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Dietary supplement

Calm Bowels Ingredients & Drug Interactions

by Dr. Gumman’s Integrative

Capsule Category: Other Combinations
Most serious interaction: Moderate
The interaction bottom line Most serious interaction: Moderate

Calm Bowels is a dietary supplement by Dr. Gumman’s Integrative with 13 active ingredients. Its ingredients are commonly taken for digestive support for protein digestion, wound cleaning (debridement of dead tissue), sore throat and inflammation.Based on those ingredients, 1,450 medications have a known interaction with it, the most serious rated moderate. The ingredients most likely to interact are TriCurmin, Deglycyrrhizinated Licorice Root Extract, Gingerine. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Calm Bowels by Dr. Gumman’s Integrative

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

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

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

Why this rating?
  • The label discloses an exact amount for 0 of its 13 active ingredients.
  • “Calm Bowels Proprietary Blend of Standardized Extracts” is a proprietary blend — the label gives one combined amount (550 mg) without saying how much of each component you get.

Calm Bowels contains 13 active ingredients: papain (a protein-digesting enzyme from papaya), bromelain (a similar enzyme from pineapple), deglycyrrhizinated licorice root extract (licorice with a key compound removed), pomegranate fruit extract, fennel seed extract, bilwin (bael fruit), boswin (frankincense), peppermint leaf extract, amlowin (Indian gooseberry), tricurmin (turmeric), androwin (andrographis), and gingerine (ginger), plus a proprietary blend of standardized extracts. The product also contains a vegan capsule as its inactive ingredient.

Does it work?

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

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

Why this rating?
  • The label markets this product for: gastrointestinal inflammatory and immune response support.
  • We looked for evidence on: Abdominal pain, Colic, Constipation, Chemotherapy-induced constipation, Chemotherapy-induced diarrhea, Chemotherapy-induced nausea and vomiting (CINV) — and 4 related terms.
  • The strongest evidence on file: Peppermint is rated "Possibly Effective" for Chemotherapy-induced nausea and vomiting (CINV) (Natural Medicines).
  • Also on file: Ginger is rated "Possibly Ineffective" for Chemotherapy-induced nausea and vomiting (CINV).
  • Also on file: Fennel is rated "Insufficient Reliable Evidence To Rate" for Constipation, Cough, Nausea and vomiting, Colic.

The evidence supporting these ingredients is mixed. Peppermint is likely effective for irritable bowel syndrome and possibly effective for indigestion and nausea.

Ginger is possibly effective for pregnancy-related nausea and vomiting, menstrual cramps, and osteoarthritis. Turmeric is possibly effective for depression, high cholesterol, hay fever, and indigestion.

Licorice is possibly effective for eczema and canker sores. Andrographis is possibly effective for ulcerative colitis, sore throat, and osteoarthritis.

Pomegranate is possibly effective for high blood pressure. Most other ingredients—papain, bromelain, fennel, bael, frankincense, and Indian gooseberry—lack reliable evidence in our data for their claimed uses, though some have insufficient evidence rather than proven ineffectiveness.

The evidence, ingredient by ingredient Papain Bromelain Licorice Maritime Pine Pomegranate Fennel Bael Frankincense

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

Most of these ingredients are generally well tolerated at typical doses. Peppermint leaf is likely safe in pregnancy; ginger is often used for morning sickness but should be discussed with your doctor first.

However, several ingredients carry pregnancy cautions: avoid concentrated papain, bromelain, fennel, bael, frankincense, and turmeric supplements during pregnancy due to limited safety data or theoretical concerns. Licorice supplements should be avoided in pregnancy.

Breastfeeding safety data is sparse for most ingredients; food amounts are generally safer than supplements. Common mild side effects include gastrointestinal upset (diarrhea, nausea, abdominal discomfort), headache, and allergic reactions in sensitive individuals.

Peppermint and ginger can cause heartburn or mouth irritation at high doses. Turmeric has rare reports of liver damage with prolonged use.

Side effects, ingredient by ingredient Papain Bromelain Licorice Maritime Pine Pomegranate Fennel Bael Frankincense

Meds to double-check

Moderate interaction found
Known Interaction Concern · database check
Moderate identified

The most serious documented interaction for these ingredients is Moderate. Check your medications for a personalized result.

Why this rating?
  • 12 of the 13 matched ingredients can interact with medications — Papain, Bael, Fennel, Pomegranate, Turmeric, among others.
  • The most serious interaction on file is rated Moderate.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; heart-rhythm medications.
  • For scale: 1,451 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 with your pharmacist or doctor before taking Calm Bowels if you're on warfarin or other blood thinners (Moderate risk from papain, bromelain, fennel, Indian gooseberry, andrographis, and ginger); diabetes medications (Moderate risk from bael, Indian gooseberry, and ginger); blood pressure drugs (Moderate risk from pomegranate and andrographis); hormonal contraceptives or hormone therapy (Moderate risk from fennel); heart medications like digoxin (Moderate risk from licorice); or any drug metabolized by cytochrome P450 enzymes, since multiple ingredients inhibit them.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFormula with limited ingredient disclosure with some supporting evidence for its stated purpose. Moderate medication interactions have been identified, and safety information is well characterized.

Calm Bowels combines digestive and anti-inflammatory herbs, but its ingredient interactions with blood thinners, diabetes medications, and hormone therapies are significant. If you take warfarin, blood pressure medication, diabetes drugs, hormonal contraceptives, or any prescription at all, run it through the interaction checker on this page before starting.

Pregnant or breastfeeding individuals should talk to their doctor or pharmacist first, as most ingredients lack robust safety data in those settings.

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

Assessment coverage: 13 of 13 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Jan 23, 2025.

This Scorecard evaluates available label information, ingredient evidence, and known medication-safety considerations. It does not independently verify product identity, purity, potency, contamination, or manufacturing quality. How these ratings are computed

At a glance

General information

Key facts about Calm Bowels, straight from the product label.

Brand Dr. Gumman’s Integrative
Barcode (UPC) 817339020957
Net contents 120 Vegan Capsule(s)
Market status On market
Date entered into DSLD Jan 23, 2025
DSLD ID 325824
Product type Other Combinations
Supplement form Capsule
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Vegan, Vegetarian, Adult (18 - 50 Years), Kosher, Halal, Dairy 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 Calm Bowels by Dr. Gumman’s Integrative, 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 Vegan Capsule(s)
Maximum serving Sizes:
2 Vegan Capsule(s)
Servings per container
120
UPC/BARCODE
817339020957
IngredientAmount% DV
Papain0 NP--
Bromelain0 NP--
Deglycyrrhizinated Licorice Root Extract0 NP--
Pine Bark Extract0 NP--
Pomegranate Fruit Extract0 NP--
Calm Bowels Proprietary Blend of Standardized Extracts550 mg--
Fennel Seed Extract0 NP--
Bilwin0 NP--
Boswin0 NP--
Peppermint Leaf Extract0 NP--
Amlowin0 NP--
TriCurmin0 NP--
Androwin0 NP--
Gingerine0 NP--

Other ingredients: Vegan Capsule

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.
Formula

Calm Bowels supports a harmonious Gastrointestinal inflammatory and immune response. It soothes and rejuvenates the Gastrointestinal tract. This powerful, synergistic formula of Dr. Gumman & team integrates the best of Modern Science, Traditional Ayurvedic, and Chinese Medicines. Calm Bowels is synergized with Gingerine, our proprietary extract of ginger to boost absorption, bioactivity, and efficacy.

Halal

Kosher

Suggested/Recommended/Usage/Directions

Suggested use: 1-2 capsules once or twice daily with or after meals or as directed by your healthcare practitioner.

Precautions

Caution: Keep out of reach of children.

Do not use if inner seal is missing or broken.

