• N&PD Moderators: Skorpio | thegreenhand

  • Neuroscience & Pharmacology Discussion Welcome Guest
    Posting Rules Bluelight Rules
    Recent Journal Articles Chemistry Mega-Thread
    FREE Chemistry Databases! Self-Education Guide

A Second Look at MAOI's?

red22 said:
As someone who's taken selegiline in the short term in very high doses, I know that that's the placebo effect.
Click to expand...

What is placebo? The effects I am experiencing after a few days? What kinda doses are you referring to here, Red? Upwards of 20mg? Once it loses selectivity, surely if you are taking huge doses, say, 50mg or such, there is some subjectively discernable changes in cognition on account of the metabolites?

The ability to sit in one place for 3 hours, abstain from smoking pot and then patiently pull apart my phone, replace a smashed touch screen and then put it back together seems like more than just placebo to me.

Yesterday was also the first time in years that I emptied the dishwasher and cleaned the kitchen before my habitual morning masturbation.
 
Something like 80 mg for about 3 or 4 days in a row. Yeah, there was a discernible effect: vasoconstriction. No well-being effect.

Sounds like placebo to me. Anyone is capable of engaging in activities like that despite their mood, it's just a matter of taking that first step, something depression usually stops you from doing. The placebo effect incited you to make that first move.

All this being said, it's possible that you could have had significant neurotransmitter modification going on; I just wanted to emphasize that selegiline didn't have a noticeable effect in me, and I know the difference between a noticeable effect and an effect you don't notice.

But once again, this is short term selegiline use. Apparently you're supposed to use it for quite a while.
 
Oral l-dep is starting to work for me. 10mg a day has almost destroyed my social anxiety altogether :)
 
I have the opportunity to be put on the Deprenyl patch. My only hesitation is the stimulation from L-methamp, as I've had experience with Adderall in the past and the levo-amphetamine was a huge part of my switch to Dexedrine.

I can choose either Dexedrine or Deprenyl for "anti-depression". I'm curious about Deprenyl for its effects, but since I know Dexedrine so well I thought I'd go back to what I know.

Any thoughts? Should I jump into the unknown?
 
Cone said:
I have the opportunity to be put on the Deprenyl patch. My only hesitation is the stimulation from L-methamp, as I've had experience with Adderall in the past and the levo-amphetamine was a huge part of my switch to Dexedrine.

I can choose either Dexedrine or Deprenyl for "anti-depression". I'm curious about Deprenyl for its effects, but since I know Dexedrine so well I thought I'd go back to what I know.

Any thoughts? Should I jump into the unknown?
Click to expand...

L-methamphetamine is not going to stimulate you very much, in fact YOU CAN BUY L-METHAMPHETAMINE OVER THE COUNTER FOR THIS REASON.
 
red22 said:
I said this on socialanxietysupport.com, a forum where the MAOI, Nardil, is very popular, and one of the members said that Nardil is way more powerful as an antidepressant than is harmine & harmaline, the two MAOIs found in ayahuasca vine and P. harmala. Interested to hear NaPD Bluelighters thoughts on this. The person admitted that he was just speculating and that he's never given harm– a fair trial.
Click to expand...
I made memantine with amphetamine when I was active there the mainstream treatment, my username Was crayzymed, I think Nardin is extremely effective but side effect wise it's not optimal compared to that combo which I'm sure is also a more sustainable solution.

red22 said:
Go with Parnate. MAO-A is much more important from what I understand and Parnate has less side effects than Nardil. Parnate does both A & B. :)

http://www.psychotropical.com/index.php/knowledge-base/97-maois/164-maois-choices
Click to expand...

Nardin is also a gaba re-take inhibitor and basically raises all neurotransmitters that can be implicated in sa, and is therefor far more effective for treatment resistant social anxiety.

Parnate, still is very sedating, that's why the addition of a low dose of a stimulant would be a good idea, the nri, action blocks the cheese response and you'd reverse the hypotension and extreme sedation.
 
