Memory Advance Ingredients & Drug Interactions
by Hawaii Pharm
What is this page for?
First and foremost: checking Memory Advance against your medications. The heart of this page is the interaction checker and the full interaction report — how this product’s ingredients may interact with prescription and over-the-counter medicines you may be taking.
Around that, we add a pharmacist’s high-level view of the product as a whole — what’s inside, the evidence for its stated use, how transparent the label is, and what safety data exists — so you can see the full picture in one place. It’s educational information from our licensed clinical databases and the clinical staff at HelloPharmacist — not medical advice — and we don’t sell or endorse products. Our editorial policy
Memory Advance is a dietary supplement by Hawaii Pharm with 7 active ingredients. Its ingredients are commonly taken for memory and cognitive support, anxiety and stress, adhd symptoms.Based on those ingredients, 1,732 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Sage Leaf Extract, Dry, Ginkgo Leaf Extract, Dry, Turmeric Rhizome Extract, Dry. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.
Check Your Meds Against Memory Advance by Hawaii Pharm
Ask about any prescription or over-the-counter medication and we check it for interactions with Memory Advance by Hawaii Pharm — and tell you which ingredient is responsible.
AI summaries are generated from our interaction database for education only — always confirm with your pharmacist. How we use AI
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HelloPharmacist Scorecard of Memory Advance by Hawaii Pharm
Our pharmacy team’s full take, with four database checks built into the cards below — a summary of what is known, not a grade of the product itself.
What’s inside
Low disclosure
Memory Advance contains 7 active ingredients in a liquid form. The three main ones are Brahmi (bacopa) whole herb extract, rosemary leaf extract, and ginkgo leaf extract — all traditional memory and cognitive support herbs.
You'll also find turmeric rhizome extract (which contains the compound curcumin), schisandra berry extract, and sage leaf extract. The product rounds out with yerba mate leaf extract, which supplies caffeine.
These are suspended in a base of alcohol, water, and glycerin.
Does it work?
Moderate evidence
The evidence for Memory Advance's ingredients is mixed. Rosemary extract shows possibly effective evidence for memory support.
Ginkgo has possibly effective evidence for dementia, hearing loss, and anxiety. Sage is possibly effective for cognitive function and menopausal symptoms.
Turmeric is possibly effective for depression and a few digestive and inflammatory conditions. For bacopa, schisandra, and yerba mate — when used specifically for cognitive and memory purposes — the evidence we hold is insufficient to rate; larger, better-designed studies would be needed to know if they truly work for those goals.
How safe is it?
Well-documented data
Bacopa is generally well tolerated but carries limited long-term safety data. It can cause gastrointestinal upset (12% to 30% of study participants reported stomach cramps, nausea, diarrhea, or bloating), and some people report drowsiness, headache, or vivid dreams.
Ginkgo is generally well tolerated for up to 6 years but raises bleeding risk — case reports link it to spontaneous bleeding and cardiac arrhythmias, though other risk factors were often present. Rosemary is safe in food amounts; concentrated extracts require caution.
Turmeric is generally safe as a food but concentrated supplements may cause constipation, nausea, or diarrhea; over 70 cases of liver damage have been reported with long-term supplement use. Sage is safe as tea or food but concentrated extracts should be used cautiously.
Schisandra is generally well tolerated short-term but can cause heartburn, appetite loss, and stomach upset. Yerba mate contains caffeine — high-dose or long-term use can cause insomnia, nervousness, tremors, and in rare cases serious effects like arrhythmias.
All six ingredients with pregnancy data advise against medicinal doses in pregnancy. For breastfeeding: bacopa and ginkgo should be avoided; rosemary and sage are okay in food amounts but avoid medicinal doses; schisandra lacks data — talk to your doctor; yerba mate caffeine passes to breast milk, so limit or avoid it.
Meds to double-check
Major interaction found
Before taking Memory Advance, double-check with your pharmacist if you take blood thinners or aspirin-type drugs (ginkgo and rosemary raise bleeding risk; this is the most serious concern). Also flag: blood pressure medications (ginkgo's talinolol interaction is major; sage may raise or lower pressure unpredictably); liver-metabolized drugs including cancer treatments, psychiatric medications, and immunosuppressants (bacopa, rosemary, turmeric, schisandra, and sage all affect liver enzyme activity); ephedrine or ephedrine-containing products (yerba mate's caffeine amplifies stimulant risk severely); diabetes drugs (rosemary raises low-blood-sugar risk); and anticonvulsants (yerba mate caffeine may reduce their effectiveness).
We could not check interactions for the proprietary extract blend component — ask your pharmacist about its ingredients.
The bottom line
Scorecard at a glanceFormula with limited ingredient disclosure with some supporting evidence for its stated purpose. Major medication interactions have been identified, and safety information is well characterized.
Memory Advance may be worth considering if you're looking for herbal cognitive support and don't take medications. However, because of the high number of drug interactions — especially with blood thinners, blood pressure drugs, cancer medications, immunosuppressants, and psychiatric drugs — you should check your exact medications with the tool on this page before starting.
If you take any prescription medication, talk to your pharmacist or doctor first.
Educational only — not medical advice; always confirm with your pharmacist. Our editorial policy · How we use AI
Assessment coverage: 7 of 7 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated May 21, 2025.
This Scorecard evaluates available label information, ingredient evidence, and known medication-safety considerations. It does not independently verify product identity, purity, potency, contamination, or manufacturing quality. How these ratings are computed
General information
Key facts about Memory Advance, straight from the product label.
| Brand | Hawaii Pharm |
|---|---|
| Barcode (UPC) | 840253669650 |
| Net contents | 4 Fluid Ounce(s); 120 mL |
| Market status | On market |
| Date entered into DSLD | May 21, 2025 |
| DSLD ID | 331998 |
| Product type | Botanical |
| Supplement form | Liquid |
| Dietary claims / uses | All Other, Structure/Function |
| Intended target group(s) | Adult (18 - 50 Years), Gluten Free |
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.
Supplement Facts
The label details for Memory Advance by Hawaii Pharm, sourced from the NIH Dietary Supplement Label Database.
Supplement Facts
| Ingredient | Amount | % DV |
|---|---|---|
| Proprietary Extract Blend | 983 mg | -- |
| Brahmi Whole Herb Extract, Dry | 0 NP | -- |
| Rosemary Leaf Extract, Dry | 0 NP | -- |
| Ginkgo Leaf Extract, Dry | 0 NP | -- |
| Turmeric Rhizome Extract, Dry | 0 NP | -- |
| Schisandra Berry Extract, Dry | 0 NP | -- |
| Sage Leaf Extract, Dry | 0 NP | -- |
| Yerba Mate Leaf Extract, Dry | 0 NP | -- |
Other ingredients: Alcohol, Water, Glycerin
Tap any ingredient to jump to its full detail below.
These statements are the manufacturer’s wording, reproduced from the product label — the label is saying it, not HelloPharmacist. We don’t verify or endorse them.
Brand IP Statement(s)
Hawaii Pharm Herbal Extract Highest quality since 2008
Suggested/Recommended/Usage/Directions
Suggested use: Shake well before using. For adults add about 20-30 drops (0.7-1 mL, one full squeeze of the dropper bulb) to some juice or water, up to 4 times a day.
Precautions
Warning: We recommend to seek expert medical advice before taking.
Do not use if you are allergic to any ingredients.
Consult your physician before giving to children under 18, during pregnancy, if nursing or taking medications.
Consult your physician before giving to children under 18, during pregnancy, if nursing or taking medications.
May affect the ability to drive and operate machinery. May have contraindications, can cause side effects and adverse reactions. Do not use if seal is broken or missing.
Keep out of the reach of children!
Storage
Store in a cool dry place.
Formulation
cGMP Made in compliance with cGMP 21 CFR 111 in an FDA registered and inspected facility.
Made in USA, Hawaii
Organic alcohol based
Only natural ingredients Identity and purity is laboratory verified
All the raw materials are gluten-free by their nature No artificial colors, flavors, or preservatives
FDA Disclaimer Statement
This product has not been evaluated by the FDA and is not intended to diagnose, treat, cure or prevent any disease.
Formula
Organic alcohol based
FDA Statement of Identity
Herbal Supplement
General Statements
Extraction rate: about 1/3-4 (up to 333 mg of dry raw material per 1 mL of extract).
Scan this QR code to get 15% discount on your next purchase Limited time deal
Seals/Symbols
USA Made in United States of America
Is this label outdated? Report a formula or label change and our pharmacy team will review it.
Memory Advance by Hawaii Pharm label
The label scan from the NIH Dietary Supplement Label Database. Tap to enlarge.
Label images are published by the NIH Dietary Supplement Label Database for the version of this product on file. Always read your actual product label.
View the full label (PDF)The Ingredients in Memory Advance by Hawaii Pharm
These are the 7 active ingredients this product is made of. Select any to open its full monograph.
Serving size0.7 mL Dosage formLiquid Servings per container120 Amounts shown are per serving.
Most supplement products combine several ingredients, and a medication can interact with the product through any one of them. Each ingredient below shows whether it has known drug interactions.
Other (inactive) ingredients: Alcohol, Water, Glycerin. These complete the product’s ingredient list but are not active constituents.
Memory Advance by Hawaii Pharm Drug Interactions
HelloPharmacist Interaction Report
Memory Advance by Hawaii Pharm contains seven active ingredients, and several of them interact with medications.
The most serious interaction we've documented is with yerba mate leaf extract and ephedrine — a stimulant combination that can raise the risk of serious, even life-threatening side effects from overstimulation.
Read the full breakdown — every affected drug type, severity by severity
Ginkgo leaf extract carries a major interaction with talinolol (a blood pressure medication), which can significantly increase talinolol levels. Ginkgo also interacts moderately with warfarin and other blood thinners, raising bleeding risk; with certain cancer drugs and HIV medications; and with the immunosuppressant tacrolimus.
Bacopa interacts moderately with four categories of drugs that are metabolized by your liver (CYP1A2, CYP2C19, CYP2C9, and CYP3A4 substrates), potentially raising their levels. It also interacts with anticholinergic and cholinergic drugs — medications used for conditions like overactive bladder and myasthenia gravis — and with the dry-mouth drug cevimeline.
Rosemary leaf extract interacts moderately with blood thinners and aspirin-like drugs (raising bleeding risk), diabetes medications (raising low-blood-sugar risk), and liver-metabolized drugs. Turmeric interacts moderately with several chemotherapy drugs, the immunosuppressant tacrolimus, the arthritis drug sulfasalazine, the cancer drug tamoxifen, and others.
Schisandra and sage leaf extract each interact with multiple liver-metabolized drug categories. Yerba mate's caffeine content also interacts moderately with anticonvulsants, disulfiram (an alcohol-use medication), and several psychiatric drugs.