Pregnant and nursing women, individuals taking medications, or persons with a health condition should consult their healthcare professional before using this product.

Storage

Protect from heat, light, and moisture.

Seals/Symbols

Harmonious and Sustainable GMP Certified GMP Manufactured GMP Certified Facility Vegan

Formulation

Vegan

Eco-Friendly

Clinical Grade Certified Lab Tested

Gastrointestinal comfort

Made with love in the USA

No: Soy, dairy, gluten, salt, sugar, artificial colors, artificial flavors or artificial sweeteners. Non-GMO. No fillers.

[Contains 550 mg active ingredients.] Color variations are natural Nothing else, pure goodness!

General Statements

O-K!

FDA Statement of Identity

Pure Herbal Supplement

Brand IP Statement(s)

Calm Bowels, Bilwin, Boswin, Amlowin, TriCurmin, Androwin, and Gingerine are trademarks of Harmony Nutraceuticals, LLC.

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.

See for yourself

Calm Bowels by Dr. Gumman’s Integrative label

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

What’s inside

The Ingredients in Calm Bowels by Dr. Gumman’s Integrative

These are the 13 active ingredients this product is made of. Select any to open its full monograph.

Serving size1 Vegan Capsule(s) Dosage formCapsule Servings per container120 Amounts shown are per serving.

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

Calm Bowels Proprietary Blend of Standardized Extracts

550 mg per serving

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

Interaction report

Calm Bowels by Dr. Gumman’s Integrative Drug Interactions

Want to check YOUR meds against Calm Bowels?

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
1,450Drugs
1,432 Moderate 18 Minor

Ingredients driving the most interactions

TriCurmin 1,133
Gingerine 1,007
Bilwin 819

Each ingredient & the kinds of drugs it affects

For each ingredient in Calm Bowels 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.

TriCurmin24 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

Deglycyrrhizinated Licorice Root Extract18 drug types · 1,040 drugs

Antihypertensive Drugs

Theoretically, licorice might reduce the effects of antihypertensive drugs.
In human research, licorice increases blood pressure in a dose-dependent manner.

Likelihood Possible Evidence B
Cisplatin (Platinol-Aq)

Theoretically, licorice might reduce the effects of cisplatin.
In animal research, licorice diminished the therapeutic efficacy of cisplatin.

Likelihood Possible Evidence D
Corticosteroids

Theoretically, concomitant use of licorice and corticosteroids might increase the side effects of corticosteroids.
Case reports suggest that concomitant use of licorice and oral corticosteroids, such as hydrocortisone, can potentiate the duration of activity and increase blood levels of corticosteroids. Additionally, in one case report, a patient with neurogenic orthostatic hypertension stabilized on fludrocortisone 0.1 mg twice daily developed pseudohyperaldosteronism after recent consumption of large amounts of black licorice.

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

Theoretically, licorice might increase levels of drugs metabolized by CYP2B6.
In vitro research shows that licorice extract and glabridin, a licorice constituent, inhibit CYP2B6 isoenzymes. Licorice extract from the species G. uralensis seems to inhibit CYP2B6 isoenzymes to a greater degree than G. glabra extract in vitro. Theoretically, these species of licorice might increase levels of drugs metabolized by CYP2B6; however, these interactions have not yet been reported in humans.

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

Theoretically, licorice might increase levels of drugs metabolized by CYP2C19.
In vitro, licorice extracts from the species G. glabra and G. uralensis inhibit CYP2C19 isoenzymes in vitro. Theoretically, these species of licorice might increase levels of drugs metabolized by CYP2C19; however, this interaction has not yet been reported in humans.

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

Theoretically, licorice might increase levels of drugs metabolized by CYP2C8.
In vitro, licorice extract from the species G. glabra and G. uralensis inhibits CYP2C8 isoenzymes. Theoretically, these species of licorice might increase levels of drugs metabolized by CYP2C8; however, this interaction has not yet been reported in humans.

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

Theoretically, licorice might increase or decrease levels of drugs metabolized by CYP2C9.
There is conflicting evidence about the effect of licorice on CYP2C9 enzyme activity. In vitro research shows that extracts from the licorice species G. glabra and G. uralensis moderately inhibit CYP2C9 isoenzymes. However, evidence from an animal model shows that licorice extract from the species G. uralensis can induce hepatic CYP2C9 activity. Until more is known, licorice should be used cautiously in people taking CYP2C9 substrates.

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

Theoretically, licorice might increase or decrease levels of drugs metabolized by CYP3A4.
Pharmacokinetic research shows that the licorice constituent glycyrrhizin, taken in a dosage of 150 mg orally twice daily for 14 days, modestly decreases the area under the concentration-time curve of midazolam by about 20%. Midazolam is a substrate of CYP3A4, suggesting that glycyrrhizin modestly induces CYP3A4 activity. Animal research also shows that licorice extract from the species G. uralensis induces CYP3A4 activity. However, licorice extract from G. glabra species appear to inhibit CYP3A4-induced metabolism of testosterone in vitro. It is thought that the G. glabra inhibits CYP3A4 due to its constituent glabridin, which is a moderate CYP3A4 inhibitor in vitro and not present in other licorice species. Until more is known, licorice should be used cautiously in people taking CYP3A4 substrates.

Likelihood Possible Evidence B
Digoxin (Lanoxin)

Theoretically, concomitant use of licorice with digoxin might increase the risk of cardiac toxicity.
Overuse or misuse of licorice with cardiac glycoside therapy might increase the risk of cardiac toxicity due to potassium loss.

Likelihood Possible Evidence D
Diuretic Drugs

Theoretically, concomitant use of licorice with diuretic drugs might increase the risk of hypokalemia.
Overuse of licorice might compound diuretic-induced potassium loss. In one case report, a 72-year-old male with a past medical history of hypertension, type 2 diabetes, hyperlipidemia, arrhythmia, stroke, and hepatic dysfunction was hospitalized with severe hypokalemia and uncontrolled hypertension due to pseudohyperaldosteronism. This was thought to be provoked by concomitant daily consumption of a product containing 225 mg of glycyrrhizin, a constituent of licorice, and hydrochlorothiazide 12.5 mg for 1 month.

Likelihood Possible Evidence D
Estrogens

Theoretically, licorice might increase or decrease the effects of estrogen therapy.
Theoretically, licorice might interfere with estrogen therapy due to estrogenic and anti-estrogenic effects.

Likelihood Possible Evidence D
Loop Diuretics

Theoretically, loop diuretics might increase the mineralocorticoid effects of licorice.
Theoretically, loop diuretics might enhance the mineralocorticoid effects of licorice by inhibiting the enzyme that converts cortisol to cortisone; however, bumetanide (Bumex) does not appear to have this effect.

Likelihood Possible Evidence D
Midazolam (Versed)

Theoretically, licorice might decrease levels of midazolam.
In humans, the licorice constituent glycyrrhizin appears to moderately induce the metabolism of midazolam. This is likely due to induction of cytochrome P450 3A4 by licorice. Until more is known, licorice should be used cautiously in people taking midazolam.

Likelihood Possible Evidence B
P-Glycoprotein Substrates

Theoretically, licorice might decrease the absorption of P-glycoprotein substrates.
In vitro research shows that licorice can increase P-glycoprotein activity.

Likelihood Possible Evidence D
Paclitaxel (Abraxane, Onxol)

Theoretically, licorice might decrease plasma levels and clinical effects of paclitaxel.
Multiple doses of licorice taken concomitantly with paclitaxel might reduce the effectiveness of paclitaxel. Animal research shows that licorice 3 grams/kg given orally for 14 days before intravenous administration of paclitaxel decreases the exposure to paclitaxel and increases its clearance. Theoretically, this occurs because licorice induces cytochrome P450 3A4 enzymes, which metabolize paclitaxel. Notably, a single dose of licorice did not affect exposure or clearance of paclitaxel.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, licorice might decrease plasma levels and clinical effects of warfarin.
Licorice seems to increase metabolism and decrease levels of warfarin in animal models. This is likely due to induction of cytochrome P450 2C9 (CYP2C9) metabolism by licorice. Advise patients taking warfarin to avoid taking licorice.

