EstroPause Ingredients & Drug Interactions
What is this page for?
First and foremost: checking EstroPause 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
EstroPause is a dietary supplement by Irwin Naturals with 14 active ingredients. Its ingredients are commonly taken for iron-deficiency anemia, low iron stores during pregnancy, fatigue from iron deficiency.Based on those ingredients, 1,679 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are St. John's Wort Extract, Asian Ginseng root extract, BioPerine. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.
Check Your Meds Against EstroPause by Irwin Naturals
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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 EstroPause by Irwin Naturals
Our pharmacy team’s full take, with four database checks built into the cards below — a summary of what is known, not a grade of the product itself.
What’s inside
Partial disclosure
EstroPause contains 13 ingredients, of which the active ones include iron, magnesium, calcium, sodium, ginger rhizome extract, black pepper (BioPerine), and red clover powder. Several of these supply minerals and nutrients; ginger and red clover are herbal extracts commonly used in women's health formulas.
The product also includes omega-3 fatty acids, Asian ginseng, chasteberry fruit extract, and isoflavones from soy and red clover. Inactive ingredients such as gelatin, glycerin, soy lecithin, and titanium dioxide serve as capsule materials and binders.
Does it work?
Not established
In the data we hold, effectiveness ratings exist only for iron, magnesium, ginger, black pepper, and calcium — not for the other active herbs in this blend. Iron is effective for iron-deficiency anemia and anemia of chronic disease, and possibly effective for heart failure.
Magnesium is effective for constipation and dyspepsia, and was studied for pre-eclampsia. Ginger is rated possibly effective for pregnancy-induced nausea and vomiting, dysmenorrhea, and osteoarthritis, though possibly ineffective for exercise-related muscle soreness.
Calcium is likely effective for osteoporosis and effective for several other conditions. Black pepper and red clover lack sufficient evidence to rate their effectiveness for the conditions we hold data on.
For chasteberry, Asian ginseng, soy isoflavones, and other herbal ingredients in this formula, we have no effectiveness ratings.
How safe is it?
Well-documented data
Iron is generally well tolerated at recommended doses, but excess iron can be toxic — use it only when there is a real need. Common side effects include abdominal pain, constipation, diarrhea, nausea, and vomiting.
Iron is often recommended in pregnancy under your prenatal care provider's guidance, and is considered acceptable while breastfeeding at appropriate doses. Magnesium is generally safe at recommended amounts and causes mostly gastrointestinal side effects like diarrhea and nausea.
Ginger is generally well tolerated; most common side effects are abdominal discomfort, heartburn, diarrhea, and a peppery aftertaste. Higher doses above 5 grams daily increase the risk of side effects.
Black pepper seems well tolerated as a food spice or single-dose supplement; concentrated supplements should be used cautiously. Calcium is well tolerated at recommended amounts and causes mainly constipation or stomach upset.
Red clover is generally well tolerated short-term; common side effects include muscle aches, nausea, and vaginal spotting. Sodium at high levels is linked to high blood pressure and heart strain — use normal dietary amounts only.
Pregnancy and lactation safety varies by ingredient: iron is likely safe in pregnancy with guidance, magnesium is likely safe, and calcium is likely safe; red clover should be avoided in pregnancy due to estrogenic effects. For ginger, black pepper, and sodium in pregnancy, safety data is limited — check with your doctor.
Meds to double-check
Major interaction found
Before taking EstroPause, check with your pharmacist if you take levodopa/carbidopa (Parkinson's disease), dolutegravir or elvitegravir (HIV), levothyroxine (thyroid), blood thinners or antiplatelet drugs, bisphosphonates (osteoporosis), quinolone or tetracycline antibiotics, blood pressure medications, antidiabetes drugs, methotrexate, or tamoxifen. The mineral content — iron, magnesium, and calcium — can reduce how much of these drugs your body absorbs, and spacing doses by 2 to 6 hours may be needed.
The bottom line
Scorecard at a glancePartially disclosed formula with no established evidence rating for its marketed use. Major medication interactions have been identified, and safety information is well characterized.
This is a multi-ingredient women's health formula that works best if you don't take medications for Parkinson's disease, blood thinning, thyroid hormone, osteoporosis, or HIV — all of which have documented interactions here. Even if you don't take those drugs, iron, magnesium, and calcium can interfere with absorption of many other medications, so spacing doses carefully is important.
Talk with your pharmacist or doctor before starting, especially if you take any prescription medication.
Educational only — not medical advice; always confirm with your pharmacist. Our editorial policy · How we use AI
Assessment coverage: 10 of 13 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Jun 22, 2023.
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 EstroPause, straight from the product label.
| Brand | Irwin Naturals |
|---|---|
| Barcode (UPC) | 710363262440 |
| Net contents | 80 Liquid Softgel(s) |
| Market status | On market |
| Date entered into DSLD | Jun 22, 2023 |
| DSLD ID | 292070 |
| Product type | Other Combinations |
| Supplement form | Softgel Capsule |
| Dietary claims / uses | Nutrient, All Other, Structure/Function |
| Intended target group(s) | Women (not pregnant or lactating), Menopause, Seniors/Mature (>50 Years) - Women ONLY |
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 EstroPause by Irwin Naturals, sourced from the NIH Dietary Supplement Label Database.
Supplement Facts
| Ingredient | Amount | % DV |
|---|---|---|
| Protein | 2 Gram(s) | -- |
| Cholesterol | 10 mg | 3% |
| Iron | 0.6 mg | 3% |
| Total Fat | 2 Gram(s) | 3% |
| Saturated Fat | 0.5 Gram(s) | 3% |
| Omega-3 Fatty Acids | 647 mg | -- |
| Calories | 35 Calorie(s) | -- |
| BioPerine Complex | 6 mg | -- |
| Total Carbohydrates | 2 Gram(s) | 1% |
| Fish Oil | 2158 mg | -- |
| Ginger Rhizome Extract | 0 NP | -- |
| BioPerine | 0 NP | -- |
| Sodium | 15 mg | 1% |
| Black Cohosh root extract | 80 mg | -- |
| Soy Isoflavones | 100 mg | -- |
| Asian Ginseng root extract | 31 mg | -- |
| Magnesium | 200 mg | 48% |
| Total Isoflavones | 5 mg | -- |
| Calcium | 500 mg | 38% |
| Chasteberry Fruit Extract | 20 mg | -- |
| St. John's Wort Extract | 300 mg | -- |
| Hypericin | 0.9 mg | -- |
| Triterpenoid Saponins | 2 mg | -- |
| Red Clover, Powder | 40 mg | -- |
Other ingredients: Gelatin, Water, Purified, Glycerin, Soy Lecithin, Titanium Dioxide, Beeswax, Lycopene, Maltodextrin
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.
Formula
EstroPause Menopause support is formulated specifically for aging women.
Minerals: Calcium and magnesium are two of the most important minerals for pre-menopausal woman and support the structure and function of bones, muscles and nerves. Botanicals: This multi-approach formula contains women's health herbs, including black cohosh, chasteberry (vitex) and red clover. Ginseng has been traditionally used as a revitalizing tonic
Calcium Magnesium Black cohosh
Promotes female health throughout all stages of menopause
Formulation
Female support: Menopause is a natural stage of life that all women must go through. To make the transition smoother and easier, many women require additional support.
EstroPause Menopause support delivers powerful ingredients to promote female health throughout all stages of menopause.
What makes us different: Liquid soft-gels - The nutrients in these easy-to-swallow Liquid Soft-Gels are released fast. Other forms of delivery can contain binders and fillers that may cause stomach upset and offer no nutritional value. Advanced Liquid Soft-Gels provide an optimum delivery system.
Quality assurance - Irwin Naturals is committed to providing the highest quality products for your health. We employ compliance testing to ensure purity and potency.
Patented BioPerine - Our special BioPerine Complex enhances the bioavailability absorption and potency of many nutrients.
Menopause Support
No preservatives added.
Seals/Symbols
Quality Tested Guaranteed Pass
FDA Disclaimer Statement
These statements have not been evaluated by the Food & Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
General Statements
Global responsibility - Over the years we have donated to organizations that support the environment and the health of our children.
Questions: Contact consumer affairs 1-800-297-3273 - Weekdays 8:00 AM to 5:00 PM (PST) [email protected] 100+ highly specialized products: www.IrwinNaturals.com
Full disclosure ingredient panel
Precautions
Usage warnings: Do not use if safety seal is broken.
St. Johns Wort can interact with medications, such as antidepressants, heart medications, blood thinners, immunosuppressants, and other medications.
Avoid excessive sun exposure as use of this product may cause your skin to be extra sensitive to UV sources. This product contains an ingredient that may affect blood sugar.
Check with your doctor before using this product if you are using medication or have any medical conditions, including heart disease and/or high/low blood pressure. Do not use if you may become pregnant, are pregnant, nursing, or taking contraceptives.
Do not exceed 90 days of continuous use of this product without a two (2) week break. Do not exceed recommended daily intake.
Not intended for use by persons under 18. Keep out of reach of children.
Contains: Fish (anchovy, sardine), soy
Storage
Store in a cool, dry place.
FDA Statement of Identity
Dietary Supplement
Suggested/Recommended/Usage/Directions
Directions: (Adult) take two (2) to four (4) liquid soft-gels a day with meals and a full glass (8oz) of water. May be taken all at once or divided throughout the day.
Brand IP Statement(s)
BioPerine is a registered trademark of Sabinsa Corporation.
Is this label outdated? Report a formula or label change and our pharmacy team will review it.
EstroPause by Irwin Naturals 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 EstroPause by Irwin Naturals
These are the 14 active ingredients this product is made of. Select any to open its full monograph.
Serving size2 Liquid Softgel(s) Dosage formSoftgel Capsule 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.
Protein
Iron
Interacts with80 drugs
Iron is an essential mineral your body needs to make hemoglobin and carry oxygen in the blood. Supplements are mainly useful for treating or preventin...
