Major interaction on record — check this product against your medications before combining. Based on 24 of 38 ingredients. Check your meds →
Dietary supplement

Chyavanprasha Kapha -9c Ingredients & Drug Interactions

by Ayurvedic Rasayanas

Other (e.g. Tea Bag) Category: Other Combinations
Most serious interaction: Major
The interaction bottom line Most serious interaction: Major

Chyavanprasha Kapha -9c is a dietary supplement by Ayurvedic Rasayanas with 38 active ingredients. Its ingredients are commonly taken for sore throat and mouth irritation, digestive upset, excessive sweating.Based on those ingredients, 1,754 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ashwagandha extract, Sage leaf extract, Green Tea leaf powder. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Chyavanprasha Kapha -9c by Ayurvedic Rasayanas

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 1 of its 36 active ingredients.
  • “Proprietary Blend of Standardized Extracts” is a proprietary blend — the label doesn't break down how much of each component you get.
  • “Proprietary Blend of Powdered Herbs” is a proprietary blend — the label doesn't break down how much of each component you get.
  • “Proprietary Blend of Pure Essential Oils” is a proprietary blend — the label doesn't break down how much of each component you get.

Chyavanprasha Kapha -9c contains 36 active ingredients — mostly traditional Ayurvedic herbs, spices, and plant extracts. The main actives include dandelion root, parsley, honey, ginger root (powder and essential oil), turmeric (powder and essential oil), coriander seed, sage leaf (extract and essential oil), Indian long pepper fruit, licorice root, brown rice syrup, cinnamon bark (powder and essential oil), tribulus (gokshura) fruit, and clove (flower powder, bud essential oil).

The product also has inactive ingredients that serve as fillers or the product form itself.

Does it work?

Not established
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
Not established

The graded evidence we hold for these ingredients covers different conditions than the ones this product is marketed for, so there's no established rating for its stated use.

Why this rating?
  • The label markets this product for: Rejuvenation, digestion, energy, and immunity support.
  • We looked for evidence on: Asthma, Bronchitis, Age-related cognitive decline, Digestive health, Metabolic support, General vitality.
  • The closest evidence on file: Indian Long Pepper is rated "Insufficient Reliable Evidence To Rate" for Bronchitis (Natural Medicines).
  • Also on file: Indian Long Pepper is rated "Insufficient Reliable Evidence To Rate" for Asthma.
  • Also on file: Sage is rated "Insufficient Reliable Evidence To Rate" for Age-related cognitive decline.

The evidence base for these ingredients is mixed. Honey is possibly effective for cold sores, cough, oral sores (oral mucositis), burns, and dry eye.

Ginger is possibly effective for pregnancy-related nausea and vomiting, period pain, and osteoarthritis, but possibly ineffective for exercise soreness and chemotherapy-related nausea. Turmeric is possibly effective for depression, high cholesterol, allergies, and indigestion.

Sage is possibly effective for hot flashes, high cholesterol, and thinking and memory. Tribulus is possibly effective for sexual dysfunction but possibly ineffective for athletic performance.

For the remaining ingredients — dandelion, parsley, coriander, cinnamon, licorice, Indian long pepper, and clove — the evidence we hold is insufficient to rate their effectiveness, or they show no proven benefit for the conditions studied.

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 22 of the 24 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 24 of 24.
  • General safety write-ups exist for 24 of 24.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Most ingredients are generally well tolerated in food amounts. However, several carry cautions at supplement doses.

Parsley is likely unsafe in pregnancy and may stimulate the uterus — stick to food amounts only. Sage is likely unsafe in pregnancy and possibly unsafe while breastfeeding due to thujone content; avoid medicinal amounts.

Dandelion and licorice lack enough safety data for pregnancy and breastfeeding — talk with your doctor. Ginger is often used for morning sickness but should be kept moderate; turmeric is likely safe in pregnancy but possibly unsafe at high doses.

Tribulus should be avoided in pregnancy and breastfeeding due to hormone effects and lack of data. Common side effects from individual ingredients include stomach upset, diarrhea, nausea, and heartburn; rare cases of allergic reactions (including anaphylaxis) have been reported with dandelion, parsley, coriander, and clove, particularly in people sensitive to the daisy (Asteraceae) family of plants.

Turmeric has been linked to rare liver damage in about 70 cases over weeks to months of supplement use.

Meds to double-check

Major interaction found
Known Interaction Concern · database check
Major identified

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

Why this rating?
  • 22 of the 24 matched ingredients can interact with medications — Elecampane, Tribulus, Coriander, Clove, Bishop's Weed, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; seizure medications; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; heart-rhythm medications; lithium.
  • For scale: 1,755 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.

Before taking this product, check your medications for interactions with blood thinners (anticoagulants and antiplatelet drugs), diabetes medications, blood pressure medications, and drugs processed by your liver's cytochrome P450 system — all are affected by multiple ingredients here. Also check if you take propranolol, theophylline, digoxin, cyclosporine, warfarin, tacrolimus, or tamoxifen, as several ingredients may alter their levels.

The interaction checker below covers these and more.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFormula with limited ingredient disclosure with no established evidence rating for its marketed use. Major medication interactions have been identified, and safety information is well characterized.

This is a complex traditional formula with many active ingredients. If you take any prescription medications — especially blood thinners, diabetes drugs, heart or blood pressure medications, or medications metabolized by your liver — you need to check each of your drugs against the interaction tool below before starting.

Pregnant or breastfeeding women should talk to their provider first; several ingredients carry cautions. People with liver disease or sensitivity to daisy-family plants should use extra care.

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

Assessment coverage: 33 of 36 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Mar 25, 2021.

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 Chyavanprasha Kapha -9c, straight from the product label.

Brand Ayurvedic Rasayanas
Net contents 10.7 Ounce(s); 300 Gram(s)
Market status On market
Date entered into DSLD Mar 25, 2021
DSLD ID 246253
Product type Other Combinations
Supplement form Other (e.g. Tea Bag)
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Adult (18 - 50 Years), Gluten Free
From the label
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.

Supplement Facts

The label details for Chyavanprasha Kapha -9c by Ayurvedic Rasayanas, sourced from the NIH Dietary Supplement Label Database.

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.
Formulation

These Rasayanas are prepared using a traditional Ayurvedic method.

Tasting the herbs while consuming them stimulates the pre-digestion process and promotes greater assimilation.

Dietary Recommendations: May support energy, digestion, metabolism, immune system and is kapha or earth balancing.

GF Certified Gluten-free

Physical Rejuv-Kapha

Formula

They’re a combination of herbs that are preserved for an indefinite amount of time in a base of honey, brown rice syrup and ghee. The word “Rasayana” means “any substance that helps to bring about rejuvenation and youthful mental and physical energy”.

Suggested/Recommended/Usage/Directions

Dosage: one teaspoon per 50lbs of weight

FDA Statement of Identity

Dietary Supplement

Precautions

Allergy Information: Contains ghee made from milk.

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.

Seals/Symbols

GF Certified Gluten-free

General Statements

Not a significant source of Vitamin A, Vitamin C, Calcium and Iron

See for yourself

Chyavanprasha Kapha -9c by Ayurvedic Rasayanas label

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

What’s inside

The Ingredients in Chyavanprasha Kapha -9c by Ayurvedic Rasayanas

These are the 38 active ingredients this product is made of. Select any to open its full monograph.

Serving size1 Teaspoon(s) Dosage formOther (e.g. Tea Bag) Servings per container50 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.

Sugar

3 Gram(s) per serving

Protein

0 Gram(s) per serving

Fat

1 Gram(s) per serving

Dietary Ingredients

1 Gram(s) per serving
Interaction report

Chyavanprasha Kapha -9c by Ayurvedic Rasayanas Drug Interactions

Want to check YOUR meds against Chyavanprasha Kapha -9c?

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
1,754Drugs
13 Major 1,738 Moderate 3 Minor

Ingredients driving the most interactions

Each ingredient & the kinds of drugs it affects

For each ingredient in Chyavanprasha Kapha -9c 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.

Ashwagandha extract10 drug types · 1,372 drugs

Antidiabetes Drugs

Theoretically, taking ashwagandha with antidiabetes drugs might increase the risk of hypoglycemia.
There is preliminary clinical evidence suggesting that ashwagandha might lower blood glucose levels. Theoretically, ashwagandha might have additive effects when used with antidiabetes drugs and increase the risk of hypoglycemia.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking ashwagandha with antihypertensive drugs might increase the risk of hypotension.
Animal research suggests that ashwagandha might lower systolic and diastolic blood pressure. Theoretically, ashwagandha might have additive effects when used with antihypertensive drugs and increase the risk of hypotension.

Likelihood Possible Evidence D
Benzodiazepines

Theoretically, taking ashwagandha might increase the sedative effects of benzodiazepines.
There is preliminary evidence that ashwagandha might have an additive effect with diazepam (Valium) and clonazepam (Klonopin). This may also occur with other benzodiazepines.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, taking ashwagandha might increase the sedative effects of CNS depressants.
Ashwagandha seems to have sedative effects. Theoretically, this may potentiate the effects of barbiturates, other sedatives, and anxiolytics.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, taking ashwagandha with hepatotoxic drugs might increase the risk of liver damage.
Ashwagandha has been linked to cases of acute hepatitis, liver failure, hepatic encephalopathy, autoimmune hepatitis, the need for liver transplantation, and death due to liver failure.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, taking ashwagandha might decrease the effects of immunosuppressants.
Ashwagandha has demonstrated immunostimulant effects in humans. Animal research has shown that ashwagandha can attenuate the immunosuppression caused by cyclophosphamide.

