Major interaction on record — check this product against your medications before combining. Based on 9 of 11 ingredients. Check your meds →
Dietary supplement

Liver Transition Formula Ingredients & Drug Interactions

by Christopher's Original Formulas

Liver Transition Formula label
See full label image
Capsule Category: Botanical
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 16, 2026 · Label data from the NIH DSLD
What is this page for?

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

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

The interaction bottom line Most serious interaction: Major

Liver Transition Formula is a dietary supplement by Christopher's Original Formulas with 11 active ingredients. Its ingredients are commonly taken for water retention (diuretic), digestive upset, liver and gallbladder support.Based on those ingredients, 1,560 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ginkgo leaf 4:1 extract powder, wildcrafted Oregon Grape, Milk Thistle seed extract powder. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

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Check Your Meds Against Liver Transition Formula by Christopher's Original Formulas

Ask about any prescription or over-the-counter medication and we check it for interactions with Liver Transition Formula by Christopher's Original Formulas — and tell you which ingredient is responsible.

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HelloPharmacist Scorecard of Liver Transition Formula by Christopher's Original Formulas

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

From our pharmacy team — supplement deep dive

Generated from HelloPharmacist’s pharmacist-curated databases and editorial rules · Last generated Aug 20, 2026

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

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

Why this rating?
  • The label discloses an exact amount for 0 of its 11 active ingredients.
  • “Proprietary Blend” is a proprietary blend — the label gives one combined amount (900 mg) without saying how much of each component you get.

Liver Transition Formula contains 11 ingredients total. The active ones are organic dandelion (listed twice), wildcrafted Oregon grape, organic rosemary, wildcrafted schisandra, ginkgo leaf 4:1 extract powder, milk thistle seed extract powder, wildcrafted wild yam, wildcrafted cramp bark, and wildcrafted American ginseng.

Organic Jurassic Green is also included but we have no interaction data on file for it. The formula is encapsulated in a plant-derived capsule.

Does it work?

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

There isn't enough reliable clinical evidence to rate this product's ingredients for its stated purpose.

Why this rating?
  • The label markets this product for: liver health and transition support.
  • We looked for evidence on: Alcohol-related liver disease, Hepatitis, Hepatitis B, Gallbladder disease, Chemotherapy-induced hepatotoxicity, Liver cirrhosis — and 3 related terms.
  • The closest evidence on file: Milk Thistle is rated "Insufficient Reliable Evidence To Rate" for Alcohol-related liver disease (Natural Medicines).
  • Also on file: Milk Thistle is rated "Insufficient Reliable Evidence To Rate" for Chemotherapy-induced hepatotoxicity, Hepatitis C, Hepatitis B, Nonalcoholic fatty liver disease (NAFLD), and more.
  • Also on file: Rosemary is rated "Insufficient Reliable Evidence To Rate" for Nonalcoholic fatty liver disease (NAFLD).

Most of the herbs in this formula lack strong evidence for their claimed uses. Ginkgo is possibly effective for hearing loss, stroke, schizophrenia, premenstrual syndrome, dementia, and anxiety.

Rosemary is possibly effective for memory. Oregon grape is possibly effective for psoriasis, and milk thistle is possibly effective for diabetes.

American ginseng appears possibly effective for upper respiratory tract infections. Dandelion, schisandra, wild yam, and cramp bark have insufficient reliable evidence in our data for their traditional uses—meaning the evidence hasn't been well established in the studies we hold.

The evidence, ingredient by ingredient Dandelion Oregon Grape Rosemary Schisandra Ginkgo Milk Thistle Wild Yam Cramp Bark

How safe is it?

Well-documented data
Safety Information · database check
Well characterized

Adverse-effect, pregnancy, and general safety data are on file for most of these ingredients.

Why this rating?
  • We hold adverse-effect (side-effect) data for 8 of the 9 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 9 of 9.
  • General safety write-ups exist for 9 of 9.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Several ingredients in this product come with caution flags. Dandelion is generally well tolerated as food but supplement-strength doses are less studied and may trigger allergies or stomach upset like diarrhea, heartburn, and discomfort.

Rare serious reactions including anaphylaxis have been reported, and people sensitive to ragweed and related plants (the Asteraceae family) should avoid it. Oregon grape should be used cautiously as oral doses are less well studied than topical use; topical use may cause itching, burning, and skin irritation.

Rosemary is safe in normal culinary amounts but concentrated extracts and undiluted oil need caution. Ginkgo is generally well tolerated but may increase bleeding risk, and cardiac arrhythmias and spontaneous bleeding have been reported—particularly concerning if you're older, have liver disease, or have had recent surgery.

Schisandra and milk thistle are generally well tolerated but long-term safety data are limited. American ginseng may cause headache.

Side effects, ingredient by ingredient Dandelion Oregon Grape Rosemary Schisandra Ginkgo Milk Thistle Wild Yam Cramp Bark

Meds to double-check

Major interaction found
Known Interaction Concern · database check
Major identified

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

Why this rating?
  • 8 of the 9 matched ingredients can interact with medications — Milk Thistle, Rosemary, Ginkgo, Schisandra, Oregon Grape, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; seizure medications; immunosuppressants / transplant drugs; diabetes medications; lithium.
  • For scale: 1,561 individual medications appear in the full list. A big number alone doesn't make a product dangerous — what matters is whether YOUR medication is on it, so run yours through the interaction checker on this page.

Check with your doctor or pharmacist before taking this product if you're on any of these: blood thinners or antiplatelet drugs like warfarin, aspirin, or clopidogrel (especially with ginkgo and dandelion); diabetes medications (dandelion, Oregon grape, rosemary, milk thistle, and American ginseng may lower blood sugar); blood pressure drugs including talinolol and other beta-blockers (ginkgo raises talinolol levels significantly); immunosuppressants like cyclosporine or tacrolimus (Oregon grape and schisandra affect these); medications metabolized by the liver including benzodiazepines, statins, and antidepressants; or lithium (dandelion may raise levels). No interactions are documented for cramp bark in our data.

