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Botanical Name: Curcuma longa L.
Pharmacopoeial Name: Curcumae longae rhizome.
Synonym: Curcuma domestica Valeton.
Common Names: Turmeric, Indian saffron.

Summary Table
Drug/Class Interaction TypeMechanism and SignificanceManagement
Cytotoxic antibiotics
Herb may reduce drug-induced pulmonary toxicity.
Clinical significance not established.
Consider coadministration only under specialist professional management.
Platinum chemotherapy compounds

Herb may reduce drug-induced renal and neurotoxicities.
Clinical significance not established.
Consider coadministration only under specialist professional management.
Alkylating agents

Herb may reduce drug-induced toxicity but may also reduce effectiveness of drug.
Conflicting data; clinical significance not established.
Avoid until further data available.
Immunosuppressive agents
/ /
Herb may enhance immunosuppressive efficacy of drug, but also risks possible reduction in drug bioavailability.
Clinical significance not established.
Consider coadministration only under specialist professional management with serum monitoring of drug levels.
Anthracycline chemotherapy
Herb protects against and reduces drug-induced cardiotoxicity and may reduce drug-induced resistance.
Effect on drug efficacy controversial.
Clinical significance not established.
Avoid coadministration, until further data available. Consider before and after chemotherapy.
Herb reduces alcohol-related pathologies in liver, pancreas, and central nervous system.
Clinical significance not established.
Incorporate into natural treatment protocols for alcohol-related conditions.
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Herb may reduce incidence and promote healing of drug-induced gastric ulceration.
Clinical trial suggests turmeric no different than antacids for healing ulcers.
Consider coadministration with ulcerogenic NSAIDs to prevent gastropathies.

Herb may chemosensitize malignant cells to drug.
Clinical significance not established.
Consider coadministration only under specialist professional management.
Vinca alkaloids

Herb may reduce drug resistance by inhibition of efflux mechanisms.Consider coadministration only under specialist professional management.
herb description



Related Species

Curcuma aromatica Salisbury, Curcuma xanthorrhiza Roxb.

Habitat and Cultivation

Native to tropical zones in India and Southeast Asia; cultivated for culinary and medicinal purposes for many centuries; now imported principally from India, China, and Indonesia.

Parts Used


Common Forms

  • Dried:   Rhizome, powdered.

Oleoresin or essential oil.

  • Tincture, Fluid Extract:   Dried or fresh rhizome, 45% ethanol.

  • Standardized Extract:   Solid extracts, concentrated and standardized to 95% curcuminoids, as curcumin.

Note: Experimental studies often use purified laboratory-grade diferuloylmethane or curcumin-I only; semisynthetic derivatives are also available.

herb in clinical practice


Although in medicinal use in Asia for more than a millennium, turmeric is probably better known in the West as a common yellow spice from the ginger family, used as a pungent flavoring ingredient in curries, which is also widely used in the U.S. food industry as a coloring agent. Until recently, Western medicine viewed turmeric primarily as a spice with minor aromatic digestive stimulant and hepatic stimulant properties, indicated but little used for functional hepatobiliary disorders. In 1985 the German Commission E approved “Turmeric Root” for dyspeptic conditions, 1 although the herb was absent from both the 1983 and the 1996 edition of the British Herbal Pharmacopoeia . The World Health Organization (WHO) monograph repeats the Commission E indications. 2

Pharmacological investigations into the anticancer and anti-inflammatory properties of the herb and its constituents began to attract research interest in the 1980s. Currently, curcumin is regarded as a natural compound of great interest and of considerable therapeutic potential because of its multiple properties, which include antioxidant, anti-inflammatory, chemopreventive, antimutagenic, anticarcinogenic, antimetastatic, antiangiogenic, and cardioprotective activities. Although this research currently constitutes a rapidly expanding body of literature, a 2003 therapeutic monograph on turmeric by the European Scientific Cooperative on Phytotherapy (ESCOP) 3 echoes the original 1985 Commission E indications for “symptomatic treatment of mild digestive disturbances and minor biliary dysfunction.” Aggarwal et al. 4 recently reviewed the chemopreventive and anticancer molecular biology of curcumin. The majority of recent scientific studies on turmeric employed purified laboratory-grade diferuloylmethane or curcumin-I, which should be noted before extrapolating to mixtures of curcuminoids or to crude whole-herb extracts.

