Major interaction on record — check this product against your medications before combining. Based on 18 of 21 ingredients. Check your meds →
Dietary supplement

Mind Full Ingredients & Drug Interactions

by Herbally Grounded

Mind Full label
See full label image
Liquid Category: Botanical
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 23, 2026 · Label data from the NIH DSLD
What is this page for?

First and foremost: checking Mind Full 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

The interaction bottom line Most serious interaction: Major

Mind Full is a dietary supplement by Herbally Grounded with 21 active ingredients. Its ingredients are commonly taken for eye and vision health, antioxidant support, diarrhea and digestive upset.Based on those ingredients, 1,706 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ginkgo, Fo-Ti, St. John's Wort. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

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Check Your Meds Against Mind Full by Herbally Grounded

Ask about any prescription or over-the-counter medication and we check it for interactions with Mind Full by Herbally Grounded — and tell you which ingredient is responsible.

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HelloPharmacist Scorecard of Mind Full by Herbally Grounded

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.

From our pharmacy team — supplement deep dive

Generated from HelloPharmacist’s pharmacist-curated databases and editorial rules · Last generated Jul 11, 2026

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

Most active ingredients don't disclose an individual amount — you can't tell how much of each you're getting.

Why this rating?
  • The label discloses an exact amount for 0 of its 20 active ingredients.
  • “Proprietary Blend” is a proprietary blend — the label gives one combined amount (2.40 mL) without saying how much of each component you get.

Mind Full contains 20 active ingredients in a proprietary blend base, including well-known herbs like ginkgo, St. John's wort, ginger, fo-ti, bilberry, and nettle, along with lesser-known ones such as motherwort, gotu kola, blessed thistle, eleuthero, rosemary, fennel, red raspberry, feverfew, alfalfa, and yellow dock.

The liquid also lists glycerin, deionized water, and apple cider vinegar as inactive ingredients.

Does it work?

Moderate evidence
Evidence for Intended Use · database check
By FDA rules, dietary supplements can’t claim to treat, cure, or prevent disease — so labels speak in careful marketing language. We discern each product’s intended use from its name, label claims, and label statements, then grade the clinical evidence for that use. How these ratings are computed
Moderate

Some clinical evidence supports this product's ingredients for its stated purpose, but it isn't conclusive.

Why this rating?
  • The label markets this product for: focus and think clearly.
  • We looked for evidence on: Attention deficit-hyperactivity disorder (ADHD), Age-related cognitive decline, Cognitive function, Cognitive impairment, Memory, Concentration — and 1 related terms.
  • The strongest evidence on file: Rosemary is rated "Possibly Effective" for Memory (Natural Medicines).
  • Also on file: Ginkgo is rated "Possibly Ineffective" for Age-related cognitive decline, Chemotherapy-related cognitive impairment.
  • Also on file: Gotu Kola is rated "Possibly Ineffective" for Cognitive function.

The evidence for Mind Full's ingredients is mixed and mostly limited. Ginkgo is possibly effective for hearing loss, stroke, schizophrenia, premenstrual syndrome, dementia, and anxiety.

St. John's Wort is likely effective for depression and possibly effective for somatic symptom disorder and menopausal symptoms.

Ginger is possibly effective for pregnancy-induced nausea, painful periods, and osteoarthritis. Rosemary is possibly effective for memory, and gotu kola is possibly effective for venous insufficiency and burns.

Nettle is possibly effective for diabetes. Most other ingredients—including bilberry, fo-ti, fennel, red raspberry, feverfew, motherwort, alfalfa, yellow dock, and eleuthero—lack reliable evidence or are rated insufficient to rate their effectiveness for the purposes listed in the product facts.

The evidence, ingredient by ingredient Bilberry Fo-ti Ginkgo Fucus Vesiculosus Fennel Red Raspberry Feverfew German Chamomile

How safe is it?

Well-documented data
Safety Information · database check
Well characterized

Adverse-effect, pregnancy, and general safety data are on file for most of these ingredients.

Why this rating?
  • We hold adverse-effect (side-effect) data for 18 of the 18 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 18 of 18.
  • General safety write-ups exist for 18 of 18.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Several ingredients in this product carry real safety concerns. Fo-ti has been linked to serious liver injury and is best avoided without professional guidance.

St. John's Wort can cause photosensitivity (sun sensitivity) and in rare cases has been linked to suicidal thoughts or psychosis.

Ginkgo increases bleeding risk and, very rarely, cardiac arrhythmias. Bilberry is generally well tolerated but may cause dark stools and flatulence.

Ginger is generally safe at typical doses but can cause heartburn, nausea, and abdominal discomfort; higher doses increase side effects. Fennel may rarely cause seizures.

Feverfew can cause mouth ulcers (especially if chewed fresh) and gastrointestinal upset, and stopping it after long-term use may cause anxiety, headache, and insomnia. Motherwort and nettle are generally tolerated but may cause stomach upset.

Yellow dock acts as a laxative and contains oxalates; raw leaves can be unsafe. Gotu kola is generally well tolerated but rare cases of liver toxicity have been reported.

Alfalfa may cause flatulence and gastrointestinal discomfort.

Side effects, ingredient by ingredient Bilberry Fo-ti Ginkgo Fucus Vesiculosus Fennel Red Raspberry Feverfew German Chamomile

Meds to double-check

Major interaction found
Known Interaction Concern · database check
Major identified

At least one ingredient has a documented Major-severity interaction. Check your medications for a personalized result.

Why this rating?
  • 18 of the 18 matched ingredients can interact with medications — Alfalfa, Blessed Thistle, Motherwort, Rosemary, Bilberry, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; seizure medications; immunosuppressants / transplant drugs; diabetes medications; heart-rhythm medications; lithium.
  • For scale: 1,707 individual medications appear in the full list. A big number alone doesn't make a product dangerous — what matters is whether YOUR medication is on it, so run yours through the interaction checker on this page.

You must double-check this product against any of the following: digoxin and other heart medications; blood thinners like warfarin and other anticoagulants or antiplatelet drugs; seizure drugs (phenytoin, phenobarbital, mephenytoin); cancer drugs (irinotecan, docetaxel); HIV protease inhibitors; immunosuppressants (tacrolimus); diabetes drugs; diuretics; and drugs processed by your liver (CYP3A4, CYP2C19, CYP2D6, CYP1A2, CYP2C9, CYP2C8, or CYP2B6 substrates). The severity ranges from Major (life-threatening) to Moderate (significant).

Check your own medication Run your meds through the checker above

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.

This is a multi-herb formula with real benefits for some people—particularly for memory, anxiety, and nausea—but it demands careful screening. If you take any blood thinners, seizure drugs, heart medications, diabetes drugs, or cancer treatments, talk to your pharmacist before starting.

The St. John's Wort and fo-ti in here are serious players and warrant professional guidance.

Check your exact medications against this product using the tool on this page.

Educational only — not medical advice; always confirm with your pharmacist. Our editorial policy · How we use AI

Assessment coverage: 18 of 20 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Sep 25, 2024.

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

At a glance

General information

Key facts about Mind Full, straight from the product label.

Brand Herbally Grounded
Barcode (UPC) 718122291229
Net contents 4 Fluid Ounce(s); 118 Milliliter(s)
Market status On market
Date entered into DSLD Sep 25, 2024
DSLD ID 318537
Product type Botanical
Supplement form Liquid
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Vegetarian, Adult (18 - 50 Years), Kosher
From the label
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 Mind Full by Herbally Grounded, sourced from the NIH Dietary Supplement Label Database.

Supplement Facts

Daily Value (DV) Target Group(s):
Adults and children 4 or more years of age
Minimum serving Sizes:
2.4 mL
Maximum serving Sizes:
2.4 mL
Servings per container
49
UPC/BARCODE
718122291229
IngredientAmount% DV
Calories5 Calorie(s)--
Proprietary Blend2.4 mL--
Carbohydrates2 Gram(s)1%
Bilberry0 NP--
Fo-Ti0 NP--
Ginkgo0 NP--
Kelp0 NP--
Fennel0 NP--
Red Raspberry0 NP--
Feverfew0 NP--
Chamomile0 NP--
Rosemary0 NP--
Nettle0 NP--
Blessed Thistle0 NP--
Motherwort0 NP--
Gotu Kola0 NP--
alfalfa0 NP--
Yellow Dock0 NP--
Eleuthero Ginseng0 NP--
St. John's Wort0 NP--
Ginger0 NP--
Lettuce, Wild0 NP--
Mung Bean0 NP--

Other ingredients: Glycerin, Water, Deionized, Apple Cider Vinegar

Tap any ingredient to jump to its full detail below.

