Major interaction on record — check this product against your medications before combining. Based on 17 of 22 ingredients. Check your meds →
Dietary supplement

Immune Force Ingredients & Drug Interactions

by BioScience International

Immune Force label
See full label image
Softgel Capsule Category: Other Combinations
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 16, 2026 · Label data from the NIH DSLD
What is this page for?

First and foremost: checking Immune Force against your medications. The heart of this page is the interaction checker and the full interaction report — how this product’s ingredients may interact with prescription and over-the-counter medicines you may be taking.

Around that, we add a pharmacist’s high-level view of the product as a whole — what’s inside, the evidence for its stated use, how transparent the label is, and what safety data exists — so you can see the full picture in one place. It’s educational information from our licensed clinical databases and the clinical staff at HelloPharmacist — not medical advice — and we don’t sell or endorse products. Our editorial policy

The interaction bottom line Most serious interaction: Major

Immune Force is a dietary supplement by BioScience International with 22 active ingredients. Its ingredients are commonly taken for antioxidant support, skin health and aging, eye health.Based on those ingredients, 1,660 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Goldenseal, Curcumin, Ginger. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

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Check Your Meds Against Immune Force by BioScience International

Ask about any prescription or over-the-counter medication and we check it for interactions with Immune Force by BioScience International — and tell you which ingredient is responsible.

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HelloPharmacist Scorecard of Immune Force by BioScience International

Our pharmacy team’s full take, with four database checks built into the cards below — a summary of what is known, not a grade of the product itself.

From our pharmacy team — supplement deep dive

Generated from HelloPharmacist’s pharmacist-curated databases and editorial rules · Last generated Jul 11, 2026

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

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

Why this rating?
  • The label discloses an exact amount for 0 of its 22 active ingredients.
  • “Proprietary Blend” is a proprietary blend — the label gives one combined amount (3.02 Gram(s)) without saying how much of each component you get.

Immune Force contains 22 active ingredients in a proprietary blend and individual components. The main actives are calcium carbonate (a mineral for bone and metabolic support), astaxanthin (a carotenoid antioxidant), ginger root, grape extract, wild yam, suma, American ginseng, burdock, bupleurum, goldenseal, schisandra (also called schizandra), sheep sorrel, grape oil, curcumin (turmeric's active compound), hyssop, maitake mushroom, poria mushroom (polyporous), and black cumin oil.

Four inactive ingredients are also present: sunflower lecithin, gelatin, ascorbic acid, and ethyl alcohol.

Does it work?

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

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

Why this rating?
  • The label markets this product for: Full spectrum immune support and natural defense.
  • We looked for evidence on: Acute respiratory distress syndrome (ARDS), Allergic rhinitis (hay fever), Bronchitis, Common cold, Influenza, General wellness.
  • The strongest evidence on file: Turmeric is rated "Possibly Effective" for Allergic rhinitis (hay fever) (Natural Medicines).
  • Also on file: Black Seed is rated "Possibly Effective" for Allergic rhinitis (hay fever).
  • Also on file: Grape is rated "Possibly Ineffective" for Allergic rhinitis (hay fever).

The evidence for most of these ingredients is limited. Calcium is rated Effective for kidney failure, dyspepsia, and low blood calcium (hypocalcemia), and Likely Effective for osteoporosis.

Ginger is Possibly Effective for pregnancy-related nausea and vomiting and for menstrual cramps (dysmenorrhea), though possibly ineffective for exercise soreness. Grape extract is Possibly Effective for chronic venous insufficiency (poor circulation in the legs).

Black cumin oil is Possibly Effective for acne, allergies, asthma, and Helicobacter pylori infection, and for blood sugar control in diabetes. Curcumin is Possibly Effective for depression, high cholesterol, allergies, and indigestion.

For the remaining ingredients — astaxanthin, wild yam, suma, American ginseng, burdock, bupleurum, goldenseal, schisandra, sheep sorrel, hyssop, maitake, and poria — the evidence is insufficient to rate them, meaning we don't have solid data showing they work for any condition.

The evidence, ingredient by ingredient Astaxanthin Calcium Ginger Grape Wild Yam Suma American Ginseng Burdock

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 16 of the 17 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 17 of 17.
  • General safety write-ups exist for 17 of 17.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Most ingredients in this product are generally well tolerated in typical amounts, though side effects can occur. Calcium at recommended doses is safe in pregnancy and breastfeeding, but high doses raise concerns.

Astaxanthin should be avoided in pregnancy and breastfeeding due to insufficient safety data. Ginger is often used for morning sickness but should be discussed with your doctor first and kept moderate; it's not safe for breastfeeding.

Wild yam lacks safety data and should be avoided in pregnancy and breastfeeding. American ginseng is not well studied in pregnancy or breastfeeding.

Goldenseal should be avoided in both pregnancy and breastfeeding because berberine (its active alkaloid) may harm the fetus or infant. Burdock used medicinally should be avoided in pregnancy and breastfeeding.

Bupleurum lacks safety information for pregnancy and breastfeeding. Black cumin oil larger doses are not proven safe in pregnancy; supplement doses should be avoided.

Hyssop is traditionally thought to stimulate the uterus and should be avoided in pregnancy. Grape extract is Likely Safe in pregnancy when used as food; concentrated supplements should be avoided.

Curcumin is generally safe as a food but concentrated supplements in pregnancy should be discussed with your doctor first. Common side effects reported across ingredients include abdominal discomfort, diarrhea, heartburn, nausea, and headache.

Side effects, ingredient by ingredient Astaxanthin Calcium Ginger Grape Wild Yam Suma American Ginseng Burdock

Meds to double-check

Major interaction found
Known Interaction Concern · database check
Major identified

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

Why this rating?
  • 15 of the 17 matched ingredients can interact with medications — Burdock, Poria Mushroom, Schisandra, Grape, Maitake Mushroom, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; heart-rhythm medications; lithium.
  • For scale: 1,661 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 Immune Force, double-check with your pharmacist if you take: HIV integrase inhibitors (dolutegravir, elvitegravir), blood thinners or anticoagulants (warfarin, other blood thinners), diabetes medications, blood pressure medications, heart medications (especially calcium channel blockers like diltiazem or nifedipine), drugs metabolized by liver enzymes (CYP3A4, CYP2D6, CYP2C9, CYP2B6, CYP2C19, CYP2E1, CYP1A2, or P-glycoprotein), tacrolimus or other immunosuppressants, thyroid medication (levothyroxine), or antibiotics like ceftriaxone. No interactions are documented for the ingredients we could not check (Eucommia, Sea Minerals, Ziziphus, and Coriolus).

Check your own medication Run your meds through the checker above

The bottom line

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

If you take any prescription medications — especially blood thinners, HIV drugs, diabetes medications, or blood pressure drugs — check your medications with the tool on this page before taking Immune Force. Pregnant or breastfeeding people should talk to their pharmacist or doctor about several of these ingredients, which lack adequate safety data.

This is a complex multi-ingredient product, so a detailed medication review is worth your time.

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

Assessment coverage: 18 of 22 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Sep 24, 2021.

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

At a glance

General information

Key facts about Immune Force, straight from the product label.

Brand BioScience International
Barcode (UPC) 748252597717
Net contents 240 Softgel(s)
Market status On market
Date entered into DSLD Sep 24, 2021
DSLD ID 258970
Product type Other Combinations
Supplement form Softgel Capsule
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Adult (18 - 50 Years), Women (not pregnant or lactating), Gluten Free, Dairy Free, Sugar Free
From the label
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.

