The corpus' own founding substance, and a jar in the average kitchen. Myristicin and elemicin are allylbenzenes; nutmeg is a documented poisoning agent with a fatal case in the literature, and myristicin has documented MAO-inhibitory activity.
Also known as: myristicin, elemicin, Myristica fragrans, mace. Category: seasoning.
What it does, mechanism by mechanism
MAO-A inhibition — inhibits, weak
Blocks monoamine oxidase A, the enzyme that breaks down serotonin, noradrenaline and dietary tyramine. Two separate hazards come off one enzyme: serotonin accumulates (toxicity) and dietary tyramine is no longer destroyed in the gut wall (pressor response).
Truitt et al. (1963) demonstrated MAO inhibition by myristicin and nutmeg. The evidence is old and largely non-human; treat it as a documented signal of uncertain human magnitude, not as an equivalent of a prescribed MAOI. Marked here deliberately as WEAK rather than dropped, because a weak documented signal in a kitchen spice is worth a reader knowing about.
Slows the enzyme that metabolises roughly half of all prescription drugs. A CYP3A4 substrate taken with a CYP3A4 inhibitor reaches higher blood levels than its dose implies.
Myristicin, elemicin and safrole are metabolised by CYP enzymes including CYP3A4 and CYP1A2; inhibiting those pathways shifts which metabolites form. This is the archive's central mechanistic claim.
Acute nutmeg poisoning is documented from roughly 5 g upward (about one to two whole nutmegs), with anticholinergic-like delirium, tachycardia, severe nausea and a 24–72 h course. A fatal case is reported in an adolescent; the Illinois Poison Center series describes 32 cases over 10 years, most in intentional-abuse context. There is no antidote — care is supportive.
A clean result means NO DOCUMENTED INTERACTION IN THIS DATASET. It does not mean safe, and it is not a clearance. Most substances are not in this dataset at all, and for many pairs that are, nobody has ever studied the combination.
Serotonergic drugs and the serotonin-toxicity mechanism
Dietary tyramine and L-dopa loads
The major cytochrome P450 pathways: CYP3A4, CYP2D6, CYP1A2, CYP2C9, CYP2C19 — inhibition and induction
P-glycoprotein inhibition and induction
11β-HSD2 inhibition (the licorice mechanism) and the potassium consequences that follow it
QT prolongation as an additive pharmacodynamic axis
Culinary seasonings and common foods with documented pharmacological activity
A selected set of narrow-therapeutic-index drugs where those shifts matter most
Not in this dataset
Any substance not named in this dataset — which is most substances. There are tens of thousands of marketed drugs and this table holds fewer than a hundred entries.
Phase-2 conjugation (UGT, SULT, NAT2, COMT) except where a specific entry names it. The oilahuasca corpus turns heavily on phase 2 and this engine models it only in passing.
Pharmacogenomics. CYP2D6 and CYP2C19 are strongly polymorphic; a poor metaboliser and an ultra-rapid metaboliser can have opposite outcomes from the same pair, and this engine does not know your genotype.
Dose, timing, duration, formulation and route — all of which change whether a documented interaction is clinically real for you.
Renal and hepatic impairment, age, pregnancy, and body composition.
Additive sedation, respiratory depression, bleeding risk, hypoglycaemia and most other pharmacodynamic axes beyond the ones listed above.
Herb–herb interactions outside the named entries, and essentially the whole botanical world: most plants have no interaction literature at all.
Allergy, intolerance, and contamination or adulteration of unregulated products.
Anything published after the last-reviewed date below.
72 substances, 20 mechanisms,
64 citations. Last reviewed .
Primary literature (every DOI resolved against the Crossref API) and FDA drug labelling. There is no free, openly-licensed, comprehensive drug-interaction dataset to draw on; NLM retired its Drug Interaction API on 2024-01-02 and DrugBank's interaction set is a commercial licence.
References
Truitt EB Jr, Duritz G, Ebersberger EM (1963). Evidence of Monoamine Oxidase Inhibition by Myristicin and Nutmeg. Proceedings of the Society for Experimental Biology and Medicine. doi:10.3181/00379727-112-28128
Beyer J, Ehlers D, Maurer HH (2006). Abuse of Nutmeg (Myristica fragrans Houtt.): Studies on the Metabolism and the Toxicologic Detection of its Ingredients Elemicin, Myristicin, and Safrole in Rat and Human Urine Using Gas Chromatography/Mass Spectrometry. Therapeutic Drug Monitoring. doi:10.1097/00007691-200608000-00013
Stein U, Greyer H, Hentschel H (2001). Nutmeg (myristicin) poisoning — report on a fatal case and a series of cases recorded by a poison information centre. Forensic Science International. doi:10.1016/S0379-0738(00)00369-8
Ehrenpreis JE, DesLauriers C, Lank P, Armstrong PK, Leikin JB (2014). Nutmeg Poisonings: A Retrospective Review of 10 Years Experience from the Illinois Poison Center, 2001-2011. Journal of Medical Toxicology. doi:10.1007/s13181-013-0379-7
Every DOI above was resolved against the Crossref API on 2026-09-09 and the returned
title checked against the one printed here. Three DOIs in the first draft resolved to real but different
papers and were corrected before publication.