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

Theoretically, licorice might decrease the levels and clinical effects of CYP1A2 substrates.
In vitro research shows that licorice induces CYP1A2 enzymes.

Likelihood Possible Evidence D
Methotrexate (Trexall, Others)

Theoretically, licorice might increase levels of methotrexate.
Animal research suggests that intravenous administration of glycyrrhizin, a licorice constituent, and high-dose methotrexate may delay methotrexate excretion and increase systemic exposure, leading to transient elevations in liver enzymes and total bilirubin. This interaction has not yet been reported in humans.

Likelihood Unlikely Evidence D

Gingerine14 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

Pomegranate Fruit Extract9 drug types · 922 drugs

Ace Inhibitors (Aceis)

Theoretically, taking pomegranate with ACEIs might increase the risk of adverse effects.
Pomegranate juice is thought to have ACE inhibitor-like effects.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking pomegranate with antihypertensive drugs might increase the risk of hypotension.
Consuming pomegranate juice can modestly lower blood pressure.

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

Theoretically, pomegranate might increase levels of drugs metabolized by CYP2D6.
In vitro, pomegranate juice inhibits CYP2D6. However, the clinical significance of this potential interaction in humans is not known.

Likelihood Possible Evidence D
Rosuvastatin (Crestor)

Theoretically, taking pomegranate with rosuvastatin might increase the risk of adverse effects.
In one case, a patient taking rosuvastatin 5 mg every other day in combination with ezetimibe 10 mg daily developed rhabdomyolysis after drinking pomegranate juice 200 mL twice weekly for 3 weeks. This patient had a history of elevated creatine kinase levels while not receiving any statin treatment. This suggests a possible underlying myopathy and predisposition to rhabdomyolysis.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, pomegranate might increase warfarin levels and increase the risk of bleeding. Also, discontinuing regular consumption of pomegranate juice might decrease warfarin levels.
In one case report, a patient had a stable, therapeutic bleeding time, as measured by international normalized ratio (INR), while taking warfarin in combination with pomegranate juice 2-3 times per week. The patient became subtherapeutic within about 10 days after discontinuing pomegranate juice, which required a warfarin dose increase. In another case report, a patient with a stable INR for over one year presented with an INR of 14. The patient noted no changes to medications or diet but did report consuming around 3 liters of pomegranate juice over the previous week. The patient's INR stabilized upon moderation of pomegranate juice consumption. The mechanism of this potential interaction is unclear.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, taking pomegranate with carbamazepine might increase the risk of adverse effects, although research suggests this interaction is unlikely to be clinically significant.
Animal research shows that pomegranate juice may inhibit cytochrome P450 3A4 (CYP3A4) metabolism of carbamazepine and increase levels of carbamazepine by 1.5 times without prolonging the elimination half-life. This suggests that pomegranate juice inhibits intestinal CYP3A4, but might not inhibit hepatic CYP3A4. However, some human research suggests that pomegranate does not significantly inhibit CYP3A4 drug metabolism in humans.

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

Theoretically, pomegranate might increase levels of drugs metabolized by CYP2C9.
Some animal and in vitro research shows that pomegranate juice inhibits intestinal, but not hepatic, CYP2C9 isoenzyme activity. However, clinical research shows that neither pomegranate juice nor pomegranate extract have a significant effect on CYP2C9 activity in humans.

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

Theoretically, pomegranate might increase levels of drugs metabolized by CYP3A4, but most research suggests this interaction is unlikely to be clinically significant.
Pomegranate contains several polyphenols that have individually been shown to inhibit CYP3A4. However, there is contradictory evidence about the effect of whole pomegranate juice on CYP3A4 activity. In vitro, pomegranate juice significantly inhibits the CYP3A4 enzyme, with comparable inhibition to grapefruit juice. In an animal model, pomegranate juice inhibits CYP3A4 metabolism of carbamazepine and increases levels of carbamazepine by 1.5 times; however, in human volunteers, drinking a single glass of pomegranate juice 240 mL or taking 200 mL daily for 2 weeks does not significantly affect levels of the CYP3A4 substrate midazolam after oral or intravenous administration. Another study in healthy volunteers shows that consuming pomegranate juice 300 mL three times daily for three days also does not significantly affect levels of simvastatin, a CYP3A4 substrate This suggests that pomegranate is unlikely to significantly affect levels of CYP3A4 substrates in humans.

Likelihood Unlikely Evidence B
Tolbutamide (Orinase)

Theoretically, pomegranate might increase levels of tolbutamide, although research suggests this interaction is unlikely to be clinically significant.
Animal research shows that pomegranate juice inhibits the cytochrome P450 2C9 (CYP2C9) metabolism of tolbutamide. Pomegranate juice increased tolbutamide levels by 1.2 times without prolonging the elimination half-life. This suggests that pomegranate juice inhibits intestinal CYP2C9, but might not inhibit hepatic CYP2C9. Despite this evidence, clinical research shows that neither pomegranate juice nor pomegranate extract have a significant effect on CYP2C9 activity in humans. This interaction does not appear to be clinically significant in humans.

Likelihood Unlikely Evidence D

Bilwin4 drug types · 819 drugs

Antidiabetes Drugs

Evidence from animal research suggests that extracts of bael seed and leaf can reduce blood glucose levels. Theoretically, bael might have additive effects with antidiabetes drugs and increase the risk of hypoglycemia. Monitor blood glucose levels closely. Dose adjustments might be necessary.
Some antidiabetes drugs include glimepiride (Amaryl), glyburide (DiaBeta, Glynase PresTab, Micronase), insulin, pioglitazone (Actos), rosiglitazone (Avandia), and others.

Likelihood Possible Evidence D
Cholinergic Drugs

Bael leaf extract shows acetylcholinesterase (AChE) inhibitory activity in vitro. Theoretically, bael might have additive effects with cholinergic drugs and increase the risk of cholinergic side effects.
Cholinergic drugs include bethanechol (Urecholine), donepezil (Aricept), echothiophate (Phospholine Iodide), edrophonium (Enlon, Reversol, Tensilon), neostigmine (Prostigmin), physostigmine (Antilirium), pyridostigmine (Mestinon, Regonol), succinylcholine (Anectine, Quelicin), and tacrine (Cognex).

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

Bael extract and its constituent marmesinin inhibited cytochrome P450 1A2 (CYP1A2) activity in vitro. So far, this interaction has not been reported in humans. Theoretically, bael might increase levels of drugs metabolized by CYP1A2.
Some drugs metabolized by CYP1A2 include amitriptyline (Elavil), haloperidol (Haldol), ondansetron (Zofran), propranolol (Inderal), theophylline (Theo-Dur, others), verapamil (Calan, Isoptin, others), and others. Use bael cautiously or avoid in patients taking these drugs.

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

Bael and its constituents marmelosin and marmesinin inhibited cytochrome P450 3A4 (CYP3A4) activity in vitro. So far, this interaction has not been reported in humans. Theoretically, bael might increase levels of drugs metabolized by CYP3A4.
Some drugs metabolized by CYP3A4 include lovastatin (Mevacor), ketoconazole (Nizoral), itraconazole (Sporanox), fexofenadine (Allegra), triazolam (Halcion), and numerous others. Use bael cautiously or avoid in patients taking these drugs.

