Curcuma longa L.

Last updated: 2016 Oct 24

Scientific Name

Curcuma longa L.

Synonyms

Amomum curcuma Jacq., Curcuma brog Valeton, Curcuma domestica Valeton, Curcuma euchroma Valeton, Curcuma ochrorhiza Valeton, Curcuma soloensis Valeton, Curcuma tinctoria Guibourt, Kua domestica Medik. [Illegitimate], Stissera curcuma Giseke. [1]

Vernacular Name

Malaysia Kunyit, temu kunyit (Malay); tius (Semang) [2]
English Turmeric, indian saffron [2] [3]
China Jiang huang huang jiang (Cantonese Wòhng gèung, Wong keong); yu jin (yu chin), yu chiu [3]
India Halud (Bengali); haldi (Hindi); arishina (Kannada); haldar, halja (Punjabi); ameshta, bahula, bhadra (Sanskrit); manjal (Tamil) [3]
Indonesia Kunyit (Indonesian); kunir (Javanese); koneng (Sundanese)[2]
Thailand Khamin (General); khamin-kaeng (Northern); khamin-chan (Central) [2]
Laos Khminz khünz [2]
Philippines Dilaw (Tagalog); duwaw (Cebuano); kalawag (Ilocano) [2]
Cambodia Rômiêt, lômiêt [2]
Vietnam Ngh[eej], u[aas]t kim [2]
France Curcuma [2].

Geographical Distributions

Curcuma longa is presumed to originate from South or South-East Asia, most probably from India. It is not known in a true wild state although in some places it appears to have become naturalised (e.g. in teak forests of East Java). C. longa has been grown in India since time immemorial. It reached China before the 7th century, East Africa in the 8th century and West Africa in the 13th century. It was introduced into Jamaica in the 18th century. Currently turmeric is widely cultivated throughout the tropics but cultivation on a considerable scale is largely confined to India and South-East Asia. [2]

Botanical Description

C. longa is classified as a member of the Zingiberaceae family. It is a robust, perennial, erect, strongly tillering herb (often cultivated as an annual), up to 1(-1.5) m tall. [2]

The rhizome is a fleshy complex with an ellipsoidal primary tuber (about 5 cm x 2.5 cm), ringed with the bases of old scale leaves and when mature bearing numerous cylindrical, lateral rhizomes (called fingers), 5-10 cm x 1-1.5 cm, the whole forming a dense clump. The rhizomes’ colour is deep orange inside and yellowish orange outside. , Its young tips are white, and it smells spicy when bruised. [2]

The leaves alternate, distichous, with sheaths forming a short pseudostem. The petiole 0.5 – 10 cm long, broadly furrowed and narrowly winged. Its blades are oblong-lanceolate to ovate-lanceolate, 7-70 cm x 3-20 cm, base cuneate to rounded, apex acute or acuminate, above dark green, below very pale green, densely studded with pellucid dots. [2]

The inflorescence is a terminal spike up to 20 cm long, erect, appearing between the leaf sheaths. The peduncle is 3-20 cm long, densely hairy, and covered by bladeless sheaths or scales. The bracts are elliptical-lanceolate, 5-7.5 cm x 2.5 cm, densely hairy, pale green to white colour. [2]

The flowers are in pairs in axils of bracts, bisexual, zygomorphic, 5-6 cm long, opening one at a time. The calyx is tubular, short, with 3 unequal teeth. The corolla is tubular at base, upper half much widened and with 3 unequal lobes, which are white in colour. The labellum (central staminode) is orbicular to obovate, 12-17 mm in diameter, with 2 small lateral lobes and a large emarginate central lobe, white with a yellow central streak, lateral staminodes 2, elliptical-oblong, 1 cm x 6 cm, creamy-white, functional stamen 1, for larger part connate with staminodes, 5-6 mm x 3 mm, anther with a broad, curved large spur at base. Ovary inferior, 3-celled, with 2 erect glands at top, style slender, passing between and held by the anther thecae, stigma expanded. [2]

The fruit is never produced. [2]

The roots are filiform, tough, sometimes very long, often swollen into an ellipsoidal tuber at the apex (2-4cm x 1-2 cm). [2]

27fig1

Figure 1: The C. longa plants are characterized by its yellowish green flowers.