Check your own medication Run your meds through the checker above

The bottom line

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

This formula contains multiple herbs that interact with common medications—particularly blood thinners, diabetes drugs, immunosuppressants, and drugs metabolized by the liver. The most serious documented interaction is between ginkgo and the blood pressure drug talinolol.

If you take any prescription medication, check each one against the drug interaction tool on this page before starting. Anyone pregnant or breastfeeding should talk with their doctor or pharmacist first, as several herbs in this formula are flagged as possibly or likely unsafe in pregnancy and lactation.

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

Assessment coverage: 10 of 11 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Apr 25, 2019.

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

At a glance

General information

Key facts about Liver Transition Formula, straight from the product label.

Brand Christopher's Original Formulas
Barcode (UPC) 084783891246
Net contents 100 Vegetarian Cap(s)
Market status On market
Date entered into DSLD Apr 25, 2019
DSLD ID 200594
Product type Botanical
Supplement form Capsule
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Adult (18 - 50 Years)
From the label
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.

Supplement Facts

The label details for Liver Transition Formula by Christopher's Original Formulas, sourced from the NIH Dietary Supplement Label Database.

Supplement Facts

Daily Value (DV) Target Group(s):
Adults and children 4 or more years of age
Minimum serving Sizes:
2 Capsule(s)
Maximum serving Sizes:
2 Capsule(s)
Servings per container
50
UPC/BARCODE
084783891246
IngredientAmount% DV
Proprietary Blend900 mg--
organic Dandelion0 NP--
wildcrafted Oregon Grape0 NP--
organic Dandelion0 NP--
organic Rosemary0 NP--
wildcrafted Schisandra0 NP--
organic Jurassic Green0 NP--
Ginkgo leaf 4:1 extract powder0 NP--
Milk Thistle seed extract powder0 NP--
wildcrafted Wild Yam0 NP--
wildcrafted Cramp Bark0 NP--
wildcrafted American Ginseng0 NP--

Other ingredients: plant-derived Capsule

Tap any ingredient to jump to its full detail below.

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

Directions: As a dietary supplement, take 2 capsules three times daily, or as directed by your health care professional.

Storage

Store in a cool dry place

General Statements

Proudly Made In The U.S.A.

450 mg each

Brand IP Statement(s)

2016 Wholistic Botanicals L.L.C. All Rights Reserved

John R. Christopher

FDA Statement of Identity

Dietary Supplement

Formulation

No Added Fillers or Chemicals

FDA Disclaimer Statement

This statement has not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent disease.

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

See for yourself

Liver Transition Formula by Christopher's Original Formulas label

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

Liver Transition Formula label

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

View the full label (PDF)
What’s inside

The Ingredients in Liver Transition Formula by Christopher's Original Formulas

These are the 11 active ingredients this product is made of. Select any to open its full monograph.

Serving size2 Capsule(s) Dosage formCapsule Servings per container50 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.

Other (inactive) ingredients: Plant-derived Capsule. These complete the product’s ingredient list but are not active constituents.

Interaction report

Liver Transition Formula by Christopher's Original Formulas Drug Interactions

Want to check YOUR meds against Liver Transition Formula?

Ask about interactions with your drugs in plain English — “Can I take it with lisinopril?” — and we find you the answer in seconds, ingredient by ingredient.

 Go to the checker
1,560Drugs
3 Major 1,551 Moderate 6 Minor

Ingredients driving the most interactions

Ginkgo leaf 4:1 extract powder 1,266
wildcrafted Oregon Grape 1,218
Milk Thistle seed extract powder 954
wildcrafted Schisandra 803
organic Dandelion 457

Individual Drug Interactions

The ingredients in Liver Transition Formula interact with 1,560 drugs. Click any drug to see the details.

8 of the 11 ingredients in Liver Transition Formula interact with drugs. Each result below shows which ingredient is responsible. Ginkgo leaf 4:1 extract powder wildcrafted Oregon Grape Milk Thistle seed extract powder wildcrafted Schisandra organic Dandelion organic Rosemary wildcrafted American Ginseng wildcrafted Wild Yam

Each ingredient & the kinds of drugs it affects

For each ingredient in Liver Transition Formula with known interactions, here are the types of medications they can affect. Open any type for the detail — or search your exact drug in the checker above.

Ginkgo leaf 4:1 extract powder23 drug types · 1,266 drugs

Talinolol

Taking ginkgo with talinolol seems to increase blood levels of talinolol.
There is some evidence that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of talinolol by 36% in healthy male individuals. However, single doses of ginkgo do not seem to affect talinolol pharmacokinetics.

Likelihood Probable Evidence B
Alprazolam (Xanax)

Theoretically, ginkgo might decrease the levels and clinical effects of alprazolam.
In clinical research, ginkgo extract (Ginkgold) 120 mg twice daily seems to decrease alprazolam levels by about 17%. However, ginkgo does not appear to decrease the elimination half-life of alprazolam. This suggests that ginkgo is more likely to decrease absorption of alprazolam rather than induce hepatic metabolism of alprazolam.

Likelihood Probable Evidence B
Anticoagulant/Antiplatelet Drugs

Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin. Theoretically, ginkgo might increase the risk of bleeding if used with other anticoagulant or antiplatelet drugs.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. However, population and clinical studies have produced mixed results. Some evidence shows that short-term use of ginkgo leaf does not significantly reduce platelet aggregation and blood clotting. A study in healthy males who took a specific ginkgo leaf extract (EGb 761) 160 mg twice daily for 7 days found no change in prothrombin time. An analysis of a large medical record database suggests that ginkgo increases the risk of a bleeding adverse event by 38% when taken concurrently with warfarin. It has been suggested that ginkgo has to be taken for at least 2-3 weeks to have a significant effect on platelet aggregation. However, a meta-analysis of 18 studies using standardized ginkgo extracts, 80-480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. In addition, a single dose of ginkgo plus clopidogrel or ticlopidine does not seem to significantly increase bleeding time or platelet aggregation. Also, taking ginkgo leaf extract daily for 8 days in conjunction with rivaroxaban does not affect anti-factor Xa activity; however, this study did not evaluate bleeding time.

