FWD 2 Expanded Commission E: Turmeric root

Herbal Medicine: Expanded Commission E

Turmeric root

Latin Name: Curcuma longa
Pharmacopeial Name: Curcumae longae rhizoma
Other Names: Curcuma, Indian saffron, Haridra (Sanskrit), Jianghuang (Chinese), Kyoo or Ukon (Japanese)


Turmeric is a perennial rhizomatous shrub native to southern Asia (Leung and Foster, 1996; Wichtl and Bisset, 1994), extensively cultivated in all parts of India (API, 1989), mainly in Madras, Bengal, and Bombay (Kapoor, 1990). It is also cultivated in southern mainland China, Taiwan, Japan, Burma, Indonesia (Yen, 1992), and throughout the African continent (Iwu, 1993). The material of commerce in Europe is obtained mainly from India, Indonesia, and somewhat from China (Wichtl, 1996). India produces most of the world supply (Leung and Foster, 1996). Turmeric is an herb of major importance in the East and, until recently, one of relatively minor importance in the West (Govindarajan, 1980). It is a member of the ginger family (Zingiberaceae); the Chinese name, jianghuang, literally means "yellow ginger."

Traditional use of turmeric has varied somewhat regionally, though its use as a digestive aid and choleretic is almost universal (Grieve, 1979). Its modern approved applications in European medicine stem from its traditional uses in Asia. Turmeric is used extensively in the Indian systems of medicine (Ayurveda, Unani, and Siddha) and is official in the Ayurvedic Pharmacopoeia of India (API, 1989; Nadkarni, 1976). In Western terms, it is used as a carminative and stomachic (Kapoor, 1990; Nadkarni, 1976) for the treatment of digestive disorders such as flatulence, bloating, and appetite loss (Schulz et al., 1998). Turmeric is prepared in a variety of internal (e.g., boiled powder, fresh juice, confection) and external (e.g., paste, oil, ointment, lotion) dosage forms, as it is also applied topically for ulcers, wounds, eczema, and inflammations (Nadkarni, 1976). In both the Ayurvedic and Siddha systems of medicine, a turmeric paste is used topically to treat ulcers and scabies (Charles and Charles, 1992). In Ayurvedic medicine, turmeric also has a long history of use for its anti-inflammatory and antiarthritic effects. According to James Duke, turmeric is a safer, more natural, and less expensive cyclooxygenase (COX) inhibitor than pharmaceutical COX-inhibitor drugs (Duke, 1999). Turmeric is also used extensively in traditional Chinese medicine. It is official in the Pharmacopoeia of the People's Republic of China (Tu, 1992) as well as in the Japanese Herbal Medicines Codex (JSHM, 1993). As in India, it is used in China, Japan, and Korea for a range of indications including abdominal fullness, kidney pain, and amenorrhea (But et al., 1997; Yen, 1992). In China, the aqueous decoction dosage form is ingested orally and applied topically (But et al., 1997).

Several clinical studies have been found in the literature. Turmeric has been investigated for its cholagogous influence on the secretion of bile, pancreatic, and gastric juices (Baumann et al., 1971; Baumann, 1975). In a multicenter, randomized, double-blind study, the efficacy of turmeric rhizome for treatment of dyspepsia was investigated. The trial was conducted in six Thai hospitals and included 116 adult patients diagnosed with acid dyspepsia, flatulent dyspepsia, and/or atonic dyspepsia. Each patient received two capsules of drug or placebo, four times daily for seven days. Eighty-seven percent of the patients receiving turmeric capsules responded favorably whereas 53% of the patients receiving placebo responded to treatment. The authors concluded that the differences in efficacy between drug and placebo were statistically significant and clinically important (Thamlikitkul et al., 1989). In a subsequent controlled clinical trial, researchers at Ratchaburi Hospital in Thailand compared the effects of turmeric against a liquid antacid drug in the treatment of gastric ulcer (Kositchaiwat et al., 1993). In a small study, the antimutagenic effects of turmeric were investigated in 16 chronic cigarette smokers in comparison with six non-smokers, who served as the control group. The smokers were given 1.5 g of turmeric per day for 30 days, which resulted in a significant reduction in the urinary excretion of mutagens. The authors concluded that regular dietary intake of turmeric provides effective antimutagen action and may be useful in chemoprevention (Polasa et al., 1992).

