Major interaction on record — check this product against your medications before combining. Check your meds →
Dietary supplement

Joint Comfort Ingredients & Drug Interactions

by Yogi

Joint Comfort label
See full label image
Other (e.g. Tea Bag) Category: Botanical
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 16, 2026 · Label data from the NIH DSLD
What is this page for?

First and foremost: checking Joint Comfort 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

Joint Comfort is a dietary supplement by Yogi with 10 active ingredients. Its ingredients are commonly taken for irritable bowel syndrome (ibs), indigestion and gas, nausea.Based on those ingredients, 1,627 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are organic decaffeinated Green Tea, organic Turmeric, Cat's Claw root extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

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Check Your Meds Against Joint Comfort by Yogi

Ask about any prescription or over-the-counter medication and we check it for interactions with Joint Comfort by Yogi — and tell you which ingredient is responsible.

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Computed from our clinical databases

HelloPharmacist Scorecard of Joint Comfort by Yogi

Four independent checks of what is known — a summary of the available information, not a grade of the product itself.

Evidence for Intended Use
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
Not assessable

The stated purpose hasn't been mapped to our evidence data yet.

Why this rating?
  • We haven't mapped this product's purpose to our evidence data yet — it'll be graded on the next content refresh.
Ingredient Transparency
Low

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

Why this rating?
  • The label discloses an exact amount for 0 of its 10 active ingredients.
  • “Proprietary Blend of Herbs” is a proprietary blend — the label gives one combined amount (1,981 mg) without saying how much of each component you get.
Known Interaction Concern
Major identified

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

Why this rating?
  • 9 of the 10 matched ingredients can interact with medications — Alfalfa, Cat's Claw, Turmeric, Peppermint, Lemongrass, 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: 1,628 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.
Safety Information
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 9 of the 10 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 10 of 10.
  • General safety write-ups exist for 10 of 10.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

HelloPharmacist summaryFormula with limited ingredient disclosure with no assessable stated purpose. Major medication interactions have been identified, and safety information is well characterized.

Assessment coverage: 10 of 10 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated May 24, 2017.

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 Joint Comfort, straight from the product label.

Brand Yogi
Barcode (UPC) 076950450332
Net contents 16 Tea Bag(s); 1.12 Oz(s); 32 Gram(s)
Market status Off market
Date entered into DSLD May 24, 2017
DSLD ID 73454
Product type Botanical
Supplement form Other (e.g. Tea Bag)
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Vegan, Vegetarian, Adult (18 - 50 Years), Kosher, Organic
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 Joint Comfort by Yogi, 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:
1 Tea Bag(s)
Maximum serving Sizes:
2 Tea Bag(s)
UPC/BARCODE
076950450332
IngredientAmount% DV
Peppermint0 NP--
Proprietary Blend of Herbs1981 mg--
Celery0 NP--
organic Turmeric0 NP--
Devil's Claw root extract0 NP--
Yucca Root Extract0 NP--
Spearmint0 NP--
organic Lemongrass0 NP--
organic decaffeinated Green Tea0 NP--
organic Alfalfa0 NP--
Cat's Claw root extract0 NP--

Other ingredients: natural Peach flavor

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.
Brand IP Statement(s)

100% recycled paperboard

2015 East West Tea Company, LLC

When you need a little Joint Comfort

General Statements

To help protect our forests and reduce landfill burden, Yogi tea cartons use 100% recycled paperboard, 55% post consumer waste, and are printed with environmentally-friendly vegetable-based inks.

Supports healthy joints

Love our tea as much as we do or we’ll gladly refund your money. Inspire us and yourself at www.yogiproducts.com

Recyclable Non-irradiated Oxygen-bleached tea bags Please recycle this box.

Yoga to spread your wings Expand our mind and your motion. Sit with soles of feet together. Hold on to feet with hands, lean forward keeping back straight and chin at 90-degree angle to chest. Breathe slowly and deeply. Continue for 1 to 3 minutes. Feel your body transform with the strength to soar through the day. Before doing this exercise or participating in any exercise program, consult your physician.