Cultivation

Soil Suitability and Climatic Requirement

C. longa thrives well in tropical and subtropical areas. The total annual rainfall of 1,000-2,000 mm or more is required for optimum growth. The plant can grow on many soil types. Sandy loam with high organic matter content is preferred. [4]

Field preparation

Land Preparation

Like other crops, C. longa needs well-prepared planting bed. This includes ploughing using disc plough and disc harrow. Pre-germination herbicide is applied prior to planting to avoid weeds smothering the area. [4]

Production of Planting Materials

C. longa is propagated using mature rhizomes. The rhizome is cut into 4-5 cm segments with 2-3 buds per segment. The rhizomes can be planted directly or after buds start to sprout. The planting material of 600-1,500 kg/ha is needed for single crop planting and 400-500 kg/ha for mixed crop planting. To reduce the incidence of fusarium disease, the planting material should be soaked in a fungicide (benomyl) solution containing 0.25% active ingredient, or 1% Bordeaux mixture for 5-10 minutes, and dried before field planting. [4]

27fig2

Figure 2: Germinated rhizomes ready for field planting.

Field Planting

On bris sandy soil, C. longa is usually planted at a planting distance of 40-60 cm on 120 cm or wider beds, with a bed height of 25-30 cm. The length of beds depends on the size of the planting area. The recommended planting distance for an area without beds is 40 cm within a row and 60 cm between rows. The rhizome is planted 5-7 cm deep in the soil. Rhizome formation starts in the 5th month and continue forming actively until it is ready for harvest at 7-9 months after field planting. Hilling at the base of the plant is recommended at 8-10 weeks after planting to encourage rhizome formation and to make sure it does not grow above the ground. [4]

27fig3

Figure 3: C. longa plant on bris soil.

Field maintenance

Fertilisation

C. longa or ‘Kunyit’ requires organic fertiliser such as cow manure or chicken manure. For bris soil, chicken manure at 10 t/ha is recommended and for mineral/inland soil, 5 t/ha is recommended. Apart from organic fertiliser, semi-organic fertiliser like Kokei (NPK=8:6:16) at the rate of 750 kg/ha is used to obtain a good growth. [4]

Weed Control

Prior to planting, pre-germination herbicide with active ingredient, alachlor, at the rate of 5.6 litres/ha should be sprayed. Weed control after germination and during growth can be done manually or by spraying cautiously. [4]

Water Management

To avoid water stress, field planting should be done at the onset of the rainy seasons. A supplementary irrigation by using sprinkler irrigation system is needed during the dry seasons. [4]

Pest and Disease Control

The main disease for the crop is leaf spot caused by the fungus Taphrina maculans. The leaf spot is 1-2 mm in diametre and causes the leaves to dry. The infection can become more serious when humidity is high. Bacterial wilt is also of significance. To avoid pest and disease, continuous planting of the crop on the same piece of land is not recommended. [4]

Harvesting

C. longa reaches maturity 7-9 months after planting. Maturity depends on the soil fertility, but maturity can be determined when the leaves dry up. The crop is harvested manually using a hoe. The rhizome is cut from the stem. The fresh weight of the harvest is 13–25 t/ha. [4]

 

27fig4

Figure 4: The matured plants that are ready for harvesting.

 

27fig5

 

Figure 5: Fully matured rhizome of C. longa is deep orange in colour.

Postharvest Handling

To market as fresh produce, the rhizomes have to be cleaned before packaging. For processing into powder, the rhizomes have to be boiled or steamed until soft. The rhizomes are then sun-dried for 10-15 days or artificially dried at 60ºC before finely ground. About 20–30% of dried C. longa is produced from the fresh rhizomes. [4]

Estimated Cost of Production

The estimated production cost per hectare of C. longa on bris soil is RM12,300. Based on fresh yield at 13,000-25,000 kg/ha, the production cost estimated to be RM0.49-RM0.95/kg. The production cost was estimated based on the cost of current inputs during writing of this article. [4]

Chemical Constituent

C. longa has been reported to contain curcuminoids (e.g. curcumin (diferuloylmethane), demethoxycurcumin, and bisdemethoxycurcumin), various volatile oils(e.g. turmerone, atlantone, and zingiberene) and. other constituents (e.g. sugars, proteins and resins) [5][6]. The curcuminoids give turmeric its bright yellow colour [5]. Turmeric contains 0.3-5.4 percent of curcumin content, which has been shown to be a primary active constituent for medicinal purposes [6].