Last edited by a moderator:
Still trying to distinguish the placebo effect from the actual improvements after close to two weeks on 10mg day of Selegiline. Improved orgasm intensity and duration, has helped general and social anxiety, but depression and executive function are no different :(:)
 
Cone said:
I have the opportunity to be put on the Deprenyl patch. My only hesitation is the stimulation from L-methamp, as I've had experience with Adderall in the past and the levo-amphetamine was a huge part of my switch to Dexedrine.

I can choose either Dexedrine or Deprenyl for "anti-depression". I'm curious about Deprenyl for its effects, but since I know Dexedrine so well I thought I'd go back to what I know.

Any thoughts? Should I jump into the unknown?
Click to expand...

You feel that the stimulation (or more accurately overstimulation in this case) was from noradrenaline? I don't wanna doubt your own experience as here in Oz we can't get the mix of salts that make up Adderall, but I would have assumed that from the 12.5% of levo amp (IIRC), you would actually get slightly less stimulation from Adderall than from Dexedrine / dextro amp.

I have never used either Desoxyn (again, not approved in Oz) nor illicit meth, but from my limited experience with Selegiline / levo deprenyl over the last fortnght and dexamp over the last 2 years (ad hoc / PRN), Selegiline is nowhere near as potent a stimulant for me personally. The highest I have dosed with Selegiline is 20mg in a day (I'd missed a few days at 10mg a day), and I was able to dose 10mg sublingually and be asleep within the hour.

Admittedly, I had high hopes for this drug, but even 2.5mg of dexamp blows 20mg of Selegiline outta the water for hyperfocus / drive etc. Ideally, I'd use the Selegiline to augment and potentiate the dexamp, but as Plato worked out yonks ago, this world ain't fucken ideal. I now regret ditching my Moclobemide script that I never filled, as it appears that Selegiline and Moclobemide concomitantly could offer similar efficacy to that of Parnate (tranylcypromine) without the hypertensive risk and dietary restrictions :)

That said, nothing like a bit of old fashioned rectal amphetamine administration to blast anhedonia away for half a day :)
 
Was on 10mg Selegiline a day leading up to last Christmas. The week before Christmas I upped that to 20mg a day. On Christmas Eve I took 20mg of dexamphetamine rectally, then 10mg orally 5 hours later. I have my BP readings taken an hour before administration of dexamp, 15 minutes and 1 hour after and then at night. I can't find them right now but the increase in blood pressure was marginal.
Just thought I'd share my anecdotal experience. Remember, as countless people before me have said, this is dangerous, even with known quantities of pharmaceutical stimulants in therapeutic doses, people can die and have died from combining MAOIs and stimulants.
Always have a BP and preferably HR monitor, some clonidine and some orange juice within arms' reach :)
All the best to everybody!
 
Apparently it's not dangerous:


Im not taking Nardil but I'm taking 80mg Parnate. Recent studies show that if you're MAOI resistant stimulants can help. I'm taking 70 mg of Vyvanse and Ritalin (not Adderal). My blood pressure is normal and the MAOI started working. Some people go as high as 120mg with stimulants. Just watch your blood pressure. Of course the higher you go the dietary restrictions become more pertinent.

7/2/2014 - MRDIGBY - http://www.socialanxietysupport.com/forum/1073591857-post542.html

NOTE: 120 mg is two times the APA maximum recommended dose and such a dose has received acknowledgement by professionals:

Jay Amsterdam at the University of Pennsylvania goes up as high as 120 mg of Parnate(tranylcypramine) and claims fewer side effects at higher doses.

This Month’s Expert: Jonathan Cole, M.D. Reflections on the Use of MAOIs | Psych Central Professional


Stimulant + MAOI journal


It's only serotonin agonists that can cause serotonin syndrome when combined with MAOIs; and I learned from a recent lecture of David Nichols' given at Psychedelic Science (www.youtube.com/watch?v=ZJtdZUy1LYE) that amphetamines don't have a significant effect on serotonin.
 
