Nutra-Disc Ingredients & Drug Interactions
What is this page for?
First and foremost: checking Nutra-Disc 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
Nutra-Disc is a dietary supplement by Anabolic Laboratories with 13 active ingredients. Its ingredients are commonly taken for morning sickness in pregnancy, premenstrual syndrome (pms), preventing or treating b6 deficiency.Based on those ingredients, 1,664 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Green Tea extract, Bioflavonoid Complex, Turmeric Root Extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.
Check Your Meds Against Nutra-Disc by Anabolic Laboratories
Ask about any prescription or over-the-counter medication and we check it for interactions with Nutra-Disc by Anabolic Laboratories — and tell you which ingredient is responsible.
AI summaries are generated from our interaction database for education only — always confirm with your pharmacist. How we use AI
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HelloPharmacist Scorecard of Nutra-Disc by Anabolic Laboratories
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.
What’s inside
Full disclosure
Nutra-Disc contains 13 active and inactive ingredients. The active components include vitamins (B6, C), minerals (magnesium, manganese, potassium), joint-support compounds (glucosamine sulfate, shark cartilage), herbal extracts (green tea, turmeric root), and animal-derived ingredients (green-lipped mussel, sea cucumber, whole adrenal).
These are blended with inactive ingredients like cellulose, glycerin, stearic acid, silica, and magnesium stearate to create the tablet form. GlucosamIne sulfate is listed at 945 mg per serving as a complex with sodium chloride, and green-lipped mussel and shark cartilage are included for joint and connective-tissue support.
The formula also provides antioxidant support through green tea and turmeric extracts.
Does it work?
Strong evidence
Evidence for this product's ingredients is mixed. Vitamin B6 is effective for sideroblastic anemia and B6 deficiency, and likely effective for hyperhomocysteinemia; it's possibly effective for pregnancy-induced nausea.
Vitamin C is effective for C deficiency and possibly effective for exercise-induced respiratory infections and cataracts. Magnesium is effective for constipation and dyspepsia, and pre-eclampsia in pregnancy.
Glucosamine is likely effective for osteoarthritis. For other ingredients, evidence is less established.
Manganese's effectiveness for anything other than manganese deficiency is insufficient to rate. Green tea is likely effective for human papillomavirus and possibly effective for ovarian cancer and high cholesterol.
Turmeric is possibly effective for depression, high cholesterol, and allergies. Green-lipped mussel, shark cartilage, whole adrenal, bioflavonoid complex, and sea cucumber all lack sufficient reliable evidence to rate their effectiveness for the conditions this product may target.
How safe is it?
Well-documented data
Individual ingredients in Nutra-Disc are generally well tolerated at normal doses. Vitamin B6 at recommended levels is safe, but high doses over time can damage nerves (sensory neuropathy).
Vitamin C is well tolerated orally at recommended amounts; high doses may cause kidney stones in susceptible people. Magnesium commonly causes diarrhea and gastrointestinal upset at higher doses.
Manganese is safe at normal dietary amounts but high doses carry a rare risk of nerve damage and Parkinson-like symptoms. Green-lipped mussel is generally well tolerated but anyone with a shellfish allergy must avoid it; it is not safe in pregnancy or breastfeeding.
Shark cartilage is poorly studied; safety is not established in pregnancy or breastfeeding. Potassium is generally safe from food but supplements can cause dangerously high blood levels, especially in people with kidney disease.
Pregnancy and breastfeeding: Vitamin B6 is likely safe in pregnancy at normal doses; Vitamin C is likely safe; magnesium is likely safe and needed in pregnancy; green-lipped mussel should be avoided in pregnancy; glucosamine should be avoided in pregnancy; shark cartilage should be avoided in pregnancy; turmeric is likely safe in pregnancy but likely unsafe at high doses. For breastfeeding, check with your doctor before use, especially regarding caffeine-containing green tea and high-dose manganese.
Meds to double-check
Major interaction found
Before taking Nutra-Disc, check with your pharmacist if you take levodopa/carbidopa (Sinemet), nadolol (Corgard), atorvastatin (Lipitor), or ephedrine — these carry Major severity interactions with magnesium or green tea. Also double-check if you take warfarin (Coumadin) or other blood thinners, as both glucosamine and high-dose vitamin C may increase bleeding risk.
Moderate-severity concerns include antihypertensive drugs (blood pressure), seizure medications (phenobarbital, phenytoin), birth control or hormone replacement (estrogens), certain antibiotics (quinolones, tetracyclines), potassium-sparing diuretics, skeletal muscle relaxants, and antipsychotic drugs. No interactions are documented for the ingredients we could not check — whole adrenal, bioflavonoid complex, and sea cucumber.
The bottom line
Scorecard at a glanceFully disclosed formula with clinical evidence supporting its stated purpose. Major medication interactions have been identified, and safety information is well characterized.
Nutra-Disc is a multi-ingredient supplement aimed at joint and connective-tissue support, with some antioxidant and vitamin components. If you take any blood thinners, seizure drugs, blood-pressure drugs, diabetes drugs, or antibiotics, or if you use birth control or hormone therapy, check your medications with the tool on this page before starting.
Anyone with kidney disease or on a potassium-restricted diet should talk to their pharmacist before use. Pregnant or breastfeeding individuals should discuss this product with their doctor given the number of ingredients and limited safety data for some of them.
Educational only — not medical advice; always confirm with your pharmacist. Our editorial policy · How we use AI
Assessment coverage: 11 of 13 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Mar 25, 2013.
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
General information
Key facts about Nutra-Disc, straight from the product label.
| Brand | Anabolic Laboratories |
|---|---|
| Barcode (UPC) | 351953279013 |
| Net contents | 60 Tablet(s) |
| Market status | Off market |
| Date entered into DSLD | Mar 25, 2013 |
| DSLD ID | 19518 |
| Product type | Other Combinations |
| Supplement form | Tablet Or Pill |
| Dietary claims / uses | All Other, Structure/Function |
| Intended target group(s) | Adult (18 - 50 Years) |
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 Nutra-Disc by Anabolic Laboratories, sourced from the NIH Dietary Supplement Label Database.
Supplement Facts
| Ingredient | Amount | % DV |
|---|---|---|
| Vitamin B6 | 10 mg | 500% |
| Vitamin C | 75 mg | 125% |
| Glucosamine Sulfate | 750 mg | -- |
| Magnesium | 48 mg | 12% |
| whole Adrenal | 10 mg | -- |
| Bioflavonoid Complex | 12 mg | -- |
| Manganese | 15 mg | 750% |
| Green Lipped Mussel extract | 37 mg | -- |
| Sea Cucumber | 700 mg | -- |
| Potassium | 44 mg | 1% |
| from 945 mg Glucosamine Sulfate 2NaCl Complex | 945 mg | -- |
| Shark Cartilage | 150 mg | -- |
| Green Tea extract | 25 mg | -- |
| Turmeric Root Extract | 100 mg | -- |
Other ingredients: Cellulose, Glycerin, Stearic Acid, Modified Cellulose, Silica, Magnesium Stearate, natural Vanilla flavor, Dextrin, Dextrose Monohydrate, Lecithin, Sodium Citrate
Tap any ingredient to jump to its full detail below.
These statements are the manufacturer’s wording, reproduced from the product label — the label is saying it, not HelloPharmacist. We don’t verify or endorse them.
Brand IP Statement(s)
NUTRA-DISC(TM) is a specially joint formula containing a unique combination of essential vitamins, minerals, glycosaminoglycans (GAG) and specialty nutrients to offer specific support for GAG synthesis and the cartilaginous structure of the disc.
General Statements
Glucosamine sulfate, a compound that helps build healthy cartilage tissue, has also been included at appropriate levels. Just three tablets daily will provide effective long-term care and six tablets daily will provide a therapeutic dosage of this focused nutritional complex for acute applications.
WE GUARANTEE OUR SUPPLEMENTS FOR POTENCY AND PURITY AVAILABLE ONLY FROM HEALTH CARE PROFESSIONALS
Professional Formula
Supports Healthy Intervertebral Discs and Joints
NDC 51953-279-01
Seals/Symbols
AL(R)
Suggested/Recommended/Usage/Directions
DIRECTIONS: Three to six tablets daily with food or as directed by your doctor.
Precautions
KEEP OUT OF THE REACH OF CHILDREN
General
2790-060D
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.
Is this label outdated? Report a formula or label change and our pharmacy team will review it.
Nutra-Disc by Anabolic Laboratories label
The label scan from the NIH Dietary Supplement Label Database. Tap to enlarge.
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)The Ingredients in Nutra-Disc by Anabolic Laboratories
These are the 13 active ingredients this product is made of. Select any to open its full monograph.
Serving size3 Tablet(s) Dosage formTablet Or Pill Amounts shown are per serving.
Most supplement products combine several ingredients, and a medication can interact with the product through any one of them. Each ingredient below shows whether it has known drug interactions.
