Turmeric

Turmeric is a perennial herb, yielding a rhizome that produces a yellow powder that gives curry its characteristic yellow colour and is used to colour French mustard and the robes of Hindu priests. Turmeric was probably first cultivated as a dye, and then as a condiment and cosmetic. It is often used as an inexpensive substitute for saffron in cooking and in the 13th century Marco Polo marveled at its similarities to saffron. Both Indian Ayurvedic and Chinese medicines use turmeric for the treatment of inflammatory and digestive disorders and turmeric has also been used in tooth powder or paste. Research has focused on turmeric’s antioxidant, hepatoprotective, anti-inflammatory, anticarcinogenic and antimicrobial properties, in addition to its use in cardiovascular disease and gastrointestinal disorders (Anon 2001).

OTHER NAMES:

Chiang huang, curcuma, curcumae longae rhizoma, curcuma rhizome, e zhu, haridra, Indian saffron, jiang huang, jiang huang curcumae rhizoma, turmeric rhizome, turmeric root, yellow root, yu jin, zedoary

BOTANICAL NAME/FAMILY:

Curcuma longa (family Zingiberaceae [ginger])

PLANT PARTS USED:

Dried secondary rhizome (containing not less than 3% curcuminoids calculated as curcumin and not less than 3% volatile oil, calculated on dry-weight basis).

CHEMICAL COMPONENTS:

Turmeric rhizome contains 5% phenolic curcuminoids (diarylheptanoids), which give turmeric the yellow colour. The most significant curcuminoid is curcumin (diferuloymethane).

It also contains up to 5% essential oil including sesquiterpene (e.g. Zingerberene), sesquiterpene alcohols and ketones, and monoterpenes.

Turmeric also contains immune stimulating polysaccharides, including acid glucans known as ukonan A, B and C (Evans 2002).

MAIN ACTIONS:

Most research has focused on a series of curcumin constituents found in the herb. Many of the animal studies; however, involve parenteral administration and oral curcumin or turmeric is likely to be far less active because curcumin is poorly absorbed by the gastrointestinal tract and only trace amounts appear in the blood after oral intake (Ammon & Wahl 1991). Curcumin may, however, have significant activity in the gastrointestinal tract, and systemic effects may take place as a consequence of local gastrointestinal effects or be associated with metabolites of the curcuminoids.

ANTIOXIDANT

Studies have shown that turmeric, as well as curcumin, has significant antioxidant activity (Shalini & Srinivas 1987, Soudamini et al 1992). Turmeric not only exerts direct free radical scavenging activity, it also appears to enhance the antioxidant activity of endogenous antioxidants, such as glutathione peroxidase, catalase and quinine reductase. Curcumin has been shown to induce phase II detoxifying enzymes (glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and catalase) (Iqbal et al 2003). Additionally, its antioxidant effects are 10-fold more potent than ascorbic acid or resveratrol (Song et al 2001). In addition to curcumin, turmeric contains the antioxidants protocatechuic acid and ferulic acid and exhibits significant protection to DNA against oxidative damage in vitro (Kumar et al 2006).

Turmeric’s antioxidant activity may mediate damage produced by myocardial ischaemia and diabetes. Turmeric has been shown to restore myocardial antioxidant status, inhibit lipid peroxidation and protect against ischaemia–reperfusion induced myocardial injuries in an animal model with enhancement of functional recovery (Mohanty et al 2004). Curcumin has also been found to prevent protein glycosylation and lipid peroxidation caused by high glucose levels in vitro (Jain et al 2006) and to improve diabetic nephropathy (Srinivasan 2005). Turmeric has also been shown to suppress cataract development and collagen cross-linking, promote wound healing, and lower blood lipids and glucose levels (Jain et al 2006).

NF-KAPPA-B INHIBITION

The many and varied effects of curcumin may be partly associated with the inhibition of transcription factor nuclear factor-kappa beta (NF-kappa-B) and induction of heat shock proteins. NF-kappa-B is a transcription factor pivotal in the regulation of inflammatory genes and is also closely associated with the heat shock response, which is a cellular defence mechanism that confers broad protection against various cytotoxic stimuli. Inhibition of NF-kappa-B may reduce inflammation and protect cells against damage (Chang 2001) and curcumin has been found to attenuate experimental colitis in animal models through a mechanism correlated with the inhibition of NFkappa- B (Salh et al 2003). The clinical significance of this is unclear.

