The data behind the verdict
The data behind the verdict
20 supplements
Cross-reference any supplement against your medications.
Warfarin (Coumadin)
Concurrent use of fish oil and anticoagulants like warfarin can increase the International Normalized Ratio (INR) and elevate the risk of bleeding.
Omega-3 fatty acids in fish oil can inhibit platelet aggregation and reduce the levels of vitamin K-dependent coagulation factors. This potentiates the anticoagulant effects of medications like warfarin.
A longer bleeding time is reported at 2 to 15 g a day of EPA and DHA combined. No upper limit has been set. The bleeding concern matters most if you take a blood thinner.
Moderate-dose omega-3 (under 3 g per day) generally safe with warfarin per published data. High doses may require INR monitoring.
EPA and DHA at over 3 g per day mildly inhibit thromboxane A2 synthesis. Mixed evidence on INR shift with warfarin.
SourcePMID 25062404
Clopidogrel (Plavix)
A longer bleeding time is reported at 2 to 15 g a day of EPA and DHA combined. No upper limit has been set. The bleeding concern matters most if you take a blood thinner.
Observational additive bleeding risk. Monitor closely.
Omega-3 fish oil high-dose additive antiplatelet effect with clopidogrel.
High-dose Aspirin
Mild bleeding risk increase.
Additive antiplatelet effects via different mechanisms. Generally safe at standard doses.
A longer bleeding time is reported at 2 to 15 g a day of EPA and DHA combined. No upper limit has been set. The bleeding concern matters most if you take a blood thinner.
Omega-3 fish oil high-dose may add to the bleeding risk of Aspirin. No study examines this pair; the supplement evidence was gathered with aspirin or warfarin. Tell your clinician you take both and stop the supplement before surgery.
Omega-3 fish oil high-dose has antiplatelet activity that is observationally additive to aspirin.
Blood pressure medications
Beneficial cardiovascular combination. Mild additive BP lowering at high doses (>3 g/day EPA+DHA).
Omega-3 fatty acids (EPA/DHA) modestly lower blood pressure and reduce vascular inflammation. Generally complementary with Lisinopril.
Beneficial cardiovascular combination. Mild additive BP lowering at high doses (>3 g/day EPA+DHA).
Omega-3 fatty acids (EPA/DHA) modestly lower blood pressure and reduce vascular inflammation. Generally complementary with Losartan.
Beneficial cardiovascular combination. Mild additive BP lowering at high doses (>3 g/day EPA+DHA).
Omega-3 fatty acids (EPA/DHA) modestly lower blood pressure and reduce vascular inflammation. Generally complementary with Ramipril.
Beneficial cardiovascular combination. Mild additive BP lowering at high doses (>3 g/day EPA+DHA).
Omega-3 fatty acids (EPA/DHA) modestly lower blood pressure and reduce vascular inflammation. Generally complementary with Valsartan.
Orlistat (Alli)
Stop 2 weeks before surgery
Bleeding risk from antiplatelet effect.
The most interaction-prone supplement in common use. St. John's Wort induces multiple drug-metabolism enzymes and can cause treatment failure across many drug classes.
SSRIs (Prozac, Zoloft, Lexapro)
Do not combine
Do not stop your medicine. Ask your prescriber before taking this supplement.
Serotonin syndrome, seizures, rhabdomyolysis.
Additive serotonergic activity. St. John's Wort inhibits serotonin reuptake similarly to SSRIs; combined use produces excessive serotonergic stimulation.
SNRIs (Effexor, Cymbalta)
Ask your prescriber first
Potentially fatal serotonin syndrome. Discuss with prescriber before either is started.
St. John's Wort is serotonergic and induces CYP3A4. Combined with SNRI's reuptake blockade: massive synaptic serotonin surge.
Oral contraceptives
Contraceptive failure and unintended pregnancy. Multiple case reports documented.
St. John's Wort is a potent CYP3A4 inducer that accelerates metabolism of estrogen and progestin components in oral contraceptives.
SourcePMID 19719333
Cyclosporine
Do not combine
Do not stop your medicine. Ask your prescriber before taking this supplement.
Acute organ rejection requiring return to dialysis; a 29-year-old kidney/pancreas transplant recipient developed chronic rejection after cyclosporine levels became subtherapeutic.
St. John's Wort induces CYP3A4 isoenzyme activity and P-glycoprotein (P-gp) expression in the liver and small intestines, accelerating cyclosporine metabolism and reducing its absorption, leading to subtherapeutic concentrations.
Do not combine
Do not stop your medicine. Ask your prescriber before taking this supplement.
ACUTE ORGAN REJECTION. Multiple case reports of transplant failure documented.
NEVER take St. John's Wort with transplant medications without explicit physician approval. Multiple case reports document acute organ rejection from CYP3A4 induction lowering immunosuppressant levels.
St. John's Wort potently induces CYP3A4 and P-glycoprotein, dropping tacrolimus / cyclosporine levels to subtherapeutic.
Warfarin
St. John's Wort significantly reduces the pharmacological effect of warfarin, leading to a decreased international normalized ratio (INR) and potentially increasing the risk of thrombosis.
St. John's Wort induces the apparent clearance of both S-warfarin and R-warfarin by inducing cytochrome P450 (CYP) enzymes, particularly CYP3A4 and CYP2C9, which are responsible for warfarin metabolism.
