In light of the thread DMT does what? Thought it would be good to make a thread about harmalas.

Apparently their mechanism of action is fairly complex. Granted much of there action is probably yet theoretical as harmalas are not well-researched (edit: pardon my ignorance ! ) but would love to learn more about what happens when harmalas are ingested.

Theyre actually quite well researched, aswell as inhibiting MAO-A and B (in large doses) they also inhibit acetylcholine esterase.
Ive found in the past that when smoking a ciarette after smoking harmalas that half way through the cigarette I am satisfied and dont want to smoke anymore of it.

Ah pardon my ignorance.

are you capable of sharing the source or pointing the way to some relevant studies?

I'm hoping to find this one :
Udenfriend, S., B. Witkop, B. G. Redfield, and H. Weissbach. 1958. Studies with reversible inhibitors of monoamine oxidase: Harmaline and related compounds. Biochemical Pharmacology 1:160–65.


But there are probably others too.

Just follow the wiki trail
Heres one reference http://link.springer.com...1007%2Fs12272-009-1910-x yes its not a study on peganum harmala hut read this bit which is relevant...

" The results of in vitro semi-quality TLC-bioautographic assay showed that harmine, harmaline and harmol displayed a similar AChE inhibitive activities comparing to galanthamine." Anyone know what a "semi-quality TLC" is?

Acetycholine is a neuromodulator itself, harmalas could possibly stop it breaking down.
Which is why I speculate that it could have a use in the treatment of nicotine addiction because the acetycholine receptors will get more acetylcholine therefore the effects of nicotine will be more pronounced and you will need less to fulfil that craving.

On a different tangent Ive noticed a significant potentiation of rue extract after taking Alpha GPC , which is a precursor to acetylcholine.

So AGPC and harmala theoretically could lead to more serotonin, dopamine, norepinethrine AND acetylcholine in the brain with the acetylcholine modulating all the others mentioned above. A sort of see-saw potentiation effect.
Im by no means an expert in the field but if I have understood the mechanism of action correctly then this is the knock-on effect I could see happening.

Please post your links I will be interested to see what you find too!

Check this out for a laundry list of effects as currently understood.

http://www.ncbi.nlm.nih....pmc/articles/PMC3841998/

Wow thats mindblowing...

That is an awesome paper! It could be of interest in several of my physical problems and possibly replace other drugs if enough research were done. I have recently become interested in it because of the obvious reason but also hopefully in my coffee and cigarette consumption. Now quite a few other possibilities by the sounds of it. I have stopped any "real" antidepressants. Cymbalta, abilify, budoprion (sp) and started using only 5-HTP, plus getting my thyroid meds to a working level with natural dessicated thyroid for hypo-thyroidism (underactive thyroid), and stopped the levothyroxine. Ill start low(er) with caapi or rue alks but does anyone see an immediate problem with these substances?

Udenfriend, S., B. Witkop, B. G. Redfield, and H. Weissbach. 1958. Studies with reversible inhibitors of monoamine oxidase: Harmaline and related compounds. Biochemical Pharmacology 1:160–65.

Thanks. Im not all that great yet with understanding some of the terms (i will continue to look them up as time allows) . It sounds like the harmaline/harmine would stop the re-uptake or quick use of serotonin? So with my 5-thp which produces or allows you to produce serotonin, I would need less to get and keep my anti depressive anti anxiety effects with regular use of extracted harmines? Or less harmines to get the desired effect? Just trying to understand, dont worry I wont treat myself on a regular basis without more reading.

LT = L tryptophan
Although no specific reports have been published, it is possible that 5-HTP, when taken in combination with either a selective serotonin reuptake inhibitor (SSRI) antidepressant such as fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), or fluvoxamine (Luvox), or an MAOI antidepressant such as phenelzine (Nardil) or tranylcypromine (Parnate) may cause a condition known as serotonin syndrome. This syndrome has been reported in patients taking LT at doses above 1200 mg/day along with MAOIs, but was not identified in a 12-month study with 5-HTP (200 mg/day) taken in conjunction with an MAOI drug.

Tryptamine derivatives and beta-Carbolines have been detected as endogenous metabolites in mammals, including humans. Methyl transferases that catalyze the synthesis of tryptamines, including DMT, 5-MeO-DMT and bufotenine, are found in human lung, brain, cerebrospinal fluid, liver and heart (McKenna & Towers 1984). In the pineal gland MAO is the primary inactivation pathway of serotonin, a neurotransmitter synthesized from the amino acid tryptophan. If MAO is blocked by harmine, harmaline or other MAO inhibitors serotonin can be converted by the methyltransferase enzymes HIOMT and INMT into psychedelic tryptamines (serotonin --(HIOMT)--> 5-MeO-trypt. --(2*INMT)--> 5-MeO-DMT).