Major interaction on record — check this product against your medications before combining. Based on 14 of 16 ingredients. Check your meds →
Dietary supplement

Elite Performance + Recovery Ingredients & Drug Interactions

by New Chapter

Elite Performance + Recovery label
See full label image
Capsule Category: Other Combinations
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 Elite Performance + Recovery 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

Elite Performance + Recovery is a dietary supplement by New Chapter with 16 active ingredients. Its ingredients are commonly taken for antioxidant support, skin health and aging, eye health.Based on those ingredients, 1,613 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are organic Green Tea (Camellia sinensis) (leaf) aqueous extract, Rhodiola (Rhodiola rosea) (root) hydroethanolic extract, organic Turmeric. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

Jump to a section

Check Your Meds Against Elite Performance + Recovery by New Chapter

Ask about any prescription or over-the-counter medication and we check it for interactions with Elite Performance + Recovery by New Chapter — and tell you which ingredient is responsible.

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HelloPharmacist Scorecard of Elite Performance + Recovery by New Chapter

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 5 of its 17 active ingredients.
  • “organic Haematococcus pluvialis” is listed as a grouped ingredient — the label gives one combined amount (60 mg) without saying how much of each component you get.
  • “Ginger” is listed as a grouped ingredient — the label gives one combined amount (120 mg) without saying how much of each component you get.
  • “Super Boosting Blend” is a proprietary blend — the label gives one combined amount (245 mg) without saying how much of each component you get.

Elite Performance + Recovery contains 17 active ingredients chosen for athletic support and overall wellness. The blend includes adaptogenic herbs like rhodiola and cordyceps, which may help with stamina and recovery; antioxidants from astaxanthin (a carotenoid pigment from algae), grape seed, green tea, and turmeric; anti-inflammatory botanicals like ginger and black seed; and nutrient-dense whole foods such as kale and broccoli.

The formula also features schisandra, maca, rosemary, and cardamom — traditional ingredients used to support energy and resilience. Inactive ingredients include olive oil, beeswax, and brown rice ferment media as delivery and stabilizing components.

Does it work?

Leans against
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
Leans against

The strongest graded evidence we hold for the stated purpose leans against a benefit.

Why this rating?
  • The label markets this product for: Athletic performance and recovery support.
  • We looked for evidence on: Athletic performance, Chronic fatigue syndrome (CFS), Exercise endurance, Muscle recovery, Stamina.
  • The closest evidence on file: Cordyceps is rated "Possibly Ineffective" for Athletic performance (Natural Medicines).
  • Also on file: Rosemary is rated "Insufficient Reliable Evidence To Rate" for Fatigue.
  • Also on file: Schisandra is rated "Insufficient Reliable Evidence To Rate" for Athletic performance.

The evidence for most ingredients in this formula is limited or mixed. Ginger shows promise for pregnancy-related nausea, period pain (dysmenorrhea), and osteoarthritis, though the evidence is rated possibly effective rather than conclusive.

Turmeric is possibly effective for depression, high cholesterol, hay fever, and indigestion. Green tea is likely effective for human papillomavirus (HPV) and possibly effective for high cholesterol.

Broccoli is possibly effective for colorectal cancer prevention. Rosemary may help with memory, and grape seed extract is possibly effective for chronic venous insufficiency.

For most other uses — athletic performance, age-related cognitive decline, sexual function, and many others — the evidence we hold is insufficient to make a reliable rating. The product is marketed for 'performance and recovery,' but the data doesn't firmly establish it for that specific purpose.

The evidence, ingredient by ingredient Astaxanthin Ginger Turmeric Grape Cordyceps Maca Rhodiola Schisandra

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 13 of the 14 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 14 of 14.
  • General safety write-ups exist for 14 of 14.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Most ingredients in this formula are generally well tolerated at typical doses. Ginger, cordyceps, maca, and black seed are all commonly consumed as foods or supplements with mild side-effect profiles — though ginger at higher doses (5+ grams daily) can cause stomach upset, heartburn, or loose stools, and cordyceps may rarely cause abdominal discomfort or diarrhea.

Turmeric is generally safe as a spice but concentrated supplements have been rarely linked to liver injury after extended use. Green tea extract in high doses has also been associated with very rare liver problems.

Astaxanthin seems well tolerated but long-term safety data are limited. For pregnancy: astaxanthin, cordyceps, maca, rhodiola, and schisandra should be avoided — there isn't enough safety data to know either way.

Ginger and black seed have some traditional use in pregnancy but warrant a doctor's approval and moderate amounts only. Broccoli, kale, rosemary, and cardamom as foods are considered safe in pregnancy.

For breastfeeding, most ingredients lack sufficient data; ginger in food amounts is likely fine, kale and broccoli are safe, but concentrated supplements should be discussed with your healthcare provider.

Side effects, ingredient by ingredient Astaxanthin Ginger Turmeric Grape Cordyceps Maca Rhodiola Schisandra

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?
  • 11 of the 14 matched ingredients can interact with medications — Rosemary, Schisandra, Grape, Cordyceps, Turmeric, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; lithium.
  • For scale: 1,614 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.

Check your medications against this product if you take blood thinners or antiplatelet drugs (warfarin, aspirin, clopidogrel), statins like atorvastatin, blood pressure medications (especially nadolol, losartan, or other antihypertensives), diabetes drugs, seizure medications (phenytoin, valproate, ethosuximide, felbamate), or any immunosuppressant (cyclosporine, tacrolimus). Green tea extract is the ingredient driving the Major-severity interactions, particularly with nadolol and atorvastatin.

If you're on any of these, don't take this product without pharmacist approval.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFormula with limited ingredient disclosure with graded evidence leaning against its stated purpose. Major medication interactions have been identified, and safety information is well characterized.

This is a multi-ingredient formula best suited to generally healthy adults interested in antioxidant and adaptogenic support — though the evidence for athletic performance specifically is not well established. If you take blood thinners, statins, diabetes medications, or blood pressure meds, you'll need to check your specific drugs against the interaction tool on this page before starting.

Pregnant or breastfeeding? Talk to your pharmacist or doctor first, as several ingredients carry insufficient safety data in those situations.

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

Assessment coverage: 17 of 17 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Sep 21, 2018.

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 Elite Performance + Recovery, straight from the product label.

Brand New Chapter
Net contents 60 Vegetarian Capsule(s)
Market status On market
Date entered into DSLD Sep 21, 2018
DSLD ID 181399
Product type Other Combinations
Supplement form Capsule
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Vegetarian, Adult (18 - 50 Years), Gluten Free
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 Elite Performance + Recovery by New Chapter, 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 Capsule(s)
Maximum serving Sizes:
2 Capsule(s)
Servings per container
30
IngredientAmount% DV
Astaxanthin4 mg--
organic Ginger supercritical extract64.8 mg--
Ginger aqueous extract55.2 mg--
organic Haematococcus pluvialis60 mg--
organic Cordyceps0 NP--
Ginger120 mg--
organic Maca0 NP--
Rhodiola (Rhodiola rosea) (root) hydroethanolic extract0 NP--
organic Schizandra0 NP--
organic Cardamom0 NP--
organic Turmeric25 mg--
Grape seed (Vitis vinifera) (seed) aqueous extract300 mg--
Super Boosting Blend245 mg--
organic Kale0 NP--
organic Broccoli0 NP--
organic Nigella (Nigella sativa) (seed) supercritical extract0 NP--
organic Nigella (Nigella sativa) (seed) aqueous extract0 NP--
organic Green Tea (Camellia sinensis) (leaf) aqueous extract0 NP--
Rosemary (Rosmarinus officinalis) (leaf) hydroethanolic extract0 NP--
Rosemary (Rosmarinus officinalis) (leaf) supercritical extract0 NP--

Other ingredients: extra-virgin Olive Oil, Hypromellose, organic yellow Beeswax, Candelilla Wax, Ferment Media, organic Brown Rice

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.
General Statements

Delivering the wisdom of nature

Proven at the cellular level to: Protect cell health by boosting antioxidant production Balance healthy inflammation response to protect cells from damage Recover ATP energy to support healthy cell activity. As shown in preclinical lab testing

Please recycle this bottle after use.

Train smart with increased athletic power, endurance & muscle health

Suggested/Recommended/Usage/Directions

Suggested Use: Two capsules daily with food.

Precautions

Not recommended for use in children.

Caution: As with any dietary supplement, a healthcare professional should be contacted before use for those with a medical condition or taking regular medication. If you are nursing, pregnant, or considering pregnancy, you should consult your healthcare professional prior to using this product.

Avoid use if known sensitivity to any of the ingredients.

Discontinue use and contact a healthcare professional if you experience an allergic reaction or side effect.

Do not exceed suggested use.

Keep out of reach of children.

Contains: Fermented soy.

Formulation

Gluten free; 100% vegetarian; no artificial flavors or colors.

Gluten free; 100% vegetarian; no artificial flavors or colors.

Non GMO

Seals/Symbols

Non GMO Project Verified 100% Vegetarian NSF Certified Gluten-free

Well Shield

Informed-sport.com Trusted by sport

FDA Disclaimer Statement

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Brand IP Statement(s)

The New Chapter Money-Back Guarantee: We proudly stand behind every product we make. However, if you are not satisfied, please visit www.newchapter.com/guarantee for refund details.

2018 New Chapter, Inc.

General

6024-A03

Formula

Synergistic blend with Grape seed, Ginger & Astaxanthin

Contains: Fermented soy.