Iron monograph & interactionsBioPerine Complex
Fish Oil
Interacts with327 drugs
Fish oil provides omega-3 fatty acids (EPA and DHA) that are best known for lowering high triglyceride levels. The evidence for other heart and health...
Fish Oil monograph & interactionsSodium
Interacts with205 drugs
Sodium is an essential mineral and electrolyte your body needs to balance fluids, support nerves, and help muscles work. Most people in modern diets g...
Sodium monograph & interactionsBlack Cohosh root extract
Interacts with652 drugs
Black cohosh is a North American plant most often used to ease menopause symptoms like hot flashes, but the research is mixed and far from settled. It...
Black Cohosh root extract monograph & interactions- › Triterpenoid Saponins
Soy Isoflavones
- › Total Isoflavones
Asian Ginseng root extract
Interacts with1,130 drugs
Panax ginseng is a popular traditional herb used to boost energy, ease stress, and support overall wellness, though scientific evidence is mixed and m...
Asian Ginseng root extract 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 & interactionsCalcium
Interacts with168 drugs
Calcium is an essential mineral your body needs for strong bones, nerve signaling, and muscle function, and supplements can help fill gaps when diet f...
Calcium monograph & interactionsChasteberry Fruit Extract
Interacts with121 drugs
Vitex (chasteberry) is an herbal remedy most often used for PMS and menstrual cycle problems, and the strongest evidence is for easing some PMS sympto...
Chasteberry Fruit Extract monograph & interactionsSt. John's Wort Extract
Interacts with1,143 drugs
St. John's wort is a well-studied herb most often used for mild to moderate depression, and some research suggests it may help with this. However, it...
St. John's Wort Extract monograph & interactions- › Hypericin
Red Clover, Powder
Interacts with867 drugs
Red clover is a plant rich in isoflavones (plant compounds with weak estrogen-like activity) that is most often used for menopause symptoms like hot f...
Red Clover, Powder monograph & interactionsOther (inactive) ingredients: Gelatin, Water, Purified, Glycerin, Soy Lecithin, Titanium Dioxide, Beeswax, Lycopene, Maltodextrin. These complete the product’s ingredient list but are not active constituents.
EstroPause by Irwin Naturals Drug Interactions
HelloPharmacist Interaction Report
EstroPause by Irwin Naturals contains several ingredients with documented interactions.
The most serious interaction involves magnesium, which can reduce levodopa/carbidopa levels by up to 35% for levodopa and 81% for carbidopa — a Major-severity effect. If you take levodopa/carbidopa for Parkinson's disease, separate this supplement from that medication by at least 2 hours.
Read the full breakdown — every affected drug type, severity by severity
Iron in this product interacts with multiple drug types at Moderate severity: levodopa, quinolone antibiotics (like ciprofloxacin), bisphosphonates (osteoporosis drugs), methyldopa (blood pressure medication), tetracycline antibiotics, levothyroxine (thyroid hormone), mycophenolate mofetil (immunosuppressant), and penicillamine (Wilson's disease treatment). Ginger and black pepper (BioPerine) also carry Moderate interactions with anticoagulant or antiplatelet drugs, antidiabetes drugs, warfarin, several others, and various heart and seizure medications.
Calcium interacts with two HIV integrase inhibitors (dolutegravir and elvitegravir) at Major severity, plus moderate interactions with levothyroxine, sotalol, and other drugs. Sodium may interfere with blood pressure control and lithium levels.
Red clover has Moderate interactions with estrogens, methotrexate, and tamoxifen.
Although we could not check omega-3 fatty acids, Asian ginseng, chasteberry, total isoflavones, or hypericin for interactions, they are blended into this product.
Altoget her, these interactions span 1,304 individual medications. Please use the interaction checker below to verify your exact medications before taking this product.
Check your own medications below · Editorial policy · How we use AI
Want to check YOUR meds against EstroPause?
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 EstroPause interact with 1,679 drugs. Click any drug to see the details.
12 of the 14 ingredients in EstroPause interact with drugs. Each result below shows which ingredient is responsible. St. John's Wort Extract Asian Ginseng root extract BioPerine Ginger Rhizome Extract Red Clover, Powder Black Cohosh root extract Fish Oil Magnesium Sodium Calcium Chasteberry Fruit Extract Iron
BrincidofovirTembexa
How Brincidofovir interacts with EstroPause — through 1 ingredient. Tap an ingredient for the detail:
Black Cohosh Root ExtractOrganic Anion-transporting Polypeptide Substrates (oatp) Minor
Interaction Summary
Black cohosh may inhibit one form of OATP, OATP2B1, which could reduce the bioavailability and clinical effects of OATP2B1 substrates.
Read the full Black Cohosh Root Extract + Brincidofovir interactionCarboplatinParaplatin
How Carboplatin interacts with EstroPause — through 1 ingredient. Tap an ingredient for the detail:
Fish OilPlatinum Agents Minor
Interaction Summary
Theoretically, taking fish oil with platinum agents can cause resistance to platinum agents, potentially decreasing their effectiveness.
Read the full Fish Oil + Carboplatin interactionChloramphenicolChloromycetin, Chloromycetin Injection, Chloromycetin Ophthalmic
How Chloramphenicol interacts with EstroPause — through 1 ingredient. Tap an ingredient for the detail:
IronChloramphenicol Minor
Interaction Summary
Theoretically, taking chloramphenicol with iron might reduce the response to iron therapy in iron deficiency anemia.
Read the full Iron + Chloramphenicol interactionCiprofloxacin, HydrocortisoneCipro HC Otic
How Ciprofloxacin, Hydrocortisone interacts with EstroPause — through 1 ingredient. Tap an ingredient for the detail:
Black Cohosh Root ExtractOrganic Anion-transporting Polypeptide Substrates (oatp) Minor
Interaction Summary
Black cohosh may inhibit one form of OATP, OATP2B1, which could reduce the bioavailability and clinical effects of OATP2B1 substrates.
Read the full Black Cohosh Root Extract + Ciprofloxacin, Hydrocortisone interactionGabapentinGralise, Neurontin
How Gabapentin interacts with EstroPause — through 1 ingredient. Tap an ingredient for the detail:
MagnesiumGabapentin (neurontin) Minor
Interaction Summary
Gabapentin absorption can be decreased by magnesium.
Read the full Magnesium + Gabapentin interactionOxaliplatinEloxatin
How Oxaliplatin interacts with EstroPause — through 1 ingredient. Tap an ingredient for the detail:
Fish OilPlatinum Agents Minor
Interaction Summary
Theoretically, taking fish oil with platinum agents can cause resistance to platinum agents, potentially decreasing their effectiveness.
Read the full Fish Oil + Oxaliplatin interactionSevelamerRenagel
How Sevelamer interacts with EstroPause — 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 interactionEach ingredient & the kinds of drugs it affects
For each ingredient in EstroPause 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.
St. John's Wort Extract
Alprazolam (Xanax)
St. John's wort increases the clearance of alprazolam and decreases its effects.
Alprazolam, which is used as a probe for cytochrome P450 3A4 (CYP3A4) activity, has a two-fold increase in clearance when given with St. John's wort. St. John's wort reduces the half-life of alprazolam from 12.4 hours to 6 hours.
Contraceptive Drugs
St. John's wort increases the clearance of contraceptive drugs and reduces their clinical effects.
Females taking St. John's wort and oral contraceptives concurrently should use an additional or alternative form of birth control. St. John's wort can decrease norethindrone and ethinyl estradiol levels by 13% to 15%, resulting in breakthrough bleeding, irregular menstrual bleeding, or unplanned pregnancy. Bleeding irregularities usually occur within a week of starting St. John's wort and regular cycles usually return when St. John's wort is discontinued. Unplanned pregnancy has occurred with concurrent use of oral contraceptives and St. John's wort extract. St. John's wort is thought to induce the cytochrome P450 1A2 (CYP1A2), 2C9 (CYP2C9), and 3A4 (CYP3A4) enzymes, which are responsible for metabolism of progestins and estrogens in contraceptives.
Cyclosporine (Neoral, Sandimmune)
St. John's wort reduces the levels and clinical effects of cyclosporine.
Concomitant use can decrease plasma cyclosporine levels by 30% to 70%. Using St. John's wort with cyclosporine in patients with heart, kidney, or liver transplants can cause subtherapeutic cyclosporine levels and acute transplant rejection. This interaction has occurred with a St. John's wort extract standardized to 0.3% hypericin and dosed at 300-600 mg per day. Withdrawal of St. John's wort can result in a 64% increase in cyclosporine levels. St. John's wort induces cytochrome P450 3A4 (CYP3A4) and the multi-drug transporter, P-glycoprotein/MDR-1, which increases cyclosporine clearance.
Cytochrome P450 3A4 (Cyp3A4) Substrates
St. John's wort increases the metabolism and reduces the levels of CYP3A4 substrates.
St. John's wort induces CYP3A4 enzymes and increases metabolism of CYP3A4 substrates. Clinically significant interactions have been reported with St. John's wort products containing hyperforin 1 mg or more.
Digoxin (Lanoxin)
St. John's wort reduces the levels and clinical effects of digoxin.
St. John's wort can reduce the bioavailability, serum levels, and therapeutic effects of digoxin. Taking an extract of St. John's wort 900 mg, containing hyperforin 7.5 mg or more, daily for 10-14 days, can reduce serum digoxin levels by 25% in healthy people. St. John's wort is thought to affect the multidrug transporter, P-glycoprotein, which mediates the absorption and elimination of digoxin and other drugs. St. John's wort products providing less than 7.5 mg of hyperforin daily do not appear to affect digoxin levels.
Docetaxel (Taxotere)
St. John's wort reduces the levels and clinical effects of docetaxel.
Clinical research shows that taking a specific St. John's wort product (Hyperiplant, VSM) 300 mg three times daily for 14 days increases docetaxel clearance by about 14%, resulting in decreased plasma concentrations of docetaxel in cancer patients. This is most likely due to induction of cytochrome P450 3A4 (CYP3A4) by St. John's wort.
Imatinib (Gleevec)
St. John's wort reduces the levels and clinical effects of imatinib.
