Horsfieldia superba is Uncontrolled in the United States, however, it is not approved for human consumption. This is a gray area of the law because the plant contains 5-MeO-DMT, which is classified as a Schedule I drug.
Addictive Potential: None
Emergency Room Visits Yearly: Unknown
Mandatory Minimum Sentence: Unknown
Mechanism of Action: AChE inhibitor; MAO inhibitor
Horsfieldia superba is found in Indonesia, Malaysia, and Singapore, and it is being threatened by habitat loss. It contains an alkaloid called horsfiline, which is reported to have analgesic effects that may help treat chronic pain. It also contains numerous other alkaloids including 5-MeO-DMT and 6-methoxy-2-methyl-1,2,3,4-tetrahydro-β-carboline, which is an MAOI.
Horsfieldia superba is currently legal to buy, sell, and possess in the United States.
The combination of 5-MeO-DMT and MAOIs has been linked to serotonin toxicity and death. Although no cases of death have been specifically associated with the consumption of Arundo donax and MAOIs, several deaths have been associated with the use of 5-MeO-DMT and MAOIs. As explained by Shen et al. (2010), “5-MeO-DMT is often co-abused with an MAOI such as harmaline to enhance hallucinations. There are two levels of interactions between harmaline and 5-MeO-DMT, pharmacokinetic and pharmacodynamic. When deamination metabolism is inhibited by harmaline, the systemic and cerebral exposure to 5-MeO-DMT, as well as to the metabolite bufotenine, is sharply elevated and prolonged. Meanwhile, harmaline and 5-MeO-DMT both act agonistically on the serotonergic systems. As a result, coadministration of harmaline potentiates 5-MeO-DMT drug responses and sometimes leads to severe or fatal serotonin toxicity…” Thus, due to the content of 5-MeO-DMT in Arundo donax, serotonin toxicity and death are potential health considerations.
General MAOI warnings. When ingested orally, MAOIs inhibit the catabolism of dietary amines. Sufficient intestinal MAO-A inhibition can lead to hypertensive crisis, when foods containing tyramine are consumed (so-called “cheese syndrome”), or hyperserotonemia if foods containing tryptophan are consumed. The amount required to cause a reaction exhibits great individual variation and depends on the degree of inhibition, which in turn depends on dosage and selectivity.
The exact mechanism by which tyramine causes a hypertensive reaction is not well understood, but it is assumed that tyramine displaces norepinephrine from the storage vesicles. This may trigger a cascade in which excessive amounts of norepinephrine can lead to a hypertensive crisis. Another theory suggests that proliferation and accumulation of catecholamines causes hypertensive crises.