ANTI-INFLAMMATORY There have been a large number of studies examining the anti-inflammatory effects of curcumin. Turmeric is a dual inhibitor of the arachidonic acid cascade. Curcumin has been shown to exert anti-inflammatory effects via phospholipase, lipo-oxygenase, COX-2, leukotrienes, thromboxane, PGs, NO, collagenase, elastase, hyaluronidase, monocyte chemoattractant protein-1, IFN-inducible protein, TNF and IL-12 (Chainani Wu 2003, Lantz et al 2005).

The anti-inflammatory effect of curcumin was tested in adjuvant-induced chronic inflammation rats which found that curcumin significantly reduced C-reactive protein, TNF-alpha, IL-1 and NO, with no significant changes observed in PGE2 and leukotriene B4 levels or lymphocyte proliferation (Banerjee et al 2003). Curcumin has also been shown to inhibit inflammation in experimental pancreatitis via inhibition of NF-kappa-B and activator protein-1 in two rat models (Gukovsky et al 2003).

GASTROINTESTINAL EFFECTS

Hepatoprotective Curcumin prevents carbon tetrachloride-induced liver injury both in vivo and in vitro (Deshpande et al 1998, Kang et al 2002), reverses aflatoxininduced liver damage in experimental animals (Soni et al 1992) and effectively suppresses the hepatic microvascular inflammatory response to lipopolysaccharides in vivo (Lukita-Atmadja et al 2002). An ethanol soluble fraction of turmeric was shown to contain three antioxidant compounds, curcumin, demethoxycurcumin and bisdemethoxycurcumin, which exert similar hepatoprotective activity to silybin and silychristin in vitro (Song et al 2001).

Several different mechanisms may contribute to turmeric’s hepatoprotective activity. Curcumin has been shown to prevent lipoperoxidation of subcellular membranes in a dosage-dependent manner, due to an antioxidant mechanism (Quiles et al 1998) and turmeric may also protect the liver via inhibition of NF-kappa-B (see above), which has been implicated in the pathogenesis of alcoholic liver disease. Curcumin also blocked endotoxin-mediated activation of NF-kappa-B and suppressed the expression of cytokines, chemokines, COX-2, and iNOS in Kupffer cells (Nanji et al 2003).

Cholagogue and hypolipidaemic Turmeric extract or curcumin extract has shown dose-dependent hypolipidaemic activity in vivo (Asai & Miyazawa 2001, Babu & Srinivasan 1997, Keshavarz 1976, Ramirez-Tortosa et al 1999, Soudamini et al 1992). One in vivo study suggests that curcumin may stimulate the conversion of cholesterol into bile acids, and therefore, increase the excretion of cholesterol (Srinivasan & Sambaiah 1991). A further study demonstrated that supplementation with turmeric reduces fatty streak development and oxidative stress (Quiles et al 2002). Oral curcumin has also been shown to stimulate contraction of the gall bladder and promote the flow of bile in healthy subjects (Rasyid & Lelo 1999).

Antispasmodic Curcuminoids exhibit smooth muscle relaxant activity possibly mediated through calcium-channel blockade, although additional mechanisms cannot be ruled out (Gilani et al 2005). Curcuminoids produced antispasmodic effects on isolated guinea pig ileum and rat uterus by receptor-dependent and independent mechanisms (Itthipanichpong et al 2003).

CANCER

Curcumin has been studied for its wide-ranging effects on tumorigenesis, angiogenesis, apoptosis and signal transduction pathways (Gururaj et al 2002, Mohan et al 2000, Thaloor et al 1998). It is known to inhibit oncogenesis during both the promotion and progression periods in a variety of cancers (Anto et al 1996, Kuttan et al 1985, Menon et al 1999, Ruby et al 1995). Recently, curcumin was found to possess chemopreventive effects against skin cancer, stomach cancer, colon cancer and oral cancer in mice. Chemoprevention

Chemoprevention refers to reversing, suppressing or preventing the process of carcinogenesis. Carcinogenesis results from the accumulation of multiple sequential mutations and alterations in nuclear and cytoplasmic molecules, culminating in invasive neoplasms. These events have traditionally been separated into three phases: initiation, promotion and progression. Typically, initiation is rapid, whereas promotion and progression can take many years. Ultimately, chemoprevention aims at preventing the growth and survival of cells already committed to becoming malignant (Gescher et al 1998, 2001).

