Major interaction on record — check this product against your medications before combining. Based on 10 of 14 ingredients. Check your meds →
Dietary supplement

Diet Detox Ingredients & Drug Interactions

by GNC BodyDynamix

Diet Detox label
See full label image
Other (e.g. Tea Bag) Category: Other Combinations
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 16, 2026 · Label data from the NIH DSLD
What is this page for?

First and foremost: checking Diet Detox 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

Diet Detox is a dietary supplement by GNC BodyDynamix with 14 active ingredients. Its ingredients are commonly taken for thinning mucus in lung conditions, acetaminophen (tylenol) overdose treatment, antioxidant and glutathione support.Based on those ingredients, 1,620 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Goldenseal Root Extract, Turmeric root extract, Milk Thistle seed extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

Jump to a section

Check Your Meds Against Diet Detox by GNC BodyDynamix

Ask about any prescription or over-the-counter medication and we check it for interactions with Diet Detox by GNC BodyDynamix — and tell you which ingredient is responsible.

Pharmacist-reviewed data Checks every ingredient Answer in seconds
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HelloPharmacist Scorecard of Diet Detox by GNC BodyDynamix

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

From our pharmacy team — supplement deep dive

Generated from HelloPharmacist’s pharmacist-curated databases and editorial rules · Last generated Jul 30, 2026

What’s inside

Full disclosure
Ingredient Transparency · database check
Full

Every active ingredient lists its own amount on the label.

Why this rating?
  • The label discloses an exact amount for 14 of its 14 active ingredients.
  • No proprietary blends here — you can verify the dose of every single component.

Diet Detox contains 14 active ingredients. The main ones are N-acetyl cysteine (a compound your body uses to make and recycle protective molecules), magnesium (a mineral involved in muscle and nerve function), theanine (an amino acid from tea), turmeric root extract (a traditional anti-inflammatory spice), potassium (an electrolyte for heart rhythm and muscle), cranberry fruit extract (long used for urinary tract health), goldenseal root extract (a traditional antimicrobial herb), picrorhiza (an herb used in Ayurvedic medicine), calcium (for bone and cell signaling), and milk thistle seed extract (traditionally used for liver support).

The product also contains several inactive ingredients—fillers, binders, and capsule materials—listed as hydroxypropylcellulose, microcrystalline cellulose, magnesium stearate, silicon dioxide, and others.

Does it work?

Strong 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

This product doesn't appear to be marketed for a specific use, so we graded its ingredients' overall clinical evidence instead.

Strong

Strong clinical evidence supports its ingredients for:

Why this rating?
  • We looked at the product name, claims, and label statements and couldn't find a stated purpose to grade.
  • Since the label doesn't commit to one use, we graded the ingredients' overall clinical evidence instead.
  • On file: Acetaminophen poisoning — rated "Effective" (N-acetyl Cysteine (nac)) (Natural Medicines).
  • On file: Atelectasis — rated "Effective" (N-acetyl Cysteine (nac)) (Natural Medicines).
  • On file: Constipation — rated "Effective" (Magnesium) (Natural Medicines).
  • On file: Dyspepsia — rated "Effective" (Calcium) (Natural Medicines).
  • On file: Hypocalcemia — rated "Effective" (Calcium) (Natural Medicines).

The evidence for this product's ingredients is mixed. N-acetyl cysteine is effective for acetaminophen poisoning and certain respiratory conditions, and possibly effective for bronchitis.

Magnesium is effective for indigestion, constipation, and the mineral deficiency it treats, and possibly effective for preventing complications in pregnancy. Theanine shows possibly effective evidence for cognitive function, but insufficient evidence exists for anxiety, cognitive decline, or Alzheimer's disease.

Turmeric is possibly effective for depression, high cholesterol, and hay fever symptoms, as well as indigestion. Cranberry shows possibly effective evidence for urinary tract infections, but insufficient evidence for cognitive decline, enlarged prostate, cancer, or fatigue.

For goldenseal, picrorhiza, and several other ingredients in this product, the evidence is either limited to insufficient or doesn't establish effectiveness for the conditions they're marketed for. Overall, if your goal is detoxification in the clinical sense, the evidence doesn't support that claim for most of these ingredients together.

The evidence, ingredient by ingredient N-acetyl Cysteine (nac) Magnesium Theanine Turmeric Potassium Cranberry Goldenseal Picrorhiza

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 10 of the 10 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 10 of 10.
  • General safety write-ups exist for 10 of 10.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Most ingredients in this product are generally well tolerated at typical doses. N-acetyl cysteine can cause diarrhea, nausea, dry mouth, and heartburn orally; intravenous use carries a higher risk of blood-clotting changes and skin rash.

Magnesium may cause diarrhea and gastrointestinal upset. Theanine may cause headaches, drowsiness, or changes in sleep.

Turmeric is associated with gastrointestinal complaints and, rarely, liver damage after weeks to months of use. Potassium can cause nausea, vomiting, and abdominal pain; dangerously high levels cause heart rhythm problems.

Cranberry can cause diarrhea and gastrointestinal discomfort, especially at very high doses. Goldenseal carries limited safety data from short-term use.

Picrorhiza may cause vomiting, rash, loss of appetite, diarrhea, itching, and dizziness. Calcium is well tolerated at recommended doses but may cause constipation or stomach upset.

Milk thistle typically causes mild gastrointestinal symptoms but is generally well tolerated. Pregnancy safety varies by ingredient: N-acetyl cysteine is possibly safe, theanine should be avoided, turmeric is likely safe early in pregnancy but likely unsafe later, goldenseal should be avoided, picrorhiza should be avoided, and milk thistle safety data are insufficient.

If you're pregnant or nursing, discuss this product with your doctor or pharmacist before use.

Side effects, ingredient by ingredient N-acetyl Cysteine (nac) Magnesium Theanine Turmeric Potassium Cranberry Goldenseal Picrorhiza

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?
  • 10 of the 10 matched ingredients can interact with medications — Milk Thistle, Turmeric, Calcium, Potassium, Goldenseal, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; heart-rhythm medications; lithium; Parkinson's medications.
  • For scale: 1,621 individual medications appear in the full list. A big number alone doesn't make a product dangerous — what matters is whether YOUR medication is on it, so run yours through the interaction checker on this page.

Before taking Diet Detox, check with your doctor or pharmacist if you take any of the following: HIV integrase inhibitors (dolutegravir, elvitegravir), the antibiotic ceftriaxone, Parkinson's medication (levodopa/carbidopa), blood thinners or antiplatelet drugs, blood pressure medications, antimalarial drugs, chemotherapy drugs, transplant rejection drugs (especially tacrolimus), cancer medications (tamoxifen, methotrexate), diabetes medications, skeletal muscle relaxants, water pills, antibiotics (especially fluoroquinolones), bone-building drugs (bisphosphonates), thyroid medication, heart rhythm drugs, or pain relievers (tramadol). These represent the categories with documented interactions.

If you're unsure whether your medication falls into any of these groups, use the drug-interaction tool on this page.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFully disclosed formula with strong clinical evidence behind its ingredients' uses. Major medication interactions have been identified, and safety information is well characterized.