FDA Statement of Identity

Dietary Supplement

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

See for yourself

Elite Performance + Recovery by New Chapter label

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

Elite Performance + Recovery 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 Elite Performance + Recovery by New Chapter

These are the 16 active ingredients this product is made of. Select any to open its full monograph.

Serving size2 Capsule(s) Dosage formCapsule Servings per container30 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.

Organic Haematococcus pluvialis

60 mg per serving

Ginger

Interacts with
1,007 drugs
120 mg per serving

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 vomi...

Ginger monograph & interactions

Organic Turmeric

Interacts with
1,133 drugs
25 mg per serving

Turmeric is a popular spice whose main active compounds, curcuminoids, are studied mostly for inflammation and joint pain. Some research is promising,...

Organic Turmeric monograph & interactions

Grape seed (Vitis vinifera) (seed) aqueous extract

Interacts with
910 drugs
300 mg per serving

Grapes and grape products like grape seed extract contain antioxidant compounds such as resveratrol and proanthocyanidins that may support heart and b...

Grape seed (Vitis vinifera) (seed) aqueous extract monograph & interactions

Other (inactive) ingredients: Extra-virgin Olive Oil, Hypromellose, Organic yellow Beeswax, Candelilla Wax, Ferment Media, Organic Brown Rice. These complete the product’s ingredient list but are not active constituents.

Interaction report

Elite Performance + Recovery by New Chapter Drug Interactions

Want to check YOUR meds against Elite Performance + Recovery?

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
1,613Drugs
13 Major 1,589 Moderate 11 Minor

Ingredients driving the most interactions

organic Green Tea (Camellia sinensis) (leaf) aqueous extract 1,293
Rhodiola (Rhodiola rosea) (root) hydroethanolic extract 1,271
organic Turmeric 1,133
Ginger 1,007
organic Nigella (Nigella sativa) (seed) supercritical extract 912

Individual Drug Interactions

The ingredients in Elite Performance + Recovery interact with 1,613 drugs. Click any drug to see the details.

11 of the 16 ingredients in Elite Performance + Recovery interact with drugs. Each result below shows which ingredient is responsible. organic Green Tea (Camellia sinensis) (leaf) aqueous extract Rhodiola (Rhodiola rosea) (root) hydroethanolic extract organic Turmeric Ginger organic Nigella (Nigella sativa) (seed) supercritical extract Grape seed (Vitis vinifera) (seed) aqueous extract organic Schizandra Astaxanthin Rosemary (Rosmarinus officinalis) (leaf) hydroethanolic extract organic Cordyceps organic Broccoli

Each ingredient & the kinds of drugs it affects

For each ingredient in Elite Performance + Recovery 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.

organic Green Tea (Camellia sinensis) (leaf) aqueous extract58 drug types · 1,293 drugs

Atorvastatin (Lipitor)

Green tea extract seems to reduce the levels and clinical effects of atorvastatin.
In healthy humans, taking green tea extract 300 mg or 600 mg along with atorvastatin reduces plasma levels of atorvastatin by approximately 24%. The elimination of atorvastatin is not affected. Atorvastatin is a substrate of organic anion-transporting polypeptides (OATPs). Research shows that two of the major catechins found in green tea, epicatechin gallate (ECG) and epigallocatechin gallate (EGCG), inhibit OATPs. Some OATPs are expressed in the small intestine and are responsible for the uptake of drugs and other compounds, which may have resulted in reduced plasma levels of atorvastatin. It is not clear if drinking green tea alters the absorption of atorvastatin.

Likelihood Likely Evidence B
Ephedrine

Theoretically, concomitant use might increase the risk for stimulant adverse effects.
Green tea contains caffeine. There is evidence that using ephedrine with caffeine might increase the risk of serious life-threatening or debilitating adverse effects such as hypertension, myocardial infarction, stroke, seizures, and death.

Likelihood Probable Evidence D
Nadolol (Corgard)

Green tea seems to reduce the levels and clinical effects of nadolol.
Preliminary clinical research shows that green tea consumption reduces plasma concentrations of nadolol. Compared to a control group, both peak levels and total drug exposure (AUC) of nadolol were reduced by approximately 85% in subjects who drank green tea daily for two weeks. Drinking green tea with nadolol also significantly reduced nadolol's systolic blood pressure lowering effect. Other clinical research shows that a single dose of green tea can affect plasma nadolol levels for at least one hour. Green tea catechins have been shown to inhibit organic anion transporting polypeptides (OATP), one of which, OATP1A2, is involved in the uptake of nadolol in the intestine The interaction is thought to be due primarily to the epigallocatechin gallate (EGCG) content of green tea.

Likelihood Likely Evidence B
5-Fluorouracil

Theoretically, high doses of green tea might increase the effects and side effects of 5-fluorouracil.
Animal research shows that taking green tea in amounts equivalent to about 6 cups daily in humans for 4 weeks prior to receiving a single injection of 5-fluorouracil increases the maximum plasma levels of 5-fluorouracil by about 2.5-fold and the area under the curve by 425%.

Likelihood Possible Evidence D
Adenosine (Adenocard)

Theoretically, green tea might decrease the vasodilatory effects of adenosine and interfere with its use prior to stress testing.
Green tea contains caffeine. Caffeine is a competitive inhibitor of adenosine at the cellular level. However, caffeine doesn't seem to affect supplemental adenosine because high interstitial levels of adenosine overcome the antagonistic effects of caffeine. It is recommended that methylxanthines and methylxanthine-containing products be stopped 24 hours prior to pharmacological stress tests. However, methylxanthines appear more likely to interfere with dipyridamole (Persantine) than adenosine-induced stress testing.

Likelihood Possible Evidence B
Anticoagulant/Antiplatelet Drugs

Theoretically, green tea may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Conflicting reports exist regarding the effect of green tea on bleeding risk when used with anticoagulant or antiplatelet drugs; however, most evidence suggests that drinking green tea in moderate amounts is unlikely to cause a significant interaction. Green tea contains small amounts of vitamin K, approximately 7 mcg per cup. Some case reports have associated the antagonism of warfarin with the vitamin K content of green tea. However, these reports are rare, and very large doses of green tea (about 8-16 cups daily) appear to be needed to cause these effects. Furthermore, the catechins and caffeine in green tea are reported to have antiplatelet activity.

Likelihood Unlikely Evidence D
Beta-Adrenergic Agonists

Green tea contains caffeine. Theoretically, concomitant use of large amounts of caffeine might increase cardiac inotropic effects of beta-agonists.

Likelihood Probable Evidence D
Bortezomib (Velcade)

Theoretically, green tea might interfere with the effects of bortezomib.
In vitro research shows that green tea polyphenols, such as epigallocatechin gallate (EGCG), interact with bortezomib and block its proteasome inhibitory action. This prevents the induction of cell death in multiple myeloma or glioblastoma cancer cell lines. Advise patients taking bortezomib, not to take green tea.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, green tea might reduce the effects of carbamazepine and increase the risk for convulsions.
Green tea contains caffeine. Animal research suggests that taking caffeine can lower the anticonvulsant effects of carbamazepine and can induce seizures when taken in doses above 400 mg/kg. Human research has shown that taking caffeine 300 mg in three divided doses along with carbamazepine 200 mg reduces the bioavailability of carbamazepine by 32% and prolongs the plasma half-life of carbamazepine 2-fold in healthy individuals.

Likelihood Possible Evidence D
Celiprolol (Celicard)

Theoretically, green tea might reduce the levels and clinical effects of celiprolol.
In a small human study, taking green tea daily for 4 days appears to decrease blood and urine levels of celiprolol by at least 98%. This interaction is possibly due to the inhibition of organic anion transporting polypeptide (OATP). Green tea catechins have been shown to inhibit organic anion transporting polypeptides (OATP), one of which, OATP1A2, is found in the intestine The interaction is thought to be due primarily to the epigallocatechin gallate (EGCG) content of green tea.

Likelihood Possible Evidence D
Cimetidine (Tagamet)

Theoretically, concomitant use might increase the effects and adverse effects of caffeine in green tea.
Green tea contains caffeine. Cimetidine can reduce caffeine clearance by 31% to 42%.

Likelihood Likely Evidence B
Clozapine (Clozaril)

Theoretically, green tea might increase the levels and adverse effects of clozapine and acutely exacerbate psychotic symptoms.
Animal research suggests that, although green tea extract does not affect the elimination of clozapine, it delays the time to reach peak concentration and reduces the peak plasma levels. Also, concomitant administration of green tea and clozapine might theoretically cause acute exacerbation of psychotic symptoms due to the caffeine in green tea. Caffeine can increase the effects and toxicity of clozapine. Caffeine doses of 400-1000 mg daily inhibit clozapine metabolism. Clozapine is metabolized by cytochrome P450 1A2 (CYP1A2). Researchers speculate that caffeine might inhibit CYP1A2. However, there is no reliable evidence that caffeine affects CYP1A2. There is also speculation that genetic factors might make some patients be more sensitive to the interaction between clozapine and caffeine.

Likelihood Possible Evidence B
Contraceptive Drugs

Theoretically, concomitant use might increase the effects and adverse effects of caffeine found in green tea.
Green tea contains caffeine. Oral contraceptives can decrease caffeine clearance by 40% to 65%.

Likelihood Probable Evidence B
Cytochrome P450 1A2 (Cyp1A2) Inhibitors

Theoretically, concomitant use might increase the levels and adverse effects of caffeine.
Green tea contains caffeine. Caffeine is metabolized by cytochrome P450 1A2 (CYP1A2),. Theoretically, drugs that inhibit CYP1A2 may decrease the clearance rate of caffeine from green tea and increase caffeine levels.