Vitamin B6
Interacts with210 drugs
Vitamin B6 (pyridoxine) is an essential water-soluble vitamin that your body needs for metabolism, brain function, and making red blood cells. It is b...
Vitamin B6 monograph & interactionsVitamin C
Interacts with207 drugs
Vitamin C (ascorbic acid) is an essential nutrient your body needs but cannot make, so you must get it from food or supplements. It's important for im...
Vitamin C monograph & interactionsGlucosamine Sulfate
Interacts with170 drugs
Glucosamine is a natural compound found in cartilage and joint fluid, and it is one of the most popular supplements for osteoarthritis, especially of...
Glucosamine Sulfate monograph & interactionsMagnesium
Interacts with295 drugs
Magnesium is an essential mineral your body needs for muscles, nerves, blood pressure, and many other functions, and supplements are useful for preven...
Magnesium monograph & interactionsWhole Adrenal
Bioflavonoid Complex
Interacts with1,169 drugs
Quercetin is a plant flavonoid with antioxidant and anti-inflammatory properties found in many common foods and sold as a supplement. While early rese...
Bioflavonoid Complex monograph & interactionsManganese
Interacts with83 drugs
Manganese is an essential trace mineral your body needs in small amounts for bone formation, metabolism, and antioxidant defense, and most people get...
Manganese monograph & interactionsGreen Lipped Mussel extract
No knowninteractions
New Zealand green-lipped mussel is a shellfish-derived supplement rich in omega-3 fats that is mostly used for joint pain and arthritis. Some studies...
Green Lipped Mussel extract monograph & interactionsSea Cucumber
Potassium
Interacts with62 drugs
Potassium is an essential mineral your body needs for nerve signals, muscle function, and a steady heartbeat, and most people get enough from a balanc...
Potassium monograph & interactionsShark Cartilage
Interacts with121 drugs
Shark cartilage is a supplement made from the skeletal tissue of sharks that was heavily promoted for cancer and joint conditions, but good-quality cl...
Shark Cartilage monograph & interactionsGreen Tea extract
Interacts with1,293 drugs
Green tea is a popular beverage rich in antioxidants called catechins, and drinking it in normal amounts is considered safe for most people. Concentra...
Green Tea extract monograph & interactionsTurmeric Root Extract
Interacts with1,133 drugs
Turmeric is a popular spice whose main active compounds, curcuminoids, are studied mostly for inflammation and joint pain. Some research is promising,...
Turmeric Root Extract monograph & interactionsOther (inactive) ingredients: Cellulose, Glycerin, Stearic Acid, Modified Cellulose, Silica, Magnesium Stearate, Natural Vanilla flavor, Dextrin, Dextrose Monohydrate, Lecithin, Sodium Citrate. These complete the product’s ingredient list but are not active constituents.
Nutra-Disc by Anabolic Laboratories Drug Interactions
HelloPharmacist Interaction Report
Nutra-Disc by Anabolic Laboratories contains 13 ingredients, several of which interact with medications.
The most serious interaction involves magnesium with levodopa/carbidopa (Sinemet) — a Major severity effect where magnesium can reduce levodopa levels by 35% and carbidopa by 81%, potentially cutting the drug's effectiveness. Green tea extract also carries Major severity interactions: it can reduce nadolol levels by roughly 85%, significantly reduce atorvastatin effectiveness, and theoretically increase serious stimulant side effects when combined with ephedrine.
Read the full breakdown — every affected drug type, severity by severity
Moderate interactions span multiple drug categories. Vitamin B6 may lower blood pressure additively with antihypertensive drugs, increase sun sensitivity from amiodarone, and reduce seizure-drug levels (phenobarbital and phenytoin) at high doses.
Vitamin C can increase estrogen levels, potentially interfering with birth control and hormone therapy, reduce warfarin (blood thinner) effectiveness at high doses, and theoretically interfere with certain chemotherapy drugs. Magnesium may enhance skeletal muscle relaxant effects, increase potassium-sparing diuretic side effects, and reduce absorption of quinolone and tetracycline antibiotics and bisphosphonates.
Potassium supplements raise the risk of dangerously high potassium levels when combined with potassium-sparing diuretics, ACE inhibitors, or ARBs. Glucosamine may increase warfarin's blood-thinning effect (Major severity), and several other ingredients — manganese, turmeric, and shark cartilage — carry moderate interactions with antipsychotics, antibiotics, immunosuppressants, and other drug classes.
We could not check whole adrenal, bioflavonoid complex, or sea cucumber for interactions.
Altogether, these interactions span 1,535 individual medications. Use the search tool below to verify your exact prescriptions before starting this product.
Check your own medications below · Editorial policy · How we use AI
Want to check YOUR meds against Nutra-Disc?
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 checkerIngredients driving the most interactions
Individual Drug Interactions
The ingredients in Nutra-Disc interact with 1,664 drugs. Click any drug to see the details.
10 of the 13 ingredients in Nutra-Disc interact with drugs. Each result below shows which ingredient is responsible. Green Tea extract Bioflavonoid Complex Turmeric Root Extract Magnesium Vitamin B6 Vitamin C Glucosamine Sulfate Shark Cartilage Manganese Potassium
ChlordiazepoxideLibrium
How Chlordiazepoxide interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Turmeric Root ExtractCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Root Extract + Chlordiazepoxide interactionChlordiazepoxide, Clidinium BromideLibrax
How Chlordiazepoxide, Clidinium Bromide interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Turmeric Root ExtractCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Root Extract + Chlordiazepoxide, Clidinium Bromide interactionEthanolEthanol
How Ethanol interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Green Tea ExtractAlcohol (ethanol) Minor
Interaction Summary
Theoretically, alcohol might increase the levels and adverse effects of caffeine.
Read the full Green Tea Extract + Ethanol interactionFenfluamineFintepla
How Fenfluamine interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Turmeric Root ExtractCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Root Extract + Fenfluamine interactionGabapentinGralise, Neurontin
How Gabapentin interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
MagnesiumGabapentin (neurontin) Minor
Interaction Summary
Gabapentin absorption can be decreased by magnesium.
Read the full Magnesium + Gabapentin interactionNaloxone, PentazocineTalwin Nx
How Naloxone, Pentazocine interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Turmeric Root ExtractCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Root Extract + Naloxone, Pentazocine interactionPentazocineTalwin
How Pentazocine interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Turmeric Root ExtractCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Root Extract + Pentazocine interactionPirfenidoneEsbriet
How Pirfenidone interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Turmeric Root ExtractCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Root Extract + Pirfenidone interactionPromethazinePhenergan
How Promethazine interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Green Tea ExtractPhenothiazines Minor
Interaction Summary
Theoretically, phenothiazines might increase the levels and adverse effects of caffeine.
Read the full Green Tea Extract + Promethazine interactionRopiniroleAdartrel, Requip
How Ropinirole interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Turmeric Root ExtractCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Root Extract + Ropinirole interactionRopivacaineNaropin
How Ropivacaine interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Turmeric Root ExtractCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Root Extract + Ropivacaine interactionSevelamerRenagel
How Sevelamer interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
MagnesiumSevelamer (renagel, Renvela) Minor
Interaction Summary
Sevelamer may increase serum magnesium levels.
Read the full Magnesium + Sevelamer interactionSodium Picosulfate, Citric Acid, Magnesium Oxide (otc Drug)Pico-Salax
How Sodium Picosulfate, Citric Acid, Magnesium Oxide (otc Drug) interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Vitamin CCholine Magnesium Trisalicylate (trilisate) Minor
Interaction Summary
Acidification of the urine by vitamin C might increase choline magnesium trisalicylate levels.
Read the full Vitamin C + Sodium Picosulfate, Citric Acid, Magnesium Oxide (otc Drug) interactionTriclabendazoleEgaten
How Triclabendazole interacts with Nutra-Disc — through 1 ingredient. Tap an ingredient for the detail:
Turmeric Root ExtractCytochrome P450 1a2 (cyp1a2) Substrates Minor
Interaction Summary
Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2.
Read the full Turmeric Root Extract + Triclabendazole interactionAcetaminophen, Dextromethorphan, DoxylamineNyQuil
How Acetaminophen, Dextromethorphan, Doxylamine interacts with Nutra-Disc — through 2 ingredients. Tap an ingredient for the detail:
From 945 Mg Glucosamine Sulfate 2nacl ComplexAcetaminophen (tylenol, Others) Minor
Interaction Summary
Acetaminophen might interfere with the activity of glucosamine sulfate by interacting with the sulfate portion.
Read the full From 945 Mg Glucosamine Sulfate 2nacl Complex + Acetaminophen, Dextromethorphan, Doxylamine interactionVitamin CAcetaminophen (tylenol, Others) Minor
Interaction Summary
High-dose vitamin C might slightly prolong the clearance of acetaminophen.