In a pilot study, conducted by the Medical and Cancer Research and Treatment Centre of Nagercoil, India, a turmeric paste was used for the treatment of scabies in 814 patients. The researchers concluded that turmeric paste is a very inexpensive, readily available, effective and acceptable mode of treatment for scabies without noticable toxicity or adverse reactions (Charles and Charles, 1992). In another study, researchers at the Swami Prakashananda Ayurveda Research Centre, in India, investigated an alcoholic extract of turmeric as well as turmeric oil and oleoresin fractions for their effects on cytogenetic damage in patients suffering from oral submucous fibrosis. All three forms of turmeric in this study were found to decrease the number of micronucleated cells in both exfoliated oral mucosal cells and in circulating lymphocytes (Hastak et al., 1997).

In Germany, turmeric is listed in the Drug Codex, approved in the Commission E monographs, and the tea form is official in the Standard License monographs (Braun et al., 1997; DAC, 1986; Wichtl and Bisset, 1994). A small amount of turmeric is used as a component in numerous multi-ingredient cholagogue and biliary remedies (Wichtl and Bisset, 1994). The German Drug Codex monograph requires turmeric to contain not less than 3.0% curcuminoids, calculated as curcumin, and not less than 3.0% volatile oil. Macroscopic and microscopic examinations and a thin-layer chromatography test are required for botanical authentication (DAC, 1986; Wichtl and Bisset, 1994). The German Standard License monograph requires that the material conform with the qualitative and quantitative requirements of the DAC (Braun et al., 1997).

Chinese pharmacopeial grade turmeric consists of the dried rhizome of Curcuma longa L., collected in the winter when the aerial part of the plant has withered. It is washed clean, boiled or steamed thoroughly, then cut into thick slices to dry in the sun, then separated from the fibrous root. It must contain not less than 7.0% (ml/g) volatile oil. Botanical identity must be confirmed by macroscopic and microscopic examinations, organoleptic evaluation, and a color reaction test using filter paper, ethanol, ether, solution of boric acid, and ammonia (Tu, 1992). Indian pharmacopeial grade turmeric consists of the dried and cured rhizomes of C. longa L., harvested after 9 to 10 months when the lower leaves turn yellow. The curing process includes boiling and drying steps. It must contain not less than 4.0% v/wvolatile oil, not less than 12% water-soluble extractive, and not less than 8% alcohol-soluble extractive. Botanical identity must be confirmed by macroscopic and microscopic examinations as well as by two different color reaction tests (API, 1989). Japanese pharmacopeial grade turmeric consists of the unpeeled or peeled (without the cork layer) rhizome of C. longa L., cured with boiling water, then sun dried. Botanical identity must be confirmed by macroscopic and organoleptic evaluations as well as by two different color reaction tests (JSHM, 1993).


Turmeric root consists of the finger-like, often tuber-like, scalded, and dried rhizomes of C. longa L. (syn. C. domestica Valeton and C. aromatica Salisbury) [Fam. Zingiberaceae] and their preparations in effective dosage. The preparation contains not less than 3% dicinnamoylmethane derivatives, calculated as curcumin, and not less than 3% volatile oil, both calculated on a dry-weight basis of the preparation.

