herb-drug interaction
12 interactions related to herb-drug interaction
aspirin + ginkgo
Ginkgo biloba can inhibit platelet-activating factor (PAF) and platelet aggregation, which can add to aspirin's irreversible inhibition of cyclooxygenase-1 and thromboxane A2. The combination may modestly increase minor bleeding events, with case reports of more serious bleeds in vulnerable patients.
rivaroxaban + ginkgo
Ginkgo biloba has antiplatelet properties and may theoretically add to the bleeding risk of rivaroxaban, although a controlled pharmacokinetic study with EGb 761 found no change in rivaroxaban plasma levels or anti-Factor Xa activity. The risk is primarily additive rather than pharmacokinetic.
apixaban + st. john's wort
St. John's wort strongly induces both CYP3A4 (apixaban's primary metabolizing enzyme) and P-glycoprotein (its efflux transporter). Co-use accelerates apixaban metabolism and clearance, lowering plasma concentrations and increasing the risk of stroke or thromboembolism.
glipizide + berberine
Berberine has potent glucose-lowering activity comparable to metformin and also inhibits CYP2C9, the enzyme responsible for clearing glipizide. The pharmacodynamic stacking plus pharmacokinetic interaction can substantially raise glipizide exposure and produce severe, prolonged hypoglycemia.
dabigatran + st. john's wort
St. John's wort is a potent inducer of P-glycoprotein (P-gp), the efflux transporter responsible for dabigatran disposition. Co-administration increases dabigatran efflux and reduces plasma concentrations, potentially leading to subtherapeutic anticoagulation and increased risk of stroke or thrombosis.
warfarin + ginkgo
Ginkgo biloba inhibits platelet-activating factor and can prolong bleeding time, adding an antiplatelet effect on top of warfarin's vitamin-K-antagonist anticoagulation. A 2025 PLOS One analysis of 2,647 prescriptions found ginkgo co-prescription was associated with a significantly higher rate of bleeding adverse events (hazard ratio ~1.38) and abnormal coagulation profiles.
clopidogrel + ginkgo
Ginkgo biloba inhibits platelet-activating factor and may add to clopidogrel's blockade of the platelet P2Y12 ADP receptor. While a healthy-volunteer study did not detect additive platelet inhibition, observational and case-report data link the combination to increased bleeding, including intracranial hemorrhage.
glipizide + bitter melon
Bitter melon (Momordica charantia) has multiple glucose-lowering mechanisms including enhanced peripheral glucose uptake and possible insulinotropic activity. Combined with the sulfonylurea glipizide, the pharmacodynamic synergism can produce significant additive hypoglycemia, particularly postprandially.
furosemide + licorice
Glycyrrhizin in licorice inhibits 11-beta-hydroxysteroid dehydrogenase type 2, allowing cortisol to act on mineralocorticoid receptors and stimulating renal potassium excretion. Combined with furosemide, this produces additive potassium wasting and a markedly higher risk of severe hypokalemia, edema, hypertension, and arrhythmia.
glipizide + ginseng
Ginseng (Panax and American) stimulates pancreatic insulin secretion through the same mechanism as glipizide. The combination is pharmacodynamically synergistic and can cause additive hypoglycemia, particularly in fasting or fed states where ginseng has demonstrated postprandial glucose reductions.
clopidogrel + garlic
Garlic supplements, especially aged garlic extract, inhibit platelet aggregation through reduced thromboxane B2 and altered platelet membrane function. Combined with clopidogrel's P2Y12 blockade, this adds antiplatelet effect and can increase bleeding risk, particularly with concentrated supplement doses.
spironolactone + licorice
Glycyrrhizin in licorice blocks 11-beta-hydroxysteroid dehydrogenase type 2 and activates mineralocorticoid receptors - the same receptors that spironolactone is designed to block. The two work in opposite directions: licorice raises blood pressure and lowers potassium while spironolactone lowers blood pressure and raises potassium, so the herb partially undoes the drug's intended therapeutic effect.