Altogether, these interactions span 1,710 individual medications. Check your exact medications with the search tool on this page before starting Memory Advance.
Check your own medications below · Editorial policy · How we use AI
Want to check YOUR meds against Memory Advance?
Ask about interactions with your drugs in plain English — “Can I take it with lisinopril?” — and we find you the answer in seconds, ingredient by ingredient.
Go to the checkerIngredients driving the most interactions
Individual Drug Interactions
The ingredients in Memory Advance interact with 1,732 drugs. Click any drug to see the details.
7 of the 7 ingredients in Memory Advance interact with drugs. Each result below shows which ingredient is responsible. Sage Leaf Extract, Dry Ginkgo Leaf Extract, Dry Turmeric Rhizome Extract, Dry Yerba Mate Leaf Extract, Dry Brahmi Whole Herb Extract, Dry Schisandra Berry Extract, Dry Rosemary Leaf Extract, Dry
Aminophylline, Amobarbital, EphedrineAmesec
How Aminophylline, Amobarbital, Ephedrine interacts with Memory Advance — through 3 ingredients. Tap an ingredient for the detail:
Yerba Mate Leaf Extract, DryStimulant Drugs, Ephedrine Major
Interaction Summary
Theoretically, concomitant use of stimulant drugs and yerba mate might increase stimulant adverse effects.
Read the full Yerba Mate Leaf Extract, Dry + Aminophylline, Amobarbital, Ephedrine interactionSage Leaf Extract, DryAnticonvulsants, Cns Depressants Moderate
Interaction Summary
Theoretically, sage might interfere with the clinical effects of anticonvulsant drugs.
Read the full Sage Leaf Extract, Dry + Aminophylline, Amobarbital, Ephedrine interactionGinkgo Leaf Extract, DryAnticonvulsants Moderate
Interaction Summary
Theoretically, ginkgo might reduce the effectiveness of anticonvulsants.
Read the full Ginkgo Leaf Extract, Dry + Aminophylline, Amobarbital, Ephedrine interactionCarbetapentane Tannate, Chlorpheniramine Tannate, Ephedrine Tannate, Phenylephrine TannateQuadratuss, Ry Tuss, Rynatuss, Tri Tannate Plus
How Carbetapentane Tannate, Chlorpheniramine Tannate, Ephedrine Tannate, Phenylephrine Tannate interacts with Memory Advance — through 6 ingredients. Tap an ingredient for the detail:
Yerba Mate Leaf Extract, DryEphedrine, Stimulant Drugs +1 Major
Interaction Summary
Theoretically, the caffeine in yerba mate might increase the risk for stimulant adverse effects when used concomitantly with ephedrine.
Read the full Yerba Mate Leaf Extract, Dry + Carbetapentane Tannate, Chlorpheniramine Tannate, Ephedrine Tannate, Phenylephrine Tannate interactionBrahmi Whole Herb Extract, DryAnticholinergic Drugs, Cytochrome P450 3a4 (cyp3a4) Substrates Moderate
Interaction Summary
Theoretically, concurrent use might decrease the effectiveness of both agents.
Read the full Brahmi Whole Herb Extract, Dry + Carbetapentane Tannate, Chlorpheniramine Tannate, Ephedrine Tannate, Phenylephrine Tannate interactionSchisandra Berry Extract, DryCytochrome P450 3a4 (cyp3a4) Substrates Moderate
Interaction Summary
Schisandra can increase the levels and clinical effects of drugs metabolized by CYP3A4.
Read the full Schisandra Berry Extract, Dry + Carbetapentane Tannate, Chlorpheniramine Tannate, Ephedrine Tannate, Phenylephrine Tannate interactionGinkgo Leaf Extract, DrySeizure Threshold Lowering Drugs, Cytochrome P450 3a4 (cyp3a4) Substrates Moderate
Interaction Summary
Theoretically, taking ginkgo with drugs that lower the seizure threshold might increase the risk for convulsions.
Read the full Ginkgo Leaf Extract, Dry + Carbetapentane Tannate, Chlorpheniramine Tannate, Ephedrine Tannate, Phenylephrine Tannate interactionSage Leaf Extract, DryCytochrome P450 3a4 (cyp3a4) Substrates, Anticholinergic Drugs Moderate
Interaction Summary
Theoretically, sage might increase the levels and clinical effects of drugs metabolized by CYP3A4.
Read the full Sage Leaf Extract, Dry + Carbetapentane Tannate, Chlorpheniramine Tannate, Ephedrine Tannate, Phenylephrine Tannate interactionTurmeric Rhizome Extract, DryCytochrome P450 3a4 (cyp3a4) Substrates Moderate
Interaction Summary
Turmeric might increase or decrease levels of drugs metabolized by CYP3A4.
Read the full Turmeric Rhizome Extract, Dry + Carbetapentane Tannate, Chlorpheniramine Tannate, Ephedrine Tannate, Phenylephrine Tannate interactionDyphylline, Ephedrine, Guaifenesin, PhenobarbitalLufyllin-EPG
How Dyphylline, Ephedrine, Guaifenesin, Phenobarbital interacts with Memory Advance — through 2 ingredients. Tap an ingredient for the detail:
Yerba Mate Leaf Extract, DryStimulant Drugs, Ephedrine +1 Major
Interaction Summary
Theoretically, concomitant use of stimulant drugs and yerba mate might increase stimulant adverse effects.
Read the full Yerba Mate Leaf Extract, Dry + Dyphylline, Ephedrine, Guaifenesin, Phenobarbital interactionSage Leaf Extract, DryCns Depressants Moderate
Interaction Summary
Theoretically, taking sage might increase the sedative and adverse effects of CNS depressants.
Read the full Sage Leaf Extract, Dry + Dyphylline, Ephedrine, Guaifenesin, Phenobarbital interactionEphedrine, Guaifenesin (otc Drug)Ephedrine Formula 400, Ephedrine Plus Tabs
How Ephedrine, Guaifenesin (otc Drug) interacts with Memory Advance — through 1 ingredient. Tap an ingredient for the detail:
Yerba Mate Leaf Extract, DryStimulant Drugs, Ephedrine Major
Interaction Summary
Theoretically, concomitant use of stimulant drugs and yerba mate might increase stimulant adverse effects.
Read the full Yerba Mate Leaf Extract, Dry + Ephedrine, Guaifenesin (otc Drug) interactionEphedrine, Guaifenesin, Phenobarbital, TheophyllineMudrane GG
How Ephedrine, Guaifenesin, Phenobarbital, Theophylline interacts with Memory Advance — through 6 ingredients. Tap an ingredient for the detail:
Yerba Mate Leaf Extract, DryEphedrine, Stimulant Drugs +2 Major
Interaction Summary
Theoretically, the caffeine in yerba mate might increase the risk for stimulant adverse effects when used concomitantly with ephedrine.
Read the full Yerba Mate Leaf Extract, Dry + Ephedrine, Guaifenesin, Phenobarbital, Theophylline interactionBrahmi Whole Herb Extract, DryCytochrome P450 1a2 (cyp1a2) Substrates Moderate
Interaction Summary
Theoretically, bacopa might increase the levels and adverse effects of CYP1A2 substrates.
Read the full Brahmi Whole Herb Extract, Dry + Ephedrine, Guaifenesin, Phenobarbital, Theophylline interactionSage Leaf Extract, DryCns Depressants Moderate
Interaction Summary
Theoretically, taking sage might increase the sedative and adverse effects of CNS depressants.
Read the full Sage Leaf Extract, Dry + Ephedrine, Guaifenesin, Phenobarbital, Theophylline interactionGinkgo Leaf Extract, DryCytochrome P450 1a2 (cyp1a2) Substrates, Seizure Threshold Lowering Drugs Moderate
Interaction Summary
Theoretically, ginkgo might increase levels of drugs metabolized by CYP1A2.
Read the full Ginkgo Leaf Extract, Dry + Ephedrine, Guaifenesin, Phenobarbital, Theophylline interactionTurmeric Rhizome Extract, DryCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Rhizome Extract, Dry + Ephedrine, Guaifenesin, Phenobarbital, Theophylline interactionRosemary Leaf Extract, DryCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, rosemary might decrease the levels and clinical effects of CYP1A2 substrates.
Read the full Rosemary Leaf Extract, Dry + Ephedrine, Guaifenesin, Phenobarbital, Theophylline interactionEphedrine, Hydroxyzine, TheophyllineAmi Rax, Marax
How Ephedrine, Hydroxyzine, Theophylline interacts with Memory Advance — through 6 ingredients. Tap an ingredient for the detail:
Yerba Mate Leaf Extract, DryStimulant Drugs, Theophylline +1 Major
Interaction Summary
Theoretically, concomitant use of stimulant drugs and yerba mate might increase stimulant adverse effects.
Read the full Yerba Mate Leaf Extract, Dry + Ephedrine, Hydroxyzine, Theophylline interactionGinkgo Leaf Extract, DrySeizure Threshold Lowering Drugs, Cytochrome P450 1a2 (cyp1a2) Substrates Moderate
Interaction Summary
Theoretically, taking ginkgo with drugs that lower the seizure threshold might increase the risk for convulsions.
Read the full Ginkgo Leaf Extract, Dry + Ephedrine, Hydroxyzine, Theophylline interactionBrahmi Whole Herb Extract, DryCytochrome P450 1a2 (cyp1a2) Substrates, Anticholinergic Drugs Moderate
Interaction Summary
Theoretically, bacopa might increase the levels and adverse effects of CYP1A2 substrates.
Read the full Brahmi Whole Herb Extract, Dry + Ephedrine, Hydroxyzine, Theophylline interactionSage Leaf Extract, DryAnticholinergic Drugs Moderate
Interaction Summary
Theoretically, sage might decrease the clinical effects of anticholinergic drugs.
Read the full Sage Leaf Extract, Dry + Ephedrine, Hydroxyzine, Theophylline interactionRosemary Leaf Extract, DryCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, rosemary might decrease the levels and clinical effects of CYP1A2 substrates.
Read the full Rosemary Leaf Extract, Dry + Ephedrine, Hydroxyzine, Theophylline interactionTurmeric Rhizome Extract, DryCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Rhizome Extract, Dry + Ephedrine, Hydroxyzine, Theophylline interactionEphedrine, Phenobarbital, Potassium Iodide, TheophyllineMudrane, Quadrinal
How Ephedrine, Phenobarbital, Potassium Iodide, Theophylline interacts with Memory Advance — through 3 ingredients. Tap an ingredient for the detail:
Yerba Mate Leaf Extract, DryPhenobarbital (luminal), Ephedrine +2 Major
Interaction Summary
Theoretically, the caffeine in yerba mate might reduce the effects of phenobarbital and increase the risk for convulsions.
