Major interaction on record — check this product against your medications before combining. Based on 10 of 15 ingredients. Check your meds →
Dietary supplement

Joint Synergy + Ingredients & Drug Interactions

by MRM Nutrition

Capsule Category: Other Combinations
Most serious interaction: Major
The interaction bottom line Most serious interaction: Major

Joint Synergy + is a dietary supplement by MRM Nutrition with 15 active ingredients. Its ingredients are commonly taken for inflammation and swelling, sinus and nasal congestion, digestion support.Based on those ingredients, 1,528 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Theracurmin Turmeric root extract, Panax ginseng Root Extract, Boswellia serrata Leaf Extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Joint Synergy + by MRM Nutrition

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

From our pharmacy team — supplement deep dive

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 15 of its 15 active ingredients.
  • No proprietary blends here — you can verify the dose of every single component.

Joint Synergy + contains 15 ingredients total. The active components include bromelain (an enzyme from pineapple), glucosamine sulfate potassium chloride, chondroitin sulfate sodium, manganese, Panax ginseng root extract, white willow bark extract, Theracurmin turmeric root extract, Boswellia serrata leaf extract, plus collagen protein complex, cetyl myristoleate complex, sea cucumber, and mineral electrolytes (sodium, chloride, potassium).

The product also contains inactive ingredients: gelatin, rice flour, and magnesium stearate.

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
Strong

Clinical evidence supports at least one of this product's ingredients for its stated purpose.

Why this rating?
  • The label markets this product for: Supports joint health.
  • We looked for evidence on: Ankylosing spondylitis, Aromatase inhibitor-induced arthralgia, Back pain, Osteoarthritis, Rheumatoid arthritis, Joint stiffness.
  • The strongest evidence on file: Glucosamine is rated "Likely Effective" for Osteoarthritis (Natural Medicines).
  • Also on file: Boswellia Serrata is rated "Possibly Effective" for Osteoarthritis.
  • Also on file: Turmeric is rated "Possibly Effective" for Osteoarthritis.

Glucosamine is rated likely effective for osteoarthritis. Chondroitin sulfate is rated possibly effective for osteoarthritis and cataracts.

Panax ginseng is rated possibly effective for erectile dysfunction, sexual arousal, influenza, cognitive function, and multiple sclerosis-related fatigue. White willow bark is rated possibly effective for back pain.

Turmeric is rated possibly effective for depression, high cholesterol (hyperlipidemia), hay fever (allergic rhinitis), and indigestion (dyspepsia). Boswellia serrata is rated possibly effective for osteoarthritis.

For bromelain and manganese, the evidence we hold shows insufficient reliable evidence to rate effectiveness for most conditions, or effectiveness only for specific uses like manganese deficiency. Potassium, sodium, and chloride have no effectiveness ratings on file.

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.

Bromelain is generally well tolerated short-term for oral use but causes diarrhea, flatulence, stomach upset, and headache in some people; it should be avoided during pregnancy and breastfeeding. Glucosamine and chondroitin are generally well tolerated orally but should be avoided in pregnancy and while breastfeeding.

Common side effects include bloating, constipation, diarrhea, nausea, and heartburn; rare reports of allergic reactions and asthma exacerbations exist. Panax ginseng is generally well tolerated short-term in healthy adults and causes insomnia most commonly; it should be avoided in pregnancy and while breastfeeding.

White willow bark acts like aspirin and should be avoided during pregnancy; it causes diarrhea, indigestion, and heartburn. Turmeric is generally well tolerated as food but concentrated supplements may cause gastrointestinal upset; it carries a caution for pregnancy and breastfeeding regarding supplement doses.

Boswellia serrata is generally well tolerated short-term and is likely safe in pregnancy but should be avoided while breastfeeding. Manganese is safe in normal dietary amounts but high-dose supplements carry a serious risk of neurotoxicity and Parkinson-like symptoms.

Sodium and potassium should be used with caution — excess sodium is linked to high blood pressure and heart strain, and potassium supplements can cause dangerously high blood levels, especially in people with kidney disease.

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 — Boswellia Serrata, Manganese, Turmeric, Chondroitin Sulfate, Glucosamine, 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.
  • For scale: 1,529 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 Joint Synergy +, double-check with your pharmacist if you take warfarin (Coumadin) or other blood thinners (anticoagulants) and antiplatelet drugs — glucosamine and several other ingredients may increase bleeding risk. Also check if you take antipsychotic drugs, insulin, furosemide (Lasix), monoamine oxidase inhibitors (MAOIs), selegiline, raltegravir, heart or blood pressure medications, potassium-sparing diuretics, ACE inhibitors, angiotensin receptor blockers, tetracycline antibiotics, quinolone antibiotics, chemotherapy drugs, methotrexate, tramadol, tacrolimus, tamoxifen, sulfasalazine, or acetaminophen.

Additionally, check if you take any medications metabolized by liver enzymes (CYP2D6, CYP2C19, CYP1A2, CYP2C9, CYP3A4) or immunosuppressants.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFully disclosed formula with clinical evidence supporting its stated purpose. Major medication interactions have been identified, and safety information is well characterized.

Joint Synergy + is a multi-ingredient joint support formula with some ingredients rated possibly or likely effective for osteoarthritis and other uses. However, the product has multiple Moderate and one Major interaction with common medications, especially blood thinners, heart medications, diabetes drugs, and psychiatric medications.

If you take any prescription medication — particularly warfarin or other anticoagulants, blood pressure drugs, diabetes medications, or psychiatric drugs — check your exact medications with the tool on this page before starting. Talk to your pharmacist or doctor about whether this product is right for you.

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

Assessment coverage: 10 of 15 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Sep 25, 2024.

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 Joint Synergy +, straight from the product label.

Brand MRM Nutrition
Barcode (UPC) 60949221008
Net contents 120 Capsule(s)
Market status On market
Date entered into DSLD Sep 25, 2024
DSLD ID 319095
Product type Other Combinations
Supplement form Capsule
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Adult (18 - 50 Years), Women (not pregnant or lactating), Gluten Free
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 Joint Synergy + by MRM Nutrition, sourced from the NIH Dietary Supplement Label Database.

Supplement Facts

Daily Value (DV) Target Group(s):
Adults and children 4 or more years of age
Minimum serving Sizes:
2 Capsule(s)
Maximum serving Sizes:
2 Capsule(s)
Servings per container
60
UPC/BARCODE
60949221008
IngredientAmount% DV
Bromelain50 mg--
Methylsulfonylmethane250 mg--
Manganese4 mg170%
Glucosamine sulfate potassium chloride400 mg--
Chondroitin Sulfate Sodium120 mg--
Panax ginseng Root Extract50 mg--
White Willow bark extract40 mg--
Cetyl Myristoleate Complex50 mg--
Collagen Protein Complex120 mg--
Theracurmin Turmeric root extract20 mg--
Sodium10 mg--
Chloride45 mg2%
Potassium50 mg--
Sea Cucumber50 mg--
Boswellia serrata Leaf Extract100 mg--

Other ingredients: Gelatin, Rice Flour, Magnesium Stearate

Tap any ingredient to jump to its full detail below.

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

Suggested usage: Take 2 capsules per day with a meal or as directed by your qualified health care provider.

Formulation

Supports Joint Health

GF (gluten free) NON GMO

Joint Health

Contains no added milk, egg, peanut, tree nut, fish, soy, wheat, or gluten ingredients.

Formula

Joint Synergy + With Theracurmin, the #1 Most Absorbable Curcumin

FDA Disclaimer Statement

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

Precautions

Warning: This product contains natural salicylates, do not use if pregnant, nursing, allergic to aspirin, or on blood thinning medication.

Warning: This product contains natural salicylates, do not use if pregnant, nursing, allergic to aspirin, or on blood thinning medication.

Contains shellfish.

Brand IP Statement(s)

Thermacurmin is a registered trademark of Theravalues Corp.

General Statements

Made from recycled materials

FDA Statement of Identity

Dietary Supplement

See for yourself

Joint Synergy + by MRM Nutrition label

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

What’s inside

The Ingredients in Joint Synergy + by MRM Nutrition

These are the 15 active ingredients this product is made of. Select any to open its full monograph.

Serving size2 Capsule(s) Dosage formCapsule Servings per container60 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.

Bromelain

Interacts with
141 drugs
50 mg per serving

Bromelain is a group of protein-digesting enzymes from pineapple that people take mainly for inflammation, swelling, and sinus problems. Some early st...

Bromelain monograph & interactions

Methylsulfonylmethane

250 mg per serving

Manganese

Interacts with
83 drugs
4 mg per serving Form: Manganese Citrate

Manganese is an essential trace mineral your body needs in small amounts for bone formation, metabolism, and antioxidant defense, and most people get...

Manganese monograph & interactions

Glucosamine sulfate potassium chloride

Interacts with
170 drugs
400 mg per serving

Glucosamine is a natural compound found in cartilage and joint fluid, and it is one of the most popular supplements for osteoarthritis, especially of...

Glucosamine sulfate potassium chloride monograph & interactions

Chondroitin Sulfate Sodium

Interacts with
2 drugs
120 mg per serving

Chondroitin sulfate is a naturally occurring building block of cartilage that is widely taken, often with glucosamine, for osteoarthritis joint pain....

Chondroitin Sulfate Sodium monograph & interactions

Panax ginseng Root Extract

Interacts with
1,130 drugs
50 mg per serving Form: Ginsenosides

Panax ginseng is a popular traditional herb used to boost energy, ease stress, and support overall wellness, though scientific evidence is mixed and m...

Panax ginseng Root Extract monograph & interactions

White Willow bark extract

Interacts with
127 drugs
40 mg per serving Form: Salicin

Willow bark is a traditional plant remedy that contains salicin, a compound related to aspirin, and is most often used for pain and inflammation. Some...

White Willow bark extract monograph & interactions

Cetyl Myristoleate Complex

50 mg per serving

Collagen Protein Complex

120 mg per serving

Theracurmin Turmeric root extract

Interacts with
1,133 drugs
20 mg per serving

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

Theracurmin Turmeric root extract monograph & interactions

Sodium

Interacts with
205 drugs
10 mg per serving Form: Chondroitin Sulfate Sodium

Sodium is an essential mineral and electrolyte your body needs to balance fluids, support nerves, and help muscles work. Most people in modern diets g...

Sodium monograph & interactions

Chloride

45 mg per serving Form: Glucosamine Sulfate Potassium Chloride

Potassium

Interacts with
62 drugs
50 mg per serving Form: Glucosamine Sulfate 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

Sea Cucumber

50 mg per serving Form: Mucopolysaccharides

Boswellia serrata Leaf Extract

Interacts with
952 drugs
100 mg per serving Form: Boswellic Acids

Boswellia serrata is a tree resin used in traditional medicine, mainly for joint pain and inflammation. Some studies suggest it may help with osteoart...

Boswellia serrata Leaf Extract monograph & interactions

Other (inactive) ingredients: Gelatin, Rice Flour, Magnesium Stearate. These complete the product’s ingredient list but are not active constituents.

Interaction report

Joint Synergy + by MRM Nutrition Drug Interactions

Want to check YOUR meds against Joint Synergy +?

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
1,528Drugs
2 Major 1,498 Moderate 28 Minor

Each ingredient & the kinds of drugs it affects

For each ingredient in Joint Synergy + 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.

Theracurmin 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

Panax ginseng Root Extract20 drug types · 1,130 drugs

Anticoagulant/Antiplatelet Drugs

Although Panax ginseng has shown antiplatelet effects in the laboratory, it is unlikely to increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro evidence suggests that ginsenoside constituents in Panax ginseng might decrease platelet aggregation. However, research in humans suggests that ginseng does not affect platelet aggregation. Animal research indicates low oral bioavailability of Rb1 and rapid elimination of Rg1, which might explain the discrepancy between in vitro and human research. Until more is known, use with caution in patients concurrently taking anticoagulant or antiplatelet drugs.

Likelihood Unlikely Evidence B
Antidiabetes Drugs

Theoretically, taking Panax ginseng with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research suggests that Panax ginseng might decrease blood glucose levels. Monitor blood glucose levels closely.

Likelihood Probable Evidence B
Caffeine

Theoretically, taking Panax ginseng with caffeine might increase the risk of adverse stimulant effects.
Panax ginseng has been shown to have stimulant effects. Theoretically, caffeine might have an additive effect on the stimulant effects of Panax ginseng.

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

Theoretically, Panax ginseng might increase levels of drugs metabolized by CYP2D6. However, research is conflicting.
There is some evidence that Panax ginseng can inhibit the CYP2D6 enzyme by approximately 6%. In addition, in animal research, Panax ginseng inhibits the metabolism of dextromethorphan, a drug metabolized by CYP2D6, by a small amount. However, contradictory research suggests Panax ginseng might not inhibit CYP2D6. Until more is known, use Panax ginseng cautiously in patients taking drugs metabolized by these enzymes.

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

Theoretically, Panax ginseng might increase or decrease levels of drugs metabolized by CYP3A4.
Panax ginseng may affect the clearance of drugs metabolized by CYP3A4. One such drug is imatinib. Inhibition of CYP3A4 was believed to be responsible for a case of imatinib-induced hepatotoxicity. In contrast, Panax ginseng has been shown to increase the clearance of midazolam, another drug metabolized by CYP3A4. Clinical research shows that Panax ginseng can reduce midazolam area under the curve by 44%, maximum plasma concentration by 26%, and time to reach maximum plasma concentration by 29%. Midazolam metabolism was also increased in animals given Panax ginseng. Until more is known, use Panax ginseng cautiously in combination with CYP3A4 substrates.

Likelihood Possible Evidence B
Estrogens

Theoretically, concomitant use of large amounts of Panax ginseng might interfere with hormone replacement therapy.
Laboratory research and some case reports suggest that Panax ginseng can have estrogenic effects due to competition for estrogen receptors. The estrogenic activity is attributed to the ginsenoside constituents of Panax ginseng.

Likelihood Possible Evidence D
Furosemide (Lasix)

Theoretically, Panax ginseng might reduce the effects of furosemide.
There is some concern that Panax ginseng might contribute to furosemide resistance. There is one case of resistance to furosemide diuresis in a patient taking a germanium-containing ginseng product.

Likelihood Possible Evidence D
Imatinib (Gleevec)

Theoretically, Panax ginseng might increase the effects and adverse effects of imatinib.
A case of imatinib-induced hepatotoxicity has been reported for a 26-year-old male with chronic myelogenous leukemia stabilized on imatinib for 7 years. The patient took imatinib 400 mg along with a Panax ginseng-containing energy drink daily for 3 months. Since imatinib-associated hepatotoxicity typically occurs within 2 years of initiating therapy, it is believed that Panax ginseng affected imatinib toxicity though inhibition of cytochrome P450 3A4. CYP3A4 is the primary enzyme involved in imatinib metabolism.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, Panax ginseng use might interfere with immunosuppressive therapy.
Panax ginseng might have immune system stimulating properties.

