Turmeric: Altmeddex® Evaluations

Alternative Medicine detail - MICROMEDEX® http://remote-lib.ui.ac.id:2232/micromedex2/librarian/CS/45E0DE/ND_...
TURMERIC
AltMedDex® Evaluations
OVERVIEW
A) TURMERIC
B) CLASS: CHOLAGOGUE, ANTI-INFLAMMATORY
C) DOSAGE:
1) IMPORTANT NOTE: Dosing of herbal preparations is highly dependent on a variety of factors,
such as growing and harvesting conditions, plant parts and extraction methods used, and the
dosage form chosen by the manufacturer. Standardization to single constituent markers has proven
unreliable. Since no official standards have been established to date to regulate the production of
herbal medicines in the United States, dosage ranges must be employed as guidelines.
2) ADULT:
a) GENERAL USE, oral:
1) fluid extract: 10 to 30 drops three times daily.
2) infusion: 15 grams of powder in 500 milliliters (mL) boiling water; dose is 15 mL of this
solution.
3) powder: 1.5 to 3 grams daily.
4) tea: 4.5 to 9 grams daily.
3) PEDIATRIC: Dosing not available.
D) ADMINISTRATION: Oral
E) HOW SUPPLIED: capsule, fluid extract, infusion, powder, tea
F) USES:
1) SCIENTIFIC EVIDENCE: Curcumin, from turmeric, has demonstrated antioxidant,
anti-inflammatory, antineoplastic, antibacterial, and antithrombotic effects in animals and in vitro.
Human clinical trials are needed to substantiate turmeric's efficacy.
2) COMPLEMENTARY AND ALTERNATIVE MEDICINE INDICATIONS: Turmeric is most often used as
an antioxidant, anti-inflammatory and antithrombotic agent in the treatment of cancer, arthritis and
atherosclerosis.
G) CONTRAINDICATIONS: Hypersensitivity to turmeric or curcumin, patients with gall bladder
obstruction, gall stones, hyperacidity, obstruction of bile passages, or stomach ulcers, or those who
are pregnant should not take these herbs.
H) ADVERSE EFFECTS: May cause skin sensitization problems and has a very bitter taste.
I) DRUG INTERACTIONS: ANTICOAGULANTS: increased risk of bleeding (theoretical);
ANTIPLATELET AGENTS: increased risk of bleeding (theoretical); LOW MOLECULAR WEIGHT
HEPARINS: increased risk of bleeding (theoretical); THROMBOLYTIC AGENTS: increased risk of
bleeding (theoretical)
J) PREGNANCY/LACTATION: Contraindicated in pregnancy. Scientific evidence for the safe use of
turmeric during lactation is not available.
K) NOTE: The safety profile of herbal medications and dietary supplements is not well known. Due
to the unregulated nature of the supplement industry in the United States, it is advised to become
familiar with manufacturers and their products before recommending them for safe and effective
use. Adulteration has been a recurring problem.
DOSING INFORMATION
1 of 21 9/23/2016 6:15 AM
DOSAGE FORMS
A) MEDICINAL COMPONENTS
1) COMMERCIAL CURCUMIN:
a) Commercial grade curcumin contains 77% curcumin, 17% demethoxycurcumin and 3%
bisdemethoxycurcumin (Huang et al, 1994).
2) RHIZOME:
a) Usually dried then ground into a powder (Garg, 1974). The powder may be used as a tea,
tincture, or fluid extract (Grieve, 1971).
3) SPICE:
a) The spice has a bitter taste (Stoner & Mukhtar, 1995).
b) Turmeric is a component of curry spice (gives it the yellow color), but in normal usage, not
enough is ingested to produce a medicinal response (McGuffin et al, 1997; Sikora et al,
1997).
4) ACTIVE INGREDIENTS
a) Curcuminoids (3% to 5%) (yellow pigments): curcumin, monodesmethoxycurcumin,
bisdesmethoxycurcumin (Bisset, 1994).
b) Volatile oils (4.2% to 14%): tumerone, zingiberen (Ammon & Wahl, 1991).
1) Tumerone (a ketone)
2) Zingiberen
B) SYNONYMS
1) CURCUMA LONGA
Amomoum curcuma
Curcuma
Curcuma aromatica Salisbury
Curcuma domestica Valet
Curcuma oil
Curcumin
E zhu
Gelbwurzel
Haldi
Indian saffron
Indian yellow root
Jiang huang
Kurkumawurzelstock
'Olena
Radix zedoaria longae
Rhizome de curcuma
Zedoary
Zitterwurzel
ADULT DOSAGE
NORMAL DOSE
IMPORTANT NOTE
1) Dosing of herbal preparations is highly dependent on a variety of factors, such
as growing and harvesting conditions, plant parts and extraction methods used,
2 of 21 9/23/2016 6:15 AM
and the dosage form chosen by the manufacturer. Standardization to single

constituent markers has proven unreliable. Since no official standards have been
established to date to regulate the production of herbal medicines in the United
States, dosage ranges must be employed as guidelines.
See Drug Consult reference:" HERBAL SUPPLEMENTS - DOSING"
See Drug Consult reference:" MEDICINAL HERBAL PREPARATIONS"
ORAL
1) GENERAL USE:
a) Fluid extract: 10 to 30 drops three times daily (Grieve, 1971).
b) Infusion: 15 grams of powder in 500 milliliters (mL) of boiling water. Dose is 15
mL of this solution (Grieve, 1971).
c) Powder: 1.5 to 3 grams daily (Blumenthal et al, 1998; McGuffin et al, 1997).
d) Tea: 4.5 to 9 grams daily (McGuffin et al, 1997).
PHARMACOKINETICS
ADME
EXCRETION
BREAST MILK
A) BREASTFEEDING: Unknown
1) Scientific evidence for the safe use of turmeric during lactation is not available.
CAUTIONS
CONTRAINDICATIONS
A) Hypersensitivity to turmeric or curcumin

B) Should not be taken by patients with gall stones or bile duct obstruction (McGuffin et al,
1997)
C) Curcuma longa should not be taken by patients with hyperacidity or with gastrointestinal
ulcers (McGuffin et al, 1997)
D) Obstruction of bile passages (Blumenthal et al, 1998)
E) Pregnancy, due to turmeric's emmenagogue and uterine stimulant effects (Brinker, 1998;
McGuffin et al, 1997)
PRECAUTIONS
A) Use with caution during excessive menstruation (McGuffin et al, 1997)

B) In case of gallstones, use only after consulting with a physician (Blumenthal et al, 1998)
ADVERSE REACTIONS
SKIN
3 of 21 9/23/2016 6:15 AM
DERMATOLOGIC EFFECTS
1) One case of acute CONTACT DERMATITIS was reported following a 6-month
occupational exposure to turmeric (Kiec-Swierczynska & Krecisz, 1998).
OTHER
TOXICITY
1) The administration of 10,000 parts per million of curcumin to rats via the diet
produced no significant toxicity (Rao et al, 1995).
TERATOGENICITY/EFFECTS IN PREGNANCY
TERATOGENICITY
1) In a study, rats and rabbits did not exhibit teratogenic effects when the animals were
administered various forms and doses of Curcuma longa (Garg, 1974).
EFFECTS IN PREGNANCY
1) ANTIFERTILITY
a) Antifertility effects (60% to 100% reduction in offspring) were seen in rats given
extracts of Curcuma longa rhizome. The petroleum ether extract also exhibited
resorption of implants. The rhizome of Curcuma longa was air dried, powdered, and
extracted with either petroleum ether, 95% ethanol, or distilled water. The extracts were
dried and suspended in gum acacia. Adult female albino rats and rabbits were mated
with male animals of proven fertility and either a placebo or one of the extracts was
given for the next 7 days. Control animals developed pregnancy in 10 of 10 rats tested.
The petroleum ether extract reduced pregnancy in 80% of animals at a dose of 100
milligrams/kilogram (mg/kg) and 100% at 200 mg/kg. The alcoholic extract reduced the
pregnancy rate by 60% and 70% respectively, and the aqueous extract prevented
pregnancy by 80% and 100% respectively (Garg, 1974).
1) No significant antiovulatory effect was noted in rabbits with 3 days of administration
of the various extracts at a dose of 100 mg/kg and 200 mg/kg (Garg, 1974).
2) None of the animals in either group exhibited teratogenicity (Garg, 1974).
2) Contraindicated during pregnancy due to its emmenagogue and abortifacient effects
from its uterine stimulant activity (Brinker, 1998; McGuffin et al, 1997).
DRUG INTERACTIONS
DRUG-DRUG COMBINATIONS
ANTICOAGULANTS
1) Summary: Theoretically, curcumin may add to the effect of anticoagulants and
increase the risk of bleeding. Curcumin inhibited platelet aggregation in animals
and in vitro (Srivastava et al, 1995; Srivastava et al, 1985), which may result in
prolonged bleeding times if taken with drugs known to affect platelet function.
2) Adverse Effect: increased risk of bleeding
3) Clinical Management: Caution is advised if curcumin and anticoagulants are
used concomitantly. Monitor bleeding time and signs and symptoms of excessive
bleeding.
4) Severity: moderate
5) Onset: delayed
6) Documentation: good
7) Probable Mechanism: inhibition of platelet aggregation by curcumin
8) Literature Report:
4 of 21 9/23/2016 6:15 AM
a) In a platelet aggregation study of blood samples obtained from healthy