This is a multi-ingredient supplement with a wide range of interactions, especially with HIV medications, blood thinners, blood pressure drugs, and several others. If you take any prescription medications—particularly for the heart, blood clotting, blood pressure, infection, or transplant—you need to check this product against your exact drug list before starting.

Even without prescriptions, the ingredients are generally tolerated but not all are well studied long-term. Talk with your own doctor or pharmacist about whether this product fits your health needs and medications.

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

Assessment coverage: 10 of 14 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Jan 7, 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 Diet Detox, straight from the product label.

Brand GNC BodyDynamix
Barcode (UPC) 048107186494
Net contents 21 Caplet(s)
Market status On market
Date entered into DSLD Jan 7, 2019
DSLD ID 182869
Product type Other Combinations
Supplement form Other (e.g. Tea Bag)
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 Diet Detox by GNC BodyDynamix, 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:
1 Caplet(s)
Maximum serving Sizes:
1 Caplet(s)
UPC/BARCODE
048107186494
IngredientAmount% DV
N-Acetyl-L-Cysteine100 mg--
Magnesium25 mg6%
Suntheanine L-Theanine100 mg--
Chloride50 mg2%
Turmeric root extract50 mg--
Potassium75 mg2%
Cranberry fruit extract25 mg--
Goldenseal Root Extract75 mg--
Betaine100 mg--
Picrorhiza kurroa root extract200 mg--
Melon Fruit Juice Concentrate10 mg--
Calcium155 mg12%
Milk Thistle seed extract100 mg--
EGCG25 mg--

Other ingredients: Hydroxypropylcellulose, Hydroxypropyl Methylcellulose, Croscarmellose Sodium, Microcrystalline Cellulose, Magnesium Stearate, Silicon Dioxide, Polyethylene Glycol, Stearic Acid, Talc, Titanium Dioxide, Chlorophyllin, Vegetable Acetoglycerides, Ethylcellulose, Polysorbate 80, Triacetin, Diacetylated Monoglycerides, Oleic Acid

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.
Precautions

Warning: Consult your physician prior to using this product if you are pregnant, nursing, taking medication, or have a medical condition.

Discontinue use two weeks prior to surgery.

Keep out of reach of children.

Brand IP Statement(s)

CurcuWIN is a registered trademark of OmniActive Health Technologies, Ltd.

Suntheanine is a registered trademark of Taiyo International Inc.

FDA Disclaimer Statement

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Storage

Store in a cool, dry place.

General Statements

Detox & Rejuvenation Formula Rejuvenates your metabolism Kick-starts your weightloss

FDA Statement of Identity

Dietary Supplement

General

CODE 484300 KSG

Suggested/Recommended/Usage/Directions

Directions: As a dietary supplement, take one caplet daily in the morning.

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

See for yourself

Diet Detox by GNC BodyDynamix label

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

Diet Detox 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 Diet Detox by GNC BodyDynamix

These are the 14 active ingredients this product is made of. Select any to open its full monograph.

Serving size1 Caplet(s) Dosage formOther (e.g. Tea Bag) 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.

N-Acetyl-L-Cysteine

Interacts with
294 drugs
100 mg per serving

N-acetyl cysteine (NAC) is a supplement form of the amino acid cysteine and a building block for the antioxidant glutathione. It has well-established...

N-Acetyl-L-Cysteine monograph & interactions

Magnesium

Interacts with
295 drugs
25 mg per serving Form: Magnesium Oxide

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 & interactions

Suntheanine L-Theanine

Interacts with
565 drugs
100 mg per serving

Theanine (usually L-theanine) is an amino acid found naturally in tea leaves that many people take to feel calmer and less stressed without strong dro...

Suntheanine L-Theanine monograph & interactions

Chloride

50 mg per serving Form: Potassium Chloride

Turmeric root extract

Interacts with
1,133 drugs
50 mg per serving Form: Curcuminoids

Turmeric is a popular spice whose main active compounds, curcuminoids, are studied mostly for inflammation and joint pain. Some research is promising,...

Turmeric root extract monograph & interactions

Potassium

Interacts with
62 drugs
75 mg per serving Form: Potassium Chloride

Potassium is an essential mineral your body needs for nerve signals, muscle function, and a steady heartbeat, and most people get enough from a balanc...

Potassium monograph & interactions

Cranberry fruit extract

Interacts with
712 drugs
25 mg per serving

Cranberry is best known for helping to prevent repeated urinary tract infections (UTIs) in some people, and the evidence here is moderate but mixed. I...

Cranberry fruit extract monograph & interactions

Goldenseal Root Extract

Interacts with
1,237 drugs
75 mg per serving

Goldenseal is a popular North American herb that contains berberine, a compound studied for antimicrobial effects. However, strong human evidence for...

Goldenseal Root Extract monograph & interactions

Betaine

100 mg per serving Form: Betaine Anhydrous

Picrorhiza kurroa root extract

Interacts with
207 drugs
200 mg per serving

Picrorhiza (Picrorhiza kurroa) is a bitter Himalayan herb used in Ayurvedic medicine, mainly for liver and digestive complaints. Early lab and small h...

Picrorhiza kurroa root extract monograph & interactions

Melon Fruit Juice Concentrate

10 mg per serving

Calcium

Interacts with
168 drugs
155 mg per serving Form: Calcium Silicate, Tricalcium Phosphate

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 & interactions

Milk Thistle seed extract

Interacts with
954 drugs
100 mg per serving Form: Silymarin

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

Milk Thistle seed extract monograph & interactions

EGCG

25 mg per serving Form: Green Tea extract

Other (inactive) ingredients: Hydroxypropylcellulose, Hydroxypropyl Methylcellulose, Croscarmellose Sodium, Microcrystalline Cellulose, Magnesium Stearate, Silicon Dioxide, Polyethylene Glycol, Stearic Acid, Talc, Titanium Dioxide, Chlorophyllin, Vegetable Acetoglycerides, Ethylcellulose, Polysorbate 80, Triacetin, Diacetylated Monoglycerides, Oleic Acid. These complete the product’s ingredient list but are not active constituents.

Interaction report

Diet Detox by GNC BodyDynamix Drug Interactions

Want to check YOUR meds against Diet Detox?

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
1,620Drugs
14 Major 1,552 Moderate 54 Minor

Ingredients driving the most interactions

Goldenseal Root Extract 1,237
Turmeric root extract 1,133
Milk Thistle seed extract 954
Cranberry fruit extract 712
Suntheanine L-Theanine 565

Individual Drug Interactions

The ingredients in Diet Detox interact with 1,620 drugs. Click any drug to see the details.

10 of the 14 ingredients in Diet Detox interact with drugs. Each result below shows which ingredient is responsible. Goldenseal Root Extract Turmeric root extract Milk Thistle seed extract Cranberry fruit extract Suntheanine L-Theanine Magnesium N-Acetyl-L-Cysteine Picrorhiza kurroa root extract Calcium Potassium

Each ingredient & the kinds of drugs it affects

For each ingredient in Diet Detox 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.