Taking St. John's wort 900 mg daily for 2 weeks reduces the bioavailability and half-life of a single dose of imatinib and decreases its serum levels by 30% in healthy volunteers. This is most likely due to induction of cytochrome P450 3A4 (CYP3A4) by St. John's wort, which increases clearance of imatinib.
Irinotecan (Camptosar)
St. John's wort reduces the levels and clinical effects of irinotecan.
St. John's wort 900 mg daily for 18 days decreases serum levels of irinotecan by at least 50%. Clearance of the active metabolite of irinotecan, SN-38, is also increased, resulting in a 42% decrease in the area under the concentration-time curve. This is thought to be due to induction of cytochrome P450 3A4 (CYP3A4) by St. John's wort.
Mephenytoin (Mesantoin)
St. John's wort reduces the levels and clinical effects of mephenytoin.
Preliminary clinical research in healthy males shows that taking St. John's wort for 14 days induces cytochrome P450 2C19 (CYP2C19) and significantly increases metabolism of mephenytoin (Mesantoin). In people with wild-type 2C19, metabolism was almost 4-fold greater in subjects who received St. John's wort compared to placebo. In contrast, patients with 2C19*2/*2 and *2/*3 genotypes did not demonstrate a similar increase in metabolism.
Non-Nucleoside Reverse Transcriptase Inhibitors (Nnrtis)
St. John's wort decreases the levels and clinical effects of NNRTIs.
St. John's wort increases the oral clearance of nevirapine (Viramune) by 35%. Subtherapeutic concentrations are associated with therapeutic failure, development of viral resistance, and development of drug class resistance. St. John's wort induces intestinal and hepatic cytochrome P450 3A4 (CYP3A4) and intestinal P-glycoprotein/MDR-1, a drug transporter.
Omeprazole (Prilosec)
St. John's wort decreases the levels and clinical effects of omeprazole.
Taking St. John's wort, 300 mg orally three times daily for 14 days, reduces serum concentrations of omeprazole by inducing its metabolism via cytochrome P450 (CYP) 2C19 and 3A4. The reduction of omeprazole serum levels is dependent on CYP2C19 genotype, with reductions up to 50% in extensive metabolizers and 38% in poor metabolizers.
Oxycodone (Oxycontin)
St. John's wort decreases the levels and clinical effects of oxycodone.
St. John's wort can increase oxycodone metabolism by inducing cytochrome P450 3A4 (CYP3A4), reducing plasma levels and analgesic activity.
P-Glycoprotein Substrates
St. John's wort decreases the levels and clinical effects of P-glycoprotein substrates.
St. John's wort induces P-glycoprotein. P-glycoprotein is a carrier mechanism responsible for transporting drugs and other substances across cell membranes. When P-glycoprotein is induced in the gastrointestinal (GI) tract, it can prevent the absorption of some medications. In addition, induction of p-glycoprotein can decrease entry of drugs into the central nervous system (CNS) and decrease access to other sites of action.
Phenobarbital (Luminal)
St. John's wort decreases the levels and clinical effects of phenobarbital.
St. John's wort may increase the metabolism of phenobarbital. Plasma concentrations of phenobarbital should be monitored carefully. The dose of phenobarbital may need to be increased when St. John's wort is started and decreased when it is stopped.
Phenprocoumon (Marcoumar, Others)
St. John's wort decreases the levels and clinical effects of phenprocoumon.
St. John's wort appears to increase the metabolism of phenprocoumon (an anticoagulant that is not available in the US) by increasing the activity of the cytochrome P450 2C9 (CYP2C9) enzyme. This may result in decreases in the anticoagulant effect and international normalized ratio (INR).
Phenytoin (Dilantin)
St. John's wort decreases the levels and clinical effects of phenytoin.
St. John's wort may increase the metabolism of phenytoin. Plasma concentrations of phenytoin should be monitored closely. The dose of phenytoin may need to be increased when St. John's wort is started and decreased when it is stopped.
Protease Inhibitors (Pis)
St. John's wort reduces the levels and clinical effects of PIs.
In healthy volunteers, St. John's wort can reduce the plasma concentrations of indinavir (Crixivan) by inducing cytochrome P450 3A4 (CYP3A4). This might result in treatment failure and viral resistance. St. John's wort also induces P-glycoprotein, which can result in decreased intracellular protease inhibitor concentrations and increased elimination.
Rivaroxaban (Xarelto)
St. John's wort decreases the levels and clinical effects of rivaroxaban.
A small pharmacokinetic study in healthy volunteers shows that taking a single dose of rivaroxaban 20 mg after using a specific St. John's wort extract (Jarsin, Vifor SA) 450 mg orally twice daily for 14 days reduces the bioavailability of rivaroxaban by 24% and reduces rivaroxaban's therapeutic inhibition of factor Xa by 20%.
Tacrolimus (Prograf)
St. John's wort decreases the levels and clinical effects of tacrolimus.
Taking a St. John's wort extract (Jarsin) 600 mg daily significantly decreases tacrolimus serum levels. Dose increases of 60% may be required to maintain therapeutic tacrolimus levels in patients taking St. John's wort. St. John's wort is thought to lower tacrolimus levels by inducing cytochrome P450 3A4 (CYP3A4) enzymes. A small clinical study in healthy adults also shows that taking St. John's wort 300 mg three times daily for 10 days decreases the total systemic exposure to tacrolimus by 27% and 33% after taking a single 5 mg dose of immediate-release or prolonged-release tacrolimus, respectively.
Warfarin (Coumadin)
St. John's wort decreases the levels and clinical effects of warfarin.
Taking St. John's wort significantly increases clearance of warfarin, including both its R- and S-isomers. This is likely due to induction of cytochrome P450 (CYP) 1A2 and CYP3A4. St. John's wort can also significantly decrease International Normalized Ratio (INR) in people taking warfarin. In addition, taking warfarin at the same time as St. John's wort might reduce warfarin bioavailability. When a dried extract is mixed with warfarin in an aqueous medium, up to 30% of warfarin is bound to particles, reducing its absorption.
Aminolevulinic Acid
St. John's wort might have additive phototoxic effects with aminolevulinic acid.
Concomitant use with St. John's wort extract may cause synergistic phototoxicity. Delta-aminolevulinic acid can cause a burning erythematous rash and severe swelling of the face, neck, and hands when taken with St. John's wort.
Bupropion (Wellbutrin)
St. John's wort might reduce the levels and effects of bupropion.
Clinical research shows that taking St. John's wort 325 mg three times daily for 14 days along with bupropion reduces the area under the concentration-time curve by approximately 14% and increases the clearance of bupropion by approximately 20%. This effect is attributed to the induction of cytochrome P450 2B6 (CYP2B6) by St. John's wort.
Clopidogrel (Plavix)
St. John's wort might increase the levels and effects of clopidogrel.
Taking St. John's wort with clopidogrel seems to increase the activity of clopidogrel. In clopidogrel non-responders, taking St. John's wort seems to induce metabolism of clopidogrel to its active metabolite by cytochrome P450 enzymes 3A4 and 2C19. This leads to increased antiplatelet activity. Theoretically, this might lead to an increased risk of bleeding in clopidogrel responders.
Clozapine (Clozaril)
St. John's wort might decrease the levels and clinical effects of clozapine.
A case report describes a female with schizophrenia controlled on clozapine who had a return of symptoms when she started taking St. John's wort. The plasma concentration of clozapine was reduced, likely because its clearance was increased due to induction of the cytochrome P450 enzymes 3A4, 1A2, 2C9, and 2C19 by St. John's wort.
Cytochrome P450 1A2 (Cyp1A2) Substrates
St. John's wort may increase the metabolism and reduce the levels of CYP1A2 substrates.
Clinical and in vitro research shows that St. John's wort induces CYP1A2, but to a lesser extent than CYP3A4.
Asian Ginseng root extract
Anticoagulant/Antiplatelet Drugs
Although Panax ginseng has shown antiplatelet effects in the laboratory, it is unlikely to increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro evidence suggests that ginsenoside constituents in Panax ginseng might decrease platelet aggregation. However, research in humans suggests that ginseng does not affect platelet aggregation. Animal research indicates low oral bioavailability of Rb1 and rapid elimination of Rg1, which might explain the discrepancy between in vitro and human research. Until more is known, use with caution in patients concurrently taking anticoagulant or antiplatelet drugs.
Antidiabetes Drugs
Theoretically, taking Panax ginseng with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research suggests that Panax ginseng might decrease blood glucose levels. Monitor blood glucose levels closely.
Caffeine
Theoretically, taking Panax ginseng with caffeine might increase the risk of adverse stimulant effects.
Panax ginseng has been shown to have stimulant effects. Theoretically, caffeine might have an additive effect on the stimulant effects of Panax ginseng.
Cytochrome P450 2D6 (Cyp2D6) Substrates
Theoretically, Panax ginseng might increase levels of drugs metabolized by CYP2D6. However, research is conflicting.
There is some evidence that Panax ginseng can inhibit the CYP2D6 enzyme by approximately 6%. In addition, in animal research, Panax ginseng inhibits the metabolism of dextromethorphan, a drug metabolized by CYP2D6, by a small amount. However, contradictory research suggests Panax ginseng might not inhibit CYP2D6. Until more is known, use Panax ginseng cautiously in patients taking drugs metabolized by these enzymes.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, Panax ginseng might increase or decrease levels of drugs metabolized by CYP3A4.
Panax ginseng may affect the clearance of drugs metabolized by CYP3A4. One such drug is imatinib. Inhibition of CYP3A4 was believed to be responsible for a case of imatinib-induced hepatotoxicity. In contrast, Panax ginseng has been shown to increase the clearance of midazolam, another drug metabolized by CYP3A4. Clinical research shows that Panax ginseng can reduce midazolam area under the curve by 44%, maximum plasma concentration by 26%, and time to reach maximum plasma concentration by 29%. Midazolam metabolism was also increased in animals given Panax ginseng. Until more is known, use Panax ginseng cautiously in combination with CYP3A4 substrates.
