Glucose Support Ingredients & Drug Interactions
What is this page for?
First and foremost: checking Glucose Support 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
Glucose Support is a dietary supplement by CHK Nutrition with 16 active ingredients. Its ingredients are commonly taken for diabetic nerve pain (neuropathy), blood sugar support in diabetes, antioxidant support.Based on those ingredients, 1,598 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ginkgo biloba leaf extract, Citrus Bioflavonoids, Milk Thistle (Silybum marianum) seed extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.
Check Your Meds Against Glucose Support by CHK Nutrition
Ask about any prescription or over-the-counter medication and we check it for interactions with Glucose Support by CHK Nutrition — 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 Glucose Support by CHK Nutrition
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
Glucose Support contains 16 active ingredients. The minerals include alpha-lipoic acid, vitamin E, manganese, vanadium, magnesium, zinc, and chromium—all involved in blood sugar regulation and antioxidant function.
The botanical extracts are gymnema sylvestre stem, ginkgo biloba leaf, bitter melon fruit, fenugreek seed, milk thistle seed, bilberry fruit, and banaba (lagerstroemia speciosa) leaf. There is also citrus bioflavonoids (from quercetin) and Jerusalem artichoke fruit extract.
Inactive ingredients include cellulose, magnesium stearate, silica, and a capsule shell.
Does it work?
Moderate evidence
The evidence for these ingredients varies widely. Alpha-lipoic acid is possibly effective for diabetic neuropathy and high cholesterol (hyperlipidemia).
Vitamin E is effective for vitamin E deficiency and possibly effective for Alzheimer's disease and several other conditions. Magnesium is effective for constipation, indigestion (dyspepsia), and pre-eclampsia.
Chromium is possibly effective for diabetes. Fenugreek and milk thistle are each possibly effective for diabetes.
For many of the other ingredients—including gymnema, ginkgo, bitter melon, bilberry, banaba, manganese, vanadium, zinc, and citrus bioflavonoids—the evidence is insufficient or not rated. We hold no effectiveness data for Jerusalem artichoke.
How safe is it?
Well-documented data
Most ingredients in this product are generally well tolerated at typical doses. Alpha-lipoic acid commonly causes headache, heartburn, nausea, or vomiting.
Vitamin E at high doses may increase bleeding risk and, in rare cases, raise the risk of hemorrhagic stroke. Magnesium can cause diarrhea, nausea, and vomiting.
Zinc may cause nausea, diarrhea, or a metallic taste. Chromium may trigger headaches, insomnia, or mood changes.
Ginkgo may cause dizziness or gastrointestinal upset and carries a small risk of bleeding. Bitter melon and fenugreek can cause stomach upset or allergic reactions.
Gymnema carries a rare but serious risk of drug-induced hepatitis. For pregnancy and breastfeeding, safety data are limited or absent for most ingredients.
Alpha-lipoic acid, citrus bioflavonoids, vanadium, and fenugreek should be avoided in pregnancy due to insufficient safety information or theoretical harm. Ginkgo and gymnema should also be avoided during pregnancy.
Breastfeeding safety is similarly unclear for many of these; discuss use with your doctor or pharmacist.
Meds to double-check
Major interaction found
Blood thinners (anticoagulants) and antiplatelet drugs: alpha-lipoic acid, vitamin E, citrus bioflavonoids, vanadium, fenugreek, and bilberry all theoretically increase bleeding risk. Antidiabetes medications (including metformin, insulin, sulfonylureas, and others): eight ingredients—alpha-lipoic acid, vanadium, chromium, gymnema, bitter melon, fenugreek, milk thistle, and bilberry—may lower blood sugar further and raise hypoglycemia risk.
Levodopa/carbidopa for Parkinson's: magnesium significantly reduces its effectiveness. Quinolone and tetracycline antibiotics: magnesium and zinc reduce their absorption.
Thyroid hormone: alpha-lipoic acid may weaken it. Chemotherapy drugs (alkylating agents, antitumor antibiotics): alpha-lipoic acid and vitamin E may theoretically reduce their activity.
Check your medications with the search tool before you start.
The bottom line
Scorecard at a glanceFully disclosed formula with some supporting evidence for its stated purpose. Major medication interactions have been identified, and safety information is well characterized.
This is a multi-ingredient glucose-support formula with some evidence backing a few of its components, especially for people managing blood sugar or neuropathy. However, it carries a substantial interaction burden—particularly with blood thinners, diabetes drugs, and Parkinson's medications—and pregnancy/breastfeeding safety is not well established.
If you take any regular medications or are pregnant or breastfeeding, check with your doctor or pharmacist before starting.
Educational only — not medical advice; always confirm with your pharmacist. Our editorial policy · How we use AI
Assessment coverage: 15 of 16 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Jun 24, 2020.
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 Glucose Support, straight from the product label.
| Brand | CHK Nutrition |
|---|---|
| Barcode (UPC) | 787500088928 |
| Net contents | 60 Capsule(s) |
| Market status | On market |
| Date entered into DSLD | Jun 24, 2020 |
| DSLD ID | 228585 |
| Product type | Other Combinations |
| Supplement form | Capsule |
| Dietary claims / uses | Nutrient, All Other, Structure/Function |
| Intended target group(s) | Adult (18 - 50 Years), Gluten Free, Sugar Free |
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 Glucose Support by CHK Nutrition, sourced from the NIH Dietary Supplement Label Database.
Supplement Facts
| Ingredient | Amount | % DV |
|---|---|---|
| Alpha Lipoic Acid | 25 mg | -- |
| Vitamin E | 67 mg | 447% |
| Citrus Bioflavonoids | 100 mg | -- |
| Manganese | 5 mg | 217% |
| Vanadium | 1 mg | -- |
| Magnesium | 400 mg | 95% |
| Zinc | 15 mg | 136% |
| Chromium | 400 mcg | 1143% |
| Gymnema sylvestre stem extract | 400 mg | -- |
| Ginkgo biloba leaf extract | 20 mg | -- |
| Bitter Melon (Momordica charantia) fruit extract | 200 mg | -- |
| Jerusalem Artichoke (Helianthus tuberosus) fruit extract | 100 mg | -- |
| Fenugreek (Trigonella foenum) seed extract | 100 mg | -- |
| Milk Thistle (Silybum marianum) seed extract | 50 mg | -- |
| Bilberry (Vaccinium myrtillus) fruit extract | 20 mg | -- |
| Lagerstroemia speciosa leaf extract | 2.7 mg | -- |
Other ingredients: Capsule, Cellulose, Magnesium Stearate, Silica
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.
Formulation
Contains no sugar, salt, yeast, wheat, gluten, preservatives, artificial colors or flavors.
Helps support normal blood sugar balance
Quality and potency guaranteed
Suggested/Recommended/Usage/Directions
Suggested use: As a dietary supplement, adults take three (3) capsules daily with meals, or as directed by a health care professional.
Storage
Store in a cool, dry place and away from direct light.
Formula
From L-OptiZinc, a patented form of zinc. From ChromeMate, a patented form of chromium. From GlucoHelp bran Lagerstroemia extract.
Brand IP Statement(s)
L-OptiZinc and ChromeMate are trademarks of InterHealth Co. GlucoHelp is a trademark of Softgel Technologies.
Precautions
Keep out of reach of children.
FDA Disclaimer Statement
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
General Statements
New day. Fresh start. Better health.
FDA Statement of Identity
Dietary Supplement
Is this label outdated? Report a formula or label change and our pharmacy team will review it.
Glucose Support by CHK Nutrition 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 Glucose Support by CHK Nutrition
These are the 16 active ingredients this product is made of. Select any to open its full monograph.
Serving size3 Capsule(s) Dosage formCapsule Servings per container20 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.
Alpha Lipoic Acid
Interacts with263 drugs
Alpha-lipoic acid (ALA) is an antioxidant made naturally by the body and found in small amounts in foods. It is most studied for diabetic nerve pain,...
Alpha Lipoic Acid monograph & interactionsVitamin E
Interacts with764 drugs
Vitamin E is an essential fat-soluble vitamin and antioxidant that most people get in adequate amounts from a normal diet. Supplements can help correc...
Vitamin E monograph & interactionsCitrus Bioflavonoids
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...
Citrus Bioflavonoids 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 & interactionsVanadium
Interacts with208 drugs
Vanadium is a trace mineral found in tiny amounts in food, and people get plenty from a normal diet. Supplement claims for diabetes, weight, and athle...