Supplement Facts

The label details for Immune Force by BioScience International, 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:
4 Softgel(s)
Maximum serving Sizes:
4 Softgel(s)
Servings per container
60
UPC/BARCODE
748252597717
IngredientAmount% DV
Astaxanthin0 NP--
Calcium Carbonate0 NP--
Proprietary Blend3.02 Gram(s)--
Ginger0 NP--
Grape extract0 NP--
Wild Yam0 NP--
Suma0 NP--
American Ginseng0 NP--
Eucommia0 NP--
Burdock0 NP--
Bupleurum0 NP--
Goldenseal0 NP--
Schizandra0 NP--
Sheep Sorrel0 NP--
Grape Oil0 NP--
Sea Minerals0 NP--
Curcumin0 NP--
Hyssop0 NP--
Ziziphus0 NP--
Maitake0 NP--
Polyporous0 NP--
Coriolus0 NP--
Black Cumin Oil0 NP--

Other ingredients: Sunflower Lecithin, Gelatin, Ascorbic Acid, Ethyl Alcohol

Tap any ingredient to jump to its full detail below.

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

Unleash the power of your immune system BioScience International's revolutionary formula is a breakthrough in cellular communication.

The result is a bio-available powerhouse of potent immune support! For seasonal challenges and year round support take Immune Force!

Gluten-free Nothing artificial Soy-free Dairy-free Non-GMO Sugar-free Corn-free

Full spectrum immune support in a liposomal delivery system Strengthens the body's natural defense system Enhances liver/gut/brain communication Supports healthy circulation and cellular regeneration Optimizes cellular detoxification

Made in Canada

Independently tested Manufactured & quality cGMP

Formula

The combination of our powerful herbal extracts, potentized mushrooms and interactive oils creates a breakthrough in immune science. Using an advanced liposomal-based delivered mechanism, IMMUNE FORCE penetrates deeply into the cells and micro capillaries to deliver nutrients in the natural form the body can recognize.

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.

General Statements

Science. Nature. Health.

FDA Statement of Identity

Dietary Supplement

Suggested/Recommended/Usage/Directions

Suggested use: Take 4 softgels, 2 times per day, 20 minutes after meals. For intensive support take 4 softgels 3 times per day.

Precautions

Warning: Keep out of reach of children.

Do not use if you are allergic to any of the ingredients.

Do not use if you are pregnant or breastfeeding.

Do not use if safety seal around top of bottle is missing or broken.

Storage

Store at room temperature. Keep out of direct sunlight.

Brand IP Statement(s)

Health Canada Product License

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

See for yourself

Immune Force by BioScience International label

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

Immune Force label

Label images are published by the NIH Dietary Supplement Label Database for the version of this product on file. Always read your actual product label.

View the full label (PDF)
What’s inside

The Ingredients in Immune Force by BioScience International

These are the 22 active ingredients this product is made of. Select any to open its full monograph.

Serving size4 Softgel(s) Dosage formSoftgel Capsule Servings per container60 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.

Proprietary Blend

3.02 Gram(s) per serving

Other (inactive) ingredients: Sunflower Lecithin, Gelatin, Ascorbic Acid, Ethyl Alcohol. These complete the product’s ingredient list but are not active constituents.

Interaction report

Immune Force by BioScience International Drug Interactions

Want to check YOUR meds against Immune Force?

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
1,660Drugs
9 Major 1,649 Moderate 2 Minor

Ingredients driving the most interactions

Goldenseal 1,237
Curcumin 1,133
Ginger 1,007
Black Cumin Oil 912
Grape extract 910

Individual Drug Interactions

The ingredients in Immune Force interact with 1,660 drugs. Click any drug to see the details.

15 of the 22 ingredients in Immune Force interact with drugs. Each result below shows which ingredient is responsible. Goldenseal Curcumin Ginger Black Cumin Oil Grape extract Schizandra Astaxanthin Polyporous Bupleurum Maitake American Ginseng Sheep Sorrel Calcium Carbonate Burdock Wild Yam

Each ingredient & the kinds of drugs it affects

For each ingredient in Immune Force 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.

Goldenseal16 drug types · 1,237 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, goldenseal might increase the risk of bleeding when used with anticoagulant or antiplatelet drugs.
Goldenseal contains berberine. In vitro and animal research shows that berberine can inhibit platelet aggregation. However, this effect has not been reported in humans.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, goldenseal might increase the risk of hypoglycemia when used with antidiabetes drugs.
Goldenseal contains berberine. Clinical research shows that berberine can lower blood glucose levels. However, this effect has not been reported with goldenseal.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, goldenseal might increase the risk of hypotension when taken with antihypertensive drugs.
Goldenseal contains berberine. Animal research shows that berberine can have hypotensive effects. Also, an analysis of clinical research shows that taking berberine in combination with amlodipine can lower systolic and diastolic blood pressure when compared with amlodipine alone. However, this effect has not been reported with goldenseal.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, goldenseal might increase the sedative effects of CNS depressants.
Goldenseal contains berberine. Animal research shows that berberine can have sedative effects. However, this effect has not been reported in humans.

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

Theoretically, goldenseal might increase serum levels of drugs metabolized by CYP2C9.
In vitro research shows that goldenseal root extract can modestly inhibit CYP2C9. This effect may be due to its alkaloid constituents, hydrastine and berberine. However, this effect has not been reported in humans.

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

Goldenseal might increase serum levels of drugs metabolized by CYP2D6.
Clinical and in vitro research shows that goldenseal can significantly inhibit CYP2D6 enzymes, potentially increasing levels of drugs metabolized by CYP2D6.

Likelihood Probable Evidence B
Cytochrome P450 2E1 (Cyp2E1) Substrates

Theoretically, goldenseal might increase serum levels of drugs metabolized by CYP2E1.
In vitro research shows that goldenseal root extract can inhibit the activity of CYP2E1. However, this effect has not been reported in humans.

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

Goldenseal might increase serum levels of drugs metabolized by CYP3A4.
Most clinical and in vitro research shows that goldenseal inhibits CYP3A4 enzyme activity and increases serum levels of CYP3A4 substrates, such as midazolam. However, in one small clinical study, goldenseal did not affect the levels of indinavir, a CYP3A4 substrate, in healthy volunteers. This is likely due to the fact that indinavir has a high oral bioavailability, making it an inadequate probe for CYP3A4 interactions and/or that it is primarily metabolized by hepatic CYP3A, while goldenseal has more potential to inhibit intestinal CYP3A enzyme activity. Both goldenseal extract and its isolated constituents berberine and hydrastine inhibit CYP3A, with hydrastine possibly having more inhibitory potential than berberine.

Likelihood Possible Evidence B
Dextromethorphan (Robitussin Dm, Others)

Theoretically, goldenseal might increase serum levels of dextromethorphan.
Goldenseal contains berberine. A small clinical study shows that berberine can inhibit cytochrome P450 2D6 (CYP2D6) activity and reduce the metabolism of dextromethorphan.