Estrogens
Theoretically, concomitant use of large amounts of Panax ginseng might interfere with hormone replacement therapy.
Laboratory research and some case reports suggest that Panax ginseng can have estrogenic effects due to competition for estrogen receptors. The estrogenic activity is attributed to the ginsenoside constituents of Panax ginseng.
Furosemide (Lasix)
Theoretically, Panax ginseng might reduce the effects of furosemide.
There is some concern that Panax ginseng might contribute to furosemide resistance. There is one case of resistance to furosemide diuresis in a patient taking a germanium-containing ginseng product.
Imatinib (Gleevec)
Theoretically, Panax ginseng might increase the effects and adverse effects of imatinib.
A case of imatinib-induced hepatotoxicity has been reported for a 26-year-old male with chronic myelogenous leukemia stabilized on imatinib for 7 years. The patient took imatinib 400 mg along with a Panax ginseng-containing energy drink daily for 3 months. Since imatinib-associated hepatotoxicity typically occurs within 2 years of initiating therapy, it is believed that Panax ginseng affected imatinib toxicity though inhibition of cytochrome P450 3A4. CYP3A4 is the primary enzyme involved in imatinib metabolism.
Immunosuppressants
Theoretically, Panax ginseng use might interfere with immunosuppressive therapy.
Panax ginseng might have immune system stimulating properties.
Insulin
Theoretically, taking Panax ginseng with insulin might increase the risk of hypoglycemia.
Clinical research suggests that Panax ginseng might decrease blood glucose levels. Insulin dose adjustments might be necessary in patients taking Panax ginseng; use with caution.
Midazolam (Versed)
Theoretically, Panax ginseng may increase the clearance of midazolam.
Midazolam is metabolized by cytochrome P450 3A4 (CYP3A4). Clinical research suggests that Panax ginseng can reduce midazolam area under the curve by 44%, maximum plasma concentration by 26%, and time to reach maximum plasma concentration by 29%. Midazolam metabolism was also increased in animals given Panax ginseng.
Monoamine Oxidase Inhibitors (Maois)
Theoretically, Panax ginseng can interfere with MAOI therapy.
Concomitant use of Panax ginseng with phenelzine (Nardil) is associated with insomnia, headache, tremors, and hypomania.
Nifedipine (Procardia)
Theoretically, taking Panax ginseng with nifedipine might increase serum levels of nifedipine and the risk of hypotension.
Preliminary clinical research shows that concomitant use can increase serum levels of nifedipine in healthy volunteers. This might cause the blood pressure lowering effects of nifedipine to be increased when taken concomitantly with Panax ginseng.
Qt Interval-Prolonging Drugs
Theoretically, Panax ginseng has an additive effect with drugs that prolong the QT interval and potentially increase the risk of ventricular arrhythmias. However, research is conflicting.
Clinical research shows that short-term use of Panax ginseng can increase the QT interval. However, no changes in QT interval have been identified with prolonged use.
Raltegravir (Isentress)
Theoretically, taking Panax ginseng with raltegravir might increase the risk of liver toxicity.
A case report suggests that concomitant use of Panax ginseng with raltegravir can increase serum levels of raltegravir, resulting in elevated liver enzymes levels.
Selegiline (Eldepryl)
Theoretically, Panax ginseng might increase or decrease levels of selegiline, possibly altering the effects and side effects of selegiline.
Animal research shows that taking selegiline with a low dose of Panax ginseng extract (1 gram/kg) reduces selegiline bioavailability, while taking a high dose of Panax ginseng extract (3 grams/kg) increases selegiline bioavailability. More research is needed to confirm these effects.
Stimulant Drugs
Theoretically, taking Panax ginseng with stimulant drugs might increase the risk of adverse stimulant effects.
Panax ginseng has been shown to have stimulant effects.
Warfarin (Coumadin)
Panax ginseng might affect the clearance of warfarin. However, this interaction appears to be unlikely.
There has been a single case report of decreased effectiveness of warfarin in a patient who also took Panax ginseng. However, it is questionable whether Panax ginseng was the cause of this decrease in warfarin effectiveness. Some research in humans and animals suggests that Panax ginseng does not affect the pharmacokinetics of warfarin. However, other research in humans suggests that Panax ginseng might modestly increase the clearance of the S-warfarin isomer. More evidence is needed to determine whether Panax ginseng causes a significant interaction with warfarin.
Fexofenadine (Allegra)
Theoretically, Panax ginseng might decrease blood levels of oral or intravenous fexofenadine.
Animal research suggests that taking Panax ginseng in combination with oral or intravenous fexofenadine may reduce the bioavailability of fexofenadine. Some scientists have attributed this effect to the ability of Panax ginseng to increase the expression of P-glycoprotein.
Lopinavir/Ritonavir (Kaletra)
Although Panax ginseng has demonstrated variable effects on cytochrome P450 3A4 (CYP3A4), which metabolizes lopinavir, Panax ginseng is unlikely to alter levels of lopinavir/ritonavir.
Lopinavir is metabolized by CYP3A4 and is administered with the CYP3A4 inhibitor ritonavir to increase its plasma concentrations. Panax ginseng has shown variable effects on CYP3A4 activity in humans. However, taking Panax ginseng (Vitamer Laboratories) 500 mg twice daily for 14 days did not alter the pharmacokinetics of lopinavir/ritonavir in 12 healthy volunteers.
BioPerine
Anticoagulant/Antiplatelet Drugs
Theoretically, black pepper might increase the risk of bleeding when taken with antiplatelet or anticoagulant drugs.
In vitro research shows that piperine, a constituent of black pepper, seems to inhibit platelet aggregation. This has not been reported in humans.
Antidiabetes Drugs
Theoretically, black pepper might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research shows that piperine, a constituent of black pepper, can reduce blood glucose levels. Monitor blood glucose levels closely. Dose adjustments might be necessary.
Atorvastatin (Lipitor)
Theoretically, black pepper might increase blood levels of atorvastatin.
Animal research shows that taking piperine, a constituent of black pepper, 35 mg/kg can increase the maximum serum concentration of atorvastatin three-fold. This has not been reported in humans.
Cyclosporine (Neoral, Sandimmune)
Theoretically, black pepper might increase the effects and side effects of cyclosporine.
In vitro research shows that piperine, a constituent of black pepper, increases the bioavailability of cyclosporine. This has not been reported in humans.
Cytochrome P450 2D6 (Cyp2D6) Substrates
Theoretically, black pepper might increase levels of drugs metabolized by CYP2D6.
In vitro research suggests that some constituents of black pepper inhibit CYP2D6. This has not been reported in humans.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, black pepper might increase levels of drugs metabolized by CYP3A4.
In vitro research and pharmacokinetic simulation data suggest that piperine, a constituent of black pepper, as well as the pepper fruit seem to inhibit CYP3A4. This has not been reported in humans.
Lithium
Theoretically, black pepper might increase blood levels of lithium due to its diuretic effects. The dose of lithium might need to be reduced.
Black pepper is thought to have diuretic properties.
Nevirapine (Viramune)
Black pepper might increase blood levels of nevirapine.
Clinical research shows that piperine, a constituent of black pepper, increases the plasma concentration of nevirapine. However, no adverse effects were observed in this study.
P-Glycoprotein Substrates
Theoretically, black pepper might increase levels of P-glycoprotein substrates.
In vitro research shows that piperine, a constituent of black pepper, seems to inhibit P-glycoprotein.
Pentobarbital (Nembutal)
Theoretically, black pepper might increase the sedative effects of pentobarbital.
Animal research shows that piperine, a constituent of black pepper, increases pentobarbital-induced sleeping time.
Phenytoin (Dilantin)
Black pepper might increase blood levels of phenytoin.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption, slow elimination, and increase levels of phenytoin. Taking a single dose of black pepper 1 gram along with phenytoin seems to double the serum concentration of phenytoin. Consuming a soup with black pepper providing piperine 44 mg/200 mL of soup along with phenytoin also seems to increase phenytoin levels when compared with consuming the same soup without black pepper.
Propranolol (Inderal)
Black pepper might increase blood levels of propranolol.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and slow elimination of propranolol.
Rifampin (Rifadin)
Black pepper might increase blood levels of rifampin.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and serum levels of rifampin.
Theophylline
Black pepper might increase blood levels of theophylline.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and slow elimination of theophylline.
Amoxicillin (Amoxil, Trimox)
Theoretically, black pepper might increase the effects and side effects of amoxicillin.
Animal research shows that taking piperine, a constituent of black pepper, with amoxicillin increases plasma levels of amoxicillin. This has not been reported in humans.
Carbamazepine (Tegretol)
Theoretically, black pepper might increase blood levels of carbamazepine, potentially increasing the effects and side effects of carbamazepine.
One clinical study in patients taking carbamazepine 300 mg or 500 mg twice daily shows that taking a single 20 mg dose of purified piperine, a constituent of black pepper, increases carbamazepine levels. Piperine may increase carbamazepine absorption by increasing blood flow to the GI tract, increasing the surface area of the small intestine, or inhibiting cytochrome P450 3A4 (CYP3A4) in the gut wall. Absorption was significantly increased by 7-10 mcg/mL/hour. The time to eliminate carbamazepine was also increased by 4-8 hours. Although carbamazepine levels were increased, this did not appear to increase side effects. In vitro research also shows that piperine can increase carbamazepine levels by 11% in a time-dependent manner.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, black pepper might decrease levels and clinical effects of drugs metabolized by CYP1A2.
In vitro research suggests that black pepper induces CYP1A2. This has not been reported in humans.
Ginger Rhizome Extract
Anticoagulant/Antiplatelet Drugs
Ginger may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Laboratory research suggests that ginger inhibits thromboxane synthetase and decreases platelet aggregation. However, this has not been demonstrated unequivocally in humans, with mixed results from clinical trials. Theoretically, excessive amounts of ginger might increase the risk of bleeding when used with anticoagulant/antiplatelet drugs.
Antidiabetes Drugs
Theoretically, taking ginger with antidiabetes drugs might increase the risk of hypoglycemia.