Label statements
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.
Suggested/Recommended/Usage/Directions

Recommended use: Take 3 dropperfuls one to six times per day as needed. One dropperful is one full squeeze of the dropper bulb.

Formula

Being able to focus and think clearly is a growing problem for adults and children alike. The brain is constantly multitasking and stimulated by many factors; therefore, it is important to nourish the brain with rich filled nutrients. The combination of herbs in this formula help support healthy brain functions such as memory, concentration, and clearer thought. Do not let the fog keep you down from everyday tasks and challenges.

K Parve (Kosher) K-1604

FDA Statement of Identity

Herbal Supplement

FDA Disclaimer Statement

The statements on this label have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure or prevent any disease.

Formulation

Vegetarian

Seals/Symbols

GMP Certified High Quality Products

K Parve (Kosher) K-1604

Is this label outdated? Report a formula or label change and our pharmacy team will review it.

See for yourself

Mind Full by Herbally Grounded label

The label scan from the NIH Dietary Supplement Label Database. Tap to enlarge.

Mind Full label

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)
What’s inside

The Ingredients in Mind Full by Herbally Grounded

These are the 21 active ingredients this product is made of. Select any to open its full monograph.

Serving size2.4 mL Dosage formLiquid Servings per container49 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.

Proprietary Blend

2.4 mL per serving

Carbohydrates

2 Gram(s) per serving

Other (inactive) ingredients: Glycerin, Water, Deionized, Apple Cider Vinegar. These complete the product’s ingredient list but are not active constituents.

Interaction report

Mind Full by Herbally Grounded Drug Interactions

Want to check YOUR meds against Mind Full?

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 checker
1,706Drugs
828 Major 863 Moderate 15 Minor

Ingredients driving the most interactions

Ginkgo 1,266
Fo-Ti 1,257
St. John's Wort 1,143
Eleuthero Ginseng 1,140
Ginger 1,007

Individual Drug Interactions

The ingredients in Mind Full interact with 1,706 drugs. Click any drug to see the details.

18 of the 21 ingredients in Mind Full interact with drugs. Each result below shows which ingredient is responsible. Ginkgo Fo-Ti St. John's Wort Eleuthero Ginseng Ginger Chamomile Feverfew Kelp Fennel alfalfa Gotu Kola Rosemary Bilberry Motherwort Nettle Red Raspberry Yellow Dock Blessed Thistle

Each ingredient & the kinds of drugs it affects

For each ingredient in Mind Full 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.

Ginkgo23 drug types · 1,266 drugs

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.

Likelihood Probable Evidence B
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.

Likelihood Probable Evidence B
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.

Likelihood Possible Evidence A
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence B
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.

Likelihood Probable Evidence B
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.

Likelihood Possible Evidence B
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.

Likelihood Probable Evidence B
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.

Likelihood Possible Evidence D
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).

Likelihood Possible Evidence B
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence B
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence D
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.

Likelihood Probable Evidence B
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence B
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.

Likelihood Possible Evidence B
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%.

Likelihood Possible Evidence B
Ginkgo full monograph & interactions

Fo-Ti17 drug types · 1,257 drugs

Anticoagulant/Antiplatelet Drugs

Fo-ti has been linked to cases of acute liver failure which can decrease clotting factor production and increase the effects of anticoagulants. In one case, a patient who had been stable on warfarin presented with acute hepatitis and an INR elevated to 14.98. The patient had been taking fo-ti for 90 days prior to admission. Discontinuation of warfarin and fo-ti lead to a decrease in the INR and full recovery. Theoretically, concomitant use of fo-ti with anticoagulant or antiplatelet drugs may increase the risk of bleeding in some patients. Until more is known, monitor patients taking fo-ti and drugs that affect bleeding.
Some of these drugs include aspirin, clopidogrel (Plavix), dalteparin (Fragmin), dipyridamole (Persantine), enoxaparin (Lovenox), heparin, ticlopidine (Ticlid), warfarin (Coumadin), and others.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, fo-ti might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Fo-ti reportedly has hypoglycemic effects.

Likelihood Possible Evidence D
Contraceptive Drugs

Theoretically, taking large amounts of fo-ti might interfere with contraceptive drugs due to competition for estrogen receptors.
In vitro research suggests that fo-ti extract has estrogenic activity.

Likelihood Probable Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, fo-ti might increase or decrease the levels and clinical effects of drugs metabolized by CYP1A2.
In vitro research suggests that fo-ti might inhibit CYP1A2. Additionally, in vitro research suggests that the degree of CYP1A2 inhibition depends on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, in an animal study, an aqueous extract of fo-ti inhibited CYP1A2 while an alcoholic extract of fo-ti induced CYP1A2. Induction or inhibition of CYP1A2 by fo-ti has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2B6 (Cyp2B6) Substrates

Theoretically, fo-ti might increase the levels and clinical effects of drugs metabolized by CYP2B6.
Animal research suggests that fo-ti might inhibit CYP2B6. One in vitro study suggests that the degree of CYP2B6 inhibition may depend on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C19 (Cyp2C19) Substrates

Theoretically, fo-ti may increase the levels and clinical effects of drugs metabolized by CYP2C19.
Animal and in vitro research suggests that fo-ti may inhibit CYP2C19. An in vitro study suggests that the degree of CYP2C19 inhibition may depend on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C8 (Cyp2C8) Substrates

Theoretically, fo-ti might increase the levels and clinical effects of drugs metabolized by CYP2C8.
In vitro research suggests that fo-ti might inhibit CYP2C8. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, fo-ti may increase the levels and clinical effects of drugs metabolized by CYP2C9.
Animal and in vitro research suggests that fo-ti may inhibit CYP2C9. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, fo-ti may increase the levels and clinical effects of drugs metabolized by CYP2D6.
Animal research suggests that fo-ti might inhibit CYP2D6. Additionally, an in vitro study suggests that the degree of CYP2D6 inhibition may depend on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, fo-ti might increase the levels and clinical effects of drugs metabolized by CYP3A4.
In vitro research suggests that fo-ti might inhibit CYP3A4. One in vitro study suggests that the degree of CYP3A4 inhibition may depend on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, this evidence conflicts with animal research suggesting that fo-ti does not inhibit CYP3A4. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Digoxin (Lanoxin)

Theoretically, fo-ti, particularly raw fo-ti root, might increase the risk of hypokalemia and cardiotoxicity when taken with digoxin.
Raw fo-ti root contains anthraquinone derivatives, which might have stimulant laxative effects. In vitro research shows that fermented and processed fo-ti root have reduced laxative effects compared with raw fo-ti root.

Likelihood Possible Evidence D
Diuretic Drugs

Theoretically, fo-ti, particularly raw fo-ti root, might increase the risk of hypokalemia when taken with diuretic drugs.
Raw fo-ti root contains anthraquinone derivatives, which might have stimulant laxative effects and compound diuretic-induced potassium loss. In vitro research shows that fermented and processed fo-ti root have reduced laxative effects compared with raw fo-ti root.

Likelihood Possible Evidence D
Estrogens

Theoretically, taking large amounts of fo-ti might interfere with hormone replacement therapy through competition for estrogen receptors.
In vitro research suggests that fo-ti extract has estrogenic activity.

Likelihood Probable Evidence D
Hepatotoxic Drugs

Theoretically, fo-ti might increase the risk of liver damage when taken with hepatotoxic drugs.
Fo-ti has been linked to liver damage in many reports.

Likelihood Possible Evidence D
Stimulant Laxatives

Theoretically, fo-ti, particularly raw fo-ti root, might increase the risk of fluid and electrolyte depletion when taken with stimulant laxatives.
Raw fo-ti root contains anthraquinone derivatives, which might have stimulant laxative effects. However, in vitro research shows that fermented and processed fo-ti root have reduced laxative effects compared with raw fo-ti root.