SourcePMID 19719333
Chemotherapy agents
Do not combine
Do not stop your medicine. Ask your prescriber before taking this supplement.
Concomitant St. John's Wort reduced imatinib AUC by 30%. Avoid the combination.
CYP3A4 induction by St. John's Wort dramatically reduces imatinib plasma levels.
HIV protease inhibitors (ritonavir, indinavir)
Digoxin
Theophylline
Triptans (sumatriptan)
Stop 2 weeks before surgery
Anesthesia interactions from CYP enzyme induction.
Fluoroquinolone antibiotics (Cipro, Levaquin)
Take at different times
Take ciprofloxacin at least 2 hours before or 6 hours after magnesium. Take levofloxacin at least 2 hours before or after magnesium. Take moxifloxacin at least 4 hours before or 8 hours after magnesium. For any other fluoroquinolone or a tetracycline, ask your pharmacist how far apart to take them, because magnesium reduces how much of the antibiotic is absorbed.
Reduced absorption and bioavailability of the antibiotic, potentially leading to decreased systemic exposure and treatment failure against bacterial infections.
Magnesium ions form insoluble chelates with fluoroquinolones and tetracyclines in the gastrointestinal tract. This complexation prevents the antibiotic from being absorbed across the intestinal mucosa.
Tetracycline antibiotics
Take at different times
Take ciprofloxacin at least 2 hours before or 6 hours after magnesium. Take levofloxacin at least 2 hours before or after magnesium. Take moxifloxacin at least 4 hours before or 8 hours after magnesium. For any other fluoroquinolone or a tetracycline, ask your pharmacist how far apart to take them, because magnesium reduces how much of the antibiotic is absorbed.
Reduced absorption and bioavailability of the antibiotic, potentially leading to decreased systemic exposure and treatment failure against bacterial infections.
Magnesium ions form insoluble chelates with fluoroquinolones and tetracyclines in the gastrointestinal tract. This complexation prevents the antibiotic from being absorbed across the intestinal mucosa.
Bisphosphonates (Fosamax, Boniva)
Take at different times
Take alendronate at least 30 minutes before magnesium. Take ibandronate at least 60 minutes before magnesium. For risedronate or any other bisphosphonate, ask your pharmacist how far apart to take them, because magnesium reduces how much of the bisphosphonate is absorbed.
Decreased absorption and bioavailability of bisphosphonates, potentially reducing their efficacy in treating osteoporosis.
Magnesium and other divalent cations physically bind to bisphosphonates in the gastrointestinal tract through chelation. This forms an insoluble complex that prevents the bisphosphonate from being absorbed into the bloodstream.
Levothyroxine (Synthroid)
Muscle relaxants and sedatives
Potassium-sparing diuretics
Timing Separation Rules
Levothyroxine (Synthroid)
Take at different times
Separate from thyroid hormone dose by at least 4 hours. Take Levothyroxine on an empty stomach 30 to 60 minutes before food, coffee, or supplements.
Concurrent administration of calcium carbonate and levothyroxine can lead to reduced levothyroxine absorption and increased serum thyrotropin levels, potentially causing hypothyroidism.
Take Levothyroxine at least 4 hours apart from calcium-containing supplements. Calcium can reduce Levothyroxine absorption by 20 to 40 percent and cause under-replacement.
Levothyroxine adsorbs to calcium carbonate in an acidic environment, such as the stomach, which reduces its bioavailability and absorption.
Calcium carbonate taken with levothyroxine significantly lowered free and total T4 and raised TSH. One in five patients moved above the normal TSH range. Separate doses by four hours.
Calcium forms an insoluble complex with levothyroxine in the gut, reducing absorption by 20-25%.
Fluoroquinolones (Cipro)
Take at different times
Take this antibiotic at a DIFFERENT time from mineral supplements. Minerals taken within 2 hours (before) or 6 hours (after) of fluoroquinolone antibiotics significantly reduce antibiotic absorption. Discuss timing with your prescriber or pharmacist.
Significant antibiotic absorption loss → treatment failure risk.
Divalent cation chelation in the gut prevents fluoroquinolone absorption.
The formation of stable fluoroquinolone-calcium chelates decreases the absorption rate and systemic exposure of the antibiotic, leading to significant reductions in pharmacokinetic parameters such as C_max and AUC, which can impair therapeutic efficacy.
Fluoroquinolones interact with multivalent metal cations like calcium in the gastrointestinal tract to form stable, insoluble chelates. This chelation reduces the oral bioavailability of the antibiotic by preventing its absorption across the intestinal mucosa.
Tetracycline and doxycycline
Iron supplements
Bisphosphonates (Fosamax)
Thiazide diuretics (HCTZ)
Timing Separation Rules
Vitamin K is the direct pharmacological antagonist of warfarin. Supplementing without cardiology supervision can cause dangerous clots.
Warfarin (Coumadin)
MK-7 supplementation may reduce warfarin effectiveness more than equivalent K1 dose due to longer tissue retention. INR monitoring required when starting or stopping MK-7.
MK-7 is more potent INR-lowering than K1 at similar doses. Avoid initiating without prescriber awareness.