Our story began in 1969 when Yogi Bhajan, an inspirational teacher of holistic living, started teaching yoga in the west. He shared with his students his wisdom and knowledge of healthy living and the beneficial properties of herbs, all while serving a comforting and aromatic spiced tea they affectionately named “Yogi Tea”.

Recyclable Compostable tea bags

Our unique blend of botanicals from Asia, Africa and America is purposefully formulated to help support the joints.

Enjoy this pleasant blend anytime during the day or when you need a little Joint Comfort.

At Yogi, it’s about more than creating deliciously purposeful teas. Learn about our efforts to do good at home and around the world at yogiproducts.com/doing-good.

General

30784-G4 D0730 201772

FDA Statement of Identity

Herbal Supplement

Formula

Made with organic turmeric root

Circle U

Naturally decaffeinated organic green tea joins organic turmeric root, used in ayurveda to promote joint health, and yucca root, traditionally used by native Americans to help support the joints. We then add cat's claw root, used for centuries by the Ashanica Indians of South America, and devil's claw root - also traditionally used to support the joints - to round out this soothing tea.

Each tea bag contains approximately 2 mg of caffeine, as compared to approximately 90 mg in 8 oz of coffee.

Seals/Symbols

Quality assurance international Certified organic

Circle U

V vegan

Certified circle B corporation

Formulation

Quality assurance international Certified organic

V vegan

FDA Disclaimer Statement

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

Suggested/Recommended/Usage/Directions

Get the most out of every cup Bring water to boiling and steep 4 to 6 minutes. For a stronger tea, use 2 tea bags. Enjoy 2 to 4 cups a day.

Precautions

Warning: Consult your healthcare provider prior to use if you are pregnant or nursing, taking any medication or if you have a medical condition.

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

See for yourself

Joint Comfort by Yogi label

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

Joint Comfort 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 Joint Comfort by Yogi

These are the 10 active ingredients this product is made of. Select any to open its full monograph.

Serving size1 Tea Bag(s) Dosage formOther (e.g. Tea Bag) Amounts shown are per serving.

Most supplement products combine several ingredients, and a medication can interact with the product through any one of them. Each ingredient below shows whether it has known drug interactions.

Other (inactive) ingredients: Natural Peach flavor. These complete the product’s ingredient list but are not active constituents.

Interaction report

Joint Comfort by Yogi Drug Interactions

Joint Comfort contains 10 ingredients, and 9 of them have known drug interactions. Altogether they interact with 1,627 medications. Here’s the picture, then you can look up your own drug.

Want to check YOUR meds against Joint Comfort?

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
1,627Drugs
15 Major 1,605 Moderate 7 Minor

Ingredients driving the most interactions

organic decaffeinated Green Tea 1,293
organic Turmeric 1,133
Cat's Claw root extract 962
Devil's Claw root extract 804
Peppermint 796

Individual Drug Interactions

The ingredients in Joint Comfort interact with 1,627 drugs. Click any drug to see the details.

9 of the 10 ingredients in Joint Comfort interact with drugs. Each result below shows which ingredient is responsible. organic decaffeinated Green Tea organic Turmeric Cat's Claw root extract Devil's Claw root extract Peppermint organic Lemongrass Celery organic Alfalfa Spearmint

Each ingredient & the kinds of drugs it affects

For each ingredient in Joint Comfort 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 decaffeinated Green Tea58 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 decaffeinated Green Tea full monograph & all 58 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

Cat's Claw root extract6 drug types · 962 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, cat's claw may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Cat's claw contains rhynchophylline and isorhynchophylline. Animal research suggests that these alkaloids can inhibit platelet aggregation. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, taking cat's claw with antihypertensive drugs might increase the risk of hypotension.
Cat's claw contains rhynchophylline. In vitro and animal research suggests that rhynchophylline can lower blood pressure. This interaction has not been reported in humans.