Likelihood Possible Evidence D
Sulindac (Clinoril)

Theoretically, fo-ti might increase or decrease the levels and clinical effects of sulindac.
Animal research suggests that the type of fo-ti extract might affect the levels of sulindac differently; the raw plant may increase levels, but processed parts may decrease levels. Induction or inhibition of CYP1A2 by fo-ti has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, fo-ti might increase the effects and adverse effects of warfarin.
Fo-ti may have stimulant laxative effects and cause diarrhea, especially when the raw or unprocessed fo-ti root is used. Diarrhea can increase the effects of warfarin, increase international normalized ratio (INR), and increase the risk of bleeding. Also, fo-ti has been linked to cases of acute liver failure which can decrease clotting factor production and increase the effects of warfarin. In one case, a patient who had been stable on warfarin presented with acute hepatitis and an INR elevated to 14.98. The patient had been taking fo-ti for 90 days prior to admission. Discontinuation of warfarin and fo-ti lead to a decrease in the INR and full recovery.

Likelihood Possible Evidence D
Fo-Ti full monograph & interactions

St. John's Wort47 drug types · 1,143 drugs

Alprazolam (Xanax)

St. John's wort increases the clearance of alprazolam and decreases its effects.
Alprazolam, which is used as a probe for cytochrome P450 3A4 (CYP3A4) activity, has a two-fold increase in clearance when given with St. John's wort. St. John's wort reduces the half-life of alprazolam from 12.4 hours to 6 hours.

Likelihood Likely Evidence B
Contraceptive Drugs

St. John's wort increases the clearance of contraceptive drugs and reduces their clinical effects.
Females taking St. John's wort and oral contraceptives concurrently should use an additional or alternative form of birth control. St. John's wort can decrease norethindrone and ethinyl estradiol levels by 13% to 15%, resulting in breakthrough bleeding, irregular menstrual bleeding, or unplanned pregnancy. Bleeding irregularities usually occur within a week of starting St. John's wort and regular cycles usually return when St. John's wort is discontinued. Unplanned pregnancy has occurred with concurrent use of oral contraceptives and St. John's wort extract. St. John's wort is thought to induce the cytochrome P450 1A2 (CYP1A2), 2C9 (CYP2C9), and 3A4 (CYP3A4) enzymes, which are responsible for metabolism of progestins and estrogens in contraceptives.

Likelihood Probable Evidence B
Cyclosporine (Neoral, Sandimmune)

St. John's wort reduces the levels and clinical effects of cyclosporine.
Concomitant use can decrease plasma cyclosporine levels by 30% to 70%. Using St. John's wort with cyclosporine in patients with heart, kidney, or liver transplants can cause subtherapeutic cyclosporine levels and acute transplant rejection. This interaction has occurred with a St. John's wort extract standardized to 0.3% hypericin and dosed at 300-600 mg per day. Withdrawal of St. John's wort can result in a 64% increase in cyclosporine levels. St. John's wort induces cytochrome P450 3A4 (CYP3A4) and the multi-drug transporter, P-glycoprotein/MDR-1, which increases cyclosporine clearance.

Likelihood Probable Evidence B
Cytochrome P450 3A4 (Cyp3A4) Substrates

St. John's wort increases the metabolism and reduces the levels of CYP3A4 substrates.
St. John's wort induces CYP3A4 enzymes and increases metabolism of CYP3A4 substrates. Clinically significant interactions have been reported with St. John's wort products containing hyperforin 1 mg or more.

Likelihood Probable Evidence B
Digoxin (Lanoxin)

St. John's wort reduces the levels and clinical effects of digoxin.
St. John's wort can reduce the bioavailability, serum levels, and therapeutic effects of digoxin. Taking an extract of St. John's wort 900 mg, containing hyperforin 7.5 mg or more, daily for 10-14 days, can reduce serum digoxin levels by 25% in healthy people. St. John's wort is thought to affect the multidrug transporter, P-glycoprotein, which mediates the absorption and elimination of digoxin and other drugs. St. John's wort products providing less than 7.5 mg of hyperforin daily do not appear to affect digoxin levels.

Likelihood Likely Evidence B
Docetaxel (Taxotere)

St. John's wort reduces the levels and clinical effects of docetaxel.
Clinical research shows that taking a specific St. John's wort product (Hyperiplant, VSM) 300 mg three times daily for 14 days increases docetaxel clearance by about 14%, resulting in decreased plasma concentrations of docetaxel in cancer patients. This is most likely due to induction of cytochrome P450 3A4 (CYP3A4) by St. John's wort.

Likelihood Probable Evidence B
Imatinib (Gleevec)

St. John's wort reduces the levels and clinical effects of imatinib.
Taking St. John's wort 900 mg daily for 2 weeks reduces the bioavailability and half-life of a single dose of imatinib and decreases its serum levels by 30% in healthy volunteers. This is most likely due to induction of cytochrome P450 3A4 (CYP3A4) by St. John's wort, which increases clearance of imatinib.

Likelihood Likely Evidence A
Irinotecan (Camptosar)

St. John's wort reduces the levels and clinical effects of irinotecan.
St. John's wort 900 mg daily for 18 days decreases serum levels of irinotecan by at least 50%. Clearance of the active metabolite of irinotecan, SN-38, is also increased, resulting in a 42% decrease in the area under the concentration-time curve. This is thought to be due to induction of cytochrome P450 3A4 (CYP3A4) by St. John's wort.

Likelihood Likely Evidence A
Mephenytoin (Mesantoin)

St. John's wort reduces the levels and clinical effects of mephenytoin.
Preliminary clinical research in healthy males shows that taking St. John's wort for 14 days induces cytochrome P450 2C19 (CYP2C19) and significantly increases metabolism of mephenytoin (Mesantoin). In people with wild-type 2C19, metabolism was almost 4-fold greater in subjects who received St. John's wort compared to placebo. In contrast, patients with 2C19*2/*2 and *2/*3 genotypes did not demonstrate a similar increase in metabolism.

Likelihood Likely Evidence B
Non-Nucleoside Reverse Transcriptase Inhibitors (Nnrtis)

St. John's wort decreases the levels and clinical effects of NNRTIs.
St. John's wort increases the oral clearance of nevirapine (Viramune) by 35%. Subtherapeutic concentrations are associated with therapeutic failure, development of viral resistance, and development of drug class resistance. St. John's wort induces intestinal and hepatic cytochrome P450 3A4 (CYP3A4) and intestinal P-glycoprotein/MDR-1, a drug transporter.

Likelihood Likely Evidence B
Omeprazole (Prilosec)

St. John's wort decreases the levels and clinical effects of omeprazole.
Taking St. John's wort, 300 mg orally three times daily for 14 days, reduces serum concentrations of omeprazole by inducing its metabolism via cytochrome P450 (CYP) 2C19 and 3A4. The reduction of omeprazole serum levels is dependent on CYP2C19 genotype, with reductions up to 50% in extensive metabolizers and 38% in poor metabolizers.

Likelihood Likely Evidence B
Oxycodone (Oxycontin)

St. John's wort decreases the levels and clinical effects of oxycodone.
St. John's wort can increase oxycodone metabolism by inducing cytochrome P450 3A4 (CYP3A4), reducing plasma levels and analgesic activity.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

St. John's wort decreases the levels and clinical effects of P-glycoprotein substrates.
St. John's wort induces P-glycoprotein. P-glycoprotein is a carrier mechanism responsible for transporting drugs and other substances across cell membranes. When P-glycoprotein is induced in the gastrointestinal (GI) tract, it can prevent the absorption of some medications. In addition, induction of p-glycoprotein can decrease entry of drugs into the central nervous system (CNS) and decrease access to other sites of action.

Likelihood Probable Evidence B
Phenobarbital (Luminal)

St. John's wort decreases the levels and clinical effects of phenobarbital.
St. John's wort may increase the metabolism of phenobarbital. Plasma concentrations of phenobarbital should be monitored carefully. The dose of phenobarbital may need to be increased when St. John's wort is started and decreased when it is stopped.

Likelihood Likely Evidence B
Phenprocoumon (Marcoumar, Others)

St. John's wort decreases the levels and clinical effects of phenprocoumon.
St. John's wort appears to increase the metabolism of phenprocoumon (an anticoagulant that is not available in the US) by increasing the activity of the cytochrome P450 2C9 (CYP2C9) enzyme. This may result in decreases in the anticoagulant effect and international normalized ratio (INR).

Likelihood Likely Evidence B
Phenytoin (Dilantin)

St. John's wort decreases the levels and clinical effects of phenytoin.
St. John's wort may increase the metabolism of phenytoin. Plasma concentrations of phenytoin should be monitored closely. The dose of phenytoin may need to be increased when St. John's wort is started and decreased when it is stopped.