Vanadium 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 & interactionsZinc
Interacts with67 drugs
Zinc is an essential mineral that your body needs for immune function, wound healing, taste, and smell. Most people get enough from food, but suppleme...
Zinc monograph & interactionsChromium
Interacts with178 drugs
Chromium is an essential trace mineral involved in how the body handles sugar and fat. Some studies suggest it may modestly help blood sugar control i...
Chromium monograph & interactionsGymnema sylvestre stem extract
Interacts with851 drugs
Gymnema is an Ayurvedic herb best known for possibly helping lower blood sugar and reducing the taste of sweetness on the tongue. Some early human stu...
Gymnema sylvestre stem extract monograph & interactionsGinkgo biloba leaf extract
Interacts with1,266 drugs
Ginkgo is one of the world's most popular herbal supplements, mostly taken to support memory and circulation. The evidence for these uses is mixed and...
Ginkgo biloba leaf extract monograph & interactionsBitter Melon (Momordica charantia) fruit extract
Interacts with282 drugs
Bitter melon is a tropical fruit eaten as food and used in traditional medicine, most often for blood sugar control. While some small studies hint it...
Bitter Melon (Momordica charantia) fruit extract monograph & interactionsJerusalem Artichoke (Helianthus tuberosus) fruit extract
Fenugreek (Trigonella foenum) seed extract
Interacts with389 drugs
Fenugreek is a common kitchen spice that is also taken as a supplement, mainly for blood sugar, cholesterol, and to support breast milk production. So...
Fenugreek (Trigonella foenum) seed extract monograph & interactionsMilk Thistle (Silybum marianum) seed extract
Interacts with954 drugs
Milk thistle is a popular herbal supplement most often used for liver health, and its main active component is a group of compounds called silymarin....
Milk Thistle (Silybum marianum) seed extract monograph & interactionsBilberry (Vaccinium myrtillus) fruit extract
Interacts with275 drugs
Bilberry is a blueberry-like fruit rich in antioxidant plant compounds called anthocyanins, and it has a long history of traditional use for eye healt...
Bilberry (Vaccinium myrtillus) fruit extract monograph & interactionsLagerstroemia speciosa leaf extract
Interacts with299 drugs
Banaba is a leaf extract most often used to help support healthy blood sugar, and small early studies suggest its active compound corosolic acid may m...
Lagerstroemia speciosa leaf extract monograph & interactionsOther (inactive) ingredients: Capsule, Cellulose, Magnesium Stearate, Silica. These complete the product’s ingredient list but are not active constituents.
Glucose Support by CHK Nutrition Drug Interactions
HelloPharmacist Interaction Report
Glucose Support by CHK Nutrition contains multiple ingredients with documented interactions: alpha-lipoic acid, vitamin E, citrus bioflavonoids (quercetin), manganese, vanadium, magnesium, zinc, chromium, gymnema, ginkgo, bitter melon, fenugreek, milk thistle, and bilberry.
The most serious interaction is magnesium with levodopa/carbidopa (a Major severity interaction)—magnesium can reduce levodopa levels by up to 35%, which may significantly weaken treatment for Parkinson's disease.
Read the full breakdown — every affected drug type, severity by severity
Beyond that, several ingredients interact with anticoagulants and antiplatelet drugs at Moderate severity: alpha-lipoic acid, vitamin E, citrus bioflavonoids, vanadium, fenugreek, and bilberry all theoretically increase bleeding risk. Antidiabetes drugs (like metformin, sulfonylureas, or insulin) are affected by alpha-lipoic acid, vanadium, chromium, gymnema, bitter melon, fenugreek, milk thistle, and bilberry—all at Moderate severity—raising the theoretical risk of low blood sugar (hypoglycemia).
Magnesium also interacts with quinolone and tetracycline antibiotics (reducing their absorption), and several ingredients affect thyroid hormone, chemotherapy drugs, and various other medication classes at Moderate severity.
We could not check Jerusalem artichoke because interaction data for it is not on file. Altogether, these interactions span 1,599 individual medications.
Before starting this product, check your exact medications using the tool on this page, and talk with your doctor or pharmacist—especially if you take blood thinners, diabetes medications, Parkinson's drugs, or chemotherapy.
Check your own medications below · Editorial policy · How we use AI
Want to check YOUR meds against Glucose Support?
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 Glucose Support interact with 1,598 drugs. Click any drug to see the details.
15 of the 16 ingredients in Glucose Support interact with drugs. Each result below shows which ingredient is responsible. Ginkgo biloba leaf extract Citrus Bioflavonoids Milk Thistle (Silybum marianum) seed extract Gymnema sylvestre stem extract Vitamin E Fenugreek (Trigonella foenum) seed extract Lagerstroemia speciosa leaf extract Magnesium Bitter Melon (Momordica charantia) fruit extract Bilberry (Vaccinium myrtillus) fruit extract Alpha Lipoic Acid Vanadium Chromium Manganese Zinc
EstroneOrtho-Est
How Estrone interacts with Glucose Support — through 1 ingredient. Tap an ingredient for the detail:
Milk Thistle (silybum Marianum) Seed ExtractEstrogens Minor
Interaction Summary
Theoretically, milk thistle might interfere with estrogen therapy through competition for estrogen receptors.
Read the full Milk Thistle (silybum Marianum) Seed Extract + Estrone interactionEstropipateOgen, Ortho EST
How Estropipate interacts with Glucose Support — through 1 ingredient. Tap an ingredient for the detail:
Milk Thistle (silybum Marianum) Seed ExtractEstrogens Minor
Interaction Summary
Theoretically, milk thistle might interfere with estrogen therapy through competition for estrogen receptors.
Read the full Milk Thistle (silybum Marianum) Seed Extract + Estropipate interactionKetorolac Tromethamine, Phenylephrine HydrochlorideOmidria
How Ketorolac Tromethamine, Phenylephrine Hydrochloride interacts with Glucose Support — through 1 ingredient. Tap an ingredient for the detail:
ChromiumNonsteroidal Anti-inflammatory Drugs (nsaids) Minor
Interaction Summary
NSAIDs might increase chromium levels in the body.
Read the full Chromium + Ketorolac Tromethamine, Phenylephrine Hydrochloride interactionNiacin (prescription Drug)Niacor, Niaspan
How Niacin (prescription Drug) interacts with Glucose Support — through 1 ingredient. Tap an ingredient for the detail:
Vitamin ENiacin Minor
Interaction Summary
Vitamin E might decrease the beneficial effects of niacin on high-density lipoprotein (HDL) cholesterol levels.
Read the full Vitamin E + Niacin (prescription Drug) interactionPrasterone (prescription Drug)Intrarosa
How Prasterone (prescription Drug) interacts with Glucose Support — through 1 ingredient. Tap an ingredient for the detail:
Milk Thistle (silybum Marianum) Seed ExtractEstrogens Minor
Interaction Summary
Theoretically, milk thistle might interfere with estrogen therapy through competition for estrogen receptors.
Read the full Milk Thistle (silybum Marianum) Seed Extract + Prasterone (prescription Drug) interactionRosuvastatinCrestor, Ezallor
How Rosuvastatin interacts with Glucose Support — through 1 ingredient. Tap an ingredient for the detail:
Milk Thistle (silybum Marianum) Seed ExtractHmg-coa Reductase Inhibitors ("statins") Minor
Interaction Summary
Theoretically, milk thistle might interfere with statin therapy by decreasing the activity of organic anion transporting polypeptide 1B1 (OATB1B1) and inhibiting breast cancer resistance protein (BCRP).
Read the full Milk Thistle (silybum Marianum) Seed Extract + Rosuvastatin interactionRosuvastatin Calcium, EzetimibeRoszet
How Rosuvastatin Calcium, Ezetimibe interacts with Glucose Support — through 1 ingredient. Tap an ingredient for the detail:
Milk Thistle (silybum Marianum) Seed ExtractHmg-coa Reductase Inhibitors ("statins") Minor
Interaction Summary
Theoretically, milk thistle might interfere with statin therapy by decreasing the activity of organic anion transporting polypeptide 1B1 (OATB1B1) and inhibiting breast cancer resistance protein (BCRP).
Read the full Milk Thistle (silybum Marianum) Seed Extract + Rosuvastatin Calcium, Ezetimibe interactionSevelamerRenagel
How Sevelamer interacts with Glucose Support — 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 interactionTiboloneLivial
How Tibolone interacts with Glucose Support — through 1 ingredient. Tap an ingredient for the detail:
Milk Thistle (silybum Marianum) Seed ExtractEstrogens Minor
Interaction Summary
Theoretically, milk thistle might interfere with estrogen therapy through competition for estrogen receptors.
