Fwiw, this i believe is the answer "We found that genetically determined CYP2D6 functionality significantly influenced the pharmacokinetics of LSD. Individuals with no functional CYP2D6 (i.e., poor metabolizers) had longer LSD half-lives and approximately 75% higher parent drug and main metabolite 2-oxo-3-hydroxy LSD area-under-the-curve blood plasma concentrations compared with carriers of functional CYP2D6. Non-functional CYP2D6 metabolizers also exhibited greater alterations of mind and longer subjective effect durations in response to LSD compared with functional CYP2D6 metabolizers. No effect on the pharmacokinetics or acute effects of LSD were observed with other CYPs. These findings indicate that genetic polymorphisms of CYP2D6 significantly influence the pharmacokinetic and subjective effects of LSD." -
https://www.nature.com/a...cles/s41598-021-90343-y
The CYP2D6 liver enzyme is potently inhibited by Harmalas, along with CYP1A2 at the least. In my experience with 2D6, as well as 1A2 substrates, there is potentiation of those substrates by the CYP inhibition of the Harmalas, as an example i take a sleep medicine at night called Tizanidine which is metabolized by CYP1A2 which the Harmalas potently inhibit, and so normally without Harmalas/CYP1A2 inhibition i'd need 8 to 10mgs of the Tizanidine for the sedative effect i'm looking for, whereas with the Harmalas/CYP1A2 inhibition i only need 2 to 4mgs of Tizanidine for the same effect, the same also applies to Caffeine but i don't have an exact dosage measurement on that, i just know a few sips of Caffeinated soda can feel more like a cup of Coffee or even 2 or 3 cups of Coffee, depending. So the same also applies to CYP2D6 substrates.
Thing about the CYP inhibition by the Harmalas though is, it moves around, depending on dosage, so as the Harmala dosage increases, the duration of the Harmalas lengthens out, and so too does the CYP inhibition timeframe, which the CYP inhibition timeframe moves with the duration and as such the potentiation is there during certain times and not there during others, which it seems there's two main CYP inhibition phases, the first is when you first take the Harmalas, and then the second one i guess after the Harmalas metabolize into their metabolites, and so the potentiation should be noticeable when the CYP substrate and the Harmalas are taken at the same time or approx close together, while the 2nd phase of inhibition is, ime, usually around the 4th hour which depending on the dosage then can go up to 5, 6, 7, 8, 9, 10 hours, haven't particularly noticed the CYP inhibition around 12 hours post-Harmalas, though it may happen, but i usually take the Harmalas regularly and let the reverse tolerance build up and the Harmala dosage just gets stronger and stronger until it eventually hits a wall of sorts (and by that time the side-effects are long gone and it feels as clean as a medicine), but i can't say i've ever noticed the heaviest dosages possible to consume inhibiting it around hour 12, i think hour 10 seems to be the cut off.
Although the timeframe for the CYP inhibition, as well as the duration of the Harmalas, could be different if you were to consume multiple Harmala dosages within a certain timeframe, but i've usually only ever dosed the Harmalas once a day until lately i've been dosing em' twice a day (12 hours apart), and a few times i did try 3 times a day, but i think if you were going to dose Harmalas multiple times to stretch out the duration and CYP inhibition, you'd have to do here and there during the main dose. Another reason could be because Harmalas themselves are metabolized by CYP2D6 and so they inhibit their own metabolization (which could also play some sort of a role in the reverse tolerance perhaps), and so if you're consuming the Harmalas during a certain timeframe you'll catch the CYP2D6 inhibition and will thus potentiate the Harmalas in terms of dosage but also in terms of duration, although the duration potentiation/lengthening seems to depend on catching the CYP inhibition at it's max, whereas a lot of the times i've noticed CYP substrates being potentiated in terms of dosage, but not duration, the increase in duration of CYP substrates is rather difficult to pin down even though the dosage is potentiated, which ime in the past i've felt that taking the CYP substrate at the same time as the Harmalas is likely the best way to go about potentiating the CYP substrate both in dosage and duration, at least for my Tizanidine.
So as far as LSD goes, i don't think the MAO-A inhibition is going to potentiate it, even Moclobemide is somewhat of a CYP2D6 inhibitor apparently, although i'm not sure how potently compared to Harmalas, so i imagine Moclobemide might be a little difficult as well to discern potentiation of LSD via MAO-A inhibition, so that to me leaves the CYP2D6 inhibition, which should be able to be put to the test via other potent CYP2D6 inhibitors, if we could find em', which i've been curious about myself for trying to potentiate the Harmalas so that maybe the duration will lengthen out and potentially even it's gut MAO-A inhibition window (which is transient and ime lasts up to about an hour and a half to two hours after a dose of Harmalas, then gut MAO-A goes back to normal, as evidenced by lack of oral DMT activation) which could allow for an extended window of being able to re-dose the oral DMT.
So all in all, it's the CYP2D6 inhibition of the Harmalas, which the CYP inhibition timeframe/window moves around depending on dosage, although ime taking them at the same time could give max potentiation, but the point is for the substrate to come into contact with the active max CYP2D6 inhibition.
PS - With my usual dosages of Harmalas (moderate to high/heavy), i've personally found hour 6 and hour 8, respectively, to be approximately the right timeframe for the 2nd phase of CYP inhibition, with heavy heavy Harmala dosages the inhibition timeframe moves up to hour 10.