Read the full Vitamin C + Acetaminophen, Dextromethorphan, Doxylamine interactionEach ingredient & the kinds of drugs it affects
For each ingredient in Nutra-Disc 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.
Green Tea extract
Atorvastatin (Lipitor)
Green tea extract seems to reduce the levels and clinical effects of atorvastatin.
In healthy humans, taking green tea extract 300 mg or 600 mg along with atorvastatin reduces plasma levels of atorvastatin by approximately 24%. The elimination of atorvastatin is not affected. Atorvastatin is a substrate of organic anion-transporting polypeptides (OATPs). Research shows that two of the major catechins found in green tea, epicatechin gallate (ECG) and epigallocatechin gallate (EGCG), inhibit OATPs. Some OATPs are expressed in the small intestine and are responsible for the uptake of drugs and other compounds, which may have resulted in reduced plasma levels of atorvastatin. It is not clear if drinking green tea alters the absorption of atorvastatin.
Ephedrine
Theoretically, concomitant use might increase the risk for stimulant adverse effects.
Green tea contains caffeine. There is evidence that using ephedrine with caffeine might increase the risk of serious life-threatening or debilitating adverse effects such as hypertension, myocardial infarction, stroke, seizures, and death.
Nadolol (Corgard)
Green tea seems to reduce the levels and clinical effects of nadolol.
Preliminary clinical research shows that green tea consumption reduces plasma concentrations of nadolol. Compared to a control group, both peak levels and total drug exposure (AUC) of nadolol were reduced by approximately 85% in subjects who drank green tea daily for two weeks. Drinking green tea with nadolol also significantly reduced nadolol's systolic blood pressure lowering effect. Other clinical research shows that a single dose of green tea can affect plasma nadolol levels for at least one hour. Green tea catechins have been shown to inhibit organic anion transporting polypeptides (OATP), one of which, OATP1A2, is involved in the uptake of nadolol in the intestine The interaction is thought to be due primarily to the epigallocatechin gallate (EGCG) content of green tea.
5-Fluorouracil
Theoretically, high doses of green tea might increase the effects and side effects of 5-fluorouracil.
Animal research shows that taking green tea in amounts equivalent to about 6 cups daily in humans for 4 weeks prior to receiving a single injection of 5-fluorouracil increases the maximum plasma levels of 5-fluorouracil by about 2.5-fold and the area under the curve by 425%.
Adenosine (Adenocard)
Theoretically, green tea might decrease the vasodilatory effects of adenosine and interfere with its use prior to stress testing.
Green tea contains caffeine. Caffeine is a competitive inhibitor of adenosine at the cellular level. However, caffeine doesn't seem to affect supplemental adenosine because high interstitial levels of adenosine overcome the antagonistic effects of caffeine. It is recommended that methylxanthines and methylxanthine-containing products be stopped 24 hours prior to pharmacological stress tests. However, methylxanthines appear more likely to interfere with dipyridamole (Persantine) than adenosine-induced stress testing.
Anticoagulant/Antiplatelet Drugs
Theoretically, green tea may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Conflicting reports exist regarding the effect of green tea on bleeding risk when used with anticoagulant or antiplatelet drugs; however, most evidence suggests that drinking green tea in moderate amounts is unlikely to cause a significant interaction. Green tea contains small amounts of vitamin K, approximately 7 mcg per cup. Some case reports have associated the antagonism of warfarin with the vitamin K content of green tea. However, these reports are rare, and very large doses of green tea (about 8-16 cups daily) appear to be needed to cause these effects. Furthermore, the catechins and caffeine in green tea are reported to have antiplatelet activity.
Beta-Adrenergic Agonists
Green tea contains caffeine. Theoretically, concomitant use of large amounts of caffeine might increase cardiac inotropic effects of beta-agonists.
Bortezomib (Velcade)
Theoretically, green tea might interfere with the effects of bortezomib.
In vitro research shows that green tea polyphenols, such as epigallocatechin gallate (EGCG), interact with bortezomib and block its proteasome inhibitory action. This prevents the induction of cell death in multiple myeloma or glioblastoma cancer cell lines. Advise patients taking bortezomib, not to take green tea.
Carbamazepine (Tegretol)
Theoretically, green tea might reduce the effects of carbamazepine and increase the risk for convulsions.
Green tea contains caffeine. Animal research suggests that taking caffeine can lower the anticonvulsant effects of carbamazepine and can induce seizures when taken in doses above 400 mg/kg. Human research has shown that taking caffeine 300 mg in three divided doses along with carbamazepine 200 mg reduces the bioavailability of carbamazepine by 32% and prolongs the plasma half-life of carbamazepine 2-fold in healthy individuals.
Celiprolol (Celicard)
Theoretically, green tea might reduce the levels and clinical effects of celiprolol.
In a small human study, taking green tea daily for 4 days appears to decrease blood and urine levels of celiprolol by at least 98%. This interaction is possibly due to the inhibition of organic anion transporting polypeptide (OATP). Green tea catechins have been shown to inhibit organic anion transporting polypeptides (OATP), one of which, OATP1A2, is found in the intestine The interaction is thought to be due primarily to the epigallocatechin gallate (EGCG) content of green tea.
Cimetidine (Tagamet)
Theoretically, concomitant use might increase the effects and adverse effects of caffeine in green tea.
Green tea contains caffeine. Cimetidine can reduce caffeine clearance by 31% to 42%.
Clozapine (Clozaril)
Theoretically, green tea might increase the levels and adverse effects of clozapine and acutely exacerbate psychotic symptoms.
Animal research suggests that, although green tea extract does not affect the elimination of clozapine, it delays the time to reach peak concentration and reduces the peak plasma levels. Also, concomitant administration of green tea and clozapine might theoretically cause acute exacerbation of psychotic symptoms due to the caffeine in green tea. Caffeine can increase the effects and toxicity of clozapine. Caffeine doses of 400-1000 mg daily inhibit clozapine metabolism. Clozapine is metabolized by cytochrome P450 1A2 (CYP1A2). Researchers speculate that caffeine might inhibit CYP1A2. However, there is no reliable evidence that caffeine affects CYP1A2. There is also speculation that genetic factors might make some patients be more sensitive to the interaction between clozapine and caffeine.
Contraceptive Drugs
Theoretically, concomitant use might increase the effects and adverse effects of caffeine found in green tea.
Green tea contains caffeine. Oral contraceptives can decrease caffeine clearance by 40% to 65%.
Cytochrome P450 1A2 (Cyp1A2) Inhibitors
Theoretically, concomitant use might increase the levels and adverse effects of caffeine.
Green tea contains caffeine. Caffeine is metabolized by cytochrome P450 1A2 (CYP1A2),. Theoretically, drugs that inhibit CYP1A2 may decrease the clearance rate of caffeine from green tea and increase caffeine levels.
Dipyridamole (Persantine)
Theoretically, green tea might decrease the vasodilatory effects of dipyridamole and interfere with its use prior to stress testing.
Green tea contains caffeine. Caffeine might inhibit dipyridamole-induced vasodilation. It is recommended that methylxanthines and methylxanthine-containing products be stopped 24 hours prior to pharmacological stress tests. Methylxanthines appear more likely to interfere with dipyridamole (Persantine) than adenosine-induced stress testing.
Disulfiram (Antabuse)
Theoretically, disulfiram might increase the risk of adverse effects from caffeine.
In human research, disulfiram decreases the clearance and increases the half-life of caffeine.
Diuretic Drugs
Theoretically, using green tea with diuretic drugs might increase the risk of hypokalemia.
Green tea contains caffeine. In excessive amounts, caffeine can reduce potassium levels due to stimulation of the sodium-potassium pump. Diuretics can also cause lower potassium levels.
Estrogens
Theoretically, estrogens might increase the levels and adverse effects of caffeine.
Green tea contains caffeine. Estrogen inhibits caffeine metabolism.
Ethosuximide (Zarontin)
Theoretically, green tea might reduce the effects of ethosuximide and increase the risk for convulsions.
Green tea contains caffeine. Animal research suggests that caffeine 92.4 mg/kg can decrease the anticonvulsant activity of ethosuximide. However, this effect has not been reported in humans.
Felbamate (Felbatol)
Theoretically, green tea might reduce the effects of felbamate and increase the risk for convulsions.
Green tea contains caffeine. Animal research suggests that a high dose of caffeine 161.7 mg/kg can decreases the anticonvulsant activity of felbamate. However, this effect has not been reported in humans.
Fexofenadine (Allegra)
Green tea can decrease blood levels of fexofenadine.
Clinical research shows that green tea can significantly decrease blood levels and excretion of fexofenadine. Taking green tea extract with a dose of fexofenadine decreased bioavailability of fexofenadine by about 30%. In vitro, green tea inhibits the cellular accumulation of fexofenadine by inhibiting the organic anion transporting polypeptide (OATP) drug transporter. Research shows that two of the major catechins found in green tea, epicatechin gallate (ECG) and epigallocatechin gallate (EGCG), inhibit OATPs, specifically OATP1A2, OATP1B1, and OATP2B1. In addition, green tea has been shown to reduce the absorption of some drugs that are OATP substrates.
