Interactions on record — worth a quick check against your medications. Based on 15 of 17 ingredients. Check your meds →
Dietary supplement

Inflamma-Less Ingredients & Drug Interactions

by Irwin Naturals

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

Inflamma-Less is a dietary supplement by Irwin Naturals with 17 active ingredients. Its ingredients are commonly taken for common cold and immune support, antioxidant support, skin health and collagen formation.Based on those ingredients, 1,586 medications have a known interaction with it, the most serious rated moderate. The ingredients most likely to interact are Quercetin, Turmeric Root Extract, BioPerine. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Inflamma-Less by Irwin Naturals

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

Partial disclosure
Ingredient Transparency · database check
Partial

Most active ingredients list an amount, but at least one is hidden in a blend or missing.

Why this rating?
  • The label discloses an exact amount for 9 of its 16 active ingredients.
  • “BioPerine Complex” is a proprietary blend — the label gives one combined amount (6 mg) without saying how much of each component you get.
  • “Turmeric Root Extract” is listed as a grouped ingredient — the label gives one combined amount (200 mg) without saying how much of each component you get.
  • “Citrus Fruit Extract” is listed as a grouped ingredient — the label gives one combined amount (90 mg) without saying how much of each component you get.

Inflamma-Less contains 16 active ingredients designed to support the body's natural inflammatory response. The formula includes vitamin C for antioxidant support; papain and bromelain, enzymes that break down proteins; pancreatin, another digestive enzyme; ginger rhizome extract, traditionally used for comfort; zinc for immune function; the polyphenol resveratrol; quercetin and hesperidin, flavonoid compounds; chymotrypsin and trypsin, additional proteolytic enzymes; black pepper extract (BioPerine) to enhance absorption; omega-3 fatty acids; curcuminoids from turmeric; and Indian frankincense gum resin extract.

Several of these are grouped in a "BioPerine Complex" and "Citrus Fruit Extract" blend. The softgel capsule also contains inactive ingredients including gelatin, glycerin, soy lecithin, and food colorants.

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: Support healthy tissue response to physical stress.
  • We looked for evidence on: Bruises, Athletic performance, Sports injury recovery, Exercise-induced inflammation, Muscle soreness, Post-exertion discomfort.
  • The closest evidence on file: Quercetin is rated "Possibly Ineffective" for Athletic performance (Natural Medicines).
  • Also on file: Ginger is rated "Possibly Ineffective" for Exercise-induced muscle soreness.
  • Also on file: Boswellia Serrata is rated "Insufficient Reliable Evidence To Rate" for Exercise-induced muscle soreness.

The evidence for Inflamma-Less's ingredients is mixed. Vitamin C is effective for preventing vitamin C deficiency and possibly effective for anemia of chronic disease, cataracts, and reducing exercise-induced respiratory infections.

Ginger is possibly effective for pregnancy-related nausea, menstrual discomfort, and osteoarthritis, though possibly ineffective for exercise-induced muscle soreness and chemotherapy nausea. Zinc is effective for zinc deficiency and likely effective for Wilson disease, with possible benefit in acne, macular degeneration, and diabetes.

For most other ingredients—papain, bromelain, chymotrypsin, trypsin, resveratrol, quercetin, hesperidin, and black pepper—the evidence we hold is insufficient to establish effectiveness for any condition, meaning these benefits are unproven based on available data.

The evidence, ingredient by ingredient Vitamin C Papain Bromelain Ginger Black Pepper Zinc Turmeric Chymotrypsin

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

Vitamin C is generally well tolerated at normal dietary amounts, though high doses can cause abdominal cramps, diarrhea, nausea, and heartburn; rare cases of kidney stones or kidney damage at very high doses have been reported. Ginger is generally well tolerated in typical amounts, though higher doses (above 5 grams daily) may cause abdominal discomfort, heartburn, and diarrhea.

Zinc is well tolerated below 40 mg daily, but higher doses can cause nausea, metallic taste, and copper deficiency with long-term use. Papain may cause allergic reactions and digestive irritation; high doses can cause esophageal perforation.

Bromelain is generally well tolerated short-term but may cause diarrhea, flatulence, and allergic reactions in sensitive people. Chymotrypsin and trypsin are generally tolerated for short-term use but can rarely cause anaphylactic reactions; trypsin may cause mild gastrointestinal upset.

Resveratrol, black pepper, hesperidin, and quercetin are generally well tolerated at typical doses, though high-dose data is limited. For pregnancy: vitamin C at normal dietary amounts is safe, but avoid high-dose supplements; ginger amounts used for morning sickness may be acceptable with your doctor's approval; papain, bromelain, chymotrypsin, and trypsin safety data advise against use; and hesperidin and quercetin lack sufficient safety information—discuss with your doctor.

For breastfeeding, data is insufficient for papain, bromelain, chymotrypsin, trypsin, resveratrol, hesperidin, and quercetin; ginger and vitamin C at normal amounts are generally acceptable.

Side effects, ingredient by ingredient Vitamin C Papain Bromelain Ginger Black Pepper Zinc Turmeric Chymotrypsin

Meds to double-check

Moderate interaction found
Known Interaction Concern · database check
Moderate identified

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

Why this rating?
  • 12 of the 14 matched ingredients can interact with medications — Boswellia Serrata, Papain, Quercetin, Resveratrol, Turmeric, among others.
  • The most serious interaction on file is rated Moderate.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; lithium.
  • For scale: 1,583 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 Inflamma-Less, check your medications for interactions with these types: blood thinners and antiplatelet drugs (warfarin, other anticoagulants) — vitamin C, papain, bromelain, ginger, resveratrol, hesperidin, and quercetin all raise bleeding risk. Antidiabetes medications — ginger may lower blood sugar too much.

Antibiotics (quinolones, tetracyclines, cephalexin) — zinc reduces their absorption. Thyroid medication (levothyroxine) — vitamin C may increase absorption.

Chemotherapy drugs — vitamin C's antioxidant effects may reduce activity. Heart and blood pressure drugs (nifedipine, losartan, propranolol, and others) — multiple ingredients interact.

HIV medications (indinavir, ritonavir, integrase inhibitors, nevirapine) — zinc and other components may reduce levels. No interactions are documented for chymotrypsin, trypsin, and several other ingredients we could not fully check.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glancePartially disclosed formula with no established evidence rating for its marketed use. Moderate medication interactions have been identified, and safety information is well characterized.

Inflamma-Less contains a blend of enzymes and plant extracts that may appeal to people seeking natural anti-inflammatory support, though proof of effectiveness for most ingredients is limited. Because this product interacts with a large number of medications—especially blood thinners, diabetes drugs, antibiotics, and heart medications—you should run your complete medication list through our checker before starting.

If you take any prescription drugs, talk to your pharmacist first.

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

Assessment coverage: 15 of 16 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Feb 23, 2025.

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

At a glance

General information

Key facts about Inflamma-Less, straight from the product label.

Brand Irwin Naturals
Barcode (UPC) 710363568191
Net contents 80 Liquid Softgel(s)
Market status On market
Date entered into DSLD Feb 23, 2025
DSLD ID 323285
Product type Other Combinations
Supplement form Softgel Capsule
Dietary claims / uses Nutrient, All Other, Structure/Function
Intended target group(s) Adult (18 - 50 Years), Women (not pregnant or lactating)
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 Inflamma-Less by Irwin Naturals, sourced from the NIH Dietary Supplement Label Database.