Likelihood Probable Evidence D
Calcium Channel Blockers

Theoretically, taking cat's claw with calcium channel blockers might increase the risk of hypotension.
Cat's claw contains various alkaloids, including rhynchophylline, isorhynchophylline, corynoxeine, and isocorynoxiene. Animal research suggests that these alkaloids can lower blood pressure by acting as calcium channel blockers. This interaction has not been reported in humans.

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

Theoretically, cat's claw might increase or decrease the levels and effects of drugs metabolized by CYP3A4.
Cat's claw may affect the clearance of drugs metabolized by CYP3A4. In vitro research shows that cat's claw can inhibit CYP3A4 enzymes. In one case report, a patient taking cat's claw (at an unspecified dose) experienced increased serum levels of atazanavir, ritonavir, and saquinavir, all of which are CYP3A4 substrates. Levels returned to normal 15 days after discontinuation of the cat's claw supplement, suggesting inhibition of CYP3A4 by cat's claw. In contrast, animal research suggests that rhynchophylline, an alkaloid contained in cat's claw, induces CYP3A expression and accelerates the metabolism of nirmatrelvir, the active component in the nirmatrelvir/ritonavir combination product.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, cat's claw might interfere with immunosuppressive therapy.
In human and laboratory research, cat's claw has been shown to have immunostimulating activity. It stimulates phagocytosis and increases respiratory cellular activity and the mobility of leukocytes. Theoretically, this could interfere with the activity of immunosuppressant medications.

Likelihood Possible Evidence D
Nirmatrelvir/Ritonavir (Paxlovid)

Theoretically, cat's claw may decrease the levels of nirmatrelvir.
Cat's claw contains rhynchophylline. Animal research suggests that this alkaloid induces CYP3A expression, thereby accelerating the metabolism of nirmatrelvir, the active component in the nirmatrelvir/ritonavir combination product. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Cat's Claw root extract full monograph & interactions

Devil's Claw root extract7 drug types · 804 drugs

Cytochrome P450 2C19 (Cyp2C19) Substrates

Theoretically, devil's claw might increase levels of drugs metabolized by CYP2C19.
In vitro research shows that devil's claw might inhibit CYP2C19, although this has not been reported in humans.

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

Theoretically, devil's claw might increase levels of drugs metabolized by CYP2C9.
In vitro research shows that devil's claw might inhibit CYP2C9, although this has not been reported in humans.

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

Theoretically, devil's claw might increase levels of drugs metabolized by CYP3A4.
In vitro research shows that devil's claw might inhibit CYP3A4, although this has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, Devil's claw might increase the activity of warfarin.
In one case report, purpura occurred in a patient taking warfarin and devil's claw concurrently. This might indicate over-anticoagulation. It is unclear if this was due to Devil's claw or other contributing factors.

Likelihood Possible Evidence D
H2-Blockers

Theoretically, devil's claw might decrease the effectiveness of H2-blockers.
Devil's claw has been reported to increase stomach acid, which might interfere with the effects of H2-blockers.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, devil's claw might increase levels of P-glycoprotein substrates.
In vitro research shows that devil's claw inhibits P-glycoprotein, which transports many drugs out of cells. This might increase intracellular levels of P-glycoprotein substrates, although it is unclear if this effect would be clinically important.

Likelihood Possible Evidence D
Proton Pump Inhibitors (Ppis)

Theoretically, devil's claw might decrease the effectiveness of PPIs.
Devil's claw has been reported to increase stomach acid, which might interfere with the effects of PPIs.

Likelihood Possible Evidence D
Devil's Claw root extract full monograph & interactions

Peppermint5 drug types · 796 drugs

Cyclosporine (Neoral, Sandimmune)

Theoretically, peppermint oil might increase the levels and adverse effects of cyclosporine.
In animal research, peppermint oil inhibits cyclosporine metabolism and increases cyclosporine levels. Inhibition of cytochrome P450 3A4 (CYP3A4) may be partially responsible for this interaction. An interaction between peppermint oil and cyclosporine has not been reported in humans.