Likelihood Possible Evidence B
Insulin

Theoretically, taking Panax ginseng with insulin might increase the risk of hypoglycemia.
Clinical research suggests that Panax ginseng might decrease blood glucose levels. Insulin dose adjustments might be necessary in patients taking Panax ginseng; use with caution.

Likelihood Probable Evidence B
Midazolam (Versed)

Theoretically, Panax ginseng may increase the clearance of midazolam.
Midazolam is metabolized by cytochrome P450 3A4 (CYP3A4). Clinical research suggests that Panax ginseng can reduce midazolam area under the curve by 44%, maximum plasma concentration by 26%, and time to reach maximum plasma concentration by 29%. Midazolam metabolism was also increased in animals given Panax ginseng.

Likelihood Probable Evidence B
Monoamine Oxidase Inhibitors (Maois)

Theoretically, Panax ginseng can interfere with MAOI therapy.
Concomitant use of Panax ginseng with phenelzine (Nardil) is associated with insomnia, headache, tremors, and hypomania.

Likelihood Probable Evidence D
Nifedipine (Procardia)

Theoretically, taking Panax ginseng with nifedipine might increase serum levels of nifedipine and the risk of hypotension.
Preliminary clinical research shows that concomitant use can increase serum levels of nifedipine in healthy volunteers. This might cause the blood pressure lowering effects of nifedipine to be increased when taken concomitantly with Panax ginseng.

Likelihood Possible Evidence B
Qt Interval-Prolonging Drugs

Theoretically, Panax ginseng has an additive effect with drugs that prolong the QT interval and potentially increase the risk of ventricular arrhythmias. However, research is conflicting.
Clinical research shows that short-term use of Panax ginseng can increase the QT interval. However, no changes in QT interval have been identified with prolonged use.

Likelihood Possible Evidence B
Raltegravir (Isentress)

Theoretically, taking Panax ginseng with raltegravir might increase the risk of liver toxicity.
A case report suggests that concomitant use of Panax ginseng with raltegravir can increase serum levels of raltegravir, resulting in elevated liver enzymes levels.

Likelihood Possible Evidence D
Selegiline (Eldepryl)

Theoretically, Panax ginseng might increase or decrease levels of selegiline, possibly altering the effects and side effects of selegiline.
Animal research shows that taking selegiline with a low dose of Panax ginseng extract (1 gram/kg) reduces selegiline bioavailability, while taking a high dose of Panax ginseng extract (3 grams/kg) increases selegiline bioavailability. More research is needed to confirm these effects.

Likelihood Possible Evidence D
Stimulant Drugs

Theoretically, taking Panax ginseng with stimulant drugs might increase the risk of adverse stimulant effects.
Panax ginseng has been shown to have stimulant effects.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Panax ginseng might affect the clearance of warfarin. However, this interaction appears to be unlikely.
There has been a single case report of decreased effectiveness of warfarin in a patient who also took Panax ginseng. However, it is questionable whether Panax ginseng was the cause of this decrease in warfarin effectiveness. Some research in humans and animals suggests that Panax ginseng does not affect the pharmacokinetics of warfarin. However, other research in humans suggests that Panax ginseng might modestly increase the clearance of the S-warfarin isomer. More evidence is needed to determine whether Panax ginseng causes a significant interaction with warfarin.

Likelihood Unlikely Evidence B
Fexofenadine (Allegra)

Theoretically, Panax ginseng might decrease blood levels of oral or intravenous fexofenadine.
Animal research suggests that taking Panax ginseng in combination with oral or intravenous fexofenadine may reduce the bioavailability of fexofenadine. Some scientists have attributed this effect to the ability of Panax ginseng to increase the expression of P-glycoprotein.

Likelihood Possible Evidence D
Lopinavir/Ritonavir (Kaletra)

Although Panax ginseng has demonstrated variable effects on cytochrome P450 3A4 (CYP3A4), which metabolizes lopinavir, Panax ginseng is unlikely to alter levels of lopinavir/ritonavir.
Lopinavir is metabolized by CYP3A4 and is administered with the CYP3A4 inhibitor ritonavir to increase its plasma concentrations. Panax ginseng has shown variable effects on CYP3A4 activity in humans. However, taking Panax ginseng (Vitamer Laboratories) 500 mg twice daily for 14 days did not alter the pharmacokinetics of lopinavir/ritonavir in 12 healthy volunteers.

Likelihood Unlikely Evidence B

Boswellia serrata Leaf Extract6 drug types · 952 drugs

Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, Boswellia serrata might increase the levels of CYP1A2 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP1A2 enzymes.

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

Theoretically, Boswellia serrata might increase the levels of CYP2C19 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP2C19 enzymes.

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

Theoretically, Boswellia serrata might increase the levels of CYP2C9 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP2C9 enzymes.

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

Theoretically, Boswellia serrata might increase the levels of CYP2D6 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP2D6 enzymes.

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

Theoretically, Boswellia serrata might increase or decrease the levels and clinical effects of CYP3A4 substrates.
In vitro research shows that Boswellia serrata gum resin inhibits CYP3A4 enzymes. Other in vitro research shows that Boswellia serrata extract inhibits CYP3A4 enzymes at most concentrations, although it may modestly induce enzyme activity at low concentrations.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, Boswellia serrata might alter the effects of immunosuppressive drugs.
Some in vitro research suggests that Boswellia serrata extracts might inhibit mediators of autoimmune disorders such as leukotrienes and reduce production of antibodies and cell-mediated immunity. However, other in vitro research suggests that, when coupled with calcium ions, boswellic acids containing the keto group have immunostimulant properties within specific cell signaling pathways.

Likelihood Possible Evidence D

Sodium7 drug types · 205 drugs

Antihypertensive Drugs

Theoretically, a high intake of dietary sodium might reduce the effectiveness of antihypertensive drugs.
High intake of dietary sodium can increase systolic and diastolic blood pressure. Also, high intake of sodium may necessitate increased use of antihypertensive medications to achieve blood pressure control in some patients, such as those with chronic kidney disease.

Likelihood Probable Evidence A
Corticosteroids

Concomitant use of mineralocorticoids and some glucocorticoids with sodium supplements might increase the risk of hypernatremia.
Mineralocorticoids and some glucocorticoids (corticosteroids) cause sodium retention. This effect is dose-related and depends on mineralocorticoid potency. It is most common with hydrocortisone, cortisone, and fludrocortisone, followed by prednisone and prednisolone.

Likelihood Possible Evidence D
Didanosine (Videx)

Concomitant use of didanosine with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia.
Didanosine formulations contain a significant amount of sodium.

Likelihood Probable Evidence C
Lithium

Altering dietary intake of sodium might alter the levels and clinical effects of lithium.
High sodium intake can reduce plasma concentrations of lithium by increasing lithium excretion. Reducing sodium intake can significantly increase plasma concentrations of lithium and cause lithium toxicity in patients being treated with lithium carbonate. Stabilizing sodium intake is shown to reduce the percentage of patients with lithium level fluctuations above 0.8 mEq/L. Patients taking lithium should avoid significant alterations in their dietary intake of sodium.

Likelihood Probable Evidence B
Sodium Phosphates

Theoretically, concomitant use of sodium phosphate with sodium supplements might increase the risk of hypernatremia.
Use of high doses (> 45 mL in 24 hours) of sodium phosphate, such as those used for bowel cleansing before surgery, can lead to serious electrolyte disturbances, including hypernatremia. The risk of hypernatremia is highest in the elderly and people with other risk factors for electrolyte disturbances.

Likelihood Possible Evidence D
Sodium-Containing Drugs

Concomitant use of sodium-containing drugs with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia and long-term sodium-related complications.
The Chronic Disease Risk Reduction (CDRR) intake level of 2.3 grams of sodium daily indicates the intake at which it is believed that chronic disease risk increases for the apparently healthy population. Some medications contain high quantities of sodium. When used in conjunction with sodium supplements or high-sodium diets, the CDRR may be exceeded. Additionally, concomitant use may increase the risk for hypernatremia; this risk is highest in the elderly and people with other risk factors for electrolyte disturbances.

Likelihood Possible Evidence D
Tolvaptan (Samsca)

Theoretically, concomitant use of tolvaptan with sodium might increase the risk of hypernatremia.
Tolvaptan is a vasopressin receptor 2 antagonist that is used to increase sodium levels in patients with hyponatremia. Patients taking tolvaptan should use caution with the use of sodium salts such as sodium chloride.

Likelihood Probable Evidence C

Glucosamine sulfate potassium chloride4 drug types · 170 drugs

Warfarin (Coumadin)

Glucosamine might increase the anticoagulant effects of warfarin and increase the risk of bruising and bleeding.
In two individual case reports, glucosamine/chondroitin combinations were associated with a significant increase in international normalized ratio (INR) in patients previously stabilized on warfarin. In one case, the increase in INR occurred only after tripling the dose of a glucosamine/chondroitin supplement from 500 mg/400 mg daily to 1500/1200 mg daily. Additionally, 20 voluntary case reports to the U.S. Food & Drug Administration (FDA) have linked glucosamine plus chondroitin with increased INR, bruising, and bleeding in patients who were also taking warfarin. There have also been 20 additional case reports to the World Health Organization (WHO) that link glucosamine alone to increased INR in patients taking warfarin. The mechanism of this interaction is unclear. Glucosamine is a small component of heparin, but is not thought to have anticoagulant activity; however, animal research suggests that it might have antiplatelet activity.

Likelihood Probable Evidence D
Topoisomerase Ii Inhibitors

Theoretically glucosamine may induce resistance to topoisomerase II inhibitors.
In vitro research suggests that glucosamine might induce resistance to etoposide (VP16, VePesid) and doxorubicin (Adriamycin) by reducing inhibition of topoisomerase II, an enzyme required for DNA replication in tumor cells. This effect has not been reported in humans.

Likelihood Possible Evidence D
Acetaminophen (Tylenol, Others)

Acetaminophen might interfere with the activity of glucosamine sulfate by interacting with the sulfate portion.
Anecdotal reports suggest that adding glucosamine to an acetaminophen regimen might decrease pain control in patients with osteoarthritis. Some research suggests that the sulfate portion of glucosamine sulfate might contribute to its effect in osteoarthritis. Since acetaminophen metabolism requires sulfur and reduces serum sulfate concentrations, acetaminophen could theoretically interfere with the action of glucosamine sulfate. Conversely, the administration of sulfate could theoretically decrease the effectiveness of acetaminophen in sulfate-deficient people by increasing its clearance.

Likelihood Possible Evidence B
Antidiabetes Drugs

Despite initial concerns, it is unlikely that glucosamine will interfere with the effects of antidiabetes drugs.
In vitro and animal research has suggested that glucosamine might increase insulin resistance or decrease insulin production. This has raised concerns that taking glucosamine might worsen diabetes and decrease the effectiveness of diabetes drugs. However, clinical research suggests that glucosamine does not have adverse effects on blood glucose or glycated hemoglobin (HbA1C) in healthy, obese, or type 2 diabetes patients.

Likelihood Unlikely Evidence B

Bromelain2 drug types · 141 drugs

Anticoagulant/Antiplatelet Drugs

Bromelain may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
There is one case report of a patient experiencing minor bruising while taking bromelain with naproxen. Bromelain is thought to have antiplatelet activity. Whether this interaction is of concern with topical bromelain is unclear. Interference with coagulation of burn wounds has been reported in a patient receiving bromelain-based enzymatic debridement. However, observational research has found that topical bromelain debridement is not associated with increases or decreases in laboratory markers of coagulation when compared with surgical debridement.

Likelihood Possible Evidence D
Tetracycline Antibiotics

Theoretically, bromelain might increase levels of tetracycline antibiotics.
Laboratory research suggests that bromelain might increase the absorption of tetracycline antibiotics. However, a study in healthy adults reported no difference in tetracycline plasma levels when a 500 mg dose was taken with or without bromelain 80 mg.

Likelihood Possible Evidence B

White Willow bark extract5 drug types · 127 drugs

Acetazolamide

Theoretically, willow bark might result in additive adverse effects associated with acetazolamide.
Willow bark contains salicin, a plant salicylate. Human case reports suggests that a combination of acetazolamide and salicylate increases unbound plasma levels of acetazolamide, as well as adverse effects related to acetazolamide.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, willow bark might increase the risk of bleeding when taken with anticoagulant/antiplatelet drugs.
Willow bark has antiplatelet effects, but less so than aspirin.

Likelihood Probable Evidence D
Aspirin

Theoretically, willow bark might increase the effects and adverse effects of aspirin.
Willow bark contains salicin, a plant salicylate. It might have an additive effect when taken with other salicylate-containing drugs such as aspirin.

Likelihood Probable Evidence D
Choline Magnesium Trisalicylate (Trilisate)

Theoretically, willow bark might increase the effects and adverse effects of choline magnesium trisalicylate.
Willow bark contains salicin, a plant salicylate. It might have an additive effect when taken with other salicylate-containing drugs such as choline magnesium trisalicylate.

Likelihood Probable Evidence D
Salsalate (Disalcid)

Theoretically, willow bark might increase the effects and adverse effects of salsalate.
Willow bark contains salicin, a plant salicylate. It might have an additive effect when taken with other salicylate-containing drugs such as salsalate.

Likelihood Probable Evidence D

Manganese3 drug types · 83 drugs

Antipsychotic Drugs

Theoretically, the risk for manganese toxicity might increase when taken with antipsychotic drugs.
Hallucinations and behavioral changes have been reported in a patient with liver disease who was taking haloperidol and manganese. Researchers speculate that taking manganese along with haloperidol, phenothiazine-derivatives, or other antipsychotic medications might increase the risk of manganese toxicity in some patients.

Likelihood Possible Evidence D
Quinolone Antibiotics

Theoretically, manganese might reduce the absorption of quinolone antibiotics.
Manganese is a multivalent cation. Interactions resulting in reduced quinolone absorption have been reported between quinolones and other multivalent cations, such as calcium and iron.

Likelihood Probable Evidence D
Tetracycline Antibiotics

Theoretically, manganese might reduce the absorption of tetracycline antibiotics.
Manganese is a multivalent cation. Interactions resulting in reduced tetracycline absorption have been reported between tetracyclines and other multivalent cations, such as calcium and iron.

Likelihood Probable Evidence D

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

Chondroitin Sulfate Sodium1 drug type · 2 drugs

Warfarin (Coumadin)

Taking chondroitin in combination with glucosamine might increase the anticoagulant effects of warfarin. However, the effect of chondroitin alone is unclear.
There have been multiple reports of increased international normalized ratio (INR) in patients taking warfarin with glucosamine, with or without chondroitin. The lack of reports with chondroitin alone seem to suggest that the interactions occurring in these reports may have been due to glucosamine. In two individual case reports, glucosamine/chondroitin combinations were associated with a significant increase in INR in patients previously stabilized on warfarin. Additionally, 20 voluntary case reports to the US Food & Drug Administration (FDA) have linked glucosamine plus chondroitin with increased INR, bruising, and bleeding in patients who were also taking warfarin. There have also been 20 additional case reports to the World Health Organization (WHO) that link glucosamine alone, without chondroitin, to increased INR in patients taking warfarin.