Goldenseal Root Extract16 drug types · 1,237 drugs

Anticoagulant/Antiplatelet Drugs

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

Likelihood Possible Evidence D
Antidiabetes Drugs

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

Likelihood Possible Evidence D
Antihypertensive Drugs

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

Likelihood Possible Evidence D
Cns Depressants

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

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

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

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

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

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

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

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

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

Likelihood Possible Evidence B
Dextromethorphan (Robitussin Dm, Others)

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

Likelihood Possible Evidence D
Digoxin (Lanoxin)

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

Likelihood Probable Evidence B
Losartan (Cozaar)

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

Likelihood Possible Evidence D
Metformin (Glucophage)

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

Likelihood Possible Evidence D
P-Glycoprotein Substrates

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

Likelihood Probable Evidence B
Pentobarbital (Nembutal)

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

Likelihood Possible Evidence D
Tacrolimus (Prograf)

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

Likelihood Possible Evidence D
Oseltamivir (Tamiflu)

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

Likelihood Possible Evidence D
Goldenseal Root Extract full monograph & interactions

Turmeric root extract24 drug types · 1,133 drugs

Alkylating Agents

Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research suggests that curcumin, a constituent of turmeric, inhibits mechlorethamine-induced apoptosis of breast cancer cells by up to 70%. Also, animal research shows that curcumin inhibits cyclophosphamide-induced tumor regression. However, some in vitro research shows that curcumin does not affect the apoptosis capacity of etoposide. Also, other laboratory research suggests that curcumin might augment the cytotoxic effects of alkylating agents. Reasons for the discrepancies may relate to the dose of curcumin and the specific chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have on alkylating agents.

Likelihood Possible Evidence D
Amlodipine (Norvasc)

Taking turmeric with amlodipine may increase levels of amlodipine.
Animal research shows that giving amlodipine 1 mg/kg as a single dose following the use of turmeric extract 200 mg/kg daily for 2 weeks increases the maximum concentration and area under the curve by 53% and 56%, respectively, when compared with amlodipine alone. Additional animal research shows that taking amlodipine 1 mg/kg with a curcumin 2 mg/kg pretreatment for 10 days increases the maximum concentration and area under the curve by about 2-fold when compared with amlodipine alone.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Turmeric may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Curcumin, a constituent of turmeric, has demonstrated antiplatelet effects in vitro. Furthermore, two case reports have found that taking turmeric along with warfarin or fluindione was associated with an increased international normalized ratio (INR). However, one clinical study in healthy volunteers shows that taking curcumin 500 mg daily for 3 weeks, alone or with aspirin 100 mg, does not increase antiplatelet effects or bleeding risk. It is possible that the dose of turmeric used in this study was too low to produce a notable effect.

Likelihood Possible Evidence B
Antidiabetes Drugs

Theoretically, taking turmeric with antidiabetes drugs might increase the risk of hypoglycemia.
Animal research and case reports suggest that curcumin, a turmeric constituent, can reduce blood glucose levels in patients with diabetes. Furthermore, clinical research in adults with type 2 diabetes shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg decreased postprandial glucose levels for up to 24 hours when compared with glyburide alone, despite the lack of a significant pharmacokinetic interaction. Other clinical studies in patients with diabetes show that taking curcumin daily can reduce blood glucose levels when compared with placebo.

Likelihood Possible Evidence B
Antitumor Antibiotics

Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro and animal research shows that curcumin, a constituent of turmeric, inhibits doxorubicin-induced apoptosis of breast cancer cells by up to 65%. However, curcumin does not seem to affect the apoptosis capacity of daunorubicin. In fact, some research shows that curcumin might augment the cytotoxic effects of antitumor antibiotics, increasing their effectiveness. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effects, if any, antioxidants such as turmeric have on antitumor antibiotics.

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

Turmeric might increase or decrease levels of drugs metabolized by CYP3A4.
In vitro and animal research show that turmeric and its constituents curcumin and curcuminoids inhibit CYP3A4. Also, 8 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking turmeric and cancer medications that are CYP3A4 substrates, including everolimus, ruxolitinib, ibrutinib, and palbociclib, and bortezomib. In another case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels after consuming turmeric powder at a dose of 15 or more spoonfuls daily for ten days prior. It was thought that turmeric increased levels of tacrolimus due to CYP3A4 inhibition.
Conversely, other in vitro research suggests that turmeric induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. An animal model suggests that induction of CYP3A4 occurs after daily curcumin use for 1 week. However, the induction of CYP3A4 by turmeric has not been reported in humans.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, turmeric might increase the risk of liver damage when taken with hepatotoxic drugs.
There is concern that turmeric might cause hepatotoxicity, especially when highly bioavailable formulations are used in high doses.

Likelihood Possible Evidence D
Methotrexate (Trexall, Others)

Theoretically, turmeric might have additive effects when used with hepatotoxic drugs such as methotrexate.
In one case report, a 39-year-old female taking methotrexate, turmeric, and linseed oil developed hepatotoxicity.

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

Theoretically, turmeric might increase blood levels of OATP4C1 substrates.
In vitro research shows that the turmeric constituent curcumin competitively inhibits OATP4C1 transport. This transporter is expressed in the kidney and facilitates the renal excretion of certain drugs. Theoretically, taking turmeric might decrease renal excretion of OATP substrates.

Likelihood Possible Evidence D
Sulfasalazine (Azulfidine)

Turmeric might increase the effects and adverse effects of sulfasalazine.
Clinical research shows that taking the turmeric constituent, curcumin, can increase blood levels of sulfasalazine by 3.2-fold.

Likelihood Probable Evidence B
Tacrolimus (Prograf)

Turmeric might increase the effects and adverse effects of tacrolimus.
In one case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels of 29 ng/mL. The patient previously had tacrolimus levels within the therapeutic range at 9.7 ng/mL. Ten days prior to presenting at the emergency room the patient started consumption of turmeric powder at a dose of 15 or more spoonfuls daily. It was thought that turmeric increased levels of tacrolimus due to cytochrome P450 3A4 (CYP3A4) inhibition. In vitro and animal research show that turmeric and its constituent curcumin inhibit CYP3A4.

Likelihood Possible Evidence D
Talinolol

Turmeric may reduce the absorption of talinolol in some situations.
Clinical research shows that taking curcumin for 6 days decreases the bioavailability of talinolol when taken together on the seventh day. The clinical significance of this effect is unclear.

Likelihood Probable Evidence B
Tamoxifen (Nolvadex)

Theoretically, turmeric might reduce the levels and clinical effects of tamoxifen.
In a small clinical trial in patients with breast cancer taking tamoxifen 20-30 mg daily, adding curcumin 1200 mg plus piperine 10 mg three times daily reduces the 24-hour area under the curve of tamoxifen and the active metabolite endoxifen by 12.8% and 12.4%, respectively, as well as the maximum concentrations of tamoxifen, when compared with tamoxifen alone. However, in the absence of piperine, the area under the curve for endoxifen and the maximum concentration of tamoxifen were not significantly reduced. Effects were most pronounced in patients who were extensive cytochrome P450 (CYP) 2D6 metabolizers.

Likelihood Possible Evidence B
Topoisomerase I Inhibitors

Turmeric has antioxidant effects. There is some concern that this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research shows that curcumin, a constituent of turmeric, inhibits camptothecin-induced apoptosis of breast cancer cells by up to 71%. However, other in vitro research shows that curcumin augments the cytotoxic effects of camptothecin. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agents. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have.