Likelihood Possible Evidence D
Thyroid Hormone

Ashwagandha might increase the effects and adverse effects of thyroid hormone.
Concomitant use of ashwagandha with thyroid hormones may cause additive therapeutic and adverse effects. Preliminary clinical research and animal studies suggest that ashwagandha boosts thyroid hormone synthesis and secretion. In one clinical study, ashwagandha increased triiodothyronine (T3) and thyroxine (T4) levels by 41.5% and 19.6%, respectively, and reduced serum TSH levels by 17.4% from baseline in adults with subclinical hypothyroidism.

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

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

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

Theoretically, ashwagandha might decrease the levels and clinical effects of CYP3A4 substrates.
In vitro research shows that ashwagandha extract induces CYP3A4 enzymes.

Likelihood Possible Evidence D
Serotonergic Drugs

Some animal studies have reported that ashwagandha can enhance serotonergic transmission by altering certain serotonin (5-HT) receptors. However, there is no evidence to suggest that ashwagandha increases the risk of serotonin-related effects, and there have been no published case reports of serotonin syndrome when combined with other serotonergic drugs. Nevertheless, due to the lack of extensive studies on the matter and the fact that ashwagandha appears to affect serotonergic pathways, it would be prudent to exercise caution when combining it with drugs that affect serotonin. [References: - Effects of Withania somnifera (Ashwaga ndha) on Stress and the Stress-Related Neuropsychiatric Disorders Anxiety, Depression, and Insomnia. Curr Neuropharmacol. 2021 Sep 14; 19: 1468–1495. - A Prospective, Randomized Double-Blind, Placebo-Controlled Study of Safety and Efficacy of a High-Concentration Full-Spectrum Extract of Ashwagandha Root in Reducing Stress and Anxiety in Adults. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573577/]

Likelihood Possible Evidence C

Sage leaf extract14 drug types · 1,296 drugs

Anticholinergic Drugs

Theoretically, sage might decrease the clinical effects of anticholinergic drugs.
In vitro evidence suggests that common sage (Salvia officinalis) and Spanish sage (Salvia lavandulaefolia) can inhibit acetylcholinesterase and might increase acetylcholine levels.

Likelihood Possible Evidence D
Anticonvulsants

Theoretically, sage might interfere with the clinical effects of anticonvulsant drugs.
Some species of sage can cause convulsions when consumed in large quantities.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking sage with antidiabetes drugs might increase the risk of hypoglycemia.
In patients with polycystic ovary syndrome (PCOS) or inadequately controlled type 2 diabetes, common sage (Salvia officinalis) has demonstrated hypoglycemic activity. However, other clinical research in patients with inadequately controlled type 2 diabetes shows that common sage extract does not lower fasting blood glucose levels.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, sage might increase or decrease the effects of antihypertensive drugs.
Animal research suggests that common sage (Salvia officinalis) can cause prolonged blood pressure reduction. However, clinical research suggests that Spanish sage (Salvia lavandulaefolia) can increase blood pressure in some people with hypertension. Until more is known, use with caution.

Likelihood Possible Evidence D
Benzodiazepines

Theoretically, taking sage might increase the sedative and adverse effects of benzodiazepines.
In vitro evidence suggests that certain components of common sage (Salvia officinalis) can bind to benzodiazepine receptors. This effect has not been reported in humans.

Likelihood Possible Evidence D
Cholinergic Drugs

Theoretically, sage might have additive effects when used with cholinergic drugs.
In vitro evidence suggests that common sage (Salvia officinalis) and Spanish sage (Salvia lavandulaefolia) can inhibit acetylcholinesterase and might increase acetylcholine levels.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, taking sage might increase the sedative and adverse effects of CNS depressants.
Some constituents of sage have CNS depressant activity.

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

Theoretically, sage might increase the levels and clinical effects of drugs metabolized by CYP2C19.
In vitro evidence suggests that aqueous extracts of sage can inhibit CYP2C19. So far, this interaction has not been reported in humans.

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

Theoretically, sage might increase the levels and clinical effects of drugs metabolized by CYP2C9.
In vitro evidence suggests that aqueous extracts of sage can inhibit CYP2C9. So far, this interaction has not been reported in humans.

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

Theoretically, sage might increase the levels and clinical effects of drugs metabolized by CYP2D6.
In vitro evidence suggests that aqueous extracts of sage can inhibit CYP2D6. So far, this interaction has not been reported in humans.

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

Theoretically, sage might decrease the levels and clinical effects of drugs metabolized by CYP2E1.
Animal research suggests that drinking common sage (Salvia officinalis) tea increases the expression of CYP2E1. So far, this interaction has not been reported in humans.

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

Theoretically, sage might increase the levels and clinical effects of drugs metabolized by CYP3A4.
In vitro evidence suggests that aqueous extracts of sage can inhibit CYP3A4. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Estrogens

Theoretically, sage might interfere with hormone therapy.
In vitro evidence suggests that geraniol, a constituent of Spanish sage (Salvia lavandulaefolia), exerts estrogenic activity. The clinical significance of this effect is unclear.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, sage might increase levels of drugs transported by P-glycoprotein.
In vitro research suggests that common sage (Salvia officinalis) can inhibit the multi-drug transporter protein, P-glycoprotein. This effect has not been reported in humans.

Likelihood Possible Evidence D

Green Tea leaf powder58 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

Turmeric root powder24 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

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

Black Pepper powder17 drug types · 1,019 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, black pepper might increase the risk of bleeding when taken with antiplatelet or anticoagulant drugs.
In vitro research shows that piperine, a constituent of black pepper, seems to inhibit platelet aggregation. This has not been reported in humans.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, black pepper might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research shows that piperine, a constituent of black pepper, can reduce blood glucose levels. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Atorvastatin (Lipitor)

Theoretically, black pepper might increase blood levels of atorvastatin.
Animal research shows that taking piperine, a constituent of black pepper, 35 mg/kg can increase the maximum serum concentration of atorvastatin three-fold. This has not been reported in humans.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, black pepper might increase the effects and side effects of cyclosporine.
In vitro research shows that piperine, a constituent of black pepper, increases the bioavailability of cyclosporine. This has not been reported in humans.

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

Theoretically, black pepper might increase levels of drugs metabolized by CYP2D6.
In vitro research suggests that some constituents of black pepper inhibit CYP2D6. This has not been reported in humans.

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

Theoretically, black pepper might increase levels of drugs metabolized by CYP3A4.
In vitro research and pharmacokinetic simulation data suggest that piperine, a constituent of black pepper, as well as the pepper fruit seem to inhibit CYP3A4. This has not been reported in humans.

Likelihood Possible Evidence D
Lithium

Theoretically, black pepper might increase blood levels of lithium due to its diuretic effects. The dose of lithium might need to be reduced.
Black pepper is thought to have diuretic properties.

Likelihood Probable Evidence D
Nevirapine (Viramune)

Black pepper might increase blood levels of nevirapine.
Clinical research shows that piperine, a constituent of black pepper, increases the plasma concentration of nevirapine. However, no adverse effects were observed in this study.

Likelihood Probable Evidence D
P-Glycoprotein Substrates

Theoretically, black pepper might increase levels of P-glycoprotein substrates.
In vitro research shows that piperine, a constituent of black pepper, seems to inhibit P-glycoprotein.

Likelihood Possible Evidence D
Pentobarbital (Nembutal)

Theoretically, black pepper might increase the sedative effects of pentobarbital.
Animal research shows that piperine, a constituent of black pepper, increases pentobarbital-induced sleeping time.

Likelihood Possible Evidence D
Phenytoin (Dilantin)

Black pepper might increase blood levels of phenytoin.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption, slow elimination, and increase levels of phenytoin. Taking a single dose of black pepper 1 gram along with phenytoin seems to double the serum concentration of phenytoin. Consuming a soup with black pepper providing piperine 44 mg/200 mL of soup along with phenytoin also seems to increase phenytoin levels when compared with consuming the same soup without black pepper.

Likelihood Possible Evidence B
Propranolol (Inderal)

Black pepper might increase blood levels of propranolol.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and slow elimination of propranolol.

Likelihood Possible Evidence B
Rifampin (Rifadin)

Black pepper might increase blood levels of rifampin.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and serum levels of rifampin.

Likelihood Possible Evidence B
Theophylline

Black pepper might increase blood levels of theophylline.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and slow elimination of theophylline.

Likelihood Possible Evidence D
Amoxicillin (Amoxil, Trimox)

Theoretically, black pepper might increase the effects and side effects of amoxicillin.
Animal research shows that taking piperine, a constituent of black pepper, with amoxicillin increases plasma levels of amoxicillin. This has not been reported in humans.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, black pepper might increase blood levels of carbamazepine, potentially increasing the effects and side effects of carbamazepine.
One clinical study in patients taking carbamazepine 300 mg or 500 mg twice daily shows that taking a single 20 mg dose of purified piperine, a constituent of black pepper, increases carbamazepine levels. Piperine may increase carbamazepine absorption by increasing blood flow to the GI tract, increasing the surface area of the small intestine, or inhibiting cytochrome P450 3A4 (CYP3A4) in the gut wall. Absorption was significantly increased by 7-10 mcg/mL/hour. The time to eliminate carbamazepine was also increased by 4-8 hours. Although carbamazepine levels were increased, this did not appear to increase side effects. In vitro research also shows that piperine can increase carbamazepine levels by 11% in a time-dependent manner.