Likelihood Unlikely Evidence D
The maker

Brand information

Manufacturer and brand details for Joint Synergy +, from the product label.

MRM Nutrition

See all MRM Nutrition products
Name
MRM
Street Address
2665 Vista Pacific Dr
City
Oceanside
State
CA
ZipCode
92056
Phone Number
1-800-948-6296
Web Address
www.mrmnutrition.com
Pharmacist Counseling Corner

Joint Synergy + by MRM Nutrition: Common Questions

Does Joint Synergy + by MRM Nutrition interact with any medications?
Yes. Based on its ingredients, Joint Synergy + has a known interaction with 1,528 medications, including 2 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Joint Synergy + contains 15 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.
Is it safe to take Joint Synergy + while I'm pregnant or breastfeeding?
Bromelain, glucosamine, chondroitin, Panax ginseng, white willow bark, and Boswellia serrata should be avoided during pregnancy — there isn't enough safety data. White willow bark specifically should be avoided because it acts like aspirin and may pose risks, especially later in pregnancy. While breastfeeding, bromelain, glucosamine, chondroitin, Panax ginseng, willow bark, and Boswellia serrata should be avoided because safety is unknown. Turmeric is likely safe during pregnancy but caution is advised with supplement doses while breastfeeding. Talk to your doctor or pharmacist before taking this product if you're pregnant or nursing.
What are the most common side effects I might experience?
The most common side effects are gastrointestinal: diarrhea, constipation, bloating, nausea, heartburn, and abdominal pain. Bromelain may cause flatulence and headache. Panax ginseng commonly causes insomnia. White willow bark may cause indigestion and vomiting. Turmeric may cause constipation, diarrhea, nausea, or vomiting. If you experience severe allergic reactions, asthma symptoms, or significant gastrointestinal bleeding, stop the product and seek medical help.
Does glucosamine actually work for joint pain and osteoarthritis?
Glucosamine is rated likely effective for osteoarthritis based on the evidence we hold. Chondroitin sulfate is rated possibly effective for osteoarthritis. Results vary between individuals, and quality of supplements differs, so your experience may differ from others.
Why is there so much sodium and potassium in this product, and could they cause problems?
Sodium and potassium are electrolytes that support normal body function. However, excess sodium is linked to high blood pressure and heart strain, especially if you take blood pressure medications. High potassium can be dangerous if you have kidney disease or take certain heart or blood pressure drugs that reduce potassium excretion. Check with your pharmacist about whether the amounts in this product are appropriate for you, especially if you have heart disease, high blood pressure, or kidney problems.
I take warfarin — can I use this product?
Glucosamine in this product may increase warfarin's effects and raise your bleeding risk — this is a Major concern. Chondroitin, Panax ginseng, and bromelain also theoretically interact with warfarin at Moderate severity. Do not take this product with warfarin without talking to your doctor or pharmacist first; your warfarin levels may need to be monitored more closely.
Can I take this with my blood pressure or heart medications?
Several ingredients in this product may interact with blood pressure and heart medications. Panax ginseng, Boswellia serrata, turmeric, sodium, and potassium all have documented interactions with these drug types. Check your exact medications with the tool on this page before starting, and talk to your pharmacist to make sure they are safe to use together.

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.

Joint Synergy + label
Go deeper

The Full Monographs Behind Joint Synergy +’s Ingredients

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

Herb & supplement monograph

Bromelain

Interacts with 141 drugs

Bromelain is a group of protein-digesting enzymes from pineapple that people take mainly for inflammation, swelling, and sinus problems. Some early studies are promising, but the overall evi...

Read the full Bromelain monograph →
Herb & supplement monograph

Manganese

Interacts with 83 drugs

Manganese is an essential trace mineral your body needs in small amounts for bone formation, metabolism, and antioxidant defense, and most people get enough from a normal diet. Supplements m...

Read the full Manganese monograph →
Herb & supplement monograph

Glucosamine

Interacts with 170 drugs

Glucosamine is a natural compound found in cartilage and joint fluid, and it is one of the most popular supplements for osteoarthritis, especially of the knee. The evidence is mixed, with so...

Read the full Glucosamine monograph →
Herb & supplement monograph

Chondroitin Sulfate

Interacts with 2 drugs

Chondroitin sulfate is a naturally occurring building block of cartilage that is widely taken, often with glucosamine, for osteoarthritis joint pain. The evidence is mixed—some people report...

Read the full Chondroitin Sulfate monograph →
Herb & supplement monograph

Panax Ginseng

Interacts with 1,130 drugs

Panax ginseng is a popular traditional herb used to boost energy, ease stress, and support overall wellness, though scientific evidence is mixed and mostly preliminary. It is generally well...

Read the full Panax Ginseng monograph →
Herb & supplement monograph

Willow Bark

Interacts with 127 drugs

Willow bark is a traditional plant remedy that contains salicin, a compound related to aspirin, and is most often used for pain and inflammation. Some evidence suggests it may modestly help...

Read the full Willow Bark 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

Sodium

Interacts with 205 drugs

Sodium is an essential mineral and electrolyte your body needs to balance fluids, support nerves, and help muscles work. Most people in modern diets get more than enough—often too much—from...

Read the full Sodium 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

Boswellia Serrata

Interacts with 952 drugs

Boswellia serrata is a tree resin used in traditional medicine, mainly for joint pain and inflammation. Some studies suggest it may help with osteoarthritis symptoms, but the overall evidenc...

Read the full Boswellia Serrata monograph →
Sources

Sources & How We Checked

Joint Synergy +'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 366 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.

Bromelain 19 references
  1. Nettis E, Napoli G, Ferrannini A, Tursi A. IgE-mediated allergy to bromelain. Allergy 2001;56:257-8. PubMed
  2. Taussig SJ, Batkin S. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol 1988;22:191-203.. PubMed
  3. Bradbrook ID, Morrison PJ, Rogers HJ. The effect of bromelain on the absorption of orally administered tetracycline. Br J Clin Pharmacol 1978;6:552-4. PubMed
  4. Bush TM, Rayburn KS, Holloway SW, et al. Adverse interactions between herbal and dietary substances and prescription medications: a clinical survey. Altern Ther Health Med 2007;13:30-5.
  5. Brien S, Lewith G, Walker AF, et al. Bromelain as an adjunctive treatment for moderate-to-severe osteoarthritis of the knee: a randomized placebo-controlled pilot study. QJM 2006;99:841-50. PubMed
  6. Mori S, Ojima Y, Hirose T, et al. The clinical effect of proteolytic enzyme containing bromelain and trypsin on urinary tract infection evaluated by double blind method. Acta Obstet Gynaecol Jpn 1972;19:147-53.
  7. Glaser D, Hilberg T. The influence of bromelain on platelet count and platelet activity in vitro. Platelets 2006;17:37-41. PubMed
  8. Heinicke R M, van der Wal L, Yokoyama M. Effect of bromelain (Ananase) on human platelet aggregation. Experientia 1972;28:844-5. PubMed
  9. Gailhofer, G., Wilders-Truschnig, M., Smolle, J., and Ludvan, M. Asthma caused by bromelain: an occupational allergy. Clin Allergy 1988;18(5):445-450. PubMed
  10. Mattei, O., Fabri, G., and Farina, G. [Occupational health experience regarding four cases of asthma due to bromelain (author's transl)]. Medicina del Lavoro 1979;70(5):404-409.
  11. Galleguillos, F. and Rodriguez, J. C. Asthma caused by bromelin inhalation. Clin Allergy 1978;8(1):21-24. PubMed
  12. Perez-Camo I, Quirce S, Duran MA, and et al. Latex allergy: evidence of cross-reactivity with papain and bromelain [abstract]. Allergy 1996;51(suppl 31):48.
  13. Martin GJ, Ehrenreich J, and Asbell N. Bromelain: pineapple proteases with anti-edema activity. Exp Med Surg 1962;20:227-247.
  14. Kasemsuk T, Saengpetch N, Sibmooh N, Unchern S. Improved WOMAC score following 16-week treatment with bromelain for knee osteoarthritis. Clin Rheumatol. 2016 Oct;35(10):2531-40. PubMed
  15. Kutlu Ö, DemirbaS A, Elmas ÖF, Güvenç U, Metin A. Fixed drug eruption: a new side effect of bromelain. Contact Dermatitis 2020. Online ahead of print. PubMed
  16. Shoham Y, Shapira E, Haik J, et al. Bromelain-based enzymatic debridement of chronic wounds: Results of a multicentre randomized controlled trial. Wound Repair Regen 2021;29(6):899-907. PubMed
  17. Pfister P, Garcia Wendel PD, Kim BS, et al. Coagulation side effects of enzymatic debridement in burned patients. Burns 2022. PubMed
  18. Hasham S, Riyat H, Fletcher A, O'Boyle CP, Alexander S. To bleed or not to bleed? Case series and discussion of haemorrhage risk with enzymatic debridement in burn injuries. Scars Burn Heal 2023;9:20595131231168333. PubMed
  19. Leelakanok N, Petchsomrit A, Janurai T, Saechan C, Sunsandee N. Efficacy and safety of bromelain: A systematic review and meta-analysis. Nutr Health 2023. PubMed

See these in context on the Bromelain monograph →

Manganese 21 references
  1. Hansten PD, Horn JR. Hansten and Horn's Drug Interactions Analysis and Management. Vancouver, CAN:Appl Therapeut, 1999.
  2. Barrington WW, Angle CR, Willcockson NK, et al. Autonomic function in manganese alloy workers. Environ Res 1998;78:50-8. PubMed
  3. Hauser RA, Zesiewicz TA, Martinez C, et al. Blood manganese correlates with brain magnetic resonance imaging changes in patients with liver disease. Can J Neurol Sci 1996;23:95-8. PubMed
  4. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2002.
  5. Lee JW. Manganese intoxication. Arch Neurol 2000;57:597-9.. PubMed
  6. Powers KM, Smith-Weller T, Franklin GM, et al. Parkinson's disease risks associated with dietary iron, manganese, and other nutrient intakes. Neurology 2003;60:1761-6.. PubMed
  7. McMillan, D. E. A brief history of the neurobehavioral toxicity of manganese: some unanswered questions. Neurotoxicology 1999;20(2-3):499-507.
  8. Gerber, G. B., Leonard, A., and Hantson, P. Carcinogenicity, mutagenicity and teratogenicity of manganese compounds. Crit Rev Oncol Hematol. 2002;42(1):25-34. PubMed
  9. Jiang, Y. and Zheng, W. Cardiovascular toxicities upon manganese exposure. Cardiovasc.Toxicol 2005;5(4):345-354. PubMed
  10. Mehta, R. and Reilly, J. J. Manganese levels in a jaundiced long-term total parenteral nutrition patient: potentiation of haloperidol toxicity? Case report and literature review. JPEN J Parenter.Enteral Nutr 1990;14(4):428-430. PubMed
  11. Nemery, B. Metal toxicity and the respiratory tract. Eur Respir.J 1990;3(2):202-219. DOI
  12. Vanek VW, Borum P, Buchman A, et al. A.S.P.E.N. position paper: recommendations for changes in commercially available parenteral multivitamin and multi-trace element products. Nutr Clin Pract. 2012;27:440-491.doi: 10.1177/0884533612446706 PubMed
  13. Schuh MJ. Possible Parkinson's disease induced by chronic manganese supplement ingestion. Consult Pharm. 2016;31(12):698-703. doi: 10.4140/TCP.n.2016.698. PubMed
  14. Baker B, Ali A, Isenring L. Recommendations for manganese supplementation to adult patients receiving long-term home parenteral nutrition: an analysis of the supporting evidence. Nutr Clin Pract 2016;31(2):180-5. doi: 10.1177/0884533615591600. PubMed
  15. Ho CSH, Ho RCM, Quek AML. Chronic manganese toxicity associated with voltage-gated potassium channel complex antibodies in a relapsing neuropsychiatric disorder. Int J Environ Res Public Health 2018;15(4). pii: E783. doi: 10.3390/ijerph15040783. PubMed
  16. Yamamoto M, Sakurai K, Eguchi A, et al.; Japan Environment and Children's Study Group: Association between blood manganese level during pregnancy and birth size: the Japan environment and children's study (JECS). Environ Res 2019;172:117-26. PubMed
  17. Li D, Ge X, Liu Z, et al. Association between long-term occupational manganese exposure and bone quality among retired workers. Environ Sci Pollut Res Int 2020;27(1):482-9. PubMed
  18. Martin KV, Sucharew H, Dietrich KN, et al. Co-exposure to manganese and lead and pediatric neurocognition in East Liverpool, Ohio. Environ Res 2021;202:111644. PubMed
  19. Racette BA, Nelson G, Dlamini WW, et al. Depression and anxiety in a manganese-exposed community. Neurotoxicology 2021;85:222-33. PubMed
  20. Ruiz-Azcona L, Fernández-Olmo I, Expósito A, et al. Impact of environmental airborne manganese exposure on cognitive and motor functions in adults: a systematic review and meta-analysis. Int J Environ Res Public Health 2021;18(8):4075. PubMed
  21. Uyar E, Gurkas E, Aksu AU, et al. Can therapeutic plasma exchange be life-saving in life-threatening manganese intoxication?. Transfus Apher Sci 2022;61(4):103417. PubMed