Animal and human research suggests that ginger might increase insulin levels and/or decrease blood glucose levels.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Ginger might increase or decrease the levels of CYP3A4 substrates.
In vitro research and some case reports suggest that ginger inhibits CYP3A4 activity. Three case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are CYP3A4 substrates (imatinib, dabrafenib, and crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.
Conversely, other in vitro research suggests that ginger induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. However, this interaction has not been reported in humans.
Losartan (Cozaar)
Theoretically, ginger might increase levels of losartan and the risk of hypotension.
In animal research, ginger increased the levels and hypotensive effects of a single dose of losartan. It is not clear if ginger alters the concentration or effects of losartan when taken continuously. Additionally, this interaction has not been shown in humans.
Nifedipine (Procardia)
Ginger may have antiplatelet effects and increase the risk of bleeding if used with nifedipine.
Clinical research shows that combined treatment with ginger 1 gram plus nifedipine 10 mg significantly inhibits platelet aggregation when compared to nifedipine or ginger alone.
P-Glycoprotein Substrates
Ginger might increase the absorption and blood levels of P-glycoprotein (P-gp) substrates.
In vitro research and case reports suggest that ginger inhibits drug efflux by P-gp, potentially increasing absorption and serum levels of P-gp substrates. Two case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are P-gp substrates (trametinib, crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.
Phenprocoumon (Marcoumar, Others)
Ginger might increase the risk of bleeding with phenprocoumon.
Phenprocoumon, a warfarin-related anticoagulant, might increase the international normalized ratio (INR) when taken with ginger. There is one case report of a 76-year-old woman with a stable INR on phenprocoumon that increased to greater than 10 when she began consuming dried ginger and ginger tea.
Warfarin (Coumadin)
Ginger might increase the risk of bleeding with warfarin.
Laboratory research suggests that ginger might inhibit thromboxane synthetase and decrease platelet aggregation. In one case report, ginger increased the INR when taken with phenprocoumon, which has similar pharmacological effects as warfarin. In another case report, ginger increased the INR when taken with a combination of warfarin, hydrochlorothiazide, and acetaminophen. A longitudinal analysis suggests that taking ginger increases the risk of bleeding in patients taking warfarin for at least 4 months. However, research in healthy people suggests that ginger has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. Until more is known, monitor INRs closely in patients taking large amounts of ginger.
Calcium Channel Blockers
Theoretically, taking ginger with calcium channel blockers might increase the risk of hypotension.
Some animal and in vitro research suggests that ginger has hypotensive and calcium channel-blocking effects. Another animal study shows that concomitant administration of ginger and the calcium channel blocker amlodipine leads to greater reductions in blood pressure when compared with amlodipine alone.
Cyclosporine (Neoral, Sandimmune)
Theoretically, when taken prior to cyclosporine, ginger might decrease cyclosporine levels.
In an animal model, ginger juice taken 2 hours prior to cyclosporine administration reduced the maximum concentration and area under the curve of cyclosporine by 51% and 40%, respectively. This effect was not observed when ginger juice and cyclosporine were administered at the same time.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, ginger might increase the levels of CYP1A2 substrates.
In vitro research shows that ginger inhibits CYP1A2 activity. However, this interaction has not been reported in humans.
Cytochrome P450 2B6 (Cyp2B6) Substrates
Theoretically, ginger might increase the levels of CYP2B6 substrates.
In vitro research shows that ginger inhibits CYP2B6 activity. However, this interaction has not been reported in humans.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, ginger might increase the levels of CYP2C9 substrates.
In vitro research shows that ginger inhibits CYP2C9 activity. However, this interaction has not been reported in humans.
Metronidazole (Flagyl)
Theoretically, ginger might increase levels of metronidazole.
In an animal model, ginger increased the absorption and plasma half-life of metronidazole. In addition, the elimination rate and clearance of metronidazole was significantly reduced.
Red Clover, Powder
Estrogens
Theoretically, concomitant use of large amounts of red clover might interfere with estrogen therapy.
Red clover contains phytoestrogens which might have estrogenic activity in some people. Theoretically, red clover might compete for estrogen receptors and interfere with estrogen-containing drug therapy.
Methotrexate (Trexall, Others)
Theoretically, red clover might increase the risk of methotrexate toxicity.
In a case report, a 52-year-old female receiving weekly methotrexate injections for psoriasis developed symptoms of methotrexate toxicity, including severe vomiting and epigastric pain, after three days of taking red clover 430 mg daily. Toxicity resolved after red clover was discontinued. However, no liver function tests or methotrexate levels were reported.
Tamoxifen (Nolvadex)
Theoretically, the phytoestrogens in red clover might interfere with tamoxifen.
In vitro and animal research suggests that genistein, a constituent of red clover, might antagonize the antitumor effects of tamoxifen. However, there is some evidence from an animal study that red clover does not reduce the efficacy of tamoxifen. Until more is known, tell patients taking tamoxifen to avoid red clover.
Anticoagulant/Antiplatelet Drugs
Although some laboratory research suggests that red clover may have anticoagulant and antiplatelet activity, clinical research has not shown this effect.
In vitro research suggests that genistein in red clover has antiplatelet effects, and historically, red clover was thought to have anticoagulant effects due to its coumarin content. However, some experts state that this is unlikely as most natural coumarins have not been shown to have anticoagulant effects, and their content in red clover is low. Additionally, some clinical research in postmenopausal patients found no effect on coagulation or prothrombin time with the use of red clover flowering tops 378 mg daily for 12 months or red clover isoflavone (Rimostil) 50 mg daily for 2 years.
Caffeine
Theoretically, soy might reduce the clearance of caffeine; however, a small clinical study found no effect.
Red clover contains genistein. Taking genistein 1 gram daily for 14 days seems to inhibit caffeine clearance and metabolism in healthy females. However, this effect does not seem to occur with the lower amounts of genistein found in red clover. A clinical study in healthy postmenopausal individuals shows that taking red clover capsules standardized to contain 60 mg isoflavones twice daily for 14 days does not affect the pharmacokinetics of caffeine.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, red clover might increase levels of drugs metabolized by CYP1A2; however, a small clinical study found no effect.
In vitro evidence shows that red clover inhibits CYP1A2. However, a clinical study in healthy postmenopausal individuals shows that taking red clover capsules standardized to contain 60 mg isoflavones twice daily for 14 days does not affect the pharmacokinetics of caffeine, a CYP1A2 probe substrate.
Cytochrome P450 2C19 (Cyp2C19) Substrates
Theoretically, red clover might increase the levels and clinical effects of drugs metabolized by CYP2C19.
In vitro evidence suggests that red clover weakly inhibits CYP2C19. This interaction has not been reported in humans.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, red clover might increase levels of drugs metabolized by CYP2C9; however, a small clinical study found no effect.
In vitro evidence suggests that red clover might inhibit CYP2C9. However, a clinical study in healthy postmenopausal individuals shows that taking red clover capsules standardized to contain 60 mg isoflavones twice daily for 14 days does not affect the pharmacokinetics of tolbutamide, a CYP2C9 probe substrate.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, red clover might increase levels of drugs metabolized by CYP3A4; however, a small clinical study found no effect.
In vitro evidence shows that red clover might inhibit CYP3A4 isoenzymes. However, a clinical study in healthy postmenopausal individuals shows that taking red clover capsules standardized to contain 60 mg isoflavones twice daily for 14 days does not affect the pharmacokinetics of alprazolam, a CYP3A4 probe substrate.
Black Cohosh root extract
Atorvastatin (Lipitor)
Taking black cohosh with atorvastatin might increase the risk for elevated liver function tests.
In one case report, a patient taking atorvastatin (Lipitor) developed significantly elevated liver function enzymes after starting black cohosh 100 mg four times daily. Liver enzymes returned to normal when black cohosh was discontinued. It is unclear whether the elevated liver enzymes were due to black cohosh itself or an interaction between atorvastatin and black cohosh.
Cisplatin (Platinol-Aq)
Theoretically, black cohosh may reduce the clinical effects of cisplatin.
Animal research suggests that black cohosh might decrease the cytotoxic effect of cisplatin on breast cancer cells.
Cytochrome P450 2D6 (Cyp2D6) Substrates
Some research suggests that black cohosh might inhibit CYP2D6, but there is conflicting evidence.
Some clinical research suggests that black cohosh might modestly inhibit CYP2D6 and increase levels of drugs metabolized by this enzyme. However, contradictory clinical research shows a specific black cohosh product (Remifemin, Enzymatic Therapy) 40 mg twice daily does not significantly inhibit metabolism of a CYP2D6 substrate in healthy study volunteers. Until more is known, use black cohosh cautiously in patients taking drugs metabolized by CYP2D6.
Estrogens
Theoretically, black cohosh may alter the effects of estrogen therapy.
Some research suggests that black cohosh has estrogenic effects. This may enhance or inhibit the effects of estrogen therapy.
Hepatotoxic Drugs
Theoretically, taking black cohosh with hepatotoxic drugs may increase the risk of liver damage.
There is concern that black cohosh might be linked to cases of liver failure and autoimmune hepatitis.
Serotonergic Drugs
Combining serotonergic drugs with black cohosh might cause additive serotonergic effects.
Black cohosh might increase the risk of serotonin syndrome when combined with other serotonergic drugs. Black cohosh acts as an agonist at several serotonin receptor subtypes and might interact with other serotonergic medications. In one case, a 55-year-old female who had been on stable treatment with sertraline 50 mg and duloxetine 60 mg daily developed serotonin syndrome after taking black cohosh extract 40 mg daily for 3 days.
Organic Anion-Transporting Polypeptide Substrates (Oatp)
Black cohosh may inhibit one form of OATP, OATP2B1, which could reduce the bioavailability and clinical effects of OATP2B1 substrates.
In vitro research shows that black cohosh modestly inhibits OATP2B1. 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.
Fish Oil
Antihypertensive Drugs
Theoretically, taking fish oil with antihypertensive drugs might increase the risk of hypotension.