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

Theoretically, black pepper might decrease levels and clinical effects of drugs metabolized by CYP1A2.
In vitro research suggests that black pepper induces CYP1A2. This has not been reported in humans.

Likelihood Possible Evidence D

Ginger root powder14 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

Clove flower powder7 drug types · 977 drugs

Antidiabetes Drugs

Theoretically, concomitant use of clove extracts with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical and laboratory research suggest that polyphenol extracts from clove flower buds might lower blood glucose levels. Dosing adjustments for insulin or oral hypoglycemic agents may be necessary when taken with clove. Monitor blood glucose levels closely.

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

Theoretically, concomitant use of clove may increase levels of drugs metabolized by CYP1A2.
In vitro research shows that eugenol, the principal constituent of clove, can inhibit CYP1A2 in a dose-dependent manner,. This effect has not been reported in humans.

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

Theoretically, concomitant use of clove may increase levels of drugs metabolized by CYP2C9.
In vitro research shows that eugenol, the principal constituent of clove, inhibits CYP2C9 in a dose-dependent manner. This effect has not been reported in humans.

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

Theoretically, concomitant use of clove may increase levels of drugs metabolized by CYP2D6.
In vitro research shows that eugenol, the principal constituent of clove, can inhibit CYP2D6 in a dose-dependent manner. This effect has not been reported in humans.

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

Theoretically, concomitant use of clove may increase levels of drugs metabolized by CYP3A4.
In vitro research shows that eugenol, the principal constituent of clove, can inhibit CYP3A4 in a dose-dependent manner. This effect has not been reported in humans.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, clove oil may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Laboratory research suggests that eugenol, a constituent of clove, has antiplatelet activity. This interaction has not been reported in humans.

Likelihood Unlikely Evidence D
Ibuprofen (Advil, Others)

Theoretically, topical application of clove oil with ibuprofen might increase the absorption and side effects of topical ibuprofen.
Laboratory research shows that topical application of clove oil increases the absorption of topical ibuprofen. This interaction has not been reported in humans.

Likelihood Possible Evidence D

Ajwain seed powder3 drug types · 954 drugs

Anticoagulant/Antiplatelet Drugs

Bergapten, a constituent of bishop's weed, has antiplatelet activity. Theoretically, bishop's weed might have additive effects with anticoagulant or antiplatelet drugs and possibly increase the risk of bleeding.
Some anticoagulant or antiplatelet drugs include aspirin, clopidogrel (Plavix), dalteparin (Fragmin), enoxaparin (Lovenox), heparin, ticlopidine (Ticlid), warfarin (Coumadin), and others.

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

Bergapten, a constituent of bishop's weed, has been shown to inhibit cytochrome P450 3A4 (CYP3A4) in vitro. Theoretically, bishop's weed might inhibit elimination and increase blood levels of drugs metabolized by CYP3A4.
Some drugs metabolized by CYP3A4 include alprazolam (Xanax), amitriptyline (Elavil), amiodarone (Cordarone), buspirone (Buspar), cerivastatin (Baycol), citalopram (Celexa), felodipine (Plendil), fexofenadine (Allegra), itraconazole (Sporanox), ketoconazole (Nizoral), lansoprazole (Prevacid), losartan (Cozaar), lovastatin (Mevacor), ondansetron (Zofran), prednisone (Deltasone, Orasone), sertraline (Zoloft), sibutramine (Meridia), sildenafil (Viagra), simvastatin (Zocor), verapamil (Calan, Covera-HS, Isoptin), and many others.

Likelihood Possible Evidence B
Photosensitizing Drugs

Bishop's weed constituents seem to cause photosensitivity. Theoretically, concomitant use of bishop's weed with photosensitizing drugs might result in increased photosensitivity.
Some drugs that cause photosensitivity include amitriptyline (Elavil), quinolones (Ciprofloxacin, others), sulfa drugs (Septra, Bactrim, others), and tetracycline.

Likelihood Possible Evidence D

Pippali fruit extract14 drug types · 896 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, Indian long pepper might increase the risk of bleeding when taken with anticoagulant/antiplatelet drugs.
In vitro research shows that Indian long pepper extract inhibits platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, Indian long pepper might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research shows that piperine, a constituent of Indian long pepper, can reduce blood glucose levels. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, Indian long pepper might increase the effects and adverse effects of cyclosporine.
In vitro research shows that piperine, a constituent of Indian long pepper, increases the bioavailability of cyclosporine.

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

Theoretically, Indian long pepper might increase the effects and adverse effects of CYP3A4 substrates.
In vitro research shows that piperine, a constituent of Indian long pepper, inhibits CYP3A4.

Likelihood Possible Evidence D
Nevirapine (Viramune)

Theoretically, Indian long pepper might increase blood levels of nevirapine.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, increases the plasma concentration and systemic exposure of nevirapine. However, no adverse effects were associated with the elevated plasma levels of nevirapine.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

Theoretically, Indian long pepper might increase levels of P-glycoprotein substrates.
In vitro research shows that piperine, a constituent of Indian long pepper, can inhibit P-glycoprotein.

Likelihood Possible Evidence D
Pentobarbital (Nembutal)

Theoretically, Indian long pepper might increase the sedative effects of pentobarbital.
Animal research shows that piperine, a constituent of Indian long pepper, can increase pentobarbitone-induced sleeping time.

Likelihood Possible Evidence D
Phenytoin (Dilantin)

Theoretically, Indian long pepper might increase blood levels of phenytoin.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, increases phenytoin serum levels and slows its elimination.

Likelihood Possible Evidence B
Propranolol (Inderal)

Theoretically, Indian long pepper might increase blood levels of propranolol.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, accelerates absorption and increases serum concentrations of propranolol.

Likelihood Possible Evidence B
Rifampin (Rifadin)

Theoretically, Indian long pepper might increase blood levels of rifampin.
Piperine, a constituent of Indian long pepper, seems to increase absorption and serum levels of rifampin.

Likelihood Possible Evidence D
Theophylline

Indian long pepper might increase blood levels of theophylline.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, increases serum concentrations and slows elimination of theophylline.

Likelihood Possible Evidence B
Amoxicillin (Amoxil, Trimox)

Theoretically, Indian long pepper might increase the effects and adverse effects of amoxicillin.
Evidence from animal research shows that piperine, a constituent of Indian long pepper, increases the plasma levels of amoxicillin when taken concomitantly.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, Indian long pepper might increase blood levels of carbamazepine.
A small pharmacokinetic study in patients taking carbamazepine 300 mg or 500 mg twice daily shows that a single 20 mg dose of purified piperine, which is a constituent of Indian long pepper, increases carbamazepine levels. Piperine may increase absorption by increasing blood flow to the GI tract, increasing the surface area of the small intestine, or by cytochrome P450 3A4 (CYP3A4) inhibition in the gut wall. Absorption was significantly increased by 7-10 mcg/mL/hour. The time to eliminate carbamazepine was also increased by 4-8 hours. Although carbamazepine levels were increased, this did not appear to increase side effects.

Likelihood Possible Evidence B
Cefotaxime (Claforan)

Theoretically, Indian long pepper might increase the effects and adverse effects of cefotaxime.
Animal research shows that piperine, a constituent of Indian long pepper, increases the plasma levels of cefotaxime when taken concomitantly.

Likelihood Possible Evidence D

Guggulu resin extract9 drug types · 757 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, guggul might increase the risk of bleeding when taken with anticoagulant/antiplatelet drugs.
In vitro research and preliminary clinical studies suggest that guggul might have antiplatelet and anticoagulant effects.

Likelihood Possible Evidence B
Contraceptive Drugs

Theoretically, guggul might increase the risk of adverse effects when taken with contraceptive drugs.
In vitro research shows that guggul has estrogen-alpha receptor agonist activity.

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

Theoretically, guggul might reduce the effects of CYP3A4 substrates.
In vitro research shows that guggul constituents known as guggulsterones can induce CYP3A4.

Likelihood Probable Evidence D
Diltiazem (Cardizem, Others)

Guggul might reduce the effects of diltiazem.
A small pharmacokinetic study shows that concomitant use of guggul with diltiazem reduces the bioavailability of diltiazem.

Likelihood Probable Evidence B
Estrogens

Theoretically, guggul might increase the risk of adverse effects when taken with estrogens.
In vitro research shows that guggul constituents known as guggulsterones have estrogen-alpha receptor agonist activity.

Likelihood Possible Evidence D
Propranolol (Inderal)

Guggul might reduce the effects of propranolol.
A small pharmacokinetic study shows that concomitant use of guggul with propranolol reduces the bioavailability of propranolol.

Likelihood Probable Evidence B
Rosuvastatin (Crestor)

Theoretically, guggul might increase the effects and adverse effects of rosuvastatin.
Animal research shows that guggul increases the bioavailability and hypolipidemic effects of rosuvastatin. The mechanism of this interaction is unclear.

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

Theoretically, guggul might interfere with tamoxifen therapy.
In vitro research shows that guggul has estrogen-alpha receptor agonist activity.

Likelihood Possible Evidence D
Thyroid Hormone

Theoretically, guggul might increase the risk for adverse effects when taken with thyroid hormone therapy.
Animal research suggests that guggul has thyroid-stimulating effects.