Likelihood Possible Evidence D
Digoxin (Lanoxin)

Goldenseal might increase serum levels of digoxin, although this effect is unlikely to be clinically significant.
Clinical research shows that goldenseal modestly increases digoxin peak levels by about 14% in healthy volunteers. However, goldenseal does not seem to affect other pharmacokinetic parameters such as area under the curve (AUC). This suggests that goldenseal does not cause a clinically significant interaction with digoxin. Digoxin is a P-glycoprotein substrate. Some evidence suggests that goldenseal constituents might affect P-glycoprotein; however, it is unclear whether these constituents inhibit or induce P-glycoprotein.

Likelihood Probable Evidence B
Losartan (Cozaar)

Theoretically, goldenseal might decrease the conversion of losartan to its active form.
Goldenseal contains berberine. A small clinical study shows that berberine inhibits cytochrome P450 2C9 (CYP2C9) activity and reduces the metabolism of losartan. However, this effect has not been reported with goldenseal.

Likelihood Possible Evidence D
Metformin (Glucophage)

Theoretically, goldenseal might reduce blood levels of metformin.
In vitro research shows that goldenseal extract decreases the bioavailability of metformin, likely by interfering with transport, intestinal permeability, or other processes involved in metformin absorption. It is unclear which, if any, of metformin's transporters are inhibited by goldenseal. Goldenseal does not appear to alter the clearance or half-life of metformin.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, goldenseal might increase or decrease serum levels of P-glycoprotein (P-gp) substrates.
There is conflicting evidence about the effect of goldenseal on P-gp. In vitro research suggests that berberine, a constituent of goldenseal, modestly inhibits P-gp efflux. Other evidence suggests that berberine induces P-gp. In healthy volunteers, goldenseal modestly increases peak levels of the P-gp substrate digoxin by about 14%. However, it does not seem to affect other pharmacokinetic parameters such as area under the curve (AUC). This suggests that goldenseal is not a potent inhibitor of P-gp-mediated drug efflux. Until more is known, goldenseal should be used cautiously with P-gp substrates.

Likelihood Probable Evidence B
Pentobarbital (Nembutal)

Theoretically, goldenseal might increase the sedative effects of pentobarbital.
Animal research shows that berberine, a constituent of goldenseal, can prolong pentobarbital-induced sleeping time. However, this effect has not been reported with goldenseal.

Likelihood Possible Evidence D
Tacrolimus (Prograf)

Theoretically, goldenseal might increase serum levels of tacrolimus.
Goldenseal contains berberine. In a 16-year-old patient with idiopathic nephrotic syndrome who was being treated with tacrolimus 6.5 mg twice daily, intake of berberine 200 mg three times daily increased the blood concentration of tacrolimus from 8 to 22 ng/mL. Following a reduction of tacrolimus dosing to 3 mg daily, blood levels of tacrolimus decreased to 12 ng/mL.

Likelihood Possible Evidence D
Oseltamivir (Tamiflu)

Theoretically, goldenseal might reduce the therapeutic effects of oseltamivir by decreasing its conversion to its active form.
In vitro evidence suggests that goldenseal reduces the formation of the active compound from the prodrug oseltamivir. The mechanism of action and clinical relevance is unclear.

Likelihood Possible Evidence D
Goldenseal full monograph & interactions

Curcumin24 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
Curcumin full monograph & interactions

Ginger14 drug types · 1,007 drugs

Anticoagulant/Antiplatelet Drugs

Ginger may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Laboratory research suggests that ginger inhibits thromboxane synthetase and decreases platelet aggregation. However, this has not been demonstrated unequivocally in humans, with mixed results from clinical trials. Theoretically, excessive amounts of ginger might increase the risk of bleeding when used with anticoagulant/antiplatelet drugs.

Likelihood Possible Evidence B
Antidiabetes Drugs

Theoretically, taking ginger with antidiabetes drugs might increase the risk of hypoglycemia.
Animal and human research suggests that ginger might increase insulin levels and/or decrease blood glucose levels.

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

Ginger might increase or decrease the levels of CYP3A4 substrates.
In vitro research and some case reports suggest that ginger inhibits CYP3A4 activity. Three case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are CYP3A4 substrates (imatinib, dabrafenib, and crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.
Conversely, other in vitro research suggests that ginger induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Losartan (Cozaar)

Theoretically, ginger might increase levels of losartan and the risk of hypotension.
In animal research, ginger increased the levels and hypotensive effects of a single dose of losartan. It is not clear if ginger alters the concentration or effects of losartan when taken continuously. Additionally, this interaction has not been shown in humans.

Likelihood Possible Evidence D
Nifedipine (Procardia)

Ginger may have antiplatelet effects and increase the risk of bleeding if used with nifedipine.
Clinical research shows that combined treatment with ginger 1 gram plus nifedipine 10 mg significantly inhibits platelet aggregation when compared to nifedipine or ginger alone.

Likelihood Possible Evidence B
P-Glycoprotein Substrates

Ginger might increase the absorption and blood levels of P-glycoprotein (P-gp) substrates.
In vitro research and case reports suggest that ginger inhibits drug efflux by P-gp, potentially increasing absorption and serum levels of P-gp substrates. Two case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are P-gp substrates (trametinib, crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.

Likelihood Possible Evidence D
Phenprocoumon (Marcoumar, Others)

Ginger might increase the risk of bleeding with phenprocoumon.
Phenprocoumon, a warfarin-related anticoagulant, might increase the international normalized ratio (INR) when taken with ginger. There is one case report of a 76-year-old woman with a stable INR on phenprocoumon that increased to greater than 10 when she began consuming dried ginger and ginger tea.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Ginger might increase the risk of bleeding with warfarin.
Laboratory research suggests that ginger might inhibit thromboxane synthetase and decrease platelet aggregation. In one case report, ginger increased the INR when taken with phenprocoumon, which has similar pharmacological effects as warfarin. In another case report, ginger increased the INR when taken with a combination of warfarin, hydrochlorothiazide, and acetaminophen. A longitudinal analysis suggests that taking ginger increases the risk of bleeding in patients taking warfarin for at least 4 months. However, research in healthy people suggests that ginger has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. Until more is known, monitor INRs closely in patients taking large amounts of ginger.

Likelihood Possible Evidence B
Calcium Channel Blockers

Theoretically, taking ginger with calcium channel blockers might increase the risk of hypotension.
Some animal and in vitro research suggests that ginger has hypotensive and calcium channel-blocking effects. Another animal study shows that concomitant administration of ginger and the calcium channel blocker amlodipine leads to greater reductions in blood pressure when compared with amlodipine alone.

Likelihood Unlikely Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, when taken prior to cyclosporine, ginger might decrease cyclosporine levels.
In an animal model, ginger juice taken 2 hours prior to cyclosporine administration reduced the maximum concentration and area under the curve of cyclosporine by 51% and 40%, respectively. This effect was not observed when ginger juice and cyclosporine were administered at the same time.

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

Theoretically, ginger might increase the levels of CYP1A2 substrates.
In vitro research shows that ginger inhibits CYP1A2 activity. However, this interaction has not been reported in humans.

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

Theoretically, ginger might increase the levels of CYP2B6 substrates.
In vitro research shows that ginger inhibits CYP2B6 activity. However, this interaction has not been reported in humans.

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

Theoretically, ginger might increase the levels of CYP2C9 substrates.
In vitro research shows that ginger inhibits CYP2C9 activity. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Metronidazole (Flagyl)

Theoretically, ginger might increase levels of metronidazole.
In an animal model, ginger increased the absorption and plasma half-life of metronidazole. In addition, the elimination rate and clearance of metronidazole was significantly reduced.

