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Turmeric/Curcumin

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

Summary Table

Drug/Class Interaction Type	Mechanism and Significance	Management
Bleomycin Cytotoxic antibiotics /	Herb may reduce drug-induced pulmonary toxicity. Clinical significance not established.	Consider coadministration only under specialist professional management.
Cisplatin Platinum chemotherapy compounds	Herb may reduce drug-induced renal and neurotoxicities. Clinical significance not established.	Consider coadministration only under specialist professional management.
Cyclophosphamide 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.
Cyclosporine 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.
Doxorubicin 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.
Ethanol /	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.
Indomethacin 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.
Paclitaxel Taxanes	Herb may chemosensitize malignant cells to drug. Clinical significance not established.	Consider coadministration only under specialist professional management.
Vinblastine Vinca alkaloids	Herb may reduce drug resistance by inhibition of efflux mechanisms.	Consider coadministration only under specialist professional management.

herb description

Family

Zingiberaceae.

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

Rhizome.

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

Overview

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

Bleomycin

Bleomycin (Blenoxane).

	Potential or Theoretical Beneficial or Supportive Interaction, with Professional Management
	Prevention or Reduction of Drug Adverse Effect

Probability: 4. Plausible
Evidence Base:

Preliminary

Effect and Mechanism of Action

Curcumin reduces the characteristic bleomycin-induced pulmonary fibrosis toxicity, according to animal data. The mechanism is not understood but may result from antioxidant and anti-inflammatory effects of curcumin.

Research

Two studies using rodent models have demonstrated that oral curcumin pretreatment for 10 days before bleomycin, and continued during the drug treatment for up to 1 month, reduces pulmonary fibrosis, inflammation, and other markers of lung toxicity, including alveolar macrophage tumor necrosis factor alpha (TNF-α) release and superoxide and nitric oxide induction. Total lung hydroxyproline was also significantly reduced with curcumin coadministration. In both studies the oral doses of curcumin were high, 300 mg/kg/day and 550 nmol/kg/day. ^39,40

Clinical Implications and Integrative Therapeutics

Pulmonary fibrosis is a well-documented adverse effect of bleomycin. Data are lacking on whether curcumin will affect the cytotoxic action of bleomycin. However, because the agent is often administered in combination with doxorubicin and vinblastine, and in vitro data suggest these agents may be more effective with curcumin administration, it may be beneficial to incorporate curcumin as an adjuvant/protective in protocols such as ABVD (Adriamycin, Blenoxane, vinblastine, dacarbazine), but clinical trial support is unavailable.

Cisplatin and Related Platinum Chemotherapy Compounds

Evidence: Cisplatin ( cis-diaminedichloroplatinum, CDDP; Platinol, Platinol-AQ).

Extrapolated, based on similar properties: Carboplatin (Paraplatin), oxaliplatin (Eloxatin).

Potential or Theoretical Beneficial or Supportive Interaction

Probability: 4. Plausible
Evidence Base:

Preliminary

Effect and Mechanism of Action

Curcumin combined with cisplatin results in synergistic antitumor activity in experimental models.

Research

Navis et al. ⁴¹ analyzed tumor markers in liver and kidney homogenates of rats with experimentally induced fibrosarcoma that was treated with cisplatin or a cisplatin-curcumin combination versus controls. Cisplatin alone reduced the markers, but the effect of the combination was to restore markers to control levels. Notarbartolo et al. ⁴² examined the antitumor effects of curcumin alone and in combination with cisplatin on a hepatocellular carcinoma line that constitutively overexpressed NF-κB. They found a sequence-dependent synergy effect of the herb-drug combination on apoptosis, which depended on pretreatment with curcumin and was not observed during simultaneous coadministration. The effect was partially reversed by adding the antioxidant N-acetylcysteine (NAC) and involved caspase-dependent and caspase-independent mechanisms, as well as reduction in the gene expression of several inhibitor of apoptosis proteins (IAPs). Interestingly, the effects of curcumin alone on NF-κB were temporally biphasic, with an initial increase followed by a decrease. The concentrations of curcumin that were effective ranged from 10 to 25 μM.