Historical/Ethnomedicine Precedent

In Ayurveda, turmeric is used internally for digestive problems and is considered a blood purifier and antimicrobial. Externally it is used for skin problems, as well as for sprains and strains. The powdered herb is often administered in a base of dietary ingredients, such as milk or honey, or in slaked lime for topical applications. 5 In classical Chinese medicine, turmeric invigorates the xue (blood) and relieves pain, especially related to liver (Gan); it clears heat and cools the blood, clears the heart (Xin) (which helps with psychological problems), and benefits the gallbladder (Dan) and treats jaundice. 6

Known or Potential Therapeutic Uses

Abdominal pain, adjunctive cancer treatment, antimicrobial, arthritis, cardiovascular disease prophylaxis, chemoprevention, chemosensitization, cholestasis, dyspepsia, ethanol-related hepatic conditions, hyperlipidemia, inflammation, jaundice, radiosensitization.

Topically for skin conditions, sprains, and strains.

Key Constituents

Curcuminoids (diferuloylmethanes), including curcumin and its methoxylated derivatives (2%-5%), are the yellow pigments and principal actives. Sometimes designated as curcumins I to IV: I, curcumin; II, desmethoxycurcumin; III, bisdesmethoxycurcumin; and IV, cyclocurcumin.

Essential oil (3% and 5%), including sesquiterpene ketones and monoterpenes.

Therapeutic Dosing Range

  • Powdered Rhizome:   Up to 12 g daily by decoction.

  • Tincture, Fluid Extract:   5 to 15 mL daily (as 1:1 equivalent).

  • Standardized Extract:   Equivalent of 400 to 600 mg curcumin three times daily.

interactions review

Strategic Considerations

No interactions with prescription drugs are noted in the available therapeutic monographs on turmeric. Both Western and Chinese herbal authorities have advised using caution when coadministering turmeric with antiplatelet or anticoagulant drugs and avoiding higher doses of the herb in such settings. 7,8No interaction with anticoagulant or antiplatelet medications has been reported clinically or described experimentally, and the suggested interaction is classified here as “overstated/speculative” (see Theoretical, Speculative, and Preliminary Interactions Research).

The primary clinical context for current use of curcumin extracts is inflammatory conditions and the integrative oncology setting. Curcumin has innumerable effects on a wide range of signal transduction pathways and molecular targets affecting cell growth, multiplication, differentiation, and apoptosis, including inhibition of nuclear factor kappa B (NF-κB) and activating protein-1 (AP-1). 4,9-13Experimental evidence is emerging for potential interactions with a variety of cytotoxic drugs, as well as radiotherapy. A novel interactions issue, unaddressed by research to date, is how curcumin, known to inhibit a number of molecular targets involved in angiogenesis, including vascular endothelial growth factor (VEGF), might interact with the newer generation of antiangiogenic agents such as the monoclonal antibody bevacizumab (Avastin). 14,15Despite the rapidly expanding basic science research on the molecular targets affected by curcumin, extrapolation to clinical settings is problematic given the lack of large-scale trial evidence. Curcumin is incorporated with other natural compounds into adjunctive anticancer protocols on an anecdotal clinical basis, and preliminary data support synergistic combination of curcumin with genistein. 16-18

Although several potentially beneficial interactions with chemotherapeutic agents are listed later, these interactions have not been well studied, particularly in vivo. One research group has questioned the advisability of combining curcumin with alkylating agents such as cyclophosphamide, which induces apoptosis through activation of Janus kinase (JNK), which may be inhibited by relatively low doses of curcumin. 19 The same authors raised concerns about the advisability of coadministering curcumin with chemotherapy agents, which increase activation of NF-κB. Even though this may reduce drug-induced NF-κB–mediated drug resistance, the activation of NF-κB may be an important (but not exclusive) part of the cytotoxic mechanism of these drugs (e.g., doxorubicin), although this study has been criticized. 20 However, until further data are available with respect to specific chemotherapy agents and specific malignancies, decisions regarding coadministration of curcumin with chemotherapy need to be made in conjunction with practitioners experienced in the integrative oncological setting. There is also evidence, not detailed here, that curcumin may have beneficial interactions with radiotherapies. 21-23

