On the MAOI list for a DIFFERENT reason from everything else on it. The pods carry L-dopa, not tyramine — which is why the restriction is specifically about the pods and about large quantities, and why calling it "a tyramine food" gets the advice wrong.
Also known as: fava bean, fava pods, broad bean pods, Vicia faba. Category: food.
What it does, mechanism by mechanism
Dietary L-dopa load — provides, moderate
Food carrying levodopa, which is converted to dopamine and noradrenaline. This is why broad-bean PODS are on the MAOI list — the mechanism is L-dopa, not tyramine, and the distinction matters because it changes which part of the plant is the problem.
The mechanism is levodopa content in the pod, converted to dopamine and noradrenaline. The shelled bean itself is a much smaller concern. Stating this correctly is the difference between a workable diet and a needlessly restrictive one.
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
Gardner DM, Shulman KI, Walker SE, Tailor SAN (1996). The making of a user friendly MAOI diet. The Journal of Clinical Psychiatry 57(3):99-104. PMID 8617704
Gillman PK, Feinberg SS, Fochtmann LJ (2018). A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine myths. Journal of Neural Transmission. doi:10.1007/s00702-018-1932-y
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.