Likelihood Possible Evidence A
Anticonvulsants

Theoretically, ginkgo might reduce the effectiveness of anticonvulsants.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking ginkgo with antidiabetes drugs might alter the response to antidiabetes drugs.
Ginkgo leaf extract seems to alter insulin secretion and metabolism, and might affect blood glucose levels in people with type 2 diabetes. The effect of ginkgo seems to differ depending on the insulin and treatment status of the patient. In diet-controlled diabetes patients with hyperinsulinemia, taking ginkgo does not seem to significantly affect insulin or blood glucose levels. In patients with hyperinsulinemia who are treated with oral hypoglycemic agents, taking ginkgo seems to decrease insulin levels and increase blood glucose following an oral glucose tolerance test. Researchers speculate that this could be due to ginkgo-enhanced hepatic metabolism of insulin. In patients with pancreatic exhaustion, taking ginkgo seems to stimulate pancreatic beta-cells, resulting in increased insulin and C-peptide levels, but with no significant change in blood glucose levels in response to an oral glucose tolerance test.

Likelihood Possible Evidence B
Atorvastatin (Lipitor)

Theoretically, ginkgo might decrease the levels and clinical effects of atorvastatin.
In humans, intake of ginkgo extract appears to increase atorvastatin clearance, reducing the area under the curve of atorvastatin by 10% to 14% and the maximum concentration by 29%. However, this interaction does not appear to affect cholesterol synthesis and absorption. Further, a model in rats with hyperlipidemia suggests that administering ginkgo extract does not impact blood levels of atorvastatin and leads to lower total cholesterol, low-density lipoprotein cholesterol, and triglycerides when compared with rats given atorvastatin alone.

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

Theoretically, ginkgo might increase levels of drugs metabolized by CYP1A2.
Laboratory research suggests that ginkgo leaf extract can mildly inhibit CYP1A2 enzymes. However, clinical research suggests ginkgo might not affect CYP1A2. Until more is known, use ginkgo cautiously in patients taking drugs metabolized by these enzymes.

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

Theoretically, ginkgo might decrease levels of drugs metabolized by CYP2C19.
Some clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce CYP2C19 enzymes and potentially decrease levels of drugs metabolized by these enzymes. However, other clinical research shows that taking ginkgo 120 mg twice daily for 12 days has no effect on levels of drugs metabolized by CYP2C19.

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

Theoretically, ginkgo might increase levels of drugs metabolized by CYP2C9.
In vitro, a specific standardized extract of ginkgo leaf (EGb 761) inhibits CYP2C9 activity . The terpenoid (ginkgolides) and flavonoid (quercetin, kaempferol, etc.) constituents seem to be responsible for this effect. Most ginkgo extracts contain some amount of these constituents. Therefore, other ginkgo leaf extracts might also inhibit the CYP2C9 enzyme. However, clinical research suggests that ginkgo might not have a significant effect on CYP2C9 in humans. Ginkgo does not seem to significantly affect the pharmacokinetics of CYP2C9 substrates diclofenac or tolbutamide.

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

Theoretically, ginkgo might decrease levels of drugs metabolized by CYP3A4.
There is conflicting evidence about whether ginkgo induces or inhibits CYP3A4. Ginkgo does not appear to affect hepatic CYP3A4. However, it is not known if ginkgo affects intestinal CYP3A4. Preliminary clinical research suggests that taking ginkgo does not significantly affect levels of donepezil, lopinavir, or ritonavir, which are all CYP3A4 substrates. Other clinical research also suggests ginkgo does not significantly affect CYP3A4 activity. However, there are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4).

Likelihood Possible Evidence B
Efavirenz (Sustiva)

Theoretically, ginkgo might decrease the levels and clinical effects of efavirenz.
There are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. In one case, an HIV-positive male experienced over a 50% decrease in efavirenz levels over the course of 14 months while taking ginkgo extract. HIV-1 RNA copies also increased substantially, from less than 50 to more than 1500. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4). In another case report, a patient stable on antiviral therapy including efavirenz for 10 years, had an increase in viral load from <50 copies/mL to 1350 copies/mL after 2 months of taking a combination of supplements including ginkgo. After stopping ginkgo, the viral load was again controlled with the same antiviral therapy regimen.

Likelihood Possible Evidence D
Ibuprofen (Advil, Others)

Theoretically, ginkgo might increase the risk of bleeding when used with ibuprofen.
Ginkgo might have antiplatelet effects and has been associated with several case reports of spontaneous bleeding. In one case, a 71-year-old male had taken a specific ginkgo extract (Gingium, Biocur) 40 mg twice daily for 2.5 years. About 4 weeks after starting ibuprofen 600 mg daily he experienced a fatal intracerebral hemorrhage. However, the antiplatelet effects of ginkgo have been questioned. A meta-analysis and other studies have not found a significant antiplatelet effect with standardized ginkgo extracts, 80 mg to 480 mg taken daily for up to 32 weeks.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, taking ginkgo with P-glycoprotein substrates might increase the levels and adverse effects of these substrates.
A small clinical study in healthy volunteers shows that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of the P-glycoprotein substrate, talinolol, by 36% in healthy male individuals. However, single doses of ginkgo do not have the same effect.

Likelihood Possible Evidence B
Risperidone (Risperdal)

Theoretically, taking ginkgo with risperidone might increase the levels and adverse effects of risperidone.
A single case of priapism has been reported for a 26-year-old male with schizophrenia who used risperidone 3 mg daily along with ginkgo extract 160 mg daily. Risperidone is metabolized by cytochrome P450 (CYP) 2D6 and CYP3A4. CYP3A4 activity might be affected by ginkgo. Theoretically, ginkgo may inhibit the metabolism of risperidone and increase the risk of adverse effects.