Likelihood Possible Evidence D

Peppermint Leaf Extract5 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

Fennel Seed Extract6 drug types · 740 drugs

Anticoagulant/Antiplatelet Drugs

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

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

Likelihood Possible Evidence D
Ciprofloxacin (Cipro)

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

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

Likelihood Probable Evidence D
Contraceptive Drugs

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

Some constituents of fennel have estrogenic activity.

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

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

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

Likelihood Possible Evidence D
Estrogens

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

Some constituents of fennel have estrogenic activity.

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

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

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

Likelihood Possible Evidence D

Androwin6 drug types · 413 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, andrographis might increase the risk of bleeding when used with anticoagulant or antiplatelet drugs.
Animal and laboratory studies suggest that andrographis has antiplatelet effects.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, andrographis might increase the risk of hypotension when used with antihypertensive drugs.
Animal research suggests that andrographis has hypotensive effects.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, andrographis might interfere with the effects of immunosuppressive drugs.
Laboratory research suggests that andrographolide has immunostimulant activity.

Likelihood Possible Evidence D
Celecoxib (Celebrex)

Theoretically, andrographis extract might increase the maximum concentration and time to peak concentration of celecoxib. The clinical significance of these changes is unclear.
Animal research suggests that andrographis extract taken orally increases the maximum concentration and time to peak concentration of celecoxib but does not appear to impact the area under the curve.

Likelihood Possible Evidence D
Etoricoxib (Arcoxia)

Theoretically, andrographis might decrease the absorption of etoricoxib, although the clinical significance is unclear.
Animal research shows that andrographis extract, or the constituent andrographolide, taken orally with etoricoxib decreases the bioavailability of etoricoxib. However, this reduced bioavailability is not correlated with a reduction in the anti-inflammatory effects of etoricoxib in arthritic mice models. The clinical significance of this interaction is unclear.

Likelihood Possible Evidence D
Glipizide (Glucotrol)

Theoretically, andrographis extract might increase the maximum concentration and area under the curve of glipizide; however, opposite effects are seen with the constituent, andrographolide. The clinical significance of this interaction is unclear.
Animal research suggests that andrographis extract taken orally with glipizide in diabetes-induced rats increases the maximum concentration and area under the curve of glipizide. However, the opposite effect is seen with the constituent, andrographolide, in which the maximum concentration and area under the curve are decreased when taken with glipizide.

Likelihood Possible Evidence D

Pine Bark Extract3 drug types · 327 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, maritime pine bark extract might increase the risk of bleeding when used with antiplatelet or anticoagulant drugs.
Clinical research suggests that maritime pine bark extract inhibits platelet aggregation. However, the clinical significance of this effect is unclear.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, maritime pine bark extract might increase the risk of hypoglycemia when used with antidiabetes drugs.
One clinical study shows that maritime pine bark extract decreases blood sugar in patients with diabetes being treated with antidiabetes agents. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence B
Immunosuppressants

Theoretically, maritime pine bark extract might decrease the effectiveness of immunosuppressant therapy.
In vitro and animal research suggests that maritime pine bark extract has immunostimulant activity. This effect has not been reported in humans.

Likelihood Possible Evidence D

Amlowin4 drug types · 208 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, Indian gooseberry may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs; however, research is conflicting.
Clinical research shows that taking Indian gooseberry 500 mg as a single dose or twice daily for 10 days reduces platelet aggregation by about 24% to 36%, increases bleeding time by about 3.8-5.9 seconds, and increases clotting time by about 9.8-12.7 seconds when compared to baseline. However, taking Indian gooseberry 500 mg along with clopidogrel 75 mg or ecosprin 75 mg, as a single dose or for 10 days, does not significantly reduce platelet aggregation or increase bleeding time or clotting time when compared with clopidogrel 75 mg or ecosprin 75 mg alone. Until more is known, use caution when taking Indian gooseberry in combination with anticoagulant/antiplatelet drugs.

Likelihood Possible Evidence B
Antidiabetes Drugs

Taking Indian gooseberry with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research shows that taking Indian gooseberry fruit or fruit extract alone or in conjunction with antidiabetes medications can lower blood glucose levels. Dose adjustments to diabetes medications might be necessary.

Likelihood Possible Evidence B
Aspirin

Theoretically, Indian gooseberry may increase the risk of bleeding if used with aspirin; however, research is conflicting.
Clinical research shows that taking Indian gooseberry 500 mg as a single dose or twice daily for 10 days reduces platelet aggregation by about 24% to 36%, increases bleeding time by about 3.8-5.9 seconds, and increases clotting time by about 9.8-12.7 seconds when compared to baseline. However, taking a single dose of Indian gooseberry 500 mg along with ecosprin 75 mg, or taking a combination of Indian gooseberry 500 mg twice daily plus ecosprin 75 mg once daily for 10 days, does not significantly reduce platelet aggregation or increase bleeding time or clotting time when compared with ecosprin 75 mg alone.

Likelihood Possible Evidence B
Clopidogrel (Plavix)

Theoretically, Indian gooseberry may increase the risk of bleeding if used with clopidogrel; however, research is conflicting.
Clinical research shows that taking Indian gooseberry 500 mg as a single dose or twice daily for 10 days reduces platelet aggregation by about 24% to 36%, increases bleeding time by about 3.8-5.9 seconds, and increases clotting time by about 9.8-12.7 seconds when compared to baseline. However, taking a single dose of Indian gooseberry 500 mg along with clopidogrel 75 mg, or taking a combination of Indian gooseberry 500 mg twice daily plus clopidogrel 75 mg once daily for 10 days, does not significantly reduce platelet aggregation or increase bleeding time or clotting time when compared with clopidogrel 75 mg alone.

Likelihood Possible Evidence B

Bromelain2 drug types · 141 drugs

Anticoagulant/Antiplatelet Drugs

Bromelain may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
There is one case report of a patient experiencing minor bruising while taking bromelain with naproxen. Bromelain is thought to have antiplatelet activity. Whether this interaction is of concern with topical bromelain is unclear. Interference with coagulation of burn wounds has been reported in a patient receiving bromelain-based enzymatic debridement. However, observational research has found that topical bromelain debridement is not associated with increases or decreases in laboratory markers of coagulation when compared with surgical debridement.

Likelihood Possible Evidence D
Tetracycline Antibiotics

Theoretically, bromelain might increase levels of tetracycline antibiotics.
Laboratory research suggests that bromelain might increase the absorption of tetracycline antibiotics. However, a study in healthy adults reported no difference in tetracycline plasma levels when a 500 mg dose was taken with or without bromelain 80 mg.

Likelihood Possible Evidence B

Papain1 drug type · 2 drugs

Warfarin (Coumadin)

Theoretically, papain might increase the effects and side effects of warfarin.
In one case report, a patient previously stable on warfarin was found to have an international normalization ratio (INR) of 7.4, which was attributed to ingestion of a supplement containing papain from papaya extract.

Likelihood Possible Evidence D
The maker

Brand information

Manufacturer and brand details for Calm Bowels, from the product label.