Supplement Facts

Daily Value (DV) Target Group(s):
Adults and children 4 or more years of age
Minimum serving Sizes:
2 Liquid Soft-Gel(s)
Maximum serving Sizes:
2 Liquid Soft-Gel(s)
Servings per container
40
UPC/BARCODE
710363568191
IngredientAmount% DV
Calories20 Calorie(s)--
Total Carbohydrates1 Gram(s)1%
Omega-3 Fatty Acids270 mg--
Vitamin C90 mg100%
Papain0 NP--
Bromelain0 NP--
Cholesterol5 mg2%
Total Fat1 Gram(s)1%
Protein1 Gram(s)--
BioPerine Complex6 mg--
Ginger Rhizome Extract0 NP--
Zinc2 mg18%
BioPerine0 NP--
Turmeric Root Extract200 mg--
Chymotrypsin0 NP--
Trypsin0 NP--
Resveratrol9 mg--
Pancreatin0 NP--
Ginger Rhizome Extract10 mg--
Hesperidin40.5 mg--
Quercetin90 mg--
Curcuminoids190 mg--
Indian Frankincense Gum Resin Extract200 mg--
Citrus Fruit Extract90 mg--
Fish Oil900 mg--

Other ingredients: Gelatin, Water, Purified, Glycerin, Soy Lecithin, Beeswax, Maltodextrin, Dextrin, Titanium Dioxide, Turmeric, Sodium Copper Chlorophyllin

Tap any ingredient to jump to its full detail below.

Label statements
These statements are the manufacturer’s wording, reproduced from the product label — the label is saying it, not HelloPharmacist. We don’t verify or endorse them.
Formula

Ayurvedic herbs: Indian botanicals have been used traditionally to support a healthy tissue response to physical stress and may positively influence feelings of discomfort due to strenuous physical activity. Proteolytic enzymes: Proteolytic enzymes are protein-digesting enzymes. When taken with meals, these enzymes can help to breakdown food nutrients. But when taken in between meals (away from food), these enzymes may have beneficial effects on tissue response to stress, overexertion, strenuous physical activity and exercise. Targeted nutrients: Vitamins, minerals and bioflavonoids can help to protect cells and support the body's own natural tissue formation. This advanced combination of ingredients also includes Omega-3 fatty acids from fish oil. What makes us different: Patented BioPerine - Our special BioPerine Complex enhances the bioavailability, absorption and potency of many nutrients.

Omega-3 oils, turmeric extract and proteolytic enzymes

Seals/Symbols

NSF Contents Certified

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.

Precautions

Usage warnings: Do not use if safety seal is broken. Do not use if you have a bile duct obstruction. Do not exceed recommended daily intake. Warning: (State of California Prop 65) This product contains a chemical known to the State of California to cause birth defects or other reproductive harm.

Check with your doctor before using this product if you are using medication or have any medical conditions. Do not use if you may become pregnant, are pregnant or nursing.

Not intended for use by persons under 18. Keep out of reach of children.

Contains: Dairy, fish (anchovy, sardine), soy

Storage

Store in a cool, dry place.

General Statements

Questions: Contact consumer affairs 100+ highly specialized products: www.IrwinNaturals.com

Formulation

Support comfort, mobility & flexibility

No preservatives added.

Inflamma-Less Nature offers a different approach to promoting comfort, mobility and flexibility. Botanical extracts, proteolytic enzymes, and targeted nutrients are combined in this product to create a powerful 3-pronged formula that supports the body's natural inflammatory response. Inflamma-Less can be used daily for health maintenance or as needed to support the body's natural inflammatory response.Liquid Soft-Gels - The nutrients in these easy-to-swallow liquid soft-gels are released fast. Other forms of delivery can contain binders and fillers that may cause stomach upset and offer no traditional value. Advanced Liquid Soft-Gels provide an optimum delivery system. Quality assurance - Irwin Naturals is committed to providing the highest quality products for your health. We employ compliance testing to ensure purity and potency. Global responsibility - Over the years we have donated to organizations that support the environment and the health of children.

FDA Statement of Identity

Dietary Supplement

Suggested/Recommended/Usage/Directions

Directions: (Adult) Take two (2) liquid soft-gels with a full glass (8oz) of water twice a day on an empty stomach as needed.

Brand IP Statement(s)

BioPerine is a registered trademark of Sabinsa Corporation.

See for yourself

Inflamma-Less by Irwin Naturals label

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

What’s inside

The Ingredients in Inflamma-Less by Irwin Naturals

These are the 17 active ingredients this product is made of. Select any to open its full monograph.

Serving size2 Liquid Soft-Gel(s) Dosage formSoftgel Capsule Servings per container40 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.

Vitamin C

Interacts with
207 drugs
90 mg per serving Form: Ascorbic Acid

Vitamin C (ascorbic acid) is an essential nutrient your body needs but cannot make, so you must get it from food or supplements. It's important for im...

Vitamin C monograph & interactions

Papain

Interacts with
2 drugs
0 NP per serving

Papain is a protein-digesting enzyme from the papaya plant that is used in digestive supplements and some topical products. While it has clear food an...

Papain monograph & interactions

Bromelain

Interacts with
141 drugs
0 NP per serving

Bromelain is a group of protein-digesting enzymes from pineapple that people take mainly for inflammation, swelling, and sinus problems. Some early st...

Bromelain monograph & interactions

Protein

1 Gram(s) per serving

BioPerine Complex

6 mg per serving

Zinc

Interacts with
67 drugs
2 mg per serving Form: Zinc Picolinate

Zinc is an essential mineral that your body needs for immune function, wound healing, taste, and smell. Most people get enough from food, but suppleme...

Zinc monograph & interactions

Turmeric Root Extract

Interacts with
1,133 drugs
200 mg per serving

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

Turmeric Root Extract monograph & interactions

Chymotrypsin

No known
interactions
0 NP per serving

Chymotrypsin is a protein-digesting (proteolytic) enzyme, usually taken from the pancreas of cattle or pigs, that is mainly used to help reduce swelli...

Chymotrypsin monograph & interactions

Trypsin

No known
interactions
0 NP per serving

Trypsin is a protein-digesting enzyme usually taken from the pancreas of animals and used either by mouth (often combined with other enzymes like chym...

Trypsin monograph & interactions

Resveratrol

Interacts with
822 drugs
9 mg per serving Form: Japanese Knotweed Root Extract

Resveratrol is a plant compound found in red grapes, berries, and peanuts that is popular for heart health, anti-aging, and antioxidant support. While...

Resveratrol monograph & interactions

Pancreatin

0 NP per serving

Ginger Rhizome Extract

Interacts with
1,007 drugs
10 mg per serving

Ginger is a widely used culinary spice with a long history in traditional medicine, and it has the strongest evidence for helping with nausea and vomi...

Ginger Rhizome Extract monograph & interactions

Quercetin

Interacts with
1,169 drugs
90 mg per serving Form: Quercetin Dihydrate

Quercetin is a plant flavonoid with antioxidant and anti-inflammatory properties found in many common foods and sold as a supplement. While early rese...

Quercetin monograph & interactions

Indian Frankincense Gum Resin Extract

Interacts with
952 drugs
200 mg per serving

Boswellia serrata is a tree resin used in traditional medicine, mainly for joint pain and inflammation. Some studies suggest it may help with osteoart...

Indian Frankincense Gum Resin Extract monograph & interactions

Citrus Fruit Extract

90 mg per serving

Fish Oil

Interacts with
327 drugs
900 mg per serving Form: Anchovy Oil, Sardine Oil

Fish oil provides omega-3 fatty acids (EPA and DHA) that are best known for lowering high triglyceride levels. The evidence for other heart and health...

Fish Oil monograph & interactions

Other (inactive) ingredients: Gelatin, Water, Purified, Glycerin, Soy Lecithin, Beeswax, Maltodextrin, Dextrin, Titanium Dioxide, Turmeric, Sodium Copper Chlorophyllin. These complete the product’s ingredient list but are not active constituents.

