Curcuminoid supplement health benefit and side effects, dosage and safety
Commercially available curcumin supplements contain a mixture of related polyphenols, collectively referred to as curcuminoids. These include the primary component curcumin along with its derivatives demethoxycurcumin and bisdemethoxycurcumin. Curcumin, a member of the curcuminoid family of compounds, is a yellow colored phenolic pigment obtained from the powdered rhizome of Curcuma longa Linn.
Curcuminoid benefits
Curcuminoids have numerous biological activities, including inhibition of cancer
related cell proliferation and reduction of amyloid plaque formation associated
with Alzheimer disease.
Curcuminoids, lead and
memory
Q. Are you familiar with the research concerning
curcuminoids to remove lead from the brain? There has been a small amount of
research. I am writing an article on lead poisoning. To date, brain damage
caused by lead ingestion has been permanent, so this would be very hopeful.
A. There has been an interesting rodent study with curcuminoids and
lead induced memory loss.
Curcuminoids, curcumin, and demethoxycurcumin reduce lead-induced memory
deficits in male Wistar rats.
J Agric Food Chem. 2007 Feb. Dairam A, Limson JL, Watkins GM, Antunes
E, Daya S. Faculty of Pharmacy, Department of Biochemistry, Microbiology, and
Biotechnology, Rhodes University, Grahamstown 6140, South Africa.
This study investigated the neuroprotective effects of curcumin and the
curcuminoids against lead-induced neurotoxicity. The results show that lead
significantly increases lipid peroxidation and reduces the viability of primary
hippocampal neurons in culture. This lead-induced toxicity was significantly
curtailed by the co-incubation of the neurons with the curcuminoids. In a whole
animal experiment, rats were trained in a water maze and thereafter dosed with
lead and/or curcuminoids, demethoxycurcumin, or bisdemethoxycurcumin for 5 days.
Animals treated with curcuminoids and demethoxycurcumin but not
bisdemethoxycurcumin had more glutathione and less oxidized proteins in the
hippocampus than those treated with lead alone. These animals also had faster
escape latencies when compared to the Pb-treated animals indicating that CURC-
and DMC-treated animals retain the spatial reference memory. The findings of
this study indicate that curcuminoids, a well-established dietary antioxidant,
is capable of playing a major role against heavy metal-induced neurotoxicity and
has neuroprotective properties.
Beta Thalassemia
Improvement in oxidative stress and antioxidant parameters in beta-thalassemia/Hb
E patients treated with curcuminoids.
Clin Biochem. 2010 Mar; Kalpravidh RW, Siritanaratkul N, Insain P,
Charoensakdi R, Panichkul N, Hatairaktham S, Srichairatanakool S, Phisalaphong
C, Rachmilewitz E, Fucharoen S. Department of Biochemistry, Faculty of Medicine
Siriraj Hospital, Mahidol University, Bangkok, Thailand.
To evaluate the hematological profile, oxidative stress, and antioxidant
parameters in beta-thalassemia / Hb E patients treated with curcuminoids for 12
months. Twenty-one beta-thalassemia/Hb E patients were given 2 capsules of 250
mg each of curcuminoids (a total of 500 mg) daily for 12 months. Blood was
collected every 2 months during treatment and 3 months after withdrawal and was
determined for complete blood count, malonyldialdehyde (MDA), superoxide
dismutase (SOD), glutathione peroxidase (GSH-Px), reduced glutathione (GSH) in
red blood cells (RBC), and non-transferrin bound iron (NTBI) in serum. The
increased oxidative stress in beta-thalassemia/Hb E patients was shown by higher
levels of MDA, SOD, GSH-Px in RBC, serum NTBI, and lower level of RBC GSH.
Curcuminoids administration resulted in improvement of all the measured
parameters as long as they were administered. After 3 months withdrawal of
treatment, all parameters returned close to baseline levels. Curcuminoids may be
used to ameliorate oxidative damage in patients with beta-thalassemia / Hb E
disease.
Cytochrome P450
metabolism
Q. Can you please tell me if curcuminoids inhibit
the action of cytochrome P450 3A4, 3A5 ? I am considering taking curcumin and
currently take verapamil which is metabolized by these enzymes. I need to know
only if curcumin and curcuminoids affect the action of these enzymes.
A. It appears that curcuminoids do inhibit the action of cytochrome
P450.
Curcuminoids inhibit multiple human cytochromes
P450, UDP-glucuronosyltransferase, and sulfotransferase enzymes, whereas
piperine is a relatively selective CYP3A4 inhibitor.
Drug Metab Dispos. 2008 August. Volak LP, Ghirmai S, Cashman JR, Court
MH. Department of Pharmacology and Experimental Therapeutics, Tufts University
School of Medicine, Boston, Massachusetts 02111, USA.
Curcuminoid extract and piperine are being evaluated for beneficial effects in
Alzheimer's disease, among other intractable disorders. Consequently, we studied
the potential for herb-drug interactions involving cytochrome P450,
UDP-glucuronosyltransferase (UGT), and sulfotransferase (SULT) enzymes. The
curcuminoid extract inhibited SULT > CYP2C19 > CYP2B6 > UGT > CYP2C9 > CYP3A
activities with IC(50), whereas CYP2D6, CYP1A2, and CYP2E1 activities were less
affected (IC(50). Inhibition of CYP3A activity by curcuminoid extract was
consistent, whereas inhibition of both CYP2C9 and CYP2C19 activities were
consistent with mixed competitive-noncompetitive inhibition. Piperine was a
relatively selective noncompetitive inhibitor of CYP3A with less effect on other
enzymes evaluated. Curcuminoid extract and piperine inhibited recombinant CYP3A4
much more potently than CYP3A5. Pure synthetic curcuminoids (curcumin,
demethoxycurcumin, and bisdemethoxycurcumin) were also evaluated for their
effects on CYP3A, CYP2C9, UGT, and SULT activities. All three curcuminoids had
similar effects on CYP3A, UGT, and SULT activity, but demethoxycurcumin was more
active against CYP2C9 than either curcumin or bisdemethoxycurcumin. Based on
these data and expected tissue concentrations of inhibitors, we predict that a
p.o. administered curcuminoid / piperine combination is most likely to inhibit
CYP3A, CYP2C9, UGT, and SULT metabolism within the intestinal mucosa.
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