volunteers, curcumin was found to inhibit platelet aggregation induced by
arachidonate, epinephrine, and collagen with IC50 values of 32 mcmol, 100
mcmol, and 344 mcmol, respectively. Curcumin (10,100, 500 mcmol) inhibited
formation of thromboxane B2 dose-dependently (IC50 equal to 63 mcmol). The
incorporation of labeled arachidonic acid into the platelet phospholipids was
inhibited by 32% with curcumin 250 mcmol (Srivastava et al, 1995).
ANTIPLATELET AGENTS
1) Summary: Theoretically, curcumin may add to the effect of antiplatelet agents
and increase the risk of bleeding. Curcumin inhibited platelet aggregation in
animals and in vitro (Srivastava et al, 1995; Srivastava et al, 1985), which may
result in increased chance of bleeding if taken with drugs known to affect platelet
function.
3) Clinical Management: Caution is advised if curcumin and antiplatelet agents are
used concomitantly. Monitor for signs and symptoms of excessive bleeding.
5) Onset: delayed
6) Documentation: fair
inhibited by 32% with curcumin 250 mcmol (Srivastava et al, 1995).
LOW MOLECULAR WEIGHT HEPARINS
1) Summary: Theoretically, curcumin may add to the effect of low molecular
weight heparins and increase the risk of bleeding. Curcumin inhibited platelet
aggregation in animals and in vitro (Srivastava et al, 1995; Srivastava et al, 1985),
which may result in prolonged bleeding times.
3) Clinical Management: Caution is advised if curcumin and low molecular weight
heparins are used concomitantly. Monitor for signs and symptoms of excessive
bleeding.
5) Onset: delayed
inhibited by 32 percent with curcumin 250 mcmol (Srivastava et al, 1995).
THROMBOLYTIC AGENTS
1) Summary: Theoretically, curcumin may add to the effect of thrombolytic agents
and increase the risk of bleeding. Curcumin inhibited platelet aggregation in
animals and in vitro (Srivastava et al, 1995; Srivastava et al, 1985), which may
result in prolonged bleeding times.
5 of 21 9/23/2016 6:15 AM