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

Theoretically, peppermint might increase the levels of CYP2C19 substrates.
In vitro research shows that peppermint oil inhibits CYP2C19. So far, this interaction has not been reported in humans.

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

Theoretically, peppermint might increase the levels of CYP2C9 substrates.
In vitro research shows that peppermint oil inhibits CYP2C9. So far, this interaction has not been reported in humans.

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

Theoretically, peppermint might increase the levels of CYP3A4 substrates.
Clinical research in healthy volunteers shows that a single dose of peppermint oil 600 mg inhibits CYP3A4 enzymes and increases the AUC of felodipine, a CYP3A4 substrate. However, in vitro research suggests that peppermint oil only inhibits CYP3A4 at very high concentrations.

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

Theoretically, peppermint might increase the levels of CYP1A2 substrates.
In vitro and animal research shows that peppermint oil and peppermint leaf inhibit CYP1A2. However, in clinical research, peppermint tea did not significantly affect the metabolism of caffeine, a CYP1A2 substrate. It is possible that the 6-day duration of treatment may have been too short to identify a difference.

Likelihood Possible Evidence B
Peppermint full monograph & interactions

organic Lemongrass3 drug types · 708 drugs

Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, lemongrass might decrease the metabolism of CYP3A4 substrates.
Animal research shows that lemongrass and its constituent citral inhibit CYP3A4.

Likelihood Possible Evidence D
Glucuronidated Drugs

Theoretically, lemongrass might increase the clearance and decrease the levels of glucuronidated drugs.
Animal research shows that lemongrass and its constituent citral induce uridine diphosphoglucuronosyl transferase (UGT), the major phase 2 enzyme that is responsible for glucuronidation.

Likelihood Possible Evidence D
Pentobarbital (Nembutal)

Theoretically, lemongrass might increase the effects and adverse effects of pentobarbital.
Animal research shows that high doses of lemongrass essential oil increases sleep time and decreases time to fall asleep in animals administered pentobarbital.

Likelihood Possible Evidence D
organic Lemongrass full monograph & interactions

Celery8 drug types · 651 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, celery root might increase the risk of bleeding when taken with anticoagulant/antiplatelet drugs.
Celery root contains the constituents falcarinol and falcarindiol. Laboratory research suggests that these constituents can inhibit platelet aggregation. This effect has not been reported in humans.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, celery seed extract might have additive effects with antihypertensive drugs.
Clinical research suggests that taking celery seed extract may reduce daytime systolic blood pressure by about 12 mmHg compared to less than 1 mmHg with placebo.

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

Theoretically, celery might increase levels of drugs metabolized by CYP1A2.
In vitro and animal research suggests that constituents of celery can inhibit CYP1A2. This effect has not been reported in humans.

Likelihood Possible Evidence D
Levothyroxine (Synthroid, Others)

Theoretically, celery seed might decrease the effects of levothyroxine.
Several cases of hypothyroidism with low T4 levels have been reported in people who were previously stabilized on levothyroxine and then started taking celery seed tablets. They presented with symptoms such as lethargy, bloating, and dry skin, and recovered when celery seed was stopped. However, celery stem and leaf has been associated with case reports of hyperthyroidism in patients with no pre-existing thyroid disorders.

Likelihood Possible Evidence D
Lithium

Theoretically, celery might reduce excretion and increase levels of lithium due to potential diuretic effects.
Celery is thought to have diuretic properties. However, this effect has not been confirmed in humans.

Likelihood Probable Evidence D
Venlafaxine (Effexor)

Theoretically, celery root extract might increase blood levels of venlafaxine.
There is one case report of a patient who experienced medication-induced bipolar disorder after beginning to take celery root extract 1000 mg daily along with venlafaxine 75 mg and St. John's wort 600 mg daily. Symptoms included confusion, speech abnormalities, manic affect, and visual hallucinations. The plasma level of venlafaxine was 476.8 ng/mL (normal range 195-400 ng/mL). It is theorized that celery root increased venlafaxine levels by inhibiting cytochrome P450 2D6.