Clinical Implications and Integrative Therapeutics

Preliminary evidence suggests that curcumin pretreatment may act as a chemosensitizer to cisplatin therapy. The clinical significance of this potentially beneficial interaction, demonstrated in vitro for hepatocellular carcinoma, remains to be established.

Cyclophosphamide

Evidence: Cyclophosphamide (Cytoxan, Endoxana, Neosar, Procytox).

Extrapolated, based on similar properties: Irinotecan (camptothecin-11, CPT-11; Campto, Camptosar); bleomycin (Blenoxane; see earlier section).

Interaction Likely but Uncertain Occurrence and Unclear Implications

Probability: 4. Plausible
Evidence Base:

Mixed

Effect and Mechanism of Action

An experimental reduction in cyclophosphamide-induced lung toxicity is likely mediated by the anti-inflammatory and antioxidant effects of curcumin. The interaction parallels that between bleomycin and curcumin. However, curcumin may reduce the effects of alkylating agent–induced apoptosis mediated through the JNK pathway.

Research

Venkatesan and Chandrakasan ⁴³ used a rodent model to show that 7 days of pretreatment with curcumin in healthy rats prevented lung damage from one intraperitoneal dose of cyclophosphamide, measured by bronchopulmonary lavage fluid levels of angiotensin-converting enzyme (ACE), lactate dehydrogenase (LDH), alkaline phosphatase, lipid peroxide, glutathione, and ascorbate. Somasundaram et al. ¹⁹ questioned the advisability of combining curcumin with alkylating agents such as cyclophosphamide, which induces apoptosis through activation of the JNK pathway, based on preliminary in vivo rodent data. Using human MCF-7 and BT-474 breast cancer cells xenografted into nude mice, oral feeding of low doses of curcumin prevented cyclophosphamide (single dose intraperitoneally) from decreasing tumor size after 24 and 48 hours. This study has been criticized for the short duration of administration of both curcumin and cyclophosphamide and the low doses of curcumin used. ²⁰ (See also Theoretical, Speculative, and Preliminary Interactions Research.)

Clinical Implications and Adaptations

Further research is needed to establish whether the potential reduction of cyclophosphamide toxicity by curcumin is demonstrable in vivo without any countervailing reduction of therapeutic effect of the compound.

Cyclosporine and Related Immunosuppressive Agents

Evidence: Cyclosporine (Ciclosporin, cyclosporin A, CsA; Neoral, Sandimmune, SangCya).

Extrapolated, based on similar properties: Mycophenolate (CellCept).

	Bimodal or Variable Interaction, with Professional Management
	Impaired Drug Absorption and Bioavailability, Precautions Appropriate
	Potential or Theoretical Beneficial or Supportive Interaction, with Professional Management

Probability: 4. Plausible
Evidence Base:

Preliminary

Effect and Mechanism of Action

In a mixed pharmacodynamic and pharmacokinetic interaction, curcumin may enhance immunosuppressive activity of cyclosporine while reducing its bioavailability. The interaction has not been demonstrated clinically to date.

Research

Chueh et al. ⁴⁴ used a rodent cardiac allograft model to demonstrate that curcumin could effectively synergize with cyclosporine. Curcumin alone prolonged survival time of allograft rats compared with controls, but when combined with subtherapeutic doses of cyclosporine, the recipient animals survived longer than those with curcumin alone. Cytokine analysis suggested reduced levels of interleukin-2 (IL-2), interferon gamma (IFN-γ), and granzyme B in both the combination and the curcumin-only animals versus controls. Ranjan et al. ⁴⁵ showed in vitro with human lymphocytes that curcumin inhibits T-cell activation through the CD28/B7 co-stimulation pathway. This pathway is resistant to cyclosporine suppression and synergistic suppression of T-cell responses. In a later study the same group showed curcumin suppressed NF-κB–mediated IL-2 release in response to mitogen activation by various stimuli. ⁴⁶