Clinical evidence indicates that fish oils can modestly lower blood pressure and might have additive effects in patients treated with antihypertensives.
Contraceptive Drugs
Theoretically, taking fish oil with contraceptive drugs might decrease the triglyceride-lowering effects of fish oil.
There is some evidence that contraceptive drugs might interfere with the triglyceride lowering effects of fish oils.
Cyclosporine (Neoral, Sandimmune)
Taking fish oil with cyclosporine might increase levels and adverse effects of cyclosporine.
In kidney transplant recipients on a general immunosuppressive regimen, taking omega-3 fatty acids daily seems to increase peak blood levels of cyclosporine when compared with placebo. This increase was as much as 20% after one month. However, the area under the curve was not significantly affected.
Orlistat (Xenical, Alli)
Theoretically, taking fish oil with orlistat might decrease the absorption of fish oil fatty acids.
Orlistat binds lipase in the gastrointestinal tract and reduces fat absorption. Theoretically, taking fish oil with orlistat might decrease absorption of fish oil fatty acids. To avoid this potential interaction, recommend separating administration of orlistat and fish oil by at least 2 hours.
Sirolimus (Rapamune)
Taking fish oil with sirolimus might increase levels and adverse effects of sirolimus.
Pharmacokinetic research shows that omega-3 fatty acids increase exposure to sirolimus in kidney transplant patients on a calcineurin inhibitor-free immunosuppressive regimen. A 25% dose reduction in sirolimus was required to keep patients within the expected trough-concentration window. Researchers hypothesize that this may be due to inhibition of cytochrome P450 3A4 (CYP3A4) by fish oil, although this has not been confirmed in clinical research.
Tacrolimus (Prograf)
Taking fish oil with tacrolimus might increase levels and adverse effects of tacrolimus.
In a small group of patients, taking fish oil 2.6 grams (Omacor) daily for 4 weeks increased the 8-hour area under the curve of tacrolimus by 25% when compared with baseline. Peak levels were increased by approximately 22%. Researchers hypothesize that this may be due either to an increase in bioavailability or to inhibition of cytochrome P450 3A4 (CYP3A4) by fish oil, although this has not been confirmed in clinical research.
Anticoagulant/Antiplatelet Drugs
Fish oil may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, evidence is conflicting.
While fish oil may not be a potent inhibitor of platelet function, high doses of fish oil might have antiplatelet effects. Theoretically, concomitant use of fish oil with anticoagulant or antiplatelet drugs may increase the risk of bleeding. However, the most rigorous research shows that short-term doses of fish oil 10 grams daily or long-term doses of 1.5 grams daily for up to 52 weeks does not increase the risk of bleeding or affect coagulation parameters in chronically ill and vulnerable patients. Other controlled research shows that fish oil does not affect platelet function or increase the risk of bleeding. Some research even suggests that perioperative fish oil use decreases bleeding risk. Some research suggests fish oil does not have additive antiplatelet effects when combined with aspirin, but other clinical evidence suggests that adding fish oil to low-dose aspirin treatment increases antiplatelet effects in patients who are aspirin-resistant. Also, some clinical research seems to show that fish oil has additive antiplatelet effects when used with aspirin and clopidogrel compared to aspirin and clopidogrel alone.
Platinum Agents
Theoretically, taking fish oil with platinum agents can cause resistance to platinum agents, potentially decreasing their effectiveness.
Platinum-induced fatty acids (PIFAs) are fatty acids secreted from human and mouse stem cells when exposed to platinum-based chemotherapy. Animal research suggests that PIFAs cause resistance to chemotherapy by stimulating lysophospholipid production in the spleen, which interferes with the DNA damage caused by certain chemotherapy drugs. One PIFA, known as 16:4(n-3), has been found in both raw fish and some commercially available fish oil products. Mackerel and herring have high PIFA concentrations, while salmon and tuna have low PIFA concentrations. Levels of PIFA in commercial fish oil products ranged from 0.2- 5.7 microMol. Animal research shows that PIFA-containing fish oil products cause resistance to cisplatin, fluorouracil, irinotecan, and oxaliplatin. It is unclear if all commercially available fish oil products contain PIFAs. Additionally, it is argued that levels of PIFA found in some fish oil products are too low to be of clinical concern. Furthermore, a lack of chemotherapy resistance in countries with high fish intake, such as Greenland, Japan, and Norway, suggest that this interaction may not be clinically significant.
Warfarin (Coumadin)
Fish oil may have antiplatelet effects and might increase the risk of bleeding if used with warfarin.
Fish oil has antiplatelet effects at high doses. Case reports show elevated INR in patients taking warfarin and fish oil 1-2 grams daily. However, some clinical research shows that taking fish oil 3-6 grams daily does not significantly increase INR in patients taking warfarin.
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.
Sodium
Antihypertensive Drugs
Theoretically, a high intake of dietary sodium might reduce the effectiveness of antihypertensive drugs.
High intake of dietary sodium can increase systolic and diastolic blood pressure. Also, high intake of sodium may necessitate increased use of antihypertensive medications to achieve blood pressure control in some patients, such as those with chronic kidney disease.
Corticosteroids
Concomitant use of mineralocorticoids and some glucocorticoids with sodium supplements might increase the risk of hypernatremia.
Mineralocorticoids and some glucocorticoids (corticosteroids) cause sodium retention. This effect is dose-related and depends on mineralocorticoid potency. It is most common with hydrocortisone, cortisone, and fludrocortisone, followed by prednisone and prednisolone.
Didanosine (Videx)
Concomitant use of didanosine with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia.
Didanosine formulations contain a significant amount of sodium.
Lithium
Altering dietary intake of sodium might alter the levels and clinical effects of lithium.
High sodium intake can reduce plasma concentrations of lithium by increasing lithium excretion. Reducing sodium intake can significantly increase plasma concentrations of lithium and cause lithium toxicity in patients being treated with lithium carbonate. Stabilizing sodium intake is shown to reduce the percentage of patients with lithium level fluctuations above 0.8 mEq/L. Patients taking lithium should avoid significant alterations in their dietary intake of sodium.
Sodium Phosphates
Theoretically, concomitant use of sodium phosphate with sodium supplements might increase the risk of hypernatremia.
Use of high doses (> 45 mL in 24 hours) of sodium phosphate, such as those used for bowel cleansing before surgery, can lead to serious electrolyte disturbances, including hypernatremia. The risk of hypernatremia is highest in the elderly and people with other risk factors for electrolyte disturbances.
Sodium-Containing Drugs
Concomitant use of sodium-containing drugs with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia and long-term sodium-related complications.
The Chronic Disease Risk Reduction (CDRR) intake level of 2.3 grams of sodium daily indicates the intake at which it is believed that chronic disease risk increases for the apparently healthy population. Some medications contain high quantities of sodium. When used in conjunction with sodium supplements or high-sodium diets, the CDRR may be exceeded. Additionally, concomitant use may increase the risk for hypernatremia; this risk is highest in the elderly and people with other risk factors for electrolyte disturbances.
Tolvaptan (Samsca)
Theoretically, concomitant use of tolvaptan with sodium might increase the risk of hypernatremia.
Tolvaptan is a vasopressin receptor 2 antagonist that is used to increase sodium levels in patients with hyponatremia. Patients taking tolvaptan should use caution with the use of sodium salts such as sodium chloride.
Calcium
Ceftriaxone (Rocephin)
Co-administration of intravenous calcium and ceftriaxone can result in precipitation of a ceftriaxone-calcium salt in the lungs and kidneys.
Avoid administering intravenous calcium in any form, such as parenteral nutrition or Lactated Ringers, within 48 hours of intravenous ceftriaxone. Case reports in neonates show that administering intravenous ceftriaxone and calcium can result in precipitation of a ceftriaxone-calcium salt in the lungs and kidneys. In several cases, neonates have died as a result of this interaction. So far there are no reports in adults; however, there is still concern that this interaction might occur in adults.
Dolutegravir (Tivicay)
Calcium seems to reduce levels of dolutegravir.
Advise patients to take dolutegravir either 2 hours before or 6 hours after taking calcium supplements. Pharmacokinetic research suggests that taking calcium carbonate 1200 mg concomitantly with dolutegravir 50 mg reduces plasma levels of dolutegravir by almost 40%. Calcium appears to decrease levels of dolutegravir through chelation.
Elvitegravir (Vitekta)
Calcium seems to reduce levels of elvitegravir.
Advise patients to take elvitegravir either 2 hours before or 2 hours after taking calcium supplements. Pharmacokinetic research suggests that taking calcium along with elvitegravir can reduce blood levels of elvitegravir through chelation.
Aluminum
Calcium citrate might increase aluminum absorption and toxicity. Other types of calcium do not increase aluminum absorption.
Calcium citrate can increase the absorption of aluminum when taken with aluminum hydroxide. The increase in aluminum levels may become toxic, particularly in individuals with kidney disease. However, the effect of calcium citrate on aluminum absorption is due to the citrate anion rather than calcium cation. Calcium acetate does not appear to increase aluminum absorption.
Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)
Calcium might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption when taken in a fasting state.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide and calcium can be taken together if taken with food. However, if taken on an empty stomach, bictegravir/emtricitabine/tenofovir alafenamide should not be taken with, or 2 hours after, calcium containing products.
Bisphosphonates
Calcium reduces the absorption of bisphosphonates.
Advise patients to take bisphosphonates at least 30 minutes before calcium, but preferably at a different time of day. Calcium supplements decrease absorption of bisphosphonates.
Calcipotriene (Dovonex)
Taking calcipotriene with calcium might increase the risk for hypercalcemia.
Calcipotriene is a vitamin D analog used topically for psoriasis. It can be absorbed in sufficient amounts to cause systemic effects, including hypercalcemia. Theoretically, combining calcipotriene with calcium supplements might increase the risk of hypercalcemia.
Digoxin (Lanoxin)
Using intravenous calcium with digoxin might increase the risk of fatal cardiac arrhythmias.