Vitamin K2 menaquinone-7 has long half-life and accumulates more than K1. Even modest MK-7 doses (45 to 180 mcg per day) can antagonize warfarin and lower INR.
High-dose vitamin K1 supplementation (over 100 mcg per day) can reverse warfarin anticoagulation, reducing INR and increasing thrombosis risk. Inconsistent vitamin K intake causes INR fluctuations. Standard advice: maintain consistent daily vitamin K intake; avoid high-dose vitamin K supplements unless prescribed for warfarin reversal.
Vitamin K1 directly antagonizes warfarin. Avoid high-dose vitamin K supplements (over 100 mcg) without prescriber guidance. Maintain consistent vitamin K dietary intake to stabilize INR.
Vitamin K1 (phylloquinone) is the direct substrate antagonized by warfarin. Warfarin inhibits VKORC1 to prevent vitamin K recycling. Exogenous vitamin K1 directly reverses warfarin anticoagulation.
Decreased sensitivity to warfarin, leading to lower INR and a requirement for higher maintenance doses of warfarin to achieve adequate anticoagulation.
Vitamin K directly antagonizes the pharmacodynamic effect of warfarin, which acts as a vitamin K antagonist by inhibiting the vitamin K epoxide reductase complex, thereby overcoming the drug's inhibition of vitamin K-dependent clotting factor synthesis.
Warfarin and other anticoagulants
The adult upper limit is 1,000 mg a day, but bleeding risk has been reported below it. Trials found more hemorrhagic stroke at 50 mg a day, and at 400 IU every other day in people who were mostly also taking aspirin. This matters most if you take a blood thinner.
High-dose vitamin E (over 400 IU per day) increases bleeding risk in warfarin users. Limit vitamin E to nutritional doses (under 100 IU) while on warfarin and monitor for bleeding signs.
Vitamin E doses over 400 IU per day increase bleeding risk with warfarin. Limit to nutritional doses (under 100 IU).
Alpha-tocopherol at over 400 IU per day inhibits platelet aggregation. Large RCT data show increased bleeding risk in anticoagulated patients.
High-dose vitamin E intake can cause serious bleeding events when taken with anticoagulants.
High-dose vitamin E intake inhibits vitamin K-derived coagulation factor synthesis.
Aspirin and NSAIDs
The adult upper limit is 1,000 mg a day, but bleeding risk has been reported below it. Trials found more hemorrhagic stroke at 50 mg a day, and at 400 IU every other day in people who were mostly also taking aspirin. This matters most if you take a blood thinner.
Observational data suggest additive bleeding risk with aspirin. Monitor for unusual bleeding.
Vitamin E high-dose has antiplatelet activity that is observationally additive to aspirin.
Chemotherapy (alkylating agents)
Do not combine
Do not stop your medicine. Ask your prescriber before taking this supplement.
May reduce chemotherapy efficacy. Avoid high-dose supplementation during active treatment.
High-dose antioxidant supplements may reduce chemotherapy efficacy. Avoid during active treatment. Discuss with your oncology team. Dietary antioxidants from food are generally acceptable.
Same antioxidant mechanism as Vitamin C; alpha-tocopherol may interfere with ROS-dependent cytotoxic effects.
Statins combined with niacin
Stop 2 weeks before surgery
High-dose bleeding risk.
Levothyroxine
Take at different times
Separate from thyroid hormone dose by at least 4 hours. Take Levothyroxine on an empty stomach 30 to 60 minutes before food, coffee, or supplements.
Simultaneous ingestion of ferrous sulfate and thyroxine causes a variable reduction in thyroxine efficacy that is clinically significant in some patients, leading to hypothyroidism.
Take Levothyroxine at least 4 hours apart from iron supplements. Iron can reduce Levothyroxine absorption by 30 to 50 percent.
Iron binds to levothyroxine in the gastrointestinal tract, forming an insoluble complex that reduces the absorption and bioavailability of the thyroid hormone.
Tetracycline and doxycycline
Take at different times
Take ciprofloxacin at least 2 hours before or 6 hours after iron. Take levofloxacin at least 2 hours before or after iron. Take moxifloxacin at least 4 hours before or 8 hours after iron. For any other fluoroquinolone or a tetracycline, ask your pharmacist how far apart to take them, because iron reduces how much of the antibiotic is absorbed.
Concomitant use of iron supplements and fluoroquinolones or tetracyclines significantly impairs the oral absorption and bioavailability of the antibiotics, potentially leading to treatment failure.
Iron forms insoluble chelates with fluoroquinolones and tetracyclines in the gastrointestinal tract. This chelation prevents the absorption of both the antibiotic and the iron into the bloodstream.
Fluoroquinolones
Take at different times
Take ciprofloxacin at least 2 hours before or 6 hours after iron. Take levofloxacin at least 2 hours before or after iron. Take moxifloxacin at least 4 hours before or 8 hours after iron. For any other fluoroquinolone or a tetracycline, ask your pharmacist how far apart to take them, because iron reduces how much of the antibiotic is absorbed.
Concomitant use of iron supplements and fluoroquinolones or tetracyclines significantly impairs the oral absorption and bioavailability of the antibiotics, potentially leading to treatment failure.
Iron forms insoluble chelates with fluoroquinolones and tetracyclines in the gastrointestinal tract. This chelation prevents the absorption of both the antibiotic and the iron into the bloodstream.