Likelihood Possible Evidence D
Acetaminophen (Tylenol, Others)

Theoretically, celery juice might increase the effects and side effects of acetaminophen.
Animal research suggests that concomitant use of celery juice plus acetaminophen prolongs the effects of acetaminophen. This effect has been attributed to a decrease in hepatic cytochrome P450 activity. However, other animal research shows that pretreatment with celery root extract protects against acetaminophen-induced acute liver failure. These effects have not been reported in humans.

Likelihood Possible Evidence D
Photosensitizing Drugs

Theoretically, celery might increase the risk of photosensitivity reactions when taken with photosensitizing drugs.
Laboratory research shows that celery contains photosensitizing agents such as phenols and psoralens.

Likelihood Possible Evidence D
Celery full monograph & interactions

organic Alfalfa6 drug types · 583 drugs

Warfarin (Coumadin)

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

Likelihood Probable Evidence D
Antidiabetes Drugs

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

Likelihood Possible Evidence D
Contraceptive Drugs

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

Likelihood Possible Evidence D
Estrogens

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

Likelihood Possible Evidence D
Immunosuppressants

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

Likelihood Possible Evidence D
Photosensitizing Drugs

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

Likelihood Possible Evidence D
organic Alfalfa full monograph & interactions

Spearmint2 drug types · 579 drugs

Cns Depressants

Theoretically, spearmint might alter the sedative effects of CNS depressants.
Animal research suggests that (-)-carvone, a major constituent of spearmint, has sedative effects. However, in humans, chewing spearmint-flavored gum induced arousal effects.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, high doses of spearmint might increase the risk of liver damage when taken with hepatotoxic drugs.
Animal research suggests that drinking spearmint tea for 30 days can increase markers of liver damage, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and cause liver degeneration and necrosis, in a dose-dependent manner. This effect has not been reported in humans.

Likelihood Possible Evidence D
Spearmint full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Joint Comfort, from the product label.

Yogi

See all Yogi products
Name
YOGI A product of East West Tea Company, LLC
Street Address
950 International Way
City
Springfield
State
OR
ZipCode
97477
Web Address
www.yogiproducts.com
Pharmacist Counseling Corner

Joint Comfort by Yogi: Common Questions

Does Joint Comfort by Yogi interact with any medications?
Yes. Based on its ingredients, Joint Comfort has a known interaction with 1,627 medications, including 15 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Joint Comfort contains 10 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.

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

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Label information is sourced from the NIH Dietary Supplement Label Database and reflects the product version on file; always read your actual product label. This page is for education only and is not a substitute for professional medical advice. Confirm with your pharmacist or doctor before combining supplements and medications.

Joint Comfort label
Go deeper

The Full Monographs Behind Joint Comfort’s Ingredients

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

Herb & supplement monograph

Peppermint

Interacts with 796 drugs

Peppermint is a popular herb with the best evidence supporting enteric-coated peppermint oil for easing IBS symptoms. It is generally well tolerated for most adults, but it can cause heartbu...

Read the full Peppermint monograph → Herb & supplement monograph

Celery

Interacts with 651 drugs

Celery is a common vegetable that is also taken as a seed extract or oil supplement, mainly for blood pressure, fluid retention, and joint discomfort. Human evidence for these supplement use...

Read the full Celery 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

Devil's Claw

Interacts with 804 drugs

Devil's claw is a southern African plant used mainly for arthritis and back pain, and some studies suggest it may help ease these types of discomfort. The evidence is moderate at best, and p...

Read the full Devil's Claw monograph → Herb & supplement monograph

Yucca

Yucca is a desert plant traditionally used for joint pain, arthritis, and digestion, and it contains compounds called saponins thought to have anti-inflammatory effects. Human evidence for t...