See these in context on the Manganese monograph →

Glucosamine 58 references
  1. Adams ME. Hype about glucosamine. Lancet 1999;354:353-4. PubMed
  2. Balkan B, Dunning BE. Glucosamine inhibits glucokinase in vitro and produces a glucose-specific impairment of in vivo insulin secretion in rats. Diabetes 1994;43:1173-9. PubMed
  3. Giaccari A, Morviducci L, Zorretta D, et al. In vivo effects of glucosamine on insulin secretion and insulin sensitivity in the rat: possible relevance to the maladaptive responses to chronic hyperglycaemia. Diabetologia 1995;38:518-24. PubMed
  4. Holmang A, Nilsson C, Niklasson M, et al. Induction of insulin resistance by glucosamine reduces blood flow but not interstitial levels of either glucose or insulin. Diabetes 1999;48:106-11. PubMed
  5. Houpt JB, McMillan R, Wein C, Paget-Dellio SD. Effect of glucosamine hydrochloride in the treatment of pain of osteoarthritis of the knee. J Rheumatol 1999;26:2423-30.
  6. Barclay TS, Tsourounis C, McCart GM. Glucosamine. Ann Pharmacother 1998;32:574-9.
  7. Shankar RR, Zhu JS, Baron AD. Glucosamine infusion in rats mimics the beta-cell dysfunction of non-insulin-dependent diabetes mellitus. Metabolism 1998;47:573-7.
  8. Almada A, Harvey P, Platt K. Effects of chronic oral glucosamine sulfate on fasting insulin resistance index (FIRI) in non-diabetic individuals. FASEB J 2000;14:A750.
  9. Reginster JY, Deroisy R, Rovati LC, et al. Long-term effects of glucosamine sulfate on osteoarthritis progression: a randomised, placebo-controlled trial. Lancet 2001;357:251-6.
  10. Does glucosamine increase serum lipid levels and blood pressure? Pharmacist's Letter/Prescriber's Letter 2001;17(11):171115.
  11. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2002.
  12. Monauni T, Zenti MG, Cretti A, et al. Effects of glucosamine infusion on insulin secretion and insulin action in humans. Diabetes 2000;49:926-35. PubMed
  13. Pouwels MJ, Jacobs JR, Span PN, et al. Short-term glucosamine infusion does not affect insulin sensitivity in humans. J Clin Endocrinol Metab 2001;86:2099-103. DOI
  14. Yun J, Tomida A, Nagata K, Tsuruo T. Glucose-regulated stresses confer resistance to VP-16 in human cancer cells through a decreased expression of DNA topoisomerase II. Oncol Res 1995;7:583-90.
  15. Pavelka K, Gatterova J, Olejarova M, et al. Glucosamine sulfate use and delay of progression of knee osteoarthritis: A 3-year, randomized, placebo-controlled, double-blind study. Arch Intern Med 2002;162:2113-23. PubMed
  16. Tallia AF, Cardone DA. Asthma exacerbation associated with glucosamine-chondroitin supplement. J Am Board Fam Pract 2002;15:481-4..
  17. Scroggie DA, Albright A, Harris MD. The effect of glucosamine-chondroitin supplementation on glycosylated hemoglobin levels in patients with type 2 diabetes mellitus: a placebo-controlled, double-blinded, randomized clinical trial. Arch Intern Med 2003; PubMed
  18. Hoffer LJ, Kaplan LN, Hamadeh MJ, et al. Sulfate could mediate the therapeutic effect of glucosamine sulfate. Metabolism 2001;50:767-70.. PubMed
  19. Yu JG, Boies SM, Olefsky JM. The effect of oral glucosamine sulfate on insulin sensitivity in human subjects. Diabetes Care 2003;26:1941-2. PubMed
  20. Danao-Camara T. Potential side effects of treatment with glucosamine and chondroitin. Arthritis Rheum 2000;43:2853. PubMed
  21. Guillaume MP, Peretz A. Possible association between glucosamine treatment and renal toxicity: comment on the letter by Danao-Camara. Arthritis Rheum 2001;44:2943-4. PubMed
  22. Rozenfeld V, Crain JL, Callahan AK. Possible augmentation of warfarin effect by glucosamine-chondroitin. Am J Health Syst Pharm 2004;61:306-307. PubMed
  23. Tannis AJ, Barban J, Conquer JA. Effect of glucosamine supplementation on fasting and non-fasting plasma glucose and serum insulin concentrations in healthy individuals. Osteoarthritis Cartilage 2004;12:506-11. PubMed
  24. Bush TM, Rayburn KS, Holloway SW, et al. Adverse interactions between herbal and dietary substances and prescription medications: a clinical survey. Altern Ther Health Med 2007;13:30-5.
  25. Stumpf JL, Lin SW. Effect of glucosamine on glucose control. Ann Pharmacother 2006;40:694-8. PubMed
  26. Pham T, Cornea A, Blick KE, et al. Oral glucosamine in doses used to treat osteoarthritis worsens insulin resistance. Am J Med Sci 2007;333:333-9. PubMed
  27. Muniyappa R, Karne RJ, Hall G, et al. Oral glucosamine for 6 weeks at standard doses does not cause or worsen insulin resistance or endothelial dysfunction in lean or obese subjects. Diabetes 2006;55:3142-50. PubMed
  28. Knudsen J, Sokol GH. Potential glucosamine-warfarin interaction resulting in increased international normalized ratio: Case report and review of the literature and MedWatch database. Pharmacotherapy 2008;28:540-8. PubMed
  29. Yue QY, Strandell J, Myrberg O. Concomitant use of glucosamine potentiates the effect of warfarin. Jan 2006. Drug Safety 29(10):911-1010. DOI
  30. Rozendaal RM, Koes BW, van Osch GJVM, et al. Effect of glucosamine sulfate on hip osteoarthritis: A randomized trial. Ann Intern Med 2008;148:268-77. PubMed
  31. Baron AD, Zhu JS, Zhu JH, et al. Glucosamine induces insulin resistance in vivo by affecting GLUT 4 translocation in skeletal muscle. Implications for glucose toxicity. J Clin Invest 1995;96(6):2792-801. PubMed
  32. Nelson BA, Robinson KA, Buse MG. High glucose and glucosamine induce insulin resistance via different mechanisms in 3T3-L1 adipocytes. Diabetes 2000;49(6):981-91. PubMed
  33. Giordano N, Fioravanti A, Papakostas P, et al. The efficacy and tolerability of glucosamine sulfate in the treatment of knee osteoarthritis: a randomized, double-blind, placebo-controlled trial. Curr Ther Res Clin Exp 2009;70(3):185-196. PubMed
  34. Shaygannejad, V., Janghorbani, M., Savoj, M. R., and Ashtari, F. Effects of adjunct glucosamine sulfate on relapsing-remitting multiple sclerosis progression: preliminary findings of a randomized, placebo-controlled trial. Neurol Res 2010;32(9):981-985. PubMed
  35. Cahlin, B. J. and Dahlstrom, L. No effect of glucosamine sulfate on osteoarthritis in the temporomandibular joints--a randomized, controlled, short-term study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;112(6):760-766. PubMed
  36. Cerda C, Bruguera M, Parés A. Hepatotoxicity associated with glucosamine and chondroitin sulfate in patients with chronic liver disease. World J Gastroenterol 2013;19(32):5381-4. PubMed
  37. Hochberg MC, Martel-Pelletier J, Monfort J, Möller I, Castillo JR, Arden N,Berenbaum F, Blanco FJ, Conaghan PG, Doménech G, Henrotin Y, Pap T, Richette P, Sawitzke A, du Souich P, Pelletier JP; on behalf of the MOVES Investigation Group. Combined chondroi
  38. von Felden J, Montani M, Kessebohm K, Stickel F. Drug-induced acute liver injury mimicking autoimmune hepatitis after intake of dietary supplements containing glucosamine and chondroitin sulfate. Int J Clin Pharmacol Ther 2013;51(3):219-23. PubMed
  39. Provenza JR, Shinjo SK, Silva JM, Peron CR, Rocha FA. Combined glucosamine and chondroitin sulfate, once or three times daily, provides clinically relevant analgesia in knee osteoarthritis. Clin Rheumatol 2015;34:1455-62. PubMed
  40. Ossendza RA, Grandval P, Chinoune F, Rocher F, Chapel F, Bernardini D. [Acute cholestatic hepatitis due to glucosamine forte]. Gastroenterol Clin Biol. 2007 Apr;31(4):449-50.
  41. Audimoolam VK, Bhandari S. Acute interstitial nephritis induced by glucosamine. Nephrol Dial Transplant 2006;21(7):2031. PubMed
  42. Greenlee H, Crew KD, Shao T, Kranwinkel G, Kalinsky K, Maurer M, Brafman L, Insel B, Tsai WY, Hershman DL. Phase II study of glucosamine with chondroitin on aromatase inhibitor-associated joint symptoms in women with breast cancer. Support Care Cancer 201 PubMed
  43. Wilkens, P., Scheel, I. B., Grundnes, O., Hellum, C., and Storheim, K. Effect of glucosamine on pain-related disability in patients with chronic low back pain and degenerative lumbar osteoarthritis: a randomized controlled trial. JAMA 2010;304(1):45-52. PubMed
  44. Simon RR, Marks V, Leeds AR, Anderson JW. A comprehensive review of oral glucosamine use and effects on glucose metabolism in normal and diabetic individuals. Diabetes Metab Res Rev 2011;27(1):14-27. PubMed
  45. Smidt D, Torpet LA, Nauntofte B, Heegaard KM, Pedersen AM. Associations between labial and whole salivary flow rates, systemic diseases and medications in a sample of older people. Community Dent Oral Epidemiol 2010;38(5):422-35. PubMed
  46. Wangroongsub Y, Tanavalee A, Wilairatana V, Ngarmukos S. Comparable clinical outcomes between glucosamine sulfate-potassium chloride and glucosamine sulfate sodium chloride in patients with mild and moderate knee osteoarthritis: a randomized, double-blind
  47. Chopra A, Saluja M, Tillu G, Venugopalan A, Sarmukaddam S, Raut AK, Bichile L, Narsimulu G, Handa R, Patwardhan B. A Randomized Controlled Exploratory Evaluation of Standardized Ayurvedic Formulations in Symptomatic Osteoarthritis Knees: A Government of I
  48. Swinburne LM. Glucosamine sulphate and osteoarthritis. Lancet 2001;357(9268):1617. PubMed
  49. Murphy RK, Ketzler L, Rice RD, Johnson SM, Doss MS, Jaccoma EH. Oral glucosamine supplements as a possible ocular hypertensive agent. JAMA Ophthalmol 2013;131(7):955-7. PubMed
  50. Kimball AB, Kaczvinsky JR, Li J, et al. Reduction in the appearance of facial hyperpigmentation after use of moisturizers with a combination of topical niacinamide and N-acetyl glucosamine: results of a randomized, double-blind, vehicle-controlled trial.
  51. Ma H, Li X, Sun D, et al. Association of habitual glucosamine use with risk of cardiovascular disease: prospective study in UK Biobank. BMJ. 2019 May 14;365:l1628. PubMed
  52. Hoban C, Byard R, Musgrave I. Hypersensitive adverse drug reactions to glucosamine and chondroitin preparations in Australia between 2000 and 2011. Postgrad Med J. 2019 Oct 9. pii: postgradmedj-2019-136957. PubMed
  53. Tenti S, Veronese N, Cheleschi S, et al. Prescription-grade crystalline glucosamine sulfate as an add-on therapy to conventional treatments in erosive osteoarthritis of the hand: results from a 6-month observational retrospective study. Aging Clin Exp Res PubMed
  54. Yu H, Wu J, Chen H, et al. Glucosamine use is associated with a higher risk of cardiovascular diseases in patients with osteoarthritis: results from a large study in 685,778 subjects. Nutrients 2022;14(18):3694. PubMed
  55. Chu EC, Huang KHK, Cheung G, Ng G, Lin A. Delayed Skin Allergy to Glucosamine Chondroitin Supplement. Cureus 2023;15(3):e36310. PubMed
  56. Lila AM, Alekseeva LI, Baranov AA, et al. Chondroitin sulfate and glucosamine combination in patients with knee and hip osteoarthritis: A long-term observational study in Russia. World J Orthop 2023;14(6):443-457. PubMed
  57. Lehrer S, Morello T, Karrasch C, Rheinstein PH, Danias J. Effect of Glucosamine on Intraocular Pressure and Risk of Developing Glaucoma. J Glaucoma 2023. PubMed
  58. Rabade A, Viswanatha GL, Nandakumar K, Kishore A. Evaluation of efficacy and safety of glucosamine sulfate, chondroitin sulfate, and their combination regimen in the management of knee osteoarthritis: a systematic review and meta-analysis. Inflammopharmac PubMed

See these in context on the Glucosamine monograph →

Chondroitin Sulfate 22 references
  1. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2002.
  2. Tallia AF, Cardone DA. Asthma exacerbation associated with glucosamine-chondroitin supplement. J Am Board Fam Pract 2002;15:481-4..
  3. Danao-Camara T. Potential side effects of treatment with glucosamine and chondroitin. Arthritis Rheum 2000;43:2853. PubMed
  4. Rozenfeld V, Crain JL, Callahan AK. Possible augmentation of warfarin effect by glucosamine-chondroitin. Am J Health Syst Pharm 2004;61:306-307. PubMed
  5. Clegg DO, Reda DJ, Harris CL, et al. Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis. N Engl J Med 2006;354:795-808. DOI
  6. Knudsen J, Sokol GH. Potential glucosamine-warfarin interaction resulting in increased international normalized ratio: Case report and review of the literature and MedWatch database. Pharmacotherapy 2008;28:540-8. PubMed
  7. Yue QY, Strandell J, Myrberg O. Concomitant use of glucosamine potentiates the effect of warfarin. Jan 2006. Drug Safety 29(10):911-1010. DOI
  8. Nordling, J. and van, Ophoven A. Intravesical glycosaminoglycan replenishment with chondroitin sulphate in chronic forms of cystitis. A multi-national, multi-centre, prospective observational clinical trial. Arzneimittelforschung. 2008;58(7):328-335. PubMed
  9. Nickel, J. C., Egerdie, B., Downey, J., Singh, R., Skehan, A., Carr, L., and Irvine-Bird, K. A real-life multicentre clinical practice study to evaluate the efficacy and safety of intravesical chondroitin sulphate for the treatment of interstitial cystit
  10. Oliviero, U., Sorrentino, G. P., De Paola, P., Tranfaglia, E., D'Alessandro, A., Carifi, S., Porfido, F. A., Cerio, R., Grasso, A. M., Policicchio, D., and . Effects of the treatment with matrix on elderly people with chronic articular degeneration. Drug
  11. Crowley, D. C., Lau, F. C., Sharma, P., Evans, M., Guthrie, N., Bagchi, M., Bagchi, D., Dey, D. K., and Raychaudhuri, S. P. Safety and efficacy of undenatured type II collagen in the treatment of osteoarthritis of the knee: a clinical trial. Int.J.Med.Sc PubMed
  12. Nickel, J. C., Egerdie, R. B., Steinhoff, G., Palmer, B., and Hanno, P. A multicenter, randomized, double-blind, parallel group pilot evaluation of the efficacy and safety of intravesical sodium chondroitin sulfate versus vehicle control in patients with
  13. Sawitzke, A. D., Shi, H., Finco, M. F., Dunlop, D. D., Harris, C. L., Singer, N. G., Bradley, J. D., Silver, D., Jackson, C. G., Lane, N. E., Oddis, C. V., Wolfe, F., Lisse, J., Furst, D. E., Bingham, C. O., Reda, D. J., Moskowitz, R. W., Williams, H. J.
  14. Wildi, L. M., Raynauld, J. P., Martel-Pelletier, J., Beaulieu, A., Bessette, L., Morin, F., Abram, F., Dorais, M., and Pelletier, J. P. Chondroitin sulphate reduces both cartilage volume loss and bone marrow lesions in knee osteoarthritis patients starti
  15. Pavelka and et al. Double-blind, dose effect study of oral cs 4 & 6 1200mg, 800mg, 200mg against placebo in the treatment of femorotibial osteoarthritis. Wular Rheumatol Liter 1998;27(suppl 2):63.
  16. Cerda C, Bruguera M, Parés A. Hepatotoxicity associated with glucosamine and chondroitin sulfate in patients with chronic liver disease. World J Gastroenterol 2013;19(32):5381-4. PubMed
  17. von Felden J, Montani M, Kessebohm K, Stickel F. Drug-induced acute liver injury mimicking autoimmune hepatitis after intake of dietary supplements containing glucosamine and chondroitin sulfate. Int J Clin Pharmacol Ther 2013;51(3):219-23. PubMed
  18. Provenza JR, Shinjo SK, Silva JM, Peron CR, Rocha FA. Combined glucosamine and chondroitin sulfate, once or three times daily, provides clinically relevant analgesia in knee osteoarthritis. Clin Rheumatol 2015;34:1455-62. PubMed
  19. Ossendza RA, Grandval P, Chinoune F, Rocher F, Chapel F, Bernardini D. [Acute cholestatic hepatitis due to glucosamine forte]. Gastroenterol Clin Biol. 2007 Apr;31(4):449-50.
  20. Greenlee H, Crew KD, Shao T, Kranwinkel G, Kalinsky K, Maurer M, Brafman L, Insel B, Tsai WY, Hershman DL. Phase II study of glucosamine with chondroitin on aromatase inhibitor-associated joint symptoms in women with breast cancer. Support Care Cancer 201 PubMed
  21. Chu EC, Huang KHK, Cheung G, Ng G, Lin A. Delayed Skin Allergy to Glucosamine Chondroitin Supplement. Cureus 2023;15(3):e36310. PubMed
  22. Lila AM, Alekseeva LI, Baranov AA, et al. Chondroitin sulfate and glucosamine combination in patients with knee and hip osteoarthritis: A long-term observational study in Russia. World J Orthop 2023;14(6):443-457. PubMed

