Yes — there is a documented interaction between these two, and it has a named mechanism.
metabolic inhibition raising the exposure of a substance with a liver signal.
Major Alcohol (ethanol) carries a liver signal, and Grapefruit slows drug metabolism
Mechanism: metabolic inhibition raising the exposure of a substance with a liver signal
These point at the same organ from two directions. One substance here has a documented hepatotoxicity signal; the others inhibit the enzymes that clear compounds through the liver. Slower clearance means higher and more prolonged exposure to the substance carrying the signal, at an unchanged dose. This is the mechanism underneath the popular idea of using a metabolic inhibitor as a potentiator: raising exposure is precisely what makes it a potentiator, and precisely what makes it a toxicology question at the same time. The two are not separable.
What to watch for. Fatigue out of proportion to the day, nausea, loss of appetite, discomfort under the right ribs, dark urine, pale stools, itching, or yellowing of the skin or the whites of the eyes. Transaminases rise before any of that is visible, which is the argument for a blood test rather than for watching for symptoms.
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
Lieber CS (1997). Cytochrome P-4502E1: its physiological and pathological role. Physiological Reviews. doi:10.1152/physrev.1997.77.2.517
Bailey DG, Dresser G, Arnold JMO (2013). Grapefruit–medication interactions: Forbidden fruit or avoidable consequences?. CMAJ (published online 2012-11-26). doi:10.1503/cmaj.120951
Bailey DG, Spence JD, Munoz C, Arnold JMO (1991). Interaction of citrus juices with felodipine and nifedipine. The Lancet. doi:10.1016/0140-6736(91)90872-M
Paine MF, Widmer WW, Hart HL, et al. (2006). A furanocoumarin-free grapefruit juice establishes furanocoumarins as the mediators of the grapefruit juice-felodipine interaction. The American Journal of Clinical Nutrition. doi:10.1093/ajcn/83.5.1097
Lown KS, Bailey DG, Fontana RJ, et al. (1997). Grapefruit juice increases felodipine oral availability in humans by decreasing intestinal CYP3A protein expression. Journal of Clinical Investigation. doi:10.1172/JCI119439
Lundahl J, Regårdh CG, Edgar B, Johnsson G (1995). Relationship between time of intake of grapefruit juice and its effect on pharmacokinetics and pharmacodynamics of felodipine in healthy subjects. European Journal of Clinical Pharmacology. doi:10.1007/BF00192360
Greenblatt DJ, von Moltke LL, Harmatz JS, et al. (2003). Time course of recovery of cytochrome p450 3A function after single doses of grapefruit juice. Clinical Pharmacology & Therapeutics. doi:10.1016/S0009-9236(03)00118-8
Edwards DJ, Bellevue FH 3rd, Woster PM (1996). Identification of 6',7'-dihydroxybergamottin, a cytochrome P450 inhibitor, in grapefruit juice. Drug Metabolism and Disposition. doi:10.1016/s0090-9556(25)08464-8
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
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.