Read the full Yucca monograph → Herb & supplement monograph

Spearmint

Interacts with 579 drugs

Spearmint is a common culinary mint that is generally safe in food and tea amounts. Early research suggests possible benefits for digestion, mild hormone-related issues (such as excess facia...

Read the full Spearmint monograph → Herb & supplement monograph

Lemongrass

Interacts with 708 drugs

Lemongrass is a fragrant tropical grass widely used as a cooking herb, a tea, and an aromatherapy oil. It is generally considered safe in the small amounts used in food, but most of its clai...

Read the full Lemongrass 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

Alfalfa

Interacts with 583 drugs

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

Read the full Alfalfa monograph → Herb & supplement monograph

Cat's Claw

Interacts with 962 drugs

Cat's claw is a South American vine traditionally used for inflammation, joint pain, and immune support. Some small studies hint it may help with arthritis symptoms, but the overall evidence...

Read the full Cat's Claw monograph →
Sources

Sources & How We Checked

Joint Comfort'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 501 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.

Peppermint 41 references
  1. Liu JH, Chen GH, Yeh HZ, et al. Enteric-coated peppermint-oil capsules in the treatment of irritable bowel syndrome: a prospective, randomized trial. J Gastroenterol 1997;32:765-8. PubMed
  2. Pittler MH, Ernst E. Peppermint oil for irritable bowel syndrome: a critical review and metaanalysis. Am J Gastroenterol 1998;93:1131-5. PubMed
  3. Kline RM, Kline JJ, Di Palma J, Barbero GJ. Enteric-coated, pH-dependent peppermint oil capsules for the treatment of irritable bowel syndrome in children. J Pediatr 2001;138:125-8. PubMed
  4. Madisch A, Heydenreich CJ, Wieland V, et al. Treatment of functional dyspepsia with a fixed peppermint oil and caraway oil combination preparation as compared to cisapride. A multicenter, reference-controlled, double-blind equivalence study. Arzneimittel
  5. May B, Kuntz HD, Kieser M, Kohler S. Efficacy of a fixed peppermint oil/caraway oil combination in non-ulcer dyspepsia. Arzneimittelforschung 1996;46:1149-53.
  6. Micklefield GH, Greving I, May B. Effects of peppermint oil and caraway oil on gastroduodenal motility. Phytother Res 2000;14:20-3. DOI
  7. Morton CA, Garioch J, Todd P, et al. Contact sensitivity to menthol and peppermint in patients with intra-oral symptoms. Contact Dermatitis 1995;32:281-4. PubMed
  8. May B, Kohler S, Schneider B. Efficacy and tolerability of a fixed combination of peppermint oil and caraway oil in patients suffering from functional dyspepsia. Aliment Pharmacol Ther 2000;14:1671-7. PubMed
  9. Nash P, Gould SR, Bernardo DE. Peppermint oil does not relieve the pain of irritable bowel syndrome. Br J Clin Pract 1986;40:292-3. DOI
  10. Rees WD, Evans BK, Rhodes J. Treating irritable bowel syndrome with peppermint oil. Br Med J 1979;2:835-6. PubMed
  11. Davies SJ, Harding LM, Baranowski AP. A novel treatment of postherpetic neuralgia using peppermint oil. Clin J Pain 2002;18:200-2. PubMed
  12. Weston CF. Anal burning and peppermint oil. Postgrad Med J 1987;63:717. PubMed
  13. Dresser GK, Wacher V, Wong S, et al. Evaluation of peppermint oil and ascorbyl palmitate as inhibitors of cytochrome P4503A4 activity in vitro and in vivo. Clin Pharmacol Ther 2002;72:247-55. PubMed
  14. Wacher VJ, Wong S, Wong HT. Peppermint oil enhances cyclosporine oral bioavailability in rats: comparison with D-alpha-tocopheryl poly(ethylene glycol 1000) succinate (TPGS) and ketoconazole. J Pharm Sci 2002;91:77-90.
  15. Lawson MJ, Knight RE, Tran K, et al. Failure of enteric-coated peppermint oil in the irritable bowel syndrome: a randomized double-blind crossover study. J Gastroenterol Hepatol 1988;3:235-8. DOI
  16. Unger M, Frank A. Simultaneous determination of the inhibitory potency of herbal extracts on the activity of six major cytochrome P450 enzymes using liquid chromatography/mass spectrometry and automated online extraction. Rapid Commun Mass Spectrom 2004;1 PubMed
  17. Maliakal PP, Wanwimolruk S. Effect of herbal teas on hepatic drug metabolizing enzymes in rats. J Pharm Pharmacol 2001;53:1323-9. PubMed