Read the full Yerba Mate Leaf Extract, Dry + Ephedrine, Phenobarbital, Potassium Iodide, Theophylline interactionGinkgo Leaf Extract, DrySeizure Threshold Lowering Drugs Moderate
Interaction Summary
Theoretically, taking ginkgo with drugs that lower the seizure threshold might increase the risk for convulsions.
Read the full Ginkgo Leaf Extract, Dry + Ephedrine, Phenobarbital, Potassium Iodide, Theophylline interactionSage Leaf Extract, DryCns Depressants Moderate
Interaction Summary
Theoretically, taking sage might increase the sedative and adverse effects of CNS depressants.
Read the full Sage Leaf Extract, Dry + Ephedrine, Phenobarbital, Potassium Iodide, Theophylline interactionEphedrine, Phenobarbital, TheophyllineTedral
How Ephedrine, Phenobarbital, Theophylline interacts with Memory Advance — through 3 ingredients. Tap an ingredient for the detail:
Yerba Mate Leaf Extract, DryStimulant Drugs, Theophylline +2 Major
Interaction Summary
Theoretically, concomitant use of stimulant drugs and yerba mate might increase stimulant adverse effects.
Read the full Yerba Mate Leaf Extract, Dry + Ephedrine, Phenobarbital, Theophylline interactionSage Leaf Extract, DryCns Depressants, Anticonvulsants Moderate
Interaction Summary
Theoretically, taking sage might increase the sedative and adverse effects of CNS depressants.
Read the full Sage Leaf Extract, Dry + Ephedrine, Phenobarbital, Theophylline interactionGinkgo Leaf Extract, DrySeizure Threshold Lowering Drugs, Anticonvulsants Moderate
Interaction Summary
Theoretically, taking ginkgo with drugs that lower the seizure threshold might increase the risk for convulsions.
Read the full Ginkgo Leaf Extract, Dry + Ephedrine, Phenobarbital, Theophylline interactionTalinololTalinolol
How Talinolol interacts with Memory Advance — through 4 ingredients. Tap an ingredient for the detail:
Ginkgo Leaf Extract, DryTalinolol Major
Interaction Summary
Taking ginkgo with talinolol seems to increase blood levels of talinolol.
Read the full Ginkgo Leaf Extract, Dry + Talinolol interactionSchisandra Berry Extract, DryTalinolol Moderate
Interaction Summary
Schisandra can increase the levels and clinical effects of talinolol.
Read the full Schisandra Berry Extract, Dry + Talinolol interactionSage Leaf Extract, DryAntihypertensive Drugs Moderate
Interaction Summary
Theoretically, sage might increase or decrease the effects of antihypertensive drugs.
Read the full Sage Leaf Extract, Dry + Talinolol interactionTurmeric Rhizome Extract, DryTalinolol Moderate
Interaction Summary
Turmeric may reduce the absorption of talinolol in some situations.
Read the full Turmeric Rhizome Extract, Dry + Talinolol interactionEach ingredient & the kinds of drugs it affects
For each ingredient in Memory Advance with known interactions, here are the types of medications they can affect. Open any type for the detail — or search your exact drug in the checker above.
Sage Leaf Extract, Dry
Anticholinergic Drugs
Theoretically, sage might decrease the clinical effects of anticholinergic drugs.
In vitro evidence suggests that common sage (Salvia officinalis) and Spanish sage (Salvia lavandulaefolia) can inhibit acetylcholinesterase and might increase acetylcholine levels.
Anticonvulsants
Theoretically, sage might interfere with the clinical effects of anticonvulsant drugs.
Some species of sage can cause convulsions when consumed in large quantities.
Antidiabetes Drugs
Theoretically, taking sage with antidiabetes drugs might increase the risk of hypoglycemia.
In patients with polycystic ovary syndrome (PCOS) or inadequately controlled type 2 diabetes, common sage (Salvia officinalis) has demonstrated hypoglycemic activity. However, other clinical research in patients with inadequately controlled type 2 diabetes shows that common sage extract does not lower fasting blood glucose levels.
Antihypertensive Drugs
Theoretically, sage might increase or decrease the effects of antihypertensive drugs.
Animal research suggests that common sage (Salvia officinalis) can cause prolonged blood pressure reduction. However, clinical research suggests that Spanish sage (Salvia lavandulaefolia) can increase blood pressure in some people with hypertension. Until more is known, use with caution.
Benzodiazepines
Theoretically, taking sage might increase the sedative and adverse effects of benzodiazepines.
In vitro evidence suggests that certain components of common sage (Salvia officinalis) can bind to benzodiazepine receptors. This effect has not been reported in humans.
Cholinergic Drugs
Theoretically, sage might have additive effects when used with cholinergic drugs.
In vitro evidence suggests that common sage (Salvia officinalis) and Spanish sage (Salvia lavandulaefolia) can inhibit acetylcholinesterase and might increase acetylcholine levels.
Cns Depressants
Theoretically, taking sage might increase the sedative and adverse effects of CNS depressants.
Some constituents of sage have CNS depressant activity.
Cytochrome P450 2C19 (Cyp2C19) Substrates
Theoretically, sage might increase the levels and clinical effects of drugs metabolized by CYP2C19.
In vitro evidence suggests that aqueous extracts of sage can inhibit CYP2C19. So far, this interaction has not been reported in humans.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, sage might increase the levels and clinical effects of drugs metabolized by CYP2C9.
In vitro evidence suggests that aqueous extracts of sage can inhibit CYP2C9. So far, this interaction has not been reported in humans.
Cytochrome P450 2D6 (Cyp2D6) Substrates
Theoretically, sage might increase the levels and clinical effects of drugs metabolized by CYP2D6.
In vitro evidence suggests that aqueous extracts of sage can inhibit CYP2D6. So far, this interaction has not been reported in humans.
Cytochrome P450 2E1 (Cyp2E1) Substrates
Theoretically, sage might decrease the levels and clinical effects of drugs metabolized by CYP2E1.
Animal research suggests that drinking common sage (Salvia officinalis) tea increases the expression of CYP2E1. So far, this interaction has not been reported in humans.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, sage might increase the levels and clinical effects of drugs metabolized by CYP3A4.
In vitro evidence suggests that aqueous extracts of sage can inhibit CYP3A4. So far, this interaction has not been reported in humans.
Estrogens
Theoretically, sage might interfere with hormone therapy.
In vitro evidence suggests that geraniol, a constituent of Spanish sage (Salvia lavandulaefolia), exerts estrogenic activity. The clinical significance of this effect is unclear.
P-Glycoprotein Substrates
Theoretically, sage might increase levels of drugs transported by P-glycoprotein.
In vitro research suggests that common sage (Salvia officinalis) can inhibit the multi-drug transporter protein, P-glycoprotein. This effect has not been reported in humans.
Ginkgo Leaf Extract, Dry
Talinolol
Taking ginkgo with talinolol seems to increase blood levels of talinolol.
There is some evidence that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of talinolol by 36% in healthy male individuals. However, single doses of ginkgo do not seem to affect talinolol pharmacokinetics.
Alprazolam (Xanax)
Theoretically, ginkgo might decrease the levels and clinical effects of alprazolam.
In clinical research, ginkgo extract (Ginkgold) 120 mg twice daily seems to decrease alprazolam levels by about 17%. However, ginkgo does not appear to decrease the elimination half-life of alprazolam. This suggests that ginkgo is more likely to decrease absorption of alprazolam rather than induce hepatic metabolism of alprazolam.
Anticoagulant/Antiplatelet Drugs
Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin. Theoretically, ginkgo might increase the risk of bleeding if used with other anticoagulant or antiplatelet drugs.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. However, population and clinical studies have produced mixed results. Some evidence shows that short-term use of ginkgo leaf does not significantly reduce platelet aggregation and blood clotting. A study in healthy males who took a specific ginkgo leaf extract (EGb 761) 160 mg twice daily for 7 days found no change in prothrombin time. An analysis of a large medical record database suggests that ginkgo increases the risk of a bleeding adverse event by 38% when taken concurrently with warfarin. It has been suggested that ginkgo has to be taken for at least 2-3 weeks to have a significant effect on platelet aggregation. However, a meta-analysis of 18 studies using standardized ginkgo extracts, 80-480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. In addition, a single dose of ginkgo plus clopidogrel or ticlopidine does not seem to significantly increase bleeding time or platelet aggregation. Also, taking ginkgo leaf extract daily for 8 days in conjunction with rivaroxaban does not affect anti-factor Xa activity; however, this study did not evaluate bleeding time.
Anticonvulsants
Theoretically, ginkgo might reduce the effectiveness of anticonvulsants.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.
Antidiabetes Drugs
Theoretically, taking ginkgo with antidiabetes drugs might alter the response to antidiabetes drugs.
Ginkgo leaf extract seems to alter insulin secretion and metabolism, and might affect blood glucose levels in people with type 2 diabetes. The effect of ginkgo seems to differ depending on the insulin and treatment status of the patient. In diet-controlled diabetes patients with hyperinsulinemia, taking ginkgo does not seem to significantly affect insulin or blood glucose levels. In patients with hyperinsulinemia who are treated with oral hypoglycemic agents, taking ginkgo seems to decrease insulin levels and increase blood glucose following an oral glucose tolerance test. Researchers speculate that this could be due to ginkgo-enhanced hepatic metabolism of insulin. In patients with pancreatic exhaustion, taking ginkgo seems to stimulate pancreatic beta-cells, resulting in increased insulin and C-peptide levels, but with no significant change in blood glucose levels in response to an oral glucose tolerance test.
Atorvastatin (Lipitor)
Theoretically, ginkgo might decrease the levels and clinical effects of atorvastatin.
In humans, intake of ginkgo extract appears to increase atorvastatin clearance, reducing the area under the curve of atorvastatin by 10% to 14% and the maximum concentration by 29%. However, this interaction does not appear to affect cholesterol synthesis and absorption. Further, a model in rats with hyperlipidemia suggests that administering ginkgo extract does not impact blood levels of atorvastatin and leads to lower total cholesterol, low-density lipoprotein cholesterol, and triglycerides when compared with rats given atorvastatin alone.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, ginkgo might increase levels of drugs metabolized by CYP1A2.
Laboratory research suggests that ginkgo leaf extract can mildly inhibit CYP1A2 enzymes. However, clinical research suggests ginkgo might not affect CYP1A2. Until more is known, use ginkgo cautiously in patients taking drugs metabolized by these enzymes.
Cytochrome P450 2C19 (Cyp2C19) Substrates
Theoretically, ginkgo might decrease levels of drugs metabolized by CYP2C19.