Curcumin has been found to effectively block carcinogen-induced skin (Azuine & Bhide 1992), colon (Rao et al 1995, 1999) and liver (Chuang et al 2000) carcinogenesis in animals. It has been suggested that the chemoprotective activity of curcumin occurs via changes in enzymes involved in both carcinogen bioactivation and oestrogen metabolism. This is supported by the findings that curcumin treatment produced changes in CYP1A, CYP3A and GST in mice (Valentine et al 2006) and alleviated the CCl4-induced inactivation of CYPs 1A, 2B, 2C and 3A isozymes in rats, possibly through its antioxidant properties, without inducing hepatic CYPs (Sugiyama et al 2006).

Oral curcumin inhibited chemically induced skin carcinogenesis in mice (Huang et al 1992) and curcumin prevented radiation-induced mammary and pituitary tumors in rats (Inano & Onoda 2002). Curcumin and genistein (from soybeans) inhibited the growth of oestrogen-positive human breast MCF-7 cells induced individually or by a mixture of the pesticides endosulfane, DDT and chlordane, or 17-beta oestradiol (Verma et al 1997).

Apoptosis Apoptosis (programmed cell death) plays a crucial role in regulating cell numbers by eliminating damaged or cancerous cells. Curcumin induced apoptosis in vitro (Kim et al 2001, Kuo et al 1996) and may act via reactive oxygen species and other mechanisms. Curcumin has been demonstrated to induce apoptosis in human basal cell carcinoma cells associated with the p53 signaling pathway, which controls intracellular redox status, levels of oxidation-damaged DNA and oxidative stress induced apoptosis (Jee et al 1998).

Curcumin has also been found to induce apoptosis in human mutant p53 melanoma cell lines and block the NF-kappa-B cell survival pathway and suppress the apoptotic inhibitor known as XIAP. Because melanoma cells with mutant p53 are strongly resistant to conventional chemotherapy, curcumin may overcome the chemoresistance of these cells and provide potential new avenues for treatment (Bush et al 2001). Curcumin has also been found to inhibit prostate cancer cell growth in mice (Dorai et al 2001) and decrease proliferation and induce apoptosis in androgen-dependent and androgen-independent prostate cancer cells in vitro. This was found to be mediated through modulation of apoptosis suppressor proteins and interference with growth factor receptor signalling pathways (Dorai et al 2000). In a further study with rats, however, curcumin did not prevent prostate carcinogenesis (Imaida et al 2001).

Antiproliferative Reduction in proliferation and/or increased apoptosis will lead to tumour regression; however, a more potent effect will be achieved if the two mechanisms occur simultaneously. Curcumin has been shown to do this. The inhibition of cell proliferation is partly related to inhibition of various kinases, such as protein kinase and phosphorylase kinase (Reddy and Aggarwal 1994), and inhibition of several oncogenes and transcription factors. For example, turmeric inhibited epidermal growth factor receptor (EGF-R) signalling via multiple mechanisms including downregulation of the EGF-R protein, inhibition of intrinsic EGF-R tyrosine kinase activity and inhibition of ligand-induced activation of the EGF-R (Dorai et al 2000).

These mechanisms may be particularly important in preventing prostate cancer cells from progressing to a hormone refractory state (Dorai et al 2000). Curcumin has also been found to suppress the growth of multiple breast cancer cell lines and deplete p185neu, the protein product of the HER2/neu proto-oncogene that is thought to be important in human carcinogenesis (Hong et al 1999).

Antimetastatic Curcumin demonstrated the ability to reduce lung metastases from melanoma cells in mice. The activity of curcumin is varied.

· In cell adhesion assays, curcumin-treated cells showed a dose-dependent reduction in their binding to four extracellular matrix proteins (binding to proteins is associated with the spreading of the cancer).

· Curcumin-treated cells showed a marked reduction in the expression of integrin receptors (integrins functionally connect the cell interior with the extracellular matrix, another process necessary for metastases).