3) Clinical Management: Caution is advised if curcumin and thrombolytic agents are
used concomitantly. Monitor for signs and symptoms of excessive bleeding.
5) Onset: delayed
8) Literature Reports:
inhibited by 32 percent with curcumin 250 mcmol (Srivastava et al, 1995).
b) In mice, thrombosis was generated in vivo with administration of 15
micrograms (mcg) collagen and 30 micromoles (mcmol) epinephrine. Aspirin or
curcumin was administered intraperitoneally one hour prior to this thrombotic
challenge. Curcumin 100 mg/kg resulted in 60 percent protection from thrombosis
versus aspirin 25 mg/kg, which resulted in 61.1 percent protection. Furthermore,
curcumin 100 mg/kg and 200 mg/kg inhibited thromboxane B2 production by 52.5
percent and 83.7 percent, respectively (Srivastava et al, 1985).
CLINICAL APPLICATIONS
MONITORING PARAMETERS
THERAPEUTIC
A) PHYSICAL EXAMINATION
1) INFLAMMATION
a) Monitor the intensity and extent of inflammation (Chevallier, 1996; (Kunchandy &
Rao, 1990).
2) TUMOR SIZE
a) Monitor size and growth (or reduction) of tumors being treated (Nagabhushan &
Bhide, 1992).
PLACE IN THERAPY
A) SUMMARY OF SCIENTIFIC EVIDENCE: Curcumin, from turmeric, has been shown to have
antioxidant properties that contribute to its antiinflammatory, antineoplastic, antibacterial, and
antithrombotic effects (Bisset, 1994; Reddy & Aggarwal, 1994; Ammon et al, 1993).
B) COMMON USES IN COMPLEMENTARY AND ALTERNATIVE MEDICINE: Turmeric has been
shown, in both clinical and laboratory settings, to be useful in treating cancer, arthritis and
atherosclerosis. Curcumin, the polyphenol which is responsible for the bright yellow pigment of
turmeric, has also demonstrated appreciable antiinflammatory and antineoplastic effects in
animal and in vitro studies. Contact dermatitis and/or skin sensitization has been reported by at
least a few individuals with direct occupational exposure to turmeric. The adverse effects of
turmeric most often apply to therapeutic doses, in the range of 1.5 grams to 3 grams per day,
6 of 21 9/23/2016 6:15 AM
not to the average amounts in culinary recipes. When using turmeric as a single herbal
medicine, 0.5 to 1 gram 3 times daily is an average dose with which to begin. As an
antioxidant and antithrombotic agent, begin with 2 grams daily. For most cancers, begin dosing
at 750 milligrams twice a day and consider increasing with positive results. At least one study
demonstrated hepatoprotective effects of turmeric. Caution should be used in patients with
liver and gallbladder disease. Therapeutic doses of turmeric should be avoided in pregnancy
and in those hoping to become pregnant, as it may act as a uterine stimulant. Because of its
strong and bitter taste, patient compliance is usually highest using standardized herbal
capsules or in tablet form along with other natural medicines.
C) HISTORICAL USES: Turmeric has been used as a spice, dye, earache cure, astringent, and
as a treatment for jaundice, digestive problems, colic, asthma, arthritis, and psoriasis
(Chevallier, 1996; Abbott, 1992; Grieve, 1971). Chinese medical uses include bruises, sores,
ringworm, chest pain, toothache, and jaundice.
D) REGULATORY/SAFETY INFORMATION: Turmeric is German Commission E approved for
dyspeptic conditions (Blumenthal et al, 1998). The American Herbal Products Association rated
Curcuma longa as Class 2b (not to be used during pregnancy) and 2d (therapeutic quantities
should not be taken by people with bile duct obstruction or gall stones; should not be
administered to patients who suffer from stomach ulcers or hyperacidity) (McGuffin et al,
1997). Turmeric is available in the United States as a spice and dietary supplement under the
Dietary Supplement Health Education Act of 1994 (DSHEA).
See Drug Consult reference:" GERMAN COMMISSION E - APPROVED HERBS"
See Drug Consult reference:" BOTANICAL SAFETY HANDBOOK TERMS - DEFINITIONS"
See Drug Consult reference:" THE DIETARY SUPPLEMENT HEALTH AND EDUCATION ACT OF
1994"
MECHANISM OF ACTION/PHARMACOLOGY
A) MECHANISM OF ACTION
1) SUMMARY: Curcuminoids have anti-inflammatory, antibacterial, antioxidant,
antihepatotoxic, antineoplastic, antithrombotic, and bile stimulant properties (Bierhaus et al,
1997; Sikora et al, 1997; Bisset, 1994; Reddy & Aggarwal, 1994). Bisdesmethoxycurcumin has
bile secretion-inhibiting properties (Bisset, 1994).
2) ANTIINFLAMMATORY EFFECTS:
a) The antiinflammatory effects of turmeric are thought to be due to inhibition of leukotriene
biosynthesis, and through this inhibition, a change in prostaglandin production (Bisset, 1994).
b) Alpha tumerone blocks the proliferation of human lymphocytes and decreases the activity
of natural killer cells (Bisset, 1994).
c) Ukonan A (a polysaccharide) has phagocytic effects when tested in mice (Bisset, 1994).
3) ANTINEOPLASTIC EFFECTS:
a) The antineoplastic effects of turmeric are due to inhibition of metabolic activation of
carcinogens and detoxification of these carcinogens (Stoner & Mukhtar, 1995). The
curcuminoids are cytotoxic and have been shown in cell cultures to be toxic to tumor cells
(Bisset, 1994; Nagabhushan & Bhide, 1992).
b) The inhibition of cell proliferation observed with curcumin may be related to inhibition of
various kinases such as protein kinase and phosphorylase kinase. Curcumin also inhibits the
expression of several proto-oncogenes (c-jun, c-fos, c-myc) in mouse skin cells and
transcription factor AP-1 (Sikora et al, 1997).
c) Turmeric binds to estradiol and progesterone receptors and may have weak estrogenic
activity in vivo. Turmeric had an estradiol binding capacity in vitro of 0.5 micrograms (mcg) of
estradiol binding equivalents per 2 grams of dried herb and 4 mcg of progesterone binding
7 of 21 9/23/2016 6:15 AM
activity per 2 grams of dried herb. After ingestion, saliva was used to obtain these
phytoestrogens and phytoprogesterones. The substances isolated were used to detect
bioavailability and bioactivity of phytoestrogens and phytoprogesterones in turmeric. Breast
cancer cell lines were used to evaluate growth rate changes induced by this herb, but the
differences were not significant (Zava et al, 1998).
d) Curcumin has antineoplastic effects through an antiproliferative mechanism. Part of this
effect may be due to curcumin's effect on various kinases. Curcumin was found to be an
inhibitor of highly purified protein kinase A (Ka), protein kinase C (Kc), protamine kinase (PK),
phosphorylase kinase (PHK), autophosphorylation-activated protein kinase (AAPK), and
pp60-tyrosine kinase (TK). The amount of inhibition varied, with phosphorylase kinase being
the most effected at lower doses of curcumin. A doses of 0.1 millimole of curcumin produced
the following reductions: PHK (98%), TK (40%), Kc (15%), Ka (10%), AAPK (1%), and PK
(0.5%). Phosphorylase kinase is a key regulatory enzyme in glycogen metabolism, which may
result in anti-proliferation effects if it is inhibited (Reddy & Aggarwal, 1994).
e) Curcumin I and curcumin III are two antineoplastic chemicals found in curcumin. Curcumin
I inhibited benzopyrene-induced forestomach and benzopyrene-initiated, tetradeconylphorbol-
acetate-promoted skin tumors in Swiss mice. Curcumin II inhibited dimethylbenzathracene-
induced skin tumors in Swiss bald mice. Both compounds demonstrated in vitro cytotoxicity
against human chronic myeloid leukemia in a dose dependent manner. Using in vivo
carcinogen metabolism enzyme studies and 3H-benzopyrene-DNA studies, curcumins were
shown to inhibit cancer at the initiation, promotion, and progression stages of development.
Altering of the activation and/or detoxification process of carcinogen metabolism was reported
(Nagabhushan & Bhide, 1992).
f) The antiproliferataive effect of curcumin on transformed and nontransformed cancer cells
was measured in vitro. In all experiments, curcumin caused slight to moderate inhibition of
the proliferation of leukemia hematopoietic cell types but not fibroblasts (Gautam et al, 1998).
g) The compound diferuloylmethane, an active component of turmeric, has been shown to
inhibit chemically induced initiation and promotion of skin tumors in mice (Gautam, et al,
1998).
4) ANTIOXIDANT EFFECTS:
a) Curcumin provides an antioxidant and anti-inflammatory effect by inhibiting the binding of
transcription factor AP-1 to DNA and activation of NF-kappaB. These two substances control
many endothelial genes such as plasminogen activator factor-1, tissue factor, endothelin-1,
and interleukin 6 & 8. Via its AP-1 inhibitory activity, curcumin inhibits both cell growth and
cell death (Bierhaus et al, 1997; Sikora et al, 1997; Singh & Aggarwal, 1995).
b) Curcumin inhibits epidermal arachidonic acid metabolism by means of lipoxygenase and
cyclooxygenase pathways and reduces the inflammatory effects of arachidonic acid and
tetradeconylphorbol-acetate (TPA) (Stoner & Mukhtar, 1995).
5) ANTITHROMBOTIC EFFECTS:
a) Curcumin is thought to provide an antithrombotic effect in precoagulation by inhibiting the
binding of transcription factor AP-1 to DNA and activation of NF-kappaB. Tumor necrosis
factor alpha induces the expression of endothelial tissue factor, which is one of the primary
initiators of coagulation cascades. This cascade is produced via actions of AP-1 and
NF-kappaB (Bierhaus et al, 1997; Sikora et al, 1997).
b) The antiproliferative effect of curcumin may be partially mediated through inhibition of
protein tyrosine kinase activity and c-myc mRNA expression. In addition, the apoptotic effect
of curcumin may partly be mediated through inhibition of protein tyrosine kinase activity,
protein kinase C activity, c-myc mRNA expression, and bcl-2 mRNA expression (Chen &
Huang, 1998).
c) Tumerone has anti-snake venom properties, blocking the hemorrhagic effects of Bothrops
venom and reducing the lethality of Crotalus venoms (Bisset, 1994). Specific studies could not
be found, maybe due to an antithrombotic effect (Bierhaus et al, 1997; Sikora et al, 1997).
d) Curcumin inhibited ADP, collagen and epinephrine induced platelet aggregation. Curcumin
did not affect prostacyclin synthesis. Curcumin may selectively inhibit thromboxane synthesis
and may produce thromboxane inhibition without prostacyclin inhibition (Srivastava et al,
1986; Srivastava et al, 1985; Mukhopadhyay et al, 1982).
8 of 21 9/23/2016 6:15 AM
6) CHOLAGOGUE EFFECTS:
a) A cholagogue stimulates bile secretion. The curcuminoids stimulate bile secretion in
general, although it has some choleresis-inhibiting properties as well, which are thought to be
due to bisdesmethoxycurcumin (Bisset, 1994).
B) REVIEW ARTICLES
1) ENGLISH:
a) A review of curcumin that includes pharmacologic and clinical trial information is presented
(Goel et al, 2008).
b) A summary of the pharmacology of Curcuma longa and a review of pharmacological or
clinical studies is available (Ammon & Wahl, 1991).
THERAPEUTIC USES
ANTIOXIDANT
1) OVERVIEW:
EFFICACY: In vitro data only
DOCUMENTATION: In vitro data only
2) SUMMARY:
- Curcumin is an antioxidant of stronger potency
than vitamin E (Chevallier, 1996)
3) IN VITRO:
a) Curcuminoids I, II, and III inhibited superoxide production in an in vitro study.
Curcuminoid III was the most potent inhibitor. Concentrations (curcumins I, II, III
respectively) of 6.25, 4.25, and 1.9 micrograms/milliliter (mcg/mL) were required for
50% inhibition of superoxide; 20, 14, and 11 grams/milliliter were required for 50%
inhibition of lipid peroxidation; and 2.3, 1.8, and 1.8 mcg/mL were required for inhibition
of 50% of hydroxyl radicals. Curcumin contains curcuminoid 1 (diferuloyl methane) as
the major portion, with 6% of curcuminoid II and 0.3% of curcuminoid III (Ruby et al,
1995).
b) The tetrahydrocurcuminoid THU1, a major metabolite of curcumin (U1), was found to
have strong anti-oxidative activity in the rabbit erythrocyte membrane ghost test, linoleic
acid in ethanol/water system, and rat liver microsomes in vitro systems. The
curcuminoids, 4-hydroxy-3-methoxycinnamoyl methane (U2) and bis-4-
hydroxycinnamoyl methane (U3), also have antioxidant properties, curcumin having the
strongest of the three. The tetrahydrocurcuminoids of U1 (THU1) and of U2 (THU2)
possessed stronger antioxidant activity than the parent U1 and U2. The lipid
peroxidation seen in the rabbit erythrocyte membrane ghost test was reduced about
70% for U1 and 82% for THU1. In the rat liver microsome system, U1 lipid peroxidation
was reduced 50% and the THU1 value was about 58% (Osawa et al, 1995).
c) Curcumin as well as the curcuminoids demethoxycurcumin, bisdemethoxycurcumin,
and acetylcurcumin (found in the Curcuma longa root) were found to be potent
inhibitors of iron-stimulated lipid peroxidation in a study of lipid peroxidation in rat brain
homogenate and rat liver microsomes. The effect was dose dependent. All of these
agents were approximately equal in action at a specific concentration. Test
concentrations varied from 0.25 micromoles (mcmol) to 20 mcmol, the percent inhibition
ranged from 2% (0.25 mcmol) to 100% (20 mcmol). All of these agents were more
active than alpha tocopherol (Sreejayan & Rao, 1994).
9 of 21 9/23/2016 6:15 AM
d) Curcumin inhibited lipid peroxidation measured in rat brain homogenates, and