Interaction report

Inflamma-Less by Irwin Naturals Drug Interactions

Want to check YOUR meds against Inflamma-Less?

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
1,586Drugs
1,580 Moderate 6 Minor

Ingredients driving the most interactions

Quercetin 1,169
BioPerine 1,019

Each ingredient & the kinds of drugs it affects

For each ingredient in Inflamma-Less 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.

Quercetin21 drug types · 1,169 drugs

Antidiabetes Drugs

Theoretically, concomitant use of quercetin and antidiabetes drugs might increase the risk of hypoglycemia.

Clinical research suggests that a combination of quercetin, myricetin, and chlorogenic acid reduce levels of fasting glucose in patients with type 2 diabetes, including those already taking antidiabetes agents. The effect of quercetin alone is unknown.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking quercetin with antihypertensive drugs might increase the risk of hypotension.

Quercetin can modestly decrease blood pressure in people with mild hypertension. Theoretically, it might have additive blood pressure lowering effects when used with antihypertensive drugs.

Likelihood Possible Evidence B
Cyclosporine (Neoral, Sandimmune)

Theoretically, concomitant use might increase the levels and adverse effects of cyclosporine.

A small study in healthy volunteers shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of a single dose of cyclosporine, possibly due to inhibition of p-glycoprotein or cytochrome P450 3A4 (CYP3A4), which metabolizes cyclosporin.

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

Theoretically, concomitant use might increase the levels and adverse effects of CYP2C8 substrates.

In vitro research shows that quercetin inhibits CYP2C8. Inhibition of paclitaxel (Taxol) metabolism via CYP2C8 has been reported in vitro. However, a small study in humans found no effect of quercetin on rosiglitazone (Avandia), which is also a CYP2C8 substrate.

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

Theoretically, concomitant use might increase the levels and adverse effects of CYP2C9 substrates.

A small clinical study in healthy volunteers shows that taking quercetin 500 mg twice daily for 10 days prior to taking diclofenac, a CYP2C9 substrate, increases diclofenac plasma levels by 75% and prolongs the half-life by 32.5%. Animal research also shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar), a substrate of CYP2C9. Furthermore, laboratory research shows that quercetin inhibits CYP2C9.

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

Theoretically, concomitant use might increase the levels and adverse effects of CYP2D6 substrates.

In vitro research show that quercetin inhibits CYP2D6. This effect has not been reported in humans.

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

Theoretically, concomitant use might alter the effects and adverse effects of CYP3A4 substrates.
A small clinical study in healthy volunteers shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of a single dose of cyclosporine (Neoral, Sandimmune), a substrate of CYP3A4. Animal research also shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar) and quetiapine (Seroquel), substrates of CYP3A4. Other laboratory research also shows that quercetin inhibits CYP3A4. However, one clinical study shows that quercetin can increase the metabolism of midazolam, a substrate of CYP3A4, and decrease serum concentrations of midazolam by about 24% in some healthy individuals, suggesting possible induction of CYP3A4.

Likelihood Possible Evidence D
Diclofenac (Voltaren, Others)

Theoretically, concomitant use might increase the levels and adverse effects of diclofenac.

A small clinical study in healthy volunteers shows that taking quercetin 500 mg twice daily for 10 days prior to taking diclofenac increases diclofenac plasma levels by 75% and prolongs the half-life by 32.5%. This is thought to be due to inhibition of CYP2C9 by quercetin.

Likelihood Probable Evidence B
Losartan (Cozaar)

Theoretically, concomitant use might increase the effects and adverse effects of losartan and decrease the effects of its active metabolite.

Animal research shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar) while decreasing plasma levels of losartan's active metabolite. This metabolite, which is around 10-fold more potent than losartan, is the result of cytochrome P450 (CYP) 2C9- and CYP3A4-mediated transformation of losartan. Additionally, in vitro research shows that quercetin may inhibit P-glycoprotein-mediated efflux of losartan from the intestines, resulting in increased absorption of losartan. These results suggest that concomitant use of quercetin and losartan might increase systemic exposure to losartan while also decreasing plasma concentrations of losartan's active and more potent metabolite.

Likelihood Possible Evidence D
Midazolam (Versed)

Theoretically, concomitant use might decrease the levels and effects of midazolam.

A small clinical study in healthy volunteers shows that quercetin can increase the metabolism of midazolam, with a decrease in AUC of about 24%.

Likelihood Possible Evidence B
Mitoxantrone

Theoretically, quercetin might increase the effects and adverse effects of mitoxantrone.
In vitro research shows that quercetin increases the intracellular accumulation and cytotoxicity of mitoxantrone, possibly through inhibition of breast cancer resistance protein (BCRP), of which mitoxantrone is a substrate. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Organic Anion Transporter 1 (Oat1) Substrates

Theoretically, concomitant use might increase the effects and adverse effects of OAT1 substrates.

In vitro research shows that quercetin is a strong non-competitive inhibitor of OAT1, with half-maximal inhibitory concentration (IC50) values less than 10 mcM. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Organic Anion Transporter 3 (Oat3) Substrates

Theoretically, concomitant use might increase the effects and adverse effects of OAT3 substrates.

In vitro research shows that quercetin is a strong non-competitive inhibitor of OAT3, with half-maximal inhibitory concentration (IC50) values as low as 0.75 mcM. So far, this interaction has not been reported in humans.

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

Theoretically, concomitant use might increase the effects and adverse effects of OATP substrates.

In vitro evidence shows that quercetin can inhibit organic anion-transporting peptide (OATP) 1B1-mediated uptake of estrone-3-sulfate and pravastatin. Furthermore, clinical research in healthy males shows that intake of quercetin along with pravastatin increases the AUC of pravastatin by 24%, prolongs its half-life by 14%, and decreases its apparent clearance by 18%, suggesting that quercetin modestly inhibits the uptake of pravastatin in hepatic cells.

Likelihood Possible Evidence B
P-Glycoprotein Substrates

Theoretically, concomitant use might alter the effects and adverse effects of P-glycoprotein substrates.

There is preliminary evidence that quercetin inhibits the gastrointestinal P-glycoprotein efflux pump, which might increase the bioavailability and serum levels of drugs transported by the pump. A small study in healthy volunteers reported that pretreatment with quercetin increased bioavailability and plasma levels after a single dose of cyclosporine (Neoral, Sandimmune). Also, two small studies have shown that quercetin might decrease the absorption of talinolol, a substrate transported by the gastrointestinal P-glycoprotein efflux pump. However, in another small study, several days of quercetin treatment did not significantly affect the pharmacokinetics of saquinavir (Invirase). The reason for these discrepancies is not entirely clear. Until more is known, use quercetin cautiously in combination with P-glycoprotein substrates.

Likelihood Possible Evidence B
Pravastatin (Pravachol)

Theoretically, concomitant use might increase the effects and adverse effects of pravastatin.
In vitro evidence shows that quercetin can inhibit OATP 1B1-mediated uptake of pravastatin. Also, preliminary clinical research in healthy males shows that intake of quercetin along with pravastatin increases the maximum concentration of pravastatin by 24%, prolongs its half-life by 14%, and decreases its apparent clearance by 18%, suggesting that quercetin modestly inhibits the uptake of pravastatin in hepatic cells.