Likelihood Possible Evidence D
Tramadol (Ultram)

Theoretically, turmeric might increase or decrease levels of tramadol.
Animal research suggests that a single dose of curcumin, a constituent of turmeric, may increase tramadol's maximum concentration (Cmax) by inhibiting metabolism, while continued daily use for 7 days may reduce the area under the curve (AUC) due to the induction of drug-metabolizing enzymes such as cytochrome P450 3A4 (CYP3A4). However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Turmeric might increase the risk of bleeding with warfarin.
One case of increased international normalized ratio (INR) has been reported for a patient taking warfarin who began taking turmeric. Prior to taking turmeric, the patient had stable INR measurements. Within a few weeks of starting turmeric supplementation, the patient's INR increased to 10. Additionally, curcumin, the active constituent in turmeric, has demonstrated antiplatelet effects in vitro, which may produce additive effects when taken with warfarin.

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

Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2. However, research is conflicting.
In vitro and animal research show that the turmeric constituent, curcumin, inhibits CYP1A2. However, other in vitro research suggests that curcumin does not significantly affect CYP1A2.

Likelihood Possible Evidence D
Docetaxel (Taxotere)

Theoretically, turmeric might increase blood levels of oral docetaxel.
Animal research suggests that the turmeric constituent, curcumin, enhances the oral bioavailability of docetaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.

Likelihood Possible Evidence D
Estrogens

Theoretically, large amounts of turmeric might interfere with hormone replacement therapy through competition for estrogen receptors.
In vitro research shows that curcumin, a constituent of turmeric, displaces the binding of estrogen to its receptors.

Likelihood Possible Evidence D
Glyburide (Diabeta, Others)

Theoretically, taking turmeric and glyburide in combination might increase the risk of hypoglycemia.
Clinical research shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg increases blood levels of glyburide by 12% at 2 hours after the dose in patients with type 2 diabetes. While maximal blood concentrations of glyburide were not affected, turmeric modestly decreased postprandial glucose levels for up to 24 hours when compared to glyburide alone, possibly due to the hypoglycemic effect of turmeric demonstrated in animal research.

Likelihood Possible Evidence B
Losartan (Cozaar)

Theoretically, turmeric might increase the effects of losartan.
Research in hypertensive rats shows that taking turmeric can increase the hypotensive effects of losartan.

Likelihood Possible Evidence D
Norfloxacin (Noroxin)

Theoretically, turmeric might increase the effects and adverse effects of norfloxacin.
Animal research shows that taking curcumin, a turmeric constituent, can increase blood levels of orally administered norfloxacin.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, turmeric might increase the absorption of P-glycoprotein substrates.
In vitro and animal research shows that curcuminoids and other constituents found in turmeric can inhibit P-glycoprotein expression and activity.

Likelihood Possible Evidence D
Paclitaxel (Abraxane, Onxol)

Theoretically, turmeric might alter blood levels of paclitaxel, although any effect may not be clinically relevant.
Clinical research in adults with breast cancer receiving intravenous paclitaxel suggests that taking turmeric may modestly alter paclitaxel pharmacokinetics. Patients received paclitaxel on day 1, followed by either no treatment or turmeric 2 grams daily from days 2-22. Pharmacokinetic modeling suggests that turmeric reduces the maximum concentration and area under the curve of paclitaxel by 12.1% and 7.7%, respectively. However, these changes are not likely to be considered clinically relevant. Conversely, animal research suggests that curcumin, a constituent of turmeric, enhances the oral bioavailability of paclitaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.

Likelihood Possible Evidence D
Turmeric root extract full monograph & interactions

Milk Thistle seed extract17 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 full monograph & interactions

Cranberry fruit extract6 drug types · 712 drugs

Atorvastatin (Lipitor)

Theoretically, cranberry might increase levels and adverse effects of atorvastatin.
In one case report, a patient taking atorvastatin experienced upper back pain, rhabdomyolysis, and abnormal liver function after drinking cranberry juice 16 ounces daily for 2 weeks. Theoretically, this may have been caused by inhibition of cytochrome P450 3A4 (CYP3A4) enzymes by cranberry juice, as atorvastatin is a CYP3A4 substrate. Creatinine kinase and liver enzymes normalized within 2 weeks of stopping cranberry juice. Patients taking atorvastatin should avoid large quantities of cranberry juice.

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

Theoretically, cranberry might increase the levels and adverse effects of CYP3A4 substrates.
A case of upper back pain, rhabdomyolysis, and abnormal liver function has been reported for a patient taking atorvastatin, a CYP3A4 substrate, in combination with cranberry juice 16 ounces daily for 2 weeks. Creatinine kinase and liver enzymes normalized within 2 weeks of stopping cranberry juice. Also, animal research suggests that cranberry juice, administered intraduodenally 30 minutes prior to nifedipine, a CYP3A4 substrate, inhibits nifedipine metabolism and increases the area under the concentration-time curve by 1.6-fold compared to control.

Likelihood Possible Evidence D
Nifedipine (Procardia)

Theoretically, cranberry might increase the levels and adverse effects of nifedipine.
Animal research suggests that cranberry juice, administered intraduodenally 30 minutes prior to nifedipine treatment, inhibits nifedipine metabolism and increases the area under the concentration-time curve by 1.6-fold compared to control. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, cranberry might increase the levels and adverse effects of warfarin. However, research is conflicting.
There is contradictory evidence about the effect of cranberry juice on warfarin. Case reports have linked cranberry juice consumption to increases in the international normalized ratio (INR) in patients taking warfarin, resulting in severe spontaneous bleeding and excessive postoperative bleeding. Daily consumption of cranberry sauce for one week has also been linked to an increase in INR in one case report. In a small study in healthy young males, taking a high dose of 3 grams of cranberry juice concentrate capsules, equivalent to 57 grams of fruit daily, for 2 weeks produced a 30% increase in the area under the INR-time curve after a single 25-mg dose of warfarin. However, 3 very small clinical studies in patients stabilized on warfarin reported that cranberry juice 250 mL once or twice daily for 7 days (27% cranberry juice or pure cranberry juice) or 240 mL once daily for 14 days does not significantly increase INR or affect plasma warfarin levels. The reasons for these discrepant findings are unclear. It is possible that the form and dose of cranberry may play a role, as cranberry extracts and juices contain different constituents. Additionally, an in vitro study evaluating 5 different cranberry juices found varying effects, with only a cranberry concentrate, and not diluted cranberry juices, inhibiting CYP2C9. However, this concentrate did not inhibit CYP2C9 activity in humans.

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

Theoretically, cranberry might increase the levels and adverse effects of CYP2C9 substrates. However, research is conflicting.
There is contradictory evidence about the effect of cranberry on CYP2C9 enzymes. In vitro evidence suggests that flavonoids in cranberry inhibit CYP2C9 enzymes. However, clinical research shows that cranberry juice does not significantly affect the levels, metabolism, or elimination of the CYP2C9 substrates flurbiprofen or diclofenac. Also, in patients stabilized on warfarin, drinking cranberry juice 250 mL daily for 7 days does not significantly increase the anticoagulant activity of warfarin, a CYP2C9 substrate. Additional pharmacokinetic research shows that cranberry juice does not increase peak plasma concentrations or area under the concentration-time curve of warfarin.