Additional, if circumstantial, evidence for immunosuppressive effects comes from the ability of curcumin extracts to inhibit experimental allergic encephalomyelitis (a standard animal model of multiple sclerosis); this was mediated by interleukin-12–signaling blockade, resulting in decreased T-cell proliferation and T helper cell type 1 (Th1) differentiation. ⁴⁷ A complication of any in vivo coadministration of cyclosporine with curcumin is that the drug is a substrate of P-gp, which is inhibited by curcumin, thus potentially decreasing bioavailability of cyclosporine. This was demonstrated, as an incidental finding, in an animal study examining the (lack of) effect of curcumin on cyclosporine-induced cholestasis and hypercholesterolemia. ⁴⁸

Clinical Implications, Adaptations, and Integrative Therapeutics

Insufficient data are available to establish the clinical significance of this interaction. However, given the practice of measuring serum values for cyclosporine concentration during immunosuppressive therapy, the problems of adjusting to pharmacokinetic variation caused by P-gp inhibition are theoretically manageable. At present, the beneficial effect of the combination shown experimentally remains to be confirmed by clinical studies. Other evidence suggests a renal-protective effect of curcumin, renal toxicity being a known effect of cyclosporine.

Jones and Shoskes ⁴⁹ showed that several plant-derived compounds reversed renal ischemia and reperfusion injury induced by mycophenolate (CellCept). Coadministration should be considered only with profession management, including monitoring of serum cyclosporine levels by the transplant providers.

Doxorubicin and Related Anthracycline Chemotherapy

Evidence: Doxorubicin (Adriamycin, Rubex).

Extrapolated, based on similar properties: Daunorubicin (Cerubidine, DaunoXome), epirubicin (Ellence, Pharmorubicin), idarubicin (Idamycin, Zavedos), mitoxantrone (Novantrone, Onkotrone).

Similar properties but evidence lacking for extrapolation: Doxorubicin, pegylated liposomal (Caelyx, Doxil, Myocet).

	Interaction Likely but Uncertain Occurrence and Unclear Implications
	Bimodal or Variable Interaction, with Professional Management

Probability: 4. Plausible
Evidence Base:

Mixed

Effect and Mechanism of Action

In this complex multifactorial interaction, curcumin may reduce the known cardiotoxicity of doxorubicin and may also counter the development of drug resistance by inhibiting doxorubicin-induced NF-κB activation. However, curcumin may lower drug efficacy under some circumstances.

Research

Rodent studies demonstrated that both acute cardiotoxicity (measured by serum creatine kinase, LDH, and malondialdehyde levels) and nephrotoxicity (measured by proteinuria, albuminuria, hypolipemia, and urinary N-acetyl-β-glucosaminidase excretion) caused by single-dose intraperitoneal Adriamycin (30 mg/kg) were significantly reduced by oral curcumin pretreatment (200 mg/kg) 7 days before and 2 days after drug administration. ^50,51 The mechanism likely involves antioxidant effects of the curcuminoids, particularly the lowering of lipid peroxidation in cardiomyocytes. Chuang et al. ⁵² used multiple human cancer cell lines to examine the various chemotherapeutic drugs clinically associated with the ability to induce drug resistance (doxorubicin, 5-fluorouracil, cisplatin, paclitaxel). Drug resistance was accompanied by transient increases in NF-κB. When doxorubicin (1 μM) was combined with curcumin (10 μM), NF-κB production was inhibited significantly more than by curcumin alone. The effect was not mediated by TNF-α, and the authors suggested that the effect of curcumin on NF-κB may be important in overcoming drug resistance. Other mechanisms, including glutathione- S-transferase modulation, may be important to the inhibition of doxorubicin resistance by curcumin. ⁵³

Another study provides conflicting data. Somasundaram et al. ¹⁹ found that doxorubicin-induced apoptosis of MCF-7 cells may be significantly reduced by curcumin at low levels in a time- and dose-dependent manner (1.0-10.0 μM). Because the curcumin concentrations used approach those found in human pharmacokinetic studies, the authors advise that patients with breast cancer (and other malignancies) should not concurrently use curcumin with chemotherapy until further investigations clarify the situation. These conclusions have been criticized as generalizations that disregard the methodology of the in vitro model, particularly the temporal kinetics based on very-short-term effects, low doses of curcumin, and a failure to account for the multifactorial mechanisms involved. ²⁰ The issues remain unresolved.