decreased the formation of conjugated dienes (reduced by 52%) and spontaneous lipid
peroxidation (about 60% at a concentration of about 50 micromoles). Lipid peroxidation
caused by ferrous ions, ferric-ascorbate, and ferric-ADP-ascorbate were also inhibited.
Curcumin reduced spontaneous lipid peroxidation by about 60%, dehydrozingerone
(from ginger) reduced it by about 14%, and DL-alpha-tocopherol (vitamin E) reduced it
by about 42%. All three agents were given at a variety of concentrations, but for these
antioxidant values, all test agents were given at a dose of 50 mcmol (Rajakumar & Rao,
1994).
e) Curcumin's anti-inflammatory effects may be due to its oxygen radical scavenging
properties. An in vitro test measured the amount of free radical scavenging. At a
concentration of 1.35 micromoles (mcmol), 33.3% of hydroxyl radical scavenging
(measured by bleaching of p-nitrosodimethylaniline) was found. The amount of
scavenging was dose dependent, the highest concentration was 27 mcmol, producing a
62.5% scavenging. At a concentration of 0.61 mcmol, curcumin actually generated
hydroxy radicals (-7.15%) rather than scavenging them (Kunchandy & Rao, 1990).
1) Curcumin was also a potent scavenger of superoxide. Levels of 2.7 micromoles
(mcmol) scavenged 1.3% of superoxide while a concentration of 54 mcmol scavenged
33%. The effect was dose dependent. At a low concentration (1.35 mcmol) the amount
of superoxide was increased (10.6%), not decreased (Kunchandy & Rao, 1990).
f) Turmeric was shown to inhibit lipid peroxidation in erythrocyte membranes. About 4
micromoles was necessary to inhibit 79% of the peroxidation. One millimole of curcumin
totally inhibited lipid peroxidation in this model. The antioxidant properties were greater
than that of vitamin E, beta-carotene, BHA, BHT, and soybean trypsin inhibitor (Salimath
et al, 1986).
CANCER
1) OVERVIEW:
EFFICACY: Animal and in vitro data only
DOCUMENTATION: Animal and in vitro data only
2) SUMMARY:
- Several tumor types in animal models and various
in vitro models have demonstrated an
antineoplastic effect of curcumin
3) ANIMAL:
a) Curcumin inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted and 7,12,-
dimethylbenz(a)anthracene (DMBA)-induced skin tumors in mice. The dose of curcumin
used was 200 nanomoles, applied topically to the skin of each mouse (Stoner &
Mukhtar, 1995).
b) Curcuminoids I, II, and III increased the life span of mice injected with Ehrlich tumor
cells (1 million cells to develop ascites). Compared to controls which received no
curcuminoids, curcumin I, II and III increased survival time in the ascites tumor test by
53.7%, 65% and 74.1% respectively. Solid tumors in mice were induced by
subcutaneous injection of Dalton's lymphoma ascites (DLA) cells into the right hind leg.
The curcuminoids (liposomally encapsulated) were given intraperitoneally 24 hours later
for the next 5 alternate days for a total dose of 50 milligrams/kilogram. Curcumin
contains curcuminoid 1 (diferuloyl methane) as the major portion, with 6% of
curcuminoid II and 0.3% of curcuminoid III (Ruby et al, 1995).
1) Tests were also done in vitro. Cytotoxicity tests were done in Ehrlich ascites cells,
Dalton's lymphoma ascites cells, and L929 cells. In vitro cytotoxicity (50% inhibition)
10 of 21 9/23/2016 6:15 AM
was seen for Ehrlich ascites cells at 10, 10, and 2 micrograms/milliliter (mcg/mL)
(curcuminoids I, II, III respectively), for DLA cells it was 6, 10 and less than 2 mcg/mL,
and for L929 cells it was 1, 1, and less than 1 mcg/mL (Ruby et al, 1995).
c) Curcumin significantly decreased the incidence of non-invasive tumors
(controls=67%, treated=37%; p less than 0.015), total number of tumors (both invasive
and non-invasive) (controls=81%, treated=47%; p less than 0.004), and size (57%) of
induced adenocarcinomas in rats. The number of invasive tumors was also reduced, but
not significantly (p equal to 0.054). This was a placebo- controlled study of rats given
either a control diet or a control diet with 2000 parts per million (ppm) of curcumin at 5
weeks of age. At 7 to 52 weeks of age, both groups were additionally given twice-
weekly subcutaneous injections of the carcinogen azoxymethane (15 milligram/kilogram
/week). Curcumin-treated animals had decreased activities of colonic mucosal and tumor
phospholipase A2 (50%), decreased phospholipase C-gamma-1(40%), and decreased
PGE2 (greater than 38%). Formation of various prostaglandins (PGE2, PGF2-alpha,
PGD2, 6-keto, PGF1-alpha) and thromboxane B was also reduced (Rao et al, 1995).
d) B(a)P-induced forestomach tumors in mice were reduced by administration of 1
milligram of curcumin by gavage (Stoner & Mukhtar, 1995).
e) Curcumin (0.5 grams/kilograms (500 parts per million (ppm)) in the diet) was found
to significantly reduce the frequency of tongue carcinoma (41% to 91%, p less than
0.05) in this placebo-controlled study of male rats who were given 4-nitroquinoline-
1-oxide (NQO) (20 ppm) to induce oral cancer. Those animals treated with curcumin had
no carcinomas, while 54% of those treated with NQO alone developed carcinomas. The
incidence of preneoplasia was also decreased in the curcumin group (p less than 0.05).
The curcumin treated group had no hyperplasia, papillary hyperplasia, or dysplasia,
while in the NQO group 96% of animals developed simple hyperplasia, 38% developed
papillary hyperplasia, and 96% developed dysplasia. The Curcumin was started at six
weeks of age, while the NQO was given in their water at 7 weeks of age and was
continued for 8 weeks. The factors measuring neoplasms were incidences of tongue
neoplasms, tongue preneoplastic lesions, polyamine levels in tongue tissue, and cell
proliferation activity estimated by bromodeoxyuridine-labeling index and by
morphometric analysis of silver-stained nucleolar organizer region proteins. The
antineoplastic effects of curcumin might be due to inhibition of cell proliferation (Tanaka
et al, 1994).
f) Mice were given a carcinogen and an initiator then administered 0.5% to 2% (0.5%
to 4% in the colon studies) of commercial grade curcumin in their diet. Effects were: (a)
Reduced number of forestomach tumors by 51% to 53% (if given during the initiation
phase), and by 47% to 67% (if given during the post-initiation phase). (b) Reduced
number of duodenal tumors per mouse by 47% to 77% in the post initiation phase. (c)
Reduced number of colon tumors per mouse by 66% (if given during the initiation
phase) and by 25% (when given during the post initiation phase). The carcinogens used
were benzoalphapyrene (forestomach), n-ethyl- N'-nitrosoquanidine (duodenum), and
azoxymethane (colon) (Huang et al, 1994).
g) Topical curcumin (3 and 10 micromoles) given 5 minutes prior to application of 20
nanomoles of the carcinogen 3-benzoalphapyrene inhibited formation of
3-benzoalphapyrene-DNA adducts in mouse epidermis by 39% and 61% respectively
(Huang et al, 1992).
h) The number tumors per mouse was decreased by 58% to 62% and the number of
mice developing tumors reduced by 18% or 25% (compared to controls) after topical
administration of curcumin 3 or 10 micromoles given five minutes prior to application of
the carcinogen benzo(alpha)pyrene (BaP). Topical administration of 20 nanomoles of
BaP to the backs of mice once weekly followed by 15 nanomoles of the tumor promoter
12-O-tetradecanoylphorbol-13-acetate (TPA) twice weekly for 21 weeks was evaluated in
both a curcumin and control group. All control mice so treated developed tumors, with
an average of 7.1 tumors per mouse (Huang et al, 1992).
i) Topical administration of 3 or 10 micromoles of curcumin five minutes prior to topical
application of 2 nanomoles of the carcinogen 7,12-dimethylbenz(alpha)anthracene
(given once per week for 10 weeks) decreased the number of tumors in mice by 37%
11 of 21 9/23/2016 6:15 AM
per mouse. One week later, administration of the tumor promoter