Antacids, PPIs, H2 blockers
Levodopa (Parkinson's)
Methyldopa
Timing Separation Rules
Fluoroquinolone antibiotics
Take at different times
Take this antibiotic at a DIFFERENT time from mineral supplements. Minerals taken within 2 hours (before) or 6 hours (after) of fluoroquinolone antibiotics significantly reduce antibiotic absorption. Discuss timing with your prescriber or pharmacist.
Reduced antibiotic absorption → treatment failure risk.
Zinc chelation in the gut prevents fluoroquinolone absorption.
Penicillamine (Wilson's disease)
Take at different times
Take penicillamine at least 1 hour apart from zinc, on an empty stomach.
Concurrent administration of zinc and penicillamine may result in decreased gastrointestinal absorption and diminished therapeutic effects of penicillamine.
Zinc, a polyvalent cation, can chelate with penicillamine in the gastrointestinal tract, forming a nonabsorbable complex that reduces the absorption of both agents.
Tetracycline antibiotics
Copper (chronic high-dose zinc)
Timing Separation Rules
Warfarin and other anticoagulants
Curcumin has antiplatelet activity in laboratory studies. No study examines it with any anticoagulant or antiplatelet drug; an additive effect is theoretical.
Curcumin and its derivatives prolong activated partial thromboplastin time (aPTT) and prothrombin time (PT) by inhibiting the generation of thrombin and activated factor X (FXa). This antiplatelet and anticoagulant activity potentiates the effects of blood-thinning medications.
This row describes concentrated turmeric or curcumin supplements rather than a specific dose, not turmeric used in cooking.
Theoretical mild additive antiplatelet effect. Limited published case reports.
Curcumin has weak antiplatelet effects and may inhibit CYP2C9 in vitro. Clinical impact at standard supplement doses uncertain.
Aspirin and NSAIDs
Curcumin has antiplatelet activity in laboratory studies. No study examines it with any anticoagulant or antiplatelet drug; an additive effect is theoretical.
Curcumin and its derivatives prolong activated partial thromboplastin time (aPTT) and prothrombin time (PT) by inhibiting the generation of thrombin and activated factor X (FXa). This antiplatelet and anticoagulant activity potentiates the effects of blood-thinning medications.
This row describes concentrated turmeric or curcumin supplements rather than a specific dose, not turmeric used in cooking.
Theoretical additive antiplatelet effect with aspirin. Monitor for bruising or unusual bleeding.
Turmeric and curcumin high-dose has antiplatelet activity that is additive to aspirin's COX-1 inhibition.
Diabetes medications (metformin, sulfonylureas)
No interaction concern with metformin. No benefit is claimed.
Curcumin has weak CYP and P-gp modulation effects in vitro. Metformin is not significantly metabolized by CYP enzymes; clinical interaction unlikely.
CYP3A4 substrates
This row describes concentrated turmeric or curcumin supplements rather than a specific dose, not turmeric used in cooking.
Generally minor. Monitor BP with high-dose supplementation.
High-dose curcumin has anti-inflammatory and mild antihypertensive activity. Weak CYP modulation in vitro.
Theoretical mild interaction. Clinically minor.
High-dose curcumin has weak CYP modulation in vitro. Bisoprolol interaction theoretical.
Tacrolimus or cyclosporine
Basis: Theoretical
Stop 2 weeks before surgery
High-dose antiplatelet effect.
Levothyroxine and thyroid medications
The interaction can lead to iatrogenic thyrotoxicosis, presenting with symptoms such as supraventricular tachycardia, due to excessive thyroid hormone levels.
Ashwagandha root extract is postulated to stimulate thyroidal activity by increasing the synthesis and/or release of thyroxine (T4) at the glandular level. Additionally, some Ashwagandha supplements may contain clinically relevant amounts of T3 and T4, further elevating thyroid hormone concentrations.
SourcePMID 28829155
Immunosuppressants (cyclosporine, tacrolimus, prednisone)
Ashwagandha may counteract the intended effects of immunosuppressant medications, leading to reduced suppression of the immune system and potential organ rejection or disease flare-ups.
Ashwagandha has immunostimulatory properties that activate both the innate and adaptive arms of the immune system, enhancing overall immune function. This immune stimulation can counteract the effects of immunosuppressive drugs like cyclophosphamide or dexamethasone.
Diabetes medications
Monitor thyroid function if both initiated together; clinically significant interaction with metformin not expected.
Ashwagandha may modulate thyroid axis (typically T4 increase) and HPA axis. No direct metformin interaction.
Sedatives and benzodiazepines (Xanax, Valium)
Blood pressure medications
Metformin
Co-administration of berberine and metformin can lead to an additive hypoglycemic effect, increasing the risk of hypoglycemia.
Berberine inhibits the transport activity of organic cation transporters (OCT1 and OCT2), which govern the disposition of metformin, thereby increasing the plasma concentration and systemic exposure of metformin.
Hypoglycemia risk. Monitor blood glucose. Consider drug-interaction effects via inhibited CYPs.
Both activate AMPK. Berberine also inhibits CYP3A4/2D6/2C9. Additive hypoglycemic effect plus altered metabolism of other drugs.