Dr. Gumman’s Integrative

See all Dr. Gumman’s Integrative products
Name
Harmony Nutraceuticals, LLC
Street Address
3701 NW 62nd Street
City
OKC
State
OK
ZipCode
73112
Phone Number
(405) 601-4518
Web Address
www.HarmonyVeda.com
Pharmacist Counseling Corner

Calm Bowels by Dr. Gumman’s Integrative: Common Questions

Does Calm Bowels by Dr. Gumman’s Integrative interact with any medications?
Yes. Based on its ingredients, Calm Bowels has a known interaction with 1,450 medications. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Calm Bowels contains 13 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 Calm Bowels if I'm on warfarin?
No, not without checking with your pharmacist first. Papain, bromelain, fennel, Indian gooseberry, and ginger in this product may all increase warfarin's blood-thinning effects and raise your bleeding risk. One case report documented a dangerous spike in bleeding time after papain use. Talk to your pharmacist before adding this product.
Is Calm Bowels safe during pregnancy?
Several ingredients—papain, bromelain, fennel, bael, frankincense, and turmeric—should be avoided in pregnancy due to limited safety data or theoretical concerns. Licorice supplements are also best avoided. Discuss this product with your doctor or pharmacist before use if you're pregnant or planning to become pregnant.
Will this product actually help my digestion or bowel problems?
The evidence is limited. Peppermint in this formula is likely effective for irritable bowel syndrome and possibly helps indigestion. Ginger is possibly effective for nausea. Most other ingredients lack reliable evidence for digestive effects in our data, though they're used traditionally for bowel health.
What are the most common side effects?
Mild gastrointestinal effects—diarrhea, nausea, abdominal discomfort, and heartburn—are most common. Some people report headache. At high doses, peppermint and ginger can cause mouth or throat irritation. Allergic reactions are rare but possible, especially in sensitive individuals.
Can I take this with my diabetes medication?
Possibly, but check first. Bael, Indian gooseberry, and ginger may lower blood sugar, so taking them with diabetes drugs could increase your risk of low blood sugar. Your doctor may need to adjust your medication dose, or you may need to monitor your blood sugar more closely.
Is this safe if I'm breastfeeding?
Safety data during breastfeeding is sparse for most ingredients. Food amounts are generally safer than supplements. Talk to your doctor or pharmacist before using this product while breastfeeding, especially the concentrated herbal extracts it contains.

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.

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Go deeper

The Full Monographs Behind Calm Bowels’s Ingredients

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

Herb & supplement monograph

Papain

Interacts with 2 drugs

Papain is a protein-digesting enzyme from the papaya plant that is used in digestive supplements and some topical products. While it has clear food and laboratory uses, strong human evidence...

Read the full Papain monograph →
Herb & supplement monograph

Bromelain

Interacts with 141 drugs

Bromelain is a group of protein-digesting enzymes from pineapple that people take mainly for inflammation, swelling, and sinus problems. Some early studies are promising, but the overall evi...

Read the full Bromelain monograph →
Herb & supplement monograph

Licorice

Interacts with 1,040 drugs

Licorice root is a traditional remedy used for sore throats, coughs, and digestive complaints, but solid human evidence is limited for most uses. Regular licorice contains glycyrrhizin, whic...

Read the full Licorice monograph →
Herb & supplement monograph

Maritime Pine

Interacts with 327 drugs

Maritime pine bark extract (often sold as Pycnogenol) is a plant-based antioxidant most studied for circulation, vein, and skin health. Some research is promising, but many studies are small...

Read the full Maritime Pine monograph →
Herb & supplement monograph

Pomegranate

Interacts with 922 drugs

Pomegranate is a nutrient-rich fruit that is high in antioxidants and is widely enjoyed as food and juice. Early research suggests it may support heart health and blood pressure, but the evi...

Read the full Pomegranate monograph →
Herb & supplement monograph

Fennel

Interacts with 740 drugs

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

Read the full Fennel monograph →
Herb & supplement monograph

Bael

Interacts with 819 drugs

Bael is a fruit-bearing tree long used in traditional Indian (Ayurvedic) medicine, mostly for digestive problems like diarrhea and indigestion. Modern human evidence for its medicinal benefi...

Read the full Bael monograph →
Herb & supplement monograph

Frankincense

Frankincense is the aromatic resin of the Boswellia tree and is best known for its boswellic acids, which may help with inflammation and joint pain. Early research is promising for condition...

Read the full Frankincense monograph →
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

Indian Gooseberry

Interacts with 208 drugs

Indian gooseberry (amla) is a vitamin C-rich fruit used in Ayurvedic medicine for many purposes, from antioxidant support to cholesterol and digestion. Early research is promising for some u...

Read the full Indian Gooseberry 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

Andrographis

Interacts with 413 drugs

Andrographis is a bitter Asian herb traditionally used for colds, flu, and infections, and some studies suggest it may ease cold symptoms and shorten how long they last. The evidence is limi...

Read the full Andrographis monograph →
Herb & supplement monograph

Ginger

Interacts with 1,007 drugs

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

Read the full Ginger monograph →
Sources

Sources & How We Checked

Calm Bowels'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 428 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.

Papain 11 references
  1. The Review of Natural Products by Facts and Comparisons. St. Louis, MO: Wolters Kluwer Co., 1999.
  2. Shaw D, Leon C, Kolev S, Murray V. Traditional remedies and food supplements: a 5-year toxicological study (1991-1995). Drug Saf 1997;17:342-56.
  3. Shuttleworth D, Hill S, Marks R, Connelly DM. Relief of experimentally induced pruritus with a novel eutectic mixture of local anaesthetic agents. Br J Dermatol 1988;119:535-40.
  4. Mansfield LE, Ting S, Haverly RW, Yoo TJ. The incidence and clinical implications of hypersensitivity to papain in an allergic population, confirmed by blinded oral challenge. Ann Allergy 1985;55:541-3.
  5. Martin, T., Uhder, K., Kurek, R., Roeddiger, S., Schneider, L., Vogt, H. G., Heyd, R., and Zamboglou, N. Does prophylactic treatment with proteolytic enzymes reduce acute toxicity of adjuvant pelvic irradiation? Results of a double-blind randomized trial PubMed
  6. Walker-Renard, P. Update on the medicinal management of phytobezoars. Am J Gastroenterol. 1993;88(10):1663-1666.
  7. Tymoszuk D, Wiszniewska M, Walusiak-Skorupa J. Papain-induced occupational rhinoconjunctivitis and asthma - A case report. Med Pr 2016;67(1):109-12. PubMed
  8. Soto-Mera MT, López-Rico MR, Filgueira JF, et al. Occupational allergy to papain. Allergy 2000;55(10):983-4. PubMed
  9. Tarlo SM, Shaikh W, Bell B, et al. Papain-induced allergic reactions. Clin Allergy 1978;8(3):207-15. PubMed
  10. Baur X, König G, Bencze K, Fruhmann G. Clinical symptoms and results of skin test, RAST and bronchial provocation test in thirty-three papain workers: Evidence for strong immunogenic potency and clinically relevant proteolytic e?ects of airborne papain. C
  11. Novey HS, Keenan WJ, Fairshter RD, Wells ID, Wilson AF, Culver BD. Pulmonary disease in workers exposed to papain: clinico-physiological and immunological studies. Clin Allergy 1980;10(6):721-31. PubMed