· Curcumin also enhanced the expression of antimetastatic proteins, tissue inhibitor metalloproteinase, non-metastatic gene 23 and E-cadherin (a cell adhesion factor) (Ray et al 2003).

Chemotherapy Curcumin enhanced the cytotoxicity of chemotherapeutic agents in prostate cancer cells in vitro by inducing the expression of certain androgen receptor and transcription factors and suppressing NF-kappa-B activation (Hour et al 2002). Curcumin also enhanced the antitumour effect of cisplatin against fibrosarcoma (Navis et al 1999).

Curcumin, however, was found to significantly inhibit cyclophosphamide-induced tumour regression in an in vivo model of human breast cancer. It is suspected that this occurred as a result of inhibition of free radical generation and blockade of JNK function. As such, curcumin intake should be limited in people undergoing treatment for breast cancer with cyclophosphamide until further investigation can clarify the significance of these findings (Somasundaram et al 2002).

Immunomodulation Curcumin administration was found to significantly increase the total white blood cell count and circulating antibodies in mice. A significant increase in macrophage phagocytic activity was also observed in curcumin-treated animals (Antony et al 1999).

However, curcumin has also been demonstrated to have some immunosuppressive activity. Curcumin inhibits PAR2- and PAR4-mediated human mast cell activation by block of ERK pathway (Baek et al 2003). An in vivo study using a cardiac transplant model found that curcumin also significantly reduced expression of IL-2, IFN-gamma and granzyme B (a serine protease associated with the activity of killer T-lymphocytes and NK cells) and increased mean survival time. Curcumin was further shown to work synergistically with the anti-rejection drug cyclosporine (Chueh et al 2003).

Curcumin also modulates other interleukins and has been shown in vitro to be a potent inhibitor of the production of the pro-inflammatory cytokine IL-8, thereby reducing tumour growth and carcinoma cell viability. Curcumin not only inhibited IL-8 production but also inhibited signal transduction through IL-8 receptors (Hidaka et al 2002) and to inhibit cell proliferation, cell-mediated cytotoxicity and cytokine production most likely by inhibiting NF-kappa-B target genes (Gao et al 2004).

CARDIOVASCULAR EFFECTS

Antiplatelet Curcumin has been shown to inhibit platelet aggregation in vivo (Srivastava et al 1985, 1986) and in vitro (Srivastava 1989, 1995). The anticoagulant effect of curcumin is weaker than that of aspirin, which is four-fold more potent than curcumin in treatment of collagen- and noradrenalin-induced thrombosis. Curcumin 100 mg/kg and aspirin 25 mg/kg resulted in 60% protection from thrombosis (Srivastava et al 1985).

Anti-atherogenic A hydro-ethanolic extract of turmeric was found to decrease LDL oxidation, have a vitamin E-sparing effect and lower the oxidation of erythrocyte and liver membranes in rabbits fed a diet high in saturated fat and cholesterol (Mesa et al 2003, Ramirez-Tortosa et al 1999). The atheroscleroprotective potential of turmeric was further demonstrated by an animal study that found turmeric lowered blood pressure and reduced the atherogenic properties of cholesterol (Zahid Ashraf et al 2005).

Dietary curcumin has also been shown to significantly lower blood cholesterol in diabetic animals. Cholesterol decrease was exclusively from the LDL-VLDL fraction. Significant decrease in blood triglyceride and phospholipids was also brought about by dietary curcumin in diabetic rats (Babu & Srinivasan 1997). In a parallel study in which diabetic animals were maintained on a high cholesterol diet, curcumin lowered cholesterol and phospholipid and countered the elevated liver and renal cholesterol and triglyceride levels seen in the diabetic animals (Babu & Srinivasan 1997).

WOUND HEALING Wound healing is a highly ordered process, requiring complex and coordinated interactions involving peptide growth factors, of which transforming growth factorbeta (TGF-beta) is one of the most important. Nitric oxide is also an important factor in healing, and its production is regulated by iNOS.