Likelihood Probable Evidence B

Honey3 drug types · 736 drugs

Phenytoin (Dilantin)

Theoretically, honey might increase levels of phenytoin.
In an animal model, the rate and extent of absorption of phenytoin was increased by honey. This effect has not been reported in humans.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, honey may increase the risk of bleeding when used with anticoagulant or antiplatelet drugs.
In vitro, honey inhibits platelet aggregation and increases the time to clotting. Furthermore, animal research suggests that feeding mice large doses of honey for 12 days increases bleeding time when compared with no intervention. However, these effects have not been reported in humans.

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

Theoretically, honey might decrease levels of drugs metabolized by CYP3A4, but research is conflicting.
Some clinical research shows that honey induces CYP3A4. However, other clinical studies found no effect on CYP3A4 activity. Different honey preparations may have different effects on CYP3A4.

Likelihood Possible Evidence B

Coriander seed powder4 drug types · 717 drugs

Antidiabetes Drugs

Theoretically, coriander might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Evidence from animal research suggests that coriander fruit and coriander extract can reduce blood glucose levels. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, coriander might increase the risk of hypotension when taken with antihypertensive drugs.
Evidence from animal research suggests that coriander fruit can lower blood pressure.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, coriander might cause additive sedative effects when taken with CNS depressants.
Evidence from animal research suggests that coriander fruit extract has sedative effects.

Likelihood Possible Evidence D
Photosensitizing Drugs

Theoretically, coriander might increase the risk of photosensitivity when taken with photosensitizing drugs.
Evidence from in vitro research suggests that coriandrin, a constituent of coriander, has photosensitizing effects.

Likelihood Possible Evidence D

Garcinia fruit extract4 drug types · 704 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, hydroxycitric acid (HCA), the main active ingredient in garcinia, might increase the risk of bleeding when used with antiplatelet or anticoagulant drugs.
HCA inhibits platelet aggregation in vitro. The inhibitory effect seems to be greater in platelets extracted from diabetic subjects than non-diabetic subjects.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, hydroxycitric acid (HCA), the main active ingredient in garcinia, might have additive effects with antidiabetes drugs and increase the risk of hypoglycemia.
HCA reduces fasting and postprandial blood glucose levels in animal models, theoretically by delaying glucose absorption. This effect has not been reported in humans.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, concomitant use with other potentially hepatotoxic drugs might increase the risk of developing liver damage.
There have been reports of acute hepatitis with elevated liver enzymes associated with garcinia, when taken alone or in combination with other ingredients. Case reports collected from the Drug Induced Liver Injury Network suggest this risk may be greater in people who carry the HLA B*35:01 allele.

Likelihood Possible Evidence D
Serotonergic Drugs

Theoretically, combining garcinia with other serotonergic drugs might increase the risk of serotonergic side effects, including serotonin syndrome.
In one report, a patient experienced serotonin syndrome after taking garcinia extract (60% hydroxycitric acid) 1000 mg daily in combination with escitalopram 20 mg, which had been taken for a year. The patient was switched to sertraline 50 mg daily and again experienced serotonin syndrome.

Likelihood Possible Evidence D

Dandelion root powder7 drug types · 457 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, taking dandelion root along with anticoagulant or antiplatelet drugs might increase the risk of bruising and bleeding.
In vitro research suggests that dandelion root inhibits platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, dandelion might increase the risk for hypoglycemia when used with antidiabetes drugs.
Laboratory research suggests that dandelion extract may have moderate alpha-glucosidase inhibitor activity and might also increase insulin secretion. Also, in a case report, a 58-year-old woman with type 2 diabetes who was being treated with insulin developed hypoglycemia 2 weeks after beginning to eat salads containing dandelion.

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

Theoretically, dandelion might increase levels of drugs metabolized by CYP1A2.
Laboratory research suggests that dandelion might inhibit CYP1A2. So far, this interaction has not been reported in humans. However, until more is known, watch for an increase in the levels of drugs metabolized by CYP1A2 in patients taking dandelion.

Likelihood Possible Evidence D
Glucuronidated Drugs

Theoretically, dandelion might increase the clearance of drugs that are UDP-glucuronosyltransferase substrates.
There is some preliminary evidence that dandelion might induce UDP-glucuronosyltransferase, a phase II enzyme.

Likelihood Possible Evidence D
Lithium

Theoretically, through diuretic effects, dandelion might reduce excretion and increase levels of lithium.
Animal research suggests that dandelion has diuretic properties. As diuretics can increase serum lithium levels, the dose of lithium might need to be decreased when taken with dandelion.

Likelihood Probable Evidence D
Potassium-Sparing Diuretics

Theoretically, dandelion might increase the risk of hyperkalemia when taken with potassium-sparing diuretics.
Dandelion contains significant amounts of potassium.

Likelihood Possible Evidence D
Quinolone Antibiotics

Theoretically, dandelion might lower fluoroquinolone levels.
Animal research shows that dandelion reduces absorption of ciprofloxacin and can lower levels by 73%. However, this effect has not been reported in humans.

Likelihood Possible Evidence D

Parsley leaf powder8 drug types · 443 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, parsley might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
Animal research suggests that parsley has antiplatelet effects.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, parsley might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research suggests that parsley might decrease blood glucose. Monitor blood glucose levels closely. Dose adjustments might be necessary.

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

Theoretically, parsley might increase serum levels of CYP1A2 substrates.
Laboratory research suggests that parsley can inhibit CYP1A2.

Likelihood Possible Evidence D
Diuretic Drugs

Theoretically, parsley might enhance or interfere with the effects of diuretic drugs.
Animal research suggests that parsley seed extract increases urine elimination. Parsley leaf and root might also interfere with diuretic therapy due their purported aquaretic effects.

Likelihood Possible Evidence D
Pentobarbital (Nembutal)

Theoretically, parsley might increase the duration of pentobarbital effects.
Animal research suggests that parsley juice prolongs the action of pentobarbital, perhaps by decreasing cytochrome P450 levels. It is not known if this occurs in humans or if this applies to other barbiturates or sedatives.

Likelihood Possible Evidence D
Sirolimus (Rapamune)

Theoretically, large quantities of parsley might increase sirolimus levels.
In one case report, an adult female with a history of kidney transplant presented with elevated blood sirolimus levels, approximately 4-7 times greater than previous measures, after daily consumption of a juice containing approximately 30 grams of parsley for 7 days. Sirolimus levels returned to normal a week after the parsley juice was discontinued.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, large amounts of parsley leaf and root might decrease the effects of warfarin.
Parlsey contains vitamin K.

Likelihood Possible Evidence D
Aspirin

Theoretically, aspirin might increase the severity of allergic reactions to parsley.
In one case, severe urticaria and swelling were reported after taking aspirin with parsley in an individual with a known mild parsley allergy.

Likelihood Unlikely Evidence D

Cinnamon bark powder2 drug types · 442 drugs

Antidiabetes Drugs

Theoretically, cassia cinnamon may have additive effects with antidiabetes drugs.
Cassia cinnamon may lower blood glucose levels, and have additive effects in patients treated with antidiabetic agents. Dose adjustments to diabetes medications might be necessary.

Likelihood Possible Evidence B
Hepatotoxic Drugs

Theoretically, large doses of cassia cinnamon might cause additive effects when used with hepatotoxic drugs.
There is some concern that ingesting large amounts of cassia cinnamon for an extended duration might cause hepatotoxicity in some people. Cassia cinnamon contains coumarin, which can cause hepatotoxicity in animal models. In humans, very high doses of coumarin from 50-7000 mg/day can result in hepatotoxicity that resolves when coumarin use is discontinued. Lower amounts might also cause liver problems in sensitive people, such as those with liver disease or those taking potentially hepatotoxic agents.

Likelihood Possible Evidence D

Gokshura fruit extract3 drug types · 259 drugs

Antidiabetes Drugs

Taking tribulus with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research shows that Tribulus can lower blood glucose levels in adults with type 2 diabetes who are taking antidiabetes medications.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, taking tribulus with antihypertensive drugs might increase the risk of hypotension.
Animal research shows that tribulus can lower blood pressure by inhibiting angiotensin-converting enzyme (ACE). Tribulus has also demonstrated hypotensive effects in pre-hypertensive adults.

Likelihood Possible Evidence D
Lithium

Theoretically, tribulus might increase the levels and clinical effects of lithium.
Tribulus is thought to have diuretic properties. Due to these potential diuretic effects, tribulus might reduce excretion and increase levels of lithium. The dose of lithium might need to be decreased.

Likelihood Probable Evidence D

Cinnamon bark essential oil2 drug types · 258 drugs

Antidiabetes Drugs

Theoretically, Ceylon cinnamon may have additive effects with antidiabetes drugs.
Ceylon cinnamon may lower blood glucose levels. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, Ceylon cinnamon might have additive effects with antihypertensive drugs and increase the risk of hypotension.
Animal research shows that Ceylon cinnamon extract has vasorelaxant properties and reduces blood pressure in rat models of hypertension, possibly via inhibition of calcium influx through L-type voltage-sensitive channels.

Likelihood Possible Evidence D

Elecampane root extract1 drug type · 248 drugs

Cns Depressants

Theoretically, elecampane may cause additive sedative effects when taken with CNS depressants.
Elecampane might have sedative effects.

Likelihood Possible Evidence D

Tulasi root extract3 drug types · 212 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, holy basil seed oil might increase the risk of bleeding when used with anticoagulant or antiplatelet drugs.
Animal research shows that holy basil seed oil can prolong bleeding time, possibly due to inhibition of platelet aggregation. However, it is not known if this occurs in humans.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, holy basil might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Small clinical studies show that taking holy basil can decrease fasting blood glucose and other measures of glycemic control in patients with type 2 diabetes.

