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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).


effects may take place as a consequence of local gastrointestinal effects or be associated with metabolites of the curcuminoids.


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

Curcuma longa (family Zingiberaceae [ginger])


Dried secondary rhizome (containing not less than

3% curcuminoids calculated as curcumin and not
less than 3% volatile oil, calculated on dry-weight

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).

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


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


wound healing, and lower blood lipids and glucose

levels (Jain et al 2006, Panchatcharam 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 NFkappa-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 NF-kappa-B (Salh et al 2003). The
clinical significance of this is unclear.

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, Rao 2007).
Due to its anti-inflammatory effects, curcumin has
shown promise in many chronic disorders such as
arthritis, colitis, allergies, arteriosclerosis, diabetes,
respiratory disorders, hepatic injury, pancreatic disease, intestinal disorders, eye diseases, neurodegenerative diseases and various cancers (Aggarwal et al
2007, Bengmark 2006).
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
Gastrointestinal effects

Extracts of both turmeric and curcumin have been

found to prevent and improve carbon tetrachloride-induced liver injury both in vivo and in vitro
(Abu-Rizq et al 2008, Deshpande et al 1998, Fu et al
2008, Kang et al 2002, Wu et al 2008), curcumin
also protects against dimethylnitrosamine-induced
liver injury (Farombi et al 2008), 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
turmerics 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 appears to
chelate hepatic and serum iron in vivo (Jiao et al
2006, 2008). Iron is pro-oxidant to the liver,
which may be problematic during hepatic disease.
Recent research also suggests that curcumin may
be useful in preventing hepatic fibrosis caused by
chronic liver disease (Fu et al 2008, OConnell &
Rushworth 2008). 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
Cholagogue and hypolipidaemic

Turmeric extract or curcumin extract has shown

dose-dependent hypolipidaemic activity in vivo
(Asai & Miyazawa 2001, Babu & Srinivasan 1997,
Keshavarz 1976, Manjunatha & Srinivasan 2007a,
2007b, 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). Curcumin
also increases LDL receptor mRNA (Peschel et al
2007). Oral curcumin has also been shown to stimulate contraction of the gall bladder and promote
the flow of bile in healthy subjects (Rasyid & Lelo

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).

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 the progression periods in a variety of
cancers (Anto et al 1996, Kuttan et al 1985, Menon
et al 1999, Ruby et al 1995). Curcumin was found
to possess chemopreventive effects against skin cancer, stomach cancer, colon cancer, prostate cancer,
breast cancer and oral cancer in mice.



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 inhibits the invasion, proliferation
and metastasis of various cancers in vivo (Kunnumakkara et al 2008). Curcumin has been found
to effectively block carcinogen-induced skin
(Azuine & Bhide 1992), colon (Rao et al 1995a,
1995b, 1995c, 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 tumours 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, dichlorodiphenyltrichloroethane (DDT) and chlordane, or 17-beta
oestradiol (Verma et al 1997). Another study found
that curcumin inhibited breast cancer metastases in
immunodeficient animals (Bachmeier et al 2007).
This may be due to curcumins ability to reduce
NF-kappa-B and therefore downregulate the two
inflammatory cytokines CXCL1 and -2 (Bachmeier
et al 2008).

Apoptosis (programmed cell death) plays a crucial

role in regulating cell numbers by eliminating damaged or cancerous cells. Curcumin has been shown
to induce apoptosis in many different cancer cell
lines, including breast, leukaemia, lymphoma,
melanoma, ovarian, colorectal, lung and pancreatic
in vitro (Kim et al 2001, Kuo et al 1996, Li et al
2007, Lin et al 2007, Lev-Ari et al 2006, Marin et al
2007, Skommer et al 2007, 2006, Tian et al 2008).
Curcumin has also increased apoptosis in breast and
ovarian cancers in vivo (Bachmeier et al 2007, Lin
et al 2007). Curcumin has been demonstrated to
induce apoptosis in human basal cell carcinoma cells
associated with the p53 signalling 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).

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).

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). Another study found that curcumin effectively suppressed COX-2, vascular endothelial growth factor and intercellular adhesion
molecules, whilst enhancing the expression of antimetastatic proteins, tissue inhibitor metalloproteases-2, non-metastatic gene 23 and E-cadherin
a transmembrane protein that plays an important
role in cell adhesion (Kuttan et al 2007).
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 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).

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 blocking the 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 antirejection 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

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

25 mg/kg resulted in 60% protection from thrombosis (Srivastava et al 1985).