Likelihood Unlikely Evidence B
Diclofenac (Voltaren, Others)

Theoretically, cranberry might modestly increase the levels and adverse effects of diclofenac.
In vitro evidence suggests that cranberry juice inhibits diclofenac metabolism by human liver microsomes. However, drinking cranberry juice does not seem to affect diclofenac metabolism in humans.

Likelihood Unlikely Evidence B
Cranberry fruit extract full monograph & interactions

Suntheanine L-Theanine3 drug types · 565 drugs

Antihypertensive Drugs

Theanine might lower blood pressure, potentiating the effects of antihypertensive drugs.
Animal research shows that theanine can lower blood pressure in spontaneously hypertensive animals. Theoretically, concomitant use of theanine and antihypertensive drugs might potentiate the antihypertensive activity.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, theanine might have additive sedative effects when used in conjunction with CNS depressants. However, it is unclear if this concern is clinically relevant.
Theoretically, theanine may compete with glutamate and/or increase plasma gamma-aminobutyric acid (GABA) levels, which could cause CNS depression. In one clinical study, some subjects taking oral theanine reported drowsiness.

Likelihood Unlikely Evidence D
Serotonergic Drugs

Clinical studies regarding the effects of L-theanine on serotonin levels are conflicting. Some studies suggest it can increase serotonin levels in the brain while others report that it may decrease them. Nevertheless, there have been no reports of l-theanine being a causative agent in serotonergic-related side effects or serotonin syndrome.

Likelihood Unlikely Evidence C
Suntheanine L-Theanine full monograph & interactions

Magnesium15 drug types · 295 drugs

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.

Likelihood Probable Evidence B
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence D
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.

Likelihood Probable Evidence D
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.

Likelihood Probable Evidence B
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.

Likelihood Possible Evidence D
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.

Likelihood Possible Evidence B
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.

Likelihood Probable Evidence D
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.

Likelihood Probable Evidence D
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.

Likelihood Probable Evidence A
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.

Likelihood Probable Evidence B
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.

Likelihood Probable Evidence D
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.

Likelihood Unlikely Evidence B
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.

Likelihood Unlikely Evidence B
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.

Likelihood Possible Evidence B
Magnesium full monograph & interactions

N-Acetyl-L-Cysteine5 drug types · 294 drugs

Nitroglycerin

N-acetyl cysteine can increase the risk for hypotension and headaches when taken with intravenous or transdermal nitroglycerin.
Clinical research shows that concomitant administration of N-acetyl cysteine and intravenous or transdermal nitroglycerin can cause severe hypotension and intolerable headaches. Furthermore, in vitro research suggests that N-acetyl cysteine increases the anticoagulant activity of nitroglycerin.

Likelihood Probable Evidence B
Activated Charcoal

N-acetyl cysteine might reduce the effects of activated charcoal, while activated charcoal might reduce the absorption of N-acetyl cysteine.
N-acetyl cysteine appears to reduce the capacity of activated charcoal to adsorb acetaminophen and salicylic acid. Conversely, although clinical research suggests that although activated charcoal can reduce the absorption of N-acetyl cysteine by up to 40%, it does not seem to reduce its clinical effects. Other clinical evidence suggests that activated charcoal does not affect the absorption of N-acetyl cysteine.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, N-acetyl cysteine might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
Clinical research suggests that intravenous N-acetyl cysteine decreases prothrombin time, prolongs coagulation time, decreases platelet aggregation, and increases blood loss in surgical patients. Furthermore, in vitro research suggests that N-acetyl cysteine increases the anticoagulant activity of nitroglycerin.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, N-acetyl cysteine might increase the risk of hypotension when taken with antihypertensive drugs.
Animal research suggests that N-acetyl cysteine potentiates the hypotensive effects of the angiotensin-converting enzyme inhibitors (ACEIs) captopril and enalaprilat. Theoretically, combining N-acetyl cysteine with other antihypertensive drugs might increase the risk of hypotension.

Likelihood Possible Evidence D
Chloroquine (Aralen)

Theoretically, N-acetyl cysteine might interfere with the antimalarial effects of chloroquine.
Animal research suggests that N-acetyl cysteine might reduce the antimalarial effects of chloroquine by increasing cellular levels of glutathione.

Likelihood Possible Evidence D
N-Acetyl-L-Cysteine full monograph & interactions

Picrorhiza kurroa root extract2 drug types · 207 drugs

Antidiabetes Drugs

Evidence from animal research suggests that an extract of picrorhiza can reduce fasting and non-fasting blood sugar levels. Theoretically, picrorhiza might have additive effects with antidiabetes drugs and increase the risk of hypoglycemia. Monitor blood glucose levels closely. Dose adjustments might be necessary. Some antidiabetes drugs include glimepiride (Amaryl), glyburide (DiaBeta, Glynase PresTab, Micronase), insulin, pioglitazone (Actos), rosiglitazone (Avandia), and others.

Likelihood Possible Evidence D
Immunosuppressants

Picrorhiza seems to have immunostimulating activity. Theoretically, picrorhiza may interfere with immunosuppressant therapy. Immunosuppressant drugs include azathioprine (Imuran), basiliximab (Simulect), cyclosporine (Neoral, Sandimmune), daclizumab (Zenapax), muromonab-CD3 (OKT3, Orthoclone OKT3), mycophenolate (CellCept), tacrolimus (FK506, Prograf), sirolimus (Rapamune), prednisone (Deltasone, Orasone), and other corticosteroids (glucocorticoids).

Likelihood Possible Evidence D
Picrorhiza kurroa root extract full monograph & interactions

Calcium18 drug types · 168 drugs

Ceftriaxone (Rocephin)

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

Likelihood Probable Evidence D
Dolutegravir (Tivicay)

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

Likelihood Probable Evidence B
Elvitegravir (Vitekta)

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

Likelihood Probable Evidence B
Aluminum

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

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

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

Likelihood Probable Evidence D
Bisphosphonates

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

Likelihood Probable Evidence C
Calcipotriene (Dovonex)

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

Likelihood Possible Evidence B
Digoxin (Lanoxin)

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

Likelihood Possible Evidence B
Diltiazem (Cardizem, Others)

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

Likelihood Probable Evidence D
Levothyroxine (Synthroid, Others)

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

Likelihood Probable Evidence B
Lithium

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

Likelihood Possible Evidence B
Quinolone Antibiotics

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

Likelihood Probable Evidence B
Raltegravir (Isentress)

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

Likelihood Possible Evidence B
Sotalol (Betapace)

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

Likelihood Possible Evidence B
Tetracycline Antibiotics

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

Likelihood Probable Evidence C
Thiazide Diuretics

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

Likelihood Probable Evidence C
Verapamil (Calan, Others)

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

Likelihood Probable Evidence D
Calcium Channel Blockers

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

Likelihood Unlikely Evidence D
Calcium full monograph & interactions

Potassium3 drug types · 62 drugs

Ace Inhibitors (Aceis)

Using ACEIs with high doses of potassium increases the risk of hyperkalemia.
ACEIs block the actions of the renin-angiotensin-aldosterone system and reduce potassium excretion. Concomitant use of these drugs with potassium supplements increases the risk of hyperkalemia. However, concomitant use of these drugs with moderate dietary potassium intake (about 3775-5200 mg daily) does not increase serum potassium levels.