Notarbartalo et al. ⁴² examined the complexity of this interaction in relation to the relative role of NF-κB and other factors using a hepatic cancer cell line. Messenger ribonucleic acid (mRNA) analysis suggested that expression of multiple genes in various pathways is modulated by the combination of agents, with effects that are in part additive and in part antagonistic.

Clinical Implications and Adaptations

Although the protective action of curcumin against doxorubicin toxicity is plausible, the effects on drug efficacy have been questioned. Extrapolations from limited in vitro data to clinical settings (especially on dose levels) are problematic, and further data are needed to characterize the interaction. Curcumin may in addition have a role in anthracycline protocols that have exhibited the emergence of drug resistance. Decisions whether to adopt concurrent use of curcumin will also likely depend on the role assigned to dietary antioxidants (vitamins A, C, and E; carotenoids) during anthracycline chemotherapy, itself a controversial topic.

Ethanol

	Prevention or Reduction of Drug Adverse Effect
	Beneficial or Supportive Interaction, with Professional Management

Probability: 1. Certain
Evidence Base:

Preliminary

Effect and Mechanism of Action

In an experimentally demonstrated interaction, curcumin treatment prevents or reduces ethanol-induced toxicities in various organs and tissues (e.g., hepatic, neural, pancreatic) through multiple mechanisms.

Research

Rodent models of experimentally induced alcoholic liver disease demonstrate the efficacy of curcumin in prevention of ethanol-induced pathology. ^54-56 Similar studies show related effects in ethanol-induced and non-ethanol-induced pancreatitis, as well as in ethanol-induced neural damage. ^57,58 Along with several in vitro investigations, these studies reveal a variety of mechanisms involved in mediating the protective effects. These include suppression of NF-κB activated proinflammatory genes, including inducible nitric oxide synthase (iNOS) and COX-2, as well as antioxidant activity and matrix metalloproteinase (MMP) inhibition. ^54,59-61

Clinical Implications and Integrative Therapeutics

Turmeric extracts and curcumin may be useful adjuncts in the treatment of acute and chronic alcohol-related liver and pancreatic disease.

Indomethacin, Related Nonsteroidal Anti-Inflammatory Drugs (NSAIDs), and Other Ulcerogenic Substances

Evidence: Indomethacin (indometacin; Indocin, Indocin-SR).

Extrapolated, based on similar properties: NSAIDs: COX-1 inhibitors:Diclofenac (Cataflam, Voltaren), combination drug: diclofenac and misoprostol (Arthrotec), diflunisal (Dolobid), etodolac (Lodine), fenoprofen (Dalfon), furbiprofen (Ansaid), ibuprofen (Advil, Excedrin IB, Motrin, Motrin IB, Nuprin, Pedia Care Fever Drops, Provel, Rufen); combination drug: hydrocodone and ibuprofen (Reprexain, Vicoprofen); ketoprofen (Orudis, Oruvail), ketorolac (Acular ophthalmic, Toradol), meclofenamate (Meclomen), mefenamic acid (Ponstel), meloxicam (Mobic), nabumetone (Relafen), naproxen (Aleve, Anaprox, Naprosyn), oxaprozin (Daypro), piroxicam (Feldene), salsalate (salicylic acid; Amigesic, Disalcid, Marthritic, Mono Gesic, Salflex, Salsitab), sulindac (Clinoril), tolmetin (Tolectin). COX-2 inhibitor:Celecoxib (Celebrex). Ethanol (see earlier section).

	Beneficial or Supportive Interaction, with Professional Management
	Prevention or Reduction of Drug Adverse Effect

Probability: 1. Certain
Evidence Base:

Preliminary

Effect and Mechanism of Action

This interaction was serendipitously discovered while using indomethacin as an ulcerogenic agent in a rodent model of acute gastric ulceration. Curcumin prevents indomethacin ulceration and accelerates ulcer healing. The mechanism is multifactorial and includes suppression of MMP-9 and iNOS (regulated by NF-κB activation).