Likelihood Possible Evidence B
Pentobarbital (Nembutal)

Theoretically, holy basil seed oil might increase the sedative effects of pentobarbital.
Animal research shows that holy basil seed oil increases pentobarbitone-induced sleeping time. However, it is not known if this occurs in humans or if this applies to other barbiturates or sedatives.

Likelihood Possible Evidence D

Shilajit extract1 drug type · 86 drugs

Antidiabetes Drugs

Taking shilajit with antidiabetes drugs might increase the risk of hypoglycemia.
Most human and animal research shows that shilajit can decrease fasting plasma glucose levels. In an animal model, shilajit 100 mg per kg daily enhanced the glucose-lowering ability of both glibenclamide and metformin when given in combination over a 4 week period. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence D
The maker

Brand information

Manufacturer and brand details for Chyavanprasha Kapha -9c, from the product label.

Ayurvedic Rasayanas

See all Ayurvedic Rasayanas products
Name
Ayurvedic Rasayanas
Street Address
P.O. Box 719
City
Ashland
State
OR
ZipCode
97520
Phone Number
541-944-7243
Web Address
www.ayurveda-herbs.com
Pharmacist Counseling Corner

Chyavanprasha Kapha -9c by Ayurvedic Rasayanas: Common Questions

Does Chyavanprasha Kapha -9c by Ayurvedic Rasayanas interact with any medications?
Yes. Based on its ingredients, Chyavanprasha Kapha -9c has a known interaction with 1,754 medications, including 13 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Chyavanprasha Kapha -9c contains 38 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.
Can I take this while pregnant?
Several ingredients carry cautions. Parsley is likely unsafe, and sage is likely unsafe in pregnancy. Dandelion, licorice, and tribulus lack enough safety data — we can't say either way. Talk with your doctor or pharmacist about whether this product is right for you during pregnancy.
Is this safe to breastfeed while taking?
Parsley and licorice lack enough safety data while breastfeeding, and sage is possibly unsafe because it's traditionally used to reduce milk supply. Honey, ginger, turmeric, and cinnamon appear safer in food amounts, but medicinal doses aren't well studied. Check with your provider before starting.
What's honey in this formula for?
Honey is possibly effective for cold sores, cough, mouth sores, burns, and dry eye. It's also a common food binder in Ayurvedic pastes and adds sweetness.
Will this help with digestion or inflammation?
Turmeric is possibly effective for indigestion, and ginger is possibly effective for nausea, which may support digestion. Licorice and dandelion have traditionally been used for digestive health, but the evidence we hold is insufficient to rate them. Talk with a pharmacist about whether this product fits your specific needs.
Are there any common side effects I should know about?
The most common side effects are mild and affect the stomach and gut — nausea, heartburn, diarrhea, constipation, and abdominal discomfort. Ginger may cause a peppery irritant feeling in the mouth or throat. Stop and call your doctor if you have signs of an allergic reaction, such as rash, swelling, or trouble breathing.
Is this product free of fillers?
This product has an 'Other' form and the facts don't list the inactive ingredients, so we can't confirm what fillers or binders are in it. Ask the manufacturer or check the full label for the complete ingredient list.

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

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Chyavanprasha Kapha -9c label
Go deeper

The Full Monographs Behind Chyavanprasha Kapha -9c’s Ingredients

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

Herb & supplement monograph

Sage

Interacts with 1,296 drugs

Sage is a common kitchen herb that is generally safe in food amounts and is traditionally used for sore throats, digestion, sweating, and memory. Some early research is encouraging for sore...

Read the full Sage monograph →
Herb & supplement monograph

Indian Long Pepper

Interacts with 896 drugs

Indian long pepper (pippali) is a spice long used in Ayurvedic medicine and is best known for its piperine content, which may increase how well the body absorbs certain other substances. Mod...

Read the full Indian Long Pepper 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

Tribulus

Interacts with 259 drugs

Tribulus is a plant supplement most often marketed to boost libido, testosterone, and athletic performance, but the human evidence behind these claims is weak and inconsistent. It is general...

Read the full Tribulus monograph →
Herb & supplement monograph

Ashwagandha

Interacts with 1,372 drugs

Ashwagandha is an Ayurvedic herb most often taken to help with stress, anxiety, and sleep, and some small studies suggest it may help, though the evidence is still limited. It is generally w...

Read the full Ashwagandha monograph →
Herb & supplement monograph

Shilajit

Interacts with 86 drugs

Shilajit is a sticky, tar-like substance found in rocks of mountain ranges like the Himalayas, used in traditional Ayurvedic medicine for energy and vitality. Human evidence is limited and m...

Read the full Shilajit monograph →
Herb & supplement monograph

Elecampane

Interacts with 248 drugs

Elecampane is a traditional herb used mainly for coughs and other respiratory complaints, and as a bitter for digestion. Modern human evidence is very limited, so it should be seen as a folk...

Read the full Elecampane monograph →
Herb & supplement monograph

Holy Basil

Interacts with 212 drugs

Holy basil (tulsi) is a traditional Ayurvedic herb most often used today for stress and general wellness, but the human evidence is mostly small and preliminary. It is generally well tolerat...

Read the full Holy Basil monograph →
Herb & supplement monograph

Garcinia

Interacts with 704 drugs

Garcinia is a tropical fruit whose rind contains hydroxycitric acid (HCA), widely marketed for weight loss and appetite control. The scientific evidence is weak and mixed, with most studies...

Read the full Garcinia monograph →
Herb & supplement monograph

Guggul

Interacts with 757 drugs

Guggul is a gum resin from the Commiphora wightii tree, long used in Ayurvedic medicine for cholesterol, joint, and skin problems. Modern studies are mixed and often low-quality, and it can...

Read the full Guggul monograph →
Herb & supplement monograph

Dandelion

Interacts with 457 drugs

Dandelion is a common plant used in food and traditional medicine, often promoted as a natural 'water pill' and digestive aid. Human evidence for these uses is very limited, so its benefits...

Read the full Dandelion monograph →
Herb & supplement monograph

Parsley

Interacts with 443 drugs

Parsley is a popular culinary herb that is safe to eat in normal food amounts and is a good source of vitamins K and C. It is traditionally used as a diuretic and for digestion, but solid hu...

Read the full Parsley monograph →
Herb & supplement monograph

Ginger

Interacts with 1,007 drugs

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

Read the full Ginger monograph →
Herb & supplement monograph

Turmeric

Interacts with 1,133 drugs

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

Read the full Turmeric monograph →
Herb & supplement monograph

Coriander

Interacts with 717 drugs

Coriander (also called cilantro) is a common cooking herb and spice that has long been used in traditional medicine for digestive complaints. As a food it is generally safe for most people,...

Read the full Coriander monograph →
Herb & supplement monograph

Cassia Cinnamon

Interacts with 442 drugs

Cassia cinnamon is the common, inexpensive cinnamon used in cooking, and it is also taken as a supplement, most often for blood sugar support. The evidence for its health benefits is mixed a...

Read the full Cassia Cinnamon monograph →
Herb & supplement monograph

Clove

Interacts with 977 drugs

Clove is a common cooking spice that is also used in traditional medicine, especially as a topical numbing agent for tooth pain thanks to its main compound, eugenol. Food amounts are general...

Read the full Clove monograph →
Herb & supplement monograph

Black Pepper

Interacts with 1,019 drugs

Black pepper is a common kitchen spice that is generally safe in the amounts used in food. Its extract, piperine, is mostly added to supplements to help the body absorb other ingredients (li...

Read the full Black Pepper monograph →
Herb & supplement monograph

Cardamom

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

Read the full Cardamom monograph →
Herb & supplement monograph

Bishop's Weed

Interacts with 954 drugs

Bishop's Weed (Ammi majus) is a flowering plant whose seeds contain natural light-sensitizing compounds called psoralens, which have been studied mainly for skin conditions like vitiligo and...

Read the full Bishop's Weed 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

Ceylon Cinnamon

Interacts with 258 drugs

Ceylon cinnamon is the so-called 'true' cinnamon, valued as a spice and used in traditional medicine for blood sugar, cholesterol, and digestion. Evidence for most health benefits is limited...

Read the full Ceylon Cinnamon monograph →
Herb & supplement monograph

Brown Rice

Brown rice is a whole grain that keeps its fiber-rich bran and nutrient-packed germ, making it more nutritious than white rice. As part of a balanced diet, it may support heart health, diges...

Read the full Brown Rice monograph →
Herb & supplement monograph

Honey

Interacts with 736 drugs

Honey is a natural food with some real, modest evidence for easing coughs and helping certain wounds, especially when special medical-grade or Manuka honey is used. It is generally safe for...

Read the full Honey monograph →
Sources

Sources & How We Checked

Chyavanprasha Kapha -9c'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 852 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.

Brown Rice 1 reference
  1. FDA, Center for Food Safety and Applied Nutrition, Office of Premarket Approval, EAFUS: A food additive database. Website: vm.cfsan.fda.gov/~dms/eafus.html (Accessed 23 February 2006).