Likelihood Possible Evidence D
Ginger full monograph & interactions

Black Cumin Oil14 drug types · 912 drugs

Anticoagulant/Antiplatelet Drugs

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

Likelihood Possible Evidence D
Antidiabetes Drugs

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

Likelihood Possible Evidence B
Antihypertensive Drugs

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

Likelihood Possible Evidence B
Clopidogrel (Plavix)

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

Likelihood Possible Evidence D
Cns Depressants

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

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

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

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

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

Likelihood Possible Evidence D
Diuretic Drugs

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

Likelihood Possible Evidence D
Immunosuppressants

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

Likelihood Possible Evidence D
Phenytoin (Dilantin)

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

Likelihood Possible Evidence D
Serotonergic Drugs

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

Likelihood Possible Evidence D
Sildenafil (Viagra)

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

Likelihood Possible Evidence D
Warfarin (Coumadin)

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

Likelihood Possible Evidence D
Prednisolone

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

Likelihood Possible Evidence D
Black Cumin Oil full monograph & interactions

Grape extract9 drug types · 910 drugs

Anticoagulant/Antiplatelet Drugs

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

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

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

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

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

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

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

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

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

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

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

Likelihood Possible Evidence D
Midazolam (Versed)

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

Likelihood Possible Evidence D
Phenacetin

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

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

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

Likelihood Unlikely Evidence D
Grape extract full monograph & interactions

Schizandra12 drug types · 803 drugs

Cyclophosphamide

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

Likelihood Probable Evidence D
Cyclosporine (Neoral, Sandimmune)

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

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

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

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

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

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

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

Likelihood Probable Evidence D
Midazolam (Versed)

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

Likelihood Probable Evidence B
P-Glycoprotein Substrates

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

Likelihood Possible Evidence D
Sirolimus (Rapamune)

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

Likelihood Probable Evidence B
Tacrolimus (Prograf)

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

Likelihood Probable Evidence B
Talinolol

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

Likelihood Probable Evidence B
Voriconazole (Vfend)

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

Likelihood Possible Evidence D
Warfarin (Coumadin)

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

Likelihood Possible Evidence D
Schizandra full monograph & interactions

Astaxanthin2 drug types · 671 drugs

Cytochrome P450 2B6 (Cyp2B6) Substrates

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

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

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

Likelihood Possible Evidence D
Astaxanthin full monograph & interactions

Polyporous3 drug types · 417 drugs

Anticholinergic Drugs

Theoretically, poria mushroom might decrease the clinical effects of anticholinergic drugs.
In animal research, poria mushroom essential oil reduces acetylcholinesterase activity. This interaction has not been shown in humans.

Likelihood Possible Evidence D
Cholinergic Drugs

Theoretically, poria mushroom might have additive effects when used with cholinergic drugs.
In animal research, poria mushroom essential oil reduces acetylcholinesterase activity. This interaction has not been shown in humans.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, taking poria mushroom extract may enhance the therapeutic and adverse effects of sedatives.
Animal research shows that poria mushroom extract has sedative properties. This interaction has not been shown in humans.

Likelihood Possible Evidence D
Polyporous full monograph & interactions

Bupleurum3 drug types · 327 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, bupleurum might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
In vitro research suggests that saikosaponins, constituents of bupleurum, can inhibit platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, bupleurum might decrease the effects of antidiabetes drugs.
Animal research suggests that saikosaponins, constituents of bupleurum, can increase blood glucose.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, bupleurum might decrease the effects of immunosuppressants.
In vitro and animal research suggests that bupleurum might stimulate immune function.

Likelihood Possible Evidence D
Bupleurum full monograph & interactions

Maitake3 drug types · 260 drugs

Antidiabetes Drugs

Theoretically, combining maitake mushroom with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research shows that taking maitake mushroom polysaccharide (MMP) can lower blood glucose levels in patients with types 2 diabetes.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, combining maitake mushroom with antihypertensive drugs might increase the risk of hypotension.
Animal research shows that maitake mushroom can lower blood pressure.

Likelihood Possible Evidence D
Warfarin (Coumadin)

There is limited evidence that maitake mushroom may increase the anticoagulant effects of warfarin.
In a case report, a patient previously stabilized on warfarin developed an elevated international normalized ratio (INR) of 5.1 after taking maitake mushroom (Grifron-Pro Maitake D-Fraction) 1 drop/kg daily in three divided doses for one week. The elevated INR resolved after holding warfarin for two days, then reducing the dose by 11%. It is thought that the beta-glucan constituent of maitake mushroom might cause warfarin dissociation from proteins, resulting in increased free warfarin levels and increased warfarin effects.

Likelihood Possible Evidence D
Maitake full monograph & interactions

American Ginseng4 drug types · 217 drugs

Warfarin (Coumadin)

American ginseng seems to decrease the effectiveness of warfarin therapy.
Healthy patients receiving warfarin 5 mg daily, who also take American ginseng 1 gram twice daily, seem to have a significantly reduced international normalized ratio (INR).

Likelihood Likely Evidence B
Antidiabetes Drugs

Theoretically, taking American ginseng with antidiabetes drugs might increase the risk of hypoglycemia.
American ginseng seems to lower postprandial blood glucose. Theoretically, concomitant use with antidiabetes drugs might enhance blood glucose lowering effects and possibly cause hypoglycemia.

Likelihood Probable Evidence B
Immunosuppressants

Theoretically, American ginseng use might interfere with immunosuppressive therapy.
American ginseng seems to stimulate immune function. Theoretically, American ginseng might decrease the effectiveness of immunosuppressant drugs.

Likelihood Possible Evidence D
Monoamine Oxidase Inhibitors (Maois)

Theoretically, American ginseng can interfere with MAOI therapy.
There is one case report of insomnia, headache, and tremors when an unspecified ginseng product was used with phenelzine (Nardil), an MAOI. There is also one case report of hypomania when an unspecified ginseng product was used with phenelzine. Theoretically, American ginseng may interfere with MAOI therapy.

Likelihood Possible Evidence D
American Ginseng full monograph & interactions

Sheep Sorrel3 drug types · 169 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, sorrel might cause additive effects and side effects when used with anticoagulant or antiplatelet drugs.
In vitro, sorrel has been shown to inhibit platelet aggregation. However, this effect has not been reported in humans.

Likelihood Possible Evidence D
Fexofenadine (Allegra)

Sorrel might reduce the effectiveness of fexofenadine by reducing its absorption from the gut.
In vitro research shows that an ethanol extract of sorrel inhibits organic anion-transporting polypeptide 1A2 (OATP1A2), which transports fexofenadine from the intestine into cells. In rats, concomitant administration of sorrel extract with fexofenadine reduces oral absorption of fexofenadine and the area under the plasma concentration-time curve (AUC).

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

Sorrel might reduce the effectiveness of OATP substrates by reducing their absorption from the gut.
In vitro research shows that sorrel inhibits OATP1A2. Theoretically it may inhibit other OATPs. The OATPs are expressed in the small intestine and liver and transport drugs into cells. Inhibition of OATP may reduce the bioavailability of oral drugs that are substrates of OATP.