Chemistry and Pharmacology

Turmeric contains 3–7.2% volatile oil, composed mainly of sesquiterpenes such as a- and b-turmerone, ar-turmerone, a-curcumen, and zingiberene, and minor amounts of monoterpenes such as cineol (Kapoor, 1990; Leung and Foster, 1996; Wichtl, 1996); 3–5% curcuminoids (dicinnomoyl derivatives), mainly curcumin (Budavari, 1996; Iwu, 1993; Wichtl, 1996), demethoxycurcumin, bisdemethoxycurcumin, and cyclocurcumin (But et al., 1997; Kiuchi et al., 1993); 3.5% minerals (e.g., potassium); carotene; vitamin C (Kapoor, 1990; Leung and Foster, 1996); a water-soluble peptide (e.g., 0.1% 5–kDa peptide–turmerin) (Srinivas et al., 1992); 45–55% gelatinized starch, composed of polysaccharides such as the immunologically active arabinogalactans (Bruneton, 1995; Wichtl, 1996), particularly the phagocytosis–activating polysaccharides ukonan A and C (Gonda et al., 1992; Gonda et al., 1993).

Note: Under proper storage conditions the volatile oil content still diminishes by approximately 0.5% per year. Therefore, product shelf life should be determined based on this known rate of volatilization, calculating the difference between the volatile oil content on the date of packaging against the minimum amount required in the drug codex or pharmacopeial monograph (Braun et al., 1997).

The Commission E reported that the choleretic action of curcumin is experimentally well documented. Further indications exist for a cholecystokinetic and a clear anti-inflammatory action.

Turmeric has anti-inflammatory and cytotoxic effects (But et al., 1997). Curcumin, isolated from turmeric, has demonstrated anti-thrombotic action while preserving prostacyclin, an inflammatory mediator (Srivastava et al., 1985; Srivastava et al., 1986). An ethereal extract of turmeric inhibited arachidonate–induced platelet aggregation in human blood platelets (Srivastava, 1989). Turmeric has also demonstrated antioxidant, antimutagen, and anticarcinogen effects in experimental animals (Polassa et al., 1992). The isolated constituent ar-turmerone has been shown to arrest the reproduction and killer activity of human lymphocytes, which may contribute to its anti-inflammatory activity (Wichtl and Bisset, 1994).Curcuminoids, isolated from turmeric, have displayed topoisomerase I and II enzyme inhibition activity (Roth et al., 1998). In vitro and in vivo experiments have found that turmeric has antihepatotoxic and antibacterial effects (Kiso et al., 1983).

While the chemistry of turmeric is well studied, its mechanism of action is not fully understood (Tyler, 1994). The rhizome contains an anti-inflammatory and choleretic volatile oil. Anti-inflammatory actions may be due to leukotriene inhibition (Ammon et al., 1992; Leung and Foster, 1996). Its curcuminoids (e.g., curcumin) and volatile oil are both partly responsible for the anti-inflammatory activity. Curcumin is, however, more effective by parenteral injection than by oral ingestion (Ammon and Wahl, 1991). The curcuminoids, despite poor absorption when taken orally, are generally thought to be responsible for the rhizome's bile-stimulating actions (Tyler, 1994). The isolated consituent curcumin has displayed anti-inflammatory and antitumor activity, and may be protective against some cancers, such as colon cancer. In laboratory tests, curcumin's antitumor actions appear to be due to interactions with arachidonate metabolism (Rao et al., 1995). Currently, turmeric is being investigated as an antioxidant. Both the rhizome, and isolated curcumin, have shown that they are able to protect DNA breakage caused by singlet oxygen. Singlet oxygen is known to have potential genotoxic and mutagenic actions. The protective, antioxidant effects of turmeric and curcumin were greater than those of vitamins E and A (Subramanian et al., 1994). An aqueous extractive of turmeric has been shown to be more effective than isolated curcumin in protecting human lymphocyte DNA from damage induced by smoke condensate (Srinivas and Shalini, 1991). A water-soluble peptide, turmerin, isolated from turmeric, has also demonstrated effective antioxidant, DNA-protectant and antimutagen actions. Turmerin contains three residues of methionine, which may be partly responsible for the antioxidant effects (Srinivas et al., 1992). More recently, an antioxidant protein has been isolated from the aqueous extract of turmeric (Selvam et al., 1995).