Topical application of curcumin accelerated wound healing in normal and diabetic rats. The wound healing is partly associated with the regulation of the growth factor TGF-beta-1 and iNOS (Mani et al 2002). Curcumin’s wound healing ability has been confirmed in several other animal studies (Sidhu et al 1998, 1999). Wounds of animals treated with curcumin showed earlier re-epithelialisation, improved neovascularisation, increased migration of various cells including dermal myofibroblasts, fibroblasts, and macrophages into the wound bed, and a higher collagen content (Sidhu et al 1999). It appears to be effective when used orally or as a local application.

Curcumin has also demonstrated powerful inhibition against hydrogen peroxide damage in human keratinocytes and fibroblasts (Phan et al 2001) and pretreatment with curcumin significantly enhanced the rate of wound contraction, decreased mean wound healing time, increased synthesis of collagen, hexosamine, DNA and NO, and improved fibroblast and vascular densities in full thickness wounds in mice exposed to whole-body [gamma]-radiation (Jagetia & Rajanikant 2004).

ANTIMICROBIAL Turmeric is used as an antimicrobial for preserving food (Jayaprakasha et al 2005) and has been found to have antifungal activity, as well as inhibiting aspergillus growth and aflatoxin production in feeds (Gowda et al 2004).

Curcumin has also been found to have dose-dependent, antiprotozoan activity against Giardia lamblia with inhibition of parasite growth and adherent capacity, induction of morphological alterations and apoptosis-like changes in vitro (Perez- Arriaga et al 2006). Curcumin has also shown in vitro and in vivo activity against malaria, with inhibition of growth of chloroquine-resistant Plasmodium falciparum in vitro and enhancement of survival in mice infected with P. berghei (Reddy et al 2005).

PSORIASIS Topical curcumin reduced the severity of active, untreated psoriasis as assessed by clinical, histological and immunohistochemical criteria in an observational study of 10 patients.

Curcumin was also found to decrease phosphorylase kinase, which is involved in signalling pathways, including those involved with cell migration and proliferation (Heng et al 2000). Topical administration of curcumin also induced normal skin formation in the modified mouse tail test (Bosman 1994).

The effects are thought to be due to immune-modulating, anti-inflammatory and cyclo-oxygenase inhibitory actions. The downregulation of pro-inflammatory cytokines supports the view that turmeric antioxidants may exert a favourable effect on psoriasis-linked inflammation. Moreover, because IL-6 and IL-8 are growth factors for keratinocytes, their inhibition by those antioxidants may reduce psoriasis-related keratinocyte hyperproliferation (Miquel et al 2002).

CLINICAL USE:

In practice turmeric and the various curcuminoids are used in many forms and administered via various routes. This review will focus mostly on those methods of use that are commonly used and preparations that are available OTC, such as oral dose forms and topical applications.

CANCER Epidemiological data suggest that curcumin reduces the rate of colorectal cancer (Hergenhahn et al 2002) and curcumin has wide-ranging chemopreventive activity in preclinical carcinogenic models (Plummer et al 2001), most notably for gastrointestinal cancers (Ireson et al 2001). To date, however, there are no controlled trials to attest to turmeric’s efficacy in cancer treatment or prevention.

In a phase 1 study, curcumin taken orally for 3 months at a starting dose of 500 mg/day was found to produce histologic improvement in cases of bladder cancer, oral leucoplakia, intestinal metaplasia of the stomach, cervical intraepithelial neoplasm and Bowen’s disease (Cheng et al 2001).

An ethanol extract of turmeric, as well as an ointment of curcumin, were found to produce remarkable symptomatic relief in patients with external cancerous lesions (Kuttan et al 1987) and there are clinical reports to suggest that curcumin could be safe and effective in the treatment of idiopathic inflammatory orbital pseudotumours (Lal et al 2000).

DYSPEPSIA/PEPTIC ULCERS A randomised, controlled, double-blind prospective multicentre pilot study compared the effects of dried extracts of greater celandine and turmeric with placebo in 76 patients with colicky abdominal pain in the right upper quadrant due to biliary dyskinesia. Abdominal pain was reduced more quickly with active treatment; however, other symptoms such as fullness, nausea and vomiting did not respond (Niederau & Gopfert 1999). Another randomised, placebo-controlled, double-blind study that investigated the efficacy of turmeric for treatment of dyspepsia and flatulence in 116 adult patients with acidic dyspepsia, flatulent dyspepsia or atonic dyspepsia found that 87% of patients receiving turmeric responded compared to 53% receiving placebo (Thamlikitkul et al 1989).

