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The Corroboree

Morris Crowley

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Posts posted by Morris Crowley

  1. Gardner, D., F. Riet-Correa, D. Lemos, K. Welch, J. Pfister, and K. Panter. 2014. Teratogenic effects of Mimosa tenuiflora in a rat model and possible role of N-methyl- and N,N-dimethyltryptamine. Journal of Agricultural and Food Chemistry, Article ASAP. doi:10.1021/jf5005176.


    The researchers fed pregnant rats with food pellets containing some M. tenuiflora leaf, seed, alkaloid extract of the leaf or seed, or purified DMT or NMT, then examined them for abnormalities at 21 days gestation. The dosage was not extreme: the greatest concentrations were in the leaf enhanced feed, which contained around 150 μg/g apiece of DMT and NMT, while the feeds enhanced with either pure DMT or NMT contained around 60 μg/g.

    Cleft palates were observed to varying degrees in all groups except for the control. Skeletal abnormalities were observed in all groups, including the control, but occurred with significantly greater frequency in the experimental feed groups. For the DMT-fed rats, skeletal deformities were observed in approximately 48% of pups, while cleft palate issues were observed in approximately 6%. For the NMT-fed rats, skeletal deformities were observed in approximately 36% of pups, while cleft palate issues were observed in approximately 19%. The group fed a mixture of DMT and NMT (at 116 and 93 μg/g feed, respectively) showed the smallest incidence of skeletal malformations of the experimental feed groups, with approximately 13%; for comparison, the incidence in the control group was approximately 9%. The combined DMT and NMT also resulted in the highest incidence of cleft palate issues, approximately 57%, and was the only feed type where any pups exhibited hard palate damage.

    There is one very curious feature about this study: the rats were not fed any monoamine oxidase inhibitors (MAOIs) during the course of the study. Under ordinary circumstances, orally-administered DMT is rapidly metabolized by monoamine oxidase (MAO) enzymes before it can enter the bloodstream. Since no MAOIs were administered and the doses do not appear sufficient to saturate the MAO enzyme, it is most likely that any effects occurred not as a direct result of DMT or NMT, but as a result of their metabolites. The primary metabolite of both DMT and NMT is indole-3-acetic acid, and has been noted as `` mutagenic for mammalian somatic cells''.

    It is also unclear why teratogenic effects would only have been noticed in rats and Brazilian cattle. They are far from the only animals that eat tryptamine-rich forage. Both sheep and cattle sometimes graze on Phalaris grass, and while they occasionally suffer phalaris staggers, no correlation between Phalaris and birth defects has been noted. And giraffes eat large quantities of tryptamine-rich Acacia foliage, apparently without issue.

    What this means for humans is unclear. While the study didn't use outlandish quantities of DMT, the dosage schedule was still very different than in a DMT-using human. For the rats, DMT was consumed throughout the day as part of every meal. In humans, DMT is not typically used on a daily basis, much less on a perpetual basis. It is difficult to draw any equivalencies between sporadic use in humans and chronic low-level use in rats. Still, it raises some concerns for any women who consume DMT while pregnant.

  2. New paper out, looking quantitatively at the alkaloid content of Tetrapterys mucronata.


    Long story short, it contains substantial amounts of bufotenine and 5-MeO-DMT, and smaller amounts of 5-MeO-NMT and 2-Me-6-MeO-THβC. That explains how it could be used without admixture as the basis of a psyhoactive brew: both bufotenine and 5-MeO-DMT have been reported active without MAOI admixture (though the authors don't seem to make that connection).

    Odd choice of plant to analyze though. T. mucronata has only been reported as the basis of an ayahuasca-like brew by one person (R. E. Schultes), and even he seems to hedge his bets about it. The language is very ambiguous both in his 1975 De plantis toxicariis... XIII article and his 1990 book The Healing Forest (coauthored with R. F. Raffauf). It's not clear, but he may be suggesting that this use was heard secondhand from a native, rather than directly observed. Or maybe his notes from the trip were just not clear... the claim dates from an expedition he took with Isidro Cabrera in the early 1950s, but he didn't publish anything about the plant until over two decades later.

    This is interesting, because recent chemical analysis of a vine sold as Tetrapterys methystica (which has been more reliably reported as the basis of an ayahuasca-like brew) did not show any known alkaloids. Then again, the vendor who sold that bark is not exactly known to be reputable... so perhaps it's a case of misidentified vine?

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  3. This is a very intriguing plant which, as far as I can tell, has never made it into cultivation. If anyone has botanically-inclined contacts in Brazil, it would be nice to change that!

    Pilocarpus pauciflorus has the potential to fill a void in the market: a viable plant source of 5-MeO-DMT. Sure, the occasional Anadenanthera seed will contain predominantly 5-MeO-DMT, but more often they contain primarily bufotenine. They simply aren't reliable. Phalaris grasses are even less reliable. Virola resin sounds like a plausible candidate, but the commercially-available bark has historically been a bust.
    Enter Pilocarpus pauciflorus, weighing in at more than 0.5% 5-MeO-DMT by weight. To be fair, that's based on a single analysis (Balsam & Voigtländer 1978). It is possible this plant may turn out to be a bust... but it could just as easily become a must-have. If you're looking for further information on the plant, most of the literature on it refers to it by the now-outdated synonym, Pilocarpus organensis.
    Any ideas on how to obtain a plant which is not currently known to be in cultivation anywhere?
    Balsam, Günter, and Hans W. Voigtländer. 1978. Ein psychotropes Alkaloid aus Pilocarpus organensis. Archiv der Pharmazie 311(12):1016-1018. DOI: 10.1002/ardp.19783111207