Likelihood Likely Evidence B
Protease Inhibitors (Pis)

St. John's wort reduces the levels and clinical effects of PIs.
In healthy volunteers, St. John's wort can reduce the plasma concentrations of indinavir (Crixivan) by inducing cytochrome P450 3A4 (CYP3A4). This might result in treatment failure and viral resistance. St. John's wort also induces P-glycoprotein, which can result in decreased intracellular protease inhibitor concentrations and increased elimination.

Likelihood Likely Evidence B
Rivaroxaban (Xarelto)

St. John's wort decreases the levels and clinical effects of rivaroxaban.
A small pharmacokinetic study in healthy volunteers shows that taking a single dose of rivaroxaban 20 mg after using a specific St. John's wort extract (Jarsin, Vifor SA) 450 mg orally twice daily for 14 days reduces the bioavailability of rivaroxaban by 24% and reduces rivaroxaban's therapeutic inhibition of factor Xa by 20%.

Likelihood Probable Evidence B
Tacrolimus (Prograf)

St. John's wort decreases the levels and clinical effects of tacrolimus.
Taking a St. John's wort extract (Jarsin) 600 mg daily significantly decreases tacrolimus serum levels. Dose increases of 60% may be required to maintain therapeutic tacrolimus levels in patients taking St. John's wort. St. John's wort is thought to lower tacrolimus levels by inducing cytochrome P450 3A4 (CYP3A4) enzymes. A small clinical study in healthy adults also shows that taking St. John's wort 300 mg three times daily for 10 days decreases the total systemic exposure to tacrolimus by 27% and 33% after taking a single 5 mg dose of immediate-release or prolonged-release tacrolimus, respectively.

Likelihood Likely Evidence B
Warfarin (Coumadin)

St. John's wort decreases the levels and clinical effects of warfarin.
Taking St. John's wort significantly increases clearance of warfarin, including both its R- and S-isomers. This is likely due to induction of cytochrome P450 (CYP) 1A2 and CYP3A4. St. John's wort can also significantly decrease International Normalized Ratio (INR) in people taking warfarin. In addition, taking warfarin at the same time as St. John's wort might reduce warfarin bioavailability. When a dried extract is mixed with warfarin in an aqueous medium, up to 30% of warfarin is bound to particles, reducing its absorption.

Likelihood Likely Evidence B
Aminolevulinic Acid

St. John's wort might have additive phototoxic effects with aminolevulinic acid.
Concomitant use with St. John's wort extract may cause synergistic phototoxicity. Delta-aminolevulinic acid can cause a burning erythematous rash and severe swelling of the face, neck, and hands when taken with St. John's wort.

Likelihood Possible Evidence D
Bupropion (Wellbutrin)

St. John's wort might reduce the levels and effects of bupropion.
Clinical research shows that taking St. John's wort 325 mg three times daily for 14 days along with bupropion reduces the area under the concentration-time curve by approximately 14% and increases the clearance of bupropion by approximately 20%. This effect is attributed to the induction of cytochrome P450 2B6 (CYP2B6) by St. John's wort.

Likelihood Probable Evidence B
Clopidogrel (Plavix)

St. John's wort might increase the levels and effects of clopidogrel.
Taking St. John's wort with clopidogrel seems to increase the activity of clopidogrel. In clopidogrel non-responders, taking St. John's wort seems to induce metabolism of clopidogrel to its active metabolite by cytochrome P450 enzymes 3A4 and 2C19. This leads to increased antiplatelet activity. Theoretically, this might lead to an increased risk of bleeding in clopidogrel responders.

Likelihood Possible Evidence B
Clozapine (Clozaril)

St. John's wort might decrease the levels and clinical effects of clozapine.
A case report describes a female with schizophrenia controlled on clozapine who had a return of symptoms when she started taking St. John's wort. The plasma concentration of clozapine was reduced, likely because its clearance was increased due to induction of the cytochrome P450 enzymes 3A4, 1A2, 2C9, and 2C19 by St. John's wort.

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

St. John's wort may increase the metabolism and reduce the levels of CYP1A2 substrates.
Clinical and in vitro research shows that St. John's wort induces CYP1A2, but to a lesser extent than CYP3A4.

Likelihood Possible Evidence B
St. John's Wort full monograph & all 47 interactions

Eleuthero Ginseng10 drug types · 1,140 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, eleuthero may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro and animal research shows that a constituent of eleuthero, dihydroxybenzoic acid, appears to inhibit platelet aggregation. Concomitant use with anticoagulant or antiplatelet drugs might increase the risk of bleeding. This effect has not been reported in humans.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, eleuthero might have additive effects when used with antidiabetes drugs.
Animal research suggests that certain constituents of eleuthero have hypoglycemic activity in both healthy and diabetic animals. A small study in adults with type 2 diabetes also shows that taking eleuthero for 3 months can lower blood glucose levels. However, one very small study in healthy individuals shows that taking powdered eleuthero 3 grams, 40 minutes prior to a 75-gram oral glucose tolerance test, significantly increases postprandial blood glucose levels when compared with placebo. These contradictory findings might be due to patient-specific variability and variability in active ingredient ratios.

Likelihood Possible Evidence B
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, eleuthero might increase levels of drugs metabolized by CYP1A2.
In vitro and animal research suggest that standardized extracts of eleuthero inhibit CYP1A2. This effect has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, eleuthero might increase levels of drugs metabolized by CYP2C9.
In vitro and animal research suggest that standardized extracts of eleuthero might inhibit CYP2C9. This effect has not been reported in humans.

Likelihood Possible Evidence D
Digoxin (Lanoxin)

Eleuthero might increase serum digoxin levels and increase the risk of side effects.
In one case report, a 74-year-old male who was stabilized on digoxin presented with an elevated serum digoxin level after starting an eleuthero supplement, without symptoms of toxicity. After stopping the supplement, serum digoxin levels returned to normal. It is not clear whether this was due to a pharmacokinetic interaction or to interference with the digoxin assay. Although the product was found to be free of digoxin and digitoxin, it was not tested for other contaminants.

Likelihood Unlikely Evidence D
Immunosuppressants

Theoretically, eleuthero might interfere with immunosuppressive drugs because of its immunostimulant activity.
Animal and in vitro research shows that eleuthero extracts have immunomodulatory effects, including increasing cellular and humoral activity.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, eleuthero might increase levels of P-glycoprotein substrates.
In vitro research suggests that eleuthero can inhibit the multi-drug transporter protein, P-glycoprotein. However, it is too soon to tell if this is clinically important. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, eleuthero might increase levels of drugs metabolized by CYP2D6.
In vitro and animal research suggest that standardized extracts of eleuthero might inhibit CYP2D6. However, research in healthy human volunteers has found that taking eleuthero 485 mg twice daily for 14 days does not inhibit CYP2D6 drug metabolism.

Likelihood Unlikely Evidence B
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, eleuthero might increase levels of drugs metabolized by CYP3A4.
In vitro and animal research suggest that standardized extracts of eleuthero might inhibit CYP3A4. However, research in healthy human volunteers has found that taking eleuthero 485 mg twice daily for 14 days does not inhibit CYP3A4 drug metabolism.

Likelihood Unlikely Evidence B
Organic Anion-Transporting Polypeptide Substrates (Oatp)

Theoretically, eleuthero might decrease levels of drugs metabolized by OATP.
In vitro research suggests that eleuthero inhibits OATP2B1, which might reduce the bioavailability of oral drugs that are substrates of OATP2B1. Due to the weak inhibitory effect identified in this study, this interaction is not likely to be clinically significant.

Likelihood Possible Evidence D
Eleuthero Ginseng full monograph & interactions

Ginger14 drug types · 1,007 drugs

Anticoagulant/Antiplatelet Drugs

Ginger may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Laboratory research suggests that ginger inhibits thromboxane synthetase and decreases platelet aggregation. However, this has not been demonstrated unequivocally in humans, with mixed results from clinical trials. Theoretically, excessive amounts of ginger might increase the risk of bleeding when used with anticoagulant/antiplatelet drugs.

Likelihood Possible Evidence B
Antidiabetes Drugs

Theoretically, taking ginger with antidiabetes drugs might increase the risk of hypoglycemia.
Animal and human research suggests that ginger might increase insulin levels and/or decrease blood glucose levels.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Ginger might increase or decrease the levels of CYP3A4 substrates.
In vitro research and some case reports suggest that ginger inhibits CYP3A4 activity. Three case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are CYP3A4 substrates (imatinib, dabrafenib, and crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.
Conversely, other in vitro research suggests that ginger induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Losartan (Cozaar)

Theoretically, ginger might increase levels of losartan and the risk of hypotension.
In animal research, ginger increased the levels and hypotensive effects of a single dose of losartan. It is not clear if ginger alters the concentration or effects of losartan when taken continuously. Additionally, this interaction has not been shown in humans.