Read the full Milk Thistle (silybum Marianum) Seed Extract + Tibolone interactionEach ingredient & the kinds of drugs it affects
For each ingredient in Glucose Support 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.
Ginkgo biloba leaf extract
Talinolol
Taking ginkgo with talinolol seems to increase blood levels of talinolol.
There is some evidence that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of talinolol by 36% in healthy male individuals. However, single doses of ginkgo do not seem to affect talinolol pharmacokinetics.
Alprazolam (Xanax)
Theoretically, ginkgo might decrease the levels and clinical effects of alprazolam.
In clinical research, ginkgo extract (Ginkgold) 120 mg twice daily seems to decrease alprazolam levels by about 17%. However, ginkgo does not appear to decrease the elimination half-life of alprazolam. This suggests that ginkgo is more likely to decrease absorption of alprazolam rather than induce hepatic metabolism of alprazolam.
Anticoagulant/Antiplatelet Drugs
Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin. Theoretically, ginkgo might increase the risk of bleeding if used with other anticoagulant or antiplatelet drugs.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. However, population and clinical studies have produced mixed results. Some evidence shows that short-term use of ginkgo leaf does not significantly reduce platelet aggregation and blood clotting. A study in healthy males who took a specific ginkgo leaf extract (EGb 761) 160 mg twice daily for 7 days found no change in prothrombin time. An analysis of a large medical record database suggests that ginkgo increases the risk of a bleeding adverse event by 38% when taken concurrently with warfarin. It has been suggested that ginkgo has to be taken for at least 2-3 weeks to have a significant effect on platelet aggregation. However, a meta-analysis of 18 studies using standardized ginkgo extracts, 80-480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. In addition, a single dose of ginkgo plus clopidogrel or ticlopidine does not seem to significantly increase bleeding time or platelet aggregation. Also, taking ginkgo leaf extract daily for 8 days in conjunction with rivaroxaban does not affect anti-factor Xa activity; however, this study did not evaluate bleeding time.
Anticonvulsants
Theoretically, ginkgo might reduce the effectiveness of anticonvulsants.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.
Antidiabetes Drugs
Theoretically, taking ginkgo with antidiabetes drugs might alter the response to antidiabetes drugs.
Ginkgo leaf extract seems to alter insulin secretion and metabolism, and might affect blood glucose levels in people with type 2 diabetes. The effect of ginkgo seems to differ depending on the insulin and treatment status of the patient. In diet-controlled diabetes patients with hyperinsulinemia, taking ginkgo does not seem to significantly affect insulin or blood glucose levels. In patients with hyperinsulinemia who are treated with oral hypoglycemic agents, taking ginkgo seems to decrease insulin levels and increase blood glucose following an oral glucose tolerance test. Researchers speculate that this could be due to ginkgo-enhanced hepatic metabolism of insulin. In patients with pancreatic exhaustion, taking ginkgo seems to stimulate pancreatic beta-cells, resulting in increased insulin and C-peptide levels, but with no significant change in blood glucose levels in response to an oral glucose tolerance test.
Atorvastatin (Lipitor)
Theoretically, ginkgo might decrease the levels and clinical effects of atorvastatin.
In humans, intake of ginkgo extract appears to increase atorvastatin clearance, reducing the area under the curve of atorvastatin by 10% to 14% and the maximum concentration by 29%. However, this interaction does not appear to affect cholesterol synthesis and absorption. Further, a model in rats with hyperlipidemia suggests that administering ginkgo extract does not impact blood levels of atorvastatin and leads to lower total cholesterol, low-density lipoprotein cholesterol, and triglycerides when compared with rats given atorvastatin alone.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, ginkgo might increase levels of drugs metabolized by CYP1A2.
Laboratory research suggests that ginkgo leaf extract can mildly inhibit CYP1A2 enzymes. However, clinical research suggests ginkgo might not affect CYP1A2. Until more is known, use ginkgo cautiously in patients taking drugs metabolized by these enzymes.
Cytochrome P450 2C19 (Cyp2C19) Substrates
Theoretically, ginkgo might decrease levels of drugs metabolized by CYP2C19.
Some clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce CYP2C19 enzymes and potentially decrease levels of drugs metabolized by these enzymes. However, other clinical research shows that taking ginkgo 120 mg twice daily for 12 days has no effect on levels of drugs metabolized by CYP2C19.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, ginkgo might increase levels of drugs metabolized by CYP2C9.
In vitro, a specific standardized extract of ginkgo leaf (EGb 761) inhibits CYP2C9 activity . The terpenoid (ginkgolides) and flavonoid (quercetin, kaempferol, etc.) constituents seem to be responsible for this effect. Most ginkgo extracts contain some amount of these constituents. Therefore, other ginkgo leaf extracts might also inhibit the CYP2C9 enzyme. However, clinical research suggests that ginkgo might not have a significant effect on CYP2C9 in humans. Ginkgo does not seem to significantly affect the pharmacokinetics of CYP2C9 substrates diclofenac or tolbutamide.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, ginkgo might decrease levels of drugs metabolized by CYP3A4.
There is conflicting evidence about whether ginkgo induces or inhibits CYP3A4. Ginkgo does not appear to affect hepatic CYP3A4. However, it is not known if ginkgo affects intestinal CYP3A4. Preliminary clinical research suggests that taking ginkgo does not significantly affect levels of donepezil, lopinavir, or ritonavir, which are all CYP3A4 substrates. Other clinical research also suggests ginkgo does not significantly affect CYP3A4 activity. However, there are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4).
Efavirenz (Sustiva)
Theoretically, ginkgo might decrease the levels and clinical effects of efavirenz.
There are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. In one case, an HIV-positive male experienced over a 50% decrease in efavirenz levels over the course of 14 months while taking ginkgo extract. HIV-1 RNA copies also increased substantially, from less than 50 to more than 1500. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4). In another case report, a patient stable on antiviral therapy including efavirenz for 10 years, had an increase in viral load from <50 copies/mL to 1350 copies/mL after 2 months of taking a combination of supplements including ginkgo. After stopping ginkgo, the viral load was again controlled with the same antiviral therapy regimen.
Ibuprofen (Advil, Others)
Theoretically, ginkgo might increase the risk of bleeding when used with ibuprofen.
Ginkgo might have antiplatelet effects and has been associated with several case reports of spontaneous bleeding. In one case, a 71-year-old male had taken a specific ginkgo extract (Gingium, Biocur) 40 mg twice daily for 2.5 years. About 4 weeks after starting ibuprofen 600 mg daily he experienced a fatal intracerebral hemorrhage. However, the antiplatelet effects of ginkgo have been questioned. A meta-analysis and other studies have not found a significant antiplatelet effect with standardized ginkgo extracts, 80 mg to 480 mg taken daily for up to 32 weeks.
P-Glycoprotein Substrates
Theoretically, taking ginkgo with P-glycoprotein substrates might increase the levels and adverse effects of these substrates.
A small clinical study in healthy volunteers shows that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of the P-glycoprotein substrate, talinolol, by 36% in healthy male individuals. However, single doses of ginkgo do not have the same effect.
Risperidone (Risperdal)
Theoretically, taking ginkgo with risperidone might increase the levels and adverse effects of risperidone.
A single case of priapism has been reported for a 26-year-old male with schizophrenia who used risperidone 3 mg daily along with ginkgo extract 160 mg daily. Risperidone is metabolized by cytochrome P450 (CYP) 2D6 and CYP3A4. CYP3A4 activity might be affected by ginkgo. Theoretically, ginkgo may inhibit the metabolism of risperidone and increase the risk of adverse effects.
Rosiglitazone (Avandia)
Theoretically, ginkgo might decrease the levels and clinical effects of rosiglitazone.
Animal research shows that ginkgo leaf extract orally 100 or 200 mg/kg daily for 10 days alters the pharmacodynamics of rosiglitazone in a dose-dependent manner. The 100 mg/kg and 200 mg/kg doses reduce the area under the concentration time curve (AUC) of rosiglitazone by 39% and 52%, respectively, and the half-life by 28% and 39%, respectively. It is hypothesized that these changes may be due to induction of cytochrome P450 2C8 by ginkgo.
Seizure Threshold Lowering Drugs
Theoretically, taking ginkgo with drugs that lower the seizure threshold might increase the risk for convulsions.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.