Flutamide (Eulexin)
Theoretically, green tea might increase the levels and adverse effects of flutamide.
Green tea contains caffeine. In vitro evidence suggests that caffeine can inhibit the metabolism of flutamide. Theoretically, concomitant use of caffeine and flutamide might increase serum concentrations of flutamide and increase the risk adverse effects.
Fluvoxamine (Luvox)
Theoretically, fluvoxamine might increase the levels and adverse effects of caffeine.
Green tea contains caffeine. Fluvoxamine reduces caffeine metabolism.
Hepatotoxic Drugs
Theoretically, concomitant use might have additive adverse hepatotoxic effects.
Green tea extract supplements have been linked to several cases of hepatotoxicity and might have additive hepatotoxic effects with other drugs..
Imatinib (Gleevec)
Theoretically, green tea might reduce the levels and clinical effects of imatinib.
In animal research, a single dose of green tea extract reduces the area under the curve (AUC) of imatinib by up to approximately 64% and its main metabolite N-desmethyl imatinib by up to approximately 81%. This interaction has not been shown in humans. The mechanism of action is unclear but may involve multiple pathways.
Bioflavonoid Complex
Antidiabetes Drugs
Theoretically, concomitant use of quercetin and antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research suggests that a combination of quercetin, myricetin, and chlorogenic acid reduce levels of fasting glucose in patients with type 2 diabetes, including those already taking antidiabetes agents. The effect of quercetin alone is unknown.
Antihypertensive Drugs
Theoretically, taking quercetin with antihypertensive drugs might increase the risk of hypotension.
Quercetin can modestly decrease blood pressure in people with mild hypertension. Theoretically, it might have additive blood pressure lowering effects when used with antihypertensive drugs.
Cyclosporine (Neoral, Sandimmune)
Theoretically, concomitant use might increase the levels and adverse effects of cyclosporine.
A small study in healthy volunteers shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of a single dose of cyclosporine, possibly due to inhibition of p-glycoprotein or cytochrome P450 3A4 (CYP3A4), which metabolizes cyclosporin.
Cytochrome P450 2C8 (Cyp2C8) Substrates
Theoretically, concomitant use might increase the levels and adverse effects of CYP2C8 substrates.
In vitro research shows that quercetin inhibits CYP2C8. Inhibition of paclitaxel (Taxol) metabolism via CYP2C8 has been reported in vitro. However, a small study in humans found no effect of quercetin on rosiglitazone (Avandia), which is also a CYP2C8 substrate.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, concomitant use might increase the levels and adverse effects of CYP2C9 substrates.
A small clinical study in healthy volunteers shows that taking quercetin 500 mg twice daily for 10 days prior to taking diclofenac, a CYP2C9 substrate, increases diclofenac plasma levels by 75% and prolongs the half-life by 32.5%. Animal research also shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar), a substrate of CYP2C9. Furthermore, laboratory research shows that quercetin inhibits CYP2C9.
Cytochrome P450 2D6 (Cyp2D6) Substrates
Theoretically, concomitant use might increase the levels and adverse effects of CYP2D6 substrates.
In vitro research show that quercetin inhibits CYP2D6. This effect has not been reported in humans.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, concomitant use might alter the effects and adverse effects of CYP3A4 substrates.
A small clinical study in healthy volunteers shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of a single dose of cyclosporine (Neoral, Sandimmune), a substrate of CYP3A4. Animal research also shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar) and quetiapine (Seroquel), substrates of CYP3A4. Other laboratory research also shows that quercetin inhibits CYP3A4. However, one clinical study shows that quercetin can increase the metabolism of midazolam, a substrate of CYP3A4, and decrease serum concentrations of midazolam by about 24% in some healthy individuals, suggesting possible induction of CYP3A4.
Diclofenac (Voltaren, Others)
Theoretically, concomitant use might increase the levels and adverse effects of diclofenac.
A small clinical study in healthy volunteers shows that taking quercetin 500 mg twice daily for 10 days prior to taking diclofenac increases diclofenac plasma levels by 75% and prolongs the half-life by 32.5%. This is thought to be due to inhibition of CYP2C9 by quercetin.
Losartan (Cozaar)
Theoretically, concomitant use might increase the effects and adverse effects of losartan and decrease the effects of its active metabolite.
Animal research shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar) while decreasing plasma levels of losartan's active metabolite. This metabolite, which is around 10-fold more potent than losartan, is the result of cytochrome P450 (CYP) 2C9- and CYP3A4-mediated transformation of losartan. Additionally, in vitro research shows that quercetin may inhibit P-glycoprotein-mediated efflux of losartan from the intestines, resulting in increased absorption of losartan. These results suggest that concomitant use of quercetin and losartan might increase systemic exposure to losartan while also decreasing plasma concentrations of losartan's active and more potent metabolite.
Midazolam (Versed)
Theoretically, concomitant use might decrease the levels and effects of midazolam.
A small clinical study in healthy volunteers shows that quercetin can increase the metabolism of midazolam, with a decrease in AUC of about 24%.
Mitoxantrone
Theoretically, quercetin might increase the effects and adverse effects of mitoxantrone.
In vitro research shows that quercetin increases the intracellular accumulation and cytotoxicity of mitoxantrone, possibly through inhibition of breast cancer resistance protein (BCRP), of which mitoxantrone is a substrate. So far, this interaction has not been reported in humans.
Organic Anion Transporter 1 (Oat1) Substrates
Theoretically, concomitant use might increase the effects and adverse effects of OAT1 substrates.
In vitro research shows that quercetin is a strong non-competitive inhibitor of OAT1, with half-maximal inhibitory concentration (IC50) values less than 10 mcM. So far, this interaction has not been reported in humans.
Organic Anion Transporter 3 (Oat3) Substrates
Theoretically, concomitant use might increase the effects and adverse effects of OAT3 substrates.
In vitro research shows that quercetin is a strong non-competitive inhibitor of OAT3, with half-maximal inhibitory concentration (IC50) values as low as 0.75 mcM. So far, this interaction has not been reported in humans.
Organic Anion-Transporting Polypeptide Substrates (Oatp)
Theoretically, concomitant use might increase the effects and adverse effects of OATP substrates.
In vitro evidence shows that quercetin can inhibit organic anion-transporting peptide (OATP) 1B1-mediated uptake of estrone-3-sulfate and pravastatin. Furthermore, clinical research in healthy males shows that intake of quercetin along with pravastatin increases the AUC of pravastatin by 24%, prolongs its half-life by 14%, and decreases its apparent clearance by 18%, suggesting that quercetin modestly inhibits the uptake of pravastatin in hepatic cells.
P-Glycoprotein Substrates
Theoretically, concomitant use might alter the effects and adverse effects of P-glycoprotein substrates.
There is preliminary evidence that quercetin inhibits the gastrointestinal P-glycoprotein efflux pump, which might increase the bioavailability and serum levels of drugs transported by the pump. A small study in healthy volunteers reported that pretreatment with quercetin increased bioavailability and plasma levels after a single dose of cyclosporine (Neoral, Sandimmune). Also, two small studies have shown that quercetin might decrease the absorption of talinolol, a substrate transported by the gastrointestinal P-glycoprotein efflux pump. However, in another small study, several days of quercetin treatment did not significantly affect the pharmacokinetics of saquinavir (Invirase). The reason for these discrepancies is not entirely clear. Until more is known, use quercetin cautiously in combination with P-glycoprotein substrates.
Pravastatin (Pravachol)
Theoretically, concomitant use might increase the effects and adverse effects of pravastatin.
In vitro evidence shows that quercetin can inhibit OATP 1B1-mediated uptake of pravastatin. Also, preliminary clinical research in healthy males shows that intake of quercetin along with pravastatin increases the maximum concentration of pravastatin by 24%, prolongs its half-life by 14%, and decreases its apparent clearance by 18%, suggesting that quercetin modestly inhibits the uptake of pravastatin in hepatic cells.
Prazosin (Minipress)
Theoretically, quercetin might increase the effects and adverse effects of prazosin.
In vitro research shows that quercetin inhibits the transcellular efflux of prazosin, possibly through inhibition of breast cancer resistance protein (BCRP), of which prazosin is a substrate. BCRP is an ATP-binding cassette efflux transporter in the intestines, kidneys, and liver. So far, this interaction has not been reported in humans.
Quetiapine (Seroquel)
Theoretically, concomitant use might increase the effects and adverse effects of quetiapine.
Animal research shows that pretreatment with quercetin can increase plasma levels of quetiapine and prolong its clearance, possibly due to inhibition of cytochrome P450 3A4 (CYP3A4) by quercetin. Additionally, the brain-to-plasma ratio of quetiapine concentrations increased, possibly due to inhibition of P-glycoprotein at the blood-brain barrier. This interaction has not been reported in humans.