SourcePMID 37439907
CYP2D6 substrates (codeine, tramadol, many antidepressants)
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Metoprolol pharmacokinetic interaction theoretical.
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Carvedilol pharmacokinetic interaction theoretical.
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Propranolol pharmacokinetic interaction theoretical.
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Nebivolol pharmacokinetic interaction theoretical.
CYP3A4 substrates (statins, calcium channel blockers)
Additive BP lowering and minor pharmacokinetic shift. Monitor blood pressure when starting or stopping berberine in losartan users.
Berberine has demonstrated mild blood pressure lowering effects and modulates CYP2C9 and CYP3A4 in vitro. Combined effect with losartan can be additive (BP) and pharmacokinetic (metabolite ratio shift).
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Bisoprolol pharmacokinetic interaction theoretical.
SourcePMID 37439907
Blood pressure medications
Additive blood pressure lowering possible. May be beneficial in some patients but increases risk of hypotension, especially at initiation or dose changes of either agent.
Berberine has demonstrated mild blood pressure lowering effects in clinical trials, likely through endothelial nitric oxide modulation and additive RAAS effects. Co-administration with lisinopril may produce additive blood pressure reduction.
Additive BP lowering and minor pharmacokinetic shift. Monitor blood pressure when starting or stopping berberine in losartan users.
Berberine has demonstrated mild blood pressure lowering effects and modulates CYP2C9 and CYP3A4 in vitro. Combined effect with losartan can be additive (BP) and pharmacokinetic (metabolite ratio shift).
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Metoprolol pharmacokinetic interaction theoretical.
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Carvedilol pharmacokinetic interaction theoretical.
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Propranolol pharmacokinetic interaction theoretical.
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Nebivolol pharmacokinetic interaction theoretical.
Theoretical mild interaction. Clinically minor at supplement doses.
Berberine has weak CYP2D6 and CYP3A4 inhibitory effects in vitro. Bisoprolol pharmacokinetic interaction theoretical.
Cyclosporine
Sulfonylureas (glipizide, glyburide)
Anticoagulants
Warfarin
The clinical outcome is a reduced responsiveness to warfarin, leading to potential treatment failure and an increased risk of thrombosis.
Coenzyme Q10 is chemically similar to K-vitamins, which allows it to exhibit procoagulant effects that counteract the anticoagulant action of warfarin. This structural similarity may explain the reduced efficacy of warfarin when co-administered with Coenzyme Q10.
Mixed case reports. Monitor INR when starting or stopping CoQ10 supplementation.
CoQ10 structurally resembles vitamin K and may have weak vitamin K-like activity. Case reports document INR reduction in some warfarin users.
Blood pressure medications
Your prescriber may recommend this
This medicine can lower your CoQ10. Ask your prescriber whether you need it.
CoQ10 supplementation may attenuate beta-blocker-associated fatigue and muscle symptoms. Beneficial co-supplementation in users developing such symptoms on Nebivolol.
Nebivolol therapy may reduce endogenous CoQ10. Discuss CoQ10 supplementation with provider if developing fatigue or muscle symptoms.
Nebivolol therapy is associated with reduced endogenous CoQ10 levels via shared mevalonate / mitochondrial pathways. Statin-like CoQ10 depletion mechanism documented in beta-blocker users with mixed but supportive observational evidence.
Your prescriber may recommend this
This medicine can lower your CoQ10. Ask your prescriber whether you need it.
CoQ10 supplementation may attenuate beta-blocker-associated fatigue and muscle symptoms. Beneficial co-supplementation in users developing such symptoms on Bisoprolol.
Bisoprolol therapy may reduce endogenous CoQ10. Discuss CoQ10 supplementation with provider if developing fatigue or muscle symptoms.
Bisoprolol therapy is associated with reduced endogenous CoQ10 levels via shared mevalonate / mitochondrial pathways. Statin-like CoQ10 depletion mechanism documented in beta-blocker users with mixed but supportive observational evidence.
Your prescriber may recommend this
This medicine can lower your CoQ10. Ask your prescriber whether you need it.
CoQ10 supplementation may attenuate beta-blocker-associated fatigue and muscle symptoms. Beneficial co-supplementation in users developing such symptoms on Labetalol.
Labetalol therapy may reduce endogenous CoQ10. Discuss CoQ10 supplementation with provider if developing fatigue or muscle symptoms.
Labetalol therapy is associated with reduced endogenous CoQ10 levels via shared mevalonate / mitochondrial pathways. Statin-like CoQ10 depletion mechanism documented in beta-blocker users with mixed but supportive observational evidence.
Your prescriber may recommend this
This medicine can lower your CoQ10. Ask your prescriber whether you need it.
CoQ10 supplementation may attenuate beta-blocker-associated fatigue and muscle symptoms. Beneficial co-supplementation in users developing such symptoms on Carvedilol.
Carvedilol therapy may reduce endogenous CoQ10. Discuss CoQ10 supplementation with provider if developing fatigue or muscle symptoms.
Carvedilol therapy is associated with reduced endogenous CoQ10 levels via shared mevalonate / mitochondrial pathways. Statin-like CoQ10 depletion mechanism documented in beta-blocker users with mixed but supportive observational evidence.
Generally well tolerated. Possible mild additive BP effect.