In a study of 24 patients with duodenal or gastric ulcers varying between 0.5 and 1.5 cm in diameter, 300 mg of turmeric given five times daily, 30–60 minutes before meals, at 1600 hours and at bedtime successfully healed 48% of ulcers after 4 weeks and 76% after 12 weeks. Of 20 patients who had erosion gastritis and dyspepsia, the same treatment produced a satisfactory reduction in abdominal pain and discomfort after the first and second week (Prucksunand et al 2001). Turmeric has also been positively compared to a liquid antacid for the treatment of gastric ulcer in a controlled clinical trial (Kositchaiwat et al 1993).

HYPERLIPIDAEMIA Turmeric may be associated with a decrease in the risk of cardiovascular disease and an intake of 200 mg of a hydro-ethanolic extract of turmeric may decrease total blood lipid peroxides and HDL- and LDL-lipid peroxidation, as well as normalise plasma fibrinogen levels and apolipoprotein B/apolipoprotein A ratio (Miquel et al 2002).

In an open trial, 10 healthy volunteers received 500 mg/day of curcumin for 7 days. A significant decrease in the level of serum lipid peroxides (33%), increase in HDL-cholesterol (29%), and a decrease in total serum cholesterol (11.63%) were noted. It also reduced serum lipid peroxides (Soni & Kuttan 1992). In a subsequent study, a 45-day intake (by healthy individuals 27–67 years of age) of a turmeric hydroalcoholic extract at a daily dose equivalent to 20 mg of curcumin resulted in a significant decrease in serum lipid peroxides (Ramirez-Bosca et al 1995).

A daily intake of turmeric equivalent to 20 mg of the phenolic antioxidant curcumin for 60 days also decreased peroxidation of both HDL and LDL in 30 healthy volunteers ranging in age from 40 to 90 years. The effect was quite striking in the persons with high baseline values of peroxidised compounds in these lipoproteins, although no apparent change took place in the persons having low baseline values (Ramirez et al 1997).

ARTHRITIS In a randomised, controlled double-blind study, curcumin 1200 mg/day was compared with phenylbutazone in subjects with RA. Curcumin was found to be effective in improving morning stiffness, walking time and joint swelling; however, the effects of phenylbutazone were stronger (Deodhar et al 1980). Curcumin combined with boswellia, withania and zinc produced a significant drop in pain and disability in OA of the knee in a randomised, double-blind, placebo controlled crossover study of 42 patients (Kulkarni et al 1991); however, the contribution of cucurmin to these results is unknown.

OTHER USES:

CHRONIC ANTERIOR UVEITIS

An open study of 32 patients found that orally administered curcumin improved symptoms and reduced recurrences of chronic anterior uveitis (a condition often associated with other autoimmune disorders) with an efficacy comparable to corticosteroid therapy, yet without significant side-effects (Lal et al 1999).

ORAL SUBMUCOUS FIBROSIS

Turmeric extract 3 g, oil 600 mg and oleoresin 600 mg effectively relieved symptoms and reduced the number of micronuclei (a sign of damage to the DNA and chromosomal integrity) in circulating lymphocytes and oral mucosal cells in patients with oral submucous fibrosis, a debilitating disease of the oral cavity mainly caused by chewing betel nut or tobacco (Hastak et al 1997).

DOSAGE RANGE:

INTERNAL USE

· Powdered turmeric: 1.5–3 g/day in water or cooking. · Liquid extract (1:1) in 45% ethanol: 5–15 mL/day. · Powdered extract standardized to 95% curcumin: 100–300 mg/day. Higher doses used for arthritis and cancer.

EXTERNAL USE

· Turmeric powder of standardized powdered extract applied as a paste or poultice — half cup of turmeric combined with 1 teaspoon of carbonate of soda and then mixed with hot water to make a paste; spread on gauze and apply to affected area.