Effects on Drug Metabolism and Bioavailability

Turmeric potentially exerts concerted effects on all three phases of drug metabolism. As with many herbs, the clinical implications of in vitro data remain to be established, and the interpretation of some studies is particularly controversial because of the extremely low bioavailability of curcumin. Biphasic effects have also been reported. In a Phase I study of 25 patients with various premalignant diagnoses, Cheng et al. 24 established that single oral doses of 8000 mg curcumin resulted in peak plasma concentrations of only 1.77. In colorectal adenocarcinoma patients who were administered curcumin for 7 days at 3600 mg/day, levels of curcumin were 2.5 times higher in malignant colorectal cells than in normal colon tissue, at 12.7 nmol/g in the form of sulfate and glucuronide conjugates. The effect of curcumin was to decrease levels of an oxidative deoxyribonucleic acid (DNA) adduct marker of cyclooxygenase-2 (COX-2) expression, which was not affected. 25,26In a rodent model, Shoba et al. 27 showed that coadministration of piperine (20 mg/kg) with curcumin increased the bioavailability of the herb by a factor of 154% in a single-dose pharmacokinetic study; in humans, 20 mg piperinen increased the bioavailability of curcumin by 2000%. 27 The low bioavailability results from rapid glucuronidation both hepatically and directly at the intestinal wall.

Effects on cytochrome P450 (CYP450) enzymes have been documented. Two different research groups used a rodent hepatocyte model to demonstrate curcumin inhibited both the induction and the activity of CYP450 1A1and 1A2, 2B1 and 2B2, and 2E1. 28-30The inhibitory effects were weak to moderate, except for 1A1/1A2, for which inhibition was more potent. These CYP450 enzymes are particularly related to metabolism of carcinogens, including the polycyclic aromatic hydrocarbons (PAHs). Using human oral mucosa cells and oral squamous cell carcinoma (SCC) cells, Rinaldi et al. 31 demonstrated induction of the nuclear translocation of the aryl hydrocarbon receptor (AhR), a process that leads to downstream activation of phase I and phase II AhR-responsive carcinogen-metabolizing enzymes. They also demonstrated increased CYP1A1 activity in oral SCC cells, combined with a decrease in carcinogen bioactivation, as well as an increase in intracellular reduced-glutathione (GSH) levels. The authors concluded that curcumin has a significant ability to modulate carcinogen activation in the human oral cavity. In a study by Raucy 32 using human hepatocytes, curcumin did not demonstrate any induction effects on CYP3A4, suggesting negligible interactions with the many drugs metabolized by this enzyme. Animal studies corroborate a significant effect of curcumin on phase II enzymes, particularly glutathione- S-transferase, and the ability of the curcuminoids to increase intracellular glutathione has been documented in several experimental models. 30,33,34

Several studies have demonstrated pronounced inhibitory effects of curcumin on P-glycoprotein (P-gp) in several cell lines, with dose-dependent effects at concentrations between 1 and 15 micromolar (μM). 35,36Anuchapreeda et al. 37 found that in human cervical carcinoma cells (KB-VI), pretreatment with curcumin at 1 to 10 μM for up to 72 hours significantly lowered MDR1 gene expression. Curcumin also inhibited rhodamine-123 efflux from these cells but had no effect on wild-type KB-3 cells that do not overexpress P-gp. The same research group later established that curcumin-I was the most effective inhibitory compound among the curcuminoids I to III, and that vinblastine sensitivity was increased in the homologous but drug-resistant KB-V1 line. 38 Nabekura et al. 36 established similar results for daunorubicin accumulation in the same drug-resistant cell line.

herb-drug interactions
Cisplatin and Related Platinum Chemotherapy Compounds
Cyclosporine and Related Immunosuppressive Agents
Doxorubicin and Related Anthracycline Chemotherapy
Indomethacin, Related Nonsteroidal Anti-Inflammatory Drugs (NSAIDs), and Other Ulcerogenic Substances
Paclitaxel and Related Taxanes
Vinblastine, Related Vinca Alkaloids, and Platinum Chemotherapy Compounds
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Anticoagulants and Antiplatelet Drugs
Irinotecan/Camptothecin, Mechlorethamine
Oral Hypoglycemic Agents and Insulin
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