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, RamirezTortosa 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). Curcumin
also inhibits the proliferation and migration of
vascular smooth muscle cells in vitro (Yang et al
Many in vivo studies have investigated the effects
of dietary curcumin on blood cholesterol in diabetic
animals (Babu & Srinivasan 1997, Manjunatha &
Srinivasan 2007a, 2007b, Pari & Murugan 2007).
The two Manjunatha and Srinivasan studies found
that curcumin significantly lowered plasma cholesterol but only lowered hepatic cholesterol in animals with normal baseline cholesterol. Additionally,
hepatic alpha-tocopherol and glutathione levels
and serum glutathione peroxidase and glutathione
transferase were increased. Babu and Srinivasan also
found a significant decrease in blood triglyceride
and phospholipid levels (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 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
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 gammaradiation (Jagetia & Rajanikant 2004).

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 dosedependent, 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).

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).

Curcumins anti-inflammatory and antioxidant

actions may be useful in preventing neurodegenerative diseases, such as Alzheimers dementia and
Parkinsons disease, and curcumin has been found
to target multiple pathogenic cascades in preclinical models (transgenic and amyloid infusion models) of AD (Cole et al 2005, Calabrese et al 2006).
Curcumin has also been found to dose-dependently
inhibit neuroglial proliferation, with low doses
being as effective as higher doses given a longer
period of treatment (Ambegaokar et al 2003). It
may also enhance immune clearance of amyloidosis
in the brain (Zhang et al 2006).
Curcumin had anti-asthmatic activity in animal
models of induced asthma. Curcumin (20 mg/kg
body weight) treatment significantly inhibited
chemical (ovalbumin)-induced airway constriction
and airway hyperreactivity. The results demonstrate that curcumin is effective in improving the
impaired airways features in ovalbumin-sensitised
guinea pigs (Ram et al 2003).


Curcumin has been found to have inhibitory

effects on P-glycoprotein in numerous test tube
studies (Anuchapreeda et al 2002, Limtrakul et al
2004, Nabekura et al 2005). The clinical significance of this observation has yet to be determined.

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 over the counter (OTC),
such as oral dose forms and topical applications.

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 turmerics
efficacy in cancer treatment or prevention.
Curcumin appears to be a well-tolerated adjunctive treatment option for patients with pancreatic cancer. Twenty-five participants took 8 g of
curcumin daily. Despite significant inter-patient
variations in blood curcumin levels, NF-kappa-B,
COX-2 and phosphorylated signal transducer and
activator of transcription 3 were all downregulated
in peripheral blood mononuclear cells (Dhillon
et al 2008).
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
Bowens disease (Cheng et al 2001).
An ethanol extract of turmeric, as well as an
ointment of curcumin, was 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,
3060 min before meals, at 4 pm 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).
Irritable bowel disease (IBD)

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.

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).
A placebo-controlled, randomised, double-blind
study investigated the effects of curcumin on the
serum lipids in 36 elderly men and women (Baum
et al 2007). The participants were randomised to
either receive 4 g/day of curcumin, 1 g/day of
curcumin or placebo for 6 months. Neither active
product significantly altered triacylglycerols or cholesterol at 1 nor 6 months; however, the concentrations of plasma curcumin and serum cholesterol
were positively and significantly correlated. This
appears to indicate that curcumin may be a mild
hypocholesterolaemic agent; however, larger trials
are needed.
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 2767 years of age) of a turmeric
hydro-alcoholic 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).

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

In a randomised, controlled double-blind study,

curcumin 1200 mg/day was compared with phenylbutazone in subjects with rheumatoid arthritis


(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 osteoarthritis (OA) of the knee in
a randomised, double-blind, placebo-controlled
crossover study of 42 patients (Kulkarni et al 1991);
however, the contribution of curcumin to these
results is unknown.
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).
Internal use

Powdered turmeric: 1.53 g/day in water or

Liquid extract (1:1) in 45% ethanol: 515 mL/day.
Powdered extract standardised to 95% curcumin:
100300 mg/day. Higher doses used for arthritis
and cancer.
External use

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

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 (Shankar


et 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) (Bhagat
& Purohit 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).

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

Theoretically, high-dose turmeric preparations may

increase the risk of bleeding when used together
with anticoagulant drugs caution is advised.

Animal studies suggest that curcumin may reduce

drug efficacy avoid.

Turmeric is contraindicated in bile duct obstruction

(Blumenthal et al 2000) and high doses are probably best avoided in males and females wanting to
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.

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
& Bhide 1986) or to be teratogenic 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.

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
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.

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 Traditional Chinese medicine (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
Turmeric has been shown to have antioxidant,
anti-inflammatory and anti-atherosclerotic activities; 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
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