Likelihood Possible Evidence D
Dipyridamole (Persantine)

Theoretically, green tea might decrease the vasodilatory effects of dipyridamole and interfere with its use prior to stress testing.
Green tea contains caffeine. Caffeine might inhibit dipyridamole-induced vasodilation. It is recommended that methylxanthines and methylxanthine-containing products be stopped 24 hours prior to pharmacological stress tests. Methylxanthines appear more likely to interfere with dipyridamole (Persantine) than adenosine-induced stress testing.

Likelihood Probable Evidence B
Disulfiram (Antabuse)

Theoretically, disulfiram might increase the risk of adverse effects from caffeine.
In human research, disulfiram decreases the clearance and increases the half-life of caffeine.

Likelihood Probable Evidence B
Diuretic Drugs

Theoretically, using green tea with diuretic drugs might increase the risk of hypokalemia.
Green tea contains caffeine. In excessive amounts, caffeine can reduce potassium levels due to stimulation of the sodium-potassium pump. Diuretics can also cause lower potassium levels.

Likelihood Possible Evidence D
Estrogens

Theoretically, estrogens might increase the levels and adverse effects of caffeine.
Green tea contains caffeine. Estrogen inhibits caffeine metabolism.

Likelihood Probable Evidence B
Ethosuximide (Zarontin)

Theoretically, green tea might reduce the effects of ethosuximide and increase the risk for convulsions.
Green tea contains caffeine. Animal research suggests that caffeine 92.4 mg/kg can decrease the anticonvulsant activity of ethosuximide. However, this effect has not been reported in humans.

Likelihood Possible Evidence D
Felbamate (Felbatol)

Theoretically, green tea might reduce the effects of felbamate and increase the risk for convulsions.
Green tea contains caffeine. Animal research suggests that a high dose of caffeine 161.7 mg/kg can decreases the anticonvulsant activity of felbamate. However, this effect has not been reported in humans.

Likelihood Possible Evidence D
Fexofenadine (Allegra)

Green tea can decrease blood levels of fexofenadine.
Clinical research shows that green tea can significantly decrease blood levels and excretion of fexofenadine. Taking green tea extract with a dose of fexofenadine decreased bioavailability of fexofenadine by about 30%. In vitro, green tea inhibits the cellular accumulation of fexofenadine by inhibiting the organic anion transporting polypeptide (OATP) drug transporter. Research shows that two of the major catechins found in green tea, epicatechin gallate (ECG) and epigallocatechin gallate (EGCG), inhibit OATPs, specifically OATP1A2, OATP1B1, and OATP2B1. In addition, green tea has been shown to reduce the absorption of some drugs that are OATP substrates.

Likelihood Probable Evidence B
Flutamide (Eulexin)

Theoretically, green tea might increase the levels and adverse effects of flutamide.
Green tea contains caffeine. In vitro evidence suggests that caffeine can inhibit the metabolism of flutamide. Theoretically, concomitant use of caffeine and flutamide might increase serum concentrations of flutamide and increase the risk adverse effects.

Likelihood Possible Evidence D
Fluvoxamine (Luvox)

Theoretically, fluvoxamine might increase the levels and adverse effects of caffeine.
Green tea contains caffeine. Fluvoxamine reduces caffeine metabolism.

Likelihood Probable Evidence D
Hepatotoxic Drugs

Theoretically, concomitant use might have additive adverse hepatotoxic effects.
Green tea extract supplements have been linked to several cases of hepatotoxicity and might have additive hepatotoxic effects with other drugs..

Likelihood Unlikely Evidence D
Imatinib (Gleevec)

Theoretically, green tea might reduce the levels and clinical effects of imatinib.
In animal research, a single dose of green tea extract reduces the area under the curve (AUC) of imatinib by up to approximately 64% and its main metabolite N-desmethyl imatinib by up to approximately 81%. This interaction has not been shown in humans. The mechanism of action is unclear but may involve multiple pathways.

Likelihood Possible Evidence D
organic Green Tea (Camellia sinensis) (leaf) aqueous extract full monograph & all 58 interactions

Rhodiola (Rhodiola rosea) (root) hydroethanolic extract10 drug types · 1,271 drugs

Antidiabetes Drugs

Theoretically, taking rhodiola with antidiabetes drugs might increase the risk of hypoglycemia.
In vitro and animal research shows that rhodiola extract can decrease blood glucose due to alpha-glucosidase activity.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, taking rhodiola with antihypertensive drugs might increase the risk of hypotension.
In vitro and animal research shows that rhodiola extract inhibits angiotensin-converting enzyme (ACE) and might lower blood pressure.

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

Theoretically, rhodiola might increase levels of drugs metabolized by CYP2C9.
In vitro research shows that rhodiola inhibits CYP2C9. This effect is highly variable and appears to be dependent on the rhodiola product studied. Also, a clinical study in healthy young males found that taking rhodiola extract 290 mg daily for 14 days reduces the metabolism of losartan, a CYP2C9 substrate, by 21% after 4 hours.

Likelihood Possible Evidence B
Immunosuppressants

Theoretically, rhodiola use might interfere with immunosuppressive therapy.
In vitro and animal research show that rhodiola has immunostimulatory effects.

Likelihood Possible Evidence D
Losartan (Cozaar)

Rhodiola might increase the levels and adverse effects of losartan.
A clinical study in healthy young males found that taking rhodiola extract 290 mg daily for 14 days reduces the metabolism of losartan, a CYP2C9 substrate, by 21% after 4 hours.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

Theoretically, rhodiola might increase levels of P-glycoprotein substrates.
In vitro research shows that rhodiola inhibits P-glycoprotein. Theoretically, using rhodiola with P-glycoprotein substrates might increase drug levels and potentially increase the risk of adverse effects.

Likelihood Possible Evidence D
Antidepressant Drugs

Theoretically, rhodiola might increase the risk of adverse effects when taken with antidepressants.
A review of adverse event reports in Poland identified cases of tachyarrhythmias, myalgia, arthralgia, gum pain, restless leg syndrome, swallowing disorders, and changes in consciousness when rhodiola was taken in combination with paroxetine, escitalopram, fluoxetine, sertraline, trazodone, and/or duloxetine.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, rhodiola might increase the risk of adverse effects when taken with CNS depressants.
A review of adverse event reports in Poland identified cases of excessive sedation, myoclonus, hypotension, and hallucinations when rhodiola was taken with haloperidol, diazepam, or alprazolam.

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

Theoretically, rhodiola might increase levels of drugs metabolized by CYP1A2.
In vitro research shows that rhodiola inhibits CYP1A2. This effect is highly variable and appears to be dependent on the rhodiola product studied. However, a clinical study in healthy young males found that taking rhodiola extract 290 mg daily for 14 days does not inhibit the metabolism of caffeine, a CYP1A2 substrate.

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

Theoretically, rhodiola might increase levels of drugs metabolized by CYP3A4.
In vitro research shows that rhodiola inhibits CYP3A4. This effect is highly variable and appears to be dependent on the rhodiola product studied. However, a clinical study in healthy young males found that taking rhodiola extract 290 mg daily for 14 days does not inhibit the metabolism of midazolam, a CYP3A4 substrate.

Likelihood Possible Evidence B
Rhodiola (Rhodiola rosea) (root) hydroethanolic extract full monograph & interactions

organic Turmeric24 drug types · 1,133 drugs

Alkylating Agents

Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research suggests that curcumin, a constituent of turmeric, inhibits mechlorethamine-induced apoptosis of breast cancer cells by up to 70%. Also, animal research shows that curcumin inhibits cyclophosphamide-induced tumor regression. However, some in vitro research shows that curcumin does not affect the apoptosis capacity of etoposide. Also, other laboratory research suggests that curcumin might augment the cytotoxic effects of alkylating agents. Reasons for the discrepancies may relate to the dose of curcumin and the specific chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have on alkylating agents.

Likelihood Possible Evidence D
Amlodipine (Norvasc)

Taking turmeric with amlodipine may increase levels of amlodipine.
Animal research shows that giving amlodipine 1 mg/kg as a single dose following the use of turmeric extract 200 mg/kg daily for 2 weeks increases the maximum concentration and area under the curve by 53% and 56%, respectively, when compared with amlodipine alone. Additional animal research shows that taking amlodipine 1 mg/kg with a curcumin 2 mg/kg pretreatment for 10 days increases the maximum concentration and area under the curve by about 2-fold when compared with amlodipine alone.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Turmeric may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Curcumin, a constituent of turmeric, has demonstrated antiplatelet effects in vitro. Furthermore, two case reports have found that taking turmeric along with warfarin or fluindione was associated with an increased international normalized ratio (INR). However, one clinical study in healthy volunteers shows that taking curcumin 500 mg daily for 3 weeks, alone or with aspirin 100 mg, does not increase antiplatelet effects or bleeding risk. It is possible that the dose of turmeric used in this study was too low to produce a notable effect.

Likelihood Possible Evidence B
Antidiabetes Drugs

Theoretically, taking turmeric with antidiabetes drugs might increase the risk of hypoglycemia.
Animal research and case reports suggest that curcumin, a turmeric constituent, can reduce blood glucose levels in patients with diabetes. Furthermore, clinical research in adults with type 2 diabetes shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg decreased postprandial glucose levels for up to 24 hours when compared with glyburide alone, despite the lack of a significant pharmacokinetic interaction. Other clinical studies in patients with diabetes show that taking curcumin daily can reduce blood glucose levels when compared with placebo.