Likelihood Likely Evidence C
Angiotensin Receptor Blockers (Arbs)

Using ARBs with high doses of potassium increases the risk of hyperkalemia.
ARBs block the actions of the renin-angiotensin-aldosterone system and reduce potassium excretion. Concomitant use of these drugs with potassium supplements increases the risk of hyperkalemia. However, concomitant use of these drugs with moderate dietary potassium intake (about 3775-5200 mg daily) does not increase serum potassium levels.

Likelihood Likely Evidence C
Potassium-Sparing Diuretics

Concomitant use increases the risk of hyperkalemia.
Using potassium-sparing diuretics with potassium supplements increases the risk of hyperkalemia.

Likelihood Likely Evidence C
Potassium full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Diet Detox, from the product label.

GNC BodyDynamix

See all GNC BodyDynamix products
Name
General Nutrition Corporation
City
Pittsburgh
State
PA
ZipCode
15222
Phone Number
1-888-462-2548
Web Address
Slimvance.com/detox
Pharmacist Counseling Corner

Diet Detox by GNC BodyDynamix: Common Questions

Does Diet Detox by GNC BodyDynamix interact with any medications?
Yes. Based on its ingredients, Diet Detox has a known interaction with 1,620 medications, including 14 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Diet Detox contains 14 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.
Does this product help me detox my body?
The term 'detox' isn't a medical claim we can verify from the ingredients' evidence. Individual components like milk thistle and turmeric have traditionally been used for liver support, and N-acetyl cysteine has real clinical uses, but the product as a whole doesn't have established evidence showing it removes toxins or 'cleanses' your system in the way the marketing suggests.
Is it safe to take this if I'm on blood pressure medication?
No, not without checking first. N-acetyl cysteine, magnesium, theanine, and goldenseal can all lower blood pressure; taking them with your medication could drop it too far. Talk with your doctor or pharmacist before starting—they may need to adjust your dose or monitor you closely.
Can I take this if I'm pregnant?
It depends on which ingredients you're asking about. Theanine and goldenseal should be avoided in pregnancy. N-acetyl cysteine is possibly safe, turmeric is likely safe early on but possibly unsafe later, and picrorhiza should be avoided. Because this is a combination product with mixed safety data, talk with your doctor or pharmacist before use in pregnancy.
What's the most common side effect?
Gastrointestinal upset—diarrhea, nausea, constipation, or stomach discomfort—is the most frequent side effect reported across most of these ingredients, especially turmeric, cranberry, potassium, and goldenseal.
Is this a substitute for treating a urinary tract infection?
No. While cranberry in this product is possibly effective for UTI prevention, it's not a substitute for medical treatment of an active infection. If you have UTI symptoms, see your doctor or pharmacist for proper diagnosis and treatment.
Can I take this with my statin (cholesterol medication)?
Potentially, but it needs checking. Cranberry in the product may increase statin levels, and turmeric may affect how your liver processes certain statins. Milk thistle may also interfere with statin metabolism. Ask your pharmacist to check your specific statin against this product before you start.

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

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

Diet Detox label
Go deeper

The Full Monographs Behind Diet Detox’s Ingredients

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

Herb & supplement monograph

N-acetyl Cysteine (nac)

Interacts with 294 drugs

N-acetyl cysteine (NAC) is a supplement form of the amino acid cysteine and a building block for the antioxidant glutathione. It has well-established prescription uses for acetaminophen over...

Read the full N-acetyl Cysteine (nac) monograph → Herb & supplement monograph

Magnesium

Interacts with 295 drugs

Magnesium 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 monograph

Theanine

Interacts with 565 drugs

Theanine (usually L-theanine) is an amino acid found naturally in tea leaves that many people take to feel calmer and less stressed without strong drowsiness. Early research suggests it may...

Read the full Theanine monograph → Herb & supplement monograph

Turmeric

Interacts with 1,133 drugs

Turmeric is a popular spice whose main active compounds, curcuminoids, are studied mostly for inflammation and joint pain. Some research is promising, but quality is mixed and curcumin is po...

Read the full Turmeric monograph → Herb & supplement monograph

Potassium

Interacts with 62 drugs

Potassium is an essential mineral your body needs for nerve signals, muscle function, and a steady heartbeat, and most people get enough from a balanced diet rich in fruits and vegetables. P...

Read the full Potassium monograph → Herb & supplement monograph

Cranberry

Interacts with 712 drugs

Cranberry is best known for helping to prevent repeated urinary tract infections (UTIs) in some people, and the evidence here is moderate but mixed. It is not a reliable treatment for an act...

Read the full Cranberry monograph → Herb & supplement monograph

Goldenseal

Interacts with 1,237 drugs

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

Read the full Goldenseal monograph → Herb & supplement monograph

Picrorhiza

Interacts with 207 drugs

Picrorhiza (Picrorhiza kurroa) is a bitter Himalayan herb used in Ayurvedic medicine, mainly for liver and digestive complaints. Early lab and small human studies suggest possible liver-prot...

Read the full Picrorhiza monograph → Herb & supplement monograph

Calcium

Interacts with 168 drugs

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

Read the full Calcium monograph → Herb & supplement monograph

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 →
Sources

Sources & How We Checked

Diet Detox'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 493 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.