The Commission E approved turmeric root for dyspeptic conditions.

The German Standard License indicates the use of turmeric tea infusion as a stomach and intestine remedy for the treatment of digestive complaints, especially functional disturbances of the gall systems (Braun et al., 1997). In both Ayurvedic and Unani medicine it is used as a stomachic and tonic (Kapoor, 1990). The Pharmacopoeia of the People's Republic of China indicates its use for treatment of pricking pain in the chest and hypochondrium (abdominal pain), mass formation in the abdomen, and amenorrhea (to stimulate menstrual discharge and relieve pain), among other conditions (Tu, 1992).


Obstruction of bile passages. In case of gallstones, first consult a physician.

Note: The Botanical Safety Handbook states that use of turmeric root should be avoided by people with bile duct obstruction or gallstones; it should not be administered to people who suffer from stomach ulcers or hyperacidity (McGuffin et al., 1997).

Side Effects

None known.

Use During Pregnancy and Lactation

Not recommended during pregnancy (McGuffin et al., 1997). No restrictions known during lactation.

Interactions with Other Drugs

None known.

Dosage and Administration

Unless otherwise prescribed: 1.5–3 g per day of cut root as well as other equivalent galenical preparations for internal use.

Powder: 1–3 g (API, 1989); 1–4 g (Kapoor, 1990); 0.5–1 g, several times daily (Wichtl and Bisset, 1994).

Infusion: Steep approximately 1.3 g root in 150 ml boiled water for 10 to 15 minutes, twice daily (Braun et al., 1997).

Fluidextract 1:1 (g/ml): 1.5–3 ml.

Tincture 1:5 (g/ml): 10 ml (Stansbury, 1999).


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Ammon, H.P., M.I. Anazodo, H. Safayhi, B.N. Dhawan, R.C. Srimal. 1992. Curcumin: a potent inhibitor of leukotriene B4 formation in rat peritoneal polymorphonuclear neutrophils. Planta Med 58(2):226.

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Baumann, J.C., K. Heintze, H.W. Muth. 1971. Klinisch-experimentelle untersuchungen der gallen-, pankreas- und magensaftsekretion unter den phytocholagogen wirkstoffen einer Carduus marianusChelidoniumCurcuma suspension [Clinico-experimental studies on the secretion of bile, pancreatic and gastric juice under the influence of phytocholagogous agents of a suspension of Carduus marianus, Chelidonium and Curcuma]. Arzneimforsch 21(1):98101.

Baumann, J.C. 1975. ber die wirkung von Chelidonium, Curcuma, Absinth und Carduus marianus auf die galle-und pankreassekretion bei hepatopathien [Effect of Chelidonium, Curcuma, Absinth and Carduus marianus on the bile and pancreatic secretion in liver diseases]. Med Monatsschr 29(4):173180.

Braun, R. et al. 1997. Standardzulassungen f r FertigarzneimittelText and Kommentar. Stuttgart: Deutscher Apotheker Verlag.

Bruneton, J. 1995. Pharmacognosy, Phytochemistry, Medicinal Plants. Paris: Lavoisier Publishing.

Budavari, S. (ed.). 1996. The Merck Index: An Encyclopedia of Chemicals, Drugs, and Biologicals, 12th ed. Whitehouse Station, N.J.: Merck & Co., Inc. 450, 1674.

But, P.P.H. et al. (eds.). 1997. International Collation of Traditional and Folk Medicine. Singapore: World Scientific. 207208.

Charles, V. and S.X. Charles. 1992. The use and efficacy of Azadirachta indica ADR (Neem') and Curcuma longa (Turmeric') in scabies. A pilot study. Trop Geogr Med 44(12):178181.

Deutscher Arzneimittel-Codex (DAC). 1986. Stuttgart: Deutscher Apotheker Verlag.

Duke, J.A. 1999. Clippings from my COX box. Journal of Medicinal Food 1(4):293298.