Quinolone Antibiotics
Theoretically, concomitant use might inhibit the effects of quinolone antibiotics.
In vitro, quercetin binds to the DNA gyrase site on bacteria, which may interfere with the activity of quinolone antibiotics.
Sulfasalazine (Azulfidine)
Theoretically, quercetin might increase the effects and adverse effects of sulfasalazine.
Animal research shows that quercetin increases the maximum serum concentration (Cmax) and area under the curve (AUC) of sulfasalazine, possibly through inhibition of breast cancer resistance protein (BCRP), of which sulfasalazine is a substrate. So far, this interaction has not been reported in humans.
Warfarin (Coumadin)
Theoretically, quercetin may increase the risk of bleeding if used with warfarin.
Animal and in vitro studies show that quercetin might increase serum levels of warfarin. Quercetin and warfarin have the same human serum albumin (HSA) binding site, and in vitro research shows that quercetin has stronger affinity for the HSA binding site and can theoretically displace warfarin, causing higher serum levels of warfarin. Animal research shows that taking quercetin for 2 weeks before initiating warfarin increases the maximum serum level of warfarin by 30%, the half-life by 10%, and the overall exposure by 63% when compared with control. Concomitant administration of quercetin and warfarin, without quercetin pre-treatment, also increased these measures, but to a lesser degree. Researchers theorize that inhibition of CYP3A4 by quercetin may explain these effects. So far, this interaction has not been reported in humans.
Turmeric Root Extract
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Magnesium
Levodopa/Carbidopa (Sinemet)
Magnesium can reduce the bioavailability of levodopa/carbidopa.
Clinical research in healthy volunteers shows that taking magnesium oxide 1000 mg with levodopa 100 mg/carbidopa 10 mg reduces the area under the curve (AUC) of levodopa by 35% and of carbidopa by 81%. In vitro and animal research shows that magnesium produces an alkaline environment in the digestive tract, which might lead to degradation and reduced bioavailability of levodopa/carbidopa.
Aminoglycoside Antibiotics
Concomitant use of aminoglycoside antibiotics and magnesium can increase the risk for neuromuscular weakness.
Both aminoglycosides and magnesium reduce presynaptic acetylcholine release, which can lead to neuromuscular blockade and possible paralysis. This is most likely to occur with high doses of magnesium given intravenously.
Antacids
Use of acid reducers may reduce the laxative effect of magnesium oxide.
A retrospective analysis shows that, in the presence of H2 receptor antagonists (H2RAs) or proton pump inhibitors (PPIs), a higher dose of magnesium oxide is needed for a laxative effect. This may also occur with antacids. Under acidic conditions, magnesium oxide is converted to magnesium chloride and then to magnesium bicarbonate, which has an osmotic laxative effect. By reducing acidity, antacids may reduce the conversion of magnesium oxide to the active bicarbonate salt.
Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)
Magnesium might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide should be taken at least 2 hours before or 6 hours after magnesium containing products.
Bisphosphonates
Magnesium can decrease absorption of bisphosphonates.
Cations, including magnesium, can decrease bisphosphonate absorption. Advise patients to separate doses of magnesium and these drugs by at least 2 hours.
Calcium Channel Blockers
Magnesium can have additive effects with calcium channel blockers, although evidence is conflicting.
Magnesium inhibits calcium entry into smooth muscle cells and may therefore have additive effects with calcium channel blockers. Severe hypotension and neuromuscular blockades may occur when nifedipine is used with intravenous magnesium, although some contradictory evidence suggests that concurrent use of magnesium with nifedipine does not increase the risk of neuromuscular weakness. High doses of magnesium could theoretically have additive effects with other calcium channel blockers.
Digoxin
Magnesium salts may reduce absorption of digoxin.
Clinical evidence suggests that treatment with oral magnesium hydroxide or magnesium trisilicate reduces absorption of digoxin from the intestines. This may reduce the blood levels of digoxin and decrease its therapeutic effects.
Potassium-Sparing Diuretics
Potassium-sparing diuretics decrease excretion of magnesium, possibly increasing magnesium levels.
Potassium-sparing diuretics also have magnesium-sparing properties, which can counteract the magnesium losses associated with loop and thiazide diuretics. Theoretically, increased magnesium levels could result from concomitant use of potassium-sparing diuretics and magnesium supplements.
Quinolone Antibiotics
Magnesium decreases absorption of quinolones.
Magnesium can form insoluble complexes with quinolones and decrease their absorption. Advise patients to take these drugs at least 2 hours before, or 4 to 6 hours after, magnesium supplements.
Skeletal Muscle Relaxants
Parenteral magnesium alters the pharmacokinetics of skeletal muscle relaxants, increasing their effects and accelerating the onset of effect.
Parenteral magnesium shortens the time to onset of skeletal muscle relaxants by about 1 minute and prolongs the duration of action by about 2 minutes. Magnesium potentiates the effects of skeletal muscle relaxants by decreasing calcium-mediated release of acetylcholine from presynaptic nerve terminals, reducing postsynaptic sensitivity to acetylcholine, and having a direct effect on the membrane potential of myocytes. Magnesium also has vasodilatory actions and increases cardiac output, allowing a greater amount of muscle relaxant to reach the motor end plate. A clinical study found that low-dose rocuronium (0.45 mg/kg), when given after administration of magnesium 30 mg/kg over 10 minutes, has an accelerated onset of effect, which matches the onset of effect seen with a full-dose rocuronium regimen (0.6 mg/kg). In another clinical study, onset times for rocuronium doses of 0.3, 0.6, and 1.2 mg/kg were 86, 76, and 50 seconds, respectively, when given alone, but were reduced to 66, 44, and 38 seconds, respectively, when the doses were given after a 15-minute infusion of magnesium sulfate 60 mg/kg. Giving intraoperative intravenous magnesium sulfate, 50 mg/kg loading dose followed by 15 mg/kg/hour, reduces the onset time of rocuronium, enhances its clinical effects, reduces the dose of intraoperative opiates, and prolongs the spontaneous recovery time. It does not affect the activity of subsequently administered neostigmine.
Sulfonylureas
Magnesium increases the systemic absorption of sulfonylureas, increasing their effects and side effects.
Clinical research shows that administration of magnesium hydroxide with glyburide increases glyburide absorption, increases maximal insulin response by 35-fold, and increases the risk of hypoglycemia, when compared with glyburide alone. A similar interaction occurs between magnesium hydroxide and glipizide. The mechanism of this effect appears to be related to the elevation of gastrointestinal pH by magnesium-based antacids, increasing solubility and enhancing absorption of sulfonylureas.
Tetracycline Antibiotics
Magnesium decreases absorption of tetracyclines.
Magnesium can form insoluble complexes with tetracyclines in the gut and decrease their absorption and antibacterial activity. Advise patients to take these drugs 1 hour before or 2 hours after magnesium supplements.
Anticoagulant/Antiplatelet Drugs
Theoretically, magnesium may have antiplatelet effects, but the evidence is conflicting.
In vitro evidence shows that magnesium sulfate inhibits platelet aggregation, even at low concentrations. Some preliminary clinical evidence shows that infusion of magnesium sulfate increases bleeding time by 48% and reduces platelet activity. However, other clinical research shows that magnesium does not affect platelet aggregation, although inhibition of platelet-dependent thrombosis can occur.
Gabapentin (Neurontin)
Gabapentin absorption can be decreased by magnesium.
Clinical research shows that giving magnesium oxide orally along with gabapentin decreases the maximum plasma concentration of gabapentin by 33%, time to maximum concentration by 36%, and area under the curve by 43%. Advise patients to take gabapentin at least 2 hours before, or 4 to 6 hours after, magnesium supplements.
Sevelamer (Renagel, Renvela)
Sevelamer may increase serum magnesium levels.
In patients on hemodialysis, sevelamer use was associated with a 0.28 mg/dL increase in serum magnesium. The mechanism of this interaction remains unclear.
Vitamin B6
Amiodarone (Cordarone)
Theoretically, vitamin B6 might increase the photosensitivity caused by amiodarone.
Despite initial case reports suggesting that pyridoxine may have a protective effect against amiodarone-induced photosensitivity, preliminary clinical research suggests that pyridoxine may actually exacerbate this adverse effect.
Antihypertensive Drugs
Theoretically, vitamin B6 may have additive effects when used with antihypertensive drugs.
Research in hypertensive rats shows that vitamin B6 can decrease systolic blood pressure. Similarly, clinical research in patients with hypertension shows that taking high doses of vitamin B6 may reduce systolic and diastolic blood pressure, possibly by reducing plasma levels of epinephrine and norepinephrine.
Phenobarbital (Luminal)
High doses of vitamin B6 may reduce the levels and clinical effects of phenobarbital.