Likelihood Possible Evidence D
Nifedipine (Procardia)

Ginger may have antiplatelet effects and increase the risk of bleeding if used with nifedipine.
Clinical research shows that combined treatment with ginger 1 gram plus nifedipine 10 mg significantly inhibits platelet aggregation when compared to nifedipine or ginger alone.

Likelihood Possible Evidence B
P-Glycoprotein Substrates

Ginger might increase the absorption and blood levels of P-glycoprotein (P-gp) substrates.
In vitro research and case reports suggest that ginger inhibits drug efflux by P-gp, potentially increasing absorption and serum levels of P-gp substrates. Two case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are P-gp substrates (trametinib, crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.

Likelihood Possible Evidence D
Phenprocoumon (Marcoumar, Others)

Ginger might increase the risk of bleeding with phenprocoumon.
Phenprocoumon, a warfarin-related anticoagulant, might increase the international normalized ratio (INR) when taken with ginger. There is one case report of a 76-year-old woman with a stable INR on phenprocoumon that increased to greater than 10 when she began consuming dried ginger and ginger tea.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Ginger might increase the risk of bleeding with warfarin.
Laboratory research suggests that ginger might inhibit thromboxane synthetase and decrease platelet aggregation. In one case report, ginger increased the INR when taken with phenprocoumon, which has similar pharmacological effects as warfarin. In another case report, ginger increased the INR when taken with a combination of warfarin, hydrochlorothiazide, and acetaminophen. A longitudinal analysis suggests that taking ginger increases the risk of bleeding in patients taking warfarin for at least 4 months. However, research in healthy people suggests that ginger has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. Until more is known, monitor INRs closely in patients taking large amounts of ginger.

Likelihood Possible Evidence B
Calcium Channel Blockers

Theoretically, taking ginger with calcium channel blockers might increase the risk of hypotension.
Some animal and in vitro research suggests that ginger has hypotensive and calcium channel-blocking effects. Another animal study shows that concomitant administration of ginger and the calcium channel blocker amlodipine leads to greater reductions in blood pressure when compared with amlodipine alone.

Likelihood Unlikely Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, when taken prior to cyclosporine, ginger might decrease cyclosporine levels.
In an animal model, ginger juice taken 2 hours prior to cyclosporine administration reduced the maximum concentration and area under the curve of cyclosporine by 51% and 40%, respectively. This effect was not observed when ginger juice and cyclosporine were administered at the same time.

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, ginger might increase the levels of CYP1A2 substrates.
In vitro research shows that ginger inhibits CYP1A2 activity. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2B6 (Cyp2B6) Substrates

Theoretically, ginger might increase the levels of CYP2B6 substrates.
In vitro research shows that ginger inhibits CYP2B6 activity. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, ginger might increase the levels of CYP2C9 substrates.
In vitro research shows that ginger inhibits CYP2C9 activity. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Metronidazole (Flagyl)

Theoretically, ginger might increase levels of metronidazole.
In an animal model, ginger increased the absorption and plasma half-life of metronidazole. In addition, the elimination rate and clearance of metronidazole was significantly reduced.

Likelihood Possible Evidence D
Ginger full monograph & interactions

Chamomile9 drug types · 960 drugs

Cns Depressants

Theoretically, German chamomile might have additive effects when used with CNS depressants.
German chamomile has mild sedative effects. Theoretically, concomitant use with drugs with sedative properties can cause additive effects and side effects.

Likelihood Possible Evidence D
Contraceptive Drugs

Theoretically, large amounts of German chamomile might reduce the effectiveness of oral contraceptives.
In vitro, German chamomile has demonstrated antiestrogenic activity. Theoretically, concomitant use of large amounts of German chamomile might interfere with contraceptive drugs through competition for estrogen receptors.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, German chamomile might inhibit CYP2C9 and increase levels of drugs metabolized by these enzymes.
In vitro evidence shows that German chamomile might inhibit CYP2C9. So far, this interaction has not been reported in humans. However, there might be an increase in the levels of drugs metabolized by CYP2C9 in patients taking German chamomile.

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, German chamomile might inhibit CYP2D6 and increase levels of drugs metabolized by these enzymes.
In vitro evidence shows that German chamomile might inhibit CYP2D6. So far, this interaction has not been reported in humans. However, there might be an increase in the levels of drugs metabolized by CYP2D6 in patients taking German chamomile.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, German chamomile might inhibit CYP3A4 and increase levels of drugs metabolized by these enzymes.
In vitro evidence shows that German chamomile might inhibit CYP3A4. So far, this interaction has not been reported in humans. However, there might be an increase in the levels of drugs metabolized by CYP3A4 in patients taking German chamomile.

Likelihood Possible Evidence D
Estrogens

Theoretically, large amounts of German chamomile might reduce the effectiveness of estrogens.
In vitro, German chamomile has demonstrated antiestrogenic activity. Theoretically, large amounts of German chamomile might interfere with hormone replacement therapy through competition for estrogen receptors.

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

Theoretically, large amounts of German chamomile might interfere with the activity of tamoxifen.
In vitro, German chamomile has demonstrated antiestrogenic activity.

Likelihood Possible Evidence D
Warfarin (Coumadin)

German chamomile might increase the effects of warfarin and increase the risk of bleeding.
In one case, a 70-year-old female taking warfarin developed retroperitoneal hematoma and bilateral recti muscle bleeding along with an INR of 7.9 following ingestion of German chamomile tea 4-5 cups daily and use of a topical chamomile-based lotion applied 4-5 times daily.

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, German chamomile might inhibit CYP1A2 and increase levels of drugs metabolized by these enzymes.
In vitro and animal research shows that German chamomile might inhibit CYP1A2. So far, this interaction has not been reported in humans. However, there might be an increase in the levels of drugs metabolized by CYP1A2 in patients taking German chamomile.

Likelihood Possible Evidence D
Chamomile full monograph & interactions

Feverfew7 drug types · 929 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, feverfew might have additive effects and increase the risk of bleeding when used with anticoagulant or antiplatelet drugs.
Laboratory research suggests that feverfew may inhibit platelet aggregation. Additionally, in one case report, a 36-year-old patient taking feverfew 2400 mg daily for 3 months experienced vaginal bleeding and a prolonged menstrual cycle, with a modest increase in partial thromboplastin time (PTT) and prothrombin time (PT).

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, feverfew might increase levels of drugs metabolized by CYP1A2.
Laboratory research shows that feverfew might inhibit CYP1A2. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C19 (Cyp2C19) Substrates

Theoretically, feverfew might increase levels of drugs metabolized by CYP2C19.
Laboratory research shows that feverfew might inhibit CYP2C19. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C8 (Cyp2C8) Substrates

Theoretically, feverfew might increase levels of drugs metabolized by CYP2C8.
Laboratory research shows that feverfew might inhibit CYP2C8. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, feverfew might increase levels of drugs metabolized by CYP2C9.
Laboratory research shows that feverfew might inhibit CYP2C9. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, feverfew might increase levels of drugs metabolized by CYP2D6.
Laboratory research shows that feverfew might inhibit CYP2D6. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, feverfew might increase levels of drugs metabolized by CYP3A4.
Laboratory research shows that feverfew might inhibit CYP3A4. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Feverfew full monograph & interactions

Kelp9 drug types · 891 drugs

Amiodarone (Cordarone)

Theoretically, combining Fucus vesiculosus with amiodarone might cause excessively high iodine levels.
Fucus vesiculosus contains high concentrations of iodine. Amiodarone contains 37.3% iodine and can increase iodine levels. Concomitant use might increase the risk of having excessive iodine levels and adversely affecting thyroid function. Monitor thyroid function.

Likelihood Probable Evidence D
Antithyroid Drugs

Due to its iodine content, Fucus vesiculosus might alter the effects of antithyroid drugs.
Fucus vesiculosus contains high concentrations of iodine. Iodine in high doses has been reported to cause both hyperthyroidism and hypothyroidism, depending on the individual's past medical history. Taking Fucus vesiculosus while using antithyroid drugs could alter the effects of the antithyroid drugs.