Likelihood Possible Evidence D
Sheep Sorrel full monograph & interactions

Calcium Carbonate18 drug types · 168 drugs

Ceftriaxone (Rocephin)

Co-administration of intravenous calcium and ceftriaxone can result in precipitation of a ceftriaxone-calcium salt in the lungs and kidneys.
Avoid administering intravenous calcium in any form, such as parenteral nutrition or Lactated Ringers, within 48 hours of intravenous ceftriaxone. Case reports in neonates show that administering intravenous ceftriaxone and calcium can result in precipitation of a ceftriaxone-calcium salt in the lungs and kidneys. In several cases, neonates have died as a result of this interaction. So far there are no reports in adults; however, there is still concern that this interaction might occur in adults.

Likelihood Probable Evidence D
Dolutegravir (Tivicay)

Calcium seems to reduce levels of dolutegravir.
Advise patients to take dolutegravir either 2 hours before or 6 hours after taking calcium supplements. Pharmacokinetic research suggests that taking calcium carbonate 1200 mg concomitantly with dolutegravir 50 mg reduces plasma levels of dolutegravir by almost 40%. Calcium appears to decrease levels of dolutegravir through chelation.

Likelihood Probable Evidence B
Elvitegravir (Vitekta)

Calcium seems to reduce levels of elvitegravir.
Advise patients to take elvitegravir either 2 hours before or 2 hours after taking calcium supplements. Pharmacokinetic research suggests that taking calcium along with elvitegravir can reduce blood levels of elvitegravir through chelation.

Likelihood Probable Evidence B
Aluminum

Calcium citrate might increase aluminum absorption and toxicity. Other types of calcium do not increase aluminum absorption.
Calcium citrate can increase the absorption of aluminum when taken with aluminum hydroxide. The increase in aluminum levels may become toxic, particularly in individuals with kidney disease. However, the effect of calcium citrate on aluminum absorption is due to the citrate anion rather than calcium cation. Calcium acetate does not appear to increase aluminum absorption.

Likelihood Possible Evidence B
Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)

Calcium might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption when taken in a fasting state.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide and calcium can be taken together if taken with food. However, if taken on an empty stomach, bictegravir/emtricitabine/tenofovir alafenamide should not be taken with, or 2 hours after, calcium containing products.

Likelihood Probable Evidence D
Bisphosphonates

Calcium reduces the absorption of bisphosphonates.
Advise patients to take bisphosphonates at least 30 minutes before calcium, but preferably at a different time of day. Calcium supplements decrease absorption of bisphosphonates.

Likelihood Probable Evidence C
Calcipotriene (Dovonex)

Taking calcipotriene with calcium might increase the risk for hypercalcemia.
Calcipotriene is a vitamin D analog used topically for psoriasis. It can be absorbed in sufficient amounts to cause systemic effects, including hypercalcemia. Theoretically, combining calcipotriene with calcium supplements might increase the risk of hypercalcemia.

Likelihood Possible Evidence B
Digoxin (Lanoxin)

Using intravenous calcium with digoxin might increase the risk of fatal cardiac arrhythmias.
Hypercalcemia increases the risk of fatal cardiac arrhythmias with digoxin. However, one retrospective analysis of clinical data suggests that intravenous calcium does not increase the risk of dysrhythmias or mortality in patients receiving digoxin.

Likelihood Possible Evidence B
Diltiazem (Cardizem, Others)

Theoretically, calcium may reduce the therapeutic effects of diltiazem.
Hypercalcemia can reduce the effectiveness of verapamil in atrial fibrillation. Theoretically, calcium might increase this risk of hypercalcemia and reduce the effectiveness of diltiazem.

Likelihood Probable Evidence D
Levothyroxine (Synthroid, Others)

Calcium seems to reduce the absorption and effectiveness of levothyroxine.
Advise patients to take levothyroxine and calcium supplements at least 4 hours apart. Calcium reduces levothyroxine absorption, probably by forming insoluble complexes. Calcium carbonate supplements reduce effectiveness of levothyroxine in patients with hypothyroidism.

Likelihood Probable Evidence B
Lithium

Theoretically, concomitant use of calcium and lithium may increase this risk of hypercalcemia.
Clinical research suggests that long-term use of lithium may cause hypercalcemia in 10% to 60% of patients. Theoretically, concomitant use of lithium and calcium supplements may further increase this risk.

Likelihood Possible Evidence B
Quinolone Antibiotics

Calcium seems to reduce the absorption of quinolone antibiotics.
Advise patients to take oral quinolones at least 2 hours before or 4-6 hours after calcium supplements or calcium-fortified foods. Taking calcium at the same time as oral quinolones can reduce quinolone absorption. Calcium binds to quinolones in the gut.

Likelihood Probable Evidence B
Raltegravir (Isentress)

Calcium may reduce levels of raltegravir.
Pharmacokinetic research shows that taking a single dose of calcium carbonate 3000 mg along with raltegravir 400 mg twice daily modestly decreases the mean area under the curve of raltegravir, but the decrease does not necessitate a dose adjustment of raltegravir. However, a case of elevated HIV-1 RNA levels and documented resistance to raltegravir has been reported for a patient taking calcium carbonate 1 gram three times daily plus vitamin D3 (cholecalciferol) 400 IU three times daily in combination with raltegravir 400 mg twice daily for 11 months. It is thought that calcium reduced raltegravir levels by chelation, leading to treatment failure.

Likelihood Possible Evidence B
Sotalol (Betapace)

Calcium seems to reduce the absorption of sotalol.
Advise patients to separate doses by at least 2 hours before or 4-6 hours after calcium. Calcium appears to reduce the absorption of sotalol, probably by forming insoluble complexes.

Likelihood Possible Evidence B
Tetracycline Antibiotics

Calcium seems to reduce the absorption of tetracycline antibiotics.
Advise patients to take oral tetracyclines at least 2 hours before, or 4-6 hours after calcium supplements. Taking calcium at the same time as oral tetracyclines can reduce tetracycline absorption. Calcium binds to tetracyclines in the gut.

Likelihood Probable Evidence C
Thiazide Diuretics

Taking calcium along with thiazides might increase the risk of hypercalcemia and renal failure.
Thiazides reduce calcium excretion by the kidneys. Using thiazides along with moderately large amounts of calcium carbonate increases the risk of milk-alkali syndrome (hypercalcemia, metabolic alkalosis, renal failure). Patients may need to have their serum calcium levels and/or parathyroid function monitored regularly.

Likelihood Probable Evidence C
Verapamil (Calan, Others)

Theoretically, calcium may reduce the therapeutic effects of verapamil.
Hypercalcemia can reduce the effectiveness of verapamil in atrial fibrillation. Theoretically, use of calcium supplements may increase this risk of hypercalcemia and reduce the effectiveness of verapamil.

Likelihood Probable Evidence D
Calcium Channel Blockers

Intravenous calcium may decrease the effects of calcium channel blockers; oral calcium is unlikely to have this effect.
Intravenous calcium is used to decrease the effects of calcium channel blockers in the management of overdose. Intravenous calcium gluconate has been used before intravenous verapamil (Isoptin) to prevent or reduce the hypotensive effects without affecting the antiarrhythmic effects. But there is no evidence that dietary or supplemental calcium when taken orally interacts with calcium channel blockers.

Likelihood Unlikely Evidence D
Calcium Carbonate full monograph & interactions

Burdock1 drug type · 122 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, taking burdock with anticoagulant or antiplatelet drugs might increase the risk of bleeding.

In vitro research shows that lignans from burdock reduce rabbit platelet aggregation by inhibiting platelet activating factor. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Burdock full monograph & interactions

Wild Yam1 drug type · 41 drugs

Estrogens

Theoretically, wild yam might increase or decrease the effects of estrogen.
Wild yam root shows estrogenic and anti-estrogenic effects in vitro. Theoretically, wild yam might interfere with hormone therapy.