Simvastatin (Zocor)
Theoretically, ginkgo might decrease the levels and clinical effects of simvastatin.
Clinical research shows that taking ginkgo extract can reduce the area under the curve and maximum concentration of simvastatin by 32% to 39%. However, ginkgo extract does not seem to affect the cholesterol-lowering ability of simvastatin.
Sofosbuvir (Sovaldi)
Theoretically, ginkgo might increase the levels and clinical effects of sofosbuvir.
Animal research in rats shows that giving a ginkgo extract 25 mg/kg orally daily for 14 days increases the area under the concentration time curve (AUC) after a single sofosbuvir dose of 40 mg/kg by 11%, increases the half-life by 60%, and increases the plasma concentration at 4 hours by 38%. This interaction appears to be related to the inhibition of intestinal P-glycoprotein by ginkgo.
Tacrolimus (Prograf)
Theoretically, ginkgo might increase the blood levels of tacrolimus.
In vitro evidence suggests that certain biflavonoids in ginkgo leaves (i.e. amentoflavone, ginkgetin, bilobetin) may inhibit the metabolism of tacrolimus by up to 50%. This interaction appears to be time-dependent and due to inhibition of cytochrome P450 (CYP) 3A4 by these bioflavonoids. In rats given tacrolimus 1 mg/kg orally, amentoflavone was shown to increase the area under the concentration time curve (AUC) of tacrolimus by 3.8-fold.
Trazodone (Desyrel)
Theoretically, ginkgo might increase the levels and clinical effects of trazodone.
In a case report, an Alzheimer patient taking trazodone 20 mg twice daily and ginkgo leaf extract 80 mg twice daily for four doses became comatose. The coma was reversed by administration of flumazenil (Romazicon). Coma might have been induced by excessive GABA-ergic activity. Ginkgo flavonoids are thought to have GABA-ergic activity and act directly on benzodiazepine receptors. Ginkgo might also increase metabolism of trazodone to active GABA-ergic metabolites, possibly by inducing cytochrome P450 3A4 (CYP3A4) metabolism.
Warfarin (Coumadin)
Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. Information from a medical database suggests that when taken concurrently with warfarin, ginkgo increases the risk of a bleeding adverse event by 38%. There is also some evidence that ginkgo leaf extract can inhibit cytochrome P450 2C9, an enzyme that metabolizes warfarin. This could result in increased warfarin levels. However, population and clinical research has produced mixed results. Clinical research in healthy people suggests that ginkgo has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. A meta-analysis of 18 studies using standardized ginkgo extracts, 80 mg to 480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. There is also some preliminary clinical research that suggests ginkgo might not significantly increase the effects of warfarin in patients that have a stable INR.
Nifedipine (Procardia)
Theoretically, taking ginkgo with oral, but not intravenous, nifedipine might increase levels and adverse effects of nifedipine.
Animal research and some clinical evidence suggests that taking ginkgo leaf extract orally in combination with oral nifedipine might increase nifedipine levels and cause increased side effects, such as headaches, dizziness, and hot flushes. However, taking ginkgo orally does not seem to affect the pharmacokinetics of intravenous nifedipine.
Omeprazole (Prilosec)
Theoretically, taking ginkgo with omeprazole might decrease the levels and clinical effects of omeprazole.
Clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce cytochrome P450 (CYP) 2C19 enzymes and decrease levels of omeprazole by about 27% to 42%.
Citrus Bioflavonoids
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.
Milk Thistle (Silybum marianum) seed extract
Antidiabetes Drugs
Taking milk thistle with antidiabetes drugs may increase the risk of hypoglycemia.
Clinical research shows that milk thistle extract, alone or along with tree turmeric extract, can lower blood glucose levels and glycated hemoglobin (HbA1c) in patients with type 2 diabetes, including those already taking antidiabetes drugs. Additionally, animal research shows that milk thistle extract increases the metformin maximum plasma concentration and area under the curve and decreases the renal clearance of metformin, due to inhibition of the multi-drug and toxin extrusion protein 1 (MATE1) renal tubular transport protein.
Cytochrome P450 2B6 (Cyp2B6) Substrates
Theoretically, milk thistle might inhibit CYP2B6.
An in vitro study shows that silybin, a constituent of milk thistle, binds to and noncompetitively inhibits CYP2B6. Additionally, silybin might downregulate the expression of CYP2B6 by decreasing mRNA and protein levels.
Glucuronidated Drugs
Theoretically, milk thistle might affect the clearance of drugs that undergo glucuronidation.
Laboratory research shows that milk thistle constituents inhibit uridine diphosphoglucuronosyl transferase (UGT), the major phase 2 enzyme that is responsible for glucuronidation. Theoretically, this could decrease the clearance and increase levels of glucuronidated drugs. Other laboratory research suggests that a milk thistle extract of silymarin might inhibit beta-glucuronidase, although the significance of this effect is unclear.
Ledipasvir
Theoretically, milk thistle might increase the levels and clinical effects of ledipasvir.
Animal research in rats shows that milk thistle increases the area under the curve (AUC) for ledipasvir and slows its elimination.
Morphine
Theoretically, concomitant use of milk thistle with morphine might affect serum levels of morphine and either increase or decrease its effects.
Animal research shows that milk thistle reduces serum levels of morphine by up to 66%. In contrast, laboratory research shows that milk thistle constituents inhibit uridine diphosphoglucuronosyl transferase (UGT), the major phase 2 enzyme that is responsible for glucuronidation. Theoretically, this could decrease the clearance and increase morphine levels. The effect of taking milk thistle on morphine metabolism in humans is not known.
Raloxifene (Evista)
Theoretically, milk thistle might decrease the clearance and increase levels of raloxifene.
Laboratory research suggests that the milk thistle constituents silibinin and silymarin inhibit the glucuronidation of raloxifene in the intestines.
Sirolimus (Rapamune)
Milk thistle might decrease the clearance of sirolimus.
Pharmacokinetic research shows that a milk thistle extract of silymarin decreases the apparent clearance of sirolimus in hepatically impaired renal transplant patients. It is unclear if this interaction occurs in patients without hepatic impairment.
Sofosbuvir (Solvaldi)
Theoretically, milk thistle might decrease the levels and clinical effects of sofosbuvir.
Animal research in rats shows that milk thistle reduces the metabolism of sofosbuvir, as well as the hepatic uptake of its active metabolite.
Tamoxifen (Nolvadex)
Theoretically, the milk thistle constituent silibinin might increase tamoxifen levels and interfere with its conversion to an active metabolite.
Animal research suggests that the milk thistle constituent silibinin might increase plasma levels of tamoxifen and alter its conversion to an active metabolite. The mechanism appears to involve inhibition of pre-systemic metabolism of tamoxifen by cytochrome P450 (CYP) 2C9 and CYP3A4, and inhibition of P-glycoprotein-mediated efflux of tamoxifen into the intestine for excretion. Whether this interaction occurs in humans is not known.
Warfarin (Coumadin)
Theoretically, milk thistle might increase the effects of warfarin.
In one case report, a man stabilized on warfarin experienced an increase in INR from 2.64 to 4.12 after taking a combination product containing milk thistle 200 mg daily, as well as dandelion, wild yam, niacinamide, and vitamin B12. Levels returned to normal after stopping the supplement. Although a direct correlation between milk thistle and the change in INR cannot be confirmed, some in vitro research suggests that milk thistle might inhibit cytochrome P450 2C9 (CYP2C9), an enzyme involved in the metabolism of various drugs, including warfarin.
Cytochrome P450 2C9 (Cyp2C9) Substrates
It is unclear if milk thistle inhibits CYP2C9; research is conflicting.
In vitro research suggests that milk thistle might inhibit CYP2C9. Additionally, 3 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking milk thistle and cancer medications that are CYP2C9 substrates, including imatinib and capecitabine. However, contradictory clinical research shows that milk thistle extract does not inhibit CYP2C9 or significantly affect levels of the CYP2C9 substrate tolbutamide. Differences in results could be due to differences in dosages or formulations utilized.
Cytochrome P450 3A4 (Cyp3A4) Substrates
It is unclear if milk thistle inhibits CYP3A4; research is conflicting.
While laboratory research shows conflicting results, pharmacokinetic research shows that taking milk thistle extract 420-1350 mg daily does not significantly affect the metabolism of the CYP3A4 substrates irinotecan, midazolam, or indinavir. However, 8 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking milk thistle and cancer medications that are CYP3A4 substrates, including gefitinib, sorafenib, doxorubicin, and vincristine.