Ubiquinol is the active reduced form of CoQ10. Same rationale as CoQ10 with Ramipril: mitochondrial and endothelial support.
Generally well tolerated. Possible mild additive BP effect.
Ubiquinol is the active reduced form of CoQ10. Same rationale as CoQ10 with Losartan: mitochondrial and endothelial support.
Generally well tolerated; possible mild additive BP effect.
CoQ10 supports mitochondrial function and endothelial health. ACE/ARB therapy is associated with improved cardiac function; CoQ10 may be complementary.
Generally well tolerated; possible mild additive BP effect.
CoQ10 supports mitochondrial function and endothelial health. ACE/ARB therapy is associated with improved cardiac function; CoQ10 may be complementary.
Generally well tolerated; possible mild additive BP effect.
CoQ10 supports mitochondrial function and endothelial health. ACE/ARB therapy is associated with improved cardiac function; CoQ10 may be complementary.
Generally well tolerated; possible mild additive BP effect.
CoQ10 supports mitochondrial function and endothelial health. ACE/ARB therapy is associated with improved cardiac function; CoQ10 may be complementary.
Generally well tolerated; possible mild additive BP effect.
CoQ10 supports mitochondrial function and endothelial health. ACE/ARB therapy is associated with improved cardiac function; CoQ10 may be complementary.
Generally well tolerated. Possible mild additive BP effect.
Ubiquinol is the active reduced form of CoQ10. Same rationale as CoQ10 with Lisinopril: mitochondrial and endothelial support.
Ubiquinol supplementation alternative to CoQ10 for beta-blocker users with absorption issues or older age.
Ubiquinol is the reduced (active) form of CoQ10 with higher bioavailability in older adults. Same mevalonate/mitochondrial rationale as CoQ10 supplementation in Atenolol users.
Ubiquinol supplementation alternative to CoQ10 for beta-blocker users with absorption issues or older age.
Ubiquinol is the reduced (active) form of CoQ10 with higher bioavailability in older adults. Same mevalonate/mitochondrial rationale as CoQ10 supplementation in Carvedilol users.
Ubiquinol supplementation alternative to CoQ10 for beta-blocker users with absorption issues or older age.
Ubiquinol is the reduced (active) form of CoQ10 with higher bioavailability in older adults. Same mevalonate/mitochondrial rationale as CoQ10 supplementation in Nebivolol users.
Ubiquinol supplementation alternative to CoQ10 for beta-blocker users with absorption issues or older age.
Ubiquinol is the reduced (active) form of CoQ10 with higher bioavailability in older adults. Same mevalonate/mitochondrial rationale as CoQ10 supplementation in Bisoprolol users.
Ubiquinol supplementation alternative to CoQ10 for beta-blocker users with absorption issues or older age.
Ubiquinol is the reduced (active) form of CoQ10 with higher bioavailability in older adults. Same mevalonate/mitochondrial rationale as CoQ10 supplementation in Labetalol users.
Ubiquinol supplementation alternative to CoQ10 for beta-blocker users with absorption issues or older age.
Ubiquinol is the reduced (active) form of CoQ10 with higher bioavailability in older adults. Same mevalonate/mitochondrial rationale as CoQ10 supplementation in Metoprolol users.
Ubiquinol supplementation alternative to CoQ10 for beta-blocker users with absorption issues or older age.
Ubiquinol is the reduced (active) form of CoQ10 with higher bioavailability in older adults. Same mevalonate/mitochondrial rationale as CoQ10 supplementation in Propranolol users.
Your prescriber may recommend this
This medicine can lower your CoQ10. Ask your prescriber whether you need it.
No interaction concern. Coenzyme Q10 and this beta-blocker are both used in migraine prevention, which is why they appear together in guidelines; evidence that CoQ10 relieves beta-blocker fatigue is not established, so no benefit is claimed.
Atenolol therapy may reduce endogenous CoQ10. Discuss CoQ10 supplementation with provider if developing fatigue or muscle symptoms.
Atenolol therapy is associated with reduced endogenous CoQ10 levels via shared mevalonate / mitochondrial pathways. Statin-like CoQ10 depletion mechanism documented in beta-blocker users with mixed but supportive observational evidence.
Your prescriber may recommend this
This medicine can lower your CoQ10. Ask your prescriber whether you need it.
No interaction concern. Coenzyme Q10 and this beta-blocker are both used in migraine prevention, which is why they appear together in guidelines; evidence that CoQ10 relieves beta-blocker fatigue is not established, so no benefit is claimed.
Metoprolol therapy may reduce endogenous CoQ10. Discuss CoQ10 supplementation with provider if developing fatigue or muscle symptoms.
Metoprolol therapy is associated with reduced endogenous CoQ10 levels via shared mevalonate / mitochondrial pathways. Statin-like CoQ10 depletion mechanism documented in beta-blocker users with mixed but supportive observational evidence.
Your prescriber may recommend this
This medicine can lower your CoQ10. Ask your prescriber whether you need it.
No interaction concern. Coenzyme Q10 and this beta-blocker are both used in migraine prevention, which is why they appear together in guidelines; evidence that CoQ10 relieves beta-blocker fatigue is not established, so no benefit is claimed.
Propranolol therapy may reduce endogenous CoQ10. Discuss CoQ10 supplementation with provider if developing fatigue or muscle symptoms.