Last edited:
red22 said:
Apparently it's not dangerous:


Im not taking Nardil but I'm taking 80mg Parnate. Recent studies show that if you're MAOI resistant stimulants can help. I'm taking 70 mg of Vyvanse and Ritalin (not Adderal). My blood pressure is normal and the MAOI started working. Some people go as high as 120mg with stimulants. Just watch your blood pressure. Of course the higher you go the dietary restrictions become more pertinent.

7/2/2014 - MRDIGBY - http://www.socialanxietysupport.com/forum/1073591857-post542.html

NOTE: 120 mg is two times the APA maximum recommended dose and such a dose has received acknowledgement by professionals:

Jay Amsterdam at the University of Pennsylvania goes up as high as 120 mg of Parnate(tranylcypramine) and claims fewer side effects at higher doses.

This Month’s Expert: Jonathan Cole, M.D. Reflections on the Use of MAOIs | Psych Central Professional


Stimulant + MAOI journal


It's only serotonin agonists that can cause serotonin syndrome when combined with MAOIs; and I learned from a recent lecture of David Nichols' given at Psychedelic Science (https://www.youtube.com/watch?v=ZJtdZUy1LYE) that amphetamines don't have a significant effect on serotonin.
Click to expand...

Serotonin syndrome isn't the only danger of combining drugs with MAOIs. MAOIs would potentiate the effects of amphetamines and that could potentially cause problems...
 
serotonin2A said:
Serotonin syndrome isn't the only danger of combining drugs with MAOIs. MAOIs would potentiate the effects of amphetamines and that could potentially cause problems...
Click to expand...

Then how's he taking 80 mg of Parnate with Vyvanse and* Ritalin?
exYibNv.gif


*He's probably varying them as they're not long-term drugs.
 
He was lucky and apparently didn't experience a great deal of potentiation. Because response to this combination varies so much, we can only infer limitedly from his experiences. This is why it is necessary to begin titrating upward from a known inactive dose of whichever stimulant. I also think that combination of stimulants and broad-spectrum MAO inhibition is insane.

ebola
 
ebola? said:
I also think that combination of stimulants and broad-spectrum MAO inhibition is insane.
Click to expand...

The nonselective principle has little to do with the risk because MAO-B is what amplifies amphetamine; MAO-A can only do so to a small extent, from what I understand.
 
red22 said:
The nonselective principle has little to do with the risk because MAO-B is what amplifies amphetamine; MAO-A can only do so to a small extent, from what I understand.
Click to expand...

Other way around. MAO-B is essentially a useless enzyme with trivial consequences from inhibition since its only notable high-affinity substrate is phenethylamine: https://en.wikipedia.org/wiki/Monoamine_oxidase_B#Effects_of_deficiency_in_humans

Amphetamine has a somewhat dynamic and not-very-well researched interaction with endogenous PEA, since PEA excretion + synthesis rate increase with amphetamine administration, at least in individuals with ADHD.

The only notable interaction I see arising from MAO-B inhibition would occur from taking amphetamine + exogenous PEA + an MAO-B inhibitor concurrently, since PEA would then augment amphetamine's more-or-less identical DAergic pharmacodynamic effects.
 
High PEA concentrations are linked with schizophrenic symptoms while low PEA concentrations are linked with depressive symptoms. As MAO-B inhibition can clearly affect PEA levels... It's not that "trivial".
 
Yes. Abnormal PEA levels is THE causal mechanism in schizophrenia and depression as opposed to just being correlated as a response or modulator variable.

The only neuropsychiatric disorder that excessive PEA signaling could induce is an addiction; and even with full MAO-B inhibition, that would still require exogenous PEA administration. So yes, elevated endogenous PEA is a trivial consequence of complete MAOB inhibition.
 
You must log in or register to reply here.
Top