Likelihood Possible Evidence B
Antitumor Antibiotics

Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro and animal research shows that curcumin, a constituent of turmeric, inhibits doxorubicin-induced apoptosis of breast cancer cells by up to 65%. However, curcumin does not seem to affect the apoptosis capacity of daunorubicin. In fact, some research shows that curcumin might augment the cytotoxic effects of antitumor antibiotics, increasing their effectiveness. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effects, if any, antioxidants such as turmeric have on antitumor antibiotics.

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

Turmeric might increase or decrease levels of drugs metabolized by CYP3A4.
In vitro and animal research show that turmeric and its constituents curcumin and curcuminoids inhibit CYP3A4. Also, 8 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking turmeric and cancer medications that are CYP3A4 substrates, including everolimus, ruxolitinib, ibrutinib, and palbociclib, and bortezomib. In another case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels after consuming turmeric powder at a dose of 15 or more spoonfuls daily for ten days prior. It was thought that turmeric increased levels of tacrolimus due to CYP3A4 inhibition.
Conversely, other in vitro research suggests that turmeric induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. An animal model suggests that induction of CYP3A4 occurs after daily curcumin use for 1 week. However, the induction of CYP3A4 by turmeric has not been reported in humans.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, turmeric might increase the risk of liver damage when taken with hepatotoxic drugs.
There is concern that turmeric might cause hepatotoxicity, especially when highly bioavailable formulations are used in high doses.

Likelihood Possible Evidence D
Methotrexate (Trexall, Others)

Theoretically, turmeric might have additive effects when used with hepatotoxic drugs such as methotrexate.
In one case report, a 39-year-old female taking methotrexate, turmeric, and linseed oil developed hepatotoxicity.

Likelihood Possible Evidence D
Organic Anion-Transporting Polypeptide Substrates (Oatp)

Theoretically, turmeric might increase blood levels of OATP4C1 substrates.
In vitro research shows that the turmeric constituent curcumin competitively inhibits OATP4C1 transport. This transporter is expressed in the kidney and facilitates the renal excretion of certain drugs. Theoretically, taking turmeric might decrease renal excretion of OATP substrates.

Likelihood Possible Evidence D
Sulfasalazine (Azulfidine)

Turmeric might increase the effects and adverse effects of sulfasalazine.
Clinical research shows that taking the turmeric constituent, curcumin, can increase blood levels of sulfasalazine by 3.2-fold.

Likelihood Probable Evidence B
Tacrolimus (Prograf)

Turmeric might increase the effects and adverse effects of tacrolimus.
In one case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels of 29 ng/mL. The patient previously had tacrolimus levels within the therapeutic range at 9.7 ng/mL. Ten days prior to presenting at the emergency room the patient started consumption of turmeric powder at a dose of 15 or more spoonfuls daily. It was thought that turmeric increased levels of tacrolimus due to cytochrome P450 3A4 (CYP3A4) inhibition. In vitro and animal research show that turmeric and its constituent curcumin inhibit CYP3A4.

Likelihood Possible Evidence D
Talinolol

Turmeric may reduce the absorption of talinolol in some situations.
Clinical research shows that taking curcumin for 6 days decreases the bioavailability of talinolol when taken together on the seventh day. The clinical significance of this effect is unclear.

Likelihood Probable Evidence B
Tamoxifen (Nolvadex)

Theoretically, turmeric might reduce the levels and clinical effects of tamoxifen.
In a small clinical trial in patients with breast cancer taking tamoxifen 20-30 mg daily, adding curcumin 1200 mg plus piperine 10 mg three times daily reduces the 24-hour area under the curve of tamoxifen and the active metabolite endoxifen by 12.8% and 12.4%, respectively, as well as the maximum concentrations of tamoxifen, when compared with tamoxifen alone. However, in the absence of piperine, the area under the curve for endoxifen and the maximum concentration of tamoxifen were not significantly reduced. Effects were most pronounced in patients who were extensive cytochrome P450 (CYP) 2D6 metabolizers.

Likelihood Possible Evidence B
Topoisomerase I Inhibitors

Turmeric has antioxidant effects. There is some concern that this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research shows that curcumin, a constituent of turmeric, inhibits camptothecin-induced apoptosis of breast cancer cells by up to 71%. However, other in vitro research shows that curcumin augments the cytotoxic effects of camptothecin. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agents. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have.

Likelihood Possible Evidence D
Tramadol (Ultram)

Theoretically, turmeric might increase or decrease levels of tramadol.
Animal research suggests that a single dose of curcumin, a constituent of turmeric, may increase tramadol's maximum concentration (Cmax) by inhibiting metabolism, while continued daily use for 7 days may reduce the area under the curve (AUC) due to the induction of drug-metabolizing enzymes such as cytochrome P450 3A4 (CYP3A4). However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Turmeric might increase the risk of bleeding with warfarin.
One case of increased international normalized ratio (INR) has been reported for a patient taking warfarin who began taking turmeric. Prior to taking turmeric, the patient had stable INR measurements. Within a few weeks of starting turmeric supplementation, the patient's INR increased to 10. Additionally, curcumin, the active constituent in turmeric, has demonstrated antiplatelet effects in vitro, which may produce additive effects when taken with warfarin.

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

Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2. However, research is conflicting.
In vitro and animal research show that the turmeric constituent, curcumin, inhibits CYP1A2. However, other in vitro research suggests that curcumin does not significantly affect CYP1A2.

Likelihood Possible Evidence D
Docetaxel (Taxotere)

Theoretically, turmeric might increase blood levels of oral docetaxel.
Animal research suggests that the turmeric constituent, curcumin, enhances the oral bioavailability of docetaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.

Likelihood Possible Evidence D
Estrogens

Theoretically, large amounts of turmeric might interfere with hormone replacement therapy through competition for estrogen receptors.
In vitro research shows that curcumin, a constituent of turmeric, displaces the binding of estrogen to its receptors.

Likelihood Possible Evidence D
Glyburide (Diabeta, Others)

Theoretically, taking turmeric and glyburide in combination might increase the risk of hypoglycemia.
Clinical research shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg increases blood levels of glyburide by 12% at 2 hours after the dose in patients with type 2 diabetes. While maximal blood concentrations of glyburide were not affected, turmeric modestly decreased postprandial glucose levels for up to 24 hours when compared to glyburide alone, possibly due to the hypoglycemic effect of turmeric demonstrated in animal research.

Likelihood Possible Evidence B
Losartan (Cozaar)

Theoretically, turmeric might increase the effects of losartan.
Research in hypertensive rats shows that taking turmeric can increase the hypotensive effects of losartan.

Likelihood Possible Evidence D
Norfloxacin (Noroxin)

Theoretically, turmeric might increase the effects and adverse effects of norfloxacin.
Animal research shows that taking curcumin, a turmeric constituent, can increase blood levels of orally administered norfloxacin.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, turmeric might increase the absorption of P-glycoprotein substrates.
In vitro and animal research shows that curcuminoids and other constituents found in turmeric can inhibit P-glycoprotein expression and activity.

Likelihood Possible Evidence D
Paclitaxel (Abraxane, Onxol)

Theoretically, turmeric might alter blood levels of paclitaxel, although any effect may not be clinically relevant.
Clinical research in adults with breast cancer receiving intravenous paclitaxel suggests that taking turmeric may modestly alter paclitaxel pharmacokinetics. Patients received paclitaxel on day 1, followed by either no treatment or turmeric 2 grams daily from days 2-22. Pharmacokinetic modeling suggests that turmeric reduces the maximum concentration and area under the curve of paclitaxel by 12.1% and 7.7%, respectively. However, these changes are not likely to be considered clinically relevant. Conversely, animal research suggests that curcumin, a constituent of turmeric, enhances the oral bioavailability of paclitaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.

Likelihood Possible Evidence D
organic Turmeric 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

organic Nigella (Nigella sativa) (seed) supercritical extract14 drug types · 912 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, black seed may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro and animal research suggests that black seed extract can inhibit platelet aggregation and clotting, and increase bleeding time. In addition, decreased platelet counts have occurred in a human case report and in animal research.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking black seed with antidiabetes drugs might increase the risk of hypoglycemia.
Some clinical research and numerous animal studies suggest that black seed, especially its constituent thymoquinone, can have hypoglycemic effects.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking black seed with antihypertensive drugs might increase the risk of hypotension.
Clinical research suggests that black seed powder and oil might reduce blood pressure by 2-3 mmHg. In animal research, black seed modestly reduces blood pressure and concomitant use of black seed and amlodipine (Norvasc) or metoprolol (Lopressor) increased the blood pressure lowering effects of these drugs.

Likelihood Possible Evidence B
Clopidogrel (Plavix)

Theoretically, black seed may increase the risk of bleeding if used with clopidogrel.
Animal research shows that taking black seed extract daily for 2 weeks prior to a single dose of clopidogrel increases maximum concentrations of clopidogrel by approximately 31% and modestly decreases oral clearance. Furthermore, bleeding time was increased by 12%. This has not been shown in humans.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, concomitant use with drugs that have sedative properties may cause additive effects.
Animal research suggests that black seed may have CNS depressant effects.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically taking black seed might reduce the levels and clinical effects of cyclosporine.
In animal research, black seed extract decreased the maximal levels of cyclosporine in the blood by 35.5%. This has not been shown in humans.

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

Theoretically, black seed might increase levels of drugs metabolized by CYP2C9.
In vitro research suggests that thymoquinone, a constituent of black seed, can decrease the metabolism of phenytoin by a mechanism possibly related to the inhibition of CYP2C9. The effect of black seed on CYP2C9 is unclear. This has not been shown in humans.