Likelihood Possible Evidence D
Rosiglitazone (Avandia)

Theoretically, ginkgo might decrease the levels and clinical effects of rosiglitazone.
Animal research shows that ginkgo leaf extract orally 100 or 200 mg/kg daily for 10 days alters the pharmacodynamics of rosiglitazone in a dose-dependent manner. The 100 mg/kg and 200 mg/kg doses reduce the area under the concentration time curve (AUC) of rosiglitazone by 39% and 52%, respectively, and the half-life by 28% and 39%, respectively. It is hypothesized that these changes may be due to induction of cytochrome P450 2C8 by ginkgo.

Likelihood Possible Evidence D
Seizure Threshold Lowering Drugs

Theoretically, taking ginkgo with drugs that lower the seizure threshold might increase the risk for convulsions.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.

Likelihood Possible Evidence D
Simvastatin (Zocor)

Theoretically, ginkgo might decrease the levels and clinical effects of simvastatin.
Clinical research shows that taking ginkgo extract can reduce the area under the curve and maximum concentration of simvastatin by 32% to 39%. However, ginkgo extract does not seem to affect the cholesterol-lowering ability of simvastatin.

Likelihood Probable Evidence B
Sofosbuvir (Sovaldi)

Theoretically, ginkgo might increase the levels and clinical effects of sofosbuvir.
Animal research in rats shows that giving a ginkgo extract 25 mg/kg orally daily for 14 days increases the area under the concentration time curve (AUC) after a single sofosbuvir dose of 40 mg/kg by 11%, increases the half-life by 60%, and increases the plasma concentration at 4 hours by 38%. This interaction appears to be related to the inhibition of intestinal P-glycoprotein by ginkgo.

Likelihood Possible Evidence D
Tacrolimus (Prograf)

Theoretically, ginkgo might increase the blood levels of tacrolimus.
In vitro evidence suggests that certain biflavonoids in ginkgo leaves (i.e. amentoflavone, ginkgetin, bilobetin) may inhibit the metabolism of tacrolimus by up to 50%. This interaction appears to be time-dependent and due to inhibition of cytochrome P450 (CYP) 3A4 by these bioflavonoids. In rats given tacrolimus 1 mg/kg orally, amentoflavone was shown to increase the area under the concentration time curve (AUC) of tacrolimus by 3.8-fold.

Likelihood Possible Evidence D
Trazodone (Desyrel)

Theoretically, ginkgo might increase the levels and clinical effects of trazodone.
In a case report, an Alzheimer patient taking trazodone 20 mg twice daily and ginkgo leaf extract 80 mg twice daily for four doses became comatose. The coma was reversed by administration of flumazenil (Romazicon). Coma might have been induced by excessive GABA-ergic activity. Ginkgo flavonoids are thought to have GABA-ergic activity and act directly on benzodiazepine receptors. Ginkgo might also increase metabolism of trazodone to active GABA-ergic metabolites, possibly by inducing cytochrome P450 3A4 (CYP3A4) metabolism.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. Information from a medical database suggests that when taken concurrently with warfarin, ginkgo increases the risk of a bleeding adverse event by 38%. There is also some evidence that ginkgo leaf extract can inhibit cytochrome P450 2C9, an enzyme that metabolizes warfarin. This could result in increased warfarin levels. However, population and clinical research has produced mixed results. Clinical research in healthy people suggests that ginkgo has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. A meta-analysis of 18 studies using standardized ginkgo extracts, 80 mg to 480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. There is also some preliminary clinical research that suggests ginkgo might not significantly increase the effects of warfarin in patients that have a stable INR.

Likelihood Possible Evidence B
Nifedipine (Procardia)

Theoretically, taking ginkgo with oral, but not intravenous, nifedipine might increase levels and adverse effects of nifedipine.
Animal research and some clinical evidence suggests that taking ginkgo leaf extract orally in combination with oral nifedipine might increase nifedipine levels and cause increased side effects, such as headaches, dizziness, and hot flushes. However, taking ginkgo orally does not seem to affect the pharmacokinetics of intravenous nifedipine.

Likelihood Possible Evidence B
Omeprazole (Prilosec)

Theoretically, taking ginkgo with omeprazole might decrease the levels and clinical effects of omeprazole.
Clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce cytochrome P450 (CYP) 2C19 enzymes and decrease levels of omeprazole by about 27% to 42%.

Likelihood Possible Evidence B
Ginkgo leaf 4:1 extract powder full monograph & interactions

wildcrafted Oregon Grape9 drug types · 1,218 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, Oregon grape might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
In vitro and in vivo research suggests that berberine, a constituent of Oregon grape, can inhibit platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, Oregon grape might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Clinical research suggests that berberine, a constituent of Oregon grape, can lower blood glucose levels.

Likelihood Possible Evidence A
Antihypertensive Drugs

Theoretically, Oregon grape might increase the risk of hypotension when taken with antihypertensive drugs.
Animal research suggests that berberine, a constituent of Oregon grape, can have hypotensive effects. Also, an analysis of clinical evidence suggests that taking berberine in combination with amlodipine (Norvasc) can lower systolic and diastolic blood pressure when compared with taking amlodipine alone.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, Oregon grape might increase the sedative effects of CNS depressants.
Animal research suggests that berberine, a constituent of Oregon grape, can have sedative effects.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, Oregon grape might increase the effects and adverse effects of cyclosporine.
Berberine, a constituent of Oregon grape, can reduce metabolism of cyclosporine and increase serum levels. It might inhibit cytochrome P450 3A4 (CYP3A4), which metabolizes cyclosporine.

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

Theoretically, Oregon grape might increase serum levels of drugs metabolized by CYP2C9.
Preliminary clinical evidence suggests that berberine, a constituent of Oregon grape, can inhibit cytochrome P450 2C9 (CYP2C9).

