Latin name; Curcuma longa
Pharmacopoeial name: Curcumae longae rhizome
Other names: Curcuma, Indian saffron
About Turmeric Root
This vibrant yellow spice, derived from the rhizome of the plant, has a long history of use in traditional medicines of China and India. The rhizome of turmeric has been crushed into a powder and used in Asian cookery, medicine, cosmetics, and fabric dying for more than 2000 years. Early European explorers to the Asian continent introduced this important spice to the Western world in the 14th century. Use of curcumin as a folk remedy continues today. As part of the ancient Indian medical system, Ayurveda, a poultice of turmeric paste is used to treat common eye infections, and to dress wounds, treat bites, burns, acne and various skin diseases. This ancient remedy is also used to treat dental diseases, digestive disorders such as dyspepsia and acidity, indigestion, flatulence and ulcers. In food and manufacturing, curcumin is currently used in perfumes and as a natural yellow colouring agent, as well as an approved food additive to flavour various types of curries and mustards.
Curcumin was first discovered about two centuries ago by Harvard College laboratory scientists Vogel and Pelletier from the rhizomes of Curcuma longa (turmeric) (1,2). Curcumin is a highly pleiotropic molecule that was first shown to exhibit antibacterial activity in 1949 (3). Since then, this polyphenol has been shown to possess anti-inflammatory, hypoglycemic, antioxidant, wound-healing, and antimicrobial activities (4). Extensive preclinical studies over the past three decades have indicated curcumin’s therapeutic potential against a wide range of human diseases (5). In addition, curcumin has been shown to directly interact with numerous signaling molecules (6). Although the therapeutic use of Curcuma was recorded as early as 1748 (7), the first article referring to the use of curcumin in human disease was published in 1937 by Oppenheimer (8). In this study, the author examined the effects of “curcumen” or “curcunat” in human biliary diseases. Since this initial identification, interest in curcumin research in human participants has increased remarkably.
Although curcumin has shown efficacy against numerous human ailments, poor bioavailability due to poor absorption, rapid metabolism, and rapid systemic elimination have been shown to limit its therapeutic efficacy (9). As a result, numerous efforts have been made to improve curcumin’s bioavailability by altering these features. The use of adjuvants that can block the metabolic pathway of curcumin is the most common strategy for increasing the bioavailability of curcumin. Other promising approaches to increase the bioavailability of curcumin in humans include the use of nanoparticles (10), liposomes (11), phospholipid complexes (12), and structural analogues (9).
Uses of Turmeric Root
One open-label study evaluated the efficacy of curcumin in patients with ulcerative proctitis and in patients
with Crohn’s disease (13). Significant decrease in symptoms as well as in inflammatory indices (erythrocyte sedimentation rate and CRP) were observed in all patients with proctitis. Only four of the five patients with Crohn’s disease, however, completed the study. There was a mean reduction of 55 points in the Crohn’s disease activity index, and reductions in erythrocyte sedimentation rate and CRP were observed in these patients. Another study evaluated the efficacy of curcumin as maintenance therapy in patients with quiescent ulcerative colitis (14). The relapse rates were 4.65% in the curcumin-treated group and 20.51% in the placebo group.
Irritable Bowel Syndrome
A partially blinded, randomized, pilot study assessed the effects of two different doses of turmeric extract on IBS symptoms in healthy adults (15). The prevalence of IBS was reduced by 53% and 60% in the one-tablet and two-tablet groups, respectively, and was associated with a marked decrease in IBS symptoms.
The potential of curcumin against arthritis was first reported in 1980 in a short-term, double-blind, crossover study involving 18 young patients with rheumatoid arthritis (16) comparing curcumin’s efficacy with that of phenylbutazone. Curcumin was well tolerated, had no adverse effects, and exerted an anti-rheumatic activity identical to that of phenylbutazone as shown by improvement in joint swelling, morning stiffness, and walking time. In recent study, curcumin alone and in combination with diclofenac sodium was found to be safe and effective in 45 patients with rheumatoid arthritis (17). Another study in patients with osteoarthritis evaluated the efficacy of curcumin (18). After 3 months of treatment, the global WOMAC score was decreased by 58%; walking distance was increased from 76 m to 332 m, and CRP levels were significantly decreased. In comparison, only modest improvement in these measurements was observed in the control group. In a subsequent study, this group investigated the long-term efficacy and safety of curcumin in a longer (8-month) study involving patients with osteoarthritis. The WOMAC score was decreased by more than 50%, whereas treadmill walking performance was increased almost threefold compared with the control. The need for hospital admissions, consultations, and tests by the patients also decreased after treatment.(19).
A randomized controlled clinical trial compared the efficacy of turmeric and liquid antacid against benign gastric ulcers (20). Of the 60 patients who participated in the study, 30 received turmeric, and the other 30 received antacid . The treatment was continued for 6 to 12 weeks. Although both antacid and turmeric improved gastric ulcers in patients, the former was better in reducing the ulcers. A phase II clinical trial evaluated the safety and efficacy of curcumin in 45 patients with peptic ulcers (21). Results after 4 weeks of treatment showed that ulcers were absent in 12 patients; after 8 weeks of treatment, ulcers were absent in 18 patients; and after 12 weeks of treatment, ulcers were absent in 19 patients. The remaining patients had symptomatic relief after turmeric treatment.
One study evaluated the effects of curcumin in reducing the serum levels of cholesterol and lipid peroxides in healthy human volunteers (22). Curcumin was administered to the volunteers for 7 days and reduced serum lipid peroxides by 33% and total serum cholesterol levels by 11.63%, and increased HDL cholesterol by 29%.