ADVERSE REACTIONS:

The safety of curcumin is demonstrated by the fact that it has been consumed for centuries at levels of up to 10 mg/day by people in certain countries (Ammon & Wahl 1991). Curcumin was not toxic to humans in doses up to 8000 mg/day when taken by mouth for 3 months (Cheng et al 2001). Multiple other human trials have also found it to be safe with no alteration of liver or renal function tests (Chainani-Wu 2003, Prucksunand et al 2001, Ramirez-Bosca et al 1995, Ramirez et al 1997, Sharma et al 2001).

Large doses of turmeric powder may cause gastrointestinal irritation in some persons (Bhavani at al 1980) and very high dosages have been shown to reduce fertility in male rats (human equivalent doses would be 35 g turmeric/70 kg adult) (Meenakshi & Ashok 2001). Normal therapeutic dosages of turmeric are not expected to affect fertility. Contact dermatitis has been reported (Hata et al 1997), as has a single case of anaphylaxis (Robinson 2003).

SIGNIFICANT INTERACTIONS:

Controlled studies are not available so interactions are based on evidence of activity and are largely theoretical and speculative.

ANTIPLATELET DRUGS

Turmeric has a theoretical interaction with antiplatelet drugs; antiplatelet properties have been demonstrated for curcumin, therefore it may produce an additive effect. The clinical significance of this interaction is unclear and likely to be dose-dependent.

ANTICOAGULANTS

Theoretically, high-dose turmeric preparations may increase the risk of bleeding when used together with anticoagulant drugs— caution is advised.

CYCLOPHOSPHAMIDE

Animal studies suggest curcumin may reduce drug efficacy— avoid.

CONTRAINDICATIONS AND PRECAUTIONS:

Turmeric is contraindicated in bile duct obstruction (Blumenthal et al 2000) and high doses are probably best avoided in males and females wanting to conceive.

Curcumin is also contraindicated in breast cancer patients treated with cyclophosphamide until the significance of an in vivo model of breast cancer, which found that curcumin reduced the tumour regression effects of chemotherapy, is clarified (Somasundaram et al 2002).

Due to antiplatelet activity and possible increased risk of bleeding, use of concentrated extracts should be suspended 1 week prior to major surgery; however, usual dietary intakes are likely to be safe.

PREGNANCY USE:

When used as a spice this herb is most likely to be safe; however, the safety of therapeutic doses has not been established. Turmeric has been demonstrated not to be mutagenic in vitro (Nagabhushan 1986) or to be teratrogenic in mice (Garg 1974, Vijayalaxmi 1980).

Constituents and/or metabolites of turmeric and curcumin were transferred to suckling pups, but no ill effect on the offspring was reported.

PRACTICE POINTS/PATIENT COUNSELLING:

· In Ayurvedic medicine, turmeric is used to strengthen the overall energy of the body, relieve gas, dispel worms, improve digestion, regulate menstruation, dissolve gallstones, relieve arthritis and purify the blood (Blumenthal et al 2000).

· In TCM, turmeric is used for bruises, sores, ringworm, chest pain, toothache and jaundice. Turmeric was also recommended for abdominal pain, mass formation in the abdomen and amenorrhoea (Blumenthal et al 2000).

· Turmeric is commonly used in foods and is likely to be a safe and healthy addition to the diet.

· Turmeric has been shown to have antioxidant, anti-inflammatory and antiatherosclerotic activity; however, further clinical evidence is needed before it can be recommended to treat specific conditions.

· Clinical evidence suggests that turmeric may provide benefit for people with dyspepsia, peptic ulcer, hyperlipidaemia, and arthritis and there is emerging evidence to suggest that turmeric may help prevent a number of cancers as well as being useful as an adjuvant in cancer treatment.

ANSWERS TO PATIENTS’ FREQUENTLY ASKED QUESTIONS:

What will this herb do for me?

In countries where people use turmeric extensively in cooking (generally in curries), the intake seems to be associated with a lower level of certain chronic conditions, possibly including cancer, gastrointestinal diseases and arthritis. There have been some encouraging studies supporting this.

When will it start to work?

In some studies the effect began to be noticed after 2 weeks. However, as most of the conditions where turmeric may be beneficial are chronic in nature, treatment with turmeric should be considered long term.

Are there any safety issues?

Turmeric is considered very safe at normal dietary or therapeutic dosages with turmeric extracts. High doses are generally not recommended during pregnancy or for those wanting to conceive.

SOURCES

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