Curcuminoids inhibit several CYPs plus the phase-2 conjugating enzymes (UGT and SULT). Phase 2 matters here: the corpus' own metabolism files turn on glucuronidation and sulfation, and this is a common seasoning that moves both.
Also known as: curcumin, Curcuma longa, curcuminoids. Category: seasoning.
What it does, mechanism by mechanism
CYP3A4 inhibition — inhibits, moderate
Slows the enzyme that metabolises roughly half of all prescription drugs. A CYP3A4 substrate taken with a CYP3A4 inhibitor reaches higher blood levels than its dose implies.
Also inhibits UGT and SULT — a phase-2 interaction, which most interaction checkers do not model at all.
This list is what is IN the table. It is not the set of substances this interacts with — that set is
larger and partly unknown, and the mechanism is the thing to carry to a substance we have not listed.
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.
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
Volak LP, Ghirmai S, Cashman JR, Court MH (2008). Curcuminoids Inhibit Multiple Human Cytochromes P450, UDP-Glucuronosyltransferase, and Sulfotransferase Enzymes, whereas Piperine is a Relatively Selective CYP3A4 Inhibitor. Drug Metabolism and Disposition. doi:10.1124/dmd.108.020552
Bahramsoltani R, Rahimi R, Farzaei MH (2017). Pharmacokinetic interactions of curcuminoids with conventional drugs: A review. Journal of Ethnopharmacology. doi:10.1016/j.jep.2017.07.022
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.