  18. Rogers SN, Pahor AL. A form of stomatitis induced by excessive peppermint consumption. Dent Update 1995;22:36-7.
  19. Cappello G, Spezzaferro M, Grossi L, et al. Peppermint oil (Mintoil) in the treatment of irritable bowel syndrome: a prospective double blind placebo-controlled randomized trial. Dig Liver Dis 2007;39:530-6. PubMed
  20. Moghadam BK, Gier R, and Thurlow T. Extensive oral mucosal ulcerations caused by misuse of a commercial mouthwash. Cutis 1999;64:131-134.
  21. Andersen, K. E. Contact allergy to toothpaste flavors. Contact Dermatitis 1978;4(4):195-198. PubMed
  22. Barnard, D. R. Repellency of essential oils to mosquitoes (Diptera: Culicidae). J Med Entomol. 1999;36(5):625-629. PubMed
  23. Tamir, S., Davidovich, Z., Attal, P., and Eliashar, R. Peppermint oil chemical burn. Otolaryngol.Head Neck Surg. 2005;133(5):801-802. PubMed
  24. Kalavala, M., Hughes, T. M., Goodwin, R. G., Anstey, A. V., and Stone, N. M. Allergic contact dermatitis to peppermint foot spray. Contact Dermatitis 2007;57(1):57-58. PubMed
  25. Vermaat, H., van Meurs, T., Rustemeyer, T., Bruynzeel, D. P., and Kirtschig, G. Vulval allergic contact dermatitis due to peppermint oil in herbal tea. Contact Dermatitis 2008;58(6):364-365. PubMed
  26. Merat, S., Khalili, S., Mostajabi, P., Ghorbani, A., Ansari, R., and Malekzadeh, R. The effect of enteric-coated, delayed-release peppermint oil on irritable bowel syndrome. Dig.Dis.Sci. 2010;55(5):1385-1390. PubMed
  27. Tran, A., Pratt, M., and DeKoven, J. Acute allergic contact dermatitis of the lips from peppermint oil in a lip balm. Dermatitis 2010;21(2):111-115. DOI
  28. Hitz, Lindenmuller, I and Lambrecht, J. T. Oral care. Curr Probl.Dermatol 2011;40:107-115.
  29. Shavakhi, A., Ardestani, S. K., Taki, M., Goli, M., and Keshteli, A. H. Premedication with peppermint oil capsules in colonoscopy: a double blind placebo-controlled randomized trial study. Acta Gastroenterol Belg 2012;75(3):349-353.
  30. Lech, Y., Olesen, K. M., Hey, H., Rask-Pedersen, E., Vilien, M., and Ostergaard, O. [Treatment of irritable bowel syndrome with peppermint oil. A double- blind study with a placebo]. Ugeskr.Laeger 10-3-1988;150(40):2388-2389.
  31. Parys, B. T. Chemical burns resulting from contact with peppermint oil mar: a case report. Burns Incl.Therm.Inj. 1983;9(5):374-375. PubMed
  32. Bayat R, Borici-Mazi R. A case of anaphylaxis to peppermint. Allergy Asthma Clin Immunol. 2014;10(1):6. PubMed
  33. Rich G, Shah A, Koloski N, et al. A randomized placebo-controlled trial on the effects of Menthacarin, a proprietary peppermint- and caraway-oil-preparation, on symptoms and quality of life in patients with functional dyspepsia. Neurogastroenterol Motil 2 PubMed
  34. Douros A, Bronder E, Andersohn F, et al. Herb-Induced Liver Injury in the Berlin Case-Control Surveillance Study. Int J Mol Sci 2016;17(1). PubMed
  35. Begas E, Tsioutsiouliti A, Kouvaras E, et al. Effects of peppermint tea consumption on the activities of CYP1A2, CYP2A6, Xanthine Oxidase, N-acetyltranferase-2 and UDP-glucuronosyltransferases-1A1/1A6 in healthy volunteers. Food Chem Toxicol 2017;100:80-9 PubMed
  36. Cash BD, Epstein MS, Shah SM. A Novel Delivery System of Peppermint Oil Is an Effective Therapy for Irritable Bowel Syndrome Symptoms. Dig Dis Sci 2016;61(2):560-71. PubMed
  37. Elsaie LT, El Mohsen AM, Ibrahim IM, Mohey-Eddin MH, Elsaie ML. Effectiveness of topical peppermint oil on symptomatic treatment of chronic pruritus. Clin Cosmet Investig Dermatol 2016;9:333-8. PubMed
  38. Wu J, Xu R, Zhan R, et al. Effective symptomatic treatment for severe and intractable pruritus associated with severe burn-induced hypertrophic scars: A prospective, multicenter, controlled trial. Burns 2016;42(5):1059-66. PubMed
  39. Weerts ZZRM, Masclee AAM, Witteman BJM, et al. Efficacy and safety of peppermint oil in a randomized, double-blind trial of patients with irritable bowel syndrome. Gastroenterology. 2020;158(1):123-136. PubMed
  40. Nee J, Ballou S, Kelley JM, et al. Peppermint Oil Treatment for Irritable Bowel Syndrome: A Randomized Placebo-Controlled Trial. Am J Gastroenterol 2021;116(11):2279-2285. PubMed
  41. Ingrosso MR, Ianiro G, Nee J, et al. Systematic review and meta-analysis: efficacy of peppermint oil in irritable bowel syndrome. Aliment Pharmacol Ther 2022;56(6):932-41. PubMed

