Teratogenic effects of Mimosa tenuiflora in a rat model... in Pharmacology, Chemistry & Medicine Posted March 17, 2015 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. http://www.ncbi.nlm.nih.gov/pubmed/24689494 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.