Likelihood Possible Evidence D
Diuretic Drugs

Theoretically, taking black seed with diuretic drugs might increase potassium loss and the risk of hypokalemia.
Black seed extract has shown diuretic effects in animals, which could theoretically increase potassium loss. This has not been shown in humans.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, black seed might interfere with immunosuppressive therapy.
Animal and in vitro studies suggest that black seed might stimulate immune function. However, other animal studies suggest that black seed may suppress immune function.

Likelihood Possible Evidence D
Phenytoin (Dilantin)

Theoretically, black seed might increase or decrease levels and effects of phenytoin.
In vitro research suggests that thymoquinone, a constituent of black seed, can decrease the metabolism of phenytoin. This effect may be due to inhibition of cytochrome P450 2C9 (CYP2C9). However, animal research shows that black seed decreases the maximum concentration of and total systemic exposure to phenytoin by 57% and 87%, respectively. This seems to be related to increased clearance and steady state volume of distribution. This interaction has not been shown in humans.

Likelihood Possible Evidence D
Serotonergic Drugs

Theoretically, combining serotonergic drugs with black seed might increase the risk of serotonergic side effects, including serotonin syndrome and cerebral vasoconstrictive disorders.
Animal research suggests that black seed can increase brain serotonin levels. In one case report, a 35-year-old man undergoing endoscopic surgery experienced immediate postoperative serotonin syndrome that was likely associated with the use of black seed oil 600 mg daily starting 4 days before surgery, and precipitated by the use of serotonergic pain medications, including fentanyl and oxycodone. Monitor patients for signs of serotonin syndrome and other serotonergic side effects if using black seed with serotonergic drugs.

Likelihood Possible Evidence D
Sildenafil (Viagra)

Theoretically, black seed might reduce plasma levels and the therapeutic effects of sildenafil.
Animal research shows that black seed reduces the total systemic exposure to sildenafil by 43%. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, black seed might increase levels of warfarin and increase the risk of bleeding.
In vitro research suggests that thymoquinone, a constituent of black seed, can decrease the metabolism of warfarin. This effect may be due to inhibition of cytochrome P450 2C9 (CYP2C9). The effect of black seed on warfarin metabolism is unclear. This has not been shown in humans.

Likelihood Possible Evidence D
Prednisolone

Theoretically black seed might reduce plasma levels and therapeutic effects of prednisolone.
In animal research, oral administration of a single dose of black seed oil 15 minutes prior to oral prednisolone decreases the prednisolone maximum plasma concentration by 65% and area under the curve by 25%. This has not been shown in humans.

Likelihood Possible Evidence D
organic Nigella (Nigella sativa) (seed) supercritical extract full monograph & interactions

Grape seed (Vitis vinifera) (seed) aqueous extract9 drug types · 910 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, grape extracts may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro evidence suggests that grape extracts might decrease platelet aggregation.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Ingesting grape juice with cyclosporine can reduce cyclosporine absorption.
A small pharmacokinetic study in healthy young adults shows that intake of purple grape juice 200 mL along with cyclosporine can decrease the absorption of cyclosporine by up to 30% when compared with water. Separate doses of grape juice and cyclosporine by at least 2 hours to avoid this interaction.

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

Theoretically, grape juice might reduce the levels of CYP1A2 substrates.
A small pharmacokinetic study in healthy adults shows that ingestion of 200 mL of grape juice decreases phenacetin plasma levels. This is thought to be due to induction of CYP1A2.

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

Theoretically, grape seed extract may increase the levels of CYP2D6 substrates.
In vitro evidence suggests that grape seed extract might inhibit CYP2D6 enzymes. However, this interaction has not been reported in humans.

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

Theoretically, grape seed extract might increase the levels of CYP2E1 substrates.
In vitro and animal research suggests that grape seed proanthocyanidin extract inhibits CYP2E1 enzymes. However, this interaction has not been reported in humans.

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

It is unclear if grape seed extract inhibits or induces CYP3A4; research is conflicting.
In vitro evidence suggests that grape seed extract might inhibit CYP3A4 enzymes. However, evidence from animal research shows that grape seed extract may induce CYP3A4 in the liver. So far, these interactions have not been reported in humans.

Likelihood Possible Evidence D
Midazolam (Versed)

Theoretically, long-term intake of grape seed extract might decrease the effects of midazolam.
Animal research shows that subchronic ingestions of grape seed extract can increase the elimination of intravenous midazolam by increasing hepatic CYP3A4 activity. Single doses of grape seed extract do not appear to affect midazolam elimination.

Likelihood Possible Evidence D
Phenacetin

Grape juice might decrease phenacetin absorption.
A small pharmacokinetic study in healthy adults shows that ingestion of 200 mL of grape juice decreases phenacetin plasma levels. This is thought to be due to induction of cytochrome P450 1A2 (CYP1A2).

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

It is unclear if grape juice or grape seed extract inhibits CYP2C9; research is conflicting.
In vitro evidence shows that grape seed extract or grape juice might inhibit CYP2C9 enzymes. However, a small pharmacokinetic study in healthy adults shows that drinking 8 ounces of grape juice once does not affect the clearance of flurbiprofen, a probe-drug for CYP2C9 metabolism. The effects of continued grape juice consumption are unclear.

Likelihood Unlikely Evidence D
Grape seed (Vitis vinifera) (seed) aqueous extract full monograph & interactions

organic Schizandra12 drug types · 803 drugs

Cyclophosphamide

Theoretically, schisandra might increase the levels and clinical effects of cyclophosphamide.
In vitro research shows that schisandra increases the concentration of cyclophosphamide, likely through inhibition of cytochrome P450 3A4. After multiple doses of the schisandra constituents schisandrin A and schisantherin A, the maximum concentration of cyclophosphamide was increased by 7% and 75%, respectively, while the overall exposure to cyclophosphamide was increased by 29% and 301%, respectively.

Likelihood Probable Evidence D
Cyclosporine (Neoral, Sandimmune)

Schisandra can increase the levels and clinical effects of cyclosporine.
A small observational study in children with aplastic anemia found that taking schisandra with cyclosporine increased cyclosporine trough levels by 93% without increasing the risk of adverse events. However, the dose of cyclosporine was reduced in 9% of children to maintain appropriate cyclosporine blood concentrations.

Likelihood Probable Evidence B
Cytochrome P450 2C19 (Cyp2C19) Substrates

Theoretically, schisandra might increase the levels and clinical effects of CYP2C19 substrates.
In vitro research shows that schisandra inhibits CYP2C19, and animal research shows that schisandra increases the concentration of voriconazole, a CYP2C19 substrate. Theoretically, schisandra may also inhibit the metabolism of other CYP2C19 substrates. This effect has not been reported in humans.

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

Theoretically, schisandra might decrease the levels and clinical effects of CYP2C9 substrates.
In vitro and animal research suggests that schisandra induces CYP2C9 enzymes. This effect has not been reported in humans.

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

Schisandra can increase the levels and clinical effects of drugs metabolized by CYP3A4.
Most clinical and laboratory research shows that schisandra, administered either as a single dose or up to twice daily for 14 days, inhibits CYP3A4 and increases the concentration of CYP3A4 substrates such as cyclophosphamide, midazolam, tacrolimus, and talinolol. Although one in vitro and animal study shows that schisandra may induce CYP3A4 metabolism, this effect appears to be overpowered by schisandra's CYP3A4 inhibitory activity and has not been reported in humans.

Likelihood Probable Evidence D
Midazolam (Versed)

Schisandra can increase the levels and clinical effects of midazolam.
A small pharmacokinetic study in healthy adults shows that taking schisandra extract (Hezheng Pharmaceutical Co.) containing deoxyschizandrin 33.75 mg twice daily for 8 days and a single dose of midazolam 15 mg on day 8 increases the overall exposure to midazolam by about 119%, increases the peak plasma level of midazolam by 86%, and decreases midazolam clearance by about 52%. This effect has been attributed to inhibition of CYP3A4 by schisandra.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

Schisandra might increase the levels and clinical effects of P-glycoprotein substrates.
In vitro research shows that schisandra extracts and constituents such as schisandrin B inhibit P-glycoprotein mediated efflux in intestinal cells and in P-glycoprotein over-expressing cell lines. Additionally, a small clinical study shows that schisandra increases the peak concentration and overall exposure to talinolol, a P-glycoprotein probe substrate. Theoretically, schisandra might inhibit the efflux of other P-glycoprotein substrates.

Likelihood Possible Evidence D
Sirolimus (Rapamune)

Schisandra can increase the levels and clinical effects of sirolimus.
A small pharmacokinetic study in healthy volunteers shows that taking 3 capsules of schisandra (Hezheng Pharmaceutical Company) containing a total of 33.75 mg deoxyschizandrin twice daily for 13 days and then taking a single dose of sirolimus 2 mg increases the overall exposure and peak level of sirolimus by two-fold. This effect is thought to be due to inhibition of cytochrome P450 3A4 by schisandra, as well as possible inhibition of the P-glycoprotein drug transporter.

Likelihood Probable Evidence B
Tacrolimus (Prograf)

Schisandra can increase the levels and clinical effects of tacrolimus.
Clinical research in healthy children and adults, transplant patients, and patients with nephrotic syndrome and various rheumatic immunologic disorders shows that taking schisandra with tacrolimus increases tacrolimus peak levels by 183% to 268%, prolongs or delays time to peak tacrolimus concentrations, increases overall exposure to tacrolimus by 126% to 343%, and decreases tacrolimus clearance by 19% to 73%. This effect is thought to be due to inhibition of P-glycoprotein drug transporter and CYP3A4 and CYP3A5 by schisandra. Some clinical and observational studies suggest that schisandra increases tacrolimus levels similarly in both expressors and non-expressors of CYP3A5, while other studies suggest it does so to a greater degree in CYP3A5 expressors than non-expressors. Animal research suggests that the greatest increase in tacrolimus levels occurs when schisandra is taken either concomitantly or up to 2 hours before tacrolimus, and clinical and observational research in humans suggests that schisandra may increase whole blood levels of tacrolimus and decrease clearance of tacrolimus in a dose-dependent manner.