See these in context on the Peppermint monograph →

Celery 48 references
  1. Newall CA, Anderson LA, Philpson JD. Herbal Medicine: A Guide for Healthcare Professionals. London, UK: The Pharmaceutical Press, 1996.
  2. The Review of Natural Products by Facts and Comparisons. St. Louis, MO: Wolters Kluwer Co., 1999.
  3. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  4. Heck AM, DeWitt BA, Lukes AL. Potential interactions between alternative therapies and warfarin. Am J Health Syst Pharm 2000;57:1221-7. DOI
  5. Gral N, Beani JC, Bonnot D, et al. [Plasma levels of psoralens after celery ingestion]. Ann Dermatol Venereol 1993;120:599-603.
  6. Moses, G. Thyroxine interacts with celery seed tablets? Australian Prescriber 2001;24:6-7. DOI
  7. Ciganda C, and Laborde A. Herbal infusions used for induced abortion. J Toxicol.Clin Toxicol. 2003;41:235-239. PubMed
  8. Jakovljevic, V., Raskovic, A., Popovic, M., and Sabo, J. The effect of celery and parsley juices on pharmacodynamic activity of drugs involving cytochrome P450 in their metabolism. Eur.J Drug Metab Pharmacokinet. 2002;27(3):153-156. PubMed
  9. Wang, L., Sterling, B., and Don, P. Berloque dermatitis induced by "Florida water". Cutis 2002;70(1):29-30.
  10. Weber, I. C., Davis, C. P., and Greeson, D. M. Phytophotodermatitis: the other "lime" disease. J Emerg.Med 1999;17(2):235-237. PubMed
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See these in context on the Celery monograph →

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Parts of this content are provided by the Therapeutic Research Center, LLC.

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.

© 2021 Therapeutic Research Center, LLC

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