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Dandelion 27 references
  1. Maliakal PP, Wanwimolruk S. Effect of herbal teas on hepatic drug metabolizing enzymes in rats. J Pharm Pharmacol 2001;53:1323-9. PubMed
  2. Williams CA, Goldstone F, Greenham J. Flavonoids, cinnamic acids and coumarins from the different tissues and medicinal preparations of Taraxacum officinale. Phytochemistry 1996;42:121-7. PubMed
  3. Hussain Z, Waheed A, Qureshi RA, et al. The effect of medicinal plants of Islamabad and Murree region of Pakistan on insulin secretion from INS-1 cells. Phytother Res 2004;18:73-7. PubMed
  4. Racz-Kotilla E, Racz G, Solomon A. The action of Taraxacum officinale extracts on the body weight and diuresis of laboratory animals. Planta Med 1974;26:212-7. PubMed
  5. Zhu M, Wong PY, Li RC. Effects of taraxacum mongolicum on the bioavailability and disposition of ciprofloxacin in rats. J Pharm Sci 1999;88:632-4. PubMed
  6. Jovanovic M, Mimica-Dukic N, Poljacki M, Boza P. Erythema multiforme due to contact with weeds: a recurrence after patch testing. Contact Dermatitis 2003;48:17-25. PubMed
  7. Chivato T, Juan F, Montoro A, Laguna R. Anaphylaxis induced by ingestion of a pollen compound. J Investig Allergol Clin Immunol 1996;6:208-9.
  8. Cohen SH, Yunginger JW, Rosenberg N, Fink JN. Acute allergic reaction after composite pollen ingestion. J Allergy Clin Immunol 1979;64:270-4. PubMed
  9. Lovell CR, Rowan M. Dandelion dermatitis. Contact Dermatitis 1991;25:185-8. PubMed
  10. Agarwal SC, Crook JR, Pepper CB. Herbal remedies -- how safe are they? A case report of polymorphic ventricular tachycardia/ventricular fibrillation induced by herbal medication used for obesity. Int J Cardiol 2006;106:260-1. PubMed
  11. Martín-Muñoz MF, Bartolome B, Caminoa M, et al. Bee pollen: a dangerous food for allergic children. Identification of responsible allergens. Allergol Immunopathol (Madr) 2010;38:263-5. PubMed
  12. Neef H, Cilli F, Declerck PJ, et al. Platelet anti-aggregating activity of Taraxacum officinale Weber. Phytotherapy Research 1996;10:s138-s140.
  13. Cuzzolin L, Zaffani S, and Benoni G. Safety implications regarding use of phytomedicines. Eur.J Clin Pharmacol. 2006;62:37-42. PubMed
  14. Posadzki, P., Watson, L. K., and Ernst, E. Adverse effects of herbal medicines: an overview of systematic reviews. Clin Med 2013;13(1):7-12. PubMed
  15. Wakelin, S. H., Marren, P., Young, E., and Shaw, S. Compositae sensitivity and chronic hand dermatitis in a seven-year-old boy. Br J Dermatol 1997;137(2):289-291. PubMed
  16. Ingber, A. Seasonal allergic contact dermatitis from Taraxacum officinale (dandelion) in an Israeli florist. Contact Dermatitis 2000;43(1):49.
  17. Rodriguez, B., Rodriguez, A., de Barrio, M., Tornero, P., and Baeza, M. L. Asthma induced by canary food mix. Allergy Asthma Proc. 2003;24(4):265-268.
  18. Syhaieva, I. A. [Efficiency of specific immunotherapy in treatment of patients with seasonal allergic rhinitis]. Lik.Sprava. 2006;(1-2):51-53.
  19. Catania, M. A., Oteri, A., Caiello, P., Russo, A., Salvo, F., Giustini, E. S., Caputi, A. P., and Polimeni, G. Hemorrhagic cystitis induced by an herbal mixture. South.Med.J. 2010;103(1):90-92. PubMed
  20. Goksu, E., Eken, C., Karadeniz, O., and Kucukyilmaz, O. First report of hypoglycemia secondary to dandelion (Taraxacum officinale) ingestion. Am J Emerg.Med 2010;28(1):111-112. PubMed
  21. Fernandez-Gonzalez, D., Gonzalez-Parrado, Z., Vega-Maray, A. M., Valencia-Barrera, R. M., Camazon-Izquierdo, B., De, Nuntiis P., and Mandrioli, P. Platanus pollen allergen, Pla a 1: quantification in the atmosphere and influence on a sensitizing populati
  22. Liang, K. L., Su, M. C., Shiao, J. Y., Wu, S. H., Li, Y. H., and Jiang, R. S. Role of pollen allergy in Taiwanese patients with allergic rhinitis. J Formos.Med Assoc. 2010;109(12):879-885. PubMed
  23. Yang, Y., Zhao, Y., Wang, C. S., Wang, X. D., and Zhang, L. [Prevalence of sensitization to aeroallergens in 10 030 patients with allergic rhinitis]. Zhonghua Er.Bi Yan.Hou Tou.Jing.Wai Ke Za Zhi 2011;46(11):914-920.
  24. Davies, M. G. and Kersey, P. J. Contact allergy to yarrow and dandelion. Contact Dermatitis 1986;14(4):256-257. PubMed
  25. Collins JM and Miller DR. Dandelion green bezoar following antrectomy and vagotomy - case report. J Kansas Med Soc 1966;67(6):303-304.
  26. Moriarty B, Pinney JH, Owen-Casey MP, Rustin MH, Deroide F, Laing C, Davenport A. Digital necrosis from dandelion tea. Br J Dermatol. 2013 Jul;169(1):227-30. PubMed
  27. Onal S, Timur S, Okutucu B, Zihnioglu F. Inhibition of alphaglucosidase by aqueous extracts of some potent antidiabetic medicinal herbs. Prep Biochem Biotechnol 2005;35:29-36.

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Parsley 21 references
  1. Newall CA, Anderson LA, Philpson JD. Herbal Medicine: A Guide for Healthcare Professionals. London, UK: The Pharmaceutical Press, 1996.
  2. Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: John Wiley & Sons, 1996.
  3. McGuffin M, Hobbs C, Upton R, Goldberg A, eds. American Herbal Products Association's Botanical Safety Handbook. Boca Raton, FL: CRC Press, LLC 1997.
  4. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  5. Robbers JE, Tyler VE. Tyler's Herbs of Choice: The Therapeutic Use of Phytomedicinals. New York, NY: The Haworth Herbal Press, 1999.
  6. Foster S, Tyler VE. Tyler's Honest Herbal, 4th ed., Binghamton, NY: Haworth Herbal Press, 1999. DOI
  7. Eberhard P, Gall HM, Muller I, Moller R. Dramatic augmentation of a food allergy by acetylsalicylic acid. J Allergy Clin Immunol 2000;105:844 PubMed
  8. Tunali T, Yarat A, Yanardag R, et al. Effect of parsley (Petroselinum crispum) on the skin of STZ induced diabetic rats. Phytother Res 1999;13:138-41.. DOI
  9. Chuang CH, Doyle P, Wang JD, et al. Herbal medicines used during the first trimester and major congenital malformations: an analysis of data from a pregnancy cohort study. Drug Saf 2006;29:537-48. PubMed
  10. Ciganda C, and Laborde A. Herbal infusions used for induced abortion. J Toxicol.Clin Toxicol. 2003;41:235-239. PubMed
  11. 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
  12. Kreydiyyeh, S. I. and Usta, J. Diuretic effect and mechanism of action of parsley. J Ethnopharmacol 2002;79(3):353-357. PubMed
  13. Yanardag, R., Bolkent, S., Tabakoglu-Oguz, A., and Ozsoy-Sacan, O. Effects of Petroselinum crispum extract on pancreatic B cells and blood glucose of streptozotocin-induced diabetic rats. Biol Pharm Bull. 2003;26(8):1206-1210. PubMed
  14. Bolkent, S., Yanardag, R., Ozsoy-Sacan, O., and Karabulut-Bulan, O. Effects of parsley (Petroselinum crispum) on the liver of diabetic rats: a morphological and biochemical study. Phytother.Res 2004;18(12):996-999.
  15. Ozsoy-Sacan, O., Yanardag, R., Orak, H., Ozgey, Y., Yarat, A., and Tunali, T. Effects of parsley (Petroselinum crispum) extract versus glibornuride on the liver of streptozotocin-induced diabetic rats. J Ethnopharmacol 3-8-2006;104(1-2):175-181. PubMed
  16. Peterson, S., Lampe, J. W., Bammler, T. K., Gross-Steinmeyer, K., and Eaton, D. L. Apiaceous vegetable constituents inhibit human cytochrome P-450 1A2 (hCYP1A2) activity and hCYP1A2-mediated mutagenicity of aflatoxin B1. Food Chem.Toxicol. 2006;44(9):147 PubMed
  17. Gadi, D., Bnouham, M., Aziz, M., Ziyyat, A., Legssyer, A., Legrand, C., Lafeve, F. F., and Mekhfi, H. Parsley extract inhibits in vitro and ex vivo platelet aggregation and prolongs bleeding time in rats. J Ethnopharmacol 8-17-2009;125(1):170-174. PubMed
  18. Arslan S, Ucar R, Caliskaner AZ. A Cases of Near-fatal Anaphylaxis: Parsley "Over-use" as an Herbal Remedy. Med Arch. 2014;68(6):426-7.
  19. Foti C, Cassano N, Mistrello G, Amato S, Romita P, Vena GA. Contact urticaria to raw arugula and parsley. Ann Allergy Asthma Immunol. 2011 May;106(5):447-8. PubMed
  20. Farzaei MH, Abbasabadi Z, Ardekani MR, Rahimi R, Farzaei F. Parsley: a review of ethnopharmacology, phytochemistry and biological activities. J Tradit Chin Med. 2013;33(6):815-26. PubMed
  21. Kurtaran M, Koc NS, Aksun MS, Yildirim T, Yilmaz SR, Erdem Y. Petroselinum crispum, a commonly consumed food, affects sirolimus level in a renal transplant recipient: a case report. Ther Adv Drug Saf 2021;12:20420986211009358.