N-acetyl Cysteine (nac) 86 references
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  2. Jepsen S, Hansen AB. The influence of N-acetylcysteine on the measurement of prothrombin time and activated partial thromboplastin time in healthy subjects. Scand J Clin Lab Invest 1994;54:543-7. PubMed
  3. van Zandwijk N, Dalesio O, Pastorino U, et al. EUROSCAN, a randomized trial of vitamin A and N-acetylcysteine in patients with head and neck cancer or lung cancer. For the European Organization for Research and Treatment of Cancer Head and Neck and Lung C DOI
  4. Horowitz RS, Dart RC, Jarvie DR, et al. Placental transfer of N-acetylcysteine following human maternal acetaminophen toxicity. J Toxicol Clin Toxicol 1997;35:447-51.
  5. Bailey B, McGuigan MA. Management of anaphylactoid reactions to intravenous N-acetylcysteine. Ann Emerg Med 1998;31:710-5. PubMed
  6. Spiller HA, Krenzelok EP, Grande GA, et al. A prospective evaluation of the effect of activated charcoal before oral N-acetylcysteine in acetaminophen overdose. Ann Emerg Med 1994;23:519-23. PubMed
  7. Ardissino D, Merlini PA, Savonitto S, et al. Effect of transdermal nitroglycerin or N-acetylcysteine, or both, in the long-term treatment of unstable angina pectoris. J Am Coll Cardiol 1997;29:941-7. PubMed
  8. Horowitz JD, Henry CA, Syrjanen ML, et al. Nitroglycerine/N-acetylcysteine in the management of unstable angina pectoris. Eur Heart J 1988;9:95-100. PubMed
  9. Louwerse ES, Weverling GJ, Bossuyt PM, et al. Randomized, double-blind, controlled trial of acetylcysteine in amyotrophic lateral sclerosis. Arch Neurol 1995;52:559-64. PubMed
  10. Wiklund O, Fager G, Andersson A, et al. N-acetylcysteine treatment lowers plasma homocysteine but not serum lipoprotein(a) levels. Atherosclerosis 1996;119:99-106. PubMed
  11. De Flora S, Grassi C, Carati L. Attenuation of influenza-like symptomatology and improvement of cell-mediated immunity with long-term N-acetylcysteine treatment. Eur Respir J 1997;10:1535-41. PubMed
  12. Iversen HK. N-acetylcysteine enhances nitroglycerin-induced headache and cranial arterial responses. Clin Pharmacol Ther 1992;52:125-33. PubMed
  13. Behr J, Maier K, Degenkolb B, et al. Antioxidative and clinical effects of high-dose N-acetylcysteine in fibrosing alveolitis. Adjunctive therapy to maintenance immunosuppression. Am J Respir Crit Care Med 1997;156:1897-901.
  14. Tenenbein PK, Sitar DS, Tenenbein M. Interaction between N-acetylcysteine and activated charcoal: implications for the treatment of acetaminophen poisoning. Pharmacotherapy 2001;21:1331-6.
  15. Arstall MA, Yang J, Stafford I, et al. N-acetylcysteine in combination with nitroglycerin and streptokinase for the treatment of evolving acute myocardial infarction. Safety and biochemical effects. Circulation 1995;92:2855-62.
  16. Estensen RD, Levy M, Klopp SJ, et al. N-acetylcysteine suppression of the proliferative index in the colon of patients with previous adenomatous colonic polyps. Cancer Lett 1999;147:109-14. PubMed
  17. Pela R, Calcagni AM, Subiaco S, et al. N-acetylcysteine reduces the exacerbation rate in patients with moderate to severe COPD. Respiration 1999;66:495-500.. PubMed
  18. Oldemeyer JB, Biddle WP, Wurdeman RL, et al. Acetylcysteine in the prevention of contrast-induced nephropathy after coronary angiography. Am Heart J 2003;146:E23. . PubMed
  19. Ekins BR, Ford DC, Thompson MI, et al. The effect of activated charcoal on N-acetylcysteine absorption in normal subjects. Am J Emerg Med. 1987;5(6):483-7. PubMed
  20. Chamberlain JM, Gorman RL, Oderda GM, Klein-Schwartz W, Klein BL. Use of activated charcoal in a simulated poisoning with acetaminophen: a new loading dose for N-acetylcysteine? Ann Emerg Med. 1993;22(9):1398-402. PubMed
  21. Renzi FP, Donovan JW, Martin TG, Morgan L, Harrison EF. Concomitant use of activated charcoal and N-acetylcysteine. Ann Emerg Med. 1985;14(6):568-72. DOI
  22. North DS, Peterson RG, Krenzelok EP. Effect of activated charcoal administration on acetylcysteine serum levels in humans. Am J Hosp Pharm. 1981;38(7):1022-4. DOI
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  24. Ruiz FJ, Salom MG, Inglés AC, et al. N-acetyl-L-cysteine potentiates depressor response to captopril and enalaprilat in SHRs. Am J Physiol. 1994;267(3 Pt 2):R767-72. PubMed
  25. Deharo E, Barkan D, Krugliak M, Golenser J, Ginsburg H. Potentiation of the antimalarial action of chloroquine in rodent malaria by drugs known to reduce cellular glutathione levels. Biochem Pharmacol. 2003;66(5):809-17. PubMed
  26. Buckley, N. A., Whyte, I. M., O'Connell, D. L., and Dawson, A. H. Oral or intravenous N-acetylcysteine: which is the treatment of choice for acetaminophen (paracetamol) poisoning? J Toxicol.Clin Toxicol. 1999;37(6):759-767.
  27. Sunman, W., Hughes, A. D., and Sever, P. S. Anaphylactoid response to intravenous acetylcysteine. Lancet 5-16-1992;339(8803):1231-1232. PubMed
  28. Reynard, K., Riley, A., and Walker, B. E. Respiratory arrest after N-acetylcysteine for paracetamol overdose. Lancet 9-12-1992;340(8820):675. PubMed
  29. BERNSTEIN, I. L. and AUSDENMOORE, R. W. IATROGENIC BRONCHOSPASM OCCURRING DURING CLINICAL TRIALS OF A NEW MUCOLYTIC AGENT, ACETYLCYSTEINE. Dis.Chest 1964;46:469-473. PubMed
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  31. Bibi, H., Seifert, B., Oullette, M., and Belik, J. Intratracheal N-acetylcysteine use in infants with chronic lung disease. Acta Paediatr. 1992;81(4):335-339. PubMed
  32. Jepsen, S., Herlevsen, P., Knudsen, P., Bud, M. I., and Klausen, N. O. Antioxidant treatment with N-acetylcysteine during adult respiratory distress syndrome: a prospective, randomized, placebo-controlled study. Crit Care Med 1992;20(7):918-923. PubMed
  33. Roes, E. M., Raijmakers, M. T., Boo, T. M., Zusterzeel, P. L., Merkus, H. M., Peters, W. H., and Steegers, E. A. Oral N-acetylcysteine administration does not stabilise the process of established severe preeclampsia. Eur.J Obstet.Gynecol.Reprod.Biol 2006
  34. Spiller, H. A., Winter, M. L., Klein-Schwartz, W., and Bangh, S. A. Efficacy of activated charcoal administered more than four hours after acetaminophen overdose. J Emerg.Med 2006;30(1):1-5. PubMed
  35. Tirouvanziam, R., Conrad, C. K., Bottiglieri, T., Herzenberg, L. A., Moss, R. B., and Herzenberg, L. A. High-dose oral N-acetylcysteine, a glutathione prodrug, modulates inflammation in cystic fibrosis. Proc Natl.Acad.Sci U.S.A 3-21-2006;103(12):4628-463
  36. Niemi, T. T., Munsterhjelm, E., Poyhia, R., Hynninen, M. S., and Salmenpera, M. T. The effect of N-acetylcysteine on blood coagulation and platelet function in patients undergoing open repair of abdominal aortic aneurysm. Blood Coagul.Fibrinolysis 2006;1 PubMed