Likelihood Possible Evidence D
Lithium

Concomitant use of Fucus vesiculosus and lithium has resulted in hyperthyroidism.
There is a case of hyperthyroidism occurring in a patient taking Fucus vesiculosus and lithium. Monitor thyroid hormones closely in patients taking lithium and Fucus vesiculosus concomitantly.

Likelihood Possible Evidence D
Thyroid Hormone

Due to its iodine content, Fucus vesiculosus might alter the effects of thyroid hormone.
Fucus vesiculosus contains high concentrations of iodine. Iodine in high doses has been reported to cause both hyperthyroidism and hypothyroidism, depending on the individual's past medical history. Taking Fucus vesiculosus while using thyroid hormone could alter the effects of thyroid hormone.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, taking Fucus vesiculosus with antiplatelet or anticoagulant drugs might increase the risk of bruising and bleeding.
In vitro evidence suggests that a constituent of Fucus vesiculosus, known as fucoidan, has anticoagulant effects. However, in clinical research, fucoidan does not seem to have significant anticoagulant activity when taken orally, possibly due to poor absorption.

Likelihood Unlikely Evidence D
Cytochrome P450 2C8 (Cyp2C8) Substrates

Theoretically, concomitant use of Fucus vesiculosus with CYP2C8 substrates might increase the risk for adverse effects.
In vitro research shows that fucoidan, a constituent of Fucus vesiculosus, inhibits CYP2C8. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, concomitant use of Fucus vesiculosus with CYP2C9 substrates might increase the risk for adverse effects.
In vitro research shows that fucoidan, a constituent of Fucus vesiculosus, inhibits CYP2C9. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, concomitant use of Fucus vesiculosus with CYP2D6 substrates might alter the effects of these substrates.
In vitro research shows that fucoidan, a constituent of Fucus vesiculosus, both inhibits and induces CYP2D6. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, concomitant use of Fucus vesiculosus with CYP3A4 substrates might increase the risk for adverse effects.
In vitro research shows that fucoidan, a constituent of Fucus vesiculosus, inhibits CYP3A4. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Kelp full monograph & interactions

Fennel6 drug types · 740 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, fennel might increase the risk of bleeding when used with antiplatelet or anticoagulant drugs.

Animal research suggests that fennel oil has antithrombotic and antiplatelet effects.

Likelihood Possible Evidence D
Ciprofloxacin (Cipro)

Theoretically, fennel might decrease the levels and clinical effects of ciprofloxacin.

Animal research shows that fennel reduces ciprofloxacin bioavailability by nearly 50%, possibly due to the metal cations such as calcium, iron, and magnesium contained in fennel. This study also found that fennel increased tissue distribution and slowed elimination of ciprofloxacin.

Likelihood Probable Evidence D
Contraceptive Drugs

Theoretically, taking large amounts of fennel might decrease the effects of contraceptive drugs due to competition for estrogen receptors.

Some constituents of fennel have estrogenic activity.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, fennel might increase levels of drugs metabolized by CYP3A4.

In vitro research suggests that fennel inhibits CYP3A4 enzyme activity. This effect has not been reported in humans.

Likelihood Possible Evidence D
Estrogens

Theoretically, taking large amounts of fennel might interfere with hormone replacement therapy due to competition for estrogen receptors.

Some constituents of fennel have estrogenic activity.

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

Theoretically, taking large amounts of fennel might decrease the antiestrogenic effect of tamoxifen.

Some constituents of fennel have estrogenic activity, which may interfere with the antiestrogenic activity of tamoxifen.

Likelihood Possible Evidence D
Fennel full monograph & interactions

alfalfa6 drug types · 583 drugs

Warfarin (Coumadin)

Theoretically, alfalfa might reduce the anticoagulant activity of warfarin.
Alfalfa contains a large amount of vitamin K. This could theoretically interfere with the activity of warfarin.

Likelihood Probable Evidence D
Antidiabetes Drugs

Theoretically, alfalfa might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research suggests that alfalfa decreases blood sugar in diabetic mice. Also, in one case report, a diabetic patient experienced hypoglycemia after consuming alfalfa extract. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Contraceptive Drugs

Theoretically, alfalfa might interfere with the activity of contraceptive drugs.
Alfalfa contains coumestrol, a phytoestrogen, and isoflavonoids, which have estrogenic effects.

Likelihood Possible Evidence D
Estrogens

Theoretically, alfalfa might interfere with hormone therapy.
Alfalfa contains coumestrol, a phytoestrogen, and isoflavonoids, which have estrogenic effects.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, alfalfa might decrease the efficacy of immunosuppressive therapy.
In vitro research and human case reports suggest that alfalfa may have immunostimulant effects.

Likelihood Possible Evidence D
Photosensitizing Drugs

Theoretically, concomitant use of alfalfa with photosensitizing drugs might have additive effects.
Animal research suggests that excessive doses of alfalfa may increase photosensitivity, possibly due to its chlorophyll content. It is unclear if this effect would be clinically relevant in humans.

Likelihood Possible Evidence D
alfalfa full monograph & interactions

Gotu Kola2 drug types · 579 drugs

Cns Depressants

Theoretically, taking gotu kola might increase the sedative effects of CNS depressants.
In vitro research suggests that gotu kola may have sedative effects via binding of GABA receptors.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, taking gotu kola with hepatotoxic drugs might have additive adverse effects.
There are at least four case reports of hepatotoxicity associated with the use of gotu kola. However, more information is needed to determine if gotu kola was the causative factor in these cases.

Likelihood Possible Evidence D
Gotu Kola full monograph & interactions

Rosemary6 drug types · 372 drugs

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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence B
Aspirin

Theoretically, rosemary might have additive effects with salicylate-containing drugs such as aspirin.
Rosemary is reported to contain salicylates.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence D
Salsalate (Disalcid)

Theoretically, rosemary might have additive effects with salicylate-containing drugs such as salsalate.
Rosemary is reported to contain salicylate.

Likelihood Possible Evidence D
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.

Likelihood Unlikely Evidence D
Rosemary full monograph & interactions

Bilberry4 drug types · 275 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, bilberry fruit extract might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
In vitro, animal, and clinical research suggest that anthocyanidin extracts from bilberry can inhibit platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, bilberry leaf or fruit extract may increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research suggests that bilberry leaf extract might have blood glucose-lowering activity. Also, one small clinical trial in patients with type 2 diabetes shows that taking bilberry fruit extract 470 mg as a single dose prior to an oral glucose tolerance test lowers plasma glucose levels when compared with placebo.

Likelihood Possible Evidence D
Cytochrome P450 2E1 (Cyp2E1) Substrates

Theoretically, bilberry fruit extract might decrease levels of drugs metabolized by CYP2E1.
Animal research shows that exposure to small concentrations of bilberry extract in drinking water for around one month increased CYP2E1 activity by 31%. However, exposure over a 2-month period did not increase CYP2E1 activity. This effect has not been reported in humans.

Likelihood Possible Evidence D
Erlotinib (Tarceva)

Theoretically, bilberry fruit extract might reduce the efficacy of erlotinib.
In vitro research suggests that bilberry fruit extract and its constituents, delphinidin and delphinidin-3-O-glucoside, inhibit the activity of erlotinib. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Bilberry full monograph & interactions

Motherwort1 drug type · 248 drugs

Cns Depressants

Theoretically, taking motherwort concomitantly with other CNS depressants may increase the risk of sedation.
Motherwort has been reported to cause CNS depression and sedation.

Likelihood Possible Evidence D
Motherwort full monograph & interactions

Nettle4 drug types · 164 drugs

Antidiabetes Drugs

Theoretically, stinging nettle might have additive effects with antidiabetes drugs.
Clinical research shows that stinging nettle might decrease blood glucose levels in patients with diabetes.

Likelihood Possible Evidence B
Diuretic Drugs

Theoretically, combining stinging nettle with diuretic drugs may have additive effects.
Animal research suggests that the above ground parts and roots of stinging nettle may have a diuretic effect.

Likelihood Possible Evidence D
Lithium

Theoretically, stinging nettle might reduce excretion and increase levels of lithium.
Animal research suggests that stinging nettle has diuretic and natriuretic properties, which could alter the excretion of lithium. The dose of lithium might need to be decreased.

Likelihood Possible Evidence D
Warfarin (Coumadin)

There is some concern that stinging nettle might decrease the effects of anticoagulant drugs such as warfarin.
Stinging nettle contains a significant amount of vitamin K. When taken in large quantities, this might interfere with the activity of warfarin.