Plant Part Used

Leaves, roots/rhizomes. [2]

Traditional Use

C. longa is cultivated for its rhizome, primarily as a dye source, as well as a culinary spice. The rhizome is usually boiled, cleaned, and dried, yielding a yellow powder. Rhizomes are also used in Africa and Asia as a cosmetic for body and face. In Asia, turmeric is widely used as an important constituent of curry powder (contains up to 25% turmeric). In Western countries, ground turmeric rhizome is widely used in the food industry, in particular as a colouring agent (E 100 in the European Union) in processed food and sauces. It is also applied as a colouring agent in pharmaceuticals, confectionery and textile dyes, and is a cheaper substitute for the true saffron (Crocus saticus L.). [2]

The young shoots and young rhizomes can be eaten fresh as a spicy vegetable. [2]

The leaves are used in preparing special medicinal bread in Nepal and India. [2]

The C. longa rhizomes are part of numerous traditional compound medicines used as stomachic, stimulant and blood purifier, and to treat liver complaints, biliousness and jaundice. Mixed with warm milk they are used to cure common cold, bronchitis and asthma. Juice from fresh rhizomes is applied against many skin infections, while a decoction is effective against eye infections. [2]

C. longa can also be applied topically in poultices to relieve pain and inflammation. [6] Turmeric also has insecticidal, fungicidal and nematicidal properties. In Madagascar ground rhizomes are mixed with grains to protect them from storage pests. [2]

Preclinical Data

Pharmacology

Pharmacokinetic study

Pharmacokinetic studies in animals have demonstrated that 40-85 percent of an oral dose of curcumin passes through the gastrointestinal tract unchanged, with most of the absorbed flavonoid being metabolized in the intestinal mucosa and liver. Due to its low rate of absorption, curcumin is often formulated with bromelain for increased absorption and enhanced anti-inflammatory effect. [7][8]

Antioxidant activity

Water- and fat-soluble extracts of turmeric and its curcumin component exhibit strong antioxidant activity, comparable to vitamins C and E [9]. Curcumin was shown to be eight times more potent than vitamin E in lipid peroxidation, and three times more powerful than vitamin C in neutralizing free radicals [10][11].

A study of ischemia in the feline heart demonstrated that curcumin pretreatment decreased ischemia-induced changes in the heart. [12]

An in vitro study measuring the effect of curcumin on endothelial heme oxygenase-1, an inducible stress protein, was conducted utilizing bovine aortic endothelial cells. Incubation (18 hours) with curcumin resulted in enhanced cellular resistance to oxidative damage. The antioxidant activity of curcumin could be mediated through antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. Curcumin has been shown to serve as a Michael acceptor, reacting with glutathione and thioredoxin. [13]

Anti-inflammatory activity

Curcumin works to inhibit the inflammatory activity and synthesis of the enzymes implicated in inflammation, such as cyclooxygenase-2 (COX-2) [14][15][16][17] and lipoxygenase [18][19][20].

It is also involved in inhibition of incorporation of arachadonic acid into membrane lipids, inhibition of prostaglandin E2, leukotriene B4, leukotriene C4, inhibition of secretion of collagenase, elastase, hyaluronidase by macrophages. [21]

It reduces inflammation by lowering histamine levels and possibly by increasing the production of natural cortisone by the adrenal glands. [18]

Oral administration of curcumin in instances of acute inflammation was found to be as effective as cortisone or phenylbutazone, and half as effective in cases of chronic inflammation. [22]

In monkeys, curcumin inhibited neutrophil aggregation associated with inflammation. [23]

A trial was performed on 18 patients with rheumatoid arthritis where all the patients received 1200 mg/d of curcumin for 2 weeks and 300 mg/d of phenylbutazone for another 2 weeks. But the sequence of administration of the two medications was randomly allocated. Compared to baseline, statistically there were significant improvement in morning stiffness, walking time, and joint swelling at the end of both treatment regimens, however the magnitude of the improvement was higher after the phenylbutazone regimen. [24]