Research

In a rodent model, turmeric extracts at an oral dose of 500 mg/kg produced significant antiulcerogenic activity in animals subjected to a variety of ulcer-inducing agents, including indomethacin and reserpine. ⁶² The mechanism has recently been shown to involve the inhibition of MMP-9 and MMP-2. ⁶³ A clinical open-label trial attempting to establish the efficacy of turmeric (1000 mg/day) compared with antacids in 50 patients over 6 weeks found that the antacid was superior to turmeric in inducing ulcer healing. However, this trial was not related to indomethacin-induced ulcers, and the mechanism may be relatively specific to ulcers caused by chemical agents (involving MMP-9 inhibition).

Clinical Implications and Integrative Therapeutics

This interaction has been cited as a demonstration of the antiulcerogenic effects of curcumin, but the available clinical trial evidence shows turmeric ineffective in healing gastric ulcers. ⁶⁴ The interaction appears is specific to ulcers caused by iatrogenic agents such as NSAIDs. Involvement of the MMPs (especially MMP-9) would predict that curcumin likely has antimetastatic activity, which has indeed been demonstrated. ⁶⁵ Similar mechanisms are involved in the protective effects of curcumin against ethanol-induced toxic damage. (See also previous ethanol-curcumin discussion.) If ulcerogenic drugs likely to induce gastropathic ulceration are administered chronically, turmeric coadministration would appear to be warranted, despite the lack of evidence for turmeric effect on stress ulcers.

Further evidence for the general applicability of these findings to iatrogenic mucosal damage is provided by a study of intestinal mucositis induced by methotrexate. The villous atrophy that resulted from methotrexate damage was partially inhibited by curcumin coadminstration. ²³ This suggests a possible role for curcumin in the amelioration of cytotoxic chemotherapy-induced mucositis.

Paclitaxel and Related Taxanes

Evidence: Paclitaxel (Paxene, Taxol).

Extrapolated, based on similar properties: Docetaxel (Taxotere); paclitaxel, protein-bound (Abraxane).

Potential or Theoretical Beneficial or Supportive Interaction, with Professional Management

Probability: 4. Plausible
Evidence Base:

Preliminary

Effect and Mechanism of Action

An experimentally demonstrated chemosensitization by curcumin to paclitaxel (Taxol)–induced cytotoxicity; the mechanism is independent of microtubule polymerization.

Research

Bava et al. ⁶⁶ tested HeLa cells with paclitaxel (Taxol) alone and Taxol in combination with curcumin and found that the combination exerted synergistic effects on cell kill, and that this was accompanied by caspase activation and cytochrome c release. Taxol-induced NF-κB activity was reduced by curcumin coadministration. There appeared to be no effect on tubulin polymerization or cyclin-dependent CdC2 activation induced by Taxol.

Clinical Implications and Integrative Therapeutics

Coadministration of curcumin with taxanes may result in increased efficacy of the drug. Clinical trial support is not available. The known pharmacology of curcumin does not suggest interference with microtubule mechanisms affected by the taxane class of chemotherapy agents.

Evidence: Vinblastine (Alkaban-AQ, Velban, Velsar).

Extrapolated, based on similar properties: Vincristine (Leurocristine, Oncovin, Vincasar PFS), vinorelbine (Navelbine); Platinum chemotherapy compounds: Carboplatin (Paraplatin), cisplatin ( cis-diaminedichloroplatinum, CDDP; Platinol, Platinol-AQ), oxaliplatin (Eloxatin).

Potential or Theoretical Beneficial or Supportive Interaction, with Professional Management

Probability: 4. Plausible
Evidence Base:

Preliminary

Effect and Mechanism of Action

In this experimentally demonstrated pharmacokinetic interaction, curcumin may increase the bioavailability of vinblastine by inhibition of P-glycoprotein.

Research

The inhibition of P-gp by curcuminoids is well documented (see Effects on Drug Metabolism and Bioavailability). Anuchapreeda et al. ³⁷ tested the ability of curcumin to decrease P-gp–mediated drug resistance in a human cervical carcinoma line and established that curcumin increased their sensitivity to vinblastine, which was consistent with an observed intracellular increase in rhodamine-123 (a P-gp substrate). ³⁷ The same group later established that curcumin-I was more effective than curcumin-II and -III in causing retention of vinblastine by the same cell line. There was no effect on a wild-type variation of the same cell line that lacked drug resistance. ³⁸