Preliminary clinical evidence suggests that vitamin B6 200 mg daily can reduce plasma levels of phenobarbital, possibly by increasing metabolism. It is not known whether lower doses have any effect. Advise people taking phenobarbital to avoid high doses of vitamin B6.
Phenytoin (Dilantin)
High doses of vitamin B6 may reduce the levels and clinical effects of phenytoin.
Preliminary clinical evidence suggests that vitamin B6 200 mg daily can reduce plasma levels of phenytoin, possibly by increasing metabolism. It is not known whether lower doses have any effect. Advise people taking phenytoin to avoid high doses of vitamin B6.
Levodopa
Vitamin B6 may increase the metabolism of levodopa when taken alone, but not when taken in conjunction with carbidopa.
Vitamin B6 (pyridoxine) enhances the metabolism of levodopa, reducing its clinical effects. However, this interaction does not occur when carbidopa is used concurrently with levodopa (Sinemet). Therefore, it is not likely to be a problem in most people.
Vitamin C
Alkylating Agents
Theoretically, antioxidant effects of vitamin C might reduce the effectiveness of alkylating agents.
The use of antioxidants like vitamin C during chemotherapy is controversial. There is concern that antioxidants could reduce the activity of chemotherapy drugs that generate free radicals, such as cyclophosphamide, chlorambucil, carmustine, busulfan, and thiotepa. In contrast, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that could interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as vitamin C have on chemotherapy.
Aluminum
Vitamin C can increase the amount of aluminum absorbed from aluminum compounds.
Research in animals and humans shows that vitamin C increases aluminum absorption, theoretically by chelating aluminum and keeping it in solution where it is available for absorption. In people with normal renal function, urinary excretion of aluminum will likely increase, making aluminum retention and toxicity unlikely. Patients with renal failure who take aluminum-containing compounds such as phosphate binders should avoid vitamin C supplements in doses above the recommended dietary allowances.
Antitumor Antibiotics
Theoretically, the antioxidant effects of vitamin C might reduce the effectiveness of antitumor antibiotics.
The use of antioxidants like vitamin C during chemotherapy is controversial. There is concern that antioxidants could reduce the activity of chemotherapy drugs which generate free radicals, such as doxorubicin. In contrast, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that could interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effects, if any, antioxidants such as vitamin C have on chemotherapy.
Estrogens
Vitamin C might increase blood levels of estrogens.
Increases in plasma estrogen levels of up to 55% occur under some circumstances when vitamin C is taken concurrently with oral contraceptives or hormone replacement therapy, including topical products. It is suggested that vitamin C prevents oxidation of estrogen in the tissues, regenerates oxidized estrogen, and reduces sulfate conjugation of estrogen in the gut wall. When tissue levels of vitamin C are high, these processes are already maximized and supplemental vitamin C does not have any effect on estrogen levels. Increases in plasma estrogen levels may occur when patients who are deficient in vitamin C take supplements. Monitor these patients for estrogen-related side effects.
Fluphenazine (Prolixin)
Theoretically, vitamin C might decrease levels of fluphenazine.
In one patient there was a clinically significant decrease in fluphenazine levels when vitamin C (500 mg twice daily) was started. The mechanism is not known, and there is no further data to confirm this interaction.
Indinavir (Crixivan)
Vitamin C can modestly reduce indinavir levels.
One pharmacokinetic study shows that taking vitamin C 1 gram orally once daily along with indinavir 800 mg orally three times daily reduces the area under the concentration-time curve of indinavir by 14%. The mechanism of this interaction is unknown, but it is unlikely to be clinically significant in most patients. The effect of higher doses of vitamin C on indinavir levels is unknown.
Levothyroxine (Synthroid, Others)
Vitamin C can increase levothyroxine absorption.
Two clinical studies in adults with poorly controlled hypothyroidism show that swallowing levothyroxine with a glass of water containing vitamin C 500-1000 mg in solution reduces thyroid stimulating hormone (TSH) levels and increases thyroxine (T4) levels when compared with taking levothyroxine alone. This suggests that vitamin C increases the oral absorption of levothyroxine, possibly due to a reduction in pH.
Warfarin (Coumadin)
High-dose vitamin C might reduce the levels and effectiveness of warfarin.
Vitamin C in high doses may cause diarrhea and possibly reduce warfarin absorption. There are reports of two people who took up to 16 grams daily of vitamin C and had a reduction in prothrombin time. Lower doses of 5-10 grams daily can also reduce warfarin absorption. In many cases, this does not seem to be clinically significant. However, a case of warfarin resistance has been reported for a patient who took vitamin C 500 mg twice daily. Cessation of vitamin C supplementation resulted in a rapid increase in international normalized ratio (INR). Tell patients taking warfarin to avoid taking vitamin C in excessively high doses (greater than 10 grams daily). Lower doses may be safe, but the anticoagulation activity of warfarin should be monitored. Patients who are stabilized on warfarin while taking vitamin C should avoid adjusting vitamin C dosage to prevent the possibility of warfarin resistance.
Acetaminophen (Tylenol, Others)
High-dose vitamin C might slightly prolong the clearance of acetaminophen.
A small pharmacokinetic study in healthy volunteers shows that taking high-dose vitamin C (3 grams) 1.5 hours after taking acetaminophen 1 gram slightly increases the apparent half-life of acetaminophen from around 2.3 hours to 3.1 hours. Ascorbic acid competitively inhibits sulfate conjugation of acetaminophen. However, to compensate, elimination of acetaminophen glucuronide and unconjugated acetaminophen increases. This effect is not likely to be clinically significant.
Aspirin
Acidification of the urine by vitamin C might increase aspirin levels.
It has been suggested that acidification of the urine by vitamin C could increase reabsorption of salicylates by the renal tubules, and increase plasma salicylate levels. However, short-term use of up to 6 grams daily of vitamin C does not seem to affect urinary pH or salicylate excretion, suggesting this interaction is not clinically significant.
Choline Magnesium Trisalicylate (Trilisate)
Acidification of the urine by vitamin C might increase choline magnesium trisalicylate levels.
It has been suggested that acidification of the urine by vitamin C could increase reabsorption of salicylates by the renal tubules, and increase plasma salicylate levels. However, short-term use of up to 6 grams daily of vitamin C does not seem to affect urinary pH or salicylate excretion, suggesting this interaction probably is not clinically significant.
Niacin
Vitamin C might decrease the beneficial effects of niacin on high-density lipoprotein (HDL) cholesterol levels.
A combination of niacin and simvastatin (Zocor) effectively raises HDL cholesterol levels in patients with coronary disease and low HDL levels. Clinical research shows that taking a combination of antioxidants (vitamin C, vitamin E, beta-carotene, and selenium) along with niacin and simvastatin (Zocor) attenuates this rise in HDL, specifically the HDL-2 and apolipoprotein A1 fractions, by more than 50% in patients with coronary disease. It is not known whether this adverse effect is due to a single antioxidant such as vitamin C, or to the combination. It also is not known whether it will occur in other patient populations.
Salsalate (Disalcid)
Acidification of the urine by vitamin C might increase salsalate levels.
It has been suggested that acidification of the urine by vitamin C could increase reabsorption of salicylates by the renal tubules, and increase plasma salicylate levels. However, short-term use of up to 6 grams/day vitamin C does not seem to affect urinary pH or salicylate excretion, suggesting this interaction probably is not clinically significant.
Glucosamine Sulfate
Warfarin (Coumadin)
Glucosamine might increase the anticoagulant effects of warfarin and increase the risk of bruising and bleeding.
In two individual case reports, glucosamine/chondroitin combinations were associated with a significant increase in international normalized ratio (INR) in patients previously stabilized on warfarin. In one case, the increase in INR occurred only after tripling the dose of a glucosamine/chondroitin supplement from 500 mg/400 mg daily to 1500/1200 mg daily. Additionally, 20 voluntary case reports to the U.S. Food & Drug Administration (FDA) have linked glucosamine plus chondroitin with increased INR, bruising, and bleeding in patients who were also taking warfarin. There have also been 20 additional case reports to the World Health Organization (WHO) that link glucosamine alone to increased INR in patients taking warfarin. The mechanism of this interaction is unclear. Glucosamine is a small component of heparin, but is not thought to have anticoagulant activity; however, animal research suggests that it might have antiplatelet activity.
Topoisomerase Ii Inhibitors
Theoretically glucosamine may induce resistance to topoisomerase II inhibitors.
In vitro research suggests that glucosamine might induce resistance to etoposide (VP16, VePesid) and doxorubicin (Adriamycin) by reducing inhibition of topoisomerase II, an enzyme required for DNA replication in tumor cells. This effect has not been reported in humans.
Acetaminophen (Tylenol, Others)
Acetaminophen might interfere with the activity of glucosamine sulfate by interacting with the sulfate portion.