See these in context on the Chondroitin Sulfate monograph →

Panax Ginseng 66 references
  1. Scaglione F, Cattaneo G, Alessandria M, Cogo R. Efficacy and safety of the standardized Ginseng extract G115 for potentiating vaccination against the influenza syndrome and protection against the common cold. Drugs Exp Clin Res 1996;22:65-72.
  2. Palmer BV, Montgomery AC, Monteiro JC, et al. Gin Seng and mastalgia [letter]. BMJ 1978;1:1284. PubMed
  3. Hopkins MP, Androff L, Benninghoff AS. Ginseng face cream and unexplained vaginal bleeding. Am J Obstet Gynecol 1988;159:1121-2. PubMed
  4. Greenspan EM. Ginseng and vaginal bleeding [letter]. JAMA 1983;249:2018.
  5. Gonzalez-Seijo JC, Ramos YM, Lastra I. Manic episode and ginseng: Report of a possible case. J Clin Psychopharmacol 1995;15:447-8.
  6. Dega H, Laporte JL, Frances C, et al. Ginseng as a cause of Stevens-Johnson syndrome. Lancet 1996;347:1344.
  7. Hamid S, Rojter S, Vierling J. Protracted cholestatic hepatitis after the use of Prostata. Ann Intern Med 1997;127:169-70.
  8. Shader RI, Greenblatt DJ. Phenelzine and the dream machine-ramblings and reflections. J Clin Psychopharmacol 1985;5:65. PubMed
  9. Jones BD, Runikis AM. Interaction of ginseng with phenelzine. J Clin Psychopharmacol 1987;7:201-2. PubMed
  10. Janetzky K, Morreale AP. Probable interaction between warfarin and ginseng. Am J Health Syst Pharm 1997;54:692-3. PubMed
  11. Becker BN. Ginseng-induced diuretic resistance. JAMA 1996;276:606-7. PubMed
  12. Gurley BJ, Gardner SF, Hubbard MA. Clinical assessment of potential cytochrome P450-mediated herb-drug interactions. AAPS Ann Mtg & Expo Indianapolis, IN: 2000; Oct 29 - Nov 2:presentation #3460.
  13. Park HJ, Lee JH, Song YB, Park KH. Effects of dietary supplementation of lipophilic fraction from Panax ginseng on cGMP and cAMP in rat platelets and on blood coagulation. Biol Pharm Bull 1996;19:1434-9. PubMed
  14. Zhu M, Chan KW, Ng LS, et al. Possible influences of ginseng on the pharmacodynamics of warfarin in rats. J Pharm Pharmacol 1999;51:175-80.
  15. Choi HK, Jung GW, Moon KH, et al. Clinical study of SS-Cream in patients with lifelong premature ejaculation. Urology 2000;55:257-61. PubMed
  16. Shin HR, Kim JY, Yun TK, et al. The cancer-preventive potential of Panax ginseng: a review of human and experimental evidence. Cancer Causes Control 2000;11:565-76. PubMed
  17. Siegel RK. Ginseng Abuse Syndrome. JAMA 1979;241:1614-5. DOI
  18. Palop-Larrea V, Gonzalvez-Perales JL, Catalan-Oliver C, et al. Metrorrhagia and ginseng. Ann Pharmacother 2000;34:1347-8. PubMed
  19. Caron MF, Hotsko AL, Robertson S, et al. Electrocardiographic and hemodynamic effects of Panax ginseng. Ann Pharmacother 2002;36:758-63..
  20. Eagon PK, Elm MS, Hunter DS, et al. Medicinal herbs: modulation of estrogen action. Era of Hope Mtg, Dept Defense; Breast Cancer Res Prog, Atlanta, GA 2000;Jun 8-11.
  21. Chan LY, Chiu PY, Lau TK. An in-vitro study of ginsenoside Rb(1)-induced teratogenicity using a whole rat embryo culture model. Hum Reprod 2003;18:2166-8..
  22. Gurley BJ, Gardner SF, Hubbard MA, et al. Cytochrome P450 phenotypic ratios for predicting herb-drug interactions in humans. Clin Pharmacol Ther 2002;72:276-87.. PubMed
  23. Wiklund IK, Mattsson LA, Lindgren R, et al. Effects of a standardized ginseng extract on quality of life and physiological parameters in symptomatic postmenopausal women: a double-blind, placebo-controlled trial. Int J Clin Pharmacol Res 1999;19:89-99..
  24. Hammond TG, Whitworth JA. Adverse reactions to ginseng [letter]. Med J Aust 1981;1:492.. PubMed
  25. Punnonen R, Lukola A. Oestrogen-like effect of ginseng. Br Med J 1980;281:1110.. PubMed
  26. Lee YJ, Jin YR, Lim WC, et al. Ginsenoside-Rb1 acts as a weak phytoestrogen in MCF-7 human breast cancer cells. Arch Pharm Res 2003;26:58-63.. PubMed
  27. Xu QF, Fang XL, Chen DF. Pharmacokinetics and bioavailability of ginsenoside Rb1 and Rg1 from Panax notoginseng in rats. J Ethnopharmacol 2003;84:187-92. PubMed
  28. Jiang X, Williams KM, Liauw WS, et al. Effect of St John's wort and ginseng on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Br J Clin Pharmacol 2004;57:592-9. PubMed
  29. Yun YP, Do JH, Ko SR, et al. Effects of Korean red ginseng and its mixed prescription on the high molecular weight dextran-induced blood stasis in rats and human platelet aggregation. J Ethnopharmacol 2001;77:259-64. PubMed
  30. Wiwanikit V, Taungjarwinai W. A case report of suspected ginseng allergy. Medscape General Medicine 6 (3), 2004. Available at: www.medscape.com/viewarticle/482833 (Accessed 17 September 2004).
  31. Kabalak AA, Soyal OB, Urfalioglu A, et al. Menometrorrhagia and tachyarrhythmia after using oral and topical ginseng. J Womens Health (Larchmt) 2004;13:830-3. PubMed
  32. Jiang X, Blair EY, McLachlan AJ. Investigation of the effects of herbal medicines on warfarin response in healthy subjects: a population pharmacokinetic-pharmacodynamic modeling approach. J Clin Pharmacol 2006;46:1370-8. PubMed
  33. Lee SH, Ahn YM, Ahn SY, et al. Interaction between warfarin and Panax ginseng in ischemic stroke patients. J Altern Complement Med 2008;14:715-721.
  34. Smith M, Lin KM, and Zheng YP. PIII-89 an open trial of nifedipine-herb interactions: Nifedipine with St. John's wort, ginseng or ginkgo biloba. Clin Pharm Ther 2001;69:P86.
  35. Mateo-Carrasco, H., Galvez-Contreras, M. C., Fernandez-Gines, F. D., and Nguyen, T. V. Elevated liver enzymes resulting from an interaction between Raltegravir and Panax ginseng: a case report and brief review. Drug Metabol.Drug Interact. 2012;27(3):171-1
  36. Oh, K. J., Chae, M. J., Lee, H. S., Hong, H. D., and Park, K. Effects of Korean red ginseng on sexual arousal in menopausal women: placebo-controlled, double-blind crossover clinical study. J Sex Med 2010;7(4 Pt 1):1469-1477. PubMed
  37. Kim, T. H., Jeon, S. H., Hahn, E. J., Paek, K. Y., Park, J. K., Youn, N. Y., and Lee, H. L. Effects of tissue-cultured mountain ginseng (Panax ginseng CA Meyer) extract on male patients with erectile dysfunction. Asian J Androl 2009;11(3):356-361. PubMed
  38. Hu, Z., Yang, X., Ho, P. C., Chan, S. Y., Heng, P. W., Chan, E., Duan, W., Koh, H. L., and Zhou, S. Herb-drug interactions: a literature review. Drugs 2005;65(9):1239-1282. PubMed
  39. Zhang, R., Jie, J., Zhou, Y., Cao, Z., and Li, W. Long-term effects of Panax ginseng on disposition of fexofenadine in rats in vivo. Am J Chin Med 2009;37(4):657-667.
  40. Lee, Y. H., Lee, B. K., Choi, Y. J., Yoon, I. K., Chang, B. C., and Gwak, H. S. Interaction between warfarin and Korean red ginseng in patients with cardiac valve replacement. Int J Cardiol. 11-19-2010;145(2):275-276. PubMed
  41. Liu, P., Yin, H., Xu, Y., Zhang, Z., Chen, K., and Li, Y. Effects of ginsenoside Rg1 on postimplantation rat and mouse embryos cultured in vitro. Toxicol In Vitro 2006;20(2):234-238. PubMed
  42. Liu, P., Xu, Y., Yin, H., Wang, J., Chen, K., and Li, Y. Developmental toxicity research of ginsenoside Rb1 using a whole mouse embryo culture model. Birth Defects Res B Dev Reprod Toxicol 2005;74(2):207-209. PubMed
  43. Gurley, B. J., Gardner, S. F., Hubbard, M. A., Williams, D. K., Gentry, W. B., Cui, Y., and Ang, C. Y. Clinical assessment of effects of botanical supplementation on cytochrome P450 phenotypes in the elderly: St John's wort, garlic oil, Panax ginseng and DOI
  44. Wesnes KA, Faleni RA, Hefting NR, and et al. The cognitive, subjective, and physical effects of a Ginkgo biloba/Panax ginseng combination in healthy volunteers with neurasthenic complaints. Psychopharmacol Bull 1997;33(4):677-683.
  45. Martínez-Mir I, Rubio E, Morales-Olivas FJ, Palop-Larrea V. Transient ischemic attack secondary to hypertensive crisis related to Panax ginseng. Ann Pharmacother 2004;38(11):1970.
  46. Kakisaka Y, Ohara T, Tozawa H, Sato S, Katayama S, Suzuki T, Hino-Fukuyo N, Kure S. Panax ginseng: a newly identified cause of gynecomastia. Tohoku J Exp Med 2012;228(2):143-5. PubMed
  47. Malati CY, Robertson SM, Hunt JD, Chairez C, Alfaro RM, Kovacs JA, Penzak SR. Influence of Panax ginseng on cytochrome P450 (CYP)3A and P-glycoprotein (P-gp) activity in healthy participants. J Clin Pharmacol 2012;52(6):932-9.
  48. Sen A. Orobuccolingual dyskinesia after long-term use of black cohosh and ginseng. J Neuropsychiatry Clin Neurosci 2013 Fall;25(4):E50. PubMed
  49. Oh MR, Park SH, Kim SY, Back HI, Kim MG, Jeon JY, Ha KC, Na WT, Cha YS, Park BH, Park TS, Chae SW. Postprandial glucose-lowering effects of fermented red ginseng in subjects with impaired fasting glucose or type 2 diabetes: a randomized, double-blind, pla
  50. Kim HG, Cho JH, Yoo SR, Lee JS, Han JM, Lee NH, Ahn YC, Son CG. Antifatigue effects of Panax ginseng C.A. Meyer: a randomised, double-blind, placebo-controlled trial. PLoS One 2013;8(4):e61271. PubMed
  51. Rhee MY, Kim YS, Bae JH, Nah DY, Kim YK, Lee MM, Kim HY. Effect of Korean red ginseng on arterial stiffness in subjects with hypertension. J Altern Complement Med 2011;17(1):45-9.
  52. Bilgi N, Bell K, Ananthakrishnan AN, Atallah E. Imatinib and Panax ginseng: a potential interaction resulting in liver toxicity. Ann Pharmacother 2010;44(5):926-8.
  53. Jalloh MA, Gregory PJ, Hein D, et al. Dietary supplement interactions with antiretrovirals: a systematic review. Int J STD AIDS. 2017 Jan;28(1):4-15. PubMed
  54. Shah SA, Occiano A, Nguyen TA, et al. Electrocardiographic and blood pressure effects of energy drinks and panax ginseng in healthy volunteers: a randomized clinical trial. Int J Cardiol. 2016 Sep 1;218:318-23. PubMed
  55. Yang L, Li CL, Tsai TH. Preclinical Herb-Drug Pharmacokinetic Interaction of Panax ginseng Extract and Selegiline in Freely Moving Rats. ACS Omega. 2020;5(9):4682-4688.
  56. Shen L, Gwak SR, Joo JC, et al. Effectiveness and safety of Panax ginseng extract on hepatic dysfunction: A randomized, double-blind, placebo-controlled clinical trial. Evid Based Complement Alternat Med. 2020;2020:2689565.
  57. Kim Y, Jo JJ, Cho P, et al. Characterization of red ginseng-drug interaction by CYP3A activity increased in high dose administration in mice. Biopharm Drug Dispos. 2020;41(7):295-306. PubMed
  58. Bessell E, Fuller NR, Markovic TP, et al. Effects of a-cyclodextrin on cholesterol control and hydrolyzed ginseng extract on glycemic control in people with prediabetes: a randomized clinical trial. JAMA Netw Open 2020 Nov 2;3(11):e2023491.
  59. Lee SR, Hur K, Cho S. Subcorneal pustular dermatosis as a cause of pityriasis amiantacea in a young child. JAAD Case Rep 2021;18:40-44. PubMed
  60. Liu J, Chang D, Cordato D, et al. A pilot randomized controlled trial of WeiNaoKang (SaiLuoTong) in treating vascular dementia. Aging Med (Milton). 2022;5(4):246-256. PubMed
  61. Shin D, Yoon BI, Bang S, et al. Safety and Efficacy Assessment of Red Ginseng Oil (RXGIN) in Men with Lower Urinary Tract Symptoms in a Randomized, Double-Blind, Placebo-Controlled Trial. World J Mens Health 2023. PubMed
  62. Shin MB, Kim SA, Lee S, et al. Pharmacokinetic Comparison of Ginsenosides between Fermented and Non-Fermented Red Ginseng in Healthy Volunteers. Pharmaceutics 2022;14(12):2807. PubMed
  63. Gao J, Shi J, Ma X, et al. Effects of ginseng berry saponins from panax ginseng on glucose metabolism of patients with prediabetes: A randomized, double-blinded, placebo-controlled, crossover trial. Phytomedicine 2024;132:155842. PubMed
  64. Cho SK, Song YJ, Han JY, Kim HW, Nam E, Sung YK. Effectiveness of Korean Red Ginseng on fatigue in patients with rheumatic diseases: a randomized, double-blind, placebo-controlled study. Korean J Intern Med 2024;39(4):680-690. PubMed
  65. Arabi SM, Shahraki-Jazinaki M, Nayyerabadi M, et al. The Effect of Ginseng Supplementation on Lipid Profile: GRADE-assessed Systematic Review and Dose-response Meta-analysis of Randomized Controlled Trials. Curr Pharm Des 2024;30(26):2047-205. PubMed
  66. Zeng X, Zhou X, Zhang A, et al. Pityriasis Rosea-Like Eruption following anti-fatigue traditional herbs: Aconitum carmichaelii Debx and Panax Ginseng suspected. BMC Complement Med Ther 2024;24(1):248. PubMed