Clinical Implications and Integrative Therapeutics

There is growing interest in the potential of natural compounds as potential modulators of drug resistance mediated by the ABC (ATP-binding cassette) family of drug transporters. Coadministration of curcumin with vinca alkaloids may reduce drug resistance to these agents, and the curcuminoids are not known to interfere with the activity of microtubule inhibitors. In vivo studies are necessary to confirm the clinical efficacy of the combination, but curcumin administration may be considered if drug resistance appears responsible for lack of efficacy in malignancies previously responsive to vinblastine.

theoretical, speculative, and preliminary interactions research, including overstated interactions claims

Anticoagulants and Antiplatelet Drugs

Several experiments using animal models (rodents and simians), as well as one study with washed human platelets, have demonstrated that curcumin can inhibit platelet aggregation induced by arachidonate, adrenaline, collagen, and platelet-activating factor (PAF) through modulation of eicosanoid biosynthesis, particularly prostaglandin I ² (PGI ² ; prostacyclin) and thromboxane A ² (TXA ² ) inhibition. ^67-69 Doses of curcumin used in rats and monkeys were between 100 and 300 mg/kg orally, and no measurements were made of bleed times or other coagulation parameters. Shah et al. ⁷⁰ found that 20- to 25-µM concentrations were effective at inhibiting PAF and arachidonic acid (AA)–induced aggregation, but that much higher doses were needed for collagen and adrenaline. ⁷⁰ These doses are higher than those likely to be attained in vivo. Studies testing combinations of turmeric or curcumin coadministration with antiplatelet or anticoagulant drugs are unavailable to date. In the absence of corroboration, extrapolated warnings that turmeric should be avoided with antiplatelet drugs can be considered speculative and overstated. ⁷

Irinotecan/Camptothecin, Mechlorethamine

Irinotecan (camptothecin-11, CPT-11; Campto, Camptosar).

Mechlorethamine (nitrogen mustard; Mustargen).

These two agents were included the in vitro but not in vivo rodent phase of a group of tests conducted by Somasundaram et al. ¹⁹ No other data are available on these particular drugs, although countervailing data exist for other agents included in this study. Apoptosis induced by the drugs was reduced by addition of curcumin. As noted earlier, because the curcumin concentrations used approach those found in human pharmacokinetic studies, the authors suggest that patients with breast cancer (and other malignancies) should not concurrently use curcumin with these chemotherapies until further studies clarify the situation. ¹⁹ Derivative sources have repeated these conclusions as definitive interactions without qualification. The Somasundaram study conclusions have been criticized as being generalizations that disregard the methodology employed in the in vitro model, particularly the temporal kinetics based on very-short-term effects, low doses of curcumin, and a failure to account for the multifactorial mechanisms. ²⁰ The situation is complex, as illustrated by the analysis of Notarbartolo et al. ⁴² (see Cyclophosphamide and Doxorubicin).

Oral Hypoglycemic Agents and Insulin

Buformin (Andromaco Gliporal, Buformina), chlorpropamide (Diabinese), glimepiride (Amaryl), glipizide (Glucotrol; Glucotrol XL), glyburide (glibenclamide; Diabeta, Glynase, Glynase Prestab, Micronase, Pres Tab), insulin (animal-source insulin: Iletin; human analog insulin: Humanlog; human insulin: Humulin, Novolin, NovoRapid, Oralin), metformin (Dianben, Glucophage, Glucophage XR); combination drugs: glipizide and metformin (Metaglip), glyburide and metformin (Glucovance); phenformin (Debeone, Fenformin), tolazamide (Tolinase), tolbutamide (Orinase, Tol-Tab).

Experimental data on diabetic mice suggest that chronic curcuminoid consumption may have beneficial effects on blood glucose levels. ^71,72 These data have been “reverse extrapolated” to imply an adverse interaction with oral hypoglycemics. The possibility of interaction may be different in acute administration versus chronic dietary curcumin consumption, and diabetic patients monitoring blood glucose are generally familiar with compensating for dietary-induced variations in blood sugar. In fact, a more appropriate characterization would be that turmeric and curcumin as dietary ingredients are protective against pathological diabetic sequelae and help maintain glucose homeostasis, as well as being hypocholesterolemic. ^73-75

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