Estrogens
Theoretically, milk thistle might interfere with estrogen therapy through competition for estrogen receptors.
Animal research suggests that a milk thistle extract of silymarin binds to estrogen receptor beta.
Hmg-Coa Reductase Inhibitors ("Statins")
Theoretically, milk thistle might interfere with statin therapy by decreasing the activity of organic anion transporting polypeptide 1B1 (OATB1B1) and inhibiting breast cancer resistance protein (BCRP).
Preliminary evidence suggests that a milk thistle extract of silymarin can decrease the activity of the OATP1B1, which transports HMG-CoA reductase inhibitors into the liver to their site of action, and animal research shows this increases the maximum plasma concentration of pitavastatin and pravastatin. The silibinin component also inhibits BCRP, which transports statins from the liver into the bile for excretion. However, in a preliminary study in healthy males, silymarin 140 mg three times daily had no effect on the pharmacokinetics of a single 10 mg dose of rosuvastatin.
Indinavir (Crixivan)
Theoretically, milk thistle may induce cytochrome P450 3A4 (CYP3A4) enzymes and increase the metabolism of indinavir; however, results are conflicting.
One pharmacokinetic study shows that taking milk thistle (Standardized Milk Thistle, General Nutrition Corp.) 175 mg three times daily in combination with multiple doses of indinavir 800 mg every 8 hours decreases the mean trough levels of indinavir by 25%. However, results from the same pharmacokinetic study show that milk thistle does not affect the overall exposure to indinavir. Furthermore, two other pharmacokinetic studies show that taking specific milk thistle extract (Legalon, Rottapharm Madaus; Thisilyn, Nature's Way) 160-450 mg every 8 hours in combination with multiple doses of indinavir 800 mg every 8 hours does not reduce levels of indinavir.
Organic Anion-Transporting Polypeptide Substrates (Oatp)
Milk thistle may inhibit one form of OATP, OATP-B1, which could reduce the bioavailability and clinical effects of OATP-B1 substrates.
In vitro research shows that milk thistle inhibits OATP-B1. Two case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking milk thistle and cancer medications that are OATP substrates, including sorafenib and methotrexate. OATPs are expressed in the small intestine and liver and are responsible for the uptake of drugs and other compounds into the body. Inhibition of OATP may reduce the bioavailability of oral drugs that are substrates of OATP.
P-Glycoprotein Substrates
Theoretically, milk thistle might increase the absorption of P-glycoprotein substrates. However, this effect does not seem to be clinically significant.
In vitro research shows that milk thistle can inhibit P-glycoprotein activity and 1 case report from the World Health Organization (WHO) adverse drug reaction database describes increased abdominal pain in a patient taking milk thistle and the cancer medication vincristine, a P-glycoprotein substrate, though this patient was also taking methotrexate. However, a small pharmacokinetic study in healthy volunteers shows that taking milk thistle (Enzymatic Therapy Inc.) 900 mg, standardized to 80% silymarin, in 3 divided doses daily for 14 days does not affect absorption of digoxin, a P-glycoprotein substrate.
Gymnema sylvestre stem extract
Antidiabetes Drugs
Theoretically, taking gymnema with antidiabetes drugs might increase the risk of hypoglycemia.
Gymnema reduces blood glucose levels in some human and animal research. In human studies, it has been shown to enhance the blood glucose lowering effects of hypoglycemic drugs. However, other research in adults with prediabetes or metabolic syndrome suggests that gymnema does not reduce fasting levels of blood glucose. Until more is known, monitor blood glucose levels closely.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, gymnema might increase levels of drugs metabolized by CYP1A2.
Animal and in vitro research shows that gymnema can inhibit the CYP1A2 enzyme. In one animal study, oral administration of gymnema for 7 days increased the plasma concentrations of phenacetin, a CYP1A2 substrate, by about 1.4-fold and reduced the clearance of phenacetin by about 29%.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, gymnema might increase or decrease levels of drugs metabolized by CYP2C9.
Animal research shows that gymnema can induce the CYP2C9 enzyme. In one animal study, gymnema caused a 2.4-fold increase in the clearance of tolbutamide, a CYP2C9 substrate, in rats. In vitro research also shows that gymnema can inhibit CYP2C9.
Phenacetin
Theoretically, taking gymnema with phenacetin might increase the levels of phenacetin.
Animal research shows that gymnema, administered orally for 7 days, decreases the clearance of phenacetin in a dose-dependent manner by about 21% to 29% and increases plasma levels about 1.3- to 1.4-fold when compared to control.
Tolbutamide (Orinase)
Theoretically, taking gymnema with tolbutamide might the decrease levels of tolbutamide.
Animal research shows that gymnema, administered orally for 7 days, increases the clearance of tolbutamide by 2.4-fold when compared to control.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, gymnema might increase levels of drugs metabolized by CYP3A4.
One in vitro study using rat liver microsomes shows that gymnema can modestly inhibit the CYP3A4 enzyme. However, other in vitro research using human liver microsomes shows that gymnema does not affect CYP3A4 activity. Animal research also shows that gymnema does not alter the function of CYP3A4. In one study in rats, oral administration of gymnema for 7 days did not alter the clearance of amlodipine, a CYP3A4 substrate.
Vitamin E
Alkylating Agents
Theoretically, antioxidant effects of vitamin E might reduce the effectiveness of alkylating agents.
There's concern that antioxidants could reduce the activity of chemotherapy drugs which generate free radicals, such as cyclophosphamide, chlorambucil, carmustine, busulfan, and thiotepa. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as vitamin E have on chemotherapy. Advise patients to consult their oncologist before using vitamin E supplements, especially in high doses.
Anticoagulant/Antiplatelet Drugs
Concomitant use of vitamin E and anticoagulant or antiplatelet agents might increase the risk of bleeding.
Vitamin E seems to inhibit of platelet aggregation and antagonize the effects of vitamin K-dependent clotting factors. These effects appear to be dose-dependent, and are probably only likely to be clinically significant with doses of at least 800 units daily. Mixed tocopherols, such as those found in food, might have a greater antiplatelet effect than alpha-tocopherol. RRR alpha-tocopherol (natural vitamin E) 1000 IU daily antagonizes vitamin K-dependent clotting factors. Advise patients to avoid high doses of vitamin E, especially in people with low vitamin K intake or other risk factors for bleeding.
Antitumor Antibiotics
Theoretically, antioxidant effects of vitamin E might reduce the effectiveness of antitumor antibiotics.
There's concern that antioxidants could reduce the activity of antitumor antibiotic drugs such as doxorubicin, which generate free radicals. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as vitamin E have on chemotherapy involving antitumor antibiotics. Advise patients to consult their oncologist before using vitamin E supplements, especially in high doses.
Cyclosporine (Neoral, Sandimmune)
A specific form of vitamin E might increase absorption and levels of cyclosporine.
There is some evidence that one specific formulation of vitamin E (D-alpha-tocopheryl-polyethylene glycol-1000 succinate, TPGS, tocophersolan, Liqui-E) might increase absorption of cyclosporine. This vitamin E formulation forms micelles which seems to increase absorption of cyclosporine by 40% to 72% in some patients. However, this interaction is unlikely to occur with the usual forms of vitamin E.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, vitamin E might induce metabolism of CYP3A4, possibly reducing the levels CYP3A4 substrates.
Vitamin E appears to bind with the nuclear receptor, pregnane X receptor (PXR), which results in increased expression of CYP3A4. Although the clinical significance of this is not known, use caution when considering concomitant use of vitamin E and other drugs affected by these enzymes.
Selumetinib (Koselugo)
Taking selumetinib with vitamin E can result in a total daily dose of vitamin E that exceeds safe limits and therefore might increase the risk of bleeding.
Selumetinib contains 48-54 IU vitamin E per capsule. The increased risk of bleeding with vitamin E appears to be dose-dependent. Be cautious when using selumetinib in combination with supplemental vitamin E, especially in patients at higher risk of bleed, such as those with chronic conditions and those taking antiplatelet drugs.
Warfarin (Coumadin)
Using vitamin E with warfarin might increase the risk of bleeding.
Due to interference with production of vitamin K-dependent clotting factors, use of more than 400 IU of vitamin E daily with warfarin might increase prothrombin time (PT), INR, and the risk of bleeding,. At a dose of 1000 IU per day, vitamin E can antagonize vitamin K-dependent clotting factors even in people not taking warfarin. Limited clinical evidence suggests that doses up to 1200 IU daily may be used safely by patients taking warfarin, but this may not be applicable in all patient populations.