Some clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce CYP2C19 enzymes and potentially decrease levels of drugs metabolized by these enzymes. However, other clinical research shows that taking ginkgo 120 mg twice daily for 12 days has no effect on levels of drugs metabolized by CYP2C19.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, ginkgo might increase levels of drugs metabolized by CYP2C9.
In vitro, a specific standardized extract of ginkgo leaf (EGb 761) inhibits CYP2C9 activity . The terpenoid (ginkgolides) and flavonoid (quercetin, kaempferol, etc.) constituents seem to be responsible for this effect. Most ginkgo extracts contain some amount of these constituents. Therefore, other ginkgo leaf extracts might also inhibit the CYP2C9 enzyme. However, clinical research suggests that ginkgo might not have a significant effect on CYP2C9 in humans. Ginkgo does not seem to significantly affect the pharmacokinetics of CYP2C9 substrates diclofenac or tolbutamide.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, ginkgo might decrease levels of drugs metabolized by CYP3A4.
There is conflicting evidence about whether ginkgo induces or inhibits CYP3A4. Ginkgo does not appear to affect hepatic CYP3A4. However, it is not known if ginkgo affects intestinal CYP3A4. Preliminary clinical research suggests that taking ginkgo does not significantly affect levels of donepezil, lopinavir, or ritonavir, which are all CYP3A4 substrates. Other clinical research also suggests ginkgo does not significantly affect CYP3A4 activity. However, there are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4).
Efavirenz (Sustiva)
Theoretically, ginkgo might decrease the levels and clinical effects of efavirenz.
There are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. In one case, an HIV-positive male experienced over a 50% decrease in efavirenz levels over the course of 14 months while taking ginkgo extract. HIV-1 RNA copies also increased substantially, from less than 50 to more than 1500. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4). In another case report, a patient stable on antiviral therapy including efavirenz for 10 years, had an increase in viral load from <50 copies/mL to 1350 copies/mL after 2 months of taking a combination of supplements including ginkgo. After stopping ginkgo, the viral load was again controlled with the same antiviral therapy regimen.
Ibuprofen (Advil, Others)
Theoretically, ginkgo might increase the risk of bleeding when used with ibuprofen.
Ginkgo might have antiplatelet effects and has been associated with several case reports of spontaneous bleeding. In one case, a 71-year-old male had taken a specific ginkgo extract (Gingium, Biocur) 40 mg twice daily for 2.5 years. About 4 weeks after starting ibuprofen 600 mg daily he experienced a fatal intracerebral hemorrhage. However, the antiplatelet effects of ginkgo have been questioned. A meta-analysis and other studies have not found a significant antiplatelet effect with standardized ginkgo extracts, 80 mg to 480 mg taken daily for up to 32 weeks.
P-Glycoprotein Substrates
Theoretically, taking ginkgo with P-glycoprotein substrates might increase the levels and adverse effects of these substrates.
A small clinical study in healthy volunteers shows that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of the P-glycoprotein substrate, talinolol, by 36% in healthy male individuals. However, single doses of ginkgo do not have the same effect.
Risperidone (Risperdal)
Theoretically, taking ginkgo with risperidone might increase the levels and adverse effects of risperidone.
A single case of priapism has been reported for a 26-year-old male with schizophrenia who used risperidone 3 mg daily along with ginkgo extract 160 mg daily. Risperidone is metabolized by cytochrome P450 (CYP) 2D6 and CYP3A4. CYP3A4 activity might be affected by ginkgo. Theoretically, ginkgo may inhibit the metabolism of risperidone and increase the risk of adverse effects.
Rosiglitazone (Avandia)
Theoretically, ginkgo might decrease the levels and clinical effects of rosiglitazone.
Animal research shows that ginkgo leaf extract orally 100 or 200 mg/kg daily for 10 days alters the pharmacodynamics of rosiglitazone in a dose-dependent manner. The 100 mg/kg and 200 mg/kg doses reduce the area under the concentration time curve (AUC) of rosiglitazone by 39% and 52%, respectively, and the half-life by 28% and 39%, respectively. It is hypothesized that these changes may be due to induction of cytochrome P450 2C8 by ginkgo.
Seizure Threshold Lowering Drugs
Theoretically, taking ginkgo with drugs that lower the seizure threshold might increase the risk for convulsions.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.
Simvastatin (Zocor)
Theoretically, ginkgo might decrease the levels and clinical effects of simvastatin.
Clinical research shows that taking ginkgo extract can reduce the area under the curve and maximum concentration of simvastatin by 32% to 39%. However, ginkgo extract does not seem to affect the cholesterol-lowering ability of simvastatin.
Sofosbuvir (Sovaldi)
Theoretically, ginkgo might increase the levels and clinical effects of sofosbuvir.
Animal research in rats shows that giving a ginkgo extract 25 mg/kg orally daily for 14 days increases the area under the concentration time curve (AUC) after a single sofosbuvir dose of 40 mg/kg by 11%, increases the half-life by 60%, and increases the plasma concentration at 4 hours by 38%. This interaction appears to be related to the inhibition of intestinal P-glycoprotein by ginkgo.
Tacrolimus (Prograf)
Theoretically, ginkgo might increase the blood levels of tacrolimus.
In vitro evidence suggests that certain biflavonoids in ginkgo leaves (i.e. amentoflavone, ginkgetin, bilobetin) may inhibit the metabolism of tacrolimus by up to 50%. This interaction appears to be time-dependent and due to inhibition of cytochrome P450 (CYP) 3A4 by these bioflavonoids. In rats given tacrolimus 1 mg/kg orally, amentoflavone was shown to increase the area under the concentration time curve (AUC) of tacrolimus by 3.8-fold.
Trazodone (Desyrel)
Theoretically, ginkgo might increase the levels and clinical effects of trazodone.
In a case report, an Alzheimer patient taking trazodone 20 mg twice daily and ginkgo leaf extract 80 mg twice daily for four doses became comatose. The coma was reversed by administration of flumazenil (Romazicon). Coma might have been induced by excessive GABA-ergic activity. Ginkgo flavonoids are thought to have GABA-ergic activity and act directly on benzodiazepine receptors. Ginkgo might also increase metabolism of trazodone to active GABA-ergic metabolites, possibly by inducing cytochrome P450 3A4 (CYP3A4) metabolism.
Warfarin (Coumadin)
Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. Information from a medical database suggests that when taken concurrently with warfarin, ginkgo increases the risk of a bleeding adverse event by 38%. There is also some evidence that ginkgo leaf extract can inhibit cytochrome P450 2C9, an enzyme that metabolizes warfarin. This could result in increased warfarin levels. However, population and clinical research has produced mixed results. Clinical research in healthy people suggests that ginkgo has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. A meta-analysis of 18 studies using standardized ginkgo extracts, 80 mg to 480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. There is also some preliminary clinical research that suggests ginkgo might not significantly increase the effects of warfarin in patients that have a stable INR.
Nifedipine (Procardia)
Theoretically, taking ginkgo with oral, but not intravenous, nifedipine might increase levels and adverse effects of nifedipine.
Animal research and some clinical evidence suggests that taking ginkgo leaf extract orally in combination with oral nifedipine might increase nifedipine levels and cause increased side effects, such as headaches, dizziness, and hot flushes. However, taking ginkgo orally does not seem to affect the pharmacokinetics of intravenous nifedipine.
Omeprazole (Prilosec)
Theoretically, taking ginkgo with omeprazole might decrease the levels and clinical effects of omeprazole.
Clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce cytochrome P450 (CYP) 2C19 enzymes and decrease levels of omeprazole by about 27% to 42%.
Turmeric Rhizome Extract, Dry
Alkylating Agents
Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research suggests that curcumin, a constituent of turmeric, inhibits mechlorethamine-induced apoptosis of breast cancer cells by up to 70%. Also, animal research shows that curcumin inhibits cyclophosphamide-induced tumor regression. However, some in vitro research shows that curcumin does not affect the apoptosis capacity of etoposide. Also, other laboratory research suggests that curcumin might augment the cytotoxic effects of alkylating agents. Reasons for the discrepancies may relate to the dose of curcumin and the specific chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have on alkylating agents.
Amlodipine (Norvasc)
Taking turmeric with amlodipine may increase levels of amlodipine.
Animal research shows that giving amlodipine 1 mg/kg as a single dose following the use of turmeric extract 200 mg/kg daily for 2 weeks increases the maximum concentration and area under the curve by 53% and 56%, respectively, when compared with amlodipine alone. Additional animal research shows that taking amlodipine 1 mg/kg with a curcumin 2 mg/kg pretreatment for 10 days increases the maximum concentration and area under the curve by about 2-fold when compared with amlodipine alone.
Anticoagulant/Antiplatelet Drugs
Turmeric may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Curcumin, a constituent of turmeric, has demonstrated antiplatelet effects in vitro. Furthermore, two case reports have found that taking turmeric along with warfarin or fluindione was associated with an increased international normalized ratio (INR). However, one clinical study in healthy volunteers shows that taking curcumin 500 mg daily for 3 weeks, alone or with aspirin 100 mg, does not increase antiplatelet effects or bleeding risk. It is possible that the dose of turmeric used in this study was too low to produce a notable effect.
Antidiabetes Drugs
Theoretically, taking turmeric with antidiabetes drugs might increase the risk of hypoglycemia.
Animal research and case reports suggest that curcumin, a turmeric constituent, can reduce blood glucose levels in patients with diabetes. Furthermore, clinical research in adults with type 2 diabetes shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg decreased postprandial glucose levels for up to 24 hours when compared with glyburide alone, despite the lack of a significant pharmacokinetic interaction. Other clinical studies in patients with diabetes show that taking curcumin daily can reduce blood glucose levels when compared with placebo.
Antitumor Antibiotics
Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro and animal research shows that curcumin, a constituent of turmeric, inhibits doxorubicin-induced apoptosis of breast cancer cells by up to 65%. However, curcumin does not seem to affect the apoptosis capacity of daunorubicin. In fact, some research shows that curcumin might augment the cytotoxic effects of antitumor antibiotics, increasing their effectiveness. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effects, if any, antioxidants such as turmeric have on antitumor antibiotics.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Turmeric might increase or decrease levels of drugs metabolized by CYP3A4.
In vitro and animal research show that turmeric and its constituents curcumin and curcuminoids inhibit CYP3A4. Also, 8 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking turmeric and cancer medications that are CYP3A4 substrates, including everolimus, ruxolitinib, ibrutinib, and palbociclib, and bortezomib. In another case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels after consuming turmeric powder at a dose of 15 or more spoonfuls daily for ten days prior. It was thought that turmeric increased levels of tacrolimus due to CYP3A4 inhibition.