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Willow Bark 12 references
  1. Chrubasik S, Eisenberg E, Balan E, et al. Treatment of low back pain exacerbations with willow bark extract: a randomized double-blind study. Am J Med 2000;109:9-14. PubMed
  2. Schmid B, Ludtke R, Selbmann HK, et al. Efficacy and tolerability of a standardized willow bark extract in patients with osteoarthritis: randomized placebo-controlled, double blind clinical trial. Phytother Res 2001;15:344-50. PubMed
  3. Biegert C, Wagner I, Ludtke R, et al. Efficacy and safety of willow bark extract in the treatment of osteoarthritis and rheumatoid arthritis: results of 2 randomized double-blind controlled trials. J Rheumatol 2004;31:2121-30.
  4. Unsworth J, d'Assis-Fonseca A, Beswick DT, Blake DR. Serum salicylate levels in a breast fed infant. Ann Rheum Dis 1987;46:638-9. PubMed
  5. Clark JH, Wilson WG. A 16-day-old breast-fed infant with metabolic acidosis caused by salicylate. Clin Pediatr (Phila) 1981;20:53-4. PubMed
  6. Chrubasik S, Kunzel O, Model A, et al. Treatment of low back pain with a herbal or synthetic anti-rheumatic: a randomized controlled study. Willow bark extract for low back pain. Rheumatology (Oxford) 2001;40:1388-93. PubMed
  7. Schmid B, Kotter I, Heide L. Pharmacokinetics of salicin after oral administration of a standardised willow bark extract. Eur J Clin Pharmacol. 2001;57:387-91. PubMed
  8. Krivoy N, Pavlotzky E, Chrubasik S, et al. Effect of salicis cortex extract on human platelet aggregation. Planta Med 2001;67:209-12. PubMed
  9. Mills SY, Jacoby RK, Chacksfield M, Willoughby M. Effect of a proprietary herbal medicine on the relief of chronic arthritic pain: a double-blind study. Br J Rheumatol 1996;35:874-8. PubMed
  10. Chrubasik, S., Kunzel, O., Black, A., Conradt, C., and Kerschbaumer, F. Potential economic impact of using a proprietary willow bark extract in outpatient treatment of low back pain: an open non-randomized study. Phytomedicine 2001;8(4):241-251. PubMed
  11. <p>Moro PA, Flacco V, Cassetti F, Clementi V, Colombo ML, Chiesa GM, Menniti-Ippolito F, Raschetti R, Santuccio C. Hypovolemic shock due to severe gastrointestinal bleeding in a child taking an herbal syrup. Ann Ist Super Sanita. 2011;47(3):278-83.</p>
  12. Sweeney, K. R., Chapron, D. J., Brandt, J. L., Gomolin, I. H., Feig, P. U., and Kramer, P. A. Toxic interaction between acetazolamide and salicylate: case reports and a pharmacokinetic explanation. Clin Pharmacol Ther 1986;40(5):518-524.

