Tyramine in aged and fermented food is normally destroyed by MAO-A in the gut wall and liver before it reaches the circulation. With MAO-A blocked it gets through, displaces noradrenaline from sympathetic nerve endings, and blood pressure rises abruptly.
Thresholds. The commonly cited figures: under about 6 mg of tyramine in a meal is generally regarded as safe on an irreversible MAOI; around 10–25 mg produces a measurable pressor response; and 25 mg or more risks a hypertensive reaction. Individual sensitivity varies several-fold, and the tyramine content of a named food varies several-fold between samples — which is why the rule is about food CATEGORIES and freshness rather than a lookup table you can trust to the milligram.
What the modern evidence changed. For an irreversible, non-selective MAOI (phenelzine, tranylcypromine, isocarboxazid) the dietary restriction is real and remains standard. What modern measurement changed is the LIST, not the principle: many foods on the 1960s lists — bottled and canned beer, ordinary soy sauce in a normal serving, fresh cheeses, chocolate, caffeine, most yoghurt — turned out to carry little tyramine, while yeast extract, aged cheese, fermented soy pastes, dried sausage and tap beer held up. Over-restriction is its own harm.
What to watch for. Sudden severe headache, usually occipital and described as pounding; palpitations; a stiff or sore neck; nausea and vomiting; sweating; visual disturbance. A hypertensive crisis is an emergency — the outcomes that matter are intracranial haemorrhage and cardiac.
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
The endocannabinoid enzymes and transport: FAAH, MAGL, endocannabinoid membrane transport, CB1 and CB2
Additive CNS depression and GABA-A positive modulation — the alcohol / benzodiazepine / opioid / kava axis
The phytocannabinoids delta-9-THC, cannabidiol and the converted cannabinoids, as both substrates and inhibitors
Synthetic full CB1 agonists as a class, and why they are pharmacologically unlike cannabis
CYP2E1, and phase-2 glucuronidation and sulfation where a specific entry names them
The sedative and potentiator botanicals of the kava literature, and dietary L-dopa from Mucuna
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.
Bleeding and antiplatelet risk, hypoglycaemia, anticholinergic load, and most other pharmacodynamic axes beyond the ones listed above. Additive CNS depression and GABA-A modulation ARE now modelled — see the covers list — but the absence of a sedation finding still only means the agents you named are not on that axis in this dataset.
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.
Bleeding and antiplatelet risk, which is the mechanism that matters most for garlic, ginkgo and several other common supplements. It is not modelled at all, so a clean result says nothing about it.
Whether any of the natural FAAH, MAGL or transport inhibition reported in vitro occurs at all at a dose a person would take. For most of these compounds nobody has measured it.
The actual contents of an unregulated cannabinoid product. This engine models named compounds; an unidentified isomer or side-product in a converted-cannabinoid product is outside it by construction.
Dose. Every cannabinoid interaction here scales with dose, and consumer product labelling for this category is repeatedly found inaccurate in published surveys.
Inhalation-specific hazards — thermal degradation products, diluents chosen for rheology rather than for inhalation toxicology, and carrier and adulterant contamination.
101 substances, 33 mechanisms,
101 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
Gillman PK (2011). Advances Pertaining to the Pharmacology and Interactions of Irreversible Nonselective Monoamine Oxidase Inhibitors. Journal of Clinical Psychopharmacology. doi:10.1097/JCP.0b013e31820469ea
Shulman KI, Walker SE (1999). Refining the MAOI Diet. The Journal of Clinical Psychiatry. doi:10.4088/jcp.v60n0308
Walker SE, Shulman KI, Tailor SAN, Gardner D (1996). Tyramine Content of Previously Restricted Foods in Monoamine Oxidase Inhibitor Diets. Journal of Clinical Psychopharmacology. doi:10.1097/00004714-199610000-00007
Blackwell B, Marley E, Price J, Taylor D (1967). Hypertensive Interactions Between Monoamine Oxidase Inhibitors and Foodstuffs. British Journal of Psychiatry. doi:10.1192/bjp.113.497.349
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.