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

Theoretically, Oregon grape might increase serum levels of drugs metabolized by CYP2D6.
In vitro research and preliminary clinical evidence suggest that berberine, a constituent of Oregon grape, can inhibit cytochrome P450 2D6 (CYP2D6).

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

Theoretically, Oregon grape might increase serum levels of drugs metabolized by CYP3A4.
In vitro research and preliminary clinical evidence suggest that berberine, a constituent of Oregon grape, moderately inhibits cytochrome P450 3A4 (CYP3A4).

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, Oregon grape might increase serum levels of drugs that are P-glycoprotein (P-gp) substrates.
In vitro research suggests that Oregon grape extracts inhibit P-gp efflux.

Likelihood Possible Evidence D
wildcrafted Oregon Grape full monograph & interactions

Milk Thistle seed extract powder17 drug types · 954 drugs

Antidiabetes Drugs

Taking milk thistle with antidiabetes drugs may increase the risk of hypoglycemia.
Clinical research shows that milk thistle extract, alone or along with tree turmeric extract, can lower blood glucose levels and glycated hemoglobin (HbA1c) in patients with type 2 diabetes, including those already taking antidiabetes drugs. Additionally, animal research shows that milk thistle extract increases the metformin maximum plasma concentration and area under the curve and decreases the renal clearance of metformin, due to inhibition of the multi-drug and toxin extrusion protein 1 (MATE1) renal tubular transport protein.

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

Theoretically, milk thistle might inhibit CYP2B6.
An in vitro study shows that silybin, a constituent of milk thistle, binds to and noncompetitively inhibits CYP2B6. Additionally, silybin might downregulate the expression of CYP2B6 by decreasing mRNA and protein levels.

Likelihood Possible Evidence D
Glucuronidated Drugs

Theoretically, milk thistle might affect the clearance of drugs that undergo glucuronidation.
Laboratory research shows that milk thistle constituents inhibit uridine diphosphoglucuronosyl transferase (UGT), the major phase 2 enzyme that is responsible for glucuronidation. Theoretically, this could decrease the clearance and increase levels of glucuronidated drugs. Other laboratory research suggests that a milk thistle extract of silymarin might inhibit beta-glucuronidase, although the significance of this effect is unclear.

Likelihood Possible Evidence D
Ledipasvir

Theoretically, milk thistle might increase the levels and clinical effects of ledipasvir.
Animal research in rats shows that milk thistle increases the area under the curve (AUC) for ledipasvir and slows its elimination.

Likelihood Possible Evidence D
Morphine

Theoretically, concomitant use of milk thistle with morphine might affect serum levels of morphine and either increase or decrease its effects.
Animal research shows that milk thistle reduces serum levels of morphine by up to 66%. In contrast, laboratory research shows that milk thistle constituents inhibit uridine diphosphoglucuronosyl transferase (UGT), the major phase 2 enzyme that is responsible for glucuronidation. Theoretically, this could decrease the clearance and increase morphine levels. The effect of taking milk thistle on morphine metabolism in humans is not known.

Likelihood Possible Evidence D
Raloxifene (Evista)

Theoretically, milk thistle might decrease the clearance and increase levels of raloxifene.
Laboratory research suggests that the milk thistle constituents silibinin and silymarin inhibit the glucuronidation of raloxifene in the intestines.

Likelihood Possible Evidence D
Sirolimus (Rapamune)

Milk thistle might decrease the clearance of sirolimus.
Pharmacokinetic research shows that a milk thistle extract of silymarin decreases the apparent clearance of sirolimus in hepatically impaired renal transplant patients. It is unclear if this interaction occurs in patients without hepatic impairment.

Likelihood Possible Evidence B
Sofosbuvir (Solvaldi)

Theoretically, milk thistle might decrease the levels and clinical effects of sofosbuvir.
Animal research in rats shows that milk thistle reduces the metabolism of sofosbuvir, as well as the hepatic uptake of its active metabolite.

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

Theoretically, the milk thistle constituent silibinin might increase tamoxifen levels and interfere with its conversion to an active metabolite.
Animal research suggests that the milk thistle constituent silibinin might increase plasma levels of tamoxifen and alter its conversion to an active metabolite. The mechanism appears to involve inhibition of pre-systemic metabolism of tamoxifen by cytochrome P450 (CYP) 2C9 and CYP3A4, and inhibition of P-glycoprotein-mediated efflux of tamoxifen into the intestine for excretion. Whether this interaction occurs in humans is not known.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, milk thistle might increase the effects of warfarin.
In one case report, a man stabilized on warfarin experienced an increase in INR from 2.64 to 4.12 after taking a combination product containing milk thistle 200 mg daily, as well as dandelion, wild yam, niacinamide, and vitamin B12. Levels returned to normal after stopping the supplement. Although a direct correlation between milk thistle and the change in INR cannot be confirmed, some in vitro research suggests that milk thistle might inhibit cytochrome P450 2C9 (CYP2C9), an enzyme involved in the metabolism of various drugs, including warfarin.

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

It is unclear if milk thistle inhibits CYP2C9; research is conflicting.
In vitro research suggests that milk thistle might inhibit CYP2C9. Additionally, 3 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking milk thistle and cancer medications that are CYP2C9 substrates, including imatinib and capecitabine. However, contradictory clinical research shows that milk thistle extract does not inhibit CYP2C9 or significantly affect levels of the CYP2C9 substrate tolbutamide. Differences in results could be due to differences in dosages or formulations utilized.

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

It is unclear if milk thistle inhibits CYP3A4; research is conflicting.
While laboratory research shows conflicting results, pharmacokinetic research shows that taking milk thistle extract 420-1350 mg daily does not significantly affect the metabolism of the CYP3A4 substrates irinotecan, midazolam, or indinavir. However, 8 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking milk thistle and cancer medications that are CYP3A4 substrates, including gefitinib, sorafenib, doxorubicin, and vincristine.

