Minute amounts of betacarbolines are known to potentials psychedelic effects, including on the mg scale of ingestion, which likely causes only traces to reach the brain.
Irreversible MAOIs were the first antidepressants to be discovered, but they fell out of favour with the advent of the discovery of safer antidepressants; these newer antidepressant drug classes have fewer adverse effects, especially the dangerous irreversible MAOI food interaction with tyramine, sometimes referred to as the 'cheese syndrome', which leads to dangerous hypertension. However, reversible MAOIs lack these hypertensive adverse effects.[25] Moclobemide, was the first reversible inhibitor of MAO-A to enter widespread clinical practice; its reversible inhibitory features give it a number of advantages over the older irreversible MAO inhibitors.[26]
That is from the Wikipedia page on MAO.
The tyramine thing is not medically or scientifically supported with Harmala alkaloids.
When I wrote that harmala alkaloids have complex action, I was referring to them in general, the alkaloids in caapi are called harmala alkaloids, harmine is a harmala alkaloid etc. harmine has very complex action, it affects GABA, glutamic acid and other things. I believe that the effects of potentiation are due to the glutamic acid related effects. I have written quite a bit on this topic and how it relates to ayahuasca additives as well elsewhere. Needless to say, Ott reported potentiation of effects of tryptamines using 5mg harmine. In the Amazon very small doses are also reported to have been taken as hunting aids, because of specific effects. I have also used slivers of caapi for this same effect, about the volume to two wooden matches, and have given this to friends as well who report specific effects. My point is that trace amounts of betacarbolines may be plenty.
I can't find cases of problems with high blood pressure for harmala alkaloids that do not involve irresponsible doses. I read one case with a ridiculous dose, it might have been that Kansas City thing you mention.
The levels of norharman and harman in nonalcoholics were unchanged after a load with ethanol (1 g/kg body weight). The norharman levels of the alcoholics were significantly higher than that of the nonalcoholic controls (99.5 +/- 26.6 pg/ml vs. 26.9 +/- 10.7 pg/ml; p less than 0.001) and did not change significantly during a 3-week detoxication period. In the subgroup of alcoholics with delirium or hallucinosis, a slight increase of norharman during detoxication could be detected while in alcoholics with vegetative withdrawal symptoms norharman levels dropped slightly over time (p = 0.07)
Norharman levels were tripled in alcoholics.
Moreover in those with delirium and hallucinations during withdraws a slight increase of norharman was observed, possibly indicating a correlation between the delirium and hallucinations and the betacarboline.
Considering that betacarbolines are considered to have effects at trace levels, and there are numerous studies for this, this is still significant, but this is only plasma levels, what about the brain, could the molecules be perhaps sequestered there? Perhaps:
Two classes of amine-aldehyde adducts, the tetrahydroisoquinoline (TIQ) and beta-carboline (THBC) compounds, have been implicated in the mechanism in the brain underlying the addictive drinking of alcohol. One part of this review focuses on the large amount of evidence unequivocally demonstrating not only the corporeal synthesis of the TIQs and THBCs but their sequestration in brain tissue as well. Experimental studies published recently have revealed that exposure to alcohol enhances markedly the endogenous formation of condensation products. Apart from their multiple neuropharmacological actions, certain adducts when delivered directly into the brain of either the rat or monkey, to circumvent the brain's blood-barrier system, can evoke an intense and dose-dependent increase in the voluntary drinking of solutions of alcohol even in noxious concentrations
Here is a quote from an abstract that says that THBC is sequestered in the brain. That alcohol enhances the formation of this markedly.
So yeah in summary:
The tyramine thing is not true, nor is the ayahuasca diet one designed to prevent hypertension, RIMAs are rather safe and this has been rather well demonstrated.
Very low amounts of betacarbolines are capable of effective potentiation.
Alcohol promotes the formation of betacarbolines, particularly in alcoholics, which are sequestered by the brain.
And of course, the potentiation effect seems due to the glutamate system in the brain, which is linked to the psychedelic activity, I have not posted much about that here but here, read post 13
Not any of this explains delayed effects that the OP reported, but it is worth addressing.