12-O-tetradecanoylphorbol-13-acetate (TPA) for 15 weeks, produced a 41% decrease in
the number of tumors per mouse (Huang et al, 1992).
j) Topically administered curcumin inhibited TPA-induced skin tumors in mice. Curcumin
was applied in doses of 0.5, 1, 3, or 10 micromoles (mcmol) with 5 nanomoles of TPA.
This topical application of curcumin inhibited TPA-induced ornithine decarboxylase
activity by 31%, 46%, 84%, and 98% respectively. When 5 nanomoles of TPA were
mixed with 1 to 10 mcmol and applied topically twice a week for 20 weeks in DMBA
treated mice, the percent inhibition was dose-dependent and ranged from 39% to 98%
(Huang et al, 1988).
4) IN VITRO:
a) Curcumin and gallic acid were compared for their cytotoxic activity in relation to their
radical modulating activity. Curcumin was more cytotoxic than gallic acid. Both curcumin
and gallic acid produced radical intensity; however, the radical intensity produced by
curcumin was always smaller than that of gallic acid. The study reveals positive
apoptosis-inducing activity for both curcumin and gallic acid; however, the mechanism
for this induction is different for each substance (Nogaki et al, 1998).
b) The antiproliferative effect of curcumin on transformed and nontransformed cancer
cells was measured in clonogenic assays, (3H)thymidine incorporation assays and DNA
fragmentation studies. In all experiments, curcumin caused slight to moderate inhibition
of the proliferation of leukemia hematopoietic cell types but not fibroblasts. To
determine the reversibility of curcumin's inhibitory effect, cells were treated with
curcumin at 6.25 to 25 micromoles (mcmol) leukemia/hematopoietic cells) or at 12.5 to
50 mcmol (fibroblasts) for 3 hours. The resulting data suggest that most cell types are
irreversibly affected by curcumin (Gautam et al, 1998).
c) Precancerous lesions, such as those induced by 7,12,-
dimethylbenz(alpha)anthracene (DMBA)-induced hyperplastic nodules in cultured rat
mammary gland tissues, were inhibited by curcumin (Stoner & Mukhtar, 1995).
d) Transcription factor NF-kappaB (TFNF) was suppressed by administration of curcumin
in a human myeloid ML-1a cell model treated with tumor necrosis factor (TNF). TFNF
and the genes it effects have been associated with acute inflammatory processes,
toxic/septic shock, graft versus host rejections, viral replication, acute-phase response,
radiation damage, atherosclerosis, and cancer. TFNF normally is inactive in the
cytoplasm of cells but can be activated by inflammatory cytokines (tumor necrosis
factor, lymphotoxin, interleukin-1) mitogens, bacterial products, protein synthesis
inhibitors, oxidative stress, ultraviolet light, and phorbol esters. When TFNF is activated,
various inflammatory cytokines and adhesion molecules are induced. This activation and
production of cytokines is blocked in vitro by administration of curcumin. In this study,
ML-1a cells were preincubated with curcumin (2 to 60 micromoles) for 60 minutes, then
incubated with 0.1 micromoles of tumor necrosis factor (Singh & Aggarwal, 1995).
CHRONIC ANTERIOR UVEITIS
1) OVERVIEW:
EFFICACY: Adult, possibly effective
DOCUMENTATION: Adult, poor
2) SUMMARY:
- Curcumin may be an effective treatment for
patients with chronic anterior uveitis
3) ADULTS:
a) Marked improvement was seen in 32 patients with chronic anterior uveitis (CAU) who
received 375 milligrams (mg) curcumin daily for 12 weeks. Patients were divided into
12 of 21 9/23/2016 6:15 AM
two groups. Group A (n=18) received topical mydriatic agents, local hot fomentation and
curcumin. Patients in group B (n=14) were treated with antitubercular drugs (rifampicin
10 mg/kilogram (kg) plus INH 5 mg/kg plus pyrazinamide 30 mg/kg daily), local
mydriatics, hot fomentation, and curcumin. In Group B, curcumin was administered for
12 weeks but antitubercular medications were continued for one year. Symptomatic
improvement was observed in both groups. Patients in group A experienced improved
vision, pain relief, decreased redness and lacrimation, regression in circumciliary
congestion, keratic precipitates, aqueous flare and vitreous turbidity. Complete remission
of CAU was observed in 12 of 14 patients in group B within 12 weeks of beginning
therapy (Lal et al, 1999).
HEPATOPROTECTANT
1) OVERVIEW:
EFFICACY: Animal data only
DOCUMENTATION: Animal data only
2) SUMMARY:
- Turmeric extract was hepatoprotective against
carbon tetrachloride in rats
3) ANIMAL:
a) A turmeric extract was hepatoprotective against carbon tetrachloride (CT) in rats.
Rats were divided into 5 groups, one of which received no treatment, another received
only the turmeric extract (5%), a third received only CT (gassed for 3 to 5 minutes with
air over a saturated solution), a fourth received the turmeric (5% in their diet)
concurrently with CT, and the last was given the turmeric for 2 weeks before the CT.
Bilirubin (BR), alkaline phosphatase (AP), alanine aminotransferase (ALT), aspartate
aminotransferase (AST), and cholesterol were measured (Deshpande et al, 1998).
1) Levels in the CT alone group were two to three times that of the no treatment,
control group. Administration of turmeric extract before the CT resulted in less of a rise
than in the CT alone group. The same was true of the concurrent turmeric
administration group, but the protection was less evident, and AP was not effected. The
results were significant at the p less than 0.001 level. At no point were the levels near
normal for any group receiving the CT (Deshpande et al, 1998).
INFECTION
1) OVERVIEW:
DOCUMENTATION: Adult, poor
2) SUMMARY:
- When applied to the skin and exposed to sunlight,
curcumin is antibacterial (Chevallier, 1996)
- Curcumin had no effect on HIV-RNA copy number

or CD4 positive lymphocyte counts
3) ADULT:
a) In a phase I/II trial, curcumin dosing of either 4800 milligrams/day (mg/day) or 2700
13 of 21 9/23/2016 6:15 AM
mg/day had no effect on the HIV-RNA copy number or CD4 positive lymphocyte cell
counts. Forty HIV patients started the study and 38 finished (2 dropped for causes
unrelated to the curcumin). The curcumin was given for 8 weeks. Positive CD4 cell
counts and HIV-RNA copy counts were taken 2 to 3 times prior to the start of the
subject in the study and at the end of the study. Curcumin was tried because in various
cell lines curcumin has been shown to inhibit tumor necrosis factor-alpha stimulation of
HIV-LTR (Hellinger et al, 1996).
4) IN VITRO:
a) An anti-integrase protein activity against human immunodeficiency virus type-1 was
shown by curcumin. The 50% inhibitory concentration for strand transfer was 40
micromoles. Integrase protein is required for viral replication (Mazumder et al, 1995).
INFLAMMATION
1) OVERVIEW:
EFFICACY: Animal and in vitro data only
DOCUMENTATION: Animal and in vitro data only
2) SUMMARY:
- Used as an anti-inflammatory, curcumin is thought
to have an action greater than
hydrocortisone (Chevallier, 1996)
- Curcumin's anti-inflammatory effects may be due

to its oxygen radical scavenging
properties (Kunchandy & Rao, 1990)
3) ANIMAL:
a) Carrageenan-induced foot pad edema in rats was lowered (36%) after oral (gavage)
treatment with curcumin (30 milligrams/kilogram). Variables altering the reported effects
were time between administration of the two agents, the concentration of the curcumin,
and the amount of dietary lipids in the animal's diet. The peak edema reducing effect
was seen if the carrageenan was injected at 3 hours post curcumin administration. If
given one hour or 12 hours after the carrageenan, the effect was reduced by 50%. The
dose of carrageenan injected was 2.5 milligrams/kilogram. Paw volume increased
linearly for 3 to 6 hours, returning to normal in 24 hours (Reddy & Lokesh, 1994).
1) Although polyunsaturated fatty acids (PUFA) are known to reduce the inflammatory
response, no additional effect from curcumin (1% weight of diet) was obtained when
the diet of these rats contained n-3 (PUFA) (10% cod liver oil), 10% peanut oil
(n6-PUFA), or 10% coconut oil (medium chain saturated fatty acids) for 10 weeks. After
being on the diet for 10 weeks, the curcumin was administered as in the experiment
above (Reddy & Lokesh, 1994).
b) No effect was seen 4 hours after carrageenin (0.05 milliliter of a 1% solution) was
injected into a rat paw then treated with 3 milligrams of curcumin injected into that paw
(Ammon & Wahl, 1991).
c) Intraperitoneal administration of Curcuma longa extracts was effective in reducing
acute carrageenin-induced rat paw edema. The effective dose 50% (ED50) of the water
extract was 4.7 milligrams/kilogram (mg/kg), the alcohol extract's ED50 was 309 mg/kg,
the petroleum ether extract's ED50 was 40.7 mg/kg, and that of curcumin itself was 8.7
mg/kg (Ammon & Wahl, 1991).
d) Ghatak & Basu reported an intraperitoneal (IP) effective dose 50% (ED50) of 2.1
milligrams/kilogram (mg/kg) for curcumin and 0.36 mg/kg for sodium curcuminate in
carrageenin-induced rat paw edema. Ten mg/kg of IP hydrocortisone inhibited edema by
14 of 21 9/23/2016 6:15 AM
47.8% (Ammon & Wahl, 1991).