Likelihood Possible Evidence B
Prazosin (Minipress)

Theoretically, quercetin might increase the effects and adverse effects of prazosin.
In vitro research shows that quercetin inhibits the transcellular efflux of prazosin, possibly through inhibition of breast cancer resistance protein (BCRP), of which prazosin is a substrate. BCRP is an ATP-binding cassette efflux transporter in the intestines, kidneys, and liver. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Quetiapine (Seroquel)

Theoretically, concomitant use might increase the effects and adverse effects of quetiapine.
Animal research shows that pretreatment with quercetin can increase plasma levels of quetiapine and prolong its clearance, possibly due to inhibition of cytochrome P450 3A4 (CYP3A4) by quercetin. Additionally, the brain-to-plasma ratio of quetiapine concentrations increased, possibly due to inhibition of P-glycoprotein at the blood-brain barrier. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Quinolone Antibiotics

Theoretically, concomitant use might inhibit the effects of quinolone antibiotics.
In vitro, quercetin binds to the DNA gyrase site on bacteria, which may interfere with the activity of quinolone antibiotics.

Likelihood Possible Evidence B
Sulfasalazine (Azulfidine)

Theoretically, quercetin might increase the effects and adverse effects of sulfasalazine.
Animal research shows that quercetin increases the maximum serum concentration (Cmax) and area under the curve (AUC) of sulfasalazine, possibly through inhibition of breast cancer resistance protein (BCRP), of which sulfasalazine is a substrate. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, quercetin may increase the risk of bleeding if used with warfarin.
Animal and in vitro studies show that quercetin might increase serum levels of warfarin. Quercetin and warfarin have the same human serum albumin (HSA) binding site, and in vitro research shows that quercetin has stronger affinity for the HSA binding site and can theoretically displace warfarin, causing higher serum levels of warfarin. Animal research shows that taking quercetin for 2 weeks before initiating warfarin increases the maximum serum level of warfarin by 30%, the half-life by 10%, and the overall exposure by 63% when compared with control. Concomitant administration of quercetin and warfarin, without quercetin pre-treatment, also increased these measures, but to a lesser degree. Researchers theorize that inhibition of CYP3A4 by quercetin may explain these effects. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D

Turmeric Root Extract24 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

BioPerine17 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 Rhizome Extract14 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

Indian Frankincense Gum Resin Extract6 drug types · 952 drugs

Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, Boswellia serrata might increase the levels of CYP1A2 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP1A2 enzymes.

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

Theoretically, Boswellia serrata might increase the levels of CYP2C19 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP2C19 enzymes.

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

Theoretically, Boswellia serrata might increase the levels of CYP2C9 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP2C9 enzymes.

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

Theoretically, Boswellia serrata might increase the levels of CYP2D6 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP2D6 enzymes.

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

Theoretically, Boswellia serrata might increase or decrease the levels and clinical effects of CYP3A4 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP3A4 enzymes. Other in vitro research shows that Boswellia serrata extract inhibits CYP3A4 enzymes at most concentrations, although it may modestly induce enzyme activity at low concentrations.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, Boswellia serrata might alter the effects of immunosuppressive drugs.
Some in vitro research suggests that Boswellia serrata extracts might inhibit mediators of autoimmune disorders such as leukotrienes and reduce production of antibodies and cell-mediated immunity. However, other in vitro research suggests that, when coupled with calcium ions, boswellic acids containing the keto group have immunostimulant properties within specific cell signaling pathways.

Likelihood Possible Evidence D

Resveratrol5 drug types · 822 drugs

Anticoagulant/Antiplatelet Drugs

Resveratrol may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Resveratrol seems to have antiplatelet effects.

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

Theoretically, resveratrol might increase levels of drugs metabolized by CYP1A2.
In vitro research shows that resveratrol can inhibit CYP1A2 enzymes. However, this interaction has not been reported in humans.

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

Theoretically, resveratrol might increase levels of drugs metabolized by CYP2C19.
In vitro research shows that resveratrol can inhibit CYP2C19 enzymes. However, this interaction has not been reported in humans.

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

Resveratrol might increase levels of drugs metabolized by CYP2E1.
In vitro research suggests that resveratrol inhibits CYP2E1 isoenzyme. Also, a pharmacokinetic study shows that taking resveratrol 500 mg daily for 10 days prior to taking a single dose of chlorzoxazone 250 mg increases the maximum concentration of chlorzoxazone by about 54%, the area under the curve of chlorzoxazone by about 72%, and the half-life of chlorzoxazone by about 35%. Chlorzoxazone is used as a probe drug for CYP2E1.

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

Theoretically, resveratrol might increase levels of drugs metabolized by CYP3A4.
In vitro research shows that resveratrol can inhibit the CYP3A4 enzyme. However, clinical research shows that taking resveratrol 3000 mg daily for 8 weeks does not necessitate dose adjustments to medications metabolized by CYP3A4.

Likelihood Possible Evidence D

Hesperidin7 drug types · 702 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, hesperidin may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Animal research suggests that hesperetin, a bioflavonoid aglycone derivative of hesperidin, may have antiplatelet activity.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, taking hesperidin with antihypertensive drugs might increase the risk of hypotension.
Some clinical and animal research shows that hesperidin can decrease blood pressure. However, other clinical research shows that hesperidin does not affect blood pressure.

Likelihood Possible Evidence D
Celiprolol (Celicard)

Theoretically, hesperidin may decrease the levels and clinical effects of celiprolol.
Animal research shows that concomitant use of hesperidin may reduce the plasma area under the curve of celiprolol by up to 75%. This effect has not been reported in humans.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, concomitant use with CNS depressants may cause additive sedative effects.
Animal studies show that hesperidin has sedative effects, due to opioid receptor activity and can increase sedation when used with diazepam. This effect has not been reported in humans.

Likelihood Possible Evidence D
Diltiazem (Cardizem, Others)

Theoretically, hesperidin may increase the levels and clinical effects of diltiazem.
Animal research suggests that hesperidin may enhance the bioavailability of diltiazem, increasing the plasma area under the curve of diltiazem by up to 65.3%. This effect has not been reported in humans.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, hesperidin might inhibit P-glycoprotein-mediated drug efflux and potentially increase levels of drugs that are substrates of P-glycoprotein.
In vitro research shows that hesperidin can inhibit P-glycoprotein efflux. This effect has not been reported in humans.

Likelihood Possible Evidence D
Verapamil (Calan, Others)

Theoretically, hesperidin might increase the levels and clinical effects of verapamil.
Animal research suggests that hesperidin may enhance the bioavailability of verapamil, increasing the plasma area under the curve of verapamil by 96.8%. This effect has not been reported in humans

Likelihood Possible Evidence D

Fish Oil9 drug types · 327 drugs

Antihypertensive Drugs

Theoretically, taking fish oil with antihypertensive drugs might increase the risk of hypotension.
Clinical evidence indicates that fish oils can modestly lower blood pressure and might have additive effects in patients treated with antihypertensives.

Likelihood Probable Evidence B
Contraceptive Drugs

Theoretically, taking fish oil with contraceptive drugs might decrease the triglyceride-lowering effects of fish oil.
There is some evidence that contraceptive drugs might interfere with the triglyceride lowering effects of fish oils.

Likelihood Probable Evidence B
Cyclosporine (Neoral, Sandimmune)

Taking fish oil with cyclosporine might increase levels and adverse effects of cyclosporine.
In kidney transplant recipients on a general immunosuppressive regimen, taking omega-3 fatty acids daily seems to increase peak blood levels of cyclosporine when compared with placebo. This increase was as much as 20% after one month. However, the area under the curve was not significantly affected.

Likelihood Probable Evidence B
Orlistat (Xenical, Alli)

Theoretically, taking fish oil with orlistat might decrease the absorption of fish oil fatty acids.
Orlistat binds lipase in the gastrointestinal tract and reduces fat absorption. Theoretically, taking fish oil with orlistat might decrease absorption of fish oil fatty acids. To avoid this potential interaction, recommend separating administration of orlistat and fish oil by at least 2 hours.