Conversely, other in vitro research suggests that turmeric induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. An animal model suggests that induction of CYP3A4 occurs after daily curcumin use for 1 week. However, the induction of CYP3A4 by turmeric has not been reported in humans.
Hepatotoxic Drugs
Theoretically, turmeric might increase the risk of liver damage when taken with hepatotoxic drugs.
There is concern that turmeric might cause hepatotoxicity, especially when highly bioavailable formulations are used in high doses.
Methotrexate (Trexall, Others)
Theoretically, turmeric might have additive effects when used with hepatotoxic drugs such as methotrexate.
In one case report, a 39-year-old female taking methotrexate, turmeric, and linseed oil developed hepatotoxicity.
Organic Anion-Transporting Polypeptide Substrates (Oatp)
Theoretically, turmeric might increase blood levels of OATP4C1 substrates.
In vitro research shows that the turmeric constituent curcumin competitively inhibits OATP4C1 transport. This transporter is expressed in the kidney and facilitates the renal excretion of certain drugs. Theoretically, taking turmeric might decrease renal excretion of OATP substrates.
Sulfasalazine (Azulfidine)
Turmeric might increase the effects and adverse effects of sulfasalazine.
Clinical research shows that taking the turmeric constituent, curcumin, can increase blood levels of sulfasalazine by 3.2-fold.
Tacrolimus (Prograf)
Turmeric might increase the effects and adverse effects of tacrolimus.
In one case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels of 29 ng/mL. The patient previously had tacrolimus levels within the therapeutic range at 9.7 ng/mL. Ten days prior to presenting at the emergency room the patient started consumption of turmeric powder at a dose of 15 or more spoonfuls daily. It was thought that turmeric increased levels of tacrolimus due to cytochrome P450 3A4 (CYP3A4) inhibition. In vitro and animal research show that turmeric and its constituent curcumin inhibit CYP3A4.
Talinolol
Turmeric may reduce the absorption of talinolol in some situations.
Clinical research shows that taking curcumin for 6 days decreases the bioavailability of talinolol when taken together on the seventh day. The clinical significance of this effect is unclear.
Tamoxifen (Nolvadex)
Theoretically, turmeric might reduce the levels and clinical effects of tamoxifen.
In a small clinical trial in patients with breast cancer taking tamoxifen 20-30 mg daily, adding curcumin 1200 mg plus piperine 10 mg three times daily reduces the 24-hour area under the curve of tamoxifen and the active metabolite endoxifen by 12.8% and 12.4%, respectively, as well as the maximum concentrations of tamoxifen, when compared with tamoxifen alone. However, in the absence of piperine, the area under the curve for endoxifen and the maximum concentration of tamoxifen were not significantly reduced. Effects were most pronounced in patients who were extensive cytochrome P450 (CYP) 2D6 metabolizers.
Topoisomerase I Inhibitors
Turmeric has antioxidant effects. There is some concern that this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research shows that curcumin, a constituent of turmeric, inhibits camptothecin-induced apoptosis of breast cancer cells by up to 71%. However, other in vitro research shows that curcumin augments the cytotoxic effects of camptothecin. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agents. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have.
Tramadol (Ultram)
Theoretically, turmeric might increase or decrease levels of tramadol.
Animal research suggests that a single dose of curcumin, a constituent of turmeric, may increase tramadol's maximum concentration (Cmax) by inhibiting metabolism, while continued daily use for 7 days may reduce the area under the curve (AUC) due to the induction of drug-metabolizing enzymes such as cytochrome P450 3A4 (CYP3A4). However, this interaction has not been reported in humans.
Warfarin (Coumadin)
Turmeric might increase the risk of bleeding with warfarin.
One case of increased international normalized ratio (INR) has been reported for a patient taking warfarin who began taking turmeric. Prior to taking turmeric, the patient had stable INR measurements. Within a few weeks of starting turmeric supplementation, the patient's INR increased to 10. Additionally, curcumin, the active constituent in turmeric, has demonstrated antiplatelet effects in vitro, which may produce additive effects when taken with warfarin.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2. However, research is conflicting.
In vitro and animal research show that the turmeric constituent, curcumin, inhibits CYP1A2. However, other in vitro research suggests that curcumin does not significantly affect CYP1A2.
Docetaxel (Taxotere)
Theoretically, turmeric might increase blood levels of oral docetaxel.
Animal research suggests that the turmeric constituent, curcumin, enhances the oral bioavailability of docetaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.
Estrogens
Theoretically, large amounts of turmeric might interfere with hormone replacement therapy through competition for estrogen receptors.
In vitro research shows that curcumin, a constituent of turmeric, displaces the binding of estrogen to its receptors.
Glyburide (Diabeta, Others)
Theoretically, taking turmeric and glyburide in combination might increase the risk of hypoglycemia.
Clinical research shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg increases blood levels of glyburide by 12% at 2 hours after the dose in patients with type 2 diabetes. While maximal blood concentrations of glyburide were not affected, turmeric modestly decreased postprandial glucose levels for up to 24 hours when compared to glyburide alone, possibly due to the hypoglycemic effect of turmeric demonstrated in animal research.
Losartan (Cozaar)
Theoretically, turmeric might increase the effects of losartan.
Research in hypertensive rats shows that taking turmeric can increase the hypotensive effects of losartan.
Norfloxacin (Noroxin)
Theoretically, turmeric might increase the effects and adverse effects of norfloxacin.
Animal research shows that taking curcumin, a turmeric constituent, can increase blood levels of orally administered norfloxacin.
P-Glycoprotein Substrates
Theoretically, turmeric might increase the absorption of P-glycoprotein substrates.
In vitro and animal research shows that curcuminoids and other constituents found in turmeric can inhibit P-glycoprotein expression and activity.
Paclitaxel (Abraxane, Onxol)
Theoretically, turmeric might alter blood levels of paclitaxel, although any effect may not be clinically relevant.
Clinical research in adults with breast cancer receiving intravenous paclitaxel suggests that taking turmeric may modestly alter paclitaxel pharmacokinetics. Patients received paclitaxel on day 1, followed by either no treatment or turmeric 2 grams daily from days 2-22. Pharmacokinetic modeling suggests that turmeric reduces the maximum concentration and area under the curve of paclitaxel by 12.1% and 7.7%, respectively. However, these changes are not likely to be considered clinically relevant. Conversely, animal research suggests that curcumin, a constituent of turmeric, enhances the oral bioavailability of paclitaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.
Yerba Mate Leaf Extract, Dry
Ephedrine
Theoretically, the caffeine in yerba mate might increase the risk for stimulant adverse effects when used concomitantly with ephedrine.
Use of ephedrine with caffeine can increase the risk of stimulatory adverse effects. There is evidence that using ephedrine with caffeine might increase the risk of serious life-threatening or debilitating adverse effects such as hypertension, myocardial infarction, stroke, seizures, and death.
Adenosine (Adenocard)
Theoretically, the caffeine in yerba mate might decrease the vasodilatory effects of adenosine and interfere with its use prior to stress testing.
Yerba mate contains caffeine. Some evidence shows that caffeine is a competitive inhibitor of adenosine and can reduce the vasodilatory effects of adenosine in humans. However, other research shows that caffeine does not seem to affect supplemental adenosine because high interstitial levels of adenosine overcome the antagonistic effects of caffeine. Still, some researchers recommend that methylxanthines, such as caffeine, as well as methylxanthine-containing products, should be stopped 24 hours prior to pharmacological stress tests. However, methylxanthines appear more likely to interfere with dipyridamole (Persantine) than adenosine-induced stress testing.
Anticoagulant/Antiplatelet Drugs
Theoretically, the caffeine in yerba mate may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Yerba mate contains caffeine. Caffeine is reported to have antiplatelet activity. Theoretically, it might increase the risk of bleeding when used concomitantly with these agents; however, this interaction has not been reported in humans.
Benzodiazepines
Theoretically, the caffeine in yerba mate might reduce the efficacy of benzodiazepines.
Yerba mate contains caffeine. Caffeine can antagonize the anxiolytic effects of benzodiazepines.
Beta-Adrenergic Agonists
Theoretically, the caffeine in yerba mate might increase the cardiac inotropic effects of beta-agonists, especially if taken in large amounts.
Yerba mate contains caffeine. Caffeine can increase cardiac inotropic effects of beta-agonists.
Carbamazepine (Tegretol)
Theoretically, the caffeine in yerba mate might reduce the effects of carbamazepine and increase the risk for convulsions.
Yerba mate contains caffeine. Animal research suggests that caffeine can lower the anticonvulsant effects of carbamazepine and can induce seizures when taken in doses above 400 mg/kg. Human research has shown that taking caffeine 300 mg in three divided doses along with carbamazepine 200 mg reduces the bioavailability of carbamazepine by 32% and prolongs the plasma half-life of carbamazepine two-fold in healthy individuals.
Cimetidine (Tagamet)
Theoretically, cimetidine might increase the levels and adverse effects of the caffeine contained in yerba mate.
Yerba mate contains caffeine. Cimetidine decreases caffeine clearance by 31% to 42%.
Clozapine (Clozaril)
Theoretically, the caffeine in yerba mate might increase the levels and adverse effects of clozapine and acutely exacerbate psychotic symptoms.
Yerba mate contains caffeine. Caffeine might increase the effects and toxicity of clozapine. Caffeine doses of 400-1000 mg per day inhibit clozapine metabolism. Clozapine is metabolized by cytochrome P450 1A2 (CYP1A2). Although researchers speculate that caffeine might inhibit CYP1A2, there is no reliable evidence that caffeine affects CYP1A2. There is also speculation that genetic factors might make some patients more sensitive to an interaction between clozapine and caffeine.
Dipyridamole (Persantine)
Theoretically, the caffeine in yerba mate might decrease the vasodilatory effects of dipyridamole and interfere with its use prior to stress testing.
Yerba mate contains caffeine. Caffeine inhibits dipyridamole-induced vasodilation. Still, some researchers recommend that methylxanthines, such as caffeine, as well as methylxanthine-containing products, should be stopped 24 hours prior to pharmacological stress. Methylxanthines appear more likely to interfere with dipyridamole (Persantine) than adenosine-induced stress testing.
Disulfiram (Antabuse)
Theoretically, disulfiram might increase the levels and adverse effects of the caffeine in yerba mate.
Yerba mate contains caffeine. Disulfiram decreases the rate of caffeine clearance.
Diuretic Drugs
Theoretically, the caffeine in yerba mate might increase the risk of hypokalemia when used concomitantly with other diuretics.
Yerba mate contains caffeine. Caffeine, especially in excessive amounts, can reduce potassium levels due to stimulation of the sodium-potassium pump. Diuretics can also cause lower potassium levels.