e) Kaolin-induced inflammation (0.05 milliliter (mL) of a 25% suspension injected into
the paw) in rats was treated by 3 milligrams/kilogram of curcumin. At 24 hours the
edema was inhibited by 19.7%; and at 48 hours, 22.4% inhibition was noted (Ammon &
Wahl, 1990).
f) Curcumin, at 3 to 10 micromoles (mcmol), was found to inhibit arachidonic
acid-induced edema by 33% to 80% (dose dependent) using a mouse ear model.
Administration of a curcumin dose of 0.4 mcmol showed a 79% inhibition; a 1 mcmol
dose showed a 97% inhibition. The curcumin was applied topically 30 minutes before
0.5 nanomoles of 12-O-tetradecanoylphorbol-13-acetate (TPA). The lower doses seemed
to be more effective (Huang et al, 1988).
g) Curcumin (diferuloyl methane) analogs were screened for anti-inflammatory effects in
carrageenin-treated (injected into the paw) rats and were found to be comparable to
phenylbutazone. The tested agents were given orally 1 hour before the injection of
carrageenin and the paw volume measured 3 hours later. Curcumin, sodium curcumin
(NaC), feruloyl 4-hydroxy cinnamoyl methane (FHM), bis(4-hydroxy cinnamoyl) methane
(BHM) and phenylbutazone were compared. BHM and FHM are natural analogs and were
administered as a 5% suspension orally. The NaC was given orally as a 5% solution.
Control rats were given water (Rao et al, 1982).
1) Phenylbutazone doses ranged from 10 to 100 milligrams/kilogram (mg/kg) (6.2% to
77.1% inhibition of paw edema (IPE) respectively.
2) FHM doses of 3 to 30 mg/kg figures were 27.1% to 75% IPE, with a 60#mg/kg dose
actually decreasing effectiveness to 43.8% IPE.
3) BHM doses of 10 to 30 mg/kg figures were 31.2% to 35.2% IPE, while a 60 mg/kg
dose increased swelling (-4.2%)
4) NaC doses of 3 to 30 mg/kg produced a 2.1% to 64.6% IPE, while the effectiveness
of 60 mg/kg dropped to 29.2%.
4) IN VITRO:
a) Ukonan C, a phagocytosis-activating polysaccharide from turmeric was shown to have
reticuloendothelial system potentiation properties. The phagocytic index of 5
milligrams/kilogram (mg/kg) of ukonan C was greater than that of 50 mg/kg (Gonda et
al, 1993).
b) Curcumin was shown to inhibit 5-lipoxygenase activity in rat peritoneal neutrophils
and to inhibit both the 12-lipoxygenase and cyclooxygenase activity in a human platelet
model. Antioxidative activity was also seen in a cell free peroxidation model (Ammon et
al, 1993).
1) The effective concentration (50%) (EC50) (in the rat peritoneal neutrophil model) of
leukotriene B4 inhibition was 30 micromoles (mcmol) (Ammon et al, 1993).
2) Activity of cyclo-oxygenase was reduced in the human platelet model, with an
EC(50) of 2 mcmol and an effective range of 1 to 10 mcmol. Lipo-oxygenase activity
was inhibited at a higher dose range (10 to 30 mcmol) (Ammon et al, 1993).
3) Curcumin antioxidant activity (EC50) in the cell free model was as low as 1 mcmol
(Ammon et al, 1993).
INFLAMMATORY BOWEL DISEASE
1) OVERVIEW:
DOCUMENTATION: Adult, good
2) SUMMARY:
- Curcumin, together with sulfasalazine or
mesalamine, prevented relapse more effectively
than placebo for patients with ulcerative
15 of 21 9/23/2016 6:15 AM
colitis in a randomized, multicenter,

double-blind, 6-month, placebo-controlled
trial(n=89) (Hanai et al, 2006).
- Curcumin reduced the inflammatory response in

patients with ulcerative proctitis and Crohn's
disease in an open label, pilot study (n=10)
(Holt et al, 2005).
3) ADULT:
a) Curcumin 1 gram (g) orally twice a day for 6 months, together with sulfasalazine or
mesalamine, prevented relapse more effectively than placebo for patients with
ULCERATIVE COLITIS (UC) in a randomized, multicenter, double-blind, placebo-
controlled trial(n=89). Patients who were in remission for UC and not taking steroids
were randomized to either curcumin capsules (n=45) or placebo (n=44) for 6 months.
Patients were also on either sulfasalazine (1 to 3 g/day) or mesalamine (1.5 to 3 g/day).
The patients were followed for an additional 6 months after curcumin was discontinued,
and maintained on sulfasalazine or mesalamine. Outcome measures included the clinical
activity index (CAI) and endoscopic index (EI), which were assessed at baseline, every 2
months (CAI), and at the end of the study. Patients with a CAI of less than or equal to 4
were considered to be in clinical remission, and relapse was defined as greater than or
equal to 5. At 6 months, 2 (4% (95% confidence interval, 0.54% to 15%)) patients on
curcumin relapsed versus 8 (15% (95% CI, 8% to 32%)) with placebo (p=0.049). At 12
months, 10 (22% (95% CI 11% to 37%)) versus 14 (31% (95% CI 18% to 48%))
patients relapsed in the curcumin and placebo groups, respectively, which was not
significant (p=0.433). The mean CAI with curcumin was improved from 1.3 +/- 1.1 at
baseline to 1 +/- 2 at 6 months (p=0.038), compared to an increase from 1 +/- 1.1 to
2.2 +/- 2.3 for placebo (p=0.0003). The EI improved for curcumin patients (baseline,
1.3 +/- 0.8; 6 months, 0.8 +/- 0.6; p=0.0001), but not for placebo patients (baseline,
1.3 +/- 1; 6 months, 1.6 +/- 1.6; p=0.0728). Nine patients receiving curcumin reported
mild adverse effects such as abdominal bloating and nausea (Hanai et al, 2006).
b) Curcumin reduced the inflammatory response in patients with ULCERATIVE
PROCTITIS and CROHN'S DISEASE in an open label, pilot study (n=10). Five patients
with ulcerative proctitis, who were currently using 5-aminosalicylic acid compounds and
corticosteroids, were given capsules of curcumin 550 milligrams (mg) orally twice daily
for 1 month, then 550 mg three times daily for a second month. C-reactive protein
(CRP), erythrocyte sedimentation rate (ESR), sigmoidoscopies, and biopsies were used
to assess degree of inflammation at baseline and 2 months. A global score was used to
assess clinical response using a standard questionnaire; scores ranged from 1 to 3,
where the higher score indicated clinical worsening, for general well-being, number of
daily stools, stool quality, stool blood, abdominal pain, rectal pain urgency, and
endoscopy. Overall, all 5 patients improved at 2 months based on the global score (p
less than 0.02), and the serologic indexes of inflammation, sedimentation rate, and CRP
returned to within normal limits. The major changes occurred in number of stools and
quality, and 4 of 5 patients reduced concomitant medications. Five additional patients
with Crohn's disease were given capsules of curcumin 360 mg orally 3 times a day for 1
month, then 360 mg 4 times a day for 2 months. The Crohn's disease activity index
(CDAI), CRP, and ESR were used to assess efficacy at baseline and 3 months. Four of 5
patients completed the study; one patient discontinued curcumin due to lack of effect.
The CDAI scores decreased by a mean of 55 points; ESR decreased by a mean of 10
mm/hr; and CRP was reduced by a mean of 0.1 mg/dL. Patients were monitored
monthly and reported an improvement in clinical symptoms: more formed stools, less
frequent bowel movements, and less abdominal pain and cramping (Holt et al, 2005).
ULCER
1) OVERVIEW:
16 of 21 9/23/2016 6:15 AM
EFFICACY: Adult, inconclusive

DOCUMENTATION: Adult, fair
2) SUMMARY:
- Turmeric was no better than placebo in treatment
of duodenal ulcers (Van Dau et al, 1998).
- Turmeric reduced drug-induced gastric mucosal

damage in rats (Rafatullah et al, 1990).
- In rabbits, turmeric treatment of dermal sterile