Likelihood Possible Evidence D
Nettle full monograph & interactions

Red Raspberry2 drug types · 135 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, taking red raspberry leaf with anticoagulant/antiplatelet drugs might increase the risk of bleeding.
In vitro research suggests that red raspberry leaf extract has antiplatelet activity and enhances the in vitro effects of the antiplatelet medication cangrelor. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Insulin

Red raspberry leaf might reduce glucose levels in patients being treated with insulin.
In one case report, a 38-year-old patient with gestational diabetes, whose blood glucose was being controlled with medical nutrition therapy and insulin, developed hypoglycemia after consuming two servings of raspberry leaf tea daily for 3 days beginning at 32 weeks' gestation. The patient required an insulin dose reduction. The hypoglycemia was considered to be probably related to use of red raspberry leaf tea.

Likelihood Possible Evidence D
Red Raspberry full monograph & interactions

Yellow Dock3 drug types · 78 drugs

Digoxin (Lanoxin)

Theoretically, yellow dock might increase the risk of digoxin toxicity when used long-term or in large amount.
When yellow dock is used chronically or in large amounts, hypokalemia may occur. This might increase the toxic effects of digoxin.

Likelihood Probable Evidence D
Diuretic Drugs

Theoretically, yellow dock might increase the risk of hypokalemia when taken with diuretics.
When yellow dock is used chronically or in large amounts, hypokalemia may occur, and overuse of yellow dock might compound diuretic-induced potassium loss.

Likelihood Probable Evidence D
Warfarin (Coumadin)

Theoretically, the laxative effects of yellow dock might increase the effects of warfarin, including the risk of bleeding.
The anthraquinones in yellow dock have a mild stimulant laxative effect. Consuming excessive amounts can cause diarrhea. Diarrhea can increase the effects of warfarin, increase international normalized ratio (INR), and increase the risk of bleeding.

Likelihood Possible Evidence D
Yellow Dock full monograph & interactions

Blessed Thistle3 drug types · 36 drugs

Antacids

Theoretically, blessed thistle might decrease the effectiveness of antacids.
There are reports that blessed thistle increases stomach acid.

Likelihood Possible Evidence D
H2-Blockers

Theoretically, blessed thistle might decrease the effectiveness of H2-blockers.
There are reports that blessed thistle increases stomach acid.

Likelihood Possible Evidence D
Proton Pump Inhibitors (Ppis)

Theoretically, blessed thistle might decrease the effectiveness of PPIs.
There are reports that blessed thistle increases stomach acid.

Likelihood Possible Evidence D
Blessed Thistle full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Mind Full, from the product label.

Herbally Grounded

See all Herbally Grounded products
Name
Herbally Grounded
City
Las Vegas
State
NV
ZipCode
89102
Phone Number
1.866.676.1410
Web Address
www.herballygrounded.com
Pharmacist Counseling Corner

Mind Full by Herbally Grounded: Common Questions

Does Mind Full by Herbally Grounded interact with any medications?
Yes. Based on its ingredients, Mind Full has a known interaction with 1,706 medications, including 828 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Mind Full contains 21 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.
Is it safe to take Mind Full while pregnant?
Several ingredients—including fo-ti, ginkgo, fennel, feverfew, motherwort, nettle, and alfalfa—lack enough safety data or have traditionally been avoided in pregnancy. St. John's Wort is best avoided due to insufficient data. Only red raspberry and ginger have any pregnancy-use history, but even ginger should be used moderately and discussed with your doctor first. Talk to your pharmacist or doctor before using this product in pregnancy.
Can I take this if I'm breastfeeding?
Safety while breastfeeding is not well established for most ingredients in this formula. St. John's Wort may pass into breast milk and affect infants. Fo-ti, ginkgo, feverfew, motherwort, and nettle lack reliable breastfeeding safety data. Yellow dock's laxative compounds may pass into milk. Check with your doctor or pharmacist before using this product while nursing.
Will this actually help my memory and focus?
Ginkgo in the formula is possibly effective for dementia and cognitive conditions, and rosemary is possibly effective for memory—though the evidence isn't strong. Most other ingredients lack reliable evidence for brain or cognitive benefits. The product contains St. John's Wort, which is likely effective for depression but is a separate concern from focus or memory support.
What are the most common side effects?
Gastrointestinal symptoms—nausea, diarrhea, heartburn, flatulence, and abdominal discomfort—are the most frequently reported across these ingredients. Ginkgo and ginger can cause dizziness. St. John's Wort may cause photodermatitis (sun sensitivity). Dark-colored stools can occur with bilberry. Feverfew chewed fresh can cause mouth ulcers. Most effects are mild, but higher doses increase the risk.
Why does fo-ti worry you?
Fo-ti has been linked to around 450 documented cases of hepatitis (liver inflammation) in medical literature. Liver damage has occurred across a range of doses, formulations, and durations—with outcomes ranging from full recovery to cirrhosis and liver failure. It's also been linked to a case where it dangerously boosted warfarin effects. The safety profile is not well established.
What if I'm on St. John's Wort already and want to add this?
This product already contains St. John's Wort, so you'd be doubling your dose, which increases all the risks. Do not combine this with a separate St. John's Wort supplement. If you're currently taking St. John's Wort for depression, talk to your doctor or pharmacist before switching to this product—they can advise on a safe transition.

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.

Mind Full label
Go deeper

The Full Monographs Behind Mind Full’s Ingredients

Every ingredient we hold a full HelloPharmacist monograph for — uses, evidence, safety, and the complete interaction list.

Herb & supplement monograph

Bilberry

Interacts with 275 drugs

Bilberry is a blueberry-like fruit rich in antioxidant plant compounds called anthocyanins, and it has a long history of traditional use for eye health, circulation, and mild diarrhea. While...

Read the full Bilberry monograph → Herb & supplement monograph

Fo-ti

Interacts with 1,257 drugs

Fo-ti (He Shou Wu) is a root used in traditional Chinese medicine, often promoted for healthy aging and hair. High-quality human evidence for these benefits is limited, and processed Fo-ti h...

Read the full Fo-ti monograph → Herb & supplement monograph

Ginkgo

Interacts with 1,266 drugs

Ginkgo 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 monograph

Fucus Vesiculosus

Interacts with 891 drugs

Fucus vesiculosus (bladderwrack) is a brown seaweed rich in iodine that has been used traditionally for thyroid concerns, weight, and skin. There is little solid human evidence to support mo...

Read the full Fucus Vesiculosus monograph → Herb & supplement monograph

Fennel

Interacts with 740 drugs

Fennel is a Mediterranean herb widely used as a food and spice, and traditionally taken for digestive complaints, colic, and menstrual cramps. Some small studies suggest possible benefit for...

Read the full Fennel monograph → Herb & supplement monograph

Red Raspberry

Interacts with 135 drugs

Red raspberry leaf is a traditional herbal remedy most often used as a tea in late pregnancy and for menstrual discomfort, but solid scientific evidence for these uses is limited. It is gene...

Read the full Red Raspberry monograph → Herb & supplement monograph

Feverfew

Interacts with 929 drugs

Feverfew is a daisy-family herb best known for migraine prevention, where some studies suggest it may modestly lower how often migraines occur, though the evidence is mixed. It is generally...

Read the full Feverfew monograph → Herb & supplement monograph

German Chamomile

Interacts with 960 drugs

German chamomile is a widely used herbal remedy taken mainly as a tea for calming, sleep, and digestive complaints. Early research suggests possible benefits for mild anxiety and some skin o...

Read the full German Chamomile monograph → Herb & supplement monograph

Rosemary

Interacts with 372 drugs

Rosemary 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 monograph

Stinging Nettle

Interacts with 164 drugs

Stinging nettle is a common plant used as food and in traditional medicine, most often for prostate symptoms, allergies, and joint pain. The evidence is mixed and mostly preliminary, so it i...

Read the full Stinging Nettle monograph → Herb & supplement monograph

Blessed Thistle

Interacts with 36 drugs

Blessed thistle is a bitter herb traditionally used to stimulate appetite and ease mild digestive complaints. High-quality human studies are lacking, so its benefits are not well proven. It...

Read the full Blessed Thistle monograph → Herb & supplement monograph

Motherwort

Interacts with 248 drugs

Motherwort is a traditional herb in the mint family long used for anxiety, heart palpitations, and women's reproductive complaints, but solid human evidence is very limited. It should be avo...