Likelihood Probable Evidence D
Sirolimus (Rapamune)

Taking fish oil with sirolimus might increase levels and adverse effects of sirolimus.
Pharmacokinetic research shows that omega-3 fatty acids increase exposure to sirolimus in kidney transplant patients on a calcineurin inhibitor-free immunosuppressive regimen. A 25% dose reduction in sirolimus was required to keep patients within the expected trough-concentration window. Researchers hypothesize that this may be due to inhibition of cytochrome P450 3A4 (CYP3A4) by fish oil, although this has not been confirmed in clinical research.

Likelihood Probable Evidence B
Tacrolimus (Prograf)

Taking fish oil with tacrolimus might increase levels and adverse effects of tacrolimus.
In a small group of patients, taking fish oil 2.6 grams (Omacor) daily for 4 weeks increased the 8-hour area under the curve of tacrolimus by 25% when compared with baseline. Peak levels were increased by approximately 22%. Researchers hypothesize that this may be due either to an increase in bioavailability or to inhibition of cytochrome P450 3A4 (CYP3A4) by fish oil, although this has not been confirmed in clinical research.

Likelihood Probable Evidence B
Anticoagulant/Antiplatelet Drugs

Fish oil may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, evidence is conflicting.
While fish oil may not be a potent inhibitor of platelet function, high doses of fish oil might have antiplatelet effects. Theoretically, concomitant use of fish oil with anticoagulant or antiplatelet drugs may increase the risk of bleeding. However, the most rigorous research shows that short-term doses of fish oil 10 grams daily or long-term doses of 1.5 grams daily for up to 52 weeks does not increase the risk of bleeding or affect coagulation parameters in chronically ill and vulnerable patients. Other controlled research shows that fish oil does not affect platelet function or increase the risk of bleeding. Some research even suggests that perioperative fish oil use decreases bleeding risk. Some research suggests fish oil does not have additive antiplatelet effects when combined with aspirin, but other clinical evidence suggests that adding fish oil to low-dose aspirin treatment increases antiplatelet effects in patients who are aspirin-resistant. Also, some clinical research seems to show that fish oil has additive antiplatelet effects when used with aspirin and clopidogrel compared to aspirin and clopidogrel alone.

Likelihood Unlikely Evidence B
Platinum Agents

Theoretically, taking fish oil with platinum agents can cause resistance to platinum agents, potentially decreasing their effectiveness.
Platinum-induced fatty acids (PIFAs) are fatty acids secreted from human and mouse stem cells when exposed to platinum-based chemotherapy. Animal research suggests that PIFAs cause resistance to chemotherapy by stimulating lysophospholipid production in the spleen, which interferes with the DNA damage caused by certain chemotherapy drugs. One PIFA, known as 16:4(n-3), has been found in both raw fish and some commercially available fish oil products. Mackerel and herring have high PIFA concentrations, while salmon and tuna have low PIFA concentrations. Levels of PIFA in commercial fish oil products ranged from 0.2- 5.7 microMol. Animal research shows that PIFA-containing fish oil products cause resistance to cisplatin, fluorouracil, irinotecan, and oxaliplatin. It is unclear if all commercially available fish oil products contain PIFAs. Additionally, it is argued that levels of PIFA found in some fish oil products are too low to be of clinical concern. Furthermore, a lack of chemotherapy resistance in countries with high fish intake, such as Greenland, Japan, and Norway, suggest that this interaction may not be clinically significant.

Likelihood Unlikely Evidence D
Warfarin (Coumadin)

Fish oil may have antiplatelet effects and might increase the risk of bleeding if used with warfarin.
Fish oil has antiplatelet effects at high doses. Case reports show elevated INR in patients taking warfarin and fish oil 1-2 grams daily. However, some clinical research shows that taking fish oil 3-6 grams daily does not significantly increase INR in patients taking warfarin.

Likelihood Unlikely Evidence B

Vitamin C13 drug types · 207 drugs

Alkylating Agents

Theoretically, antioxidant effects of vitamin C might reduce the effectiveness of alkylating agents.
The use of antioxidants like vitamin C during chemotherapy is controversial. There is concern that antioxidants could reduce the activity of chemotherapy drugs that generate free radicals, such as cyclophosphamide, chlorambucil, carmustine, busulfan, and thiotepa. In contrast, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that could interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as vitamin C have on chemotherapy.

Likelihood Possible Evidence D
Aluminum

Vitamin C can increase the amount of aluminum absorbed from aluminum compounds.
Research in animals and humans shows that vitamin C increases aluminum absorption, theoretically by chelating aluminum and keeping it in solution where it is available for absorption. In people with normal renal function, urinary excretion of aluminum will likely increase, making aluminum retention and toxicity unlikely. Patients with renal failure who take aluminum-containing compounds such as phosphate binders should avoid vitamin C supplements in doses above the recommended dietary allowances.

Likelihood Probable Evidence B
Antitumor Antibiotics

Theoretically, the antioxidant effects of vitamin C might reduce the effectiveness of antitumor antibiotics.
The use of antioxidants like vitamin C during chemotherapy is controversial. There is concern that antioxidants could reduce the activity of chemotherapy drugs which generate free radicals, such as doxorubicin. In contrast, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that could interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effects, if any, antioxidants such as vitamin C have on chemotherapy.

Likelihood Possible Evidence D
Estrogens

Vitamin C might increase blood levels of estrogens.
Increases in plasma estrogen levels of up to 55% occur under some circumstances when vitamin C is taken concurrently with oral contraceptives or hormone replacement therapy, including topical products. It is suggested that vitamin C prevents oxidation of estrogen in the tissues, regenerates oxidized estrogen, and reduces sulfate conjugation of estrogen in the gut wall. When tissue levels of vitamin C are high, these processes are already maximized and supplemental vitamin C does not have any effect on estrogen levels. Increases in plasma estrogen levels may occur when patients who are deficient in vitamin C take supplements. Monitor these patients for estrogen-related side effects.

Likelihood Probable Evidence B
Fluphenazine (Prolixin)

Theoretically, vitamin C might decrease levels of fluphenazine.
In one patient there was a clinically significant decrease in fluphenazine levels when vitamin C (500 mg twice daily) was started. The mechanism is not known, and there is no further data to confirm this interaction.

Likelihood Possible Evidence D
Indinavir (Crixivan)

Vitamin C can modestly reduce indinavir levels.
One pharmacokinetic study shows that taking vitamin C 1 gram orally once daily along with indinavir 800 mg orally three times daily reduces the area under the concentration-time curve of indinavir by 14%. The mechanism of this interaction is unknown, but it is unlikely to be clinically significant in most patients. The effect of higher doses of vitamin C on indinavir levels is unknown.

Likelihood Probable Evidence B
Levothyroxine (Synthroid, Others)

Vitamin C can increase levothyroxine absorption.
Two clinical studies in adults with poorly controlled hypothyroidism show that swallowing levothyroxine with a glass of water containing vitamin C 500-1000 mg in solution reduces thyroid stimulating hormone (TSH) levels and increases thyroxine (T4) levels when compared with taking levothyroxine alone. This suggests that vitamin C increases the oral absorption of levothyroxine, possibly due to a reduction in pH.