and septic ulcers produced enhanced healing
(Gujral et al, 1953).
3) ADULT:
a) Turmeric was no better than controls in healing DUODENAL ULCERS. The study was a
double-blind, prospective, placebo-controlled, multicenter trial of 118 patients who
received 6 grams/day of tumeric. No H2-receptor antagonists, anticholinergics or other
antiulcer drugs were used during the study or for a week before the study began. The
follow-up endoscopy and x-rays were done after 28 and 56 days. The ulcer healing rate
of placebo was 29% and that of turmeric was 27% (Van Dau et al, 1998).
4) ANIMAL:
a) Turmeric treatment of ulcers produced a 23% increase in accelerated healing of
aseptic ulcers in three rabbits, and a 26% acceleration of septic ulcers on three others.
The DERMAL ULCERS were created by placing a hot disk on the rabbit's skin. A treated
ulcer and control ulcer were placed on the same animal. Septic ulcers were created by
injection of a drop of a 24 hour-old Staphylococcus aureas culture. Turmeric powder was
combined with a small amount of water and the paste applied to the ulcers. When six
rats were used, there was a 24.2% accelerated healing (Gujral et al, 1953).
b) Oral administration of an ethanol extract of turmeric produced significant anti-ulcer
and cytoprotective effects in rats. Turmeric extract given orally at a dose of 500
milligrams/kilogram 30 minutes before the administration of an ulcerogenic agent,
produced a significant reduction in the gastric mucosal damage induced by indomethacin
and reserpine. Duodenal ulcers were reduced as well, but was not statistically significant
(Rafatullah et al, 1990).
COMPARATIVE EFFICACY
CAPSAICIN
1) SUMMARY:
a) Curcumin was more effective than capsaicin in reducing rat paw edema (Reddy &
Lokesh, 1994).
2) INFLAMMATION:
a) In one experimental model, foot pad edema was lower with curcumin-treated rats
than with capsaicin-treated rats. Male Wistar rats were injected in the foot with 2.5
milligrams/kilogram of carrageenan and the amount of foot pad edema measured after
administration (gavage) of curcumin or capsaicin. Doses of 0.5 and 1 milligram/kilogram
(mg/kg) reduced inflammation by 20% and 29% respectively, while doses of 15 to 30
mg/kg of curcumin reduced inflammation by 23% to 36%. Higher curcumin doses
decreased the anti-inflammatory effect (Reddy & Lokesh, 1994).
17 of 21 9/23/2016 6:15 AM
EUGENOL
1) SUMMARY:
a) Eugenol was more effective than curcumin in reducing rat paw edema (Reddy &
Lokesh, 1994).
2) INFLAMMATION:
a) In one experimental model, foot pad edema was lower with eugenol-treated rats than
with curcumin-treated rats. Male Wistar rats were injected in the foot with 2.5
milligrams/kilogram (mg/kg) of carrageenan and the amount of foot pad edema
measured after administration (gavage) of curcumin or eugenol. Doses of 100 to 250
mg/kg of eugenol reduced inflammation 51 to 53%, while doses of 15 to 30 mg/kg of
curcumin reduced inflammation by 23 to 36%. Higher curcumin doses decreased the
effect (Reddy & Lokesh, 1994).
GALLIC ACID
1) SUMMARY:
a) Curcumin was more cytotoxic than gallic acid (Nogaki et al, 1998).
2) APOPTOSIS:
a) The cytotoxic activity of curcumin was significantly higher than that of gallic acid in
an in vitro analysis. The activity of curcumin was not affected by catalase, unlike gallic
acid, whose apoptosis-inducing activity was completely eliminated by catalase (Nogaki et
al, 1998).
HYDROCORTISONE
1) SUMMARY:
a) Curcumin was as effective as hydrocortisone in treating rat paw edema (Ammon &
Wahl, 1991).
2) INFLAMMATION:
a) Ghatak & Basu reported an intraperitoneal (IP) effective dose of 50% (ED50) of 2.1
milligrams/kilogram (mg/kg) for curcumin and 0.36 mg/kg for sodium curcuminate in
carrageenin-induced rat paw edema. Ten mg/kg of IP hydrocortisone inhibited edema by
47.8% (Ammon & Wahl, 1991).
JAVANESE TURMERIC
1) SUMMARY:
a) The bile-stimulating effects of curcumin xanthorrhizae and curcumin domestica are
about equal (Bisset, 1994).
2) CHOLAGOGUE:
a) The effect of turmeric (C domestica) is only slightly less than that of Javanese
turmeric (C xanthorrhizae) (Bisset, 1994).
PHENYLBUTAZONE
1) SUMMARY:
a) In a study of rat paw edema, the effect of curcumin was found to be comparable with
that of phenylbutazone (Rao et al, 1982).
2) INFLAMMATION:
a) Curcumin (diferuloyl methane) analogs were screened for antiinflammatory effects in
carrageenin-treated (injected into the paw) rats and were found to be comparable to
phenylbutazone. The tested agents were given orally 1 hour before the injection of
carrageenin and the paw volume measured 3 hours later. Curcumin, sodium curcumin
(NaC), feruloyl 4-hydroxy cinnamoyl methane (FHM), bis(4-hydroxy cinnamoyl) methane
(BHM), and phenylbutazone were compared. BHM and FHM are natural analogs and
were administered as a 5% suspension orally. The NaC was given orally as a 5%
solution. Control rats were given water (Rao et al, 1982).
18 of 21 9/23/2016 6:15 AM
1) Phenylbutazone doses ranged from 10 to 100 milligrams/kilogram, with 6.2% to

