Drug, food and seasoning interactions

Most interaction checkers are pair lookup tables, and the pairs nobody typed in are invisible. This one is built the other way round: on mechanisms. CYP3A4 inhibition is one rule and it covers grapefruit, ketoconazole, ritonavir, clarithromycin and the piperine in black pepper. A mechanism generalises to a substance that is not in the table yet. A pair list cannot.

It is also why the seasoning shelf is here rather than as a curiosity. Nutmeg, grapefruit, black pepper, licorice, cinnamon and star anise are not folk warnings — they are documented pharmacology, and the enzymes they move are the same ones your prescriptions are cleared by.

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 2026-09-09. 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.

By mechanism

CYP1A2 inhibition
Slows the caffeine/clozapine/olanzapine/theophylline enzyme.
CYP2C19 inhibition
Slows the enzyme handling clopidogrel activation, PPIs and some benzodiazepines.
CYP2C9 inhibition
Slows the enzyme handling S-warfarin, phenytoin and NSAIDs.
CYP2D6 inhibition
Slows the enzyme handling many antidepressants, antipsychotics, opioids and psilocin.
CYP3A4 inhibition
Slows the enzyme that metabolises roughly half of all prescription drugs.
Additive hepatotoxicity
Two or more agents with documented liver injury signals taken together.
MAO-A inhibition
Blocks monoamine oxidase A, the enzyme that breaks down serotonin, noradrenaline and dietary tyramine.
11β-HSD2 inhibition (pseudohyperaldosteronism)
Blocks the enzyme that inactivates cortisol in the kidney, so cortisol acts on the mineralocorticoid receptor.
P-glycoprotein inhibition
Blocks the efflux pump that ejects drugs back into the gut lumen and out of the brain.
QT prolongation
Delays cardiac repolarisation, usually by blocking the hERG potassium channel.
Seizure-threshold lowering
Agents that make a seizure more likely, additively.
Serotonin reuptake inhibition
Blocks the serotonin transporter (SERT), raising synaptic serotonin.
Dietary tyramine load
Food that carries pressor amines produced by bacterial decarboxylation during ageing or fermentation.

By substance

Specific combinations

96 combination pages exist because there is documented, cited, substance-specific material to put on them. 2460 further combinations were deliberately not given a page: a page with nothing on it is worse than no page, both for the reader and for the site.

Last reviewed 2026-09-09. All interaction pages.