Estrogens
Theoretically, estrogens might increase the levels and adverse effects of the caffeine in yerba mate.
Yerba mate contains caffeine. Estrogen inhibits caffeine metabolism.
Ethosuximide (Zarontin)
Theoretically, the caffeine in yerba mate might reduce the effects of ethosuximide and increase the risk for convulsion.
Yerba mate contains caffeine. Animal research shows that caffeine 92.4 mg/kg can decrease the anticonvulsant activity of ethosuximide. However, this effect has not been reported in humans.
Felbamate (Felbatol)
Theoretically, the caffeine in yerba mate might reduce the effects of felbamate and increase the risk for convulsion.
Yerba mate contains caffeine. Animal research shows that a high dose of caffeine 161.7 mg/kg can decreases the anticonvulsant activity of felbamate. However, this effect has not been reported in humans.
Flutamide (Eulexin)
Theoretically, the caffeine in yerba mate might increase the levels and adverse effects of flutamide.
Yerba mate contains caffeine. In vitro evidence suggests that caffeine can inhibit the metabolism of flutamide. However, this effect has not been reported in humans.
Fluvoxamine (Luvox)
Theoretically, fluvoxamine might increase the levels and adverse effects of the caffeine in yerba mate.
Yerba mate contains caffeine. Fluvoxamine reduces caffeine metabolism.
Lithium
Theoretically, abrupt withdrawal of the caffeine in yerba mate might increase serum lithium levels.
Yerba mate contains caffeine, which has diuretic activity. When abruptly discontinued, it might alter the clearance of lithium. There are two case reports of lithium tremor that worsened upon abrupt coffee withdrawal.
Midazolam (Versed)
Theoretically, use of yerba mate with midazolam might increase midazolam metabolite levels and adverse effects.
In vitro research shows that yerba mate extract containing 6.75% chlorogenic acid significantly inhibits the metabolism of midazolam via inhibition of cytochrome P450 3A4 (CYP3A4).
Monoamine Oxidase Inhibitors (Maois)
Theoretically, the caffeine in yerba mate might increase risk of a hypertensive crisis when used concomitantly with MAOIs.
Yerba mate contains caffeine. Caffeine has been shown to inhibit monoamine oxidase (MAO) A and B in laboratory studies. Concomitant intake of large amounts of caffeine with MAOIs might precipitate a hypertensive crisis. In a case report, a patient that consumed 10-12 cups of caffeinated coffee and took the MAOI tranylcypromine presented with severe hypertension. Hypertension was resolved after the patient switched to drinking decaffeinated coffee.
Nicotine
Theoretically, the caffeine in yerba mate might increase risk of hypertension when used concomitantly with nicotine.
Yerba mate contains caffeine. Concomitant use of caffeine and nicotine has been shown to have additive cardiovascular effects, including increased heart rate and blood pressure. Blood pressure was increased by 10.8/12.4 mmHg when the agents were used concomitantly.
Pentobarbital (Nembutal)
Theoretically, the caffeine in yerba mate might decrease the effects of pentobarbital.
The caffeine in yerba mate might negate the hypnotic effects of pentobarbital.
Phenobarbital (Luminal)
Theoretically, the caffeine in yerba mate might reduce the effects of phenobarbital and increase the risk for convulsions.
Yerba mate contains caffeine. Animal research suggests that caffeine can decrease the anticonvulsant activity of phenobarbital. However, the exact mechanism of this interaction is unclear.
Phenylpropanolamine
Theoretically, phenylpropanolamine might increase the risk of hypertension as well as the levels and adverse effects of the caffeine in yerba mate.
Yerba mate contains caffeine. Concomitant use of phenylpropanolamine and caffeine might cause an additive increase in blood pressure. Phenylpropanolamine also seems to increase caffeine serum levels.
Phenytoin (Dilantin)
Theoretically, the caffeine in yerba mate might reduce the effects of phenytoin and increase the risk for convulsions.
Yerba mate contains caffeine. Animal research suggests that caffeine can decrease the anticonvulsant activity of phenytoin. The effect does not seem to be related to the seizure threshold-lowering effects of caffeine. However, the exact mechanism of this interaction is unclear.
Pioglitazone (Actos)
Theoretically, the caffeine in yerba mate might increase the levels and clinical effects of pioglitazone.
Yerba mate contains caffeine. Animal research suggests that caffeine can modestly increase the maximum concentration, area under the curve, and half-life of pioglitazone, and also reduce its clearance. This increased the antidiabetic effects of pioglitazone. However, the exact mechanism of this interaction is unclear.
Brahmi Whole Herb Extract, Dry
Anticholinergic Drugs
Theoretically, concurrent use might decrease the effectiveness of both agents.
Bacopa seems to inhibit acetylcholinesterase and might increase acetylcholine levels, which could counteract the effects of anticholinergic drugs. Similarly, anticholinergic drugs might counteract the cholinergic effects of bacopa.
Cevimeline (Evoxac)
Theoretically, bacopa might increase the effects and adverse effects of cevimeline.
In one case, a 58-year-old female taking cevimeline long-term for Sjogren syndrome experienced hyperhidrosis, malaise, nausea, and tachycardia shortly after taking a single dose of bacopa. Symptoms resolved after two days. Cevimeline is metabolized by cytochrome P450 (CYP) 2D6 and CYP3A4, and researchers theorize that bacopa may have inhibited these isoenzymes. However, it is unclear if bacopa causes clinically significant inhibition of either CYP2D6 or CYP3A4.
Cholinergic Drugs
Theoretically, concurrent use of bacopa with other cholinergic drugs might have additive effects.
Bacopa seems to inhibit acetylcholinesterase and might increase acetylcholine levels. Theoretically, this could result in additive cholinergic effects when used with cholinergic drugs.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, bacopa might increase the levels and adverse effects of CYP1A2 substrates.
Research on the effects of bacopa extracts on CYP1A2 enzymes is conflicting. Some in vitro evidence shows that bacopa extract can moderately and non-competitively inhibit CYP1A2, while other in vitro evidence suggests that any effect is unlikely to be clinically significant.
Cytochrome P450 2C19 (Cyp2C19) Substrates
Theoretically, bacopa might increase the levels and adverse effects of CYP2C19 substrates.
In vitro evidence suggests that bacopa extract can moderately and non-competitively inhibit CYP2C19 enzymes. It is not known whether this is clinically significant.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, bacopa might increase the levels and adverse effects of CYP2C9 substrates.
Research on the effect of bacopa extracts on CYP2C9 enzymes is conflicting. Some in vitro evidence suggests that bacopa extract can moderately and non-competitively inhibit CYP2C9, while other in vitro evidence suggests that any effect is unlikely to be clinically significant.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, bacopa might increase the levels and adverse effects of CYP3A4 substrates.
Research on the effects of bacopa extracts on CYP3A4 enzymes is conflicting. Some in vitro evidence suggests that bacopa extract can moderately and competitively inhibit CYP3A4, while other in vitro evidence suggests that any effect is unlikely to be clinically significant.
Thyroid Hormone
Theoretically, bacopa might have additive effects when used with thyroid hormone.
Animal research suggests that bacopa increases thyroxine (T4) levels in mice by about 40%.
Schisandra Berry Extract, Dry
Cyclophosphamide
Theoretically, schisandra might increase the levels and clinical effects of cyclophosphamide.
In vitro research shows that schisandra increases the concentration of cyclophosphamide, likely through inhibition of cytochrome P450 3A4. After multiple doses of the schisandra constituents schisandrin A and schisantherin A, the maximum concentration of cyclophosphamide was increased by 7% and 75%, respectively, while the overall exposure to cyclophosphamide was increased by 29% and 301%, respectively.
Cyclosporine (Neoral, Sandimmune)
Schisandra can increase the levels and clinical effects of cyclosporine.
A small observational study in children with aplastic anemia found that taking schisandra with cyclosporine increased cyclosporine trough levels by 93% without increasing the risk of adverse events. However, the dose of cyclosporine was reduced in 9% of children to maintain appropriate cyclosporine blood concentrations.
Cytochrome P450 2C19 (Cyp2C19) Substrates
Theoretically, schisandra might increase the levels and clinical effects of CYP2C19 substrates.
In vitro research shows that schisandra inhibits CYP2C19, and animal research shows that schisandra increases the concentration of voriconazole, a CYP2C19 substrate. Theoretically, schisandra may also inhibit the metabolism of other CYP2C19 substrates. This effect has not been reported in humans.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, schisandra might decrease the levels and clinical effects of CYP2C9 substrates.
In vitro and animal research suggests that schisandra induces CYP2C9 enzymes. This effect has not been reported in humans.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Schisandra can increase the levels and clinical effects of drugs metabolized by CYP3A4.
Most clinical and laboratory research shows that schisandra, administered either as a single dose or up to twice daily for 14 days, inhibits CYP3A4 and increases the concentration of CYP3A4 substrates such as cyclophosphamide, midazolam, tacrolimus, and talinolol. Although one in vitro and animal study shows that schisandra may induce CYP3A4 metabolism, this effect appears to be overpowered by schisandra's CYP3A4 inhibitory activity and has not been reported in humans.
Midazolam (Versed)
Schisandra can increase the levels and clinical effects of midazolam.
A small pharmacokinetic study in healthy adults shows that taking schisandra extract (Hezheng Pharmaceutical Co.) containing deoxyschizandrin 33.75 mg twice daily for 8 days and a single dose of midazolam 15 mg on day 8 increases the overall exposure to midazolam by about 119%, increases the peak plasma level of midazolam by 86%, and decreases midazolam clearance by about 52%. This effect has been attributed to inhibition of CYP3A4 by schisandra.
P-Glycoprotein Substrates
Schisandra might increase the levels and clinical effects of P-glycoprotein substrates.
In vitro research shows that schisandra extracts and constituents such as schisandrin B inhibit P-glycoprotein mediated efflux in intestinal cells and in P-glycoprotein over-expressing cell lines. Additionally, a small clinical study shows that schisandra increases the peak concentration and overall exposure to talinolol, a P-glycoprotein probe substrate. Theoretically, schisandra might inhibit the efflux of other P-glycoprotein substrates.
Sirolimus (Rapamune)
Schisandra can increase the levels and clinical effects of sirolimus.
A small pharmacokinetic study in healthy volunteers shows that taking 3 capsules of schisandra (Hezheng Pharmaceutical Company) containing a total of 33.75 mg deoxyschizandrin twice daily for 13 days and then taking a single dose of sirolimus 2 mg increases the overall exposure and peak level of sirolimus by two-fold. This effect is thought to be due to inhibition of cytochrome P450 3A4 by schisandra, as well as possible inhibition of the P-glycoprotein drug transporter.