Another trial was conducted on 45 postsurgical patients (hernia or hydrocele) where all the patients were randomly assigned to receive curcumin (1200 mg/d), phenylbutazone (300 mg/d), or placebo for 5 days. Four clinical parameters of inflammation and pain were evaluated: spermatic cord edema, spermatic cord tenderness, pain at operative site, and tenderness at operative site. These were evaluated using a semi-quantitative scale of 0, absent; 1, mild; 2, moderate; and 3, severe. Addition of these gave a total intensity scale ranging from 0 to 12. Mean reduction in total intensity score at day 6 for curcumin was 2.38 (standard error [SE] 0.59, p , 0.01), for phenylbutazone was 1.57 (SE: 0.55, p , 0.05), and for placebo was 1.0 (SE: 0.79, not significant [NS]). Curcumin was demonstrated to be efficacious in reducing these parameters of postoperative inflammation. [25]

Anticarcinogenic activity

Animal studies involving rats and mice as well as in vitro studies utilizing human cell lines have demonstrated curcumin’s ability to inhibit carcinogenesis at three stages: Tumour promotion [26], angiogenesis [27] and tumour growth [28]. In two studies of colon and prostate cancer, curcumin inhibited cell proliferation and tumour growth.

Turmeric and curcumin compounds have been found to induce apoptosis in lung and colon tumour cell lines [29][30]. Curcumin inhibited AK-5 tumor growth and induced apoptosis in AK-5 cells [31].

Curcumin’s ability to protect against damage to DNA was demonstrated in a study in a community with a high content of groundwater arsenic [32]. Arsenic is extremely carcinogenic because it causes severe oxidative damage to DNA. Blood samples before curcumin supplementation showed severe DNA damage, with increased levels of free radicals and lipid peroxidation. Three months of curcumin intervention reduced the DNA damage, retarded free radical formation and lipid peroxidation, and raised the level of antioxidant activity. In another study, cigarette smokers receiving turmeric demonstrated a significant reduction in the level of urinary-excreted mutagens – an indication of the ability of the body to rid cancer-causing compounds via detoxification mechanisms. For many reasons, curcumin is emerging as a very important agent in the battle against cancer [33].

Hepatoprotective activity

Turmeric's hepatoprotective effect is mainly a result of its antioxidant properties as well as its ability to decrease the formation of proinflammatory cytokines. It protects the liver from a number of toxic compounds such as carbon tetrachloride (CCl4) [34][35], galactosamine [36], acetaminophen (paracetamol) [37], and Aspergillus aflatoxin [38]. Sodium curcuminate, a salt of curcumin, also exerts choleretic effects by increasing biliary excretion of bile salts, cholesterol, and bilirubin as well as by increasing bile solubility, therefore, possibly preventing and treating cholelithiasis. Curcumin has choleretic activity that increases bile output and solubility, which may be helpful in treating gallstones [39].

Antimicrobial activity

Antibacterial activity

Both curcumin and the oil fraction suppress growth of several bacteria like Streptococcus, Staphylococcus, Lactobacillus, etc. [40]. The aqueous extract of turmeric rhizomes has antibacterial effects [41]. Curcumin also prevents growth of Helicobacter pylori CagA+ strains in vitro [42].

Antiviral activity

Curcumin acts as an efficient inhibitor of Epstein-Barr virus (EBV) key activator Bam H fragment z left frame 1 (BZLF1) protein transcription in Raji DR-LUC cells. EBV inducers such as 12-0-tetradecanoylphorbol- 13-acetate, sodium butyrate and transforming growth factor-beta increase the level of BZLF1 m-RNA at 12–48 h after treatment in these cells, which is effectively blocked by curcumin. [43]

Curcumin also shows anti-HIV (human immunodeficiency virus) activity by inhibiting the HIV-1 integrase needed for viral replication [44][45]. It also inhibits UV light induced HIV gene expression [46].

Antiprotozoan activity

The ethanol extract of the rhizomes has anti-Entamoeba histolytica activity. Curcumin has anti-Leishmania activity in vitro. [47] Several synthetic derivatives of curcumin have anti-L. amazonensis effect [48]. Anti-Plasmodium falciparum and anti-L. major effects of curcumin have also been reported [49].

Antifungal activity

Ether and chloroform extracts and oil of C. longa have antifungal effects [50][51][52]. Crude ethanol extract also possesses antifungal activity [53]. Turmeric oil is also active against Aspergillus flavus, A. parasiticus, Fusarium moniliforme and Penicillium digitatum [54].