Likelihood Probable Evidence B
Talinolol

Schisandra can increase the levels and clinical effects of talinolol.
A small pharmacokinetic study in healthy volunteers shows that taking schisandra extract 300 mg twice daily for 14 days with a single dose of talinolol 100 mg on day 14 increases the peak talinolol level by 51% and the overall exposure to talinolol by 47%. This effect is thought to be due to the possible inhibition of cytochrome P450 3A4 and P-glycoprotein by schisandra. tly.

Likelihood Probable Evidence B
Voriconazole (Vfend)

Theoretically, schisandra might increase the levels and clinical effects of voriconazole.
Animal research shows that oral schisandra given daily for 1 or 14 days increases levels of intravenously administered voriconazole, a cytochrome P450 (CYP) 2C19 substrate. This effect is thought to be due to inhibition of CYP2C19 by schisandra. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, schisandra might decrease the levels and clinical effects of warfarin.
Animal research suggests that oral schisandra extract, given daily for 6 days, reduces levels of intravenously administered warfarin. This effect might be due to the induction of cytochrome P450 (CYP) 2C9 metabolism by schisandra. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
organic Schizandra full monograph & interactions

Astaxanthin2 drug types · 671 drugs

Cytochrome P450 2B6 (Cyp2B6) Substrates

Theoretically, astaxanthin may decrease levels of drugs metabolized by CYP2B6.
In vitro research shows that astaxanthin induces cytochrome CYP2B6 enzyme activity in human hepatocytes. This effect has not been reported in humans.

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

Theoretically, astaxanthin may decrease levels of drugs metabolized by CYP3A4.
In vitro research shows that astaxanthin induces CYP3A4 enzyme activity in human hepatocytes. This effect has not been reported in humans.

Likelihood Possible Evidence D
Astaxanthin full monograph & interactions

Rosemary (Rosmarinus officinalis) (leaf) hydroethanolic extract6 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 (Rosmarinus officinalis) (leaf) hydroethanolic extract full monograph & interactions

organic Cordyceps3 drug types · 249 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, cordyceps may increase the risk of bleeding when used with antiplatelet or anticoagulant drugs.
In vitro and animal research suggests that cordyceps extract inhibits platelet aggregation and function. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, concurrent use of cordyceps might interfere with immunosuppressive therapy.
Animal and in vitro research suggests that cordyceps stimulates the immune system. However, limited clinical research suggests that taking cordyceps may lower the necessary therapeutic dose of the immunosuppressant cyclosporine, which suggests that cordyceps may have an immunosuppressive effect.

Likelihood Possible Evidence B
Testosterone

Theoretically, concurrent use of cordyceps and testosterone might have additive effects.
Animal research suggests that cordyceps can increase testosterone levels. The clinical significance of this finding is unclear.

Likelihood Possible Evidence D
organic Cordyceps full monograph & interactions

organic Broccoli2 drug types · 187 drugs

Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, broccoli might reduce the levels and effects of drugs metabolized by CYP1A2.
Pharmacokinetic research in humans shows that eating 500 grams of fresh broccoli daily for 6-12 days can increase CYP1A2 activity by 10% to 200%. Induction of CYP1A2 activity by broccoli is attributed to its glucosinolate constituents.

Likelihood Possible Evidence B
Cytochrome P450 2A6 (Cyp2A6) Substrates

Theoretically, broccoli might reduce the levels and effects of drugs metabolized by CYP2A6.
Pharmacokinetic research in humans shows that eating 500 grams of broccoli daily for 6 days increases CYP2A6 activity by 135% to 550%. Induction of CYP2A6 activity is attributed to its glucosinolate constituents.

Likelihood Possible Evidence B
organic Broccoli full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Elite Performance + Recovery, from the product label.

New Chapter

See all New Chapter products
Name
New Chapter, Inc.
Street Address
90 Technology Drive
City
Brattleboro
State
VT
ZipCode
05301
Phone Number
888-874-4461
Pharmacist Counseling Corner

Elite Performance + Recovery by New Chapter: Common Questions

Does Elite Performance + Recovery by New Chapter interact with any medications?
Yes. Based on its ingredients, Elite Performance + Recovery has a known interaction with 1,613 medications, including 13 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Elite Performance + Recovery contains 16 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.
Can I take this if I'm pregnant or breastfeeding?
Several ingredients — astaxanthin, cordyceps, maca, rhodiola, and schisandra — lack enough safety data, so they should be avoided in pregnancy. Ginger and black seed have some traditional pregnancy use but need your doctor's okay and modest amounts. Broccoli, kale, and rosemary as foods are generally safe. For breastfeeding, green tea passes caffeine into milk, so keep intake moderate. Talk to your OB or pharmacist about each ingredient based on your situation.
Will this help my athletic performance?
The formula contains cordyceps and rhodiola, which are marketed for athletic support, but the data we hold rates both as having insufficient reliable evidence or possibly ineffective for athletic performance specifically. Ginger shows possibly ineffective for exercise-induced muscle soreness. If athletic gains are your main goal, the evidence doesn't yet back that claim.
What are the most common side effects?
Ginger may cause stomach discomfort, heartburn, or loose stools at higher doses. Black seed and cordyceps can cause mild abdominal upset or diarrhea. Green tea extract may trigger nausea or constipation. Turmeric might cause digestive issues or, rarely, liver problems with long-term high-dose use. Most people taking normal doses tolerate the formula well.
Does this product contain any fillers?
The product contains inactive ingredients: olive oil, beeswax, candelilla wax, and brown rice ferment media as delivery and stabilizing agents. These are standard excipients, not fillers in the sense of 'nothing else' — they serve to protect and deliver the active ingredients.
Can I take this with my blood thinner?
Ginger, black seed, and grape seed extract in this formula may increase bleeding risk when combined with blood thinners like warfarin or antiplatelet drugs like aspirin. Do not take this product with blood thinners without checking your exact medications against the interaction tool on this page and getting pharmacist approval first.
Is green tea safe to take with my statin?
Green tea extract can reduce atorvastatin (Lipitor) levels by about 24%, which may reduce the statin's effectiveness at lowering cholesterol. If you take atorvastatin or another statin, talk to your pharmacist before adding this product — the interaction is significant.

Written and reviewed by the HelloPharmacist editorial staff. Our editorial policy

Not sure if Elite Performance + Recovery is safe with your meds?

Our pharmacists answer your medication & supplement questions — free.

Ask a pharmacist

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.

Elite Performance + Recovery label
Go deeper

The Full Monographs Behind Elite Performance + Recovery’s Ingredients

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

Herb & supplement monograph

Astaxanthin

Interacts with 671 drugs

Astaxanthin is a reddish carotenoid pigment with strong antioxidant activity in the lab, and it is widely promoted for skin, eye, heart, and exercise benefits. Early human studies are promis...

Read the full Astaxanthin 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 → Herb & supplement monograph

Turmeric

Interacts with 1,133 drugs

Turmeric is a popular spice whose main active compounds, curcuminoids, are studied mostly for inflammation and joint pain. Some research is promising, but quality is mixed and curcumin is po...

Read the full Turmeric monograph → Herb & supplement monograph

Grape

Interacts with 910 drugs

Grapes and grape products like grape seed extract contain antioxidant compounds such as resveratrol and proanthocyanidins that may support heart and blood vessel health. While the food is he...

Read the full Grape monograph → Herb & supplement monograph

Cordyceps

Interacts with 249 drugs

Cordyceps is a fungus used in traditional Chinese medicine for energy, exercise performance, and lung and immune support. Human research is limited and mostly low quality, so its benefits ar...

Read the full Cordyceps monograph → Herb & supplement monograph

Maca

Maca is a nutrient-rich Andean root often used for energy, libido, and menopause symptoms. Early studies suggest it may modestly help sexual desire and some menopause symptoms, but the evide...

Read the full Maca monograph → Herb & supplement monograph

Rhodiola

Interacts with 1,271 drugs

Rhodiola is an herb traditionally used to fight fatigue and help the body cope with stress. Some small studies suggest it may modestly reduce fatigue and improve mood, but the evidence is li...

Read the full Rhodiola monograph → Herb & supplement monograph

Schisandra

Interacts with 803 drugs

Schisandra is a traditional Chinese medicine berry used as an adaptogen for stress, fatigue, and liver support. Human evidence is limited and most claims are not well proven, but it appears...

Read the full Schisandra monograph → Herb & supplement monograph

Cardamom

Cardamom is a popular cooking spice that has long been used in traditional medicine for digestion and fresh breath. As a food, it is generally safe for most people, but high-dose supplements...

Read the full Cardamom monograph → Herb & supplement monograph

Kale

Kale is a nutrient-dense leafy green vegetable that is rich in vitamins, minerals, fiber, and antioxidants. Eaten as a normal food it is very healthy for most people, but it is a whole food...

Read the full Kale monograph → Herb & supplement monograph

Broccoli

Interacts with 187 drugs

Broccoli is a nutritious cruciferous vegetable rich in fiber, vitamins, and plant compounds like sulforaphane that have drawn scientific interest for health benefits. Eating broccoli as food...