Gonda, R., M. Tomoda, K. Takada, N. Ohara, N. Shimizu. 1992. The core structure of ukonan A, a phagocytosis-activating polysaccharide from the rhizome of Curcuma longa, and immunological activities of degradation products. Chem Pharm Bull (Tokyo) 40(4):990993.

Gonda, R., M. Tomoda, N. Ohara, K. Takada. 1993. Arabinogalactan core structure and immunological activities of ukonan C, an acidic polysaccharide from the rhizome of Curcuma longa. Biol Pharm Bull 16(3):235238.

Govindarajan, V.S. 1980. Turmericchemistry, technology, and quality. Crit Rev Food Sci Nutr 12(3):199301.

Grieve, M. 1979. A Modern Herbal. New York: Dover Publications, Inc.

Hastak, K. et al. 1997. Effect of turmeric oil and turmeric oleoresin on cytogenetic damage in patients suffering from oral submucous fibrosis. Cancer Lett 116(2):265269.

Iwu, M.M. 1993. Handbook of African Medicinal Plants. Boca Raton: CRC Press. 164166.

The Japanese Standards for Herbal Medicines (JSHM). 1993. Tokyo: Yakuji Nippo, Ltd. 279.

Kapoor, L.D. 1990. CRC Handbook of Ayurvedic Medicinal Plants. Boca Raton: CRC Press. 149150.

Kiso, Y., Y. Suzuki, N. Watanabe, Y. Oshima, H. Hikino. 1983. Antihepatotoxic principles of Curcuma longa rhizomes. Planta Med 49(3):185187.

Kiuchi, F. et al. 1993. Nematocidal activity of turmeric: synergistic action of curcuminoids. Chem Pharm Bull (Tokyo) 41(9):16401643.

Kositchaiwat, C., S. Kositchaiwat, J. Havanondha. 1993. Curcuma longa Linn. in the treatment of gastric ulcer comparison to liquid antacid: a controlled clinical trial. J Med Assoc Thai 76(11):601605.

Leung, A.Y. and S. Foster. 1996. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics, 2nd ed. New York: John Wiley & Sons, Inc. 499501.

McGuffin, M., C. Hobbs, R. Upton, A. Goldberg. 1997. American Herbal Product Association's Botanical Safety Handbook. Boca Raton: CRC Press. 39.

Nadkarni, K.M. 1976. Indian Materia Medica. Bombay: Popular Prakashan. 414418.

Polasa, K., T.C. Raghuram, T.P. Krishna, K. Krishnaswamy. 1992. Effect of turmeric on urinary mutagens in smokers. Mutagenesis 7(2):107109.

Rao, C.V., A. Rivenson, B. Simi, B.S. Reddy. 1995. Chemoprevention of colon carcinogenesis by dietary curcumin, a naturally occurring plant phenolic compound. Cancer Res 55(2):259266.

Roth, G.N., A. Chandra, M.G. Nair. 1998. Novel bioactivities of Curcuma longa constituents. J Nat Prod 61(4):542545.

Schulz, V., R. Hnsel, V.E. Tyler. 1998. Rational Phytotherapy: A Physicians' Guide to Herbal Medicine. New York: Springer.

Selvam, R., L. Subramanian, R. Gayathri, N. Angayarkanni. 1995. The anti-oxidant activity of turmeric (Curcuma longa). J Ethnopharmacol 47(2):5967.

Srinivas, L. and V.K. Shalini. 1991. DNA damage by smoke: protection by turmeric and other inhibitors of ROS. Free Radic Biol Med 11(3):277283.

Srinivas, L., V.K. Shalini, M. Shylaja. 1992. Turmerin: a water-soluble antioxidant peptide from turmeric (Curcuma longa). Arch Biochem Biophys 292(2):617623.

Srivastava, K.C. 1989. Extracts from two frequently consumed spicescumin (Cucinum cyminum) and turmeric (Curcuma longa)inhibit platelet aggregation and alter eicosanoid biosynthesis in human blood platelets. Prostaglandins Leukot Essent Fatty Acids 37(1):5764.