Likelihood Possible Evidence D
Wild Yam full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Immune Force, from the product label.

BioScience International

See all BioScience International products
Name
BioScience International
Street Address
3250 Hatch Road
City
Cedar Park
State
Texas
ZipCode
78613
Phone Number
(877) 958-9030
Web Address
www.bioscienceinternational.com
Pharmacist Counseling Corner

Immune Force by BioScience International: Common Questions

Does Immune Force by BioScience International interact with any medications?
Yes. Based on its ingredients, Immune Force has a known interaction with 1,660 medications, including 9 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Immune Force contains 22 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 Immune Force if I'm pregnant?
Several ingredients in this product should be avoided in pregnancy due to insufficient safety data: astaxanthin, wild yam, American ginseng, goldenseal, bupleurum, and burdock. Ginger and hyssop are traditionally thought to affect the uterus. Talk with your doctor or pharmacist before taking this product during pregnancy — it's not a simple yes or no.
Can I take Immune Force while breastfeeding?
Goldenseal should be avoided because berberine can pass to your infant and cause harm. Astaxanthin, wild yam, American ginseng, bupleurum, burdock, hyssop, maitake, and poria all lack sufficient safety data for breastfeeding. Check with your pharmacist before using this product.
What are the most common side effects?
The ingredients most likely to cause side effects are ginger (which can cause heartburn, diarrhea, and a peppery feeling in the mouth at higher doses) and calcium (constipation, diarrhea, and stomach upset). Black cumin oil can cause nausea, vomiting, constipation, and stomach burning. Most side effects are mild and more common at higher doses.
Does this product actually work for immune support?
The effectiveness data we hold show that American ginseng is Possibly Effective for upper respiratory infections, and black cumin oil is Possibly Effective for allergies and asthma — both relevant to immunity. For the majority of the other ingredients, we don't have solid evidence they work for any specific condition.
Is this product safe if I don't take any medications?
For healthy people not taking medications, Immune Force is likely well tolerated in the recommended dose. The most common side effects are gastrointestinal (diarrhea, heartburn, nausea). However, if you have a bleeding disorder, diabetes, high blood pressure, or thyroid disease, check with your pharmacist first — several ingredients can affect these conditions.
Why does this product have alcohol in it?
Ethyl alcohol is listed as an inactive ingredient and is likely present as a preservative or extraction solvent. The amount in the final product is typically small, but if you avoid alcohol, you may want to contact the manufacturer to confirm the concentration.

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

Not sure if Immune Force is safe with your meds?

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

Immune Force label
Go deeper

The Full Monographs Behind Immune Force’s Ingredients

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

Herb & supplement monograph

Astaxanthin

Interacts with 671 drugs

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

Read the full Astaxanthin monograph → Herb & supplement monograph

Calcium

Interacts with 168 drugs

Calcium is an essential mineral your body needs for strong bones, nerve signaling, and muscle function, and supplements can help fill gaps when diet falls short. Most people do best getting...

Read the full Calcium 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

Grape

Interacts with 910 drugs

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

Read the full Grape monograph → Herb & supplement monograph

Wild Yam

Interacts with 41 drugs

Wild yam is a root traditionally used for menopausal symptoms, cramps, and as a so-called 'natural' hormone supplement, but solid human evidence for these uses is lacking. Despite popular cl...

Read the full Wild Yam monograph → Herb & supplement monograph

Suma

Suma is a South American root often marketed as a 'Brazilian ginseng' and used as an adaptogen for energy, stamina, and stress. Human evidence is very limited, and most claims come from trad...

Read the full Suma monograph → Herb & supplement monograph

American Ginseng

Interacts with 217 drugs

American ginseng is an herbal root used as an 'adaptogen' to support energy, stress, immune function, and blood sugar. Some uses—such as reducing the chance or length of colds and modestly l...

Read the full American Ginseng monograph → Herb & supplement monograph

Burdock

Interacts with 122 drugs

Burdock is a traditional herb most often used for skin problems and as a so-called 'blood purifier,' but high-quality human studies are lacking and most claims are not well proven. It is wid...

Read the full Burdock monograph → Herb & supplement monograph

Bupleurum

Interacts with 327 drugs

Bupleurum (Chai Hu) is a root used in traditional Chinese medicine, usually as part of multi-herb formulas, for liver, digestive, and fever-related complaints. High-quality human evidence fo...

Read the full Bupleurum monograph → Herb & supplement monograph

Goldenseal

Interacts with 1,237 drugs

Goldenseal is a popular North American herb that contains berberine, a compound studied for antimicrobial effects. However, strong human evidence for its many traditional uses is largely lac...

Read the full Goldenseal monograph → Herb & supplement monograph

Schisandra

Interacts with 803 drugs

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

Read the full Schisandra monograph → Herb & supplement monograph

Sorrel

Interacts with 169 drugs

Sorrel is a tangy, leafy herb used in cooking and traditional medicine, often for congestion, digestion, and inflammation. Solid human evidence for any health benefit is limited, and its hig...

Read the full Sorrel 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

Hyssop

Hyssop is a Mediterranean mint-family herb traditionally used for coughs, colds, and digestive complaints, but solid human evidence for these uses is lacking. The dried herb in tea is genera...

Read the full Hyssop monograph → Herb & supplement monograph

Maitake Mushroom

Interacts with 260 drugs

Maitake is an edible mushroom long used as food and in traditional Japanese medicine, and it is being studied for possible immune, blood sugar, and blood pressure effects. The human evidence...

Read the full Maitake Mushroom monograph → Herb & supplement monograph

Poria Mushroom

Interacts with 417 drugs

Poria mushroom (Fu Ling) is a fungus long used in Traditional Chinese Medicine, mainly as a mild diuretic and digestive and calming aid. Modern scientific evidence in humans is very limited,...

Read the full Poria Mushroom monograph → Herb & supplement monograph

Black Seed

Interacts with 912 drugs

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

Read the full Black Seed monograph →
Sources

Sources & How We Checked

Immune Force'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 455 references behind this product’s interaction data

Every citation that drives the interaction findings for this product’s ingredients, from the evidence-graded Natural Medicines (TRC Healthcare) database. Open an ingredient to browse its citations — links open the study on PubMed or the publisher’s site.

