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
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 ß-carbolines, 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--but will say no more at this time, pending resolution of yet-outstanding mysteries--that the psychoptic pharmacology of the tryptamines neither begins nor ends with the hallowed ayahuasca effect, exploration of which constitutes only scratching the surface of a broad and intricate, far-ranging topic, rife with scientific, commercial and political significance which has yet to dawn on psychonauts, much less ayahuasqueros, governmental sanatory authorities or pharmaceutical-corporation scientists. -- JONATHAN OTT, México
[One of the ENTHEOBOTANY instructors] at the seminar in Uxmál said that Mimosa [tenuiflora] could be used in a quick, cold water extraction. 15 minutes?! My two experiments were not successful. Maybe my Peganum harmala extract wasn't sufficient. In any case, I would like to know more about this as a possible reliable ayahuasca method. -- T.C., OR
We had heard through the grapevine that JONATHAN OTT announced at the PSYCHOACTIVITY conference in Amsterdam last year that Mimosa tenuiflora root-bark was active by itself at the 35 gm dose. In a letter regarding this, Mr. OTT confirmed what he stated above about this, noting that M. tenuiflora:
OTT, J. 1999. Personal correspondence.
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 ß-carbolines, 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--but will say no more at this time, pending resolution of yet-outstanding mysteries--that the psychoptic pharmacology of the tryptamines neither begins nor ends with the hallowed ayahuasca effect, exploration of which constitutes only scratching the surface of a broad and intricate, far-ranging topic, rife with scientific, commercial and political significance which has yet to dawn on psychonauts, much less ayahuasqueros, governmental sanatory authorities or pharmaceutical-corporation scientists. -- JONATHAN OTT, México
On the topic of Mimosa tenuiflora we also received the following question:
[One of the ENTHEOBOTANY instructors] at the seminar in Uxmál said that Mimosa [tenuiflora] could be used in a quick, cold water extraction. 15 minutes?! My two experiments were not successful. Maybe my Peganum harmala extract wasn't sufficient. In any case, I would like to know more about this as a possible reliable ayahuasca method. -- T.C., OR
We had heard through the grapevine that JONATHAN OTT announced at the PSYCHOACTIVITY conference in Amsterdam last year that Mimosa tenuiflora root-bark was active by itself at the 35 gm dose. In a letter regarding this, Mr. OTT confirmed what he stated above about this, noting that M. tenuiflora:
...is indeed active neat, with no cooking nor additives, simply by hand-squeezing briefly the pounded root-bark in water--25 g twice infused for less than an hour and minimally squeezed in 125 ml cold, neutral water each time was quite distinctly visionary and pharmahuasca-DMT-like, albeit with a slightly accelerated pharmacodynamic all-'round, which militates in favor of the directly-orally-active DMT-adduct-theory, as opposed to some endo-MAOI from same (OTT 1999).Without knowing any more details (such as amount of the Mimosa tenuiflora used, whether or not is was root-bark or stem bark, potency of whatever plant-part was used, exact length of infusion, etc.), it is hard to say what went wrong with the two experiments performed by T.C., OR. What is clear is that the case has been made by Mr. OTT that T.C., OR needn't have used any Peganum harmala extract at all, in order to experience effects. Thought we doubted not Mr. OTT'S claims, it seemed only reasonable to get a second opinion. DAVID AARDVARK stepped forth for the bioassay:
25 grams of Mimosa tenuiflora root-bark was powdered in a coffee bean grinder. The fine dust that wafted upwards when the lid was removed smelled quite strongly of DMT. (Indeed, if one burns a piece of M. tenuiflora root-bark, one can also notice the pungent odor of burning DMT.) The root-bark powder was placed into a tupperware container with 125 ml of cold tap water, shaken, and left to sit for an hour. It was then strained through a "French press" coffee filter, and soaked a second time in a fresh 125 ml of water for another hour. This was strained and the two extracts were combined and drunk. The taste was quite bitter and astringent, but didn't evoke a gag response until the final few swallows (which had a bit of fine particulate matter in them, like the last sips of Greek-style coffee might). I later learned that it was apparently traditional to add honey to this infusion, to cut the astringent bitterness (GONÇALVES DE LIMA 1946). There was some very mild stomach upset at the onset, but no real nausea to speak of at all, and no diarrhea. I was amazed that I started to feel the first effects in about 15 minutes after consumption. These built up over the next 20 minutes or so to a solid "plus 2" on the SHULGIN scale. The effects were indistinguishable from smoked DMT. I felt as though I had smoked about 25-30 mg, the only difference being the more gradual onset, and the longer duration. After hitting the peak, there was a fairly rapid decline to near baseline. This all within one hour. I was surprised to find myself almost sober for about 5-10 minutes (I could have easily driven a car), and then I started going up again! I peaked a second time, equally as high, but for perhaps a slightly shorter period of time, and came back down. Again 5-10 minutes passed where I felt almost totally sober, and again I started going up for a third time. This third peak was not as high, and did not last as long. The trip was completely over within two hours, and I felt a pleasant afterglow. I was (and am) amazed by the whole experience, and eager to try this again at a higher dose. (I'm tempted to double the dose, but will probably step up more slowly, in 10 gram increments.) There was virtually no "body load," and the whole experience was quite pleasant. I am at a loss to explain the wavelike nature of the experience with the three peaks and returns. I'd also be quite interested to know how much DMT is left in the marc from this experiment, and if this root-bark might be used a second time if it were cooked in acidified water and taken with a MAOI? More experiments are obviously needed, and I encourage ER readers to see for themselves that this astonishingly simple preparation can produce an effective, enjoyable, and brief entheogenic voyage.
References
GONÇALVES DE LIMA, O. 1946. "Observações sôbre o Vinho da Jurema' utilizado pelos índios Pancarú de Tacaratú (Pernambuco)," Ariquivos do Instituto de Pesquisas Agronómicas 4: 45-80.OTT, J. 1999. Personal correspondence.