See these in context on the Papain monograph →

Bromelain 19 references
  1. Nettis E, Napoli G, Ferrannini A, Tursi A. IgE-mediated allergy to bromelain. Allergy 2001;56:257-8. PubMed
  2. Taussig SJ, Batkin S. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol 1988;22:191-203.. PubMed
  3. Bradbrook ID, Morrison PJ, Rogers HJ. The effect of bromelain on the absorption of orally administered tetracycline. Br J Clin Pharmacol 1978;6:552-4. PubMed
  4. Bush TM, Rayburn KS, Holloway SW, et al. Adverse interactions between herbal and dietary substances and prescription medications: a clinical survey. Altern Ther Health Med 2007;13:30-5.
  5. Brien S, Lewith G, Walker AF, et al. Bromelain as an adjunctive treatment for moderate-to-severe osteoarthritis of the knee: a randomized placebo-controlled pilot study. QJM 2006;99:841-50. PubMed
  6. Mori S, Ojima Y, Hirose T, et al. The clinical effect of proteolytic enzyme containing bromelain and trypsin on urinary tract infection evaluated by double blind method. Acta Obstet Gynaecol Jpn 1972;19:147-53.
  7. Glaser D, Hilberg T. The influence of bromelain on platelet count and platelet activity in vitro. Platelets 2006;17:37-41. PubMed
  8. Heinicke R M, van der Wal L, Yokoyama M. Effect of bromelain (Ananase) on human platelet aggregation. Experientia 1972;28:844-5. PubMed
  9. Gailhofer, G., Wilders-Truschnig, M., Smolle, J., and Ludvan, M. Asthma caused by bromelain: an occupational allergy. Clin Allergy 1988;18(5):445-450. PubMed
  10. Mattei, O., Fabri, G., and Farina, G. [Occupational health experience regarding four cases of asthma due to bromelain (author's transl)]. Medicina del Lavoro 1979;70(5):404-409.
  11. Galleguillos, F. and Rodriguez, J. C. Asthma caused by bromelin inhalation. Clin Allergy 1978;8(1):21-24. PubMed
  12. Perez-Camo I, Quirce S, Duran MA, and et al. Latex allergy: evidence of cross-reactivity with papain and bromelain [abstract]. Allergy 1996;51(suppl 31):48.
  13. Martin GJ, Ehrenreich J, and Asbell N. Bromelain: pineapple proteases with anti-edema activity. Exp Med Surg 1962;20:227-247.
  14. Kasemsuk T, Saengpetch N, Sibmooh N, Unchern S. Improved WOMAC score following 16-week treatment with bromelain for knee osteoarthritis. Clin Rheumatol. 2016 Oct;35(10):2531-40. PubMed
  15. Kutlu Ö, DemirbaS A, Elmas ÖF, Güvenç U, Metin A. Fixed drug eruption: a new side effect of bromelain. Contact Dermatitis 2020. Online ahead of print. PubMed
  16. Shoham Y, Shapira E, Haik J, et al. Bromelain-based enzymatic debridement of chronic wounds: Results of a multicentre randomized controlled trial. Wound Repair Regen 2021;29(6):899-907. PubMed
  17. Pfister P, Garcia Wendel PD, Kim BS, et al. Coagulation side effects of enzymatic debridement in burned patients. Burns 2022. PubMed
  18. Hasham S, Riyat H, Fletcher A, O'Boyle CP, Alexander S. To bleed or not to bleed? Case series and discussion of haemorrhage risk with enzymatic debridement in burn injuries. Scars Burn Heal 2023;9:20595131231168333. PubMed
  19. Leelakanok N, Petchsomrit A, Janurai T, Saechan C, Sunsandee N. Efficacy and safety of bromelain: A systematic review and meta-analysis. Nutr Health 2023. PubMed