Cardiovascular effects and its effects on lipid metabolism

Curcumin decreases the severity of pathological changes and thus protects from damage caused by myocardial infarction [55]. Curcumin improves Ca2+-transport and its slippage from the cardiac muscle sarcoplasmic reticulum, thereby raising the possibility of pharmacological interventions to correct the defective Ca2+ homeostasis in the cardiac muscle [56]. Curcumin has significant hypocholesteremic effect in hypercholesteremic rats [57]. It protective effects on the cardiovascular system include lowering cholesterol and triglyceride levels, decreasing susceptibility of low density lipoprotein (LDL) to lipid peroxidation [58], and inhibiting platelet aggregation [59]. These effects have been noted even with low doses [58]. Turmeric extract’s effect on cholesterol levels may be due to decreased cholesterol uptake in the intestines and increased conversion of cholesterol to bile acids in the liver [60].

Gastrointestinal effects

It increases mucin secretion in rabbits and may thus act as gastro protectant against irritants [61]. Both antiulcer [62] and ulcerogenic [63][64] effects of curcumin have been reported but detailed studies are still lacking. It also protects from 5-hydroxytryptamine- induced ulceration at 20 mg/kg dose [65][66]. In fact, at higher doses of 50 mg/ kg and 100 mg/kg, it produces ulcers in rats [64]. It also enhances intestinal lipase, sucrase and maltase activity [67].

Anticoagulant effect

Inhibition of platelet aggregation by curcumin constituents is thought to be via potentiation of prostacyclin synthesis and inhibition of thromboxane synthesis. [59]

Curcumin shows anticoagulant activity by inhibiting collagen and adrenaline-induced platelet aggregation in vitro as well as in vivo in rat thoracic aorta. [68]

Toxicity

No documentation.

Clinical Data

Clinical findings

Uveitis

A 12 week pilot study conducted in India enrolled 53 patients with chronic anterior uveitis. The subjects received orally administered curcumin derived from Curcuma longa. 32 patients completed the trial. Patients with a strong PPD reaction received anti-tubercular treatment in addition to the curcumin. Both groups demonstrated improvement beginning after 2 weeks of treatment; 86% of the group also receiving anti-tubercular treatment improved and 100% of the curcumin alone group improved. Follow-up for 3 years indicated a recurrence of 55% in the curcumin alone group and 36% in the curcumin and anti-tubercular medication group. These results are comparable to corticosteroid therapy, the standard treatment for this disease. [69]

In 2010, curcumin was studied in a clinical trial of 122 patients with recurrent anterior uveitis. This nonrandomized study utilized a daily dose of 1200 mg of a curcumin phosphatidylcholine complex in addition to prior conventional steroid and anti-infective therapy for one year. Symptomatic improvement and the frequency of relapse were studied. The study found that after a few weeks of treatment, symptoms of eye pain, blurring of vision, and pericorneal hyperemia significantly improved in more than 80% of subjects. Additionally, after one year of treatment with the curcumin phosphatidylcholine complex, the frequency of relapse decreased significantly (p<0.001). [70]

There were 275 relapses 1 year before the treatment and only 36 relapses at the end of the year follow-up period after treatment with the curcumin complex. Overall, of the 128 subjects, 7 worsened and 15 dropped out due to noncompliance and the remainder (88%) demonstrated subjective and objective improvements at one year. [70]

Pancreatic Cancer

A phase I/II clinical trial enrolled 21 gemcitabine (Gemzar) resistant patients with advanced pancreatic cancer. All patients received 8 g curcumin daily in combination with gemcitabine. The agent used contained curcuminoids with 73% curcumin, 22% demethoxycurcumin, 4% disdemethoxycurcumin. Plasma curcumin levels ranged from 29 – 412 ng/mL. No dose-limiting toxicities were observed and the toxicity profile was comparable with that of gemcitabine, therefore the combination was determined not to increase toxicity. In contrast, several subjects reported an improvement of cancer or chemotherapy-related symptoms after starting curcumin. The median survival after initiation of curcumin was 161 days (95% CI 109-223). The one-year survival rate was 19% (95% CI 4.4% – 41.4%). However, median survival after failure of first-line gemcitabine is 70 days, which makes the results of this study significant [71]. Of note, a prior clinical study failed to demonstrate clinical response in 17 patients with advanced pancreatic cancer with an 8000mg dose of curcumin concurrent with gemcitabine [72]. More clinical study is needed for this indication.