See these in context on the Parsley monograph →

Honey 40 references
  1. The Review of Natural Products by Facts and Comparisons. St. Louis, MO: Wolters Kluwer Co., 1999.
  2. Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: John Wiley & Sons, 1996.
  3. Bose B. Honey or sugar in treatment of infected wounds? Lancet 1982;1:963. PubMed
  4. Ozhan H, Akdemir R, Yazici M, et al. Cardiac emergencies caused by honey ingestion: a single centre experience. Emerg Med J 2004;21:742-4. PubMed
  5. Centers for Disease Control. Botulism in the Unites Sates, 1899-1996. Handbook for epidemiologists, clinicians, and laboratory workers, 1998. Available online: http://www.cdc.gov/ncidod/dbmd/diseaseinfo/botulism.PDF.
  6. Simon A, Traynor K, Santos K, et al. Medical honey for wound care - still the 'latest resort'? Evid Based Complement Alternat Med 2009;6:165-73. PubMed
  7. Gethin G, Cowman S. Case series of use of Manuka honey in leg ulceration. Int Wound J 2005;2:10-15. PubMed
  8. Ingle R, Levin J, Polinder K. Wound healing with honey - a randomised controlled trial. S Afr Med J 2006;96:831-5.
  9. Johnson DW, van Eps C, Mudge DW, et al. Randomized, controlled trial of topical exit-site application of honey (Medihoney) versus mupirocin for the prevention of catheter-associated infections in hemodialysis patients. J Am Soc Nephrol 2005;16:1456-62. PubMed
  10. Sukriti and Garg, S. K. Influence of honey on the pharmacokinetics of phenytoin in rabbits. Ind J Pharmacol 2002;34(147).
  11. Jung, A. and Ottosson, J. [Infantile botulism caused by honey]. Ugeskr Laeger 2001;163(2):169.
  12. Gunduz, A., Turedi, S., Uzun, H., and Topbas, M. Mad honey poisoning. Am J Emerg.Med 2006;24(5):595-598.
  13. van der Vorst, M. M., Jamal, W., Rotimi, V. O., and Moosa, A. Infant botulism due to consumption of contaminated commercially prepared honey. First report from the Arabian Gulf States. Med Princ.Pract. 2006;15(6):456-458. PubMed
  14. Tushar, T., Vinod, T., Rajan, S., Shashindran, C., and Adithan, C. Effect of honey on CYP3A4, CYP2D6 and CYP2C19 enzyme activity in healthy human volunteers. Basic Clin Pharmacol Toxicol 2007;100(4):269-272. PubMed
  15. Nilforoushzadeh, M. A., Jaffary, F., Moradi, S., Derakhshan, R., and Haftbaradaran, E. Effect of topical honey application along with intralesional injection of glucantime in the treatment of cutaneous leishmaniasis. BMC Complement Altern Med 2007;7:13. PubMed
  16. Koca, I. and Koca, A. F. Poisoning by mad honey: a brief review. Food Chem Toxicol 2007;45(8):1315-1318. PubMed
  17. Akinci, S., Arslan, U., Karakurt, K., and Cengel, A. An unusual presentation of mad honey poisoning: acute myocardial infarction. Int J Cardiol 2008;129(2):e56-e58. PubMed
  18. Yildirim, N., Aydin, M., Cam, F., and Celik, O. Clinical presentation of non-ST-segment elevation myocardial infarction in the course of intoxication with mad honey. Am J Emerg Med 2008;26(1):108.e-2. PubMed
  19. Shrestha, P., Vaidya, R., and Sherpa, K. Mad honey poisoning: a rare case report of seven cases. Nepal Med Coll J 2009;11(3):212-213.
  20. Fetzner, L., Burhenne, J., Weiss, J., Völker, M., Unger, M., Mikus, G., and Haefeli, W. E. Daily honey consumption does not change CYP3A activity in humans. J Clin Pharmacol 2011;51(8):1223-1232. PubMed
  21. Thamboo, A., Thamboo, A., Philpott, C., Javer, A., and Clark, A. Single-blind study of manuka honey in allergic fungal rhinosinusitis. J Otolaryngol Head Neck Surg 2011;40(3):238-243.
  22. Ahmed, A., Khan, R. A., Azim, M. K., Saeed, S. A., Mesaik, M. A., Ahmed, S., and Imran, I. Effect of natural honey on human platelets and blood coagulation proteins. Pak.J Pharm Sci 2011;24(3):389-397.
  23. Yarlioglues, M., Akpek, M., Ardic, I., Elcik, D., Sahin, O., and Kaya, M. G. Mad-honey sexual activity and acute inferior myocardial infarctions in a married couple. Tex.Heart Inst.J 2011;38(5):577-580.
  24. Biberoglu, S., Biberoglu, K., and Komsuoglu, B. Mad honey. JAMA 4-1-1988;259(13):1943.
  25. Biberoglu, K., Biberoglu, S., and Komsuoglu, B. Transient Wolff-Parkinson-White syndrome during honey intoxication. Isr.J.Med.Sci. 1988;24(4-5):253-254.
  26. Gössinger, H., Hruby, K., Pohl, A., Davogg, S., Sutterlütti, G., and Mathis, G. [Poisoning with andromedotoxin-containing honey]. Dtsch Med Wochenschr 1983;108(41):1555-1558.
  27. Fenicia, L., Ferrini, A. M., Aureli, P., and Pocecco, M. A case of infant botulism associated with honey feeding in Italy. Eur J Epidemiol 1993;9(6):671-673. PubMed
  28. Sutlupinar, N., Mat, A., and Satganoglu, Y. Poisoning by toxic honey in Turkey. Arch.Toxicol. 1993;67(2):148-150. PubMed
  29. von Malottki, K. and Wiechmann, H. W. [Acute life-threatening bradycardia: food poisoning by Turkish wild honey]. Dtsch.Med.Wochenschr. 7-26-1996;121(30):936-938.
  30. Abdulla CO, Ayubi A, Zulfiquer F, Santhanam G, Ahmed MA, Deeb J. Infant botulism following honey ingestion. BMJ Case Rep. 2012 Sep 7;2012.
  31. Johnson DW, Badve SV, Pascoe EM, Beller E, Cass A, Clark C, de Zoysa J, Isbel NM, McTaggart S, Morrish AT, Playford EG, Scaria A, Snelling P, Vergara LA, Hawley CM; HONEYPOT Study Collaborative Group. Antibacterial honey for the prevention of peritoneal-d
  32. Matos D, Serrano P, Menezes Brandão F. A case of allergic contact dermatitis caused by propolis-enriched honey. Contact Dermatitis. 2015 Jan;72(1):59-60. PubMed
  33. Oduwole O, Meremikwu MM, Oyo-Ita A, Udoh EE. Honey for acute cough in children. Cochrane Database Syst Rev. 2014 Dec 23;12:CD007094. PubMed
  34. Vezir E, Kaya A, Toyran M, Azkur D, Dibek Misirlioglu E, Kocabas CN. Anaphylaxis/angioedema caused by honey ingestion. Allergy Asthma Proc. 2014 Jan-Feb;35(1):71-4. PubMed
  35. Wang YT, Qi Y, Tang FY, et al. The effect of cupping therapy for low back pain: A meta-analysis based on existing randomized controlled trials. J Back Musculoskelet Rehabil. 2017;30(6):1187-1195. PubMed
  36. Oduwole O, Udoh EE, Oyo-Ita A, Meremikwu MM. Honey for acute cough in children. Cochrane Database Syst Rev. 2018;4:CD007094. PubMed
  37. Wong D, Albietz JM, Tran H, et al. Treatment of contact lens related dry eye with antibacterial honey. Cont Lens Anterior Eye. 2017;40(6):389-393. PubMed
  38. Martina SJ, Ramar LAP, Silaban MRI, Luthfi M, Govindan PAP. Antiplatelet Effectivity between Aspirin with Honey on Cardiovascular Disease Based on Bleeding Time Taken on Mice. Open Access Maced J Med Sci. 2019 Oct 14;7(20):3416-3420. PubMed
  39. Jhawar N, Gonzalez-Estrada A. Honey-induced anaphylaxis in an adult. QJM 2022;115(5):325-326. PubMed
  40. Di Costanzo M, De Paulis N, Peveri S, Montagni M, Berni Canani R, Biasucci G. Anaphylaxis caused by artisanal honey in a child: a case report. J Med Case Rep 2021;15(1):235. PubMed