See these in context on the Bromelain monograph →

Licorice 92 references
  1. Farese RV Jr, Biglieri EG, Shackleton CH, et al. Licorice-induced hypermineralocorticoidism. N Engl J Med 1991;325:1223-7. PubMed
  2. Sigurjonsdottir HA, Ragnarsson J, Franzson L, Sigurdsson G. Is blood pressure commonly raised by moderate consumption of liquorice? J Hum Hypertens 1995;9:345-8.
  3. Armanini D, Lewicka S, Pratesi C, et al. Further studies on the mechanism of the mineralocorticoid action of licorice in humans. J Endocrinol Invest 1996;19:624-9. PubMed
  4. Zhang YD, Lorenzo B, Reidenberg MM. Inhibition of 11 beta hydroxysteroid dehydrogenase obtained from guinea pig kidney by furosemide, naringenin and some other compounds. J Steroid Biochem Mol Biol 1994;49:81-5.
  5. Strandberg TE, Jarvenpaa AL, Vanhanen H, McKeigue PM. Birth outcome in relation to licorice consumption during pregnancy. Am J Epidemiol 2001;153:1085-8. PubMed
  6. Sigurjonsdottir HA, Franzson L, Manhem K, et al. Liquorice-induced rise in blood pressure: a linear dose-response relationship. J Hum Hypertens 2001;15:549-52. PubMed
  7. Amato P, Christophe S, Mellon PL. Estrogenic activity of herbs commonly used as remedies for menopausal symptoms. Menopause 2002;9:145-50. PubMed
  8. Kent UM, Aviram M, Rosenblat M, Hollenberg PF. The licorice root derived isoflavan glabridin inhibits the activities of human cytochrome P450S 3A4, 2B6, and 2C9. Drug Metab Dispos 2002;30:709-15.. PubMed
  9. Yoshida S, Takayama Y. Licorice-induced hypokalemia as a treatable cause of dropped head syndrome. Clin Neurol Neurosurg 2003;105:286-7.. PubMed
  10. Strandberg TE, Andersson S, Jarvenpaa AL, et al. Preterm birth and licorice consumption during pregnancy. Am J Epidemiol 2002;156:803-5.. PubMed
  11. Hussain RM. The sweet cake that reaches parts other cakes can't! Postgrad Med J 2003;79:115-6.. PubMed
  12. Morris DJ, Davis E, Latif SA. Licorice, tobacco chewing, and hypertension. N Engl J Med 1990;322:849-50. PubMed
  13. Quinkler M, Stewart PM. Hypertension and the cortisol-cortisone shuttle. J Clin Endocrinol Metab 2003;88:2384-92. PubMed
  14. Westman EC, Guthrie GP. Licorice, tobacco chewing, and hypertension. N Engl J Med 1990;322:850. PubMed
  15. Mu Y, Zhang J, Zhang S, et al. Traditional Chinese medicines Wu Wei Zi (Schisandra chinensis Baill) and Gan Cao (Glycyrrhiza uralensis Fisch) activate pregnane X receptor and increase warfarin clearance in rats. J Pharmacol Exp Ther 2006;316:1369-77. PubMed
  16. Yasue H, Itoh T, Mizuno Y, Harada E. Severe hypokalemia, rhabdomyolysis, muscle paralysis, and respiratory impairment in a hypertensive patient taking herbal medicines containing licorice. Intern Med 2007;46:575-8. PubMed
  17. Brayley J, Jones J. Life-threatening hypokalemia associated with excessive licorice ingestion (letter). Am J Psychiatry 1994;151:617-8. PubMed
  18. de Klerk GJ, Nieuwenhuis G, Beutler JJ. Hypokalaemia and hypertension associated with use of liquorice flavoured chewing gum. BMJ 1997;314:731-2.
  19. Dellow EL, Unwin RJ, Honour JW. Pontefract cakes can be bad for you: refractory hypertension and liquorice excess. Nephol Dial Transplant 1999;14:218-20. PubMed
  20. Elinav E, Chajek-Shaul T. Licorice consumption causing severe hypokalemic paralysis. Mayo Clin Proc 2003;78:767-8. PubMed
  21. Eriksson JW, Carlberg B, Hillom V. Life-threatening ventricular tachycardia due to liquorice-induced hypokalemia. J Intern Med 1999;245:307-10.
  22. Janse A, van Iersel M, Hoefnagels WH, Olde Rikker MG. The old lady who liked liquorice: hypertension due to chronic intoxication in a memory-impaired patient. Neth J Med 2005;63:149-50.
  23. Lin SH, Yang SS, Chau T, Halperin ML. An unusual cause of hypokalemic paralysis: chronic licorice ingestion. Am J Med Sci 2003;325:153-6. PubMed
  24. van den Bosch AE, van der Klooster JM, Zuidgeest DM, et al. Severe hypokalemic paralysis and rhabdomyolysis due to ingestion of liquorice. Neth J Med 2005;63:146-8.
  25. van Uum SH. Liquorice and hypertension. Neth J Med 2005;63:119-20.
  26. Russo S, Mastropasqua M, Mosetti MA, et al. Low doses of liquorice can induce hypertension encephalopathy. Am J Nephrol 2000;20:145-8. PubMed
  27. Stormer FC, Reistad R, Alexander J. Glycyrrhizic acid in liquorice - evaluation of health hazard. Food Chem Toxicol 1993;31:303-12. PubMed
  28. Sontia B, Mooney J, Gaudet L, Touyz RM. Pseudohyperaldosteronism, liquorice, and hypertension. J Clin Hypertens (Greenwich) 2008;10:153-7. PubMed
  29. Francini-Pesenti F, Puato M, Piccoli A, Brocadello F. Liquorice-induced hypokalaemia and water retention in the absence of hypertension. Phytother Res 2008;22:563-5. PubMed
  30. Lapi F, Gallo E, Bernasconi S, et al. Myopathies associated with red yeast rice and liquorice: spontaneous reports from the Italian Surveillance System of Natural Health Products. Br J Clin Pharmacol 2008;66:572-4. PubMed
  31. Chen MF, Shimada F, Kato H, Yano S, Kanaoka M. Effect of glycyrrhizin on the pharmacokinetics of prednisolone following low dosage of prednisolone hemisuccinate. Endocrinol Jpn 1990;37:331-41. PubMed
  32. Teelucksingh S, Mackie AD, Burt D, McIntyre MA, Brett L, Edwards CR. Potentiation of hydrocortisone activity in skin by glycyrrhetinic acid. Lancet 1990;335(8697):1060-3. PubMed
  33. Heidemann HT, Kreuzfelder E. Hypokalemic rhabdomyolysis with myoglobinuria due to licorice ingestion and diuretic treatment. Klin Wochenschr 1983;61:303-5. PubMed
  34. Hukkanen J, Ukkola O, Savolainen MJ. Effects of low-dose liquorice alone or in combination with hydrochlorothiazide on the plasma potassium in healthy volunteers. Blood Press 2009;18:192-5. PubMed
  35. Bisogni V, Rossi GP, Calò LA. Apparent mineralcorticoid excess syndrome, an often forgotten or unrecognized cause of hypokalemia and hypertension: case report and appraisal of the pathophysiology. Blood Press. 2014 Jun;23(3):189-92. PubMed
  36. Dehours E, Vallé B, Rougé-Bugat ME, Florent B, Bounes V, Franchitto N. Suspected hypokalaemia following liquorice ingestion on board ship. J Telemed Telecare. 2013 Jun;19(4):227-8. PubMed
  37. Kormann R, Languille E, Amiot HM, Hertig A. Dying for a cup of tea. BMJ Case Rep. 2012 Oct 19;2012. PubMed
  38. Panduranga P, Al-Rawahi N. Licorice-induced severe hypokalemia with recurrent torsade de pointes. Ann Noninvasive Electrocardiol. 2013 Nov;18(6):593-6. PubMed
  39. Räikkönen K, Seckl JR, Heinonen K, Pyhälä R, Feldt K, Jones A, Pesonen AK, Phillips DI, Lahti J, Järvenpää AL, Eriksson JG, Matthews KA, Strandberg TE, Kajantie E. Maternal prenatal licorice consumption alters hypothalamic-pituitary-adrenocortical axis fu
  40. Robles BJ, Sandoval AR, Dardon JD, Blas CA. Lethal liquorice lollies (liquorice abuse causing pseudohyperaldosteronism). BMJ Case Rep. 2013 Sep 19;2013. PubMed
  41. Chamberlain, J. J. and Abolnik, I. Z. Pulmonary edema following a licorice binge. West J Med 1997;167(3):184-185.
  42. Barrella, M., Lauria, G., Quatrale, R., and Paolino, E. Hypokaliemic rhabdomyolysis associated with liquorice ingestion: report of an atypical case. Ital.J Neurol.Sci 1997;18(4):217-220. PubMed
  43. Fugh-Berman, A. Herb-drug interactions. Lancet 2000;355(9198):134-138. PubMed
  44. Hasegawa, J., Suyama, Y., Kinugawa, T., Morisawa, T., and Kishimoto, Y. Echocardiographic findings of the heart resembling dilated cardiomyopathy during hypokalemic myopathy due to licorice-induced pseudoaldosteronism. Cardiovasc.Drugs Ther 1998;12(6):59 PubMed
  45. van Rossum, T. G., Vulto, A. G., Hop, W. C., Brouwer, J. T., Niesters, H. G., and Schalm, S. W. Intravenous glycyrrhizin for the treatment of chronic hepatitis C: a double-blind, randomized, placebo-controlled phase I/II trial. J Gastroenterol Hepatol 199 PubMed
  46. Lozano, P., Flores, D., Martinez, S., Artigues, I., Rimbau, E. M., and Gomez, F. Upper limb ischemia induced by chronic licorice ingestion. J Cardiovasc.Surg (Torino) 2000;41(4):631-632.
  47. Brouwers, A. J. and van der, Meulen J. ['Licorice hypertension' also caused by licorice tea]. Ned.Tijdschr Geneeskd. 4-14-2001;145(15):744-747.
  48. van Rossum, T. G., Vulto, A. G., Hop, W. C., and Schalm, S. W. Glycyrrhizin-induced reduction of ALT in European patients with chronic hepatitis C. Am J Gastroenterol 2001;96(8):2432-2437. PubMed
  49. Sigurjonsdottir, H. A., Manhem, K., Axelson, M., and Wallerstedt, S. Subjects with essential hypertension are more sensitive to the inhibition of 11 beta-HSD by liquorice. J Hum Hypertens 2003;17(2):125-131.