Niacin
Vitamin E might decrease the beneficial effects of niacin on high-density lipoprotein (HDL) cholesterol levels.
A combination of niacin and simvastatin (Zocor) effectively raises high-density lipoprotein (HDL) cholesterol levels in people 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%. Vitamin E alone combined with a statin does not seem to decrease HDL levels. It is not known whether the adverse effect on HDL is due to one of the other antioxidants or to the combination. It also is not known whether it will occur in other patient populations.
Fenugreek (Trigonella foenum) seed extract
Anticoagulant/Antiplatelet Drugs
Theoretically, fenugreek might have additive effects when used with anticoagulant or antiplatelet drugs.
Some of the constituents in fenugreek have antiplatelet effects in animal and in vitro research. However, common fenugreek products might not contain sufficient concentrations of these constituents for clinical effects. A clinical study in patients with coronary artery disease or diabetes shows that taking fenugreek seed powder 2.5 grams twice daily for 3 months does not affect platelet aggregation, fibrinolytic activity, or fibrinogen levels .
Antidiabetes Drugs
Theoretically, fenugreek seed might have additive hypoglycemic effects when used with antidiabetes drugs.
Clinical research shows that fenugreek seed can reduce fasting blood glucose and 2-hour postprandial glucose levels in adults with type 2 diabetes.
Clopidogrel (Plavix)
Theoretically, fenugreek seed might alter the clinical effects of clopidogrel by inhibiting its conversion to the active form.
Animal research shows that fenugreek seed 200 mg/kg daily for 14 days increases the maximum serum concentration of clopidogrel by 21%. It is unclear how this affects the pharmacokinetics of the active metabolite of clopidogrel; however, this study found that concomitant use of fenugreek seed and clopidogrel prolonged bleeding time by an additional 11%.
Metoprolol (Toprol)
Theoretically, fenugreek seed might have additive hypotensive effects when used with metoprolol.
Animal research shows that fenugreek seed 300 mg/kg daily for 2 weeks decreases systolic and diastolic blood pressure by 9% and 11%, respectively, when administered alone, and by 15% and 22%, respectively, when given with metoprolol 10 mg/kg.
Phenytoin (Dilantin)
Theoretically, fenugreek might decrease plasma levels of phenytoin.
Animal research shows that taking fenugreek seeds for 1 week decreases maximum concentrations and the area under the curve of a single dose of phenytoin by 44% and 72%, respectively. This seems to be related to increased clearance. So far, this interaction has not been reported in humans.
Sildenafil (Viagra)
Theoretically, concurrent use of sildenafil and fenugreek might reduce levels and therapeutic effects of sildenafil.
Animal research shows that taking fenugreek seeds for 1 week reduces maximum concentrations and the area under the curve of a single dose of sildenafil by 27% and 48%, respectively. So far, this interaction has not been reported in humans.
Theophylline
Theoretically, fenugreek may reduce the levels and clinical effects of theophylline.
Animal research shows that fenugreek 50 grams daily for 7 days reduces the maximum serum concentration (Cmax) of theophylline by 28% and the area under the plasma drug concentration-time curve (AUC) by 22%.
Warfarin (Coumadin)
Theoretically, fenugreek might have additive effects with warfarin and increase the international normalized ratio (INR).
Some fenugreek constituents have antiplatelet effects, although these might not be present in concentrations that are clinically significant. In one case report, a patient taking warfarin experienced an increased INR when starting to take fenugreek in combination with boldo.
Antihypertensive Drugs
Fenugreek may also have an additive effect on blood pressure-lowering medications. Studies on animals have shown that fenugreek seed can decrease both systolic and diastolic blood pressure by up to 22% when combined with metoprolol. Therefore, it is essential to monitor your blood pressure regularly if you are taking fenugreek and metoprolol together or any other antihypertensive drugs.
Lagerstroemia speciosa leaf extract
Antidiabetes Drugs
Theoretically, concomitant use of banaba and hypoglycemic drugs might have additive effects.
Human and animal research suggests that banaba can lower blood glucose levels.
Antihypertensive Drugs
Theoretically, concomitant use of banaba and antihypertensive drugs might cause additive effects.
Human and animal research suggests that banaba can lower blood pressure.
Organic Anion-Transporting Polypeptide Substrates (Oatp)
Theoretically, concomitant use of banaba with substrates of OATP might reduce the bioavailability of the OATP substrate.
In vitro research shows that banaba inhibits OATP, particularly OATP2B1. OATPs are expressed in the small intestine and liver and are responsible for the absorption of drugs and other compounds.
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.
Bitter Melon (Momordica charantia) fruit extract
Antidiabetes Drugs
Taking bitter melon with antidiabetes drugs might increase the risk of hypoglycemia.
Bitter melon can lower blood glucose levels and might have additive effects when used with antidiabetes drugs. This might increase the risk of hypoglycemia in some patients. Monitor blood glucose levels closely.
P-Glycoprotein Substrates
Theoretically, bitter melon might increase levels of P-glycoprotein substrates.
Bitter melon might inhibit the p-glycoprotein (P-gp) intestinal pump and increase intracellular levels of P-gp substrates. In vitro research in intestinal cells shows that 1-monopalmitin, a constituent of bitter melon, increases levels of daunomycin, a P-gp substrate. Additionally, drinking bitter melon juice has been associated with a case of acute pancreatitis in a patient who had been taking pazopanib, a P-gp substrate, for 8 years. Researchers theorize that inhibition of P-gp led to increased levels of pazopanib, resulting in pazopanib-induced pancreatitis.
Pazopanib (Votrient)
Theoretically, bitter melon might increase levels of pazopanib, potentially increasing the risk of adverse effects.
In one case, a 65-year-old patient taking pazopanib for 8 years for renal cell carcinoma experienced signs and symptoms consistent with acute pancreatitis 4 days after drinking bitter melon juice at a dose of 100-150 mL daily. The patient's symptoms, amylase levels, and lipase levels improved upon discontinuation of bitter melon and pazopanib. Pazopanib treatment was re-initiated with no further evidence of pancreatitis. Researchers theorize that inhibition of P-glycoprotein by bitter melon led to increased levels of pazopanib, a P-glycoprotein substrate, resulting in pazopanib-induced pancreatitis.
Bilberry (Vaccinium myrtillus) fruit extract
Anticoagulant/Antiplatelet Drugs
Theoretically, bilberry fruit extract might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
In vitro, animal, and clinical research suggest that anthocyanidin extracts from bilberry can inhibit platelet aggregation.
Antidiabetes Drugs
Theoretically, bilberry leaf or fruit extract may increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research suggests that bilberry leaf extract might have blood glucose-lowering activity. Also, one small clinical trial in patients with type 2 diabetes shows that taking bilberry fruit extract 470 mg as a single dose prior to an oral glucose tolerance test lowers plasma glucose levels when compared with placebo.
Cytochrome P450 2E1 (Cyp2E1) Substrates
Theoretically, bilberry fruit extract might decrease levels of drugs metabolized by CYP2E1.
Animal research shows that exposure to small concentrations of bilberry extract in drinking water for around one month increased CYP2E1 activity by 31%. However, exposure over a 2-month period did not increase CYP2E1 activity. This effect has not been reported in humans.
Erlotinib (Tarceva)
Theoretically, bilberry fruit extract might reduce the efficacy of erlotinib.
In vitro research suggests that bilberry fruit extract and its constituents, delphinidin and delphinidin-3-O-glucoside, inhibit the activity of erlotinib. This interaction has not been reported in humans.
Alpha Lipoic Acid
Alkylating Agents
Theoretically, the antioxidant effects of alpha-lipoic acid might alter the effectiveness of alkylating agents.
The use of antioxidants like alpha-lipoic acid during chemotherapy is controversial. There are concerns that antioxidants could reduce the activity of chemotherapy drugs that generate free radicals. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as alpha-lipoic acid have on chemotherapy. Advise patients to consult their oncologist before using alpha-lipoic acid.
Anticoagulant/Antiplatelet Drugs
Theoretically, alpha-lipoic acid may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro, alpha-lipoic acid inhibits platelet aggregation.
Antitumor Antibiotics
Theoretically, the antioxidant effects of alpha-lipoic acid might alter the effectiveness of antitumor antibiotics.
