Isocarboxazid and Aged and mature cheese

Yes — there is a documented interaction between these two, and it has a named mechanism. tyramine pressor response (hypertensive reaction).

Critical Isocarboxazid + Aged and mature cheese — dietary tyramine with MAO-A inhibition

Mechanism: tyramine pressor response (hypertensive reaction)

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.

Sources: Gillman PK 2011, Walker SE 1996, Shulman KI 1999, Blackwell B 1963, Blackwell B 1967, Gillman PK 2018

The mechanism, generalised

Read the mechanism page and you can apply this to substances that are not on it: MAO-A inhibition, Dietary tyramine load.

Substance pages: Isocarboxazid · Aged and mature cheese.

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

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

  1. 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
  2. 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
  3. Shulman KI, Walker SE (1999). Refining the MAOI Diet. The Journal of Clinical Psychiatry. doi:10.4088/jcp.v60n0308
  4. Blackwell B (1963). Hypertensive crisis due to monoamine-oxidase inhibitors. The Lancet. doi:10.1016/S0140-6736(63)92743-0
  5. 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
  6. 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.

Last reviewed . All interaction pages.