Srivastava, R., M. Dikshit, R.C. Srimal, B.N. Dhawan. 1985. Anti-thrombotic effect of curcumin. Thrombosis Res 40(3):413417.

Srivastava, R., V. Puri, R.C. Srimal, B.N. Dhawan. 1986. Effect of curcumin on platelet aggregation and vascular prostacyclin synthesis. Arzneimforsch 36(4):715717.

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Subramanian, M., M. Sreejayan, N. Rao, T.P. Devasagayam, B.B. Singh. 1994. Diminution of singlet oxygen-induced DNA damage by curcumin and related antioxidants. Mutat Res 311(2):249255.

Thamlikitkul, V. et al. 1989. Randomized double blind study of Curcuma domestica Val. for dyspepsia. J Med Assoc Thai 72(11):613620.

Tu, G. (ed.). 1992. Pharmacopoeia of the People's Republic of China (English Edition 1992). Beijing: Guangdong Science and Technology Press. 202203.

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Additional Resources

Ferreira, L.A. et al. 1992. Antivenom and biological effects of ar-turmerone isolated from Curcuma longa. Toxicon 30(10):12111218.

Jentzsch, K., T. Gonda, H. Hller. 1959. Papierchromatographische Unterscheidung von Curcuma domestica Val. und Curcuma xanthorrhiza Roxb. Pharm Acta Helv 34(4):181188.

Jiangsu Institute of Modern Medicine. 1977. Zhong Yao Da Ci Dian (Encyclopedia of Chinese Materia Medica), Vol. 3. Shanghai: Shanghai Scientific and Technical Publications.

Leung, A.Y. 1984. Chinese Herbal Remedies. New York: Universe Books. [Republished as: Chinese Healing Foods and Herbs. 1993. Glen Rock: AYSL Corp.]

Qureshi, S., A.H. Shah, A.M. Ageel. 1992. Toxicity studies on Alpinia galanga and Curcuma longa. Planta Med 58(2):124127.

Randhawa, G.S. and R.K. Mahey. 1988. Herbs, Spices, and Medicinal Plants: Recent Advances in Botany, Horticulture, and Pharmacology, Vol. 3. Phoenix: Oryx Press.

Srimal, R.C. and B.N. Dhawan. 1973. Pharmacology of diferuloyl methane (curcumin), a non-steroidal anti-inflammatory agent. J Pharm Pharmacol 25(6):447452.

This material was adapted from The Complete German Commission E MonographsTherapeutic Guide to Herbal Medicines. M. Blumenthal, W.R. Busse, A. Goldberg, J. Gruenwald, T. Hall, C.W. Riggins, R.S. Rister (eds.) S. Klein and R.S. Rister (trans.). 1998. Austin: American Botanical Council; Boston: Integrative Medicine Communications.

1) The Overview section is new information.

2) Description, Chemistry and Pharmacology, Uses, Contraindications, Side Effects, Interactions with Other Drugs, and Dosage sections have been drawn from the original work. Additional information has been added in some or all of these sections, as noted with references.

3) The dosage for equivalent preparations (tea infusion, fluidextract, and tincture) have been provided based on the following example:

  • Unless otherwise prescribed: 2 g per day of [powdered, crushed, cut or whole] [plant part]
  • Infusion: 2 g in 150 ml of water
  • Fluidextract 1:1 (g/ml): 2 ml
  • Tincture 1:5 (g/ml): 10 ml

4) The References and Additional Resources sections are new sections. Additional Resources are not cited in the monograph but are included for research purposes.

This monograph, published by the Commission E in 1994, was modified based on new scientific research. It contains more extensive pharmacological and therapeutic information taken directly from the Commission E.

Excerpt from Herbal Medicine: Expanded Commission E Monographs
Copyright 2000 American Botanical Council
Published by Integrative Medicine Communications
Available from the American Botanical Council.