The use of antioxidants like alpha-lipoic acid during chemotherapy is controversial. There are concerns that antioxidants could reduce the activity of antitumor antibiotic drugs, which work by generating free radicals. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as alpha-lipoic acid have on chemotherapy involving antitumor antibiotics. Advise patients to consult their oncologist before using alpha-lipoic acid.
Thyroid Hormone
Theoretically, alpha-lipoic acid might decrease the effects of thyroid hormone drugs.
Animal research suggests that co-administration of thyroxine with alpha-lipoic acid reduces conversion into the active T3 form.
Antidiabetes Drugs
Theoretically, taking alpha-lipoic acid with antidiabetes drugs might increase the risk of hypoglycemia.
Although some small clinical studies have suggested that alpha-lipoic acid can lower blood glucose levels, larger clinical studies in patients with diabetes have shown no clinically meaningful effect. Additionally, co-administration of single doses of alpha-lipoic acid and glyburide or acarbose did not cause detectable drug interactions in healthy volunteers.
Vanadium
Anticoagulant/Antiplatelet Drugs
Theoretically, vanadium might increase the risk of bleeding when taken with anticoagulant/antiplatelet drugs.
In vitro research shows that the sodium orthovanadate form of vanadium prolongs clotting time, likely through inhibition of thrombin and factor Xa.
Antidiabetes Drugs
Theoretically, vanadium might increase the risk of hypoglycemia when taken with antidiabetes drugs.
A few very small clinical studies in patients with type 2 diabetes show that the vanadyl sulfate form of vanadium increases insulin sensitivity and might lower blood glucose levels.
Chromium
Antidiabetes Drugs
Theoretically, chromium may have additive effects with antidiabetic agents and increase the risk of hypoglycemia.
Some research shows that taking chromium might lower blood glucose levels, especially in patients with poorly controlled type 2 diabetes.
Insulin
Theoretically, concomitant use of chromium and insulin might increase the risk of hypoglycemia.
In clinical research, chromium has been shown to increase insulin sensitivity,
Levothyroxine (Synthroid, Others)
Chromium might bind levothyroxine in the intestinal tract and decrease levothyroxine absorption.
Clinical research in healthy volunteers shows that taking chromium picolinate 1000 mcg with levothyroxine 1 mg decreases serum levels of levothyroxine by 17% when compared to taking levothyroxine alone. Advise patients to take levothyroxine at least 30 minutes before or 3-4 hours after taking chromium.
Aspirin
Theoretically, aspirin might increase chromium absorption.
Animal research suggests that aspirin may increase chromium absorption and chromium levels in the blood.
Nonsteroidal Anti-Inflammatory Drugs (Nsaids)
NSAIDs might increase chromium levels in the body.
Drugs that are prostaglandin inhibitors, such as NSAIDs, seem to increase chromium absorption and retention.
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.
Zinc
Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)
Theoretically, zinc might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide should be taken at least 2 hours before or 6 hours after zinc containing products.
Cephalexin (Keflex)
Zinc might decrease cephalexin levels by chelating with cephalexin in the gut and preventing its absorption.
A pharmacokinetic study shows that zinc sulfate 250 mg taken concomitantly with cephalexin 500 mg decreases peak levels of cephalexin by 31% and reduces the exposure to cephalexin by 27%. Also, taking zinc sulfate 3 hours before cephalexin decreases peak levels of cephalexin by 11% and reduces the exposure to cephalexin by 18%. By decreasing cephalexin levels, zinc might increase the risk of treatment failure. This effect does not occur when zinc is taken 3 hours after the cephalexin dose. To avoid an interaction, advise patients take zinc sulfate 3 hours after taking cephalexin.
Cisplatin (Platinol-Aq)
Theoretically, zinc might interfere with the therapeutic effects of cisplatin.
Animal research suggests that zinc stimulates tumor cell production of the protein metallothionein, which binds and inactivates cisplatin. It is not known whether zinc supplements or high dietary zinc intake can cause clinically significant interference with cisplatin therapy. Cisplatin might also increase zinc excretion.
Integrase Inhibitors
Theoretically, taking zinc along with integrase inhibitors might decrease the levels and clinical effects of these drugs.
Zinc is a divalent cation. Pharmacokinetic studies have shown that other divalent cations such as calcium and iron can decrease blood levels of the integrase inhibitor dolutegravir through chelation.
Penicillamine (Cuprimine, Depen)
Zinc might reduce the levels and clinical effects of penicillamine.
By forming an insoluble complex with penicillamine, zinc interferes with penicillamine absorption and activity. Zinc supplements reduce the efficacy of low-dose penicillamine (0.5-1 gram/day), but do not seem to affect higher doses (1-2.75 gram/day), provided dosing times are separated. Advise patients to take zinc and penicillamine at least 2 hours apart.
Quinolone Antibiotics
Zinc can decrease the levels and clinical effects of quinolones antibiotics.
Quinolones form complexes with zinc in the gastrointestinal tract, reducing absorption of both the quinolone and zinc if taken at the same time. Advise patients to take these drugs at least 2 hours before, or 4-6 hours after, zinc supplements.
Ritonavir (Norvir)
Zinc modestly reduces levels of ritonavir.
Clinical research shows that zinc might reduce serum ritonavir levels by chelating with ritonavir in the gut and preventing its absorption. In patients with HIV, ritonavir is taken with atazanavir to prevent the metabolism and increase the effects of atazanavir. A pharmacokinetic study shows that, in patients being treated with atazanavir/ritonavir, co-administration of zinc sulfate (Solvazinc tablets) 125 mg as a single dose or as multiple daily doses for 2 weeks reduces plasma levels of ritonavir by about 16%. However, atazanavir levels still remains high enough to prevent HIV virus replication. Therefore, the decrease in ritonavir levels is not likely to be clinically significant.
Tetracycline Antibiotics
Zinc might reduce levels of tetracycline antibiotics.
Tetracyclines form complexes with zinc in the gastrointestinal tract, which can reduce absorption of both the tetracycline and zinc when taken at the same time. Taking zinc sulfate 200 mg with tetracycline reduces absorption of the antibiotic by 30% to 40%. Demeclocycline and minocycline cause a similar interaction. However, doxycycline does not seem to interact significantly with zinc. Advise patients to take tetracyclines at least 2 hours before, or 4-6 hours after, zinc supplements to avoid any interactions.
Amiloride (Midamor)
Amiloride can modestly reduce zinc excretion and increase zinc levels.
Clinical research shows that amiloride can reduce urinary zinc excretion, especially at doses of 10 mg per day or more. This zinc-sparing effect can help to counteract zinc losses caused by thiazide diuretics, but it is unlikely to cause zinc toxicity at usual amiloride doses. The other potassium-sparing diuretics, spironolactone (Aldactone) and triamterene (Dyrenium), do not seem to have a zinc-sparing effect.
Atazanavir (Reyataz)
Zinc modestly reduces levels of atazanavir, although this effect does not seem to be clinically significant.
Clinical research shows that zinc might decrease serum atazanavir levels by chelating with atazanavir in the gut and preventing its absorption. Although a single dose of zinc sulfate (Solvazinc tablets) 125 mg orally does not affect atazanavir concentrations in patients being treated with atazanavir/ritonavir, co-administration of zinc sulfate 125 mg daily for 2 weeks reduces plasma levels of atazanavir by about 22% in these patients. However, despite this decrease, atazanavir levels still remain at high enough concentrations for the prevention of HIV virus replication.
Brand information
Manufacturer and brand details for Glucose Support, from the product label.
CHK Nutrition
See all CHK Nutrition products- Name
- CHK Nutrition
- Street Address
- 3930 E Calvary Rd
- City
- Duluth
- State
- MN
- ZipCode
- 55803
- Phone Number
- 877-538-8388
Glucose Support by CHK Nutrition: Common Questions
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Written and reviewed by the HelloPharmacist editorial staff. Our editorial policy
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Label information is sourced from the NIH Dietary Supplement Label Database and reflects the product version on file; always read your actual product label. This page is for education only and is not a substitute for professional medical advice. Confirm with your pharmacist or doctor before combining supplements and medications.
The Full Monographs Behind Glucose Support’s Ingredients
Every ingredient we hold a full HelloPharmacist monograph for — uses, evidence, safety, and the complete interaction list.
Alpha-lipoic Acid
Interacts with 263 drugsAlpha-lipoic acid (ALA) is an antioxidant made naturally by the body and found in small amounts in foods. It is most studied for diabetic nerve pain, where some evidence suggests it may help...