Propranolol therapy is associated with reduced endogenous CoQ10 levels via shared mevalonate / mitochondrial pathways. Statin-like CoQ10 depletion mechanism documented in beta-blocker users with mixed but supportive observational evidence.
Insulin and diabetes medications
Mitochondrial support option for metformin users.
Ubiquinol is the reduced form of CoQ10 with potentially higher bioavailability in older adults.
No interaction concern. No benefit from combining them is claimed.
Metformin acts on mitochondrial complex I, potentially affecting CoQ10 utilization. CoQ10 supplementation may support mitochondrial function.
Chemotherapy
Basis: Theoretical
Warfarin and other anticoagulants
Two controlled studies in healthy volunteers found ginkgo did not alter warfarin pharmacokinetics or INR. Bleeding case reports exist; stop before surgery and tell your clinician. For DOACs no study exists and the same low posture applies (mechanism_inference).
Ginkgolides inhibit platelet activating factor (PAF). Case reports document spontaneous bleeding (intracranial, subdural, retinal) in patients on warfarin plus Ginkgo.
Aspirin and NSAIDs
Increased risk of bleeding and abnormal coagulation profiles.
Ginkgo biloba extract inhibits platelet-activating factor (PAF), leading to synergistic antiplatelet effects when combined with antiplatelet drugs.
Case reports of bleeding events. Monitor for unusual bleeding when combining.
Ginkgolides inhibit platelet activating factor (PAF). Additive antiplatelet effect with aspirin's COX-1 inhibition.
CYP2C9 substrates
Possible minor additive vascular effects. Monitor if combined with other antiplatelet or antihypertensive agents.
Ginkgo biloba has mild vasodilatory and antiplatelet activity. Generally minor interaction with Losartan.
Seizure medications (valproate, phenytoin)
Basis: Case reports
Stop 2 weeks before surgery
Bleeding risk from PAF inhibition.
Diabetes medications
Melatonin supplementation may alter blood glucose levels and interfere with the effectiveness of diabetes medications, requiring potential dosage adjustments.
Melatonin decreases insulin secretion by inhibiting cAMP and cGMP pathways while activating the phospholipaseC/IP3 pathway via MT1 and MT2 receptors. This interference with insulin secretion can affect glucose regulation and the efficacy of antidiabetic drugs.
Warfarin and other anticoagulants
Basis: Case reports
Immunosuppressants
Sedatives and benzodiazepines
Fluvoxamine (Luvox)
SourcePMID 11270913
Nitroglycerin
Activated charcoal
Anticoagulants
Timing Separation Rules
Nadolol (beta-blocker)
Warfarin
Iron supplements
Stimulant medications (Adderall, Ritalin)
MAOIs
Timing Separation Rules
Thiazide diuretics (HCTZ)
Concurrent use of vitamin D and thiazide diuretics can lead to symptomatic hypercalcemia, which may present with nausea, vomiting, abdominal pain, muscle weakness, and altered mental status.
Thiazide diuretics decrease urinary calcium excretion. When combined with vitamin D supplementation, which increases intestinal calcium absorption, the additive effect can result in elevated serum calcium levels (hypercalcemia).
Steroids (prednisone)
Long-term glucocorticoids cause bone loss. Guidelines recommend calcium and vitamin D alongside them; take as advised. The guideline names glucocorticoids as a class; prednisone is the prototypical one.
All patients on corticosteroids for more than 3 months should receive calcium 1000-1200 mg/day AND vitamin D3 800-2000 IU/day per ACR guidelines. Risk of fracture begins at doses as low as 2.5 mg prednisone/day. Discuss with your prescriber.
Corticosteroids reduce vitamin D activation and 25-OH vitamin D levels.
Orlistat (Alli)
Cholestyramine (bile acid sequestrant)
Levodopa (without carbidopa)
SourceFDA label
Phenytoin (Dilantin)
Methotrexate
Your prescriber may recommend this
This medicine can lower your folate. Ask your prescriber whether you need it.
Folic acid supplementation reduces the incidence of methotrexate-induced gastrointestinal and hepatic toxicity without significantly compromising its clinical efficacy in rheumatoid arthritis.
Methotrexate is a folate antagonist that inhibits dihydrofolate reductase, leading to depletion of intracellular folate and subsequent inhibition of purine and pyrimidine synthesis. Folic acid supplementation replenishes folate stores, counteracting the toxic effects of methotrexate on healthy rapidly dividing cells.
Folic acid is routinely prescribed alongside methotrexate. In a double-blind placebo-controlled trial it did not reduce methotrexate's efficacy and lowered toxicity scores. Take it as prescribed.
DUAL ROLE: For CANCER use, folic acid may reduce methotrexate efficacy and is generally avoided unless prescribed. For RA / autoimmune use, folic acid 1 mg/day is standard of care to reduce methotrexate toxicity. Context is critical, discuss with your prescriber.
Methotrexate inhibits dihydrofolate reductase. Folic acid bypasses this inhibition.
Phenytoin (Dilantin)
Ask your prescriber first
Enzyme-inducing anti-seizure medicines lower folate and supplementation is routinely advised, especially before and during pregnancy. High-dose folic acid can lower phenytoin levels and reduce seizure control, so doses above the usual supplement range need monitoring.