Colorectal Cancer

A placebo-controlled clinical trial randomized 126 patients with colorectal cancer to either receive curcumin or placebo. [73]

All patients also received surgery followed by radiotherapy, chemotherapy, chemoradiotherapy, or no additional therapy. The curcumin group received 360mg curcumin three times daily pre-surgery (10 – 30 days). Blood (pre- and post) and tissue samples were analyzed. The body weight of Curcumin patients increased (approx. 4%) vs. weight loss of 6% in placebo group (p<0.05). This was thought to be due to a significant 60% reduction of TNF-α in the curcumin group (p<0.5), as TNF-α causes cancer cachexia. Furthermore, in the resected colon tissue, curcumin increased the prevalence of apoptosis (associated with increased Bax and inhibited Bcl-2) and p53 expression (major tumor suppressor gene) over tissue from placebo group. [73]

Another phase IIa clinical trial assessed the impact of two different doses of curcumin on the prevention of colorectal neoplasia. [74]

The effects of oral curcumin (2g or 4 g per day for 30 days) on the number of aberrant crypt foci was assessed in a nonrandomized, open-label clinical trial in 44 eligible smokers with eight or more aberrant crypt foci on screening colonoscopy. Forty-one subjects completed the study. There was a 40% reduction in aberrant crypt foci number in the 4g group (p<0.005), whereas no significant reduction was observed in the 2 g dose group. The reduction in crypts corresponded to increased plasma curcumin/conjugate levels. [74]

Multiple Myeloma

Monoclonal Gammopathy of Undetermined Significance (MGUS) and Smoldering Multiple Myeloma (SMM) are asymptomatic plasma cell disorders which can progress to multiple myeloma (MM) over a long period (up to 20 years). Abnormal serum free light chain ratio increases risk of progression. An abnormal ratio is indicative of an excess of one light chain over the other, indicating clonal (neoplastic) expansion. Curcumin has been shown in-vitro to inhibit proliferation of MM cells by down-regulating IL-6 and NFkB, inhibiting osteoclastogenesis and reducing bone turnover by suppressing RANKL signaling. A randomized, double-blinded placebo-controlled cross-over trial with curcumin enrolled 19 patients with MGUS and 17 patients with SMM. [75]  

Nineteen patients completed 4 g curcumin daily cross-over study and 18 patients completed 8g curcumin daily cross-over study. Both 4 and 8 g daily doses reduced the serum-free light chain ratio (35% and 36% respectively) and reduced total serum protein (P=0.04) in the urine in both MGUS and SMM patients. Patients with abnormal serum free light chain ratios at study onset had the greatest response. Curcumin also decreased markers of bone turnover (urinary DPYD) and excretion of crosslinked N-telopeptides by more than 25%. [75]

Cardiovascular disease

Age-related cardiovascular decline in postmenopausal women is characterized,by increased left ventricular afterload, an indication of vascular dysfunction and hypertension. An 8 week pilot study randomized 45 postmenopausal women to one of four interventions: placebo, 150mg curcumin, exercise training plus placebo or exercise training plus curcumin. [76]  

Only in the exercise and curcumin group did the aortic brachial systolic pressure, a measure of left ventricular afterload, decrease significantly (p<0.05). This study suggests that adding curcumin to regular exercise provides enhanced cardiovascular fitness in postmenopausal women. [76]

Arthritis

The long-term efficacy and safety of curcuminoid and phosphatidylcholine extract was investigated in an 8 month long pilot study involving 100 osteoarthritis patients. [77]  

Patients served as controls (standard conventional treatment only) or received additional treatment of 1000mg curcuma extract providing 200mg curcumin daily. The composition of the test material was a natural curcuminoid mixture (20%), phosphatidyl- choline (40%), and microcrystalline cellulose (40%). The clinical end points included the scores on various validated assessment tools, as well as selected inflammatory biomarkers. Five patients in the treatment group and six patients in the control group left the study for non-medical reasons. At the conclusion of the study, all subjective and objective parameters were improved in the treatment group over the control group (p<0.05). The curcumin group had improved scores for joint pain and stiffness, physical function, and social and emotional function. [77]

Diabetes

A randomized, parallel-group, placebo-controlled 8-week study randomized 72 patients with type 2 diabetes to receive either 300mg curcumin twice daily, atorvastatin 10mg daily or placebo. [78]