Tacrolimus (Prograf)
Schisandra can increase the levels and clinical effects of tacrolimus.
Clinical research in healthy children and adults, transplant patients, and patients with nephrotic syndrome and various rheumatic immunologic disorders shows that taking schisandra with tacrolimus increases tacrolimus peak levels by 183% to 268%, prolongs or delays time to peak tacrolimus concentrations, increases overall exposure to tacrolimus by 126% to 343%, and decreases tacrolimus clearance by 19% to 73%. This effect is thought to be due to inhibition of P-glycoprotein drug transporter and CYP3A4 and CYP3A5 by schisandra. Some clinical and observational studies suggest that schisandra increases tacrolimus levels similarly in both expressors and non-expressors of CYP3A5, while other studies suggest it does so to a greater degree in CYP3A5 expressors than non-expressors. Animal research suggests that the greatest increase in tacrolimus levels occurs when schisandra is taken either concomitantly or up to 2 hours before tacrolimus, and clinical and observational research in humans suggests that schisandra may increase whole blood levels of tacrolimus and decrease clearance of tacrolimus in a dose-dependent manner.
Talinolol
Schisandra can increase the levels and clinical effects of talinolol.
A small pharmacokinetic study in healthy volunteers shows that taking schisandra extract 300 mg twice daily for 14 days with a single dose of talinolol 100 mg on day 14 increases the peak talinolol level by 51% and the overall exposure to talinolol by 47%. This effect is thought to be due to the possible inhibition of cytochrome P450 3A4 and P-glycoprotein by schisandra.
tly.
Voriconazole (Vfend)
Theoretically, schisandra might increase the levels and clinical effects of voriconazole.
Animal research shows that oral schisandra given daily for 1 or 14 days increases levels of intravenously administered voriconazole, a cytochrome P450 (CYP) 2C19 substrate. This effect is thought to be due to inhibition of CYP2C19 by schisandra. However, this interaction has not been reported in humans.
Warfarin (Coumadin)
Theoretically, schisandra might decrease the levels and clinical effects of warfarin.
Animal research suggests that oral schisandra extract, given daily for 6 days, reduces levels of intravenously administered warfarin. This effect might be due to the induction of cytochrome P450 (CYP) 2C9 metabolism by schisandra. However, this interaction has not been reported in humans.
Rosemary Leaf Extract, Dry
Anticoagulant/Antiplatelet Drugs
Theoretically, rosemary may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro and animal research suggests that rosemary inhibits platelet aggregation.
Antidiabetes Drugs
Theoretically, taking rosemary with antidiabetes drugs might increase the risk of hypoglycemia.
Animal research shows that rosemary extract can decrease blood glucose levels in diabetic models. However, research in humans is conflicting. Although rosemary powder decreased blood glucose levels in healthy adults, no change in blood glucose levels was seen in adults with type 2 diabetes, most of whom were taking antidiabetes drugs.
Aspirin
Theoretically, rosemary might have additive effects with salicylate-containing drugs such as aspirin.
Rosemary is reported to contain salicylates.
Choline Magnesium Trisalicylate (Trilisate)
Theoretically, rosemary might have additive effects with salicylate-containing drugs such as choline magnesium trisalicylate.
Rosemary is reported to contain salicylate.
Salsalate (Disalcid)
Theoretically, rosemary might have additive effects with salicylate-containing drugs such as salsalate.
Rosemary is reported to contain salicylate.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, rosemary might decrease the levels and clinical effects of CYP1A2 substrates.
In vitro research shows that rosemary induces CYP1A2 enzymes. This effect has not been reported in humans.
Brand information
Manufacturer and brand details for Memory Advance, from the product label.
Hawaii Pharm
See all Hawaii Pharm products- Name
- Hawaii Pharm LLC
- Street Address
- 510 Sumner St 613
- City
- Honolulu
- State
- HI
- ZipCode
- 96817
- Phone Number
- 1-808-385-6076
- Web Address
- www.hawaiipharm.com
Memory Advance by Hawaii Pharm: Common Questions
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Written and reviewed by the HelloPharmacist editorial staff. Our editorial policy
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Label information is sourced from the NIH Dietary Supplement Label Database and reflects the product version on file; always read your actual product label. This page is for education only and is not a substitute for professional medical advice. Confirm with your pharmacist or doctor before combining supplements and medications.
The Full Monographs Behind Memory Advance’s Ingredients
Every ingredient we hold a full HelloPharmacist monograph for — uses, evidence, safety, and the complete interaction list.
Bacopa
Interacts with 930 drugsBacopa is an Ayurvedic herb most often used for memory and thinking. Some small studies suggest it may modestly help memory when taken regularly for several weeks, but the evidence is limite...
Read the full Bacopa monograph → Herb & supplement monographRosemary
Interacts with 372 drugsRosemary is a fragrant Mediterranean herb that is safe and flavorful in normal food amounts. Some early research suggests possible benefits for memory, mood, and hair growth, but the evidenc...
Read the full Rosemary monograph → Herb & supplement monographGinkgo
Interacts with 1,266 drugsGinkgo is one of the world's most popular herbal supplements, mostly taken to support memory and circulation. The evidence for these uses is mixed and generally weak, and it is not proven to...
Read the full Ginkgo monograph → Herb & supplement monographTurmeric
Interacts with 1,133 drugsTurmeric is a popular spice whose main active compounds, curcuminoids, are studied mostly for inflammation and joint pain. Some research is promising, but quality is mixed and curcumin is po...
Read the full Turmeric monograph → Herb & supplement monographSchisandra
Interacts with 803 drugsSchisandra is a traditional Chinese medicine berry used as an adaptogen for stress, fatigue, and liver support. Human evidence is limited and most claims are not well proven, but it appears...
Read the full Schisandra monograph → Herb & supplement monographSage
Interacts with 1,296 drugsSage is a common kitchen herb that is generally safe in food amounts and is traditionally used for sore throats, digestion, sweating, and memory. Some early research is encouraging for sore...
Read the full Sage monograph → Herb & supplement monographYerba Mate
Interacts with 1,086 drugsYerba mate is a caffeine-containing herbal beverage from South America that is widely enjoyed for its stimulating, coffee-like effects. While it is rich in antioxidants and is being studied...
Read the full Yerba Mate monograph →Sources & How We Checked
Memory Advance's label data comes from the NIH Dietary Supplement Label Database; the ingredient interaction data is from the Natural Medicines database, reviewed by our pharmacists.
- NIH Dietary Supplement Label Database (DSLD) — The official product label on file for this supplement.
- Natural Medicines (Therapeutic Research Center) — Evidence-graded clinical reference behind the ingredient interaction data.
Content is written and reviewed by licensed HelloPharmacist pharmacists. See our data sources and editorial standards for how this information is built and checked.
The 407 references behind this product’s interaction data
Every citation that drives the interaction findings for this product’s ingredients, from the evidence-graded Natural Medicines (TRC Healthcare) database. Open an ingredient to browse its citations — links open the study on PubMed or the publisher’s site.
Bacopa 12 references
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- Yadav SK, Jain AK, Tripathi SN, Gupta JP. Irritable bowel syndrome: therapeutic evaluation of indigenous drugs. Indian J Med Res 1989;90:496-503..
- Morgan A, Stevens J. Does Bacopa monnieri improve memory performance in older persons? Results of a randomized, placebo-controlled, double-blind trial. J Altern Complement Med 2010;16:753-9.
- Kar, A., Panda, S., and Bharti, S. Relative efficacy of three medicinal plant extracts in the alteration of thyroid hormone concentrations in male mice. J Ethnopharmacol. 2002;81(2):281-285. PubMed
- Mukherjee, G. D. and Dey, C. D. Clinical trial on Brahmi. I. J.Exp.Med.Sci. 1966;10(1):5-11.
- Kar A, Pandit S, Mukherjee K, Bahadur S, Mukherjee PK. Safety assessment of selected medicinal food plants used in Ayurveda through CYP450 enzyme inhibition study. J Sci Food Agric 2017;97(1):333-40. doi: 10.1002/jsfa.7739. PubMed
- Kongkeaw C, Dilokthornsakul P, Thanarangsarit P, et al. Meta-analysis of randomized controlled trials on cognitive effects of Bacopa monnieri extract. J Ethnopharmacol 2014;151(1):528-35. PubMed
- Ramasamy S, Kiew LV, Chung LY. Inhibition of human cytochrome P450 enzymes by Bacopa monnieri standardized extract and constituents. Molecules 2014;19(2):2588-601. PubMed
- Prabhakar S, Vishnu VY, Modi M, et al. Efficacy of Bacopa monnieri (Brahmi) and donepezil in Alzheimer's disease and mild cognitive impairment: a randomized double-blind parallel phase 2b study. Ann Indian Acad Neurol 2020;23(6):767-73. PubMed
- Acquarulo B, Tandon P, Macica CM. Suspected cholinergic toxicity due to cevimeline hydrochloride and Bacopa monnieri interaction: a case report. J Med Case Rep 2022;16(1):253. PubMed
- Keegan AP, Stough C, Paris D, et al. Bacopa monnieri supplementation has no effect on serum brain-derived neurotrophic factor levels but beneficially modulates nuclear factor kappa B and cyclic AMP response element-binding protein levels in healthy elderl
- Yaworski AM, Blyumin M, Chang T, Mammen AL, Greene M. Necrotizing myopathy with elevated anti-HMGCR antibodies following exposure to the supplement Bacopa. Muscle Nerve 2023;67(2):E1-E3.
Rosemary 20 references
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- Foster S, Tyler VE. Tyler's Honest Herbal: A Sensible Guide to the Use of Herbs and Related Remedies. 3rd ed., Binghamton, NY: Haworth Herbal Press, 1993.
- The Review of Natural Products by Facts and Comparisons. St. Louis, MO: Wolters Kluwer Co., 1999.
- McGuffin M, Hobbs C, Upton R, Goldberg A, eds. American Herbal Products Association's Botanical Safety Handbook. Boca Raton, FL: CRC Press, LLC 1997.
- Gruenwald J, Brendler T, Jaenicke C. PDR for Herbal Medicines. 1st ed. Montvale, NJ: Medical Economics Company, Inc., 1998.