  50. Shintani, S., Murase, H., Tsukagoshi, H., and Shiigai, T. Glycyrrhizin (licorice)-induced hypokalemic myopathy. Report of 2 cases and review of the literature. Eur Neurol 1992;32(1):44-51. PubMed
  51. Chen, M. F., Shimada, F., Kato, H., Yano, S., and Kanaoka, M. Effect of oral administration of glycyrrhizin on the pharmacokinetics of prednisolone. Endocrinol Jpn 1991;38(2):167-174. PubMed
  52. Lee, C. K., Park, K. K., Lim, S. S., Park, J. H., and Chung, W. Y. Effects of the licorice extract against tumor growth and cisplatin-induced toxicity in a mouse xenograft model of colon cancer. Biol Pharm Bull 2007;30(11):2191-2195. PubMed
  53. Isaia, G. C., Pellissetto, C., Ravazzoli, M., and Tamone, C. Acute adrenal crisis and hypercalcemia in a patient assuming high liquorice doses. Minerva Med 2008;99(1):91-94.
  54. Bocker, D. and Breithardt, G. [Induction of arrhythmia by licorice abuse]. Z Kardiol 1991;80(6):389-391.
  55. Tacconi, P., Paribello, A., Cannas, A., and Marrosu, M. G. Carpal tunnel syndrome triggered by excessive licorice consumption. J Peripher.Nerv.Syst. 2009;14(1):64-65. PubMed
  56. Tu, J. H., He, Y. J., Chen, Y., Fan, L., Zhang, W., Tan, Z. R., Huang, Y. F., Guo, D., Hu, D. L., Wang, D., and Hong-Hao Zhou. Effect of glycyrrhizin on the activity of CYP3A enzyme in humans. Eur J Clin Pharmacol 2010;66(8):805-810. PubMed
  57. Goultschin, J., Palmon, S., Shapira, L., Brayer, L., and Gedalia, I. Effect of glycyrrhizin-containing toothpaste on dental plaque reduction and gingival health in humans. A pilot study. J Clin Periodontol 1991;18(3):210-212. PubMed
  58. Scali, M., Pratesi, C., Zennaro, M. C., Zampollo, V., and Armanini, D. Pseudohyperaldosteronism from liquorice-containing laxatives. J Endocrinol Invest 1990;13(10):847-848. PubMed
  59. Chatterjee, N., Domoto-Reilly, K., Fecci, P. E., Schwamm, L. H., and Singhal, A. B. Licorice-associated reversible cerebral vasoconstriction with PRES. Neurology 2010;75(21):1939-1941. PubMed
  60. Imtiaz, K. E. Sweet root, bitter pill: liquorice-induced hyperaldosteronism. QJM 2011;104(12):1093-1095. PubMed
  61. van Beers, E. J., Stam, J., and van den Bergh, W. M. Licorice consumption as a cause of posterior reversible encephalopathy syndrome: a case report. Crit Care 2011;15(1):R64. PubMed
  62. MacKenzie, M. A., Hoefnagels, W. H., Jansen, R. W., Benraad, T. J., and Kloppenborg, P. W. The influence of glycyrrhetinic acid on plasma cortisol and cortisone in healthy young volunteers. J Clin Endocrinol Metab 1990;70(6):1637-1643. PubMed
  63. Bardhan, K. D., Cumberland, D. C., Dixon, R. A., and Holdsworth, C. D. Clinical trial of deglycyrrhizinised liquorice in gastric ulcer. Gut 1978;19(9):779-782. PubMed
  64. Koster, M. and David, G. K. Reversible severe hypertension due to licorice ingestion. N Engl J Med 1968;278(25):1381-1383. PubMed
  65. Corse, F. M., Galgani, S., Gasparini, C., Giacanelli, M., and Piazza, G. Acute hypokalemic myopathy due to chronic licorice ingestion: report of a case. Ital J Neurol Sci 1983;4(4):493-497. PubMed
  66. Berlango Jimenez A., Jimenez Murillo L., Montero Perez F. J., Munoz Avila J. A., Torres Murillo J., and Calderon de la Barca Gazquez J. M. [Acute rhabdomyolysis and tetraparesis secondary to hypokalemia due to ingested licorice]. An Med Interna 1995;12(1)
  67. Bernardi, M., D'Intino, P. E., Trevisani, F., Cantelli-Forti, G., Raggi, M. A., Turchetto, E., and Gasbarrini, G. Effects of prolonged ingestion of graded doses of licorice by healthy volunteers. Life Sci 1994;55(11):863-872. PubMed
  68. van der Zwan A. Hypertension encephalopathy after liquorice ingestion. Clin Neurol Neurosurg 1993;95(1):35-37. PubMed
  69. Werner, S., Brismar, K., and Olsson, S. Hyperprolactinaemia and liquorice. Lancet 2-10-1979;1(8111):319.
  70. Nishioka, K. and Seguchi, T. Contact allergy due to oil-soluble licorice extracts in cosmetic products. Contact Dermatitis 1999;40(1):56. PubMed
  71. Yoshino T, Yanagawa T, Watanabe K. Risk factors for pseudoaldosteronism with rhabdomyolysis caused by consumption of drugs containing licorice and differences between incidence of these conditions in Japan and other countries: case report and literature r
  72. Li G, Simmler C, Chen L, et al. Cytochrome P450 inhibition by three licorice species and fourteen licorice constituents. Eur J Pharm Sci. 2017;109:182-190. PubMed
  73. Li J, Fan X, Wang Q. Hypertensive crisis with 2 target organ impairment induced by glycyrrhizin: a case report. Medicine (Baltimore) 2018;97(11):e0073. PubMed
  74. Foster CA, Church KS, Poddar M, Van Uum SH, Spaic T. Licorice-induced hypertension: a case of pseudohyperaldosteronism due to jelly bean ingestion. Postgrad Med 2017;129(3):329-31. PubMed
  75. Gallacher SD, Tsokolas G, Dimitropoulos I. Liquorice-induced apparent mineralocorticoid excess presenting in the emergency department. Clin Med (Lond) 2017;17(1):43-5. PubMed
  76. Dai DW, Singh I, Hershman JM. Lozenge-induced hypermineralcorticoid state--a unique case of licorice lozenges resulting in hypertension and hypokalemia. J Clin Hypertens (Greenwich) 2016;18(2):159-60.
  77. O'Connell K, Kinsella J, McMahon C, Holian J, O'Riordan S. Posterior reversible encephalopathy syndrome (PRES) associated with liquorice consumption. Ir J Med Sci 2016;185(4):945-7. PubMed
  78. Hataya Y, Oba A, Yamashita T, Komatsu Y. Hyponatremia in an elderly patient due to isolated hypoaldosteronism occurring after licorice withdrawal. Intern Med 2017;56(2):175-9. PubMed
  79. Ha Y, Wang T, Li J, et al. Herb-Drug Interaction Potential of Licorice Extract and Paclitaxel: A Pharmacokinetic Study in Rats. Eur J Drug Metab Pharmacokinet. 2020;45(2):257-264. PubMed
  80. Edelman ER, Butala NM, Avery LL, Lundquist AL, Dighe AS. Case 30-2020: A 54-Year-Old Man with Sudden Cardiac Arrest. N Engl J Med. 2020;383(13):1263-1275. PubMed
  81. Wang H, Dong L, Qu F, et al. Effects of glycyrrhizin on the pharmacokinetics of nobiletin in rats and its potential mechanism. Pharm Biol. 2020 Dec;58(1):352-356. PubMed
  82. Attou R, Redant S, Honore PM, Preseau T, Hantson P, De Bels D. Liquorice intoxication can lead to cardiac arrest! Case Rep Emerg Med. 2020;2020:3727682. PubMed
  83. Benge E, Shah P, Yamaguchi L, Josef V. Trick or Treat? Licorice-Induced Hypokalemia: A Case Report. Cureus 2020;12(11):e11656. PubMed
  84. Abe K, Higurashi T, Takahashi M, et al. Concomitant Use of High-dose Methotrexate and Glycyrrhizin Affects Pharmacokinetics of Methotrexate, Resulting in Hepatic Toxicity. In Vivo 2021;35(4):2163-2169. PubMed
  85. Awad N, Makar G, Burroughs V, Ravi P, Burroughs SR. Licorice-induced apparent mineralocorticoid excess causing persistent hypertension and hypokalemia. Acta Endocrinol (Buchar) 2020;16(4):508-510. PubMed
  86. Patel P, Aknouk M, Dawson A, et al. How Much Is Too Much? Exploring Pseudohyperaldosteronism in Glycyrrhizic Acid Toxicity From Chronic Licorice Root Consumption. Cureus 2021;13(7):e16454. PubMed
  87. Fan ZJ, Liu JM, Li XX, et al. Glycyrrhizin-Induced Pseudohyperaldosteronism: A Case Report. Chin J Integr Med 2022. PubMed
  88. Gatica-Ortega ME, Pastor-Nieto MA. Allergic contact dermatitis to Glycyrrhiza inflata root extract in an anti-acne cosmetic product. Contact Dermatitis 2021;85(4):454-455.
  89. Wang JB, Huang A, Wang Y, et al. Corticosteroid plus glycyrrhizin therapy for chronic drug- or herb-induced liver injury achieves biochemical and histological improvements: a randomised open-label trial. Aliment Pharmacol Ther 2022;55(10):1297-1310. PubMed
  90. Puaratanaarunkon T, Washrawirul C, Chuenboonngarm N, Noppakun N, Asawanonda P, Kumtornrut C. Efficacy and safety of a facial serum containing snail secretion filtrate, Calendula officinalis, and Glycyrrhiza glaba root extract in the treatment of maskne: A
  91. 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
  92. Han EJ, Park JS. Lethal Arrhythmia Induced by Licorice. J Korean Med Sci 2023;38(12):e107. PubMed

See these in context on the Licorice monograph →

Maritime Pine 14 references
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Pomegranate 27 references
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Fennel 17 references
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Bael 7 references
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Frankincense 2 references
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Peppermint 41 references
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Indian Gooseberry 6 references
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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.

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