Read the full Motherwort monograph → Herb & supplement monograph

Gotu Kola

Interacts with 579 drugs

Gotu kola is a traditional Ayurvedic and Asian herb that people use for wound healing, circulation, skin problems, and as a calming or memory-supporting herb. Some early studies suggest poss...

Read the full Gotu Kola monograph → Herb & supplement monograph

Alfalfa

Interacts with 583 drugs

Alfalfa is a nutrient-rich legume that people use for high cholesterol, menopause symptoms, and general wellness, but solid human evidence for most of these uses is limited. It is best avoid...

Read the full Alfalfa monograph → Herb & supplement monograph

Yellow Dock

Interacts with 78 drugs

Yellow dock is a traditional herb used mostly as a mild laxative and a digestive and skin tonic. Good-quality human studies are lacking, so its benefits are largely unproven, and its natural...

Read the full Yellow Dock monograph → Herb & supplement monograph

Eleuthero

Interacts with 1,140 drugs

Eleuthero is an herb traditionally used as an 'adaptogen' to fight fatigue, boost energy, and help the body handle stress. The scientific evidence behind these uses is limited and mixed, so...

Read the full Eleuthero monograph → Herb & supplement monograph

St. John's Wort

Interacts with 1,143 drugs

St. John's wort is a well-studied herb most often used for mild to moderate depression, and some research suggests it may help with this. However, it has many serious interactions with presc...

Read the full St. John's Wort monograph → Herb & supplement monograph

Ginger

Interacts with 1,007 drugs

Ginger is a widely used culinary spice with a long history in traditional medicine, and it has the strongest evidence for helping with nausea and vomiting, including from motion sickness, pr...

Read the full Ginger monograph →
Sources

Sources & How We Checked

Mind Full'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.

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 561 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.

Bilberry 14 references
  1. Cignarella A, Nastasi M, Cavalli E, Puglisi L. Novel lipid-lowering properties of Vaccinium myrtillus L. leaves, a traditional antidiabetic treatment, in several models of rat dyslipidaemia: a comparison with ciprofibrate. Thromb Res 1996;84:311-22. PubMed
  2. Morazzoni P, Magistretti MJ. Activity of Myrtocyan, an anthosyanoside complex from Vaccinium myrtillus (VMA), on platelet aggregation and adhesiveness. Fitoterapia 1990;61:13-21.
  3. Erlund, I., Koli, R., Alfthan, G., Marniemi, J., Puukka, P., Mustonen, P., Mattila, P., and Jula, A. Favorable effects of berry consumption on platelet function, blood pressure, and HDL cholesterol. Am J Clin Nutr 2008;87(2):323-331. PubMed
  4. Hawrelak, J. A. and Myers, S. P. Effects of two natural medicine formulations on irritable bowel syndrome symptoms: a pilot study. J Altern Complement Med 2010;16(10):1065-1071. PubMed
  5. Morazzoni P and Magistretti MJ. Effects of Vaccinium myrtillus anthocyanosides on prostacyclin-like activity in rat arterial issue. Fitoterapia 1986;57:11-14.
  6. Pulliero G, Montin S, Bettini V, and et al. Ex vivo study of the inhibitory effects of Vaccinium myrtillus anthocyanosides on human platelet aggregation. Fitoterapia 1989;60:69-75.
  7. Bottecchia D. Preliminary report on the inhibitory effect of vaccinium myrtillus anthocyanosides on platelet aggregation and clot retraction. Fitoterapia 1987;48:3-8.
  8. Fdez, M., Zaragoza, F., and Alvarez, P. In vitro platelet aggregation effects of anthocyanosides of vaccinium myrtilus L. Anales de la Real Academia de Farmacia 1983;49:79-90.
  9. Biedermann L, Mwinyi J, Scharl M, Frei P, Zeitz J, Kullak-Ublick GA, et al. Bilberry ingestion improves disease activity in mild to moderate ulcerative colitis-an open pilot study. 2013 May;7(4):271-9. PubMed
  10. Hoggard N, Cruickshank M, Moar KM, Bestwick C, Holst J, Russell W, et al. A single supplement of a standardized bilberry (Vaccinium myrtillus L.) extract (36% wet weight anthocyanins) modifies glycaemic response in individuals with type 2 diabetes control
  11. Aichinger G, Pahlke G, Nagel LJ, Berger W, Marko D. Bilberry extract, its major phenolic compounds, and soy isoflavone genistein antagonize the cytostatic drug erlotinib in human epithelial cells. Food Funct 2016;7(8):3628-36.
  12. Prokop J, Ln&ecaron;ni&ccaron;kov&aacute; K, Cibicek N, et al. Effect of bilberry extract (Vaccinium myrtillus L.) on drug-metabolizing enzymes in rats. Food Chem Toxicol 2019;129:382-90. PubMed
  13. Chan SW, Chu TTW, Choi SW, Benzie IFF, Tomlinson B. Impact of short-term bilberry supplementation on glycemic control, cardiovascular disease risk factors, and antioxidant status in Chinese patients with type 2 diabetes. Phytother Res 2021. Online ahead o PubMed
  14. Bøhn SK, Myhrstad MCW, Thoresen M, et al. Bilberry/red grape juice decreases plasma biomarkers of inflammation and tissue damage in aged men with subjective memory impairment -a randomized clinical trial. BMC Nutr 2021;7(1):75. PubMed

See these in context on the Bilberry monograph →

Fo-ti 28 references
  1. 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.
  2. McGuffin M, Hobbs C, Upton R, Goldberg A, eds. American Herbal Products Association's Botanical Safety Handbook. Boca Raton, FL: CRC Press, LLC 1997.
  3. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  4. Covington TR, et al. Handbook of Nonprescription Drugs. 11th ed. Washington, DC: American Pharmaceutical Association, 1996.
  5. Park GJ, Mann SP, Ngu MC. Acute hepatitis induced by Shou-Wu-Pian, a herbal product derived from Polygonum multiflorum. J Gastroenterol Hepatol 2001;16:115-7.
  6. But PP, Tomlinson B, Lee KL. Hepatitis related to the Chinese medicine Shou-wu-pian manufactured from Polygonum multiflorum. Vet Hum Toxicol 1996;38:280-2.
  7. Oerter Klein KO, Janfaza M, Wong JA, Chang RJ. Estrogen bioactivity in Fo-Ti and other herbs used for their estrogen-like effects as determined by a recombinant cell bioassay. J Clin Endocrinol Metab 2003;88:4077-9.. PubMed
  8. Unger M, Frank A. Simultaneous determination of the inhibitory potency of herbal extracts on the activity of six major cytochrome P450 enzymes using liquid chromatography/mass spectrometry and automated online extraction. Rapid Commun Mass Spectrom 2004;1 PubMed
  9. UK Medicines and Healthcare Products Regulatory Agency. Polygonum multiflorum and liver reactions. April 2006. Available at: www.mhra.gov.uk/home/idcplg?IdcService= SS_GET_PAGE&useSecondary=true&ssDocName= CON2023590&ssTargetNodeId= 833 (Accessed 10 May 2
  10. Panis B, Wong DR, Hooymans PM, De Smet PA, Rosias PP. Recurrent toxic hepatitis in a Caucasian girl related to the use of Shou-Wu-Pian, a Chinese herbal preparation. J Pediatr Gastroenterol Nutr 2005;41:256-8. PubMed
  11. Mazzanti G, Battinelli L, Daniele C, et al. New case of acute hepatitis following the consumption of Shou Wu Pian, a Chinese herbal product derived from Polygonum multiflorum. Ann Intern Med 2004;140:E589-90.
  12. Cardenas A, Restrepo JC, Sierra F, Correa G. Acute hepatitis due to shen-min: a herbal product derived from Polygonum multiflorum. J Clin Gastroenterol 2006;40:629-32. PubMed
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Red Raspberry 8 references
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Feverfew 18 references
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German Chamomile 15 references
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Rosemary 20 references
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Stinging Nettle 23 references
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Blessed Thistle 2 references
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Motherwort 6 references
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Gotu Kola 18 references
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Alfalfa 32 references
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DISCLAIMER: Currently this does not check for drug-drug interactions. This is not an all-inclusive comprehensive list of potential interactions and is for informational purposes only. Not all interactions are known or well-reported in the scientific literature, and new interactions are continually being reported. Input is needed from a qualified healthcare provider including a pharmacist before starting any therapy. Application of clinical judgment is necessary.

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