Likelihood Unlikely Evidence D
Estrogens

Theoretically, milk thistle might interfere with estrogen therapy through competition for estrogen receptors.
Animal research suggests that a milk thistle extract of silymarin binds to estrogen receptor beta.

Likelihood Possible Evidence D
Hmg-Coa Reductase Inhibitors ("Statins")

Theoretically, milk thistle might interfere with statin therapy by decreasing the activity of organic anion transporting polypeptide 1B1 (OATB1B1) and inhibiting breast cancer resistance protein (BCRP).
Preliminary evidence suggests that a milk thistle extract of silymarin can decrease the activity of the OATP1B1, which transports HMG-CoA reductase inhibitors into the liver to their site of action, and animal research shows this increases the maximum plasma concentration of pitavastatin and pravastatin. The silibinin component also inhibits BCRP, which transports statins from the liver into the bile for excretion. However, in a preliminary study in healthy males, silymarin 140 mg three times daily had no effect on the pharmacokinetics of a single 10 mg dose of rosuvastatin.

Likelihood Unlikely Evidence D
Indinavir (Crixivan)

Theoretically, milk thistle may induce cytochrome P450 3A4 (CYP3A4) enzymes and increase the metabolism of indinavir; however, results are conflicting.
One pharmacokinetic study shows that taking milk thistle (Standardized Milk Thistle, General Nutrition Corp.) 175 mg three times daily in combination with multiple doses of indinavir 800 mg every 8 hours decreases the mean trough levels of indinavir by 25%. However, results from the same pharmacokinetic study show that milk thistle does not affect the overall exposure to indinavir. Furthermore, two other pharmacokinetic studies show that taking specific milk thistle extract (Legalon, Rottapharm Madaus; Thisilyn, Nature's Way) 160-450 mg every 8 hours in combination with multiple doses of indinavir 800 mg every 8 hours does not reduce levels of indinavir.

Likelihood Unlikely Evidence B
Organic Anion-Transporting Polypeptide Substrates (Oatp)

Milk thistle may inhibit one form of OATP, OATP-B1, which could reduce the bioavailability and clinical effects of OATP-B1 substrates.
In vitro research shows that milk thistle inhibits OATP-B1. Two case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking milk thistle and cancer medications that are OATP substrates, including sorafenib and methotrexate. OATPs are expressed in the small intestine and liver and are responsible for the uptake of drugs and other compounds into the body. Inhibition of OATP may reduce the bioavailability of oral drugs that are substrates of OATP.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, milk thistle might increase the absorption of P-glycoprotein substrates. However, this effect does not seem to be clinically significant.
In vitro research shows that milk thistle can inhibit P-glycoprotein activity and 1 case report from the World Health Organization (WHO) adverse drug reaction database describes increased abdominal pain in a patient taking milk thistle and the cancer medication vincristine, a P-glycoprotein substrate, though this patient was also taking methotrexate. However, a small pharmacokinetic study in healthy volunteers shows that taking milk thistle (Enzymatic Therapy Inc.) 900 mg, standardized to 80% silymarin, in 3 divided doses daily for 14 days does not affect absorption of digoxin, a P-glycoprotein substrate.

Likelihood Unlikely Evidence B
Milk Thistle seed extract powder full monograph & interactions

wildcrafted Schisandra12 drug types · 803 drugs

Cyclophosphamide

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

Likelihood Probable Evidence D
Cyclosporine (Neoral, Sandimmune)

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

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

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

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

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

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

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

Likelihood Probable Evidence D
Midazolam (Versed)

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

Likelihood Probable Evidence B
P-Glycoprotein Substrates

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

Likelihood Possible Evidence D
Sirolimus (Rapamune)

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

Likelihood Probable Evidence B
Tacrolimus (Prograf)

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

Likelihood Probable Evidence B
Talinolol

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

Likelihood Probable Evidence B
Voriconazole (Vfend)

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

Likelihood Possible Evidence D
Warfarin (Coumadin)

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

Likelihood Possible Evidence D
wildcrafted Schisandra full monograph & interactions

organic Dandelion7 drug types · 457 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, taking dandelion root along with anticoagulant or antiplatelet drugs might increase the risk of bruising and bleeding.
In vitro research suggests that dandelion root inhibits platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, dandelion might increase the risk for hypoglycemia when used with antidiabetes drugs.
Laboratory research suggests that dandelion extract may have moderate alpha-glucosidase inhibitor activity and might also increase insulin secretion. Also, in a case report, a 58-year-old woman with type 2 diabetes who was being treated with insulin developed hypoglycemia 2 weeks after beginning to eat salads containing dandelion.

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

Theoretically, dandelion might increase levels of drugs metabolized by CYP1A2.
Laboratory research suggests that dandelion might inhibit CYP1A2. So far, this interaction has not been reported in humans. However, until more is known, watch for an increase in the levels of drugs metabolized by CYP1A2 in patients taking dandelion.

Likelihood Possible Evidence D
Glucuronidated Drugs

Theoretically, dandelion might increase the clearance of drugs that are UDP-glucuronosyltransferase substrates.
There is some preliminary evidence that dandelion might induce UDP-glucuronosyltransferase, a phase II enzyme.

Likelihood Possible Evidence D
Lithium

Theoretically, through diuretic effects, dandelion might reduce excretion and increase levels of lithium.
Animal research suggests that dandelion has diuretic properties. As diuretics can increase serum lithium levels, the dose of lithium might need to be decreased when taken with dandelion.

Likelihood Probable Evidence D
Potassium-Sparing Diuretics

Theoretically, dandelion might increase the risk of hyperkalemia when taken with potassium-sparing diuretics.
Dandelion contains significant amounts of potassium.

