 2 weeks and found it to be an effective pro-motivational antidepressant and nootropic. Swim took 30 mg 4-HO-MiPT HCl orally. (This was a substance and a doseage level with which Swim was familiar, albeit not in combination with Selegiline. On a number of prior occasions, 30 mg 4-HO-MiPT had provided a gratifyingly involving "signature" tryptamine experience comparable for Swim to perhaps 5-7 grams dried psilocybe cubensis mushrooms. 4-HO-MiPT is Swim's favorite tryptamine, extremely vibrant and positive.) In combination with the Selegiline, the 4-HO-MiPT was quite a bit stronger than it had been in previous excursions. The intensity of the experience significantly exceeded that described in the 20 mg report in TiHKAL, and could only be described as revelatory. http://www.erowid.org/library/books_online/tihkal/tihkal22.shtml For approximately 90 minutes, Swim had what could be described as massive ecstatic out-of-body ego dissolution. In contrast to Swim's previous psychedelic experiences, Swim was disinclined to move or communicate with others at all, though it was possible with great mental effort. Throughout the experience, Swim had a carcinoid flush and noticeable pressor symptoms. These physical effects were not present without Selegiline, and were unpleasant. Despite the vast and unexpected strength of the mental effects, and the appearance of unwanted physical side effects, for Swim the experience was extremely positive overall. With a different set /or setting, or a different individual, the results could have easily been doubleplus ungood. A last note; the length of the 4-HO-MiPT experience was substantially unchanged by Selegiline; that is to say the plateau lasted about 4 hours with a 2-4 hour afterglow. boot from the shadow of a broken mirror



		Psiloman (Stranger) 10-29-04 14:10 No 538536				Very Nice!
						Very Nice information guys! Yes,with phenethylamines bad reactions can be explainable... So as i see there was some interaction between the tryptamine and selegiline! What i can comment on was that you were on a high dose regimen of selegiline,so you could possibly have had full MAOB inhibition. Maybe the experience profile would differ if it was a one time administration or if harmine/harmaline was addes as in an ayahuasca! Thank you very much for the information if someone has mor feedback i would appreciate it!

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