Likelihood Probable Evidence B
Warfarin (Coumadin)

High-dose vitamin C might reduce the levels and effectiveness of warfarin.
Vitamin C in high doses may cause diarrhea and possibly reduce warfarin absorption. There are reports of two people who took up to 16 grams daily of vitamin C and had a reduction in prothrombin time. Lower doses of 5-10 grams daily can also reduce warfarin absorption. In many cases, this does not seem to be clinically significant. However, a case of warfarin resistance has been reported for a patient who took vitamin C 500 mg twice daily. Cessation of vitamin C supplementation resulted in a rapid increase in international normalized ratio (INR). Tell patients taking warfarin to avoid taking vitamin C in excessively high doses (greater than 10 grams daily). Lower doses may be safe, but the anticoagulation activity of warfarin should be monitored. Patients who are stabilized on warfarin while taking vitamin C should avoid adjusting vitamin C dosage to prevent the possibility of warfarin resistance.

Likelihood Possible Evidence D
Acetaminophen (Tylenol, Others)

High-dose vitamin C might slightly prolong the clearance of acetaminophen.
A small pharmacokinetic study in healthy volunteers shows that taking high-dose vitamin C (3 grams) 1.5 hours after taking acetaminophen 1 gram slightly increases the apparent half-life of acetaminophen from around 2.3 hours to 3.1 hours. Ascorbic acid competitively inhibits sulfate conjugation of acetaminophen. However, to compensate, elimination of acetaminophen glucuronide and unconjugated acetaminophen increases. This effect is not likely to be clinically significant.

Likelihood Probable Evidence B
Aspirin

Acidification of the urine by vitamin C might increase aspirin levels.
It has been suggested that acidification of the urine by vitamin C could increase reabsorption of salicylates by the renal tubules, and increase plasma salicylate levels. However, short-term use of up to 6 grams daily of vitamin C does not seem to affect urinary pH or salicylate excretion, suggesting this interaction is not clinically significant.

Likelihood Possible Evidence B
Choline Magnesium Trisalicylate (Trilisate)

Acidification of the urine by vitamin C might increase choline magnesium trisalicylate levels.
It has been suggested that acidification of the urine by vitamin C could increase reabsorption of salicylates by the renal tubules, and increase plasma salicylate levels. However, short-term use of up to 6 grams daily of vitamin C does not seem to affect urinary pH or salicylate excretion, suggesting this interaction probably is not clinically significant.

Likelihood Possible Evidence B
Niacin

Vitamin C might decrease the beneficial effects of niacin on high-density lipoprotein (HDL) cholesterol levels.
A combination of niacin and simvastatin (Zocor) effectively raises HDL cholesterol levels in patients with coronary disease and low HDL levels. Clinical research shows that taking a combination of antioxidants (vitamin C, vitamin E, beta-carotene, and selenium) along with niacin and simvastatin (Zocor) attenuates this rise in HDL, specifically the HDL-2 and apolipoprotein A1 fractions, by more than 50% in patients with coronary disease. It is not known whether this adverse effect is due to a single antioxidant such as vitamin C, or to the combination. It also is not known whether it will occur in other patient populations.

Likelihood Possible Evidence A
Salsalate (Disalcid)

Acidification of the urine by vitamin C might increase salsalate levels.
It has been suggested that acidification of the urine by vitamin C could increase reabsorption of salicylates by the renal tubules, and increase plasma salicylate levels. However, short-term use of up to 6 grams/day vitamin C does not seem to affect urinary pH or salicylate excretion, suggesting this interaction probably is not clinically significant.

Likelihood Possible Evidence B

Bromelain2 drug types · 141 drugs

Anticoagulant/Antiplatelet Drugs

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

Likelihood Possible Evidence D
Tetracycline Antibiotics

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

Likelihood Possible Evidence B

Zinc10 drug types · 67 drugs

Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)

Theoretically, zinc might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide should be taken at least 2 hours before or 6 hours after zinc containing products.

Likelihood Probable Evidence D
Cephalexin (Keflex)

Zinc might decrease cephalexin levels by chelating with cephalexin in the gut and preventing its absorption.
A pharmacokinetic study shows that zinc sulfate 250 mg taken concomitantly with cephalexin 500 mg decreases peak levels of cephalexin by 31% and reduces the exposure to cephalexin by 27%. Also, taking zinc sulfate 3 hours before cephalexin decreases peak levels of cephalexin by 11% and reduces the exposure to cephalexin by 18%. By decreasing cephalexin levels, zinc might increase the risk of treatment failure. This effect does not occur when zinc is taken 3 hours after the cephalexin dose. To avoid an interaction, advise patients take zinc sulfate 3 hours after taking cephalexin.

Likelihood Probable Evidence B
Cisplatin (Platinol-Aq)

Theoretically, zinc might interfere with the therapeutic effects of cisplatin.
Animal research suggests that zinc stimulates tumor cell production of the protein metallothionein, which binds and inactivates cisplatin. It is not known whether zinc supplements or high dietary zinc intake can cause clinically significant interference with cisplatin therapy. Cisplatin might also increase zinc excretion.

Likelihood Possible Evidence D
Integrase Inhibitors

Theoretically, taking zinc along with integrase inhibitors might decrease the levels and clinical effects of these drugs.
Zinc is a divalent cation. Pharmacokinetic studies have shown that other divalent cations such as calcium and iron can decrease blood levels of the integrase inhibitor dolutegravir through chelation.

Likelihood Possible Evidence D
Penicillamine (Cuprimine, Depen)

Zinc might reduce the levels and clinical effects of penicillamine.
By forming an insoluble complex with penicillamine, zinc interferes with penicillamine absorption and activity. Zinc supplements reduce the efficacy of low-dose penicillamine (0.5-1 gram/day), but do not seem to affect higher doses (1-2.75 gram/day), provided dosing times are separated. Advise patients to take zinc and penicillamine at least 2 hours apart.

Likelihood Probable Evidence B
Quinolone Antibiotics

Zinc can decrease the levels and clinical effects of quinolones antibiotics.
Quinolones form complexes with zinc in the gastrointestinal tract, reducing absorption of both the quinolone and zinc if taken at the same time. Advise patients to take these drugs at least 2 hours before, or 4-6 hours after, zinc supplements.

Likelihood Probable Evidence B
Ritonavir (Norvir)

Zinc modestly reduces levels of ritonavir.
Clinical research shows that zinc might reduce serum ritonavir levels by chelating with ritonavir in the gut and preventing its absorption. In patients with HIV, ritonavir is taken with atazanavir to prevent the metabolism and increase the effects of atazanavir. A pharmacokinetic study shows that, in patients being treated with atazanavir/ritonavir, co-administration of zinc sulfate (Solvazinc tablets) 125 mg as a single dose or as multiple daily doses for 2 weeks reduces plasma levels of ritonavir by about 16%. However, atazanavir levels still remains high enough to prevent HIV virus replication. Therefore, the decrease in ritonavir levels is not likely to be clinically significant.

Likelihood Probable Evidence B
Tetracycline Antibiotics

Zinc might reduce levels of tetracycline antibiotics.
Tetracyclines form complexes with zinc in the gastrointestinal tract, which can reduce absorption of both the tetracycline and zinc when taken at the same time. Taking zinc sulfate 200 mg with tetracycline reduces absorption of the antibiotic by 30% to 40%. Demeclocycline and minocycline cause a similar interaction. However, doxycycline does not seem to interact significantly with zinc. Advise patients to take tetracyclines at least 2 hours before, or 4-6 hours after, zinc supplements to avoid any interactions.

Likelihood Probable Evidence B
Amiloride (Midamor)

Amiloride can modestly reduce zinc excretion and increase zinc levels.
Clinical research shows that amiloride can reduce urinary zinc excretion, especially at doses of 10 mg per day or more. This zinc-sparing effect can help to counteract zinc losses caused by thiazide diuretics, but it is unlikely to cause zinc toxicity at usual amiloride doses. The other potassium-sparing diuretics, spironolactone (Aldactone) and triamterene (Dyrenium), do not seem to have a zinc-sparing effect.