Likelihood Possible Evidence D
Quinolone Antibiotics

Theoretically, dandelion might lower fluoroquinolone levels.
Animal research shows that dandelion reduces absorption of ciprofloxacin and can lower levels by 73%. However, this effect has not been reported in humans.

Likelihood Possible Evidence D
organic Dandelion full monograph & interactions

organic Rosemary6 drug types · 372 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, rosemary may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro and animal research suggests that rosemary inhibits platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking rosemary with antidiabetes drugs might increase the risk of hypoglycemia.
Animal research shows that rosemary extract can decrease blood glucose levels in diabetic models. However, research in humans is conflicting. Although rosemary powder decreased blood glucose levels in healthy adults, no change in blood glucose levels was seen in adults with type 2 diabetes, most of whom were taking antidiabetes drugs.

Likelihood Possible Evidence B
Aspirin

Theoretically, rosemary might have additive effects with salicylate-containing drugs such as aspirin.
Rosemary is reported to contain salicylates.

Likelihood Possible Evidence D
Choline Magnesium Trisalicylate (Trilisate)

Theoretically, rosemary might have additive effects with salicylate-containing drugs such as choline magnesium trisalicylate.
Rosemary is reported to contain salicylate.

Likelihood Possible Evidence D
Salsalate (Disalcid)

Theoretically, rosemary might have additive effects with salicylate-containing drugs such as salsalate.
Rosemary is reported to contain salicylate.

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

Theoretically, rosemary might decrease the levels and clinical effects of CYP1A2 substrates.
In vitro research shows that rosemary induces CYP1A2 enzymes. This effect has not been reported in humans.

Likelihood Unlikely Evidence D
organic Rosemary full monograph & interactions

wildcrafted American Ginseng4 drug types · 217 drugs

Warfarin (Coumadin)

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

Likelihood Likely Evidence B
Antidiabetes Drugs

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

Likelihood Probable Evidence B
Immunosuppressants

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

Likelihood Possible Evidence D
Monoamine Oxidase Inhibitors (Maois)

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

Likelihood Possible Evidence D
wildcrafted American Ginseng full monograph & interactions

wildcrafted Wild Yam1 drug type · 41 drugs

Estrogens

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

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

Brand information

Manufacturer and brand details for Liver Transition Formula, from the product label.

Christopher's Original Formulas

See all Christopher's Original Formulas products
Name
Wholistic Botanicals L.L.C.
City
Spanish Fork
State
UT
ZipCode
84660
Phone Number
1-800-453-1406
Web Address
www.drchristopher.com
Pharmacist Counseling Corner

Liver Transition Formula by Christopher's Original Formulas: Common Questions

Does Liver Transition Formula by Christopher's Original Formulas interact with any medications?
Yes. Based on its ingredients, Liver Transition Formula has a known interaction with 1,560 medications, including 3 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Liver Transition Formula contains 11 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.
Can I take this if I'm pregnant or breastfeeding?
Several herbs in this formula—Oregon grape, schisandra, ginkgo, and wild yam—are flagged as possibly or likely unsafe during pregnancy or breastfeeding based on available safety data. Dandelion, rosemary, milk thistle, and cramp bark have insufficient safety information. Talk with your doctor or pharmacist about whether this formula is right for you.
Will this help my liver?
The evidence in our data shows milk thistle is possibly effective for diabetes and ginkgo is possibly effective for several conditions, but for most of the other herbs—including dandelion, schisandra, wild yam, and cramp bark—the evidence isn't established. Your doctor can advise whether this formula fits your specific needs.
What side effects might I experience?
Common side effects from dandelion include diarrhea, heartburn, and stomach discomfort. Ginkgo may cause dizziness and gastrointestinal symptoms. Milk thistle may cause bloating, diarrhea, nausea, and gas. Rosemary in high amounts or as an oil could theoretically cause seizures. Rare but serious reactions like anaphylaxis have been reported with dandelion, wild yam, and milk thistle in sensitive people.
Is this safe if I'm allergic to ragweed?
Dandelion is a member of the ragweed family (Asteraceae), so if you're sensitive to ragweed, chrysanthemums, or daisies, you should avoid this formula—allergic reactions including anaphylaxis have been reported.
Can I use this with my blood pressure or cholesterol medication?
Ginkgo in this formula may lower levels of simvastatin (a cholesterol drug) and has a documented interaction with the blood pressure drug talinolol. Other ingredients also interact with blood pressure and heart medications. Check each of your medications with the tool on this page or ask your pharmacist before starting.
What's Jurassic Green?
Jurassic Green is included in this formula, but we have no interaction data on file for it, so we cannot tell you how it might interact with your medications.

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

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Liver Transition Formula label
Go deeper

The Full Monographs Behind Liver Transition Formula’s Ingredients

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

Herb & supplement monograph

Dandelion

Interacts with 457 drugs

Dandelion is a common plant used in food and traditional medicine, often promoted as a natural 'water pill' and digestive aid. Human evidence for these uses is very limited, so its benefits...

Read the full Dandelion monograph → Herb & supplement monograph

Oregon Grape

Interacts with 1,218 drugs

Oregon grape is a shrub whose root contains berberine and related compounds. The strongest (though still modest) evidence is for topical creams that may slightly ease psoriasis; evidence for...

Read the full Oregon Grape monograph → Herb & supplement monograph

Rosemary

Interacts with 372 drugs

Rosemary is a fragrant Mediterranean herb that is safe and flavorful in normal food amounts. Some early research suggests possible benefits for memory, mood, and hair growth, but the evidenc...

Read the full Rosemary monograph → Herb & supplement monograph

Schisandra

Interacts with 803 drugs

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

Read the full Schisandra monograph → Herb & supplement monograph

Ginkgo

Interacts with 1,266 drugs

Ginkgo is one of the world's most popular herbal supplements, mostly taken to support memory and circulation. The evidence for these uses is mixed and generally weak, and it is not proven to...