Read the full Alpha-lipoic Acid monograph → Herb & supplement monographVitamin E
Interacts with 764 drugsVitamin E is an essential fat-soluble vitamin and antioxidant that most people get in adequate amounts from a normal diet. Supplements can help correct a true deficiency, but high-dose vitam...
Read the full Vitamin E 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 monographVanadium
Interacts with 208 drugsVanadium is a trace mineral found in tiny amounts in food, and people get plenty from a normal diet. Supplement claims for diabetes, weight, and athletic performance are not well proven, and...
Read the full Vanadium 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 monographZinc
Interacts with 67 drugsZinc is an essential mineral that your body needs for immune function, wound healing, taste, and smell. Most people get enough from food, but supplements can help correct or prevent a defici...
Read the full Zinc monograph → Herb & supplement monographChromium
Interacts with 178 drugsChromium is an essential trace mineral involved in how the body handles sugar and fat. Some studies suggest it may modestly help blood sugar control in certain people with type 2 diabetes, b...
Read the full Chromium monograph → Herb & supplement monographGymnema
Interacts with 851 drugsGymnema is an Ayurvedic herb best known for possibly helping lower blood sugar and reducing the taste of sweetness on the tongue. Some early human studies are encouraging for blood sugar sup...
Read the full Gymnema monograph → Herb & supplement monographGinkgo
Interacts with 1,266 drugsGinkgo is one of the world's most popular herbal supplements, mostly taken to support memory and circulation. The evidence for these uses is mixed and generally weak, and it is not proven to...
Read the full Ginkgo monograph → Herb & supplement monographBitter Melon
Interacts with 282 drugsBitter melon is a tropical fruit eaten as food and used in traditional medicine, most often for blood sugar control. While some small studies hint it may modestly lower blood sugar, the evid...
Read the full Bitter Melon monograph → Herb & supplement monographFenugreek
Interacts with 389 drugsFenugreek is a common kitchen spice that is also taken as a supplement, mainly for blood sugar, cholesterol, and to support breast milk production. Some early research is encouraging for blo...
Read the full Fenugreek monograph → Herb & supplement monographMilk Thistle
Interacts with 954 drugsMilk thistle is a popular herbal supplement most often used for liver health, and its main active component is a group of compounds called silymarin. While it is generally well tolerated, th...
Read the full Milk Thistle monograph → Herb & supplement monographBilberry
Interacts with 275 drugsBilberry is a blueberry-like fruit rich in antioxidant plant compounds called anthocyanins, and it has a long history of traditional use for eye health, circulation, and mild diarrhea. While...
Read the full Bilberry monograph → Herb & supplement monographBanaba
Interacts with 299 drugsBanaba is a leaf extract most often used to help support healthy blood sugar, and small early studies suggest its active compound corosolic acid may modestly lower glucose. The overall evide...
Read the full Banaba monograph →Sources & How We Checked
Glucose Support'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 644 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.
Alpha-lipoic Acid 48 references
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- Konrad T, Vicini P, Kusterer K, et al. Alpha-lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with Type 2 diabetes. Diabetes Care 1999;22:280-7. PubMed
- Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic peripheral neuropathy with the antioxidant alpha-lipoic acid: A 3-week, multicentre randomized controlled trial (ALADIN Study). Diabetologia 1995;38:1425-33.
- Gleiter CH, Schreeb KH, Freudenthaler S, et al. Lack of interaction between thioctic acid, glibenclamide and acarbose. Br J Clin Pharmacol 1999;48:819-25. PubMed
- Jacob S, Henriksen EJ, Tritschler HJ, et al. Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid. Exp Clin Endocrinol Diabet 1996;104:284-8. PubMed
- Jacob S, Henriksen EJ, Schiemann AL, et al. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung 1995;45:872-4.
- Jacob S, Ruus P, Hermann R, et al. Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled, pilot trial. Free Rad Biol Med 1999;27:309-14.
- Segermann J, Hotze A, Ulrich H, Rao GS. Effect of alpha-lipoic acid on the peripheral conversion of thyroxine to triiodothyronine and on serum lipid-, protein- and glucose levels. Arzneimittelforschung 1991;41:1294-8.
- Beitner H. Randomized, placebo controlled, double-blind study on the clinical efficacy of a cream containing 5% alpha-lipoic acid related to photoaging of facial skin. Br J Dermatol 2003;149:841-9.
- Ziegler D, Nowak H, Kempler P, et al. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: A meta-analysis. Diabet Med 2004;21:114-21.
- 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
- Conklin KA. Cancer chemotherapy and antioxidants. J Nutr 2004;134:3201S-3204S. PubMed
- Vincent HK, Bourguignon CM, Vincent KR, Taylor AG. Effects of alpha-lipoic acid supplementation in peripheral arterial disease: a pilot study. J Alt Complement Med 2007;13:577-84. PubMed
- Furukawa N, Miyamura N, Nishida K, et al. Possible relevance of alpha lipoic acid contained in a health supplement in a case of insulin autoimmune syndrome. Diabetes Res Clin Pract 2007;75:366-7. PubMed
- Ziegler D., Ametov A., Barinov A., Dyck P. J., Gurieva I., Low P. A., Munzel U., Yakhno N., Raz I., Novosadova M., Maus J., Samigullin, R. Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: the SYDNEY 2 trial. Diabetes Car
- Gu X. M., Zhang S. S., Wu J. C., Tang Z. Y., Lu Z. Q., Li H., Liu C., Chen L., Ning, G. [Efficacy and safety of high-dose a-lipoic acid in the treatment of diabetic polyneuropathy]. Zhonghua Yi Xue Za Zhi 2010;90(35):2473-2476.
- Porasuphatana S., Suddee S., Nartnampong A., Konsil J., Harnwong B., Santaweesuk A. Glycemic and oxidative status of patients with type 2 diabetes mellitus following oral administration of alpha-lipoic acid: a randomized double-blinded placebo-controlled
- Ansar H., Mazloom Z., Kazemi F., Hejazi N. Effect of alpha-lipoic acid on blood glucose, insulin resistance and glutathione peroxidase of type 2 diabetic patients. Saudi Med J 2011;32(6):584-588. DOI
- de Oliveira A. M., Rondó P. H., Luzia L. A., D'Abronzo F. H., Illison V. K. The effects of lipoic acid and a-tocopherol supplementation on the lipid profile and insulin sensitivity of patients with type 2 diabetes mellitus: a randomized, double-blind, pla
- Mazloom Z., Ansar H. The Effect of Alpha-Lipoic Acid on Blood Pressure in Type 2 Diabetics. Iranian Journal of Endocrinology and Metabolism 2009;11(3):245-250.
- Volchegorskii I. A., Rassokhina L. M., Koliadich M. I., Alekseev M. I. [Comparative study of alpha-lipoic acid and mexidol effects on affective status, cognitive functions and quality of life in diabetes mellitus patients]. Eksp Klin Farmakol 2011;74(11):
- Cavalcanti D. R., da Silveira F. R. Alpha lipoic acid in burning mouth syndrome--a randomized double-blind placebo-controlled trial. J Oral Pathol Med 2009;38(3):254-261. PubMed
- Koh E. H., Lee W. J., Lee S. A., Kim E. H., Cho E. H., Jeong E., Kim D. W., Kim M. S., Park J. Y., Park K. G., Lee H. J., Lee I. K., Lim S., Jang H. C., Lee K. H., Lee K. U. Effects of alpha-lipoic Acid on body weight in obese subjects. Am J Med 2011;124( PubMed
- Bergqvist-Karlsson, A., Thelin, I., and Bergendorff, O. Contact dermatitis to alpha-lipoic acid in an anti-wrinkle cream. Contact Dermatitis 2006;55(1):56-57.
- Tang, J., Wingerchuk, D. M., Crum, B. A., Rubin, D. I., and Demaerschalk, B. M. Alpha-lipoic acid may improve symptomatic diabetic polyneuropathy. Neurologist. 2007;13(3):164-167. PubMed
- Hegazy SK, Tolba OA, Mostafa TM, Eid MA, El-Afify DR. Alpha-lipoic acid improves subclinical left ventricular dysfunction in asymptomatic patients with type 1 diabetes. Rev Diabet Stud 2013;10(1):58-67. PubMed
- Huang Z, Wan X, Liu J, et al. Short-term continuous subcutaneous insulin infusion combined with insulin sensitizers rosiglitazone, metformin, or antioxidant a-lipoic acid in patients with newly diagnosed type 2 diabetes mellitus. Diabetes Technol Ther 201
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