Read the full Broccoli monograph → Herb & supplement monograph

Black Seed

Interacts with 912 drugs

Black seed (Nigella sativa) is a traditional spice and remedy that has been studied for asthma, blood sugar, cholesterol, and blood pressure, with early research showing some promise but no...

Read the full Black Seed monograph → Herb & supplement monograph

Green Tea

Interacts with 1,293 drugs

Green tea is a popular beverage rich in antioxidants called catechins, and drinking it in normal amounts is considered safe for most people. Concentrated green tea extracts are a different s...

Read the full Green Tea 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 →
Sources

Sources & How We Checked

Elite Performance + Recovery'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 565 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.

Astaxanthin 3 references
  1. Kupcinskas L, Lafolie P, Lignell A, et al. Efficacy of the natural antioxidant astaxanthin in the treatment of functional dyspepsia in patients with or without Helicobacter pylori infection: A prospective, randomized, double blind, and placebo-controlled
  2. Kistler, A., Liechti, H., Pichard, L., Wolz, E., Oesterhelt, G., Hayes, A., and Maurel, P. Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. Arch.Toxicol. 2002;75(11-12):665-675. PubMed
  3. Choi HD, Youn YK, Shin WG. Positive effects of astaxanthin on lipid profiles and oxidative stress in overweight subjects. Plant Foods Hum Nutr. 2011;66:363-369. PubMed

See these in context on the Astaxanthin monograph →

Ginger 64 references
  1. Fischer-Rasmussen W, Kjaer SK, Dahl C, Asping U. Ginger treatment of hyperemesis gravidarum. Eur J Obstet Gynecol Reprod Biol 1991;38:19-24. PubMed
  2. Jewell D, Young G. Interventions for nausea and vomiting in early pregnancy. Cochrane Database Syst Rev 2000;(2):CD000145. PubMed
  3. Vutyavanich T, Kraisarin T, Ruangsri R. Ginger for nausea and vomiting in pregnancy: randomized, double-masked, placebo-controlled trial. Obstet Gynecol 2001;97:577-82. DOI
  4. Backon J. Ginger in preventing nausea and vomiting of pregnancy; a caveat due to its thromboxane synthetase activity and effect on testosterone binding. Eur J Obstet Gynecol Reprod Biol 1991;42:163-4. PubMed
  5. Srivastava KC. Effect of onion and ginger consumption on platelet thromboxane production in humans. Prostaglandins Leukot Essent Fatty Acids 1989;35:183-5. PubMed
  6. Stewart JJ, Wood MJ, Wood CD, Mims ME. Effects of ginger on motion sickness susceptibility and gastric function. Pharmacology 1991;42:111-20. PubMed
  7. Smith C, Crowther C, Willson K, et al. A randomized controlled trial of ginger to treat nausea and vomiting in pregnancy. Obstet Gynecol 2004;103:639-45. PubMed
  8. Portnoi G, Chng LA, Karimi-Tabesh L, et al. Prospective comparative study of the safety and effectiveness of ginger for the treatment of nausea and vomiting in pregnancy. Am J Obstet Gynecol 2003;189:1374-7.. PubMed
  9. Wigler I, Grotto I, Caspi D, Yaron M. The effects of Zintona EC (a ginger extract) on symptomatic gonarthritis. Osteoarthritis Cartilage 2003;11:783-9. PubMed
  10. Ghayur MN, Gilani AH. Ginger lowers blood pressure through blockade of voltage-dependent calcium channels. J Cardiovasc Pharmacol 2005;45:74-80. PubMed
  11. Thomson M, Al-Qattan KK, Al-Sawan SM, et al. The use of ginger (Zingiber officinale Rosc.) as a potential anti-inflammatory and antithrombotic agent. Prostaglandins Leukot Essent Fatty Acids 2002;67:475-8. PubMed
  12. Kanerva L, Estlander T, Jolanki R. Occupational allergic contact dermatitis from spices. Contact Dermatitis 1996;35:157-62. PubMed
  13. Akhani SP, Vishwakarma SL, Goyal RK. Anti-diabetic activity of Zingiber officinale in streptozotocin-induced type I diabetic rats. J Pharm Pharmacol 2004;56:101-5.
  14. Kruth P, Brosi E, Fux R, et al. Ginger-associated overanticoagulation by phenprocoumon. Ann Pharmacother 2004;38:257-60. PubMed
  15. Jiang X, Williams KM, Liauw WS, et al. Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Br J Clin Pharmacol 2005;59:425-32. PubMed
  16. Borrelli F, Capasso R, Aviello G, et al. Effectiveness and safety of ginger in the treatment of pregnancy-induced nausea and vomiting. Obstet Gynecol 2005;105:849-56. PubMed
  17. Smith C, Crowther C, Wilson K et al. A randomized controlled trial of ginger to treat nausea and vomiting in pregnancy. Obstet Gynecol 2004;103:639-45. PubMed
  18. Jiang X, Blair EY, McLachlan AJ. Investigation of the effects of herbal medicines on warfarin response in healthy subjects: a population pharmacokinetic-pharmacodynamic modeling approach. J Clin Pharmacol 2006;46:1370-8. PubMed
  19. Chittumma P, Kaewkiattikun K, Wiriyasiriwach B. Comparison of the effectiveness of ginger and vitamin B6 for treatment of nausea and vomiting in early pregnancy: a randomized double-blind controlled trial. J Med Assoc Thai 2007;90:15-20.
  20. Ozgoli G, Goli M, Moattar F. Comparison of effects of ginger, mefenamic acid, and ibuprofen on pain in women with primary dysmenorrhea. J Altern Complement Med 2009;15:129-32. PubMed
  21. Black CD, Herring MP, Hurley DJ, O'Connor PJ. Ginger (Zingiber officinale) reduces muscle pain caused by eccentric exercise. J Pain 2010;11:894-903. PubMed
  22. Heitmann K, Nordeng H, Holst L. Safety of ginger use in pregnancy: results from a large population-based cohort study. Eur J Clin Pharmacol 2012 Jun 17. PubMed
  23. Ryan JL, Heckler CE, Roscoe JA, et al. Ginger (Zingiber officinale) reduces acute chemotherapy-induced nausea: a URCC CCOP study of 576 patients. Support Care Cancer. 2012;20:1479-89. PubMed
  24. Backon J. Ginger as an antiemetic: possible side effects due to its thromboxane synthetase activity. Anaesthesia. 1991;46(8):705-6.. PubMed
  25. Abebe W. Herbal medication: potential for adverse interactions with analgesic drugs. J Clin Pharm Ther. 2002;27:391-401. PubMed
  26. Argento A, Tiraferri E, Marzaloni M. [Oral anticoagulants and medicinal plants. An emerging interaction]. Ann Ital Med Int. 2000;15:139-43.
  27. Young HY, Liao JC, Chang YS, et al. Synergistic effect of ginger and nifedipine on human platelet aggregation: a study in hypertensive patients and normal volunteers. Am J Chin Med. 2006;34:545-51. PubMed
  28. Greenway FL, Liu Z, Martin CK, et al. Safety and efficacy of NT, an herbal supplement, in treating human obesity. Int J Obes (Lond). 2006;30:1737-41. PubMed
  29. Shalansky S, Lynd L, Richardson K, et al. Risk of warfarin-related bleeding events and supratherapeutic international normalized ratios associated with complementary and alternative medicine: a longitudinal analysis. Pharmacotherapy. 2007;27:1237-47. PubMed
  30. Lesho EP, Saullo L, Udvari-Nagy S. A 76-year-old woman with erratic anticoagulation. Cleve Clin J Med. 2004;71:651-6. PubMed
  31. Okonta JM, Uboh M, Obonga WO. Herb-Drug Interaction: A Case Study of Effect of Ginger on the Pharmacokinetic of Metronidazole in Rabbit. Indian Journal of Pharmaceutical Sciences (India) 2008;70(230):232. PubMed
  32. Chiang HM, Chao PD, Hsiu SL, et al. Ginger significantly decreased the oral bioavailability of cyclosporine in rats. Am J Chin Med. 2006;34:845-55. PubMed
  33. Bhandari U, Kanojia R, Pillai KK. Effect of ethanolic extract of Zingiber officinale on dyslipidaemia in diabetic rats. J Ethnopharmacol. 2005;97:227-30. PubMed
  34. Ojewole JA. Analgesic, antiinflammatory and hypoglycaemic effects of ethanol extract of Zingiber officinale (Roscoe) rhizomes (Zingiberaceae) in mice and rats. Phytother Res. 2006;20:764-72.
  35. Al-Amin ZM, Thomson M, Al-Qattan KK, et al. Anti-diabetic and hypolipidaemic properties of ginger (Zingiber officinale) in streptozotocin-induced diabetic rats. Br J Nutr. 2006;96:660-6.
  36. Islam MS, Choi H. Comparative effects of dietary ginger (Zingiber officinale) and garlic (Allium sativum) investigated in a type 2 diabetes model of rats. J Med Food. 2008;11:152-9.
  37. Cady RK, Goldstein J, Nett R, et al. A double-blind placebo-controlled pilot study of sublingual feverfew and ginger (LipiGesic M) in the treatment of migraine. Headache 2011;51:1078-86.
  38. Futrell, J. M. and Rietschel, R. L. Spice allergy evaluated by results of patch tests. Cutis 1993;52(5):288-290.
  39. Sripramote, M. and Lekhyananda, N. A randomized comparison of ginger and vitamin B6 in the treatment of nausea and vomiting of pregnancy. J Med Assoc.Thai. 2003;86(9):846-853.
  40. Lohsiriwat, S., Rukkiat, M., Chaikomin, R., and Leelakusolvong, S. Effect of ginger on lower esophageal sphincter pressure. J.Med.Assoc.Thai. 2010;93(3):366-372.
  41. Liu, P. H. and Ho, H. L. Ginger and drug bezoar induced small bowel obstruction. J R.Coll.Surg.Edinb. 1983;28(6):397-398.
  42. Maghbooli M, Golipour F, Moghimi Esfandabadi A, Yousefi M. Comparison between the efficacy of ginger and sumatriptan in the ablative treatment of the common migraine. Phytother Res 2014;28(3):412-5. PubMed
  43. Mahluji S, Attari VE, Mobasseri M, Payahoo L, Ostadrahimi A, Golzari SE. Effects of ginger (Zingiber officinale) on plasma glucose level, HbA1c and insulin sensitivity in type 2 diabetic patients. Int J Food Sci Nutr 2013;64(6):682-6.
  44. Mozaffari-Khosravi H, Talaei B, Jalali BA, Najarzadeh A, Mozayan MR. The effect of ginger powder supplementation on insulin resistance and glycemic indices in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled trial. Complement PubMed
  45. Paramdeep G. Efficacy and tolerability of ginger (Zingiber officinale) in patients of osteoarthritis of knee. Indian J Physiol Pharmacol 2013;57(2):177-83.
  46. Rahnama P, Montazeri A, Huseini HF, Kianbakht S, Naseri M. Effect of Zingiber officinale R. rhizomes (ginger) on pain relief in primary dysmenorrhea: a placebo randomized trial. BMC Complement Altern Med 2012;12:92. PubMed
  47. Viljoen E, Visser J, Koen N, Musekiwa A. A systematic review and meta-analysis of the effect and safety of ginger in the treatment of pregnancy-associated nausea and vomiting. Nutr J 2014;13:20. PubMed
  48. Bartels EM, Folmer VN, Bliddal H, et al. Efficacy and safety of ginger in osteoarthritis patients: a meta-analysis of randomized placebo-controlled trials. Osteoarthritis Cartilage. 2015;23(1):13-21. PubMed
  49. Choi JS, Han JY, Ahn HK, et al. Assessment of fetal and neonatal outcomes in the offspring of women who had been treated with dried ginger (Zingiberis rhizoma siccus) for a variety of illnesses during pregnancy. J Obstet Gynaecol. 2015;35(2):125-30.
  50. Marx W, McKavanagh D, McCarthy AL, Bird R, Ried K, Chan A, Isenring L. The effect of ginger (Zingiber officinale) on platelet aggregation: A systematic literature review. PLoS One. 2015;10(10):e0141119. PubMed
  51. Crichton M, Marshall S, Marx W, McCarthy AL, Isenring E. Efficacy of ginger (Zingiber officinale) in ameliorating chemotherapy-induced nausea and vomiting and chemotherapy-related outcomes: A systematic review update and meta-analysis. J Acad Nutr Diet. 2 PubMed
  52. Martins LB, Rodrigues AMDS, Monteze NM, et al. Double-blind placebo-controlled randomized clinical trial of ginger (Zingiber officinale Rosc.) in the prophylactic treatment of migraine. Cephalalgia. 2020;40(1):88-95.
  53. Martins LB, Rodrigues AMDS, Rodrigues DF, Dos Santos LC, Teixeira AL, Ferreira AVM. Double-blind placebo-controlled randomized clinical trial of ginger (Zingiber officinale Rosc.) addition in migraine acute treatment. Cephalalgia. 2019;39(1):68-76.
  54. Ahad A, Raish M, Bin Jardan YA, Alam MA, Al-Mohizea AM, Al-Jenoobi FI. Effect of Hibiscus sabdariffa and Zingiber officinale on the antihypertensive activity and pharmacokinetic of losartan in hypertensive rats. Xenobiotica. 2020:1-11.
  55. Okuhira H, Nakatani Y, Furukawa F, Kanazawa N. Anaphylaxis to ginger induced by herbal medicine. Allergol Int. 2020;69(1):159-160. PubMed
  56. Yamprasert R, Chanvimalueng W, Mukkasombut N, Itharat A. Ginger extract versus Loratadine in the treatment of allergic rhinitis: a randomized controlled trial. BMC Complement Med Ther. 2020;20(1):116. PubMed
  57. Ebrahimzadeh A, Ebrahimzadeh A, Mirghazanfari SM, Hazrati E, Hadi S, Milajerdi A. The effect of ginger supplementation on metabolic profiles in patients with type 2 diabetes mellitus: a systematic review and meta-analysis of randomized controlled trials. PubMed
  58. Alam MA, Bin Jardan YA, Alzenaidy B, et al. Effect of Hibiscus sabdariffa and Zingiber officinale on pharmacokinetics and pharmacodynamics of amlodipine. J Pharm Pharmacol 2021;73(9):1151-60.
  59. Akbarzadeh E, Heydari M, Atarzadeh F, Jaladat AM. Chronic dysuria following ginger (Zingiber officinale) use: a case report. Galen Med J 2018;7:e1086. DOI
  60. Haron MH, Dale O, Martin K, et al. Evaluation of the Herb-Drug Interaction Potential of Commonly Used Botanicals on the US Market with Regard to PXR- and AhR-Mediated Influences on CYP3A4 and CYP1A2. J Diet Suppl 2022. PubMed
  61. Rostamkhani H, Veisi P, Niknafs B, Jafarabadi MA, Ghoreishi Z. The effect of zingiber officinale on prooxidant-antioxidant balance and glycemic control in diabetic patients with ESRD undergoing hemodialysis: a double-blind randomized control trial. BMC Co PubMed
  62. Husain I, Dale OR, Idrisi M, et al. Evaluation of the Herb-Drug Interaction (HDI) Potential of Zingiber officinale and Its Major Phytoconstituents. J Agric Food Chem. 2023;71(19):7521-7534.
  63. Committee on Practice Bulletins-Obstetrics. ACOG Practice Bulletin No. 189: Nausea And Vomiting Of Pregnancy. Obstet Gynecol. 2018;131(1):e15-e30. PubMed
  64. Pochet S, Lechon AS, Lescrainier C, et al. Herb-anticancer drug interactions in real life based on VigiBase, the WHO global database. Sci Rep 2022;12(1):14178. PubMed