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Ginger 64 references
  1. Fischer-Rasmussen W, Kjaer SK, Dahl C, Asping U. Ginger treatment of hyperemesis gravidarum. Eur J Obstet Gynecol Reprod Biol 1991;38:19-24. PubMed
  2. Jewell D, Young G. Interventions for nausea and vomiting in early pregnancy. Cochrane Database Syst Rev 2000;(2):CD000145. PubMed
  3. Vutyavanich T, Kraisarin T, Ruangsri R. Ginger for nausea and vomiting in pregnancy: randomized, double-masked, placebo-controlled trial. Obstet Gynecol 2001;97:577-82. DOI
  4. Backon J. Ginger in preventing nausea and vomiting of pregnancy; a caveat due to its thromboxane synthetase activity and effect on testosterone binding. Eur J Obstet Gynecol Reprod Biol 1991;42:163-4. PubMed
  5. Srivastava KC. Effect of onion and ginger consumption on platelet thromboxane production in humans. Prostaglandins Leukot Essent Fatty Acids 1989;35:183-5. PubMed
  6. Stewart JJ, Wood MJ, Wood CD, Mims ME. Effects of ginger on motion sickness susceptibility and gastric function. Pharmacology 1991;42:111-20. PubMed
  7. Smith C, Crowther C, Willson K, et al. A randomized controlled trial of ginger to treat nausea and vomiting in pregnancy. Obstet Gynecol 2004;103:639-45. PubMed
  8. Portnoi G, Chng LA, Karimi-Tabesh L, et al. Prospective comparative study of the safety and effectiveness of ginger for the treatment of nausea and vomiting in pregnancy. Am J Obstet Gynecol 2003;189:1374-7.. PubMed
  9. Wigler I, Grotto I, Caspi D, Yaron M. The effects of Zintona EC (a ginger extract) on symptomatic gonarthritis. Osteoarthritis Cartilage 2003;11:783-9. PubMed
  10. Ghayur MN, Gilani AH. Ginger lowers blood pressure through blockade of voltage-dependent calcium channels. J Cardiovasc Pharmacol 2005;45:74-80. PubMed
  11. Thomson M, Al-Qattan KK, Al-Sawan SM, et al. The use of ginger (Zingiber officinale Rosc.) as a potential anti-inflammatory and antithrombotic agent. Prostaglandins Leukot Essent Fatty Acids 2002;67:475-8. PubMed
  12. Kanerva L, Estlander T, Jolanki R. Occupational allergic contact dermatitis from spices. Contact Dermatitis 1996;35:157-62. PubMed
  13. Akhani SP, Vishwakarma SL, Goyal RK. Anti-diabetic activity of Zingiber officinale in streptozotocin-induced type I diabetic rats. J Pharm Pharmacol 2004;56:101-5.
  14. Kruth P, Brosi E, Fux R, et al. Ginger-associated overanticoagulation by phenprocoumon. Ann Pharmacother 2004;38:257-60. PubMed
  15. Jiang X, Williams KM, Liauw WS, et al. Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Br J Clin Pharmacol 2005;59:425-32. PubMed
  16. Borrelli F, Capasso R, Aviello G, et al. Effectiveness and safety of ginger in the treatment of pregnancy-induced nausea and vomiting. Obstet Gynecol 2005;105:849-56. PubMed
  17. Smith C, Crowther C, Wilson K et al. A randomized controlled trial of ginger to treat nausea and vomiting in pregnancy. Obstet Gynecol 2004;103:639-45. PubMed
  18. Jiang X, Blair EY, McLachlan AJ. Investigation of the effects of herbal medicines on warfarin response in healthy subjects: a population pharmacokinetic-pharmacodynamic modeling approach. J Clin Pharmacol 2006;46:1370-8. PubMed
  19. Chittumma P, Kaewkiattikun K, Wiriyasiriwach B. Comparison of the effectiveness of ginger and vitamin B6 for treatment of nausea and vomiting in early pregnancy: a randomized double-blind controlled trial. J Med Assoc Thai 2007;90:15-20.
  20. Ozgoli G, Goli M, Moattar F. Comparison of effects of ginger, mefenamic acid, and ibuprofen on pain in women with primary dysmenorrhea. J Altern Complement Med 2009;15:129-32. PubMed
  21. Black CD, Herring MP, Hurley DJ, O'Connor PJ. Ginger (Zingiber officinale) reduces muscle pain caused by eccentric exercise. J Pain 2010;11:894-903. PubMed
  22. Heitmann K, Nordeng H, Holst L. Safety of ginger use in pregnancy: results from a large population-based cohort study. Eur J Clin Pharmacol 2012 Jun 17. PubMed
  23. Ryan JL, Heckler CE, Roscoe JA, et al. Ginger (Zingiber officinale) reduces acute chemotherapy-induced nausea: a URCC CCOP study of 576 patients. Support Care Cancer. 2012;20:1479-89. PubMed
  24. Backon J. Ginger as an antiemetic: possible side effects due to its thromboxane synthetase activity. Anaesthesia. 1991;46(8):705-6.. PubMed
  25. Abebe W. Herbal medication: potential for adverse interactions with analgesic drugs. J Clin Pharm Ther. 2002;27:391-401. PubMed
  26. Argento A, Tiraferri E, Marzaloni M. [Oral anticoagulants and medicinal plants. An emerging interaction]. Ann Ital Med Int. 2000;15:139-43.
  27. Young HY, Liao JC, Chang YS, et al. Synergistic effect of ginger and nifedipine on human platelet aggregation: a study in hypertensive patients and normal volunteers. Am J Chin Med. 2006;34:545-51. PubMed
  28. Greenway FL, Liu Z, Martin CK, et al. Safety and efficacy of NT, an herbal supplement, in treating human obesity. Int J Obes (Lond). 2006;30:1737-41. PubMed
  29. Shalansky S, Lynd L, Richardson K, et al. Risk of warfarin-related bleeding events and supratherapeutic international normalized ratios associated with complementary and alternative medicine: a longitudinal analysis. Pharmacotherapy. 2007;27:1237-47. PubMed
  30. Lesho EP, Saullo L, Udvari-Nagy S. A 76-year-old woman with erratic anticoagulation. Cleve Clin J Med. 2004;71:651-6. PubMed
  31. Okonta JM, Uboh M, Obonga WO. Herb-Drug Interaction: A Case Study of Effect of Ginger on the Pharmacokinetic of Metronidazole in Rabbit. Indian Journal of Pharmaceutical Sciences (India) 2008;70(230):232. PubMed
  32. Chiang HM, Chao PD, Hsiu SL, et al. Ginger significantly decreased the oral bioavailability of cyclosporine in rats. Am J Chin Med. 2006;34:845-55. PubMed
  33. Bhandari U, Kanojia R, Pillai KK. Effect of ethanolic extract of Zingiber officinale on dyslipidaemia in diabetic rats. J Ethnopharmacol. 2005;97:227-30. PubMed
  34. Ojewole JA. Analgesic, antiinflammatory and hypoglycaemic effects of ethanol extract of Zingiber officinale (Roscoe) rhizomes (Zingiberaceae) in mice and rats. Phytother Res. 2006;20:764-72.
  35. Al-Amin ZM, Thomson M, Al-Qattan KK, et al. Anti-diabetic and hypolipidaemic properties of ginger (Zingiber officinale) in streptozotocin-induced diabetic rats. Br J Nutr. 2006;96:660-6.
  36. Islam MS, Choi H. Comparative effects of dietary ginger (Zingiber officinale) and garlic (Allium sativum) investigated in a type 2 diabetes model of rats. J Med Food. 2008;11:152-9.
  37. Cady RK, Goldstein J, Nett R, et al. A double-blind placebo-controlled pilot study of sublingual feverfew and ginger (LipiGesic M) in the treatment of migraine. Headache 2011;51:1078-86.
  38. Futrell, J. M. and Rietschel, R. L. Spice allergy evaluated by results of patch tests. Cutis 1993;52(5):288-290.
  39. Sripramote, M. and Lekhyananda, N. A randomized comparison of ginger and vitamin B6 in the treatment of nausea and vomiting of pregnancy. J Med Assoc.Thai. 2003;86(9):846-853.
  40. Lohsiriwat, S., Rukkiat, M., Chaikomin, R., and Leelakusolvong, S. Effect of ginger on lower esophageal sphincter pressure. J.Med.Assoc.Thai. 2010;93(3):366-372.
  41. Liu, P. H. and Ho, H. L. Ginger and drug bezoar induced small bowel obstruction. J R.Coll.Surg.Edinb. 1983;28(6):397-398.
  42. Maghbooli M, Golipour F, Moghimi Esfandabadi A, Yousefi M. Comparison between the efficacy of ginger and sumatriptan in the ablative treatment of the common migraine. Phytother Res 2014;28(3):412-5. PubMed
  43. Mahluji S, Attari VE, Mobasseri M, Payahoo L, Ostadrahimi A, Golzari SE. Effects of ginger (Zingiber officinale) on plasma glucose level, HbA1c and insulin sensitivity in type 2 diabetic patients. Int J Food Sci Nutr 2013;64(6):682-6.
  44. Mozaffari-Khosravi H, Talaei B, Jalali BA, Najarzadeh A, Mozayan MR. The effect of ginger powder supplementation on insulin resistance and glycemic indices in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled trial. Complement PubMed
  45. Paramdeep G. Efficacy and tolerability of ginger (Zingiber officinale) in patients of osteoarthritis of knee. Indian J Physiol Pharmacol 2013;57(2):177-83.
  46. Rahnama P, Montazeri A, Huseini HF, Kianbakht S, Naseri M. Effect of Zingiber officinale R. rhizomes (ginger) on pain relief in primary dysmenorrhea: a placebo randomized trial. BMC Complement Altern Med 2012;12:92. PubMed
  47. Viljoen E, Visser J, Koen N, Musekiwa A. A systematic review and meta-analysis of the effect and safety of ginger in the treatment of pregnancy-associated nausea and vomiting. Nutr J 2014;13:20. PubMed
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Sage 27 references
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Ceylon Cinnamon 22 references
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Cassia Cinnamon 20 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.

© 2021 Therapeutic Research Center, LLC

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