- Cartier LC, Lehrer A, Malo JL. Occupational asthma caused by aromatic herbs. Allergy 1996;51:647-9. DOI
- Burkhard PR, Burkhardt K, Haenggeli CA, Landis T. Plant-induced seizures: reappearance of an old problem. J Neurol 1999;246:667-70. PubMed
- Swain AR, Dutton SP, Truswell AS. Salicylates in foods. J Am Diet.Assoc 1985;85(8):950-60. DOI
- Zhu BT, Loder DP, Cai MX, et al. Dietary administration of an extract from rosemary leaves enhances the liver microsomal metabolism of endogenous estrogens and decreases their uterotropic action in CD-1 mice. Carcinogenesis 1998;19(10):1821-7. PubMed
- Debersac P, Heydel JM, Amiot MJ, et al. Induction of cytochrome P450 and/or detoxication enzymes by various extracts of rosemary: description of specific patterns. Food Chem Toxicol 2001;39(9):907-18. PubMed
- Debersac P, Vernevaut MF, Amiot MJ, et al. Effects of a water-soluble extract of rosemary and its purified component rosmarinic acid on xenobiotic-metabolizing enzymes in rat liver. Food Chem Toxicol 2001;39(2):109-17. PubMed
- Lee JJ, Jin YR, Lee JH, et al. Antiplatelet activity of carnosic acid, a phenolic diterpene from Rosmarinus officinalis. Planta Med 2007;73(2):121-7.
- Yamamoto J, Yamada K, Naemura A, et al. Testing various herbs for antithrombotic effect. Nutrition 2005;21(5):580-7. PubMed
- Naemura A, Ura M, Yamashita T, et al. Long-term intake of rosemary and common thyme herbs inhibits experimental thrombosis without prolongation of bleeding time. Thromb Res 2008;122(4):517-22. PubMed
- Lee JJ, Jin YR, Lim Y, et al. Antiplatelet activity of carnosol is mediated by the inhibition of TXA2 receptor and cytosolic calcium mobilization. Vascul Pharmacol 2006;45:148-53. PubMed
- Bakirel, T., Bakirel, U., Keles, O. U., Ulgen, S. G., and Yardibi, H. In vivo assessment of antidiabetic and antioxidant activities of rosemary (Rosmarinus officinalis) in alloxan-diabetic rabbits. J Ethnopharmacol 2-28-2008;116(1):64-73. PubMed
- Erenmemisoglu, A., Saraymen, R., and Ustun, S. Effect of a Rosmarinus officinalis leave extract on plasma glucose levels in normoglycaemic and diabetic mice. Pharmazie 1997;52(8):645-646.
- Valones MAA, Silva ICG, Gueiros LAM, Leão JC, Caldas AF Jr, Carvalho AAT. Clinical assessment of rosemary-based toothpaste (Rosmarinus officinalis Linn.): A randomized controlled double-blind study. Braz Dent J. 2019;30(2):146-151. PubMed
- Quirarte-Báez SM, Zamora-Perez AL, Reyes-Estrada CA, et al. A shortened treatment with rosemary tea (rosmarinus officinalis) instead of glucose in patients with diabetes mellitus type 2 (TSD). J Popul Ther Clin Pharmacol. 2019;26(4):e18-e28.
- Al Jamal A. Effect of rosemary (Rosmarinus officinalis) on lipid profiles and blood glucose in human diabetic patients (type-2). African J. Biochem. Res. 2014;8(8):147-50. DOI
Ginkgo 97 references
- Davydov L, Stirling AL. Stevens-Johnson syndrome with Ginkgo biloba. J Herb Pharmacother 2001;1:65-9. DOI
- Benjamin J, Muir T, Briggs K, Pentland B. A case of cerebral haemorrhage-can Ginkgo biloba be implicated? Postgrad Med J 2001;77:112-3.
- Matthews, MK. Association of Ginkgo biloba with intracerebral hemorrhage. Neurology 1998;50:1934.
- Rowin J, Lewis SL. Spontaneous bilateral subdural hemotomas with chronic Ginkgo biloba ingestion. Neurology 1996;46:1775-6.
- Rosenblatt M, Mindel T. Spontaneous hyphema associated with ingestion of Ginkgo biloba extract. N Engl J Med 1997;336:1108.
- Fessenden JM, Wittenborn W, Clarke L. Gingko biloba: a case report of herbal medicine and bleeding postoperatively from a laparoscopic cholecystectomy. Am Surg 2001;67:33-5. DOI
- Gurley BJ, Gardner SF, Hubbard MA. Clinical assessment of potential cytochrome P450-mediated herb-drug interactions. AAPS Ann Mtg & Expo Indianapolis, IN: 2000; Oct 29 - Nov 2:presentation #3460.
- Cohen AJ, Bartlik B. Ginkgo biloba for antidepressant-induced sexual dysfunction. J Sex Marital Ther 1998;24:139-43. PubMed
- Kudolo GB. The effect of 3-month ingestion of Ginkgo biloba extract on pancreatic beta-cell function in response to glucose loading in normal glucose tolerant individuals. J Clin Pharmacol 2000;40:647-54.
- Heck AM, DeWitt BA, Lukes AL. Potential interactions between alternative therapies and warfarin. Am J Health Syst Pharm 2000;57:1221-7. DOI
- Cesarani A, Meloni F, Alpini D, et al. Ginkgo biloba (EGb 761) in the treatment of equilibrium disorders. Adv Ther 1998;15:291-304.
- Galluzzi S, Zanetti O, Binetti G, et al. Coma in a patient with Alzheimer's disease taking low dose trazodone and Ginkgo biloba. J Neurol Neurosurg Psychiatry 2000;68:679-80. DOI
- Budzinski JW, Foster BC, Vandenhoek S, Arnason JT. An in vitro evaluation of human cytochrome P450 3A4 inhibition by selected commercial herbal extracts and tinctures. Phytomedicine 2000;7:273-82. PubMed
- Gregory PJ. Seizure associated with Ginkgo biloba? Ann Intern Med 2001;134:344.
- Granger AS. Ginkgo biloba precipitating epileptic seizures. Age Ageing 2001;30:523-5. PubMed
- Kajiyama Y, Fujii K, Takeuchi H, Manabe Y. Ginkgo seed poisoning. Pediatrics 2002;109:325-7. PubMed
- Miwa H, Iijima M, Tanaka S, Mizuno Y. Generalized convulsions after consuming a large amount of gingko nuts. Epilepsia 2001;42:280-1. DOI
- Burschka MA, Hassan HA, Reineke T, et al. Effect of treatment with Ginkgo biloba extract EGb 761 (oral) on unilateral idiopathic sudden hearing loss in a prospective randomized double-blind study of 106 outpatients. Eur Arch Otorhinolaryngol 2001;258:213- PubMed
- Miller LG, Freeman B. Possible subdural hematoma associated with Ginkgo biloba. J Herb Pharmacother 2002;2:57-63.
- Kudolo GB, Dorsey S, Blodgett J. Effect of the ingestion of Ginkgo biloba extract on platelet aggregation and urinary prostanoid excretion in healthy and Type 2 diabetic subjects. Thromb Res 2002;108:151-60.. PubMed
- Fong KC, Kinnear PE. Retrobulbar haemorrhage associated with chronic Ginkgo biloba ingestion. Postgrad Med J 2003;79:531-2..
- Gurley BJ, Gardner SF, Hubbard MA, et al. Cytochrome P450 phenotypic ratios for predicting herb-drug interactions in humans. Clin Pharmacol Ther 2002;72:276-87.. PubMed
- Kang BJ, Lee SJ, Kim MD, Cho MJ. A placebo-controlled, double-blind trial of Ginkgo biloba for antidepressant-induced sexual dysfunction. Hum Psychopharmacol 2002;17:279-84.
- Yale SH, Glurich I. Analysis of the inhibitory potential of Ginkgo biloba, Echinacea purpurea, and Serenoa repens on the metabolic activity of cytochrome P450 3A4, 2D6, and 2C9. J Altern Complement Med 2005;11:433-9.
- Yasui-Furukori N, Furukori H, Kaneda A, et al. The effects of Ginkgo biloba extracts on the pharmacokinetics and pharmacodynamics of donepezil. J Clin Pharmacol 2004;44:538-42.
- Markowitz JS, Donovan JL, Lindsay DeVane C, et al. Multiple-dose administration of Ginkgo biloba did not affect cytochrome P-450 2D6 or 3A4 activity in normal volunteers. J Clin Psychopharmacol 2003;23:576-81. PubMed
- Arenz A, Kelin M, Flehe K, et al. Occurrence of neurotoxic 4'-O-methylpyridoxine in ginkgo biloba leaves, ginkgo medications and Japanese ginkgo food. Planta Med 1996;62:548-51.
- Engelsen J, Nielsen JD, Winther K. Effect of coenzyme Q10 and Ginkgo biloba on warfarin dosage in stable, long-term warfarin treated outpatients. A randomised, double blind, placebo-crossover trial. Thromb Haemost 2002;87:1075-6. DOI
- Gaudineau C, Beckerman R, Welbourn S, Auclair K. Inhibition of human P450 enzymes by multiple constituents of the Ginkgo biloba extract. Biochem Biophys Res Comm 2004;318:1072–8. PubMed
- Kohler S, Funk P, Kieser M. Influence of a 7-day treatment with Ginkgo biloba special extract EGb 761 on bleeding time and coagulation: a randomized, placebo-controlled, double-blind study in healthy volunteers. Blood Coagul Fibrinolysis 2004;15:303–9. PubMed
- Jiang X, Williams KM, Liauw WS, et al. Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Br J Clin Pharmacol 2005;59:425-32. PubMed
- Destro MW, Speranzini MB, Cavalheiro Filho C, et al. Bilateral haematoma after rhytidoplasty and blepharoplasty following chronic use of Ginkgo biloba. Br J Plast Surg 2005;58:100-1. PubMed
- Yin OQ, Tomlinson B, Waye MM, et al. Pharmacogenetics and herb-drug interactions: experience with Ginkgo biloba and omeprazole. Pharmacogenetics 2004;14:841-50. PubMed
- Bent S, Goldberg H, Padula A, Avins AL. Spontaneous bleeding associated with Ginkgo biloba: a case report and systematic review of the literature. J Gen Intern Med 2005;20;657-61. DOI
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- Hauser D, Gayowski T, Singh N. Bleeding complications precipitated by unrecognized Gingko biloba use after liver transplantation. Transpl Int 2002;15:377-9. DOI
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- Kudolo GB. The effect of 3-month ingestion of Ginkgo biloba extract (EGb 761) on pancreatic beta-cell function in response to glucose loading in individuals with non-insulin-dependent diabetes mellitus. J Clin Pharmacol 2001;41:600-11.
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- Kellermann AJ, Kloft C. Is there a risk of bleeding associated with standardized ginkgo biloba extract therapy? A systematic review and meta-analysis. Pharmacotherapy 2011;31:490-502.
- Kuller LH, Ives DG, Fitzpatrick AL, et al. Does Ginkgo biloba reduce the risk of cardiovascular events? Circ Cardiovasc Qual Outcomes 2010;3:41-7.
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