MIMOSA ACTIVE WITHOUT MAOI? (Vol. VIII, No. 1) Jonathan Ott seems to think that Mimosa hostilis is active without MAOI added. The ingredient, kokusaginine, which is morphine-like in structure, may possess MAOI properties such as the other well-known MAOI morphine-like compound, moclobemide, does. I would suggest that the kokusaginine, supposedly insoluble in water, is nonetheless extracted enough—especially with heat—to allow for sufficient MAOI effect. However, if M. hostilis is taken whole, the quantity of kokusaginine causes excess MAOI effects coupled with morphine-like effects, producing the reputed bad effects. One could make a fat extraction and if the Mimosa hostilis aqueous extraction then proved inactive, this would imply that the kokusaginine is the contributing MAOI factor. Does anyone know, for certain, what the effects of kokusaginine are? Those who are chemistry smart might check this out. — J.S., OR I have only heard of kokusaginine reported from the Rutaceae. I know nothing about its activity except for the fact a related compound was reported to be antagonistic to Ditran. I would like to hear more on all of this. I suspect tannins are what cause people problems when they ingest the actual powdered bark. (Perhaps worth noting, I’ve heard one report that someone ended up in an emergency room from ingesting powdered Mimosa tenuiflora root-bark directly.) “Morphine-like,” I love that phrase—what does it mean though? Mescaline is sometimes defined as being morphine-like because of the similarity of the subjects to an observer. I suspect this is in reference to its action in your usage. I did notice a very strong stuporous component with one bioassay of M. tenuiflora root-bark and a MAOI, that I did not in the others. JONATHAN would be the best one to talk with about this. — K. TROUT We asked Mr. OTT what his thoughts on this matter were, and he responded: It isn’t so much that I “seem to think that Mimosa [tenuiflora (Willd.) Poir. = M.] hostilis [(Mart.) Benth.—let’s get this taxonomic orthography straight for good and all] is active without MAOI added,” but rather that I know this, having felt it in my own body in the only valid scientific analysis I know: the psychonautic bioassay. This ought not be surprising, and I have always known in my bones it were so—all the scant ethnographic evidence is entirely consistent with this, and there is absolutely no evidence for some lost or missing ingredient, all the sterile and uninformed scientific speculation in this regard notwithstanding. I’ve no idea whence derives the querist’s notion that kokusaginine occurs in M. tenuiflora, and I am in agreement with K. Trout’s remark in this regard, while it is a mystery to me why it would be assumed this compound possesses MAOI activity, nor indeed how this compound—or moclobemide, with which it is structurally unrelated— is “morphine-like,” none of which has anything to do with the recondite pharmacology of jurema preta/ tepescohuite, in any case. Perhaps there is some confusion here between the rutaceous kokusaginine [found in New Caledonian Dutaillyea spp., among others] and the socalled “kukulkanins” reported from powdered stem-bark of Mexican tepescohuite [misreported as Mimosa tenuefolia L. (sic): Journal of Natural Products 52(4): 864– 867, 1989], also of obscure pharmacology. There is no reason to suppose this compound or any of the diverse saponins likewise reported from bark of Mexican tepescohuite [Phytochemistry 30(7): 2357–2360, 1991; JNP 54(5): 1247–1253, 1991; Journal of Ethnopharmacology 38(2,3): 153–157, 1993] show MAOI activity, and at least five phytochemical analyses of Brazilian jurema preta [mostly unpublished] have failed to show presence of ßcarbolines nor any other category of potent MAO. Moreover, pharmacologically and pharmacodynamically, the psychoptic effects of cold-water, hand squeezed and short-time-infused, aqueous extracts of simple pounded jurema preta root-bark prepared according to the traditional manner as documented in several Brazilian reports, bears no relation to the—to me—well-known pharmacology of the ß-carbolines and other MAOI, such as the artificial isocarboxazid and moclobemide, and others. Preliminary chemical evidence reveals rather the presence of several novel and yet-unidentified DMTadducts in jurema preta root-bark, apart from free DMT itself. Either these compounds show oral activity per se, not being substrate to gastric MAO, or rather show a higher affinity for the enzyme[s], serving thus as competitive inhibitors respective to DMT for its active site[s], in the manner that the ß-carbolines do. My current work strongly suggests the former conjecture is the more parsimonious. Remember, the simple, short-acting tryptamines are themselves MAOI, albeit far weaker than harmine and harmaline in this regard. The reported enhancements of psilocybian effects by concomitant administration of ß-carbolines suggests that even psilocine, with its dramatic oral activity, is a significant substrate for gastric MAO, as this synergy, if it is borne out scientifically, yet to be done, would almost certainly be due to inhibition of gastric MAO, as all evidence suggests that in the brain, the MAOI [at least in the case of ßcarbolines, probably via a general inhibitory effect at the GABAA receptor combined with competitive inhibition of tryptamine-binding at 5-HT receptor subtypes]; including the artificial, medicinal agents like iproniazid, etc., markedly inhibits effects of DMT and its cogeners, not to mention LSD [vide my article in MAPS VI(3): 32– 35, 1996 for references and the new edition of Ayahuasca Analogues for a discussion of this phenomenon; vide item: The Heffter Review 1: 65–77, 1998; recall also that cerebral MAO is found inside nerve-terminals, not in synapses]. Finally, why this undue and exaggerated emphasis on the ayahuasca effect in attempting to rationalize the pharmacology of jurema preta? I can assure you… — Continued — THE ENTHEOGEN REVIEW, POB 19820, SACRAMENTO, CA 95819-0820, USA