Read the full Ginkgo monograph → Herb & supplement monograph

Milk Thistle

Interacts with 954 drugs

Milk thistle is a popular herbal supplement most often used for liver health, and its main active component is a group of compounds called silymarin. While it is generally well tolerated, th...

Read the full Milk Thistle monograph → Herb & supplement monograph

Wild Yam

Interacts with 41 drugs

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

Read the full Wild Yam monograph → Herb & supplement monograph

Cramp Bark

Cramp Bark is the dried bark of Viburnum opulus, traditionally used to ease muscle and menstrual cramps. Modern, high-quality human studies are very limited, so its effectiveness is not well...

Read the full Cramp Bark monograph → Herb & supplement monograph

American Ginseng

Interacts with 217 drugs

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

Read the full American Ginseng monograph →
Sources

Sources & How We Checked

Liver Transition Formula's label data comes from the NIH Dietary Supplement Label Database; the ingredient interaction data is from the Natural Medicines database, reviewed by our pharmacists.

Content is written and reviewed by licensed HelloPharmacist pharmacists. See our data sources and editorial standards for how this information is built and checked.

The 279 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.

Dandelion 27 references
  1. Maliakal PP, Wanwimolruk S. Effect of herbal teas on hepatic drug metabolizing enzymes in rats. J Pharm Pharmacol 2001;53:1323-9. PubMed
  2. Williams CA, Goldstone F, Greenham J. Flavonoids, cinnamic acids and coumarins from the different tissues and medicinal preparations of Taraxacum officinale. Phytochemistry 1996;42:121-7. PubMed
  3. Hussain Z, Waheed A, Qureshi RA, et al. The effect of medicinal plants of Islamabad and Murree region of Pakistan on insulin secretion from INS-1 cells. Phytother Res 2004;18:73-7. PubMed
  4. Racz-Kotilla E, Racz G, Solomon A. The action of Taraxacum officinale extracts on the body weight and diuresis of laboratory animals. Planta Med 1974;26:212-7. PubMed
  5. Zhu M, Wong PY, Li RC. Effects of taraxacum mongolicum on the bioavailability and disposition of ciprofloxacin in rats. J Pharm Sci 1999;88:632-4. PubMed
  6. Jovanovic M, Mimica-Dukic N, Poljacki M, Boza P. Erythema multiforme due to contact with weeds: a recurrence after patch testing. Contact Dermatitis 2003;48:17-25. PubMed
  7. Chivato T, Juan F, Montoro A, Laguna R. Anaphylaxis induced by ingestion of a pollen compound. J Investig Allergol Clin Immunol 1996;6:208-9.
  8. Cohen SH, Yunginger JW, Rosenberg N, Fink JN. Acute allergic reaction after composite pollen ingestion. J Allergy Clin Immunol 1979;64:270-4. PubMed
  9. Lovell CR, Rowan M. Dandelion dermatitis. Contact Dermatitis 1991;25:185-8. PubMed
  10. Agarwal SC, Crook JR, Pepper CB. Herbal remedies -- how safe are they? A case report of polymorphic ventricular tachycardia/ventricular fibrillation induced by herbal medication used for obesity. Int J Cardiol 2006;106:260-1. PubMed
  11. Martín-Muñoz MF, Bartolome B, Caminoa M, et al. Bee pollen: a dangerous food for allergic children. Identification of responsible allergens. Allergol Immunopathol (Madr) 2010;38:263-5. PubMed
  12. Neef H, Cilli F, Declerck PJ, et al. Platelet anti-aggregating activity of Taraxacum officinale Weber. Phytotherapy Research 1996;10:s138-s140.
  13. Cuzzolin L, Zaffani S, and Benoni G. Safety implications regarding use of phytomedicines. Eur.J Clin Pharmacol. 2006;62:37-42. PubMed
  14. Posadzki, P., Watson, L. K., and Ernst, E. Adverse effects of herbal medicines: an overview of systematic reviews. Clin Med 2013;13(1):7-12. PubMed
  15. Wakelin, S. H., Marren, P., Young, E., and Shaw, S. Compositae sensitivity and chronic hand dermatitis in a seven-year-old boy. Br J Dermatol 1997;137(2):289-291. PubMed
  16. Ingber, A. Seasonal allergic contact dermatitis from Taraxacum officinale (dandelion) in an Israeli florist. Contact Dermatitis 2000;43(1):49.
  17. Rodriguez, B., Rodriguez, A., de Barrio, M., Tornero, P., and Baeza, M. L. Asthma induced by canary food mix. Allergy Asthma Proc. 2003;24(4):265-268.
  18. Syhaieva, I. A. [Efficiency of specific immunotherapy in treatment of patients with seasonal allergic rhinitis]. Lik.Sprava. 2006;(1-2):51-53.
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  8. Yuan CS, Wei G, Dey L, et al. American ginseng reduces warfarin's effect in healthy patients: a randomized, controlled trial. Ann Intern Med 2004;141:23-7.
  9. Predy GN, Goel V, Lovlin R, et al. Efficacy of an extract of North American ginseng containing poly-furanosyl-pyranosyl-saccharides for preventing upper respiratory tract infections: a randomized controlled trial. CMAJ 2005;173:1043-8.. PubMed
  10. McElhaney JE, Goel V, Toane B, et al. Efficacy of COLD-fX in the prevention of respiratory symptoms in community-dwelling adults: a randomized, double-blinded, placebo controlled trial. J Altern Complement Med 2006;12:153-7. PubMed
  11. Predy GN, Goel V, Lovlin RE, et al. Immune modulating effects of daily supplementation of COLD-fX (a proprietary extract of North American ginseng) in healthy adults. J Clin Biochem Nutr 2006;39:162-167. DOI
  12. Stavro PM, Woo M, Leiter LA, et al. Long-term intake of North American ginseng has no effect on 24-hour blood pressure and renal function. Hypertension 2006;47(4):791-6. PubMed

See these in context on the American Ginseng monograph →

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

© 2021 Therapeutic Research Center, LLC

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