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Turmeric 102 references
  1. McGuffin M, Hobbs C, Upton R, Goldberg A, eds. American Herbal Products Association's Botanical Safety Handbook. Boca Raton, FL: CRC Press, LLC 1997.
  2. Sharma RA, McLelland HR, Hill KA, et al. Pharmacodynamic and pharmacokinetic study of oral Curcuma extract in patients with colorectal cancer. Clin Cancer Res 2001;7:1894-900..
  3. Shah BH, Nawaz Z, Pertani SA. Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling. Biochem Pharmacol 1 PubMed
  4. Hata M, Sasaki E, Ota M, et al . Allergic contact dermatitis from curcumin (turmeric). Contact Dermatitis 1997;36:107-8. PubMed
  5. Kuttan R, Sudheeran PC, Josph CD. Turmeric and curcumin as topical agents in cancer therapy. Tumori 1987;73:29-31.. PubMed
  6. Thapliyal R, Deshpande SS, Maru GB. Mechanism(s) of turmeric-mediated protective effects against benzo(a)pyrene-derived DNA adducts. Cancer Lett 2002;175:79-88. PubMed
  7. Lee SW, Nah SS, Byon JS, et al. Transient complete atrioventricular block associated with curcumin intake. Int J Cardiol 2011;150:e50-2. PubMed
  8. Kuptniratsaikul V, Thanakhumtorn S, Chinswangwatanakul P, et al. Efficacy and safety of Curcuma domestica extracts in patients with knee osteoarthritis. J Altern Complement Med 2009;15:891-7.
  9. Carroll RE, Benya RV, Turgeon DK, et al. Phase IIa clinical trial of curcumin for the prevention of colorectal neoplasia. Cancer Prev Res (Phila) 2011;4:354-64. PubMed
  10. Junyaprasert, V. B., Soonthornchareonnon, N., Thongpraditchote, S., Murakami, T., and Takano, M. Inhibitory effect of Thai plant extracts on P-glycoprotein mediated efflux. Phytother.Res 2006;20(1):79-81. PubMed
  11. Ampasavate, C., Sotanaphun, U., Phattanawasin, P., and Piyapolrungroj, N. Effects of Curcuma spp. on P-glycoprotein function. Phytomedicine. 2010;17(7):506-512. PubMed
  12. Hou, X. L., Takahashi, K., Tanaka, K., Tougou, K., Qiu, F., Komatsu, K., Takahashi, K., and Azuma, J. Curcuma drugs and curcumin regulate the expression and function of P-gp in Caco-2 cells in completely opposite ways. Int.J Pharm 6-24-2008;358(1-2):224-2 PubMed
  13. Choi, B. H., Kim, C. G., Lim, Y., Shin, S. Y., and Lee, Y. H. Curcumin down-regulates the multidrug-resistance mdr1b gene by inhibiting the PI3K/Akt/NF kappa B pathway. Cancer Lett. 1-18-2008;259(1):111-118.
  14. Zhang, W., Tan, T. M., and Lim, L. Y. Impact of curcumin-induced changes in P-glycoprotein and CYP3A expression on the pharmacokinetics of peroral celiprolol and midazolam in rats. Drug Metab Dispos. 2007;35(1):110-115. PubMed
  15. Limtrakul, P., Chearwae, W., Shukla, S., Phisalphong, C., and Ambudkar, S. V. Modulation of function of three ABC drug transporters, P-glycoprotein (ABCB1), mitoxantrone resistance protein (ABCG2) and multidrug resistance protein 1 (ABCC1) by tetrahydrocu
  16. Holland, M. L., Panetta, J. A., Hoskins, J. M., Bebawy, M., Roufogalis, B. D., Allen, J. D., and Arnold, J. C. The effects of cannabinoids on P-glycoprotein transport and expression in multidrug resistant cells. Biochem.Pharmacol 4-14-2006;71(8):1146-1154 PubMed
  17. Tang, X. Q., Bi, H., Feng, J. Q., and Cao, J. G. Effect of curcumin on multidrug resistance in resistant human gastric carcinoma cell line SGC7901/VCR. Acta Pharmacol Sin. 2005;26(8):1009-1016. PubMed
  18. Nabekura, T., Kamiyama, S., and Kitagawa, S. Effects of dietary chemopreventive phytochemicals on P-glycoprotein function. Biochem.Biophys.Res Commun. 2-18-2005;327(3):866-870. PubMed
  19. Romiti, N., Tongiani, R., Cervelli, F., and Chieli, E. Effects of curcumin on P-glycoprotein in primary cultures of rat hepatocytes. Life Sci. 1998;62(25):2349-2358. PubMed
  20. Yue, G. G., Cheng, S. W., Yu, H., Xu, Z. S., Lee, J. K., Hon, P. M., Lee, M. Y., Kennelly, E. J., Deng, G., Yeung, S. K., Cassileth, B. R., Fung, K. P., Leung, P. C., and Lau, C. B. The role of turmerones on curcumin transportation and P-glycoprotein acti
  21. Shenouda, N. S., Zhou, C., Browning, J. D., Ansell, P. J., Sakla, M. S., Lubahn, D. B., and MacDonald, R. S. Phytoestrogens in common herbs regulate prostate cancer cell growth in vitro. Nutr.Cancer 2004;49(2):200-208. PubMed
  22. Appiah-Opong, R., Commandeur, J. N., Vugt-Lussenburg, B., and Vermeulen, N. P. Inhibition of human recombinant cytochrome P450s by curcumin and curcumin decomposition products. Toxicology 6-3-2007;235(1-2):83-91. PubMed
  23. Hou, X. L., Takahashi, K., Kinoshita, N., Qiu, F., Tanaka, K., Komatsu, K., Takahashi, K., and Azuma, J. Possible inhibitory mechanism of Curcuma drugs on CYP3A4 in 1alpha,25 dihydroxyvitamin D3 treated Caco-2 cells. Int.J Pharm 6-7-2007;337(1-2):169-177.
  24. Valentine, S. P., Le Nedelec, M. J., Menzies, A. R., Scandlyn, M. J., Goodin, M. G., and Rosengren, R. J. Curcumin modulates drug metabolizing enzymes in the female Swiss Webster mouse. Life Sci. 4-11-2006;78(20):2391-2398. PubMed
  25. Price, R. J., Scott, M. P., Giddings, A. M., Walters, D. G., Stierum, R. H., Meredith, C., and Lake, B. G. Effect of butylated hydroxytoluene, curcumin, propyl gallate and thiabendazole on cytochrome P450 forms in cultured human hepatocytes. Xenobiotica 2 PubMed
  26. Ganta, S., Devalapally, H., and Amiji, M. Curcumin enhances oral bioavailability and anti-tumor therapeutic efficacy of paclitaxel upon administration in nanoemulsion formulation. J Pharm Sci 2010;99(11):4630-4641. PubMed
  27. Lamb, S. R. and Wilkinson, S. M. Contact allergy to tetrahydrocurcumin. Contact Dermatitis 2003;48(4):227. PubMed
  28. Joshi, J., Ghaisas, S., Vaidya, A., Vaidya, R., Kamat, D. V., Bhagwat, A. N., and Bhide, S. Early human safety study of turmeric oil (Curcuma longa oil) administered orally in healthy volunteers. J Assoc.Physicians India 2003;51:1055-1060.
  29. Mahesh, T., Balasubashini, M. S., and Menon, V. P. Effect of photo-irradiated curcumin treatment against oxidative stress in streptozotocin-induced diabetic rats. J Med.Food 2005;8(2):251-255. PubMed
  30. Thompson, D. A. and Tan, B. B. Tetrahydracurcumin-related allergic contact dermatitis. Contact Dermatitis 2006;55(4):254-255. PubMed
  31. Patumraj, S., Wongeakin, N., Sridulyakul, P., Jariyapongskul, A., Futrakul, N., and Bunnag, S. Combined effects of curcumin and vitamin C to protect endothelial dysfunction in the iris tissue of STZ-induced diabetic rats. Clin Hemorheol.Microcirc. 2006;3
  32. Liddle, M., Hull, C., Liu, C., and Powell, D. Contact urticaria from curcumin. Dermatitis 2006;17(4):196-197. PubMed
  33. Juan, H., Terhaag, B., Cong, Z., Bi-Kui, Z., Rong-Hua, Z., Feng, W., Fen-Li, S., Juan, S., Jing, T., and Wen-Xing, P. Unexpected effect of concomitantly administered curcumin on the pharmacokinetics of talinolol in healthy Chinese volunteers. Eur.J Clin PubMed
  34. Murugan, P. and Pari, L. Influence of tetrahydrocurcumin on erythrocyte membrane bound enzymes and antioxidant status in experimental type 2 diabetic rats. J Ethnopharmacol. 9-25-2007;113(3):479-486. PubMed
  35. Seo, K. I., Choi, M. S., Jung, U. J., Kim, H. J., Yeo, J., Jeon, S. M., and Lee, M. K. Effect of curcumin supplementation on blood glucose, plasma insulin, and glucose homeostasis related enzyme activities in diabetic db/db mice. Mol.Nutr.Food Res 2008;5
  36. Weisberg, S. P., Leibel, R., and Tortoriello, D. V. Dietary curcumin significantly improves obesity-associated inflammation and diabetes in mouse models of diabesity. Endocrinology 2008;149(7):3549-3558. PubMed
  37. Jain, S. K., Rains, J., Croad, J., Larson, B., and Jones, K. Curcumin supplementation lowers TNF-alpha, IL-6, IL-8, and MCP-1 secretion in high glucose-treated cultured monocytes and blood levels of TNF-alpha, IL-6, MCP-1, glucose, and glycosylated hemog
  38. Yu, Y., Hu, S. K., and Yan, H. [The study of insulin resistance and leptin resistance on the model of simplicity obesity rats by curcumin]. Zhonghua Yu Fang Yi.Xue.Za Zhi. 2008;42(11):818-822.
  39. Pavithra, B. H., Prakash, N., and Jayakumar, K. Modification of pharmacokinetics of norfloxacin following oral administration of curcumin in rabbits. J Vet.Sci. 2009;10(4):293-297. PubMed
  40. Yan, Y. D., Kim, D. H., Sung, J. H., Yong, C. S., and Choi, H. G. Enhanced oral bioavailability of docetaxel in rats by four consecutive days of pre-treatment with curcumin. Int J Pharm 10-31-2010;399(1-2):116-120. PubMed
  41. Epelbaum, R., Schaffer, M., Vizel, B., Badmaev, V., and Bar-Sela, G. Curcumin and gemcitabine in patients with advanced pancreatic cancer. Nutr Cancer 2010;62(8):1137-1141. PubMed
  42. Madkor, H. R., Mansour, S. W., and Ramadan, G. Modulatory effects of garlic, ginger, turmeric and their mixture on hyperglycaemia, dyslipidaemia and oxidative stress in streptozotocin-nicotinamide diabetic rats. Br J Nutr 2011;105(8):1210-1217. PubMed
  43. Pungcharoenkul, K. and Thongnopnua, P. Effect of different curcuminoid supplement dosages on total in vivo antioxidant capacity and cholesterol levels of healthy human subjects. Phytother Res 2011;25(11):1721-1726.
  44. Kusuhara, H., Furuie, H., Inano, A., Sunagawa, A., Yamada, S., Wu, C., Fukizawa, S., Morimoto, N., Ieiri, I., Morishita, M., Sumita, K., Mayahara, H., Fujita, T., Maeda, K., and Sugiyama, Y. Pharmacokinetic interaction study of sulphasalazine in healthy
  45. Mohammadi, A., Sahebkar, A., Iranshahi, M., Amini, M., Khojasteh, R., Ghayour-Mobarhan, M., and Ferns, G. A. Effects of supplementation with curcuminoids on dyslipidemia in obese patients: a randomized crossover trial. Phytother Res 2013;27(3):374-379. PubMed
  46. Chuengsamarn, S., Rattanamongkolgul, S., Luechapudiporn, R., Phisalaphong, C., and Jirawatnotai, S. Curcumin extract for prevention of type 2 diabetes. Diabetes Care 2012;35(11):2121-2127. PubMed
  47. Goh, C. L. and Ng, S. K. Allergic contact dermatitis to Curcuma longa (turmeric). Contact Dermatitis 1987;17(3):186. PubMed
  48. Srivastava, R., Puri, V., Srimal, R. C., and Dhawan, B. N. Effect of curcumin on platelet aggregation and vascular prostacyclin synthesis. Arzneimittelforschung. 1986;36(4):715-717.
  49. Srinivasan, M. Effect of curcumin on blood sugar as seen in a diabetic subject. Indian J Med Sci 1972;26(4):269-270.
  50. Srivastava, K. C., Bordia, A., and Verma, S. K. Curcumin, a major component of food spice turmeric (Curcuma longa) inhibits aggregation and alters eicosanoid metabolism in human blood platelets. Prostaglandins Leukot.Essent.Fatty Acids 1995;52(4):223-227 PubMed
  51. Oetari, S., Sudibyo, M., Commandeur, J. N., Samhoedi, R., and Vermeulen, N. P. Effects of curcumin on cytochrome P450 and glutathione S-transferase activities in rat liver. Biochem Pharmacol 1-12-1996;51(1):39-45. PubMed
  52. Kiec-Swierczynska, M. and Krecisz, B. Occupational allergic contact dermatitis due to curcumin food colour in a pasta factory worker. Contact Dermatitis 1998;39(1):30-31. PubMed
  53. Van Dau N, Ngoc Ham N, Huy Khac D, and et al. The effects of a traditional drug, tumeric (Curcuma longa), and placebo on the healing of duodenal ulcer. Phytomed 1998;5(1):29-34.
  54. Daveluy A, Géniaux H, Thibaud L, Mallaret M, Miremont-Salamé G, Haramburu F. Probable interaction between an oral vitamin K antagonist and turmeric (Curcuma longa). Therapie. 2014 Nov-Dec;69(6):519-20. PubMed
  55. Kuptniratsaikul V, Dajpratham P, Taechaarpornkul W, Buntragulpoontawee M, Lukkanapichonchut P, Chootip C, Saengsuwan J, Tantayakom K, Laongpech S. Efficacy and safety of Curcuma domestica extracts compared with ibuprofen in patients with knee osteoarthrit
  56. Madhu K, Chanda K, Saji MJ. Safety and efficacy of Curcuma longa extract in the treatment of painful knee osteoarthritis: a randomized placebo-controlled trial. Inflammopharmacology 2013;21(2):129-36. PubMed
  57. Mali AM, Behal R, Gilda SS. Comparative evaluation of 0.1% turmeric mouthwash with 0.2% chlorhexidine gluconate in prevention of plaque and gingivitis: A clinical and microbiological study. J Indian Soc Periodontol 2012;16(3):386-91. PubMed
  58. Sanmukhani J, Satodia V, Trivedi J, Patel T, Tiwari D, Panchal B, Goel A, Tripathi CB. Efficacy and safety of curcumin in major depressive disorder: a randomized controlled trial. Phytother Res 2014;28(4):579-85. PubMed
  59. Nayeri A, Wu S, Adams E, et al. Acute Calcineurin Inhibitor Nephrotoxicity Secondary to Turmeric Intake: A Case Report. Transplant Proc. 2017;49(1):198-200. PubMed
  60. Mitchell TM. Correspondence re: Somasundaram et al., Dietary curcumin inhibits chemotherapy-induced apoptosis in models of human breast cancer. Cancer Res. 2003;63(16):5165-6; author reply 5166-7.
  61. Somasundaram S, Edmund NA, Moore DT, Small GW, Shi YY, Orlowski RZ. Dietary curcumin inhibits chemotherapy-induced apoptosis in models of human breast cancer. Cancer Res. 2002;62(13):3868-75.
  62. Haroyan A, Mukuchyan V, Mkrtchyan N, et al. Efficacy and safety of curcumin and its combination with boswellic acid in osteoarthritis: a comparative, randomized, double-blind, placebo-controlled study. BMC Complement Altern Med. 2018;18(1):7. PubMed
  63. Al-Karawi D, Al Mamoori DA, Tayyar Y. The role of curcumin administration in patients with major depressive disorder: Mini meta-analysis of clinical trials. Phytother Res. 2016;30(2):175-83. PubMed
  64. Neerati P, Devde R, Gangi AK. Evaluation of the effect of curcumin capsules on glyburide therapy in patients with type-2 diabetes mellitus. Phytother Res. 2014;28(12):1796-800. PubMed
  65. Simental-Mendía LE, Pirro M, Gotto AM Jr, et al. Lipid-modifying activity of curcuminoids: A systematic review and meta-analysis of randomized controlled trials. Crit Rev Food Sci Nutr. 2017:1-10. PubMed
  66. Fung FY, Wong WH, Ang SK, et al. A randomized, double-blind, placebo- controlled study on the anti-haemostatic effects of Curcuma longa, Angelica sinensis and Panax ginseng. Phytomedicine. 2017;32:88-96. PubMed
  67. Small GW, Siddarth P, Li Z, et al. Memory and brain amyloid and tau effects of a bioavailable form of curcumin in non-demented adults: A double-blind, placebo-controlled 18-month trial. Am J Geriatr Psychiatry. 2018;26(3):266-277.
  68. Cruz-Correa M, Hylind LM, Marrero JH, et al. Efficacy and safety of curcumin in treatment of intestinal adenomas in patients with familial adenomatous polyposis. Gastroenterology. 2018 May 23. Pii:S0016-5085(18)34564-5. [Epub ahead of print] PubMed
  69. Rahmani S, Asgary S, Askari G, et al. Treatment of non-alcoholic fatty liver disease with curcumin: a randomized placebo-controlled trial. Phytother Res. 2016 Sep;30(9):1540-8. PubMed
  70. Lopez-Villafuerte L, CLores KH. Contact dermatitis caused by turmeric in a massage oil. Contact Dermatitis. 2016 Jul;75(1):52-3. PubMed
  71. Lukefahr AL, McEvoy S, Alfafara C, Funk JL. Drug-induced autoimmune hepatitis associated with turmeric dietary supplement use. BMJ Case Rep. 2018. pii: bcr-2018-224611. PubMed
  72. Medsafe Safety Communication- Turmeric/Curcumin Interaction with Warfarin. April 30, 2018. Accessed at: https://medsafe.govt.nz/safety/EWS/2018/Turmeric.asp.
  73. Imam Z, Khasawneh M, Jomaa D, Iftikhar H, Sayedahmad Z. Drug induced liver injury attributed to a curcumin supplement. Case Rep Gastrointest Med 2019 Oct 20;2019:6029403. doi: 10.1155/2019/6029403. PubMed
  74. Chand S, Hair C, Beswick L. A rare case of turmeric-induced hepatotoxicity. Intern Med J. 2020;50(2):258-259. PubMed
  75. Jiang N, Zhang M, Meng X, Sun B. Effects of Curcumin on the Pharmacokinetics of Amlodipine in Rats and Its Potential Mechanism. Pharm Biol. 2020;58(1):465-468. PubMed
  76. Lee BS, Bhatia T, Chaya CT, Wen R, Taira MT, Lim BS. Autoimmune Hepatitis Associated With Turmeric Consumption. ACG Case Rep J. 2020;7(3):e00320. PubMed
  77. Lombardi N, Crescioli G, Maggini V, et al. Acute liver injury following turmeric use in Tuscany: an analysis of the Italian Phytovigilance database and systematic review of case reports. Br J Clin Pharmacol. 2020. PubMed
  78. Suhail FK, Masood U, Sharma A, John S, Dhamoon A. Turmeric supplement induced hepatotoxicity: a rare complication of a poorly regulated substance. Clin Toxicol (Phila). 2020;58(3):216-217. PubMed
  79. Nakagawa Y, Mukai S, Yamada S, et al. The efficacy and safety of highly-bioavailable curcumin for treating knee osteoarthritis: a 6-month open-labeled prospective study. Clin Med Insights Arthritis Musculoskelet Disord. 2020;13:1179544120948471. PubMed
  80. Shafabakhsh R, Asemi Z, Reiner Z, Soleimani A, Aghadavod E, Bahmani F. The effects of nano-curcumin on metabolic status in patients with diabetes on hemodialysis, a randomized, double blind, placebo-controlled trial. Iran J Kidney Dis. 2020;14(4):290-9.
  81. Allegri P, Rosa R, Masala A, et al. Clinical effectiveness of a new oral curcumin formulation in acute non-infectious uveitic macular edema: a 12-month observational study. Eur Rev Med Pharmacol Sci 2022;26(1):46-53.
  82. Tsai IC, Hsu CW, Chang CH, Tseng PT, Chang KV. The effect of curcumin differs on individual cognitive domains across different patient populations: A systematic review and meta-analysis. Pharmaceuticals (Basel) 2021;14(12):1235. PubMed
  83. Alam MA, Bin Jardan YA, Raish M, Al-Mohizea AM, Ahad A, Al-Jenoobi FI. Herb-drug interaction: Pharmacokinetics and pharmacodynamics of anti-hypertensive drug amlodipine besylate in presence of lepidium sativum and curcuma longa. Xenobiotica 2022;1-9.
  84. Sohal A, Alhankawi D, Sandhu S, Chintanaboina J. Turmeric-induced hepatotoxicity: Report of 2 cases. Int Med Case Rep J 2021;14:849-852. PubMed
  85. Hussaarts KGAM, Hurkmans DP, Oomen-de Hoop E, et al. Impact of curcumin (with or without piperine) on the pharmacokinetics of tamoxifen. Cancers (Basel). 2019;11(3):403. PubMed
  86. Kalluru H, Mallayasamy SR, Kondaveeti SS, Chandrasekhar V, Kalachaveedu M. Effect of turmeric supplementation on the pharmacokinetics of paclitaxel in breast cancer patients: A study with population pharmacokinetics approach. Phytother Res 2022;36(4):1761 PubMed
  87. 109288 Halegoua-DeMarzio D, Navarro V, Ahmad J, et al. Liver injury associated with turmeric-A growing problem: Ten cases from the drug-induced liver injury network [DILIN]. Am J Med. 2022:S0002-9343(22)00740-9. PubMed
  88. Arzallus T, Izagirre A, Castiella A, Torrente S, Garmendia M, Zapata EM. Drug induced autoimmune hepatitis after turmeric intake. Gastroenterol Hepatol 2023. PubMed
  89. Gilad O, Rosner G, Ivancovsky-Wajcman D, et al. Efficacy of wholistic turmeric supplement on adenomatous polyps in patients with familial adenomatous polyposis-A randomized, double-blinded, placebo-controlled study. Genes (Basel) 2022;13(12):2182. PubMed
  90. Ahad A, Raish M, Abdelrahman IA, et al. Changes in pharmacokinetics and pharmacodynamics of losartan in experimental diseased rats treated with Curcuma longa and Lepidium sativum. Pharmaceuticals (Basel) 2022;16(1):33. PubMed
  91. Haron MH, Dale O, Martin K, et al. Evaluation of the Herb-Drug Interaction Potential of Commonly Used Botanicals on the US Market with Regard to PXR- and AhR-Mediated Influences on CYP3A4 and CYP1A2. J Diet Suppl 2022. PubMed
  92. Pochet S, Lechon AS, Lescrainier C, et al. Herb-anticancer drug interactions in real life based on VigiBase, the WHO global database. Sci Rep 2022;12(1):14178. PubMed
  93. Kou H, Huang L, Jin M, He Q, Zhang R, Ma J. Effect of curcumin on rheumatoid arthritis: a systematic review and meta-analysis. Front Immunol 2023;14:1121655. PubMed
  94. Qiu L, Gao C, Wang H, et al. Effects of dietary polyphenol curcumin supplementation on metabolic, inflammatory, and oxidative stress indices in patients with metabolic syndrome: a systematic review and meta-analysis of randomized controlled trials. Front PubMed
  95. Sato T, Yagi A, Yamauchi M, et al. The use of an antioxidant enables accurate evaluation of the interaction of curcumin on organic anion-transporting polypeptides 4C1 by preventing auto-oxidation. Int J Mol Sci 2024;25(2):991. PubMed
  96. Washington O, Robinson E, Simh D, et al. Oxalate nephropathy and chronic turmeric supplementation: a case report. J Bras Nefrol 2024;46(1):99-106. PubMed
  97. Munshi R, Karande-Patil S, Kumbhar D, Deshmukh A, Hingorani L. A randomized, controlled, comparative, proof-of-concept study to evaluate the efficacy and safety of Nisha-Amalaki capsules in prediabetic patients for preventing progression to diabetes. J Ay PubMed
  98. Sharifi Razavi A, Mohajerani F, Niksolat F, Karimi N. Efficacy of topical curcumin on mild to moderate carpal tunnel syndrome: a randomized double-blind, placebo-controlled clinical trial. Pain Med 2024;25(5):327-333. PubMed
  99. Yaikwawong M, Jansarikit L, Jirawatnotai S, Chuengsamarn S. Curcumin Reduces Depression in Obese Patients with Type 2 Diabetes: A Randomized Controlled Trial. Nutrients 2024;16(15):2414. PubMed
  100. Tehrani SD, Hosseini A, Shahzamani M, et al. Evaluation of the effectiveness of curcumin and piperine co-supplementation on inflammatory factors, cardiac biomarkers, atrial fibrillation, and clinical outcomes after coronary artery bypass graft surgery. Cl PubMed
  101. Yaikwawong M, Jansarikit L, Jirawatnotai S, Chuengsamarn S. The Effect of Curcumin on Reducing Atherogenic Risks in Obese Patients with Type 2 Diabetes: A Randomized Controlled Trial. Nutrients 2024;16(15):2441. PubMed
  102. Dibaei M, Hosseini A, Lavasani H, Kiani-Dehkordi B, Rouini M. Assessment of metabolic interaction between curcumin and tramadol using the isolated perfused rat liver. Heliyon 2024;10(15):e35070. PubMed