See these in context on the Ginger monograph →

Cordyceps 14 references
  1. Zhu JS, Halpern GM, Jones K. The scientific rediscovery of an ancient Chinese herbal medicine: Cordyceps sinensis: part I. J Altern Complement Med 1998;4:289-303.
  2. Zhu JS, Halpern GM, Jones K. The scientific rediscovery of a precious ancient Chinese herbal regimen: Cordyceps sinensis: part II. J Altern Complement Med 1998;4:429-57.
  3. Chen YJ, Shiao MS, Lee SS, Wang SY. Effect of Cordyceps sinensis on the proliferation and differentiation of human leukemic U937 cells. Life Sci 1997;60:2349-59. PubMed
  4. Zhao Y. [Inhibitory effects of alcoholic extract of Cordyceps sinensis on abdominal aortic thrombus formation in rabbits]. Chung Hua I Hsueh Tsa Chih (Taipei) 1991;71:612-5, 42.
  5. Chen GZ, Chen GL, Sun T, et al. Effects of Cordyceps sinensis on murine T lymphocyte subsets. Chin Med J (English) 1991;104:4-8.
  6. Zhu XY, Yu HY. [Immunosuppressive effect of cultured Cordyceps sinensis on cellular immune response]. Chung Hsi I Chieh Ho Tsa Chih 1990;10:485-7, 454.
  7. Hsu, C. C., Huang, Y. L., Tsai, S. J., Sheu, C. C., and Huang, B. M. In vivo and in vitro stimulatory effects of Cordyceps sinensis on testosterone production in mouse Leydig cells. Life Sci 9-5-2003;73(16):2127-2136. PubMed
  8. Ikumoto, T., Sasaki, S., Namba, H., Toyama, R., Moritoki, H., and Mouri, T. [Physiologically active compounds in the extracts from tochukaso and cultured mycelia of Cordyceps and Isaria]. Yakugaku Zasshi 1991;111(9):504-509. PubMed
  9. Wu, T. N., Yang, K. C., Wang, C. M., Lai, J. S., Ko, K. N., Chang, P. Y., and Liou, S. H. Lead poisoning caused by contaminated Cordyceps, a Chinese herbal medicine: two case reports. Sci.Total Environ. 4-5-1996;182(1-3):193-195. PubMed
  10. Hong T, Zhang M, Fan J. Cordyceps sinensis (a traditional Chinese medicine) for kidney transplant recipients (Review). Cochrane Database Syst Rev. 2015;(10):CD009698. doi: 10.1002/14651858.CD009698.pub2.
  11. Zhang HW, Lin ZX, Tung YS, Kwan TH, Mok CK, Leung C, Chan LS. Cordyceps sinensis (a traditional Chinese medicine) for treating chronic kidney disease (Review). Cochrane Database Syst Rev. 2014;(12):CD008353. doi: 10.1002/14651858.CD008353.pub2. PubMed
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Grape 34 references
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Kale 2 references
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Broccoli 5 references
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See these in context on the Broccoli monograph →

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  59. Abutaima R, Al-Ebini Y, Alkofahi A, et al. In vivo assessment of black seed oil single dose on prednisolone pharmacokinetics. J Pharm Pharmacol 2024;76(1):57-63.
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See these in context on the Black Seed monograph →

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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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