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

See these in context on the Astaxanthin monograph →

Calcium 62 references
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  2. Hernandez-Avila M, Gonzalez-Cossio T, Hernandez-Avila JE, et al. Dietary calcium supplements to lower blood lead levels in lactating women: a randomized placebo-controlled trial. Epidemiology 2003;14:206-12.. PubMed
  3. Thys-Jacobs S, Ceccarelli S, Bierman A, et al. Calcium supplementation in premenstrual syndrome: a randomized crossover trial. J Gen Intern Med 1989;4:183-9. PubMed
  4. Maton PN, Burton ME. Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use. Drugs 1999;57:855-70.
  5. Clemens JD, Feinstein AR. Calcium carbonate and constipation: a historical review of medical mythopoeia. Gastroenterology 1977;72:957-61. DOI
  6. Saunders D, Sillery J, Chapman R. Effect of calcium carbonate and aluminum hydroxide on human intestinal function. Dig Dis Sci 1988;33:409-13. PubMed
  7. Friedman PA, Bushinsky DA. Diuretic effects on calcium metabolism. Semin Nephrol 1999;19:551-6.
  8. Koo WK, Walters JC, Esterlitz J, et al. Maternal calcium supplementation and fetal bone mineralization. Obstet Gynecol 1999;94:577-82. DOI
  9. Raman L, Rajalakshmi K, Krishnamachari KAVR, et al. Effect of calcium supplementation to undernourished mothers during pregnancy on the bone density of the neonates. Am J Clin Nutr 1978; 31:466-9. DOI
  10. Murry JJ, Healy MD. Drug-mineral interactions: a new responsibility for the hospital dietician. J Am Diet Assoc 1991;91:66-73.
  11. Chan JM, Giovannucci E, Andersson SO, et al. Dairy products, calcium, phosphorous, vitamin D, and risk of prostate cancer. Cancer Causes Control 1998;9:559-66.
  12. Butner LE, Fulco PP, Feldman G, et al. Calcium carbonate-induced hypothyroidism. Ann Intern Med 2000:132:595. PubMed
  13. Schneyer CR. Calcium carbonate and reduction of levothyroxine efficacy. JAMA 1998;279:750. PubMed
  14. Moser LR, Smythe MA, Tisdale JE. The use of calcium salts in the prevention and management of verapamil-induced hypotension. Ann Pharmacother 2000;34:622-9. PubMed
  15. Singh N, Singh PN, Hershman JM. Effect of calcium carbonate on the absorption of levothyroxine. JAMA 2000;283:2822-5. PubMed
  16. Kahela P, Anttila M, Tikkanen R, Sundquist H. Effect of food, food constituents and fluid volume on the bioavailability of sotalol. Acta Pharmacol Toxicol (Copenh) 1979;44:7-12.. PubMed
  17. Pletz MW, Petzold P, Allen A, et al. Effect of calcium carbonate on bioavailability of orally administered gemifloxacin. Antimicrob Agents Chemother 2003;47:2158-60.. PubMed
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  19. Decktor DL, Robinson M, Maton PN, et al. Effects of aluminum/magnesium hydroxide and calcium carbonate on esophageal and gastric pH in subjects with heartburn. Am J Ther 1995;2:546-52. PubMed
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  21. Peters ML, Leonard M, Licata AA. Role of alendronate and risedronate in preventing and treating osteoporosis. Cleve Clin J Med 2001;68:945-51. PubMed
  22. Bourke JF, Mumford R, Whittaker P, et al. The effects of topical calcipotriol on systemic calcium homeostasis in patients with chronic plaque psoriasis. J Am Acad Dermatol 1997;37:929-34.
  23. Gueguen L, Pointillart A. The bioavailability of dietary calcium. J Am Coll Nutr 2000;19:119s-136s. PubMed
  24. Vella A, Gerber TC, Hayes DL, Reeder GS. Digoxin, hypercalcaemia, and cardiac conduction. Postgrad Med J 1999;75:554-6. PubMed
  25. Bania TC, Blaufeux B, Hughes S, et al. Calcium and digoxin vs. calcium alone for severe verapamil toxicity. Acad Emerg Med 2000;7:1089-96. PubMed
  26. Tseng M, Breslow RA, Graubard BI, Ziegler RG. Dairy, calcium, and vitamin D intakes and prostate cancer risk in the National Health and Nutrition Examination Epidemiologic Follow-up Study cohort. Am J Clin Nutr 2005;81:1147-54. PubMed
  27. Weingarten MA, Zalmanovici A, Yaphe J. Dietary calcium supplementation for preventing colorectal cancer and adenomatous polyps. Cochrane Database Syst Rev 2004;(1):CD003548. PubMed
  28. Tavani A, Bertuccio P, Bosetti C, et al. Dietary intake of calcium, vitamin D, phosphorus and the risk of prostate cancer. Eur Urol 2005;48:27-33. PubMed
  29. Giovannucci E, Liu Y, Stampfer MJ, Willett WC. A prospective study of calcium intake and incident and fatal prostate cancer. Cancer Epidemiol Biomarkers Prev 2006;15:203-10. PubMed
  30. Rocephin (ceftriaxone) and calcium interaction. Pharmacist's Letter / Prescriber's Letter 2007;23(10):231005.
  31. Bolland MJ, Barber PA, Doughty RN, et al. Vascular events in healthy older women receiving calcium supplementation: randomised control trial. BMJ 2008;336:262-6.
  32. Bolland MJ, Avenell A, Baron JA, et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ 2010;341:c3691. PubMed
  33. Calcium supplementation and vascular events. Pharmacist's Letter / Prescriber's Letter 2008;24(3):240306.
  34. Dietary reference intakes for calcium and vitamin D. Institute of Medicine, November 30, 2010. Available at: http://www.iom.edu/~/media/Files/Report%20Files/2010/Dietary-Reference-Intakes-for-Calcium-and-Vitamin-D/Vitamin%20D%20and%20Calcium%202010%20Repo
  35. Coburn JW, Mischel MG, Goodman WG, et al. Calcium citrate markedly enhances aluminum absorption from aluminum hydroxide. Am J Kidney Dis. 1991;17(6):708-11. PubMed
  36. Bradley JS, Wassel RT, Lee L, et al. Intravenous ceftriaxone and calcium in the neonate: assessing the risk for cardiopulmonary adverse events. Pediatrics. 2009;123(4):e609-13. PubMed
  37. Kays MB, Overholser BR, Mueller BA, et al. Effects of sevelamer hydrochloride and calcium acetate on the oral bioavailability of ciprofloxacin. Am J Kidney Dis. 2003;42(6):1253-9. PubMed
  38. Neuhofel, A. L., Wilton, J. H., Victory, J. M., Hejmanowsk, L. G., and Amsden, G. W. Lack of bioequivalence of ciprofloxacin when administered with calcium-fortified orange juice: a new twist on an old interaction. J Clin Pharmacol. 2002;42(4):461-466. DOI
  39. Dickinson, H. O., Nicolson, D. J., Cook, J. V., Campbell, F., Beyer, F. R., Ford, G. A., and Mason, J. Calcium supplementation for the management of primary hypertension in adults. Cochrane.Database.Syst.Rev. 2006;(2):CD004639. PubMed
  40. Jones, B. J. and Twomey, P. J. Requesting patterns for serum calcium concentration in patients on long-term lithium therapy. Int J Clin Pract. 2009;63(1):170-172. PubMed
  41. Levine, M., Nikkanen, H., and Pallin, D. J. The effects of intravenous calcium in patients with digoxin toxicity. J Emerg.Med. 2011;40(1):41-46. PubMed
  42. Castelo-Branco, C., Ciria-Recasens, M., Cancelo-Hidalgo, M. J., Palacios, S., Haya-Palazuelos, J., Carbonell-Abello, J., Blanch-Rubio, J., Martinez-Zapata, M. J., Manasanch, J., and Perez-Edo, L. Efficacy of ossein-hydroxyapatite complex compared with ca
  43. Li K, Kaaks R, Linseisen J, Rohrmann S. Associations of dietary calcium intake and calcium supplementation with myocardial infarction and stroke risk and overall cardiovascular mortality in the Heidelberg cohort of the European Prospective Investigation i
  44. Chung M, Tang AM, Fu Z. Calcium Intake and Cardiovascular Disease Risk: An Updated Systematic Review and Meta-analysis. Ann Intern Med. 2016 Oct 25. PubMed
  45. Nolan CR, Califano JR, Butzin CA. Influence of calcium acetate or calcium citrate on intestinal aluminum absorption. Kidney Int. 1990;38(5):937-41. PubMed
  46. Lewis JR, Radavelli-Bagatini S, Rejnmark L, et al. The effects of calcium supplementation on verified coronary heart disease hospitalization and death in postmenopausal women: a collaborative meta-analysis of randomized controlled trials. J Bone Miner Res PubMed
  47. Jalloh MA, Gregory PJ, Hein D, et al. Dietary supplement interactions with antiretrovirals: a systematic review. Int J STD AIDS. 2017 Jan;28(1):4-15. PubMed
  48. Lappe J, Watson P, Travers-Gustafson D, Recker R, Garland C, Gorham E, Baggerly K, McDonnell SL. Effect of Vitamin D and Calcium Supplementation on Cancer Incidence in Older Women: A Randomized Clinical Trial. JAMA. 2017 Mar 28;317(12):1234-1243. PubMed
  49. Grove ML, Cook D. Calcium and heart attacks. Doesn't apply to most calcium prescriptions. BMJ. 2010;341:c5003. PubMed
  50. Insentress [package insert]. Whitehouse Station, NJ: Merck Sharp & Dohme Corp.; 2014.
  51. Roberts JL, Kiser JJ, Hindman JT, Meditz AL. Virologic failure with a raltegravir-containing antiretroviral regimen and concomitant calcium administration. Pharmacotherapy 2011;31(10):298e-302e. DOI
  52. Vitekta [package insert]. Foster City, CA: Gilead Sciences, Inc.; 2014.
  53. Storan ER, O'Gorman SM, Murphy A, Laing M. Case Report of Calciphylaxis Secondary to Calcium and Vitamin D<sub>3</sub> Supplementation. J Cutan Med Surg. 2017;21(2):162-163. DOI
  54. Jenkins DJA, Spence JD, Giovannucci EL, et al. Supplemental vitamins and minerals for CVD prevention and treatment. J Am Coll Cardiol 2018;71(22):2570-84. PubMed
  55. Borkenhagen JF, Connor EL, Stafstrom CE. Neonatal hypocalcemic seizures due to excessive maternal calcium ingestion. Pediatr Neurol 2013;48(6):469-71. PubMed
  56. WHO recommendations on antenatal care for a positive pregnancy experience. Geneva: World Health Organization; 2016 (http://www.who.int/reproductivehealth/publications/maternal_perinatal_health/ anc-positive-pregnancy-experience/en/).
  57. Aune D, Navarro Rosenblatt DA, Chan DS, et al. Dairy products, calcium, and prostate cancer risk: a systematic review and meta-analysis of cohort studies. Am J Clin Nutr. 2015;101(1):87-117. PubMed
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See these in context on the Calcium monograph →