Hypercalcemia increases the risk of fatal cardiac arrhythmias with digoxin. However, one retrospective analysis of clinical data suggests that intravenous calcium does not increase the risk of dysrhythmias or mortality in patients receiving digoxin.
Diltiazem (Cardizem, Others)
Theoretically, calcium may reduce the therapeutic effects of diltiazem.
Hypercalcemia can reduce the effectiveness of verapamil in atrial fibrillation. Theoretically, calcium might increase this risk of hypercalcemia and reduce the effectiveness of diltiazem.
Levothyroxine (Synthroid, Others)
Calcium seems to reduce the absorption and effectiveness of levothyroxine.
Advise patients to take levothyroxine and calcium supplements at least 4 hours apart. Calcium reduces levothyroxine absorption, probably by forming insoluble complexes. Calcium carbonate supplements reduce effectiveness of levothyroxine in patients with hypothyroidism.
Lithium
Theoretically, concomitant use of calcium and lithium may increase this risk of hypercalcemia.
Clinical research suggests that long-term use of lithium may cause hypercalcemia in 10% to 60% of patients. Theoretically, concomitant use of lithium and calcium supplements may further increase this risk.
Quinolone Antibiotics
Calcium seems to reduce the absorption of quinolone antibiotics.
Advise patients to take oral quinolones at least 2 hours before or 4-6 hours after calcium supplements or calcium-fortified foods. Taking calcium at the same time as oral quinolones can reduce quinolone absorption. Calcium binds to quinolones in the gut.
Raltegravir (Isentress)
Calcium may reduce levels of raltegravir.
Pharmacokinetic research shows that taking a single dose of calcium carbonate 3000 mg along with raltegravir 400 mg twice daily modestly decreases the mean area under the curve of raltegravir, but the decrease does not necessitate a dose adjustment of raltegravir. However, a case of elevated HIV-1 RNA levels and documented resistance to raltegravir has been reported for a patient taking calcium carbonate 1 gram three times daily plus vitamin D3 (cholecalciferol) 400 IU three times daily in combination with raltegravir 400 mg twice daily for 11 months. It is thought that calcium reduced raltegravir levels by chelation, leading to treatment failure.
Sotalol (Betapace)
Calcium seems to reduce the absorption of sotalol.
Advise patients to separate doses by at least 2 hours before or 4-6 hours after calcium. Calcium appears to reduce the absorption of sotalol, probably by forming insoluble complexes.
Tetracycline Antibiotics
Calcium seems to reduce the absorption of tetracycline antibiotics.
Advise patients to take oral tetracyclines at least 2 hours before, or 4-6 hours after calcium supplements. Taking calcium at the same time as oral tetracyclines can reduce tetracycline absorption. Calcium binds to tetracyclines in the gut.
Thiazide Diuretics
Taking calcium along with thiazides might increase the risk of hypercalcemia and renal failure.
Thiazides reduce calcium excretion by the kidneys. Using thiazides along with moderately large amounts of calcium carbonate increases the risk of milk-alkali syndrome (hypercalcemia, metabolic alkalosis, renal failure). Patients may need to have their serum calcium levels and/or parathyroid function monitored regularly.
Verapamil (Calan, Others)
Theoretically, calcium may reduce the therapeutic effects of verapamil.
Hypercalcemia can reduce the effectiveness of verapamil in atrial fibrillation. Theoretically, use of calcium supplements may increase this risk of hypercalcemia and reduce the effectiveness of verapamil.
Calcium Channel Blockers
Intravenous calcium may decrease the effects of calcium channel blockers; oral calcium is unlikely to have this effect.
Intravenous calcium is used to decrease the effects of calcium channel blockers in the management of overdose. Intravenous calcium gluconate has been used before intravenous verapamil (Isoptin) to prevent or reduce the hypotensive effects without affecting the antiarrhythmic effects. But there is no evidence that dietary or supplemental calcium when taken orally interacts with calcium channel blockers.
Chasteberry Fruit Extract
Antipsychotic Drugs
Theoretically, vitex agnus-castus could interfere with the activity of antipsychotic drugs.
Vitex agnus-castus might interfere with the action of dopamine antagonists such as antipsychotic drugs due to its dopamine agonist effects.
Contraceptive Drugs
Theoretically, vitex agnus-castus could interfere with oral contraceptives.
Vitex agnus-castus might interfere with the efficacy of oral contraceptives due to possible hormone modulating activity.
Dopamine Agonists
Theoretically, vitex agnus-castus could interfere with dopamine agonists.
Vitex agnus-castus might potentiate the actions of dopaminergic agonists due to possible dopaminergic effects.
Estrogens
Theoretically, vitex agnus-castus could interfere with the activity of estrogens.
Vitex agnus-castus has hormone modulating activity that can interfere with the efficacy of hormone replacement therapy.
Metoclopramide (Reglan)
Theoretically, dopaminergic effects of vitex agnus-castus could interfere with metoclopramide.
Vitex agnus-castus might interfere with the action of dopamine antagonists such as metoclopramide due to its possible dopaminergic effects.
Iron
Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)
Iron might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption when taken in a fasting state.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide and iron can be taken together if taken with food. However, if taken on an empty stomach, bictegravir/emtricitabine/tenofovir alafenamide should not be taken with, or 2 hours after, iron containing products.
Bisphosphonates
Iron reduces the absorption of bisphosphonates.
Advise patients that doses of bisphosphonates should be separated by at least two hours from doses of all other medications, including supplements such as iron. Divalent cations, including iron, can decrease absorption of bisphosphonates by forming insoluble complexes in the gastrointestinal tract.
Denosumab (Prolia, Others)
Administration of intravenous iron within one month of denosumab administration might increase the risk of severe hypophosphatemia and hypocalcemia.
A case of severe hypocalcemia (albumin corrected calcium 6.88 mg/dL, ionized calcium 3.68 mg/dL) and hypophosphatemia (<0.5 mg/dL) with respiratory acidosis, QT interval prolongation, and nonsustained ventricular tachycardia was reported in a 76-year-old male who had received an iron polymaltose infusion within 2 weeks of a subcutaneous injection of denosumab. Serum parathyroid hormone was also elevated (348 pg/mL). Subsequent iron infusions with iron polymaltose and ferric carboxymaltose were followed by transient hypophosphatemia, but without hypocalcemia. Additionally, a literature review describes 6 additional cases of hypophosphatemia and hypocalcemia in patients 52-92 years of age who had been administered intravenous iron as either ferric carboxymaltose or iron polymaltose and subcutaneous denosumab within 1-4 weeks of each other.
Dolutegravir (Tivicay)
Iron might decrease dolutegravir levels by reducing its absorption.
Advise patients to take dolutegravir at least 2 hours before or 6 hours after taking iron. Pharmacokinetic research shows that iron can decrease the absorption of dolutegravir from the gastrointestinal tract through chelation. When taken under fasting conditions, a single dose of ferrous fumarate 324 mg orally along with dolutegravir 50 mg reduces overall exposure to dolutegravir by 54%.
Integrase Inhibitors
Theoretically, taking iron along with integrase inhibitors might decrease the levels and clinical effects of these drugs.
Iron is a divalent cation. There is concern that iron may decrease the absorption of integrase inhibitors from the gastrointestinal tract through chelation. One pharmacokinetic study shows that iron can decrease blood levels of the specific integrase inhibitor dolutegravir through chelation. Also, other pharmacokinetic research shows that other divalent cations such as calcium can decrease the absorption and levels of some integrase inhibitors through chelation.
Levodopa
Iron might decrease levodopa levels by reducing its absorption.
Advise patients to separate doses of levodopa and iron as much as possible. There is some evidence in healthy people that iron forms chelates with levodopa, reducing the amount of levodopa absorbed by around 50%. The clinical significance of this hasn't been determined.
Levothyroxine (Synthroid, Others)
Iron might decrease levothyroxine levels by reducing its absorption.
Advise patients to separate levothyroxine and iron doses by at least 2 hours. Iron can decrease the absorption and efficacy of levothyroxine by forming insoluble complexes in the gastrointestinal tract.
Methyldopa (Aldomet)
Iron might decrease methyldopa levels by reducing its absorption.
Advise patients to separate methyldopa and iron doses by at least 2 hours. Iron can decrease the absorption of methyldopa from the gastrointestinal tract through chelation, resulting in increases in blood pressure.
Mycophenolate Mofetil (Cellcept)
Theoretically, iron might decrease mycophenolate mofetil levels by reducing its absorption.
Advise patients to take iron 4-6 hours before, or 2 hours after, mycophenolate mofetil. It has been suggested that a decrease of absorption is possible, probably by forming nonabsorbable chelates. However, mycophenolate pharmacokinetics are not affected by iron supplementation in available clinical research.
Penicillamine (Cuprimine, Depen)
Iron might decrease penicillamine levels by reducing its absorption.
Advise patients to separate penicillamine and iron doses by at least 2 hours. Oral iron supplements can reduce absorption of penicillamine by 30% to 70%, probably due to chelate formation. In people with Wilson's disease, this interaction has led to reduced efficacy of penicillamine.
Quinolone Antibiotics
Iron might decrease levels of quinolone antibiotics by reducing their absorption.
Advise patients to separate quinolone antibiotics and iron doses by at least 2 hours. Iron decreases the absorption of quinolones due to formation of insoluble complexes in the gastrointestinal tract.
Tetracycline Antibiotics
Iron might decrease levels of tetracycline antibiotics by reducing their absorption.
Advise patients to take iron at least 2 hours before or 4 hours after tetracycline antibiotics. Concomitant use can decrease absorption of tetracycline antibiotics from the gastrointestinal tract by 50% to 90%.
Chloramphenicol
Theoretically, taking chloramphenicol with iron might reduce the response to iron therapy in iron deficiency anemia.
Chloramphenicol interferes with erythrocyte maturation. However, since chloramphenicol isn't usually taken for prolonged periods, this isn't likely to be clinically significant.
Brand information
Manufacturer and brand details for EstroPause, from the product label.