ALL women of childbearing potential on antiepileptic drugs MUST take folic acid 4-5mg/day (10x standard prenatal dose). Start BEFORE conception.
AEDs deplete folate via multiple mechanisms (CYP induction, gut absorption interference). Folate deficiency multiplies neural-tube-defect risk in pregnancy.
Your prescriber may recommend this
This medicine can lower your folate. Ask your prescriber whether you need it.
Enzyme-inducing anti-seizure medicines lower folate and supplementation is routinely advised, especially before and during pregnancy. Evidence is class-level for enzyme-inducing AEDs; the phenytoin-level-lowering caveat is phenytoin-specific and omitted here.
ALL women of childbearing potential on antiepileptic drugs MUST take folic acid 4-5mg/day (10x standard prenatal dose). Start BEFORE conception.
AEDs deplete folate via multiple mechanisms (CYP induction, gut absorption interference). Folate deficiency multiplies neural-tube-defect risk in pregnancy.
5-Fluorouracil (5-FU)
Warfarin and other anticoagulants
Applies to concentrated garlic supplements and extracts, not to garlic eaten as food. The sources reviewed describe this risk by form rather than by a dose cutoff. Garlic supplements may add to the effect of blood thinners, so tell your surgeon or prescriber if you take them.
Case reports of INR elevation and bleeding events on warfarin with high-dose garlic supplements. Culinary garlic intake unlikely to cause issue.
High-dose garlic (allicin, ajoene) has antiplatelet effects via thromboxane synthesis inhibition. Some case reports also suggest CYP2C9 modulation affecting warfarin levels.
Concomitant use of garlic and anticoagulants may increase the risk of bleeding.
Garlic contains compounds like ajoene and allicin that inhibit platelet aggregation and alter coagulation. This can enhance the pharmacological effect of anticoagulants.
Controlled trials found no significant effect on INR. Bleeding case reports involving garlic did not involve patients taking warfarin.
Garlic has theoretical antiplatelet activity.
HIV protease inhibitors (saquinavir)
Do not combine
Do not stop your medicine. Ask your prescriber before taking this supplement.
Significant protease-inhibitor underexposure → virologic failure risk. DIETARY garlic in food is generally safe; only garlic supplements cause this interaction.
Garlic supplements (capsules, aged garlic extract, allicin) reduce saquinavir AUC by ~51% in clinical study; mechanism likely involves CYP3A4/intestinal P-glycoprotein modulation.
Blood pressure medications
Applies to concentrated garlic supplements and extracts, not to garlic eaten as food. The sources reviewed describe this risk by form rather than by a dose cutoff. Garlic supplements may add to the effect of blood thinners, so tell your surgeon or prescriber if you take them.
Additive blood pressure lowering with Metoprolol. Monitor blood pressure when starting or stopping garlic supplements.
High-dose garlic has documented blood pressure lowering effects via nitric oxide synthase modulation and H2S signaling.
Additive blood pressure lowering with Atenolol. Monitor blood pressure when starting or stopping garlic supplements.
High-dose garlic has documented blood pressure lowering effects via nitric oxide synthase modulation and H2S signaling.
Additive blood pressure lowering with Bisoprolol. Monitor blood pressure when starting or stopping garlic supplements.
High-dose garlic has documented blood pressure lowering effects via nitric oxide synthase modulation and H2S signaling.
Additive blood pressure lowering with Carvedilol. Monitor blood pressure when starting or stopping garlic supplements.
High-dose garlic has documented blood pressure lowering effects via nitric oxide synthase modulation and H2S signaling.
Additive blood pressure lowering with Labetalol. Monitor blood pressure when starting or stopping garlic supplements.
High-dose garlic has documented blood pressure lowering effects via nitric oxide synthase modulation and H2S signaling.
Additive blood pressure lowering with Nebivolol. Monitor blood pressure when starting or stopping garlic supplements.
High-dose garlic has documented blood pressure lowering effects via nitric oxide synthase modulation and H2S signaling.
Additive blood pressure lowering with Propranolol. Monitor blood pressure when starting or stopping garlic supplements.
High-dose garlic has documented blood pressure lowering effects via nitric oxide synthase modulation and H2S signaling.
Possible additive BP lowering. Generally minor; monitor blood pressure if starting high-dose garlic supplementation.
High-dose garlic extract has mild antihypertensive effects via NO and vascular pathways. May be additive with Lisinopril.
Possible additive BP lowering. Generally minor; monitor blood pressure if starting high-dose garlic supplementation.
High-dose garlic extract has mild antihypertensive effects via NO and vascular pathways. May be additive with Enalapril.
Possible additive BP lowering. Generally minor; monitor blood pressure if starting high-dose garlic supplementation.
High-dose garlic extract has mild antihypertensive effects via NO and vascular pathways. May be additive with Losartan.
Possible additive BP lowering. Generally minor; monitor blood pressure if starting high-dose garlic supplementation.
High-dose garlic extract has mild antihypertensive effects via NO and vascular pathways. May be additive with Telmisartan.
Isoniazid (TB treatment)
Stop 2 weeks before surgery
Bleeding risk from antiplatelet effect.
Informational only. Always consult your pharmacist or physician before combining supplements with medications.