Dietary tyramine load
Dietary tyramine load. Food that carries pressor amines produced by bacterial decarboxylation during ageing or fermentation. Harmless when gut and liver MAO-A destroy it. Not harmless when that enzyme is blocked.
Dietary L-dopa load. 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.
What acts on it
- Aged and mature cheese
— provides, strong
Walker et al. measured wide variation: many aged cheeses well above 6 mg per serving, some samples far higher, with the same named cheese varying between samples. Variability is the hazard — you cannot tell by looking. - Cured, dried and fermented meat
— provides, strong
Fermented and air-dried sausages are consistently high. Fresh meat is not a source; spoiled or improperly stored meat is. - Soy sauce and fermented soy
— provides, variable
Highly variable between products and brands. Ordinary soy sauce in a normal serving is usually modest; fermented soybean pastes and fermented bean curd can be high. - Yeast extract and brewer's yeast — provides, strong
- Tap (draught) and unpasteurised beer
— provides, variable
Bottled/canned commercial beer: low, and two standard drinks are generally regarded as acceptable in modern MAOI guidance. Tap, cask and home-brewed beer: unpredictable and occasionally high. Tailor et al. re-analysed the classic phenelzine + tap beer hypertensive case and confirmed pressor amines in the beer. - Sauerkraut, kimchi and fermented vegetables — provides, moderate
- Broad bean (fava) PODS
— provides, moderate
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. - Anything aged, fermented, pickled, smoked or spoiled
— provides, variable
Tyramine is produced by bacterial decarboxylation of tyrosine. Freshness is the variable that matters; a food that was low last week can be high after poor storage. - Mucuna pruriens (L-dopa)
— provides, strong
L-dopa is decarboxylated to dopamine and onward to noradrenaline. With a monoamine oxidase inhibitor present the pressor response is not destroyed, and that is a documented hypertensive hazard — the same mechanism that puts broad-bean pods rather than broad beans on the MAOI list. Mucuna delivers far more L-dopa than any food does. - Cacao / chocolate
— provides, weak
Chocolate appears on older MAOI diet lists. The revised tyramine literature puts its content low enough that it is no longer generally restricted, and the honest statement is that the restriction was relaxed rather than that it was always wrong.
What is affected by it
- Nothing in this dataset.
What a clean result means here
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.
In this dataset
- Monoamine oxidase inhibition (prescription MAOIs, RIMAs, linezolid, methylene blue, harmala alkaloids)
- 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
- 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
- Shulman KI, Walker SE (1999). Refining the MAOI Diet. The Journal of Clinical Psychiatry. doi:10.4088/jcp.v60n0308
- Blackwell B (1963). Hypertensive crisis due to monoamine-oxidase inhibitors. The Lancet. doi:10.1016/S0140-6736(63)92743-0
- 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
- 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
- Shulman KI, Tailor SAN, Walker SE, Gardner DM (1997). Tap (Draft) Beer and Monoamine Oxidase Inhibitor Dietary Restrictions. The Canadian Journal of Psychiatry. doi:10.1177/070674379704200311
- Tailor SAN, Shulman KI, Walker SE, Moss J, Gardner D (1994). Hypertensive Episode Associated with Phenelzine and Tap Beer — A Reanalysis of the Role of Pressor Amines in Beer. Journal of Clinical Psychopharmacology. doi:10.1097/00004714-199402000-00002
- Katzenschlager R, Evans A, Manson A, et al. (2004). Mucuna pruriens in Parkinson's disease: a double blind clinical and pharmacological study. Journal of Neurology, Neurosurgery & Psychiatry. doi:10.1136/jnnp.2003.028761
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.
Last reviewed . All interaction pages.