  37. Komisarof, J. A., Gilkey, G. M., Peters, D. M., Koudelka, C. W., Meyer, M. M., and Smith, S. M. N-acetylcysteine for patients with prolonged hypotension as prophylaxis for acute renal failure (NEPHRON). Crit Care Med 2007;35(2):435-441. PubMed
  38. Grimble, G. K. Adverse gastrointestinal effects of arginine and related amino acids. J Nutr 2007;137(6 Suppl 2):1693S-1701S. PubMed
  39. Berk, M., Copolov, D. L., Dean, O., Lu, K., Jeavons, S., Schapkaitz, I., Anderson-Hunt, M., and Bush, A. I. N-acetyl cysteine for depressive symptoms in bipolar disorder--a double-blind randomized placebo-controlled trial. Biol Psychiatry 9-15-2008;64(6) PubMed
  40. Shahin, A. Y., Hassanin, I. M., Ismail, A. M., Kruessel, J. S., and Hirchenhain, J. Effect of oral N-acetyl cysteine on recurrent preterm labor following treatment for bacterial vaginosis. Int J Gynaecol.Obstet. 2009;104(1):44-48. PubMed
  41. Nigwekar, S. U. and Kandula, P. N-acetylcysteine in cardiovascular-surgery-associated renal failure: a meta-analysis. Ann Thorac.Surg 2009;87(1):139-147. PubMed
  42. Sandilands, E. A. and Bateman, D. N. Adverse reactions associated with acetylcysteine. Clin Toxicol.(Phila) 2009;47(2):81-88. PubMed
  43. Wijeysundera, D. N., Karkouti, K., Rao, V., Granton, J. T., Chan, C. T., Raban, R., Carroll, J., Poonawala, H., and Beattie, W. S. N-acetylcysteine is associated with increased blood loss and blood product utilization during cardiac surgery. Crit Care Me PubMed
  44. Holdiness, M. R. Clinical pharmacokinetics of N-acetylcysteine. Clin Pharmacokinet. 1991;20(2):123-134. PubMed
  45. Dawson, A. H., Henry, D. A., and McEwen, J. Adverse reactions to N-acetylcysteine during treatment for paracetamol poisoning. Med J Aust. 3-20-1989;150(6):329-331.
  46. Rasmussen, J. B. and Glennow, C. Reduction in days of illness after long-term treatment with N-acetylcysteine controlled-release tablets in patients with chronic bronchitis. Eur.Respir.J 1988;1(4):351-355. DOI
  47. Walters, M. T., Rubin, C. E., Keightley, S. J., Ward, C. D., and Cawley, M. I. A double-blind, cross-over, study of oral N-acetylcysteine in Sjogren's syndrome. Scand J Rheumatol.Suppl 1986;61:253-258.
  48. Cato, A., Goldstein, I., and Millman, M. A double-blind parallel study of acetylcysteine-isoproterenol and saline-isoproterenol in patients with chronic obstructive lung disease. J Int Med Res 1977;5(3):175-183. PubMed
  49. Parr, G. D. and Huitson, A. Oral Fabrol (oral N-acetyl-cysteine) in chronic bronchitis. Br.J.Dis.Chest 1987;81(4):341-348.
  50. Dano, G. Bronchospasm caused by acetylcysteine in children with bronchial asthma. Acta Allergol. 1971;26(3):181-190. DOI
  51. Howatt, W. F. and DeMuth, G. R. A double-blind study of the use of acetylcysteine in patients with cystic fibrosis. Univ Mich.Med Cent.J 1966;32(2):82-85.
  52. Millman, M. and Grundon, W. Use of acetylcysteine in bronchial asthma and emphysema. J Asthma Res 1969;6(4):199-209. PubMed
  53. Vale, J. A. and Wheeler, D. C. Anaphylactoid reaction to acetylcysteine. Lancet 10-30-1982;2(8305):988.
  54. Mant, T. G., Tempowski, J. H., Volans, G. N., and Talbot, J. C. Adverse reactions to acetylcysteine and effects of overdose. Br Med J (Clin Res Ed) 7-28-1984;289(6439):217-219. PubMed
  55. Myers, C., Bonow, R., Palmeri, S., Jenkins, J., Corden, B., Locker, G., Doroshow, J., and Epstein, S. A randomized controlled trial assessing the prevention of doxorubicin cardiomyopathy by N-acetylcysteine. Semin.Oncol 1983;10(1 Suppl 1):53-55.
  56. Miller, L. F. and Rumack, B. H. Clinical safety of high oral doses of acetylcysteine. Semin.Oncol 1983;10(1 Suppl 1):76-85.
  57. Boman, G., Backer, U., Larsson, S., Melander, B., and Wahlander, L. Oral acetylcysteine reduces exacerbation rate in chronic bronchitis: report of a trial organized by the Swedish Society for Pulmonary Diseases. Eur J Respir.Dis 1983;64(6):405-415.
  58. Tattersall, A. B., Bridgman, K. M., and Huitson, A. Irish general practice study of acetylcysteine (Fabrol) in chronic bronchitis. J Int Med Res 1984;12(2):96-101. PubMed
  59. Jackson, I. M., Barnes, J., and Cooksey, P. Efficacy and tolerability of oral acetylcysteine (Fabrol) in chronic bronchitis: a double-blind placebo controlled study. J Int Med Res 1984;12(3):198-206. PubMed
  60. Ho, S. W. and Beilin, L. J. Asthma associated with N-acetylcysteine infusion and paracetamol poisoning: report of two cases. Br Med J (Clin Res Ed) 9-24-1983;287(6396):876-877. PubMed
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  62. Bateman, D. N., Woodhouse, K. W., and Rawlins, M. D. Adverse reactions to N-acetylcysteine. Hum Toxicol. 1984;3(5):393-398. PubMed
  63. Gervais, S., Lussier-Labelle, F., and Beaudet, G. Anaphylactoid reaction to acetylcysteine. Clin Pharm 1984;3(6):586-587.
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  65. Casola, G. and vanSonnenberg, E. Skin damage from acetylcysteine leak during percutaneous abscess drainage. Radiology 1984;152(1):233. PubMed
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  69. Hansen, N. C., Skriver, A., Brorsen-Riis, L., Balslov, S., Evald, T., Maltbaek, N., Gunnersen, G., Garsdal, P., Sander, P., Pedersen, J. Z., and . Orally administered N-acetylcysteine may improve general well-being in patients with mild chronic bronchiti
  70. Reid, M. B., Stokic, D. S., Koch, S. M., Khawli, F. A., and Leis, A. A. N-acetylcysteine inhibits muscle fatigue in humans. J Clin Invest 1994;94(6):2468-2474. PubMed
  71. Chirkov, Y. Y. and Horowitz, J. D. N-Acetylcysteine potentiates nitroglycerin-induced reversal of platelet aggregation. J Cardiovasc.Pharmacol 1996;28(3):375-380. PubMed
  72. Hershkovitz, E., Shorer, Z., Levitas, A., and Tal, A. Status epilepticus following intravenous N-acetylcysteine therapy. Isr.J Med Sci 1996;32(11):1102-1104.
  73. Stavem, K. [Anaphylactic reaction to N-acetylcysteine after poisoning with paracetamol]. Tidsskr.Nor Laegeforen. 5-30-1997;117(14):2038-2039.
  74. Walton, N. G., Mann, T. A., and Shaw, K. M. Anaphylactoid reaction to N-acetylcysteine. Lancet 12-15-1979;2(8155):1298. PubMed
  75. Perry, H. E. and Shannon, M. W. Efficacy of oral versus intravenous N-acetylcysteine in acetaminophen overdose: results of an open-label, clinical trial. J Pediatr 1998;132(1):149-152. PubMed
  76. Kory, R. C., Hirsch, S. R., and Giraldo, J. Nebulization of N-acetylcysteine combined with a bronchodilator in patients with chronic bronchitis. A controlled study. Chest 1968;54(6):504-509. PubMed
  77. Nahir, A. M., Scharf, J. M., and Szargel, R. Effects of oral N-acetylcysteine on both ocular and oral manifestations of Sjogren's Syndrome. Curr Ther Res 1989;46:187-192.
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Magnesium 82 references
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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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