Ginger 64 references
  1. Fischer-Rasmussen W, Kjaer SK, Dahl C, Asping U. Ginger treatment of hyperemesis gravidarum. Eur J Obstet Gynecol Reprod Biol 1991;38:19-24. PubMed
  2. Jewell D, Young G. Interventions for nausea and vomiting in early pregnancy. Cochrane Database Syst Rev 2000;(2):CD000145. PubMed
  3. Vutyavanich T, Kraisarin T, Ruangsri R. Ginger for nausea and vomiting in pregnancy: randomized, double-masked, placebo-controlled trial. Obstet Gynecol 2001;97:577-82. DOI
  4. Backon J. Ginger in preventing nausea and vomiting of pregnancy; a caveat due to its thromboxane synthetase activity and effect on testosterone binding. Eur J Obstet Gynecol Reprod Biol 1991;42:163-4. PubMed
  5. Srivastava KC. Effect of onion and ginger consumption on platelet thromboxane production in humans. Prostaglandins Leukot Essent Fatty Acids 1989;35:183-5. PubMed
  6. Stewart JJ, Wood MJ, Wood CD, Mims ME. Effects of ginger on motion sickness susceptibility and gastric function. Pharmacology 1991;42:111-20. PubMed
  7. Smith C, Crowther C, Willson K, et al. A randomized controlled trial of ginger to treat nausea and vomiting in pregnancy. Obstet Gynecol 2004;103:639-45. PubMed
  8. Portnoi G, Chng LA, Karimi-Tabesh L, et al. Prospective comparative study of the safety and effectiveness of ginger for the treatment of nausea and vomiting in pregnancy. Am J Obstet Gynecol 2003;189:1374-7.. PubMed
  9. Wigler I, Grotto I, Caspi D, Yaron M. The effects of Zintona EC (a ginger extract) on symptomatic gonarthritis. Osteoarthritis Cartilage 2003;11:783-9. PubMed
  10. Ghayur MN, Gilani AH. Ginger lowers blood pressure through blockade of voltage-dependent calcium channels. J Cardiovasc Pharmacol 2005;45:74-80. PubMed
  11. Thomson M, Al-Qattan KK, Al-Sawan SM, et al. The use of ginger (Zingiber officinale Rosc.) as a potential anti-inflammatory and antithrombotic agent. Prostaglandins Leukot Essent Fatty Acids 2002;67:475-8. PubMed
  12. Kanerva L, Estlander T, Jolanki R. Occupational allergic contact dermatitis from spices. Contact Dermatitis 1996;35:157-62. PubMed
  13. Akhani SP, Vishwakarma SL, Goyal RK. Anti-diabetic activity of Zingiber officinale in streptozotocin-induced type I diabetic rats. J Pharm Pharmacol 2004;56:101-5.
  14. Kruth P, Brosi E, Fux R, et al. Ginger-associated overanticoagulation by phenprocoumon. Ann Pharmacother 2004;38:257-60. PubMed
  15. Jiang X, Williams KM, Liauw WS, et al. Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Br J Clin Pharmacol 2005;59:425-32. PubMed
  16. Borrelli F, Capasso R, Aviello G, et al. Effectiveness and safety of ginger in the treatment of pregnancy-induced nausea and vomiting. Obstet Gynecol 2005;105:849-56. PubMed
  17. Smith C, Crowther C, Wilson K et al. A randomized controlled trial of ginger to treat nausea and vomiting in pregnancy. Obstet Gynecol 2004;103:639-45. PubMed
  18. Jiang X, Blair EY, McLachlan AJ. Investigation of the effects of herbal medicines on warfarin response in healthy subjects: a population pharmacokinetic-pharmacodynamic modeling approach. J Clin Pharmacol 2006;46:1370-8. PubMed
  19. Chittumma P, Kaewkiattikun K, Wiriyasiriwach B. Comparison of the effectiveness of ginger and vitamin B6 for treatment of nausea and vomiting in early pregnancy: a randomized double-blind controlled trial. J Med Assoc Thai 2007;90:15-20.
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Wild Yam 7 references
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Suma 3 references
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American Ginseng 12 references
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Burdock 11 references
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Bupleurum 17 references
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Goldenseal 34 references
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Parts of this content are provided by the Therapeutic Research Center, LLC.

DISCLAIMER: Currently this does not check for drug-drug interactions. This is not an all-inclusive comprehensive list of potential interactions and is for informational purposes only. Not all interactions are known or well-reported in the scientific literature, and new interactions are continually being reported. Input is needed from a qualified healthcare provider including a pharmacist before starting any therapy. Application of clinical judgment is necessary.

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