Irwin Naturals
See all Irwin Naturals products- Name
- Irwin Naturals
- Street Address
- 5310 Beethoven Street
- City
- Los Angeles
- State
- CA
- ZipCode
- 90066
- Phone Number
- 1-800-297-3273
- Web Address
- www.IrwinNaturals.com
EstroPause by Irwin Naturals: Common Questions
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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 EstroPause’s Ingredients
Every ingredient we hold a full HelloPharmacist monograph for — uses, evidence, safety, and the complete interaction list.
Iron
Interacts with 80 drugsIron is an essential mineral your body needs to make hemoglobin and carry oxygen in the blood. Supplements are mainly useful for treating or preventing iron deficiency and iron-deficiency an...
Read the full Iron monograph → Herb & supplement monographGinger
Interacts with 1,007 drugsGinger is a widely used culinary spice with a long history in traditional medicine, and it has the strongest evidence for helping with nausea and vomiting, including from motion sickness, pr...
Read the full Ginger monograph → Herb & supplement monographBlack Pepper
Interacts with 1,019 drugsBlack pepper is a common kitchen spice that is generally safe in the amounts used in food. Its extract, piperine, is mostly added to supplements to help the body absorb other ingredients (li...
Read the full Black Pepper monograph → Herb & supplement monographFish Oil
Interacts with 327 drugsFish oil provides omega-3 fatty acids (EPA and DHA) that are best known for lowering high triglyceride levels. The evidence for other heart and health benefits is mixed, and it is generally...
Read the full Fish Oil monograph → Herb & supplement monographDocosahexaenoic Acid (dha)
Interacts with 375 drugsDHA is an omega-3 fatty acid found in fatty fish and algae that is a building block for the brain, nervous system, and eyes. It is widely used and generally well tolerated, with the stronges...
Read the full Docosahexaenoic Acid (dha) monograph → Herb & supplement monographSodium
Interacts with 205 drugsSodium is an essential mineral and electrolyte your body needs to balance fluids, support nerves, and help muscles work. Most people in modern diets get more than enough—often too much—from...
Read the full Sodium monograph → Herb & supplement monographBlack Cohosh
Interacts with 652 drugsBlack cohosh is a North American plant most often used to ease menopause symptoms like hot flashes, but the research is mixed and far from settled. It is generally well tolerated for short-t...
Read the full Black Cohosh monograph → Herb & supplement monographPanax Ginseng
Interacts with 1,130 drugsPanax ginseng is a popular traditional herb used to boost energy, ease stress, and support overall wellness, though scientific evidence is mixed and mostly preliminary. It is generally well...
Read the full Panax Ginseng 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 monographCalcium
Interacts with 168 drugsCalcium is an essential mineral your body needs for strong bones, nerve signaling, and muscle function, and supplements can help fill gaps when diet falls short. Most people do best getting...
Read the full Calcium monograph → Herb & supplement monographVitex Agnus-castus
Interacts with 121 drugsVitex (chasteberry) is an herbal remedy most often used for PMS and menstrual cycle problems, and the strongest evidence is for easing some PMS symptoms. It is generally well tolerated by ma...
Read the full Vitex Agnus-castus monograph → Herb & supplement monographSt. John's Wort
Interacts with 1,143 drugsSt. John's wort is a well-studied herb most often used for mild to moderate depression, and some research suggests it may help with this. However, it has many serious interactions with presc...
Read the full St. John's Wort monograph → Herb & supplement monographRed Clover
Interacts with 867 drugsRed clover is a plant rich in isoflavones (plant compounds with weak estrogen-like activity) that is most often used for menopause symptoms like hot flashes. The evidence is mixed and genera...
Read the full Red Clover monograph →Sources & How We Checked
EstroPause'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 886 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.
Iron 72 references
- McEvoy GK, ed. AHFS Drug Information. Bethesda, MD: American Society of Health-System Pharmacists, 1998.
- Bruner AB, Joffe A, Duggan AK, et al. Randomized study of cognitive effects of iron supplementation in non- anaemic iron-deficient adolescent girls. Lancet 1996;348:992-6.
- Ullen H, Augustsson K, Gustavsson C, Steineck G. Supplementary iron intake and risk of cancer: reversed causality? Cancer Lett 1997;114:215-6.
- Reunanen A, Takkunen H, Knekt P, et al. Body iron stores, dietary iron intake and coronary heart disease mortality. J Intern Med 1995;238:223-30. PubMed
- Lund EK, Wharf SG, Fairweather-Tait SJ, Johnson IT. Oral ferrous sulfate supplements increase the free radical-generating capacity of feces from healthy volunteers. Am J Clin Nutr 1999;69:250-5.
- Rehman A, Collis CS, Yang M, et al. The effects of iron and vitamin C co-supplementation on oxidative damage to DNA in healthy volunteers. Biochem Biophys Res Comm 1998;246:293-8. PubMed
- Klipstein-Grobusch K, Grobbee DE, den Breeijen JH, et al. Dietary iron and risk of myocardial infarction in the Rotterdam Study. Am J Epidemiol 1999;149:421-8. PubMed
- Hansten PD, Horn JR. Drug Interactions Analysis and Management. Vancouver, WA: Applied Therapeutics Inc., 1997 and updates.
- Tatro DS, ed. Drug Interactions Facts. Facts and Comparisons Inc., St. Louis, MO. 1999.
- Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2002.
- Campbell N, Paddock V, Sundaram R. Alteration of methyldopa absorption, metabolism, and blood pressure control by ferrous sulfate and ferrous gluconate. Clin Pharmacol Ther 1988;43:381-6..
- Schumann K, Borch-Iohnsen B, Hentze MW, Marx JJ. Tolerable upper intakes for dietary iron set by the US Food and Nutrition Board (commentary). Am J Clin Nutr 2002;76:499-500. PubMed
- Tuomainen TP, Punnonen K, Nyyssonen K, Salonen JT. Association between body iron stores and the risk of acute myocardial infarction in men. Circulation 1998;97:1461-6.. PubMed
- Salonen JT, Nyyssonen K, Korpela H, et al. High stored iron levels are associated with excess risk of myocardial infarction in Eastern Finnish men. Circulation 1992;86:803-11.. PubMed
- Campbell NRC, Hasinoff B. Ferrous sulfate reduces levodopa bioavailability: Chelation as a possible mechanism. Clin Pharmacol Ther 1989;45:220-5.. PubMed
- Campbell NRC, Hasinoff BB, Stalts H, et al. Ferrous sulfate reduces thyroxine efficacy in patients with hypothyroidism. Ann Int Med 1992;117:1010-3.. PubMed
- Kiechl S, Willeit J, Egger G, et al. Body iron stores and the risk of carotid atherosclerosis: prospective results from the Bruneck study. Circulation 1997;96:3300-07. PubMed
- Comparison of oral iron supplements. Pharmacist's Letter / Prescriber's Letter 2008;24(8):240811.
- Tran T., Wax J. R., Philput C., Steinfeld J. D., Ingardia C. J. Intentional iron overdose in pregnancy--management and outcome. J Emerg Med 2000;18(2):225-228. PubMed
- Toblli J. E., Brignoli, R. Iron(III)-hydroxide polymaltose complex in iron deficiency anemia / review and meta-analysis. Arzneimittelforschung 2007;57(6A):431-438. PubMed
- Köpcke W., Sauerland M. C. Meta-analysis of efficacy and tolerability data on iron proteinsuccinylate in patients with iron deficiency anemia of different severity. Arzneimittelforschung 1995;45(11):1211-1216.
- Campbell N. R., Campbell R. R., Hasinoff B. B. Ferrous sulfate reduces methyldopa absorption: methyldopa: iron complex formation as a likely mechanism. Clin Invest Med 1990;13(6):329-332.
- Morii M., Ueno K., Ogawa A., Kato R., Yoshimura H., Wada K., Hashimoto H., Takada M., Tanaka K., Nakatani T., Shibakawa M. Impairment of mycophenolate mofetil absorption by iron ion. Clin Pharmacol Ther 2000;68(6):613-616. PubMed
- Gelone D. K., Park J. M., Lake K. D. Lack of an effect of oral iron administration on mycophenolic acid pharmacokinetics in stable renal transplant recipients. Pharmacotherapy 2007;27(9):1272-1278. PubMed
- Ducray P. S., Banken L., Gerber M., Boutouyrie B., Zandt H. Absence of an interaction between iron and mycophenolate mofetil absorption. Br J Clin Pharmacol 2006;62(4):492-495. PubMed
- Lorenz M., Wolzt M., Weigel G., Puttinger H., Hörl W. H., Födinger M., Speiser W., Sunder-Plassmann G. Ferrous sulfate does not affect mycophenolic acid pharmacokinetics in kidney transplant patients. Am J Kidney Dis 2004;43(6):1098-1103. PubMed
- Osman M. A., Patel R. B., Schuna A., Sundstrom W. R., Welling P. G. Reduction in oral penicillamine absorption by food, antacid, and ferrous sulfate. Clin Pharmacol Ther 1983;33(4):465-470. PubMed
- Michael, B., Coyne, D. W., Fishbane, S., Folkert, V., Lynn, R., Nissenson, A. R., Agarwal, R., Eschbach, J. W., Fadem, S. Z., Trout, J. R., Strobos, J., and Warnock, D. G. Sodium ferric gluconate complex in hemodialysis patients: adverse reactions compar
- Zhang, X., Ouyang, J., Wieczorek, R., and DeSoto, F. Iron medication-induced gastric mucosal injury. Pathol.Res Pract 2009;205(8):579-581. PubMed
- Barbieri, P. G. [To-day exposure to occupational carcinogens and their effects. The experience of the rubber industry, iron metallurgy, asphalt work and aviculture]. Epidemiol.Prev 2009;33(4-5 Suppl 2):94-105.
- Macedo, A. and Cardoso, S. [Routine iron supplementation in pregnancy]. Acta Med Port. 2010;23(5):785-792.
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Docosahexaenoic Acid (dha) 49 references
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See these in context on the Docosahexaenoic Acid (dha) monograph →
Fish Oil 157 references
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