Anecdotal reports suggest that adding glucosamine to an acetaminophen regimen might decrease pain control in patients with osteoarthritis. Some research suggests that the sulfate portion of glucosamine sulfate might contribute to its effect in osteoarthritis. Since acetaminophen metabolism requires sulfur and reduces serum sulfate concentrations, acetaminophen could theoretically interfere with the action of glucosamine sulfate. Conversely, the administration of sulfate could theoretically decrease the effectiveness of acetaminophen in sulfate-deficient people by increasing its clearance.
Antidiabetes Drugs
Despite initial concerns, it is unlikely that glucosamine will interfere with the effects of antidiabetes drugs.
In vitro and animal research has suggested that glucosamine might increase insulin resistance or decrease insulin production. This has raised concerns that taking glucosamine might worsen diabetes and decrease the effectiveness of diabetes drugs. However, clinical research suggests that glucosamine does not have adverse effects on blood glucose or glycated hemoglobin (HbA1C) in healthy, obese, or type 2 diabetes patients.
Shark Cartilage
Immunosuppressants
Theoretically, shark cartilage might interfere with immunosuppressive therapy.
In vitro evidence suggests that shark cartilage might stimulate immune responses. This effect has not been reported in humans.
Manganese
Antipsychotic Drugs
Theoretically, the risk for manganese toxicity might increase when taken with antipsychotic drugs.
Hallucinations and behavioral changes have been reported in a patient with liver disease who was taking haloperidol and manganese. Researchers speculate that taking manganese along with haloperidol, phenothiazine-derivatives, or other antipsychotic medications might increase the risk of manganese toxicity in some patients.
Quinolone Antibiotics
Theoretically, manganese might reduce the absorption of quinolone antibiotics.
Manganese is a multivalent cation. Interactions resulting in reduced quinolone absorption have been reported between quinolones and other multivalent cations, such as calcium and iron.
Tetracycline Antibiotics
Theoretically, manganese might reduce the absorption of tetracycline antibiotics.
Manganese is a multivalent cation. Interactions resulting in reduced tetracycline absorption have been reported between tetracyclines and other multivalent cations, such as calcium and iron.
Potassium
Ace Inhibitors (Aceis)
Using ACEIs with high doses of potassium increases the risk of hyperkalemia.
ACEIs block the actions of the renin-angiotensin-aldosterone system and reduce potassium excretion. Concomitant use of these drugs with potassium supplements increases the risk of hyperkalemia. However, concomitant use of these drugs with moderate dietary potassium intake (about 3775-5200 mg daily) does not increase serum potassium levels.
Angiotensin Receptor Blockers (Arbs)
Using ARBs with high doses of potassium increases the risk of hyperkalemia.
ARBs block the actions of the renin-angiotensin-aldosterone system and reduce potassium excretion. Concomitant use of these drugs with potassium supplements increases the risk of hyperkalemia. However, concomitant use of these drugs with moderate dietary potassium intake (about 3775-5200 mg daily) does not increase serum potassium levels.
Potassium-Sparing Diuretics
Concomitant use increases the risk of hyperkalemia.
Using potassium-sparing diuretics with potassium supplements increases the risk of hyperkalemia.
Brand information
Manufacturer and brand details for Nutra-Disc, from the product label.
Anabolic Laboratories
See all Anabolic Laboratories products- Name
- Anabolic Laboratories
- City
- Irvine
- State
- CA
- ZipCode
- 92614
- Web Address
- www.anaboliclabs.com
Nutra-Disc by Anabolic Laboratories: Common Questions
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Written and reviewed by the HelloPharmacist editorial staff. Our editorial policy
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The Full Monographs Behind Nutra-Disc’s Ingredients
Every ingredient we hold a full HelloPharmacist monograph for — uses, evidence, safety, and the complete interaction list.
Vitamin B6
Interacts with 210 drugsVitamin B6 (pyridoxine) is an essential water-soluble vitamin that your body needs for metabolism, brain function, and making red blood cells. It is best known for helping with pregnancy-rel...
Read the full Vitamin B6 monograph → Herb & supplement monographVitamin C
Interacts with 207 drugsVitamin C (ascorbic acid) is an essential nutrient your body needs but cannot make, so you must get it from food or supplements. It's important for immune function, collagen, and acts as an...
Read the full Vitamin C monograph → Herb & supplement monographGlucosamine
Interacts with 170 drugsGlucosamine is a natural compound found in cartilage and joint fluid, and it is one of the most popular supplements for osteoarthritis, especially of the knee. The evidence is mixed, with so...
Read the full Glucosamine monograph → Herb & supplement monographMagnesium
Interacts with 295 drugsMagnesium is an essential mineral your body needs for muscles, nerves, blood pressure, and many other functions, and supplements are useful for preventing or correcting deficiency. Some othe...
Read the full Magnesium monograph → Herb & supplement monographQuercetin
Interacts with 1,169 drugsQuercetin is a plant flavonoid with antioxidant and anti-inflammatory properties found in many common foods and sold as a supplement. While early research is interesting for allergies, blood...
Read the full Quercetin monograph → Herb & supplement monographManganese
Interacts with 83 drugsManganese is an essential trace mineral your body needs in small amounts for bone formation, metabolism, and antioxidant defense, and most people get enough from a normal diet. Supplements m...
Read the full Manganese monograph → Herb & supplement monographNew Zealand Green-lipped Mussel
New Zealand green-lipped mussel is a shellfish-derived supplement rich in omega-3 fats that is mostly used for joint pain and arthritis. Some studies suggest a modest benefit for osteoarthri...
Read the full New Zealand Green-lipped Mussel monograph → Herb & supplement monographPotassium
Interacts with 62 drugsPotassium is an essential mineral your body needs for nerve signals, muscle function, and a steady heartbeat, and most people get enough from a balanced diet rich in fruits and vegetables. P...
Read the full Potassium monograph → Herb & supplement monographShark Cartilage
Interacts with 121 drugsShark cartilage is a supplement made from the skeletal tissue of sharks that was heavily promoted for cancer and joint conditions, but good-quality clinical trials have not shown meaningful...
Read the full Shark Cartilage monograph → Herb & supplement monographGreen Tea
Interacts with 1,293 drugsGreen tea is a popular beverage rich in antioxidants called catechins, and drinking it in normal amounts is considered safe for most people. Concentrated green tea extracts are a different s...
Read the full Green Tea monograph → Herb & supplement monographTurmeric
Interacts with 1,133 drugsTurmeric 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 →Sources & How We Checked
Nutra-Disc'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.
- NIH Dietary Supplement Label Database (DSLD) — The official product label on file for this supplement.
- Natural Medicines (Therapeutic Research Center) — Evidence-graded clinical reference behind the ingredient interaction data.
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 627 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.
Vitamin B6 32 references
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- de, Vogel S., Dindore, V., van, Engeland M., Goldbohm, R. A., van den Brandt, P. A., and Weijenberg, M. P. Dietary folate, methionine, riboflavin, and vitamin B-6 and risk of sporadic colorectal cancer. J Nutr 2008;138(12):2372-2378. PubMed
- Hagen, I., Nesheim, B. I., and Tuntland, T. No effect of vitamin B-6 against premenstrual tension. A controlled clinical study. Acta Obstet.Gynecol.Scand. 1985;64(8):667-670. PubMed
- Aybak, M., Sermet, A., Ayyildiz, M. O., and Karakilcik, A. Z. Effect of oral pyridoxine hydrochloride supplementation on arterial blood pressure in patients with essential hypertension. Arzneimittelforschung. 1995;45(12):1271-1273.
- Lal, K. J., Dakshinamurti, K., and Thliveris, J. The effect of vitamin B6 on the systolic blood pressure of rats in various animal models of hypertension. J Hypertens. 1996;14(3):355-363. PubMed
- Lauritzen CH, Reuter HD, Repges R, Bohnert K, and Schmidt U. Treatment of premenstrual tension syndrome with Vitex agnus castus. Controlled, double-blind study versus pyridoxine. Phytomed 1997;4(3):183-189. PubMed
- Fonseca VA, Lavery LA, Thethi TK, et al. Metanx in type 2 diabetes with peripheral neuropathy: A randomized trial. Am J Med 2013;126(2):141-9. PubMed
- Hankey GJ, Eikelboom JW, Yi Q, et al. Treatment with B vitamins and incidence of cancer in patients with previous stroke or transient ischemic attack: Results of a randomized placebo-controlled trial. Stroke 2012;43(6):1572-7. PubMed
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- Mahmoud A, Tabassum S, Al Enazi S, et al. Amelioration of levetiracetam-induced behavioral side effects by pyridoxine. A randomized double blind controlled study. Pediatr Neurol 2021;119:15-21. PubMed
- Gupta M, Gallante B, Bamberger JN, et al. Prospective randomized evaluation of idiopathic hyperoxaluria treatments. J Endourol 2021;35(12):1844-1851. PubMed
- Li H, Chen M, Liang S, et al. Excessive vitamin B6 during treatment is related to poor prognosis of patients with nasopharyngeal carcinoma: A U-shaped distribution suggests low dose supplement. Clin Nutr 2021;40(4):2293-2300. PubMed
- Tanigawa J, Nabatame S, Tominaga K, et al. High-dose pyridoxine treatment for inherited glycosylphosphatidylinositol deficiency. Brain Dev 2021;43(6):680-687. PubMed
- Committee on Practice Bulletins-Obstetrics. ACOG Practice Bulletin No. 189: Nausea And Vomiting Of Pregnancy. Obstet Gynecol. 2018;131(1):e15-e30. PubMed
Vitamin C 51 references
- McEvoy GK, ed. AHFS Drug Information. Bethesda, MD: American Society of Health-System Pharmacists, 1998.