Because of its anti-inflammatory property, curcumin represents a promising therapeutic option for type 2 diabetes mellitus. (T2DM). Curcumin’s ability to decrease blood sugar levels in human patients was first reported in 1972 (23).
Usharani et al. (24) evaluated the potential of a standardized preparation of curcuminoids against various oxidative stress and inflammatory markers in patients with T2DM. Curcumin treatment significantly improved endothelial function and reduced oxidative stress (MDA) and inflammatory markers (IL-6, TNFα, endothelin-1) in these patients. More recently, a randomized, double-blind, placebo controlled clinical trial assessed the efficacy of curcumin in delaying development of T2DM in a pre-diabetes population (25). Changes in β cell functions (homeostasis model assessment [HOMA]-β, C-peptide, and proinsulin/insulin), insulin resistance (HOMA-IR), and anti-inflammatory cytokine (adiponectin) levels were monitored. After 9 months of treatment, 16.4% of participants in the placebo group were diagnosed with T2DM, whereas none were diagnosed with T2DM in the curcumin-treated group. In addition, the participants of curcumin-treated group showed a better overall function of β cells, with higher HOMA-β and lower C-peptide levels. The curcumin-treated participants also exhibited a lower level of HOMA-IR and higher adiponectin.
Type 2 Diabetic Nephropathy
The study consisted of 40 patients with overt type 2 diabetic nephropathy who were randomly assigned to either the trial group or the control group. Each patient in the trial group received curcumin or placebo. Serum concentrations of TGF-β and IL-8 and urinary protein excretion and IL-8 were significantly decreased after turmeric supplementation in comparison with the pre-supplementation values. No adverse effects related to turmeric supplementation were observed during the trial. The authors of this study concluded that short-term turmeric supplementation can attenuate proteinuria, TGF-β, and IL-8 in patients with overt type 2 diabetic nephropathy and can be administered as a safe adjuvant therapy for these patients (26).
Keywords: IBD, IBS, arthritis, peptic ulcer, atherosclerosis, diabetes, type 2 diabetic nephropathy
1. Vogel A, Pelletier J. J Pharm. 1815;1:289–300.
2. Gupta SC, Patchva S, Koh W, Aggarwal BB. Clin Exp Pharmacol Physiol. 2012;39 (3):283–99.
3. Schraufstatter E, Bernt H. Nature. 1949;164(4167):456.
4. Aggarwal BB, Sung B. Trends Pharmacol Sci. 2009;30(2):85–94.
5. Aggarwal BB, Harikumar KB. Int J Biochem Cell Biol. 2009;41(1):40–59.
6. Gupta SC, Prasad S, Kim JH, Patchva S, Webb LJ, Priyadarsini IK, et al. Nat Prod Rep. 2011;28(12):1937–55.
7. Loeber CC. De curcuma officinarum. diss Inaug Halae. 1748.
8. Oppenheimer A. Lancet. 1937;229:619–21.
9. Anand P, Kunnumakkara AB, Newman RA, Aggarwal BB. Mol Pharm. 2007;4(6):807–18.
10. Sasaki H, Sunagawa Y, Takahashi K, Imaizumi A, Fukuda, H, Hashimoto T, et al. Biol Pharm Bull. 2011;34 (5):660–5.
11. Gota VS, Maru GB, Soni TG, Gandhi TR, Kochar N, Agarwal MG. J Agric Food Chem. 2010;58(4):2095–9.
12. Cuomo J, Appendino G, Dern AS, Schneider E, McKinnon TP, Brown MJ, et al. J Nat Prod. 2011;74(4):664–9.
13. Holt PR, Katz S, Kirshoff R. Dig Dis Sci. 2005;50(11):2191–3.
14. Hanai H, Iida T, Takeuchi K, Watanabe F, Maruyama Y, Andoh A, et al. Clin Gastroenterol Hepatol. 2006;4(12):1502–6..
15. Bundy R, Walker AF, Middleton RW, Booth J. J Altern Complement Med. 2004;10(6):1015–8.
16. Deodhar SD, Sethi R, Srimal RC. Indian J Med Res. 1980;71:632–4.
17. Chandran B, Goel A. Phytother Res. 2012;26(11):1719–25.
18. Belcaro G, Cesarone MR, Dugall M, Pellegrini L, Ledda A,
19. Grossi MG, et al. Panminerva Med. 2010;52(2 Suppl 1):55–62.
20. Kositchaiwat C, Kositchaiwat S, Havanondha J. J Med Assoc Thail. 1993;76 (11):601–5.
21. Prucksunand C, Indrasukhsri B, Leethochawalit M, Hungspreugs K. Southeast Asian J Trop Med Public Health. 2001;32(1):208–15.
22. Soni KB, Kuttan R. Indian J Physiol Pharmacol. 1992;36(4):273–5.
23. Srinivasan M. Indian J Med Sci. 1972;26(4):269–70.
24. Usharani P, Mateen AA, Naidu MU, Raju YS, Chandra N. Drugs R D. 2008;9(4):243–50.
25. Chuengsamarn S, Rattanamongkolgul S, Luechapudiporn R, Phisalaphong C, Jirawatnotai S. Diabetes Care. 2012;35(11):2121–7.
26. Khajehdehi P, Pakfetrat M, Javidnia K, Azad F, Malekmakan L, Nasab MH, et al. Scand J Urol Nephrol. 2011;45(5):365–70.