See these in context on the Turmeric monograph →

Sodium 38 references
  1. Garabedian-Ruffalo SM, Ruffalo RL. Drug and nutrient interactions. Am Fam Physician 1986;33:165-74.
  2. Food and Drug Administration Science Background: Safety of Sodium Phosphates Oral Solution. September 17, 2001. Available at: http://www.fda.gov/cder/drug/safety/sodiumphospate.htm
  3. Coton T, Mallaret C, Coilliot C, Carre D, Guisset M. Severe acute ulcerated gastritis induced by salt. Presse Med 2009;38(3):499-500. PubMed
  4. Frings-Meuthen P, Buehlmeier J, Baecker N, et al. High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses. J Appl Physiol 2011;111(2):537-542. PubMed
  5. Frings-Meuthen P, Baecker N, Heer M. Low-grade metabolic acidosis may be the cause of sodium chloride-induced exaggerated bone resorption. J Bone Miner Res 2008;23(4):517-524. PubMed
  6. Alam S, Johnson AG. A meta-analysis of randomised controlled trials (RCT) among healthy normotensive and essential hypertensive elderly patients to determine the effect of high salt (NaCl) diet of blood pressure. J Hum Hypertens 1999;13(6):367-74.
  7. Boudville N, Ward S, Benaroia M, House AA. Increased sodium intake correlates with greater use of antihypertensive agents by subjects with chronic kidney disease. Am J Hypertens 2005;18(10):1300-5. PubMed
  8. Bennett WM. Drug interactions and consequences of sodium restriction. Am J Clin Nutr 1997;65(2 Suppl):678S-681S. PubMed
  9. Okusa MD, Crystal LJ. Clinical manifestations and management of acute lithium intoxication. Am J Med 1994;97(4):383-9. PubMed
  10. Food and Nutrition Board, Institute of Medicine. Dietary reference intakes for water, potassium, sodium, chloride, and sulfate. Washington, DC: National Academy Press, 2005. Available at: http://www.nap.edu/openbook.php?record_id=10925. DOI
  11. D'Elia L, Rossi G, Ippolito R, Cappuccio FP, Strazzullo P. Habitual salt intake and risk of gastric cancer: a meta-analysis of prospective studies. Clin Nutr 2012;31(4):489-98. PubMed
  12. Goldsmith SR. Hyponatremia in heart failure: time for a trial. J Card Fail 2013;19(6):398-400. PubMed
  13. Willocks L, Brettle R, Keen J, Valentine C, Pinching AJ. Formulations of didanosine (ddI) and salt overload. Lancet 1992;339(8786):190.
  14. Chen L, Zhang Z, Chen W, Whelton PK, Appel LJ. Lower Sodium Intake and Risk of Headaches: Results From the Trial of Nonpharmacologic Interventions in the Elderly. Am J Public Health. 2016;106(7):1270-5. PubMed
  15. Cook NR, Appel LJ, Whelton PK. Lower levels of sodium intake and reduced cardiovascular risk. Circulation. 2014;129(9):981-9. PubMed
  16. Cook NR, Appel LJ, Whelton PK. Sodium Intake and All-Cause Mortality Over 20 Years in the Trials of Hypertension Prevention. J Am Coll Cardiol. 2016;68(15):1609-1617. PubMed
  17. Mente A, O'Donnell M, Rangarajan S, et al. Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies. Lancet. 2016;388(10043):465-75. PubMed
  18. Moosavian SP, Haghighatdoost F, Surkan PJ, Azadbakht L. Salt and obesity: a systematic review and meta-analysis of observational studies. Int J Food Sci Nutr. 2017;68(3):265-277. PubMed
  19. O'Donnell M, Mente A, Rangarajan S, et al. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med. 2014;371(7):612-23. DOI
  20. Poggio R, Gutierrez L, Matta MG, Elorriaga N, Irazola V, Rubinstein A. Daily sodium consumption and CVD mortality in the general population: systematic review and meta-analysis of prospective studies. Public Health Nutr. 2015;18(4):695-704. PubMed
  21. Stallings VA, Harrison M, Oria M; Committee to Review the Dietary Reference Intakes for Sodium and Potassium, Food and Nutrition Board, Health and Medicine Division, National Academies of Sciences, Engineering, and Medicine. Washington (DC): National Acad
  22. Mahtani KR, Heneghan C, Onakpoya I, et al. Reduced Salt Intake for Heart Failure: A Systematic Review. JAMA Intern Med. 2018 Dec 1;178(12):1693-1700. PubMed
  23. Yancy CW. Sodium Restriction in Heart Failure: Too Much Uncertainty-Do the Trials. JAMA Intern Med. 2018 Dec 1;178(12):1700-1701. PubMed
  24. He FJ, Campbell NRC, Ma Y, MacGregor GA, Cogswell ME, Cook NR. Errors in estimating usual sodium intake by the Kawasaki formula alter its relationship with mortality: implications for public health. Int J Epidemiol. 2018;47(6):1784-1795. PubMed
  25. Murthy K, Ondrey GJ, Malkani N, et al. THE EFFECTS OF HYPONATREMIA ON BONE DENSITY AND FRACTURES: A SYSTEMATIC REVIEW AND META-ANALYSIS. Endocr Pract. 2019;25(4):366-378. PubMed
  26. Messerli FH, Hofstetter L, Syrogiannouli L, et al. Sodium intake, life expectancy, and all-cause mortality. Eur Heart J 2021;42(21):2103-2112. PubMed
  27. Graudal NA, Hubeck-Graudal T, Jurgens G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Cochrane Database Syst Rev 2020;12(12):CD004022. PubMed
  28. Giatti S, Santos RB, Aielo AN, et al. Association of sodium with obstructive sleep apnea. The ELSA-Brasil study. Ann Am Thorac Soc 2021;18(3):502-510. PubMed
  29. Nan X, Lu H, Wu J, et al. The interactive association between sodium intake, alcohol consumption and hypertension among elderly in northern China: a cross-sectional study. BMC Geriatr 2021;21(1):135. PubMed
  30. Kyozuka H, Fukusda T, Murata T, et al. Impact of preconception sodium intake on hypertensive disorders of pregnancy: The Japan Environment and Children's study. Pregnancy Hypertens 2021;23:66-72. PubMed
  31. Zhao L, Ogden CL, Yang Q, et al. Association of usual sodium intake with obesity among US children and adolescents, NHANES 2009-2016. Obesity (Silver Spring) 2021;29(3):587-594. PubMed
  32. Ma Y, He FJ, Sun Q, et al. 24-Hour urinary sodium and potassium excretion and cardiovascular risk. N Engl J Med 2022;386(3):252-263. PubMed
  33. Liu J, Yang X, Zhang P, et al. Association of urinary sodium excretion and left ventricular hypertrophy in people with type 2 diabetes mellitus: A cross-sectional study. Front Endocrinol (Lausanne) 2021;12:728493. PubMed
  34. Filippini T, Malavolti M, Whelton PK, Vinceti M. Sodium intake and risk of hypertension: A systematic review and dose-response meta-analysis of observational cohort studies. Curr Hypertens Rep 2022;24(5):133-144. PubMed
  35. Wang DD, Li Y, Nguyen XT, et al. Dietary sodium and potassium intake and risk of non-fatal cardiovascular diseases: The million veteran program. Nutrients 2022;14(5):1121. PubMed
  36. Kwak JH, Park CH, Eun CS, et al. The associations of dietary intake of high sodium and low zinc with gastric cancer mortality: A prospective cohort study in Korea. Nutr Cancer 2022;74(10):3501-3508. PubMed
  37. George S, Maiti R, Mishra BR, Jena M, Mohapatra D. Effect of regulated add-on sodium chloride intake on stabilization of serum lithium concentration in bipolar disorder: A randomized controlled trial. Bipolar Disord 2023;25(1):66-75. PubMed
  38. Zhou TL, Schütten MTJ, Kroon AA, et al. Urinary Sodium Excretion and Salt Intake Are Not Associated With Blood Pressure Variability in a White General Population. J Am Heart Assoc 2023;12(1):e026578. PubMed

See these in context on the Sodium monograph →

Potassium 12 references
  1. McEvoy GK, ed. AHFS Drug Information. Bethesda, MD: American Society of Health-System Pharmacists, 1998.
  2. Gennaro A. Remington: The Science and Practice of Pharmacy. 19th ed. Lippincott: Williams & Wilkins, 1996.
  3. Whelton PK, He J, Cutler JA, et al. Effects of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical trials. JAMA 1997;277:1624-32. PubMed
  4. Phillips, C. O., Kashani, A., Ko, D. K., Francis, G., and Krumholz, H. M. Adverse effects of combination angiotensin II receptor blockers plus angiotensin-converting enzyme inhibitors for left ventricular dysfunction: a quantitative review of data from ra DOI
  5. Altieri, P. I., Herrero, C., Suero, R., and Ortiz, A. Bleeding duodenal ulcer in a patient taking slow-releasing potassium tablets. Bol.Asoc.Med P.R. 1977;69(8):276.
  6. Raf, L. E. Enteric-coated potassium chloride tablets and ulcer of the small intestine. Acta Chir Scand Suppl 1967;(374):1-87.
  7. Potassium chloride oral solution [package insert]. Allentown, PA: Lehigh Valley Technologies, Inc.; 2014.
  8. Potassium chloride injection [package insert]. Lake Forest, IL: Hospira Inc.; 2009.
  9. Patel RB, Tannenbaum S, Viana-Tejedor A, et al. Serum potassium levels, cardiac arrhythmias, and mortality following non-ST-elevation myocardial infarction or unstable angina: insights from MERLIN-TIMI 36. Eur Heart J Acute Cardiovasc Care 2017 Feb;6(1):1 PubMed
  10. Malta D, Arcand J, Ravindran A, Floras V, Allard JP, Newton GE. Adequate intake of potassium does not cause hyperkalemia in hypertensive individuals taking medications that antagonize the renin angiotensin aldosterone system. Am J Clin Nutr 2016 Oct;104(4 PubMed
  11. Keskin M, Kaya A, Tatlisu MA, et al. The effect of serum potassium level on in-hospital and long-term mortality in ST elevation myocardial infarction. Int J cardiol. 2016 Oct 15;221:505-10.
  12. Stallings VA, Harrison M, Oria M; Committee to Review the Dietary Reference Intakes for Sodium and Potassium, Food and Nutrition Board, Health and Medicine Division, National Academies of Sciences, Engineering, and Medicine. Washington (DC): National Acad

See these in context on the Potassium monograph →

Boswellia Serrata 16 references
  1. Gupta I, Gupta V, Parihar A, et al. Effects of Boswellia serrata gum resin in patients with bronchial asthma: results of a double-blind, placebo-controlled, 6-week clinical study. Eur J Med Res 1998;3:511-4.
  2. Electronic Code of Federal Regulations. Title 21. Part 182 -- Substances Generally Recognized As Safe. Available at: https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?CFRPart=182
  3. Kimmatkar N, Thawani V, Hingorani L, et al. Efficacy and tolerability of Boswellia serrata extract in treatment of osteoarthritis of knee--a randomized double blind placebo controlled trial. Phytomedicine 2003;10:3-7. PubMed
  4. Liu JJ, Nilsson A, Oredsson S, et al. Boswellic acids trigger apoptosis via a pathway dependent on caspase-8 activation but independent on Fas/Fas ligand interaction in colon cancer HT-29 cells. Carcinogenesis 2002;23:2087-93. PubMed
  5. Wildfeuer A, Neu IS, Safayhi H, et al. Effects of boswellic acids extracted from a herbal medicine on the biosynthesis of leukotrienes and the course of experimental autoimmune encephalomyelitis. Arzneimittelforschung 1998;48:668-74.
  6. Gupta I, Parihar A, Malhotra P, et al. Effects of gum resin of Boswellia serrata in patients with chronic colitis. Planta Med 2001;67:391-5. PubMed
  7. Sengupta K, Alluri KV, Satish AR, et al. A double blind, randomized, placebo controlled study of the efficacy and safety of 5-Loxin. Arthritis Res Ther 2008;10:R85.
  8. Sengupta K, Krishnaraju AV, Vishal AA, et al. Comparative efficacy and tolerability of 5-Loxin and Aflapin against osteoarthritis of the knee: a double blind, randomized, placebo controlled clinical study. Int J Med Sci 2010;7:366-77.
  9. Ernst E. Frankincense: systematic review. BMJ 2008;337:a2813. PubMed
  10. Kirste S, Treier M, Wehrle SJ, et al. Boswellia serratea extract acts on cerebral edema in patients irradiated for brain tumors: a prospective, randomized, placebo-controlled, double-blind pilot trial. Cancer 2011;117:3788-95.
  11. Frank A, Unger M. Analysis of frankincense from various Boswellia species with inhibitory activity on human drug metabolising cytochrome P450 enzymes using liquid chromatography mass spectrometry after automated on-line extraction. J Chromatogr A 2006;111 PubMed
  12. Altmann A, Poeckel D, Fischer L, et al. Coupling of boswellic acid-incuded Ca2+ mobilisation and MAPK activation to lipid metabolism and peroxide formation in human leucocytes. Br J Pharmacol 2004;141:223-32.
  13. El Fortia, M., Badi, H., Elalem, Kh, Kadiki, O., and Topov, Y. Olibanum bezoar: complication of a traditional popular medicine. East Mediterr.Health J 2006;12(6):927-929.
  14. Meshkat S, Mahmoodi Baram S, Rajaei S, et al. Boswellia serrata extract shows cognitive benefits in a double-blind, randomized, placebo-controlled pilot clinical trial in individuals who suffered traumatic brain injury. Brain Inj 2022;36(4):553-559. PubMed
  15. Haron MH, Dale O, Martin K, et al. Evaluation of the Herb-Drug Interaction Potential of Commonly Used Botanicals on the US Market with Regard to PXR- and AhR-Mediated Influences on CYP3A4 and CYP1A2. J Diet Suppl 2022. PubMed
  16. Valente IVB, Garcia D, Abbott A, et al. The anti-proliferative effects of a frankincense extract in a window of opportunity phase ia clinical trial for patients with breast cancer. Breast Cancer Res Treat 2024;204(3):521-530. PubMed

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

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