77.1% inhibition of paw edema (IPE) respectively.
2) FHM doses of 3 to 30 mg/kg figures were 27.1% to 75% IPE, with a 60 mg/kg dose
actually decreasing effectiveness to 43.8% IPE.
3) BHM doses of 10 to 30 mg/kg figures were 31.2% to 35.2% IPE, while a 60 mg/kg
dose increased swelling (-4.2%).
4) NaC doses of 3 to 30 mg/kg produced a 2.1% to 64.6% IPE, while the effectiveness
of 60 mg/kg dropped to 29.2%.
POLYUNSATURATED FATTY ACIDS
1) SUMMARY:
a) No additional antiinflammatory effects were noted when curcumin was given to rats
already treated with polyunsaturated fatty acids (Reddy & Lokesh, 1994).
2) INFLAMMATION:
a) Although polyunsaturated fatty acids (PUFA) are known to reduce the inflammatory
response, no additional effect from curcumin (1% weight of diet) was obtained when the
diet of these rats contained n-3 PUFA (10% cod liver oil), 10% peanut oil (n6-PUFA), or
10% coconut oil (medium chain saturated fatty acids) for 10 weeks. After being on the
diet for 10 weeks, curcumin was administered without additional beneficial effects
(Reddy & Lokesh, 1994).
VITAMIN E
1) SUMMARY:
a) Vitamin E was not as effective as curcumin in a rat paw-edema model (Reddy &
Lokesh, 1994).
2) INFLAMMATION:
a) In one experimental model, foot pad edema was less with curcumin-treated rats than
with vitamin-E treated rats. Male Wistar rats were injected in the foot with 2.5
milligrams/kilogram (mg/kg) of carrageenan and the amount of foot pad edema
measured after administration (gavage) of curcumin or vitamin E. Two, 4, and 15
international units of vitamin E reduced inflammation by 24%, 30%, and 18%
respectively, while doses of 15 to 30 mg/kg of curcumin reduced inflammation by 23%
to 36%. Higher curcumin doses decreased the antiinflammatory effect (Reddy & Lokesh,
1994).
REFERENCES
1) Abbott IA: La'au Hawai'i. Traditional Hawaiian Uses of Plants. Bishop Museum Press, Manoa,
Hawaii; 1992.
2) Ammon HP, Safayhi H, Mack T et al: Mechanism of antiinflammatory actions of curcumin and
boswellic acids. J Ethnopharmacol 1993; 38(2-3):113-119.
3) Ammon HPT & Wahl MA: Pharmacology of Curcuma longa. Planta Med 1991; 57(1):1-7.
4) Bierhaus A, Zhang Y, Quehenberger et al: The dietary pigment curcumin reduces endothelial
tissue factor gene expression by inhibitingbinding of AP-1 to the DNA and activaton of NF-kappaB.
Thromb Haemost 1997; 77(4):772-782.
5) Bisset NG (ed): Herbal Drugs and Phytopharmaceuticals: A Handbook for Practice on a Scientific
Basis. CRC Press, Boca Raton, FL; 1994.
6) Blumenthal M, Busse WR, Goldberg A et al: The Complete German Commission E Monographs:
Therapeutic Guide to Herbal Medicines. American Botanical Council and Boston; Integrative Medicine
Communications, Austin, TX; 1998.
7) Brinker F: Herb Contraindications and Drug Interactions. Eclectic Medical Publications, Sandy,
19 of 21 9/23/2016 6:15 AM
OR; 1998.
8) Chen HW & Huang HC: Effect of curcumin on cell cycle progression and apoptosis in vascular
smooth muscle cells. Br J Pharm 1998; 124(6):1029-1040.
9) Chevallier A: The Encyclopedia of Medicinal Plants. DK Publishing Company, New York, NY; 1996.
10) Deshpande UR, Gadre SG, Raste AS et al: Protective effect of turmeric (Curcuma longa L)
extract on carbon tetrachloride-induced liver damage in rats. Indian J Exp Biol 1998; 36(6):573-577.
11) Garg SK: Effect of Curcuma longa (rhizomes) on fertility in experimental animals. Planta Med
1974; 26(3):225-227.
12) Gautam SC, Xu YX, Pindolia KR et al: Nonselective inhibition of proliferation of transformed and
nontransformed cells by the anticancer agent curcumin (diferuloylmethane). Biochem Pharm 1998;
55(8):1333-1337.
13) Goel A, Kunnumakkara AB & Aggarwal BB: Curcumin as "Curecumin": from kitchen to clinic.
Biochem Pharmacol 2008; 75(4):787-809.
14) Gonda R, Tomoda M, Ohara N et al: Arabinogalactan core structure and immunological activity
of ukonan-C, and acidic polysaccharide from the rhizome of Curcuma longa. Biol Pharm Bull 1993;
16(3):235-238.
15) Grieve M: A Modern Herbal. Dover Publications, Inc., New York, NY; 1971.
16) Gujral ML, Chowdhury NK & Saxena PN: The effect of certain indigenous remedies on the
healing of wounds and ulcers. J Indian Med Assoc 1953; 23:273-276.
17) Hanai H, Iida T, Takeuchi K et al: Curcumin maintenance therapy for ulcerative colitis:
randomized, multicenter, double-blind, placebo-controlled trial. Clin Gastroenterol Hepatol 2006;
4(12):1502-1506.
18) Hellinger JA, Cohen CJ, Dugan ME et al: Phase III randomized, open-label study of oral
curcumin safety, and antiviral effects on HIV-RT PCR in HIV positive individuals. 3rd Conf Retro and
Opportun Infect 1996; Jan:78.
19) Holt PR, Katz S & Kirshoff R: Curcumin therapy in inflammatory bowel disease: a pilot study.
Dig Dis Sci 2005; 50(11):2191-2193.
20) Huang MT, Lou YR, Ma W et al: Inhibitory effects of dietary curcumin on fore-stomach,
duodenal, and colon carcinogenesis in mice. Cancer Res 1994; 54(22):5841-5847.
21) Huang MT, Smart RC, Wong CQ et al: Inhibitory effect of curcumin, chlorogenic acid, caffeic
acid, ferulic acid on tumor promotion in mouse skin by 12-O-tetradecanoylphorbol-13-acetate.
Cancer Res 1988; 48(21):5941-5946.
22) Huang MT, Wang ZY, Georgiadis CA et al: Inhibitory effects of curcumin on tumor initiation by
benzo(alpha)pyrene and 7,12-dimethylbenz(alpha)anthracene. Carcinogenesis 1992;
13(11):2183-2186.
23) Kiec-Swierczynska M & Krecisz B: Occupational allergic contact dermatitis due to curcumin food
colour in a pasta factory worker. Contact Dermatitis 1998; 39(1):30-31.
24) Kunchandy E & Rao MNA: Oxygen radical scavenging activity of curcumin. Int J Pharmaceutics
1990; 58:237-240.
25) Lal B, Kapoor AK, Asthana OP et al: Efficacy of curcumin in the management of chronic anterior
uveitis. Phytother Res 1999; 13:318-322.
26) Mazumder A, Raghavan K, Weinstein J et al: Inhibition of human immunodeficiency virus type-1
integrase by curcumin. Biochem Pharmacol 1995; 49(8):1165-1170.
27) McGuffin M, Hobbs C, Upton R et al: Botanical Safety Handbook. CRC Press, Boca Raton, FL;
1997.
28) Mukhopadhyay A, Basu N, Ghatak N et al: Anti-inflammatory and irritant activities of curcumin
analogues in rats. Agents Actions 1982; 12(4):508-515.
20 of 21 9/23/2016 6:15 AM
29) Nagabhushan M & Bhide SV: Curcumin as an inhibitor of cancer. J Am Coll Nutr 1992;
11(2):192-198.
30) Nogaki A, Satoh K, Iwasaka K et al: Radial intensity and cytotoxic activity of curcumin and gallic
acid. Anticancer Res 1998; 18(5A):3487-3491.
31) Osawa T, Sugiyama Y, Inayoshi M et al: Antioxidative activity of tetrahydrocurcuminoids. Biosci
Biotechnol Biochem 1995; 59(9):1609-1612.
32) Rafatullah M, Tariq M, Al-Yahya MA et al: Evaluation of turmeric (Curcuma longa) for gastric
and duodenal antiulcer activity in rats. J Ethnopharmacol 1990; 29(1):25-34.
33) Rajakumar DV & Rao MN: Antioxidant properties of dehydrozingerone and curcumin in rat brain
homogenates. Mol Cell Biochem 1994; 140(1):73-79.
34) Rao C, Rivenson A, Simi B et al: Chemoprevention of colon carcinogenesis by dietary curcumin,
a naturally occurring plant phenolic compound. Cancer Res 1995; 55(2):259-266.
35) Rao TS, Basu N & Siddiqui HH: Anti-inflammatory activity of curcumin analogues. Indian J Med
Res 1982; 75(Apr):574-578.
36) Reddy ACP & Lokesh BR: Studies on anti-inflammatory activity of spice principles and dietary
n-3 polyunsaturated fatty acids on carrageenan-induced inflammation in rats. Ann Nutr Metab 1994;
38(6):349-358.
37) Reddy S & Aggarwal BB: Curcumin is a non-competitive and selective inhibitor of phosphorylase
kinase. FEBS Lett 1994; 341(1):19-22.
38) Salimath BP, Sundaresh CS, Srinivas L et al: Dietary components inhibit lipid peroxidation in
erythrocyte membrane. Nutr Res 1986; 6:1171-1178.
39) Sikora E, Bielak-Zmijewska A, Piwocka K et al: Inhibition of proliferation and apoptosis of
human and rat T lymphocytes by curcumin, a curry pigment. Biochem Pharm 1997; 54(8):899-907.
40) Singh S & Aggarwal BB: Activation of transcription factor NF-kappaB is suppressed by curcumin.
J Biol Chem 1995; 270(42):24995-25000.
41) Sreejayan & Rao MNA: Curcuminoids as potent inhibitors of lipid peroxidation. J Pharm
Pharmacol 1994; 46(12):1013-1016.
42) Srivastava KC, Bordia A & Verma SK: Curcumin, a major component of food spice tumeric
(Curcuma longa) inhibits aggregation and alters eicosanoid metabolism in human blood platelets.
Prostgland Leukotr Ess Fatty Acids 1995; 52:223-227.
43) Srivastava R, Dikshit M, Srimal RC et al: Anti-thrombotic effect of curcumin. Thromb Res 1985;
40(3):413-417.
44) Srivastava R, Puri V, Srimal RC et al: Effect of curcumin on platelet aggregation and vascular
prostacyclin synthesis. Arnzmittelforschung 1986; 36(4):715-717.
45) Stoner GD & Muktar H: Polyphenols as cancer chemopreventive agents. J Cell Biochem Suppl
1995; 22:169-180.
46) Tanaka T, Makita H, Ohnishi M et al: Chemoprevention of 4-nitroquinoline 1-oxide-induced oral
carcinogenesis by dietary curcumin and hesperidin: comparison with the protective effect of
beta-carotene. Cancer Res 1994; 54(17):4653-4659.
47) Van Dau N, Ham NN, Khac DH et al: The effects of a traditional drug, turmeric (Curcuma
longa), and placebo on the healing of duodenal ulcers. Phytomedicine 1998; 5:29-34.
48) Werbach M & Murray M: Botanical Influences on Illness: A Sourcebook of Clinical Research.
Third Line Press, Tarzana, CA; 1994.
49) Zava DT, Dollbaum CM & Blen M: Estrogen and progestin bioactivity of foods, herbs, and
spices. Proc Soc Exp Biol Med 1998; 217(3):369-378.
©2016 Truven Health Analytics Inc.
21 of 21 9/23/2016 6:15 AM

Turmeric: Altmeddex® Evaluations

Transféré par

Informations du document

Titre original

Copyright

Formats disponibles

Partager ce document

Partager ou intégrer le document

Options de partage

Avez-vous trouvé ce document utile ?

Ce contenu est-il inapproprié ?

Droits d'auteur :

Formats disponibles

Turmeric: Altmeddex® Evaluations

Transféré par

Droits d'auteur :

Formats disponibles

Alternative Medicine detail - MICROMEDEX® http://remote-lib.ui.ac.id:2232/micromedex2/librarian/CS/45E0DE/ND_...

and the dosage form chosen by the manufacturer. Standardization to single

A) Hypersensitivity to turmeric or curcumin

A) Use with caution during excessive menstruation (McGuffin et al, 1997)

a) In a platelet aggregation study of blood samples obtained from healthy

2) Adverse Effect: increased risk of bleeding

d) Curcumin inhibited lipid peroxidation measured in rat brain homogenates, and

per mouse. One week later, administration of the tumor promoter

- Curcumin had no effect on HIV-RNA copy number

- Curcumin's anti-inflammatory effects may be due

47.8% (Ammon & Wahl, 1991).

colitis in a randomized, multicenter,

- Curcumin reduced the inflammatory response in

EFFICACY: Adult, inconclusive

- Turmeric reduced drug-induced gastric mucosal

- In rabbits, turmeric treatment of dermal sterile

1) Phenylbutazone doses ranged from 10 to 100 milligrams/kilogram, with 6.2% to

©2016 Truven Health Analytics Inc.

Vous aimerez peut-être aussi