Turmeric
Turmeric
Turmeric
897
Turmeric
HISTORICAL NOTE 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 marvelled 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 turmerics
antioxidant, hepatoprotective, anti-inflammatory, anticarcinogenic and antimicrobial properties, in addition to its
use in cardiovascular disease and gastrointestinal disorders (National Library of Medicine 2001).
COMMON NAME
Turmeric
effects may take place as a consequence of local gastrointestinal effects or be associated with metabolites of the curcuminoids.
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
Turmeric rhizome contains 5% phenolic curcuminoids (diarylheptanoids), which give turmeric the
yellow colour. The most significant curcuminoid is
curcumin (diferuloylmethane).
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
Antioxidant
Studies have shown that turmeric, as well as curcumin, has significant antioxidant activity (Ak &
Gulcin 2008, Bengmark 2006, Menon & Sudheer
2007, 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).
Turmerics antioxidant activity may mediate
damage produced by myocardial and cerebral ischaemia (Al-Omar et al 2006, Fiorillo et al 2008,
Shukla et al 2008) and diabetes (Farhangkhoee et al
2006, Jain et al 2006; Kowluru & Kanwar 2007).
Turmeric has been shown to restore myocardial antioxidant status, inhibit lipid peroxidation and protect
against ischaemiareperfusion-induced myocardial
injuries in two animal studies (Fiorillo et al 2008,
Mohanty et al 2004). The mechanism is likely due
to curcumins antioxidant and anti-inflammatory
effects. 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) and retinopathy (Kowluru & Kanwar 2007).
Turmeric has also been shown to suppress cataract
development and collagen cross-linking, promote
TURMERIC
Chemoprevention
899
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 & 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
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 enhanced
the antitumour effect of cisplatin against fibrosarcoma
(Navis et al 1999), fluorouracil and oxaliplatin in
colorectal cancer (Du et al 2006, Li et al 2007) and
gemcitabine and paclitaxel in bladder cancer (Kamat
et al 2007). Curcumin also attenuated multidrug resistance in a non-small cell lung cancer cell line (Andjelkovic et al 2008) and acted as a radiosensitiser for
cervical cancer in vitro (Javvadi et al 2008).
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 has been shown to inhibit platelet aggregation in vivo (Chen et al 2007, Srivastava et al
1985, 1986) and in vitro (Jantan et al 2008, Srivastava 1989, Srivastava et al 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
Wound healing is a highly ordered process, requiring complex and coordinated interactions involving peptide growth factors, of which transforming
growth factor-beta (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). Curcumins 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
TURMERIC
901
Turmeric extract shows promise in the symptomatic treatment of IBD, according to a partially
blinded, randomised study by Bundy et al (2004).
The study of 207 volunteers with diagnosed irritable bowel syndrome (IBS) complying with the
Rome II criteria were randomly assigned to receive
either 72 mg or 144 mg of turmeric a day or placebo for 8 weeks (Bundy et al 2004). The group
receiving the lower dose (72 mg/day) experienced
a significant 53% decrease in irritable bowel symptoms, whereas higher treatment (144 mg/day)
resulted in a 60% decrease when compared to placebo
(P < 0.001). Abdominal discomfort was also
reduced by 22% and 25% of patients in the 72 mg
and 144 mg groups, respectively (P < 0.001).
Approximately two-thirds of the participants in the
active groups reported overall symptom improvement and had better quality-of-life scores.
Inflammatory bowel disease
An open-label pilot study has produced preliminary data to suggest that curcumin may be effective
in inflammatory bowel disease (Holt et al 2005).
Five patients with Crohns disease received 360
mg of curcumin 3 times a day for 1 month, followed by 4 times a day for another 2 months. The
Crohns disease activity index (CDAI), C-reactive
protein (CRP) and erythrocyte sedimentation rate
(ESR) fell significantly in 4 out of 5 patients. Five
patients with ulcerative proctitis were also enrolled
and received 550 mg of curcumin twice a day for 1
month, then three times a day for another month.
Overall, stool quality was greatly improved and
frequency was significantly reduced. Two patients
were able to eliminate their concomitant medications altogether, whilst another two patients were
able to reduce them. The CRP and ESR also
returned to within normal limits by the cessation
of the study.
A randomised, double-blind, multicentre trial of
89 patients examined the efficacy of curcumin as
a maintenance therapy in ulcerative colitis (Hanai
et al 2006). Patients in the active group received
1 g of curcumin, twice a day with sulfasalazine or
mesalazine as compared to placebo plus sulfasalazine or mesalazine. At the end of the study period,
4.65% of patients in the curcumin group relapsed
during treatment as compared to 20.51% in the placebo group (P = 0.040). The clinical activity index
(P = 0.038) and endoscopic index (P = 0.0001)
were also significantly improved. This is a promising result that may have great clinical significance.
Hyperlipidaemia
A phase 2, non-blinded, open-label trial investigated the effect of curcuminoid C3 complex (500
mg, 3 capsules 3 times a day) in 12 patients with
plaque psoriasis for 12 weeks followed by a 4-week
observation period (Kurd et al 2008). Results were
poor with the intention-to-treat analysis response
rate only reaching 16.7%. Of the eight patients
who completed the trial the two participants who
responded achieved good results (83% and 88%
improvement in symptoms), however this could
be due to a placebo effect. Overall, the medication
was well tolerated with only mild side effects being
reported, due to either gastrointestinal upset or hot
flushing.
Arthritis
TURMERIC
Turmeric powder of standardised 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
903
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