Endothelial function was assessed at baseline and post-treatment. Additionally, blood levels of biomarkers IL-6, TNF-alpha, malondialdehyde and endothelin-1 were measured pre- and post-treatment. 67 patients completed the study. Compared with baseline, there was significant and comparable improvement in endothelial function in both the atorvastatin and the curcumin groups. Additionally all biomarkers decreased in both treatment groups, whereas no improvements were seen in the placebo group. [78]

Digestive disorders

A pilot demonstrated improved symptoms and reduced medications from oral curcumin in patients with ulcerative colitis and Chrohn’s disease. [79]

An open, phase II trial was performed on 25 patients with endoscopically-diagnosed gastric ulcer. Participants were given 600mg powdered turmeric five times daily. After 4 weeks, ulcers had completely healed in 48 percent of patients. The success rate increased over time, with 76 percent being ulcer free after 12 weeks of treatment. No significant adverse reactions or blood abnormalities were noted. [80]

A partially blinded, randomized, two-dose pilot study randomized 207 healthy subjects to receive one to two tablets of turmeric extract for 8 weeks. The prevalence of IBS decreased by 41% in the one-tablet group and 57% in the two-tablet group. Additional, abdominal pain and discomfort decreased by 22% and 25% in the two groups. [81]

A pilot study of 25 patients positive for H. pylori and functional dyspepsia assessed the efficacy of non-antibiotic therapy. Subjects received 20 mg of pantoprazole twice daily along with 600mg twice daily of N-acetylcysteine, 100 mg twice daily of lactoferrin and 30 mg twice daily of curcumin. These three agents were administered orally for 7 days. Assessments included: H.pylori status, assessed by (13)C-urea breath test, a scale of upper gastrointestinal symptoms, and blood levels of pepsinogens, gastrin, and anti-H. pylori IgG antibodies. Twelve percent (3/25) patients were cured of H. pylori infection. There was significant improvement in gastrointestinal symptoms (p<0.001) and in pepsinogen levels (p<0.001) in treated patients. IgG and gastrin levels did not change significantly. The study suggests that this regimen is effective in reducing dyspeptic symptoms associated with H. pylori without eradicating the H. pylori infection. [82]

Precautions

No side effects are observed when used in the recommended dosage.

In addition, curcumin should be used with caution in patients with gallstones, because it can stimulate gallbladder contractions. [83]

Pregnancy/Breast Feeding

No documentation.

Age limitation

No documentation.

Adverse reaction

Humans appear to be able to tolerate high doses of curcumin without significant side-effects. [84]

Two patients with AIDS reported gastric irritation, of whom one had a past history of peptic ulcers. [85]

Interaction & Depletion

Interaction with drug

In one human study, 300 mg of curcumin reduced the absorption of the beta-blocker talinolol by roughly 35%. [86]

In rabbits, pretreatment with curcumin resulted in increased plasma elimination half-life, thereby reducing the dosage of norfloxacin. [87]

In an experimental model, curcumin was shown to inhibit apoptosis produced by a number of chemotherapy agents, including camptothecin, mechlorethamine, and doxorubicin. [88]

Some theoretic concern has been raised that curcumin might increase the risk of bleeding of anticoagulant drugs due to its ability to decrease platelet aggregation. [89]

Interaction with other Herbs

No documentation.

Contraindications

No documentation.

Case Report

No documentation.

Dosage

Mode of Administration:

Whole, cut and powdered drug available as capsules, solution, coated tablets and compound preparations. [89]

Preparation:

To prepare a tea, scald 0.5 to 1 gm drug in boiling water, cover, draw for 5 minutes and then strain. [89]

The tincture strength is 1:10. [89]

Storage: Turmeric should be protected from light. [89]

Dosage Range

The average dose is 1.5 to 3 gm of drug. [89]

Most Common Dosage

The powder should be taken 2 to 3 times daily after meals. [89]

The tea (2 to 3 cups) should be taken between meals. [89]

The tincture dose is 10 to 15 drops 2 to 3 times daily. [89]

Standardisation

No documentation.

Poisonous

No documentation.

Line drawing

27

 

Figure 6: The line drawing of C. longa [2]

References

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  3. Porcher MH. Multilingual Multiscript Plant Name Database. Sorting Curcuma names. [homepage on the Internet]. Melbourne: The University of Melbourne; c1995-2020 [updated 2006 Jan 29; cited 2015 Mar 11]. Available from: http://www.plantnames.unimelb.edu.au/Sorting/Curcuma.html#longa
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