Likelihood Probable Evidence B
Atazanavir (Reyataz)

Zinc modestly reduces levels of atazanavir, although this effect does not seem to be clinically significant.
Clinical research shows that zinc might decrease serum atazanavir levels by chelating with atazanavir in the gut and preventing its absorption. Although a single dose of zinc sulfate (Solvazinc tablets) 125 mg orally does not affect atazanavir concentrations in patients being treated with atazanavir/ritonavir, co-administration of zinc sulfate 125 mg daily for 2 weeks reduces plasma levels of atazanavir by about 22% in these patients. However, despite this decrease, atazanavir levels still remain at high enough concentrations for the prevention of HIV virus replication.

Likelihood Probable Evidence B

Papain1 drug type · 2 drugs

Warfarin (Coumadin)

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

Likelihood Possible Evidence D
The maker

Brand information

Manufacturer and brand details for Inflamma-Less, from the product label.

Irwin Naturals

See all Irwin Naturals products
Name
Irwin Naturals
Street Address
5310 Beethoven Street
City
Los Angeles
State
CA
ZipCode
90066
Phone Number
1-800-297-3273
Web Address
www.IrwinNaturals.com
Pharmacist Counseling Corner

Inflamma-Less by Irwin Naturals: Common Questions

Does Inflamma-Less by Irwin Naturals interact with any medications?
Yes. Based on its ingredients, Inflamma-Less has a known interaction with 1,586 medications. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Inflamma-Less contains 17 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 Inflamma-Less if I'm on a blood thinner like warfarin?
No—this product contains multiple ingredients (vitamin C, papain, bromelain, ginger, resveratrol, hesperidin, and quercetin) that may increase bleeding risk with warfarin and other blood thinners. You must talk to your pharmacist or doctor before starting Inflamma-Less if you take any blood thinner or antiplatelet drug.
Is ginger in this product safe for pregnancy nausea?
Ginger is sometimes used for morning sickness, and the safety data we hold rates it as likely safe at modest amounts in pregnancy. But check with your doctor first about the right dose and whether this product's full formula is appropriate for you.
What do the enzymes (papain, bromelain, chymotrypsin, trypsin) do?
These are proteases—they break down proteins. Papain and bromelain are plant-derived enzymes; chymotrypsin and trypsin are animal-derived. They're traditionally used to support the body's inflammatory response, but the evidence we hold is insufficient to confirm their effectiveness for any specific condition.
Will this supplement interfere with my diabetes or thyroid medications?
Possibly. Ginger may increase insulin and lower blood glucose, raising the risk of low blood sugar with diabetes drugs. Vitamin C can increase levothyroxine absorption, which may affect thyroid hormone levels. Check your exact medications in our tool and talk to your pharmacist.
Is this product safe to take long-term?
Short-term use of most ingredients is generally well tolerated, but quality evidence on long-term safety is limited for many of them (especially bromelain, resveratrol, hesperidin, and quercetin). Talk to your pharmacist about safe duration based on your individual needs.
Does this product contain any allergens?
Papain and bromelain can trigger allergic reactions in sensitive people. The softgel capsule contains gelatin (animal-derived) and soy lecithin. If you have known allergies to these or pineapple/papaya enzymes, avoid this product.

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

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Inflamma-Less label
Go deeper

The Full Monographs Behind Inflamma-Less’s Ingredients

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

Herb & supplement monograph

Vitamin C

Interacts with 207 drugs

Vitamin C (ascorbic acid) is an essential nutrient your body needs but cannot make, so you must get it from food or supplements. It's important for immune function, collagen, and acts as an...

Read the full Vitamin C monograph →
Herb & supplement monograph

Papain

Interacts with 2 drugs

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

Read the full Papain monograph →
Herb & supplement monograph

Bromelain

Interacts with 141 drugs

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

Read the full Bromelain monograph →
Herb & supplement monograph

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

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

Zinc

Interacts with 67 drugs

Zinc is an essential mineral that your body needs for immune function, wound healing, taste, and smell. Most people get enough from food, but supplements can help correct or prevent a defici...

Read the full Zinc 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

Chymotrypsin

Chymotrypsin is a protein-digesting (proteolytic) enzyme, usually taken from the pancreas of cattle or pigs, that is mainly used to help reduce swelling and support healing after injury or s...

Read the full Chymotrypsin monograph →
Herb & supplement monograph

Trypsin

Trypsin is a protein-digesting enzyme usually taken from the pancreas of animals and used either by mouth (often combined with other enzymes like chymotrypsin and bromelain) for swelling and...

Read the full Trypsin monograph →
Herb & supplement monograph

Resveratrol

Interacts with 822 drugs

Resveratrol is a plant compound found in red grapes, berries, and peanuts that is popular for heart health, anti-aging, and antioxidant support. While lab and animal studies are promising, s...

Read the full Resveratrol monograph →
Herb & supplement monograph

Quercetin

Interacts with 1,169 drugs

Quercetin is a plant flavonoid with antioxidant and anti-inflammatory properties found in many common foods and sold as a supplement. While early research is interesting for allergies, blood...

Read the full Quercetin monograph →
Herb & supplement monograph

Boswellia Serrata

Interacts with 952 drugs

Boswellia serrata is a tree resin used in traditional medicine, mainly for joint pain and inflammation. Some studies suggest it may help with osteoarthritis symptoms, but the overall evidenc...

Read the full Boswellia Serrata monograph →
Herb & supplement monograph

Hesperidin

Interacts with 702 drugs

Hesperidin is a flavonoid found in citrus fruits that is often combined with diosmin and used for vein and circulation problems like hemorrhoids and varicose veins. Some evidence supports th...

Read the full Hesperidin monograph →
Herb & supplement monograph

Fish Oil

Interacts with 327 drugs

Fish oil provides omega-3 fatty acids (EPA and DHA) that are best known for lowering high triglyceride levels. The evidence for other heart and health benefits is mixed, and it is generally...

Read the full Fish Oil monograph →
Herb & supplement monograph

Docosahexaenoic Acid (dha)

Interacts with 375 drugs

DHA is an omega-3 fatty acid found in fatty fish and algae that is a building block for the brain, nervous system, and eyes. It is widely used and generally well tolerated, with the stronges...

Read the full Docosahexaenoic Acid (dha) monograph →
Sources

Sources & How We Checked

Inflamma-Less'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 673 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.