- Back DJ, Breckenridge AM, MacIver M, et al. Interaction of ethinyloestradiol with ascorbic acid in man. Br Med J (Clin Res Ed) 1981;282:1516.
- Morris JC, Beeley L, Ballantine N. Interaction of ethinyloestradiol with ascorbic acid in man [letter]. Br Med J (Clin Res Ed) 1981;283:503.
- Labriola D, Livingston R. Possible interactions between dietary antioxidants and chemotherapy. Oncology 1999;13:1003-8.
- Dwyer JH, Merz NB, Shirocre AM, et al. Progression of early atherosclerosis and intake of vitamin C and vitamin E from supplements and food. The Los Angeles Atherosclerosis Study. 41st Annual Conference on Cardiovascular Disease Epidemiology and Prevent
- Levine M, Rumsey SC, Daruwala R, et al. Criteria and recommendations for vitamin C intake. JAMA 1999;281:1415-23. PubMed
- Hansten PD, Horn JR. Drug Interactions Analysis and Management. Vancouver, WA: Applied Therapeutics Inc., 1997 and updates.
- Segal S, Kaminski S. Drug-nutrient interactions. American Druggist 1996 Jul;42-8.
- Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC: National Academy Press, 2000. Available at: http://www.nap.edu/books/0309069351/html/.
- Houston JB, Levy G. Drug biotransformation interactions in man VI: Acetaminophen and ascorbic acid. J Pharm Sci 1976;65:1218-21. PubMed
- Brown BG, Zhao XQ, Chait A, et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med 2001;345:1583-93. DOI
- Rosenthal G. Interaction of ascorbic acid and warfarin. JAMA 1971;215:1671. DOI
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- Domingo JL, Gomez M, Llobet JM, Richart C. Effect of ascorbic acid on gastrointestinal aluminum absorption (letter). Lancet 1991;338:1467.
- Domingo JL, Gomez M, Llobet JM, Corbella J. Influence of some dietary constituents on aluminum absorption and retention in rats. Kidney Int 1991;39:598-601. PubMed
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- Mc Leod DC, Nahata MC. Inefficacy of ascorbic acid as a urinary acidifier (letter). N Engl J Med 1977;296:1413. DOI
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- Vihtamaki T, Parantainen J, Koivisto AM, et al. Oral ascorbic acid increases plasma oestradiol during postmenopausal hormone replacement therapy. Maturitas 2002;42:129-35. PubMed
- Slain D, Amsden JR, Khakoo RA, et al. Effect of high-dose vitamin C on the steady-state pharmacokinetics of the protease inhibitor indinavir in healthy volunteers. Pharmacotherapy 2005;25:165-70. PubMed
- Cheung MC, Zhao XQ, Chait A, et al. Antioxidant supplements block the response of HDL to simvastatin-niacin therapy in patients with coronary artery disease and low HDL. Arterioscler Thromb Vasc Biol 2001;21:1320-6. PubMed
- Feetam CL, Leach RH, Meynell MJ. Lack of a clinically important interaction between warfarin and ascorbic acid. Toxicol Appl Pharmacol 1975;31:544-7. PubMed
- Weintraub M, Griner PF. Warfarin and ascorbic acid: lack of evidence for a drug interaction. Toxicol Appl Pharmacol 1974;28:53-6. PubMed
- Lee DH, Folsom AR, Harnack L, et al. Does supplemental vitamin C increase cardiovascular disease risk in women with diabetes? Am J Clin Nutr 2004;80:1194-200. PubMed
- Taylor EN, Stampfer MJ, Curhan GC. Dietary factors and the risk of incident kidney stones in men: new insights after 14 years of follow-up. J Am Soc Nephrol 2004;15:3225-32. PubMed
- Ward NC, Hodgson JM, Croft KD, et al. The combination of vitamin C and grape-seed polyphenols increases blood pressure: a randomized, double-blind, placebo-controlled trial. J Hypertens 2005;23:427-34.. PubMed
- Prasad KN. Rationale for using high-dose multiple dietary antioxidants as an adjunct to radiation therapy and chemotherapy. J Nutr 2004;134:3182S-3S. PubMed
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- Fairweather-Tait S, Hickson K, McGaw B, et al. Orange juice enhances aluminium absorption from antacid preparation. Eur J Clin Nutr. 1994;48(1):71-3.
- Gruenwald, J., Graubaum, H. J., Busch, R., and Bentley, C. Safety and tolerance of ester-C compared with regular ascorbic acid. Adv.Ther. 2006;23(1):171-178.
- Rahimi, R., Nikfar, S., Rezaie, A., and Abdollahi, M. A meta-analysis on the efficacy and safety of combined vitamin C and E supplementation in preeclamptic women. Hypertens.Pregnancy. 2009;28(4):417-434. PubMed
- Einerson, B., Nathorn, C., Kitiyakara, C., Sirada, M., and Thamlikitkul, V. The efficacy of ascorbic acid in suboptimal responsive anemic hemodialysis patients receiving erythropoietin: a meta-analysis. J Med.Assoc.Thai. 2011;94 Suppl 1:S134-S146.
- Li, G., Li, L., Yu, C., and Chen, L. Effect of vitamins C and E supplementation on Helicobacter pylori eradication: a meta-analysis. Br.J Nutr 2011;106(11):1632-1637.
- Chen X, Shen L, Gu X, et al. High-dose supplementation with vitamin C--induced pediatric urolithiasis: the first case report in a child and literature review. Urology. 2014;84(4):922-4. PubMed
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- Yaich S, Chaabouni Y, Charfeddine K, et al. Secondary oxalosis due to excess vitamin C intake: a cause of graft loss in a renal transplant recipient. Saudi J Kidney Dis Transpl. 2014;25(1):113-6. PubMed
- 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
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- Seo MS, Kim JK, Shim JY. High-dose vitamin C promotes regression of multiple pulmonary metastases originating from hepatocellular carcinoma. Yonsei Med J. 2015;56(5):1449-52. PubMed
- Skelin M, Lucijanic T, Amidzic Klaric D, et al. Factors Affecting Gastrointestinal Absorption of Levothyroxine: A Review. Clin Ther. 2017 Feb;39(2):378-403. PubMed
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Glucosamine 58 references
- Adams ME. Hype about glucosamine. Lancet 1999;354:353-4. PubMed
- Balkan B, Dunning BE. Glucosamine inhibits glucokinase in vitro and produces a glucose-specific impairment of in vivo insulin secretion in rats. Diabetes 1994;43:1173-9. PubMed
- Giaccari A, Morviducci L, Zorretta D, et al. In vivo effects of glucosamine on insulin secretion and insulin sensitivity in the rat: possible relevance to the maladaptive responses to chronic hyperglycaemia. Diabetologia 1995;38:518-24. PubMed
- Holmang A, Nilsson C, Niklasson M, et al. Induction of insulin resistance by glucosamine reduces blood flow but not interstitial levels of either glucose or insulin. Diabetes 1999;48:106-11. PubMed
- Houpt JB, McMillan R, Wein C, Paget-Dellio SD. Effect of glucosamine hydrochloride in the treatment of pain of osteoarthritis of the knee. J Rheumatol 1999;26:2423-30.
- Barclay TS, Tsourounis C, McCart GM. Glucosamine. Ann Pharmacother 1998;32:574-9.
- Shankar RR, Zhu JS, Baron AD. Glucosamine infusion in rats mimics the beta-cell dysfunction of non-insulin-dependent diabetes mellitus. Metabolism 1998;47:573-7.
- Almada A, Harvey P, Platt K. Effects of chronic oral glucosamine sulfate on fasting insulin resistance index (FIRI) in non-diabetic individuals. FASEB J 2000;14:A750.
- Reginster JY, Deroisy R, Rovati LC, et al. Long-term effects of glucosamine sulfate on osteoarthritis progression: a randomised, placebo-controlled trial. Lancet 2001;357:251-6.
- Does glucosamine increase serum lipid levels and blood pressure? Pharmacist's Letter/Prescriber's Letter 2001;17(11):171115.
- Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2002.
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See these in context on the New Zealand Green-lipped Mussel monograph →
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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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