Docosahexaenoic Acid (dha) 49 references
  1. Akedo I, Ishikawa H, Nakamura T, et al. Three cases with familial adenomatous polyposis diagnosed as having malignant lesions in the course of a long-term trial using docosahexanoic acid (DHA)-concentrated fish oil capsules (abstract). Jpn J Clin Oncol PubMed
  2. Prisco D, Paniccia R, Bandinelli B, et al. Effect of medium-term supplementation with a moderate dose of n-3 polyunsaturated fatty acids on blood pressure in mild hypertensive patients. Thromb Res 1998;1:105-12.
  3. Grimsgaard S, Bonaa KH, Hansen JB, Nordoy A. Highly purified eicosapentaenoic acid and docosahexaenoic acid in humans have similar triacylglycerol-lowering effects but divergent effects on serum fatty acids. Am J Clin Nutr 1997;66:649-59.
  4. Toft I, Bonaa KH, Ingebretsen OC, et al. Effects of n-3 polyunsaturated fatty acids on glucose homeostasis and blood pressure in essential hypertension. A randomized, controlled trial. Ann Intern Med 1995;123:911-8.
  5. Sacks FM, Hebert P, Appel LJ, et al. Short report: the effect of fish oil on blood pressure and high-density lipoprotein-cholesterol levels in phase I of the trials of hypertension prevention. J Hypertens 1994;12:209-13.
  6. Vandongen R, Mori TA, Burke V, et al. Effects on blood pressure of omega 3 fats in subjects at increased risk of cardiovascular disease. Hypertension 1993;22:371-9. PubMed
  7. FDA. Center for Food Safety and Applied Nutrition. Letter regarding dietary supplement health claim for omega-3 fatty acids and coronary heart disease. Available at: http://www.fda.gov/ohrms/dockets/dockets/95s0316/95s-0316-Rpt0272-38-Appendix-D-Reference
  8. Pedersen HS, Mulvad G, Seidelin KN, et al. N-3 fatty acids as a risk factor for haemorrhagic stroke. Lancet 1999;353:812-3. PubMed
  9. Ito Y, Suzuki K, Imai H, et al. Effects of polyunsaturated fatty acids on atrophic gastritis in a Japanese population. Cancer Lett 2001;163:171-8. PubMed
  10. Kris-Ehterton PM, Harris WS, Appel LJ, et al. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation 2002;106:2747-57. PubMed
  11. Woodman RJ, Mori TA, Burke V, et al. Effects of purified eicosapentaenoic and docosahexaenoic acids on glycemic control, blood pressure, and serum lipids in type 2 diabetic patients with treated hypertension. Am J Clin Nutr 2002;76:1007-15.. PubMed
  12. Marangell LB, Martinez JM, Zboyan HA, et al. A double-blind, placebo-controlled study of the omega-3 fatty acid docosahexaenoic acid in the treatment of major depression. Am J Psychiatry 2003;160:996-8.. PubMed
  13. Leng GC, Smith FB, Fowkes FG, et al. Relationship between plasma essential fatty acids and smoking, serum lipids, blood pressure and haemostatic and rheological factors. Prostaglandins Leukot Essent Fatty Acids 1994;51:101-8. PubMed
  14. Nelson GJ, Schmidt PS, Bartolini GL, et al. The effect of dietary docosahexaenoic acid on platelet function, platelet fatty acid composition, and blood coagulation in humans. Lipids 1997;32:1129-36. PubMed
  15. Wheaton DH, Hoffman DR, Locke KG, et al. Biological safety assessment of docosahexaenoic acid supplementation in a randomized clinical trial for X-linked retinitis pigmentosa. Arch Ophthalmol 2003;121:1269-78. PubMed
  16. Malcolm CA, McCulloch DL, Montgomery C, et al. Maternal docosahexaenoic acid supplementation during pregnancy and visual evoked potential development in term infants: a double blind, prospective, randomised trial. Arch Dis Child Fetal Neonatal Ed 2003;88: DOI
  17. Sanjurjo P, Ruiz-Sanz JI, Jimeno P, et al. Supplementation with docosahexaenoic acid in the last trimester of pregnancy: maternal-fetal biochemical findings. J Perinat Med 2004;32:132-6.
  18. Montgomery C, Speake BK, Cameron A, et al. Maternal docosahexaenoic acid supplementation and fetal accretion. Br J Nutr 2003;90:135-45. DOI
  19. Lauritzen L, Hoppe C, Straarup EM, Michaelsen KF. Maternal fish oil supplementation in lactation and growth during the first 2.5 years of life. Pediatr Res 2005;58:235-42. PubMed
  20. Hawkes JS, Bryan DL, Makrides M, et al. A randomized trial of supplementation with docosahexaenoic acid-rich tuna oil and its effects on the human milk cytokines interleukin 1 beta, interleukin 6, and tumor necrosis factor alpha. Am J Clin Nutr 2002;75:75
  21. Uauy R, Hoffman DR, Mena P, et al. Term infant studies of DHA and ARA supplementation on neurodevelopment: Results of randomized controlled trials. J Pediatr 2003;143:S17-25. PubMed
  22. Decsi, T., Campoy, C., and Koletzko, B. Effect of N-3 polyunsaturated fatty acid supplementation in pregnancy: the Nuheal trial. Adv.Exp Med Biol 2005;569:109-113. PubMed
  23. Mori, T. A., Bao, D. Q., Burke, V., Puddey, I. B., and Beilin, L. J. Docosahexaenoic acid but not eicosapentaenoic acid lowers ambulatory blood pressure and heart rate in humans. Hypertension 1999;34(2):253-260. PubMed
  24. Otto, S. J., van Houwelingen, A. C., and Hornstra, G. The effect of supplementation with docosahexaenoic and arachidonic acid derived from single cell oils on plasma and erythrocyte fatty acids of pregnant women in the second trimester. Prostaglandins Le PubMed
  25. Helland, I. B., Saugstad, O. D., Smith, L., Saarem, K., Solvoll, K., Ganes, T., and Drevon, C. A. Similar effects on infants of n-3 and n-6 fatty acids supplementation to pregnant and lactating women. Pediatrics 2001;108(5):E82. PubMed
  26. Nestel, P., Shige, H., Pomeroy, S., Cehun, M., Abbey, M., and Raederstorff, D. The n-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid increase systemic arterial compliance in humans. Am.J.Clin.Nutr. 2002;76(2):326-330. PubMed
  27. Woodman, R. J., Mori, T. A., Burke, V., Puddey, I. B., Barden, A., Watts, G. F., and Beilin, L. J. Effects of purified eicosapentaenoic acid and docosahexaenoic acid on platelet, fibrinolytic and vascular function in hypertensive type 2 diabetic patients PubMed
  28. Jensen, C. L., Voigt, R. G., Prager, T. C., Zou, Y. L., Fraley, J. K., Rozelle, J. C., Turcich, M. R., Llorente, A. M., Anderson, R. E., and Heird, W. C. Effects of maternal docosahexaenoic acid intake on visual function and neurodevelopment in breastfed
  29. Theobald, H. E., Goodall, A. H., Sattar, N., Talbot, D. C., Chowienczyk, P. J., and Sanders, T. A. Low-dose docosahexaenoic acid lowers diastolic blood pressure in middle-aged men and women. J Nutr 2007;137(4):973-978.
  30. Mischoulon D, Best-Popescu C, Laposata M, et al. A double-blind dose-finding pilot study of docosahexaenoic acid (DHA) for major depressive disorder. Eur Neuropsychopharmacol. 2008;18(9):639-645. PubMed
  31. Birch EE, Carlson SE, Hoffman DR, et al. The DIAMOND (DHA Intake And Measurement Of Neural Development) Study: a double-masked, randomized controlled clinical trial of the maturation of infant visual acuity as a function of the dietary level of docosahexa
  32. Carlson SE, Colombo J, Gajewski BJ, Gustafson KM, Mundy D, Yeast J, Georgieff MK, Markley LA, Kerling EH, Shaddy DJ. DHA supplementation and pregnancy outcomes. Am J Clin Nutr. 2013 Apr;97(4):808-15. PubMed
  33. Escamilla-Nuñez MC, Barraza-Villarreal A, Hernández-Cadena L, Navarro-Olivos E, Sly PD, Romieu I. Omega-3 fatty acid supplementation during pregnancy and respiratory symptoms in children. Chest. 2014 Aug;146(2):373-82. PubMed
  34. Fu YQ, Zheng JS, Yang B, Li D. Effect of individual omega-3 fatty acids on the risk of prostate cancer: a systematic review and dose-response meta-analysis of prospective cohort studies. J Epidemiol. 2015;25(4):261-74. PubMed
  35. Imhoff-Kunsch B, Stein AD, Villalpando S, Martorell R, Ramakrishnan U. Docosahexaenoic acid supplementation from mid-pregnancy to parturition influenced breast milk fatty acid concentrations at 1 month postpartum in Mexican women. J Nutr. 2011 Feb;141(2): PubMed
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