[The message below is from Robert Rolen. It was within another unrelated post
and needed to be separated to here. --Paul]

I also thought you might be interested in something I ran across that
might allow you to lower your aspirin dose.

[I and Kitty take aspirin for many more reasons than its ability to inhibit
inflammatory and coagulative eicosanoid production. One of those major reasons
is the antiglycative properties of aspirin, with respect to which more is
better. we only keep our dose as low as it is, distributed and with food, in
order to minimize the possibility of negative intestinal effects and too much
anticoagulation. --Paul]


With the recent COX-2 inhibitor scandals, many people are starting to
add COX-1 inhibitors to their cocktails in order to keep thromboxane
TXA2/TXB2 down. COX-2 inhibitors seem to inhibit prostacyclin PGI2
but not TXA2/TXB2 and COX-1 inhibitors vice versa.

[While both COX-1 and COX-2 inhibitors inhibit PGI2, TXA2 and TXB2, Robert is
correct that COX-2 is largely responsible for PGI2 synthesis (particularly in
endothelial cells) while COX-1 is largely responsible for TXA2 and TXB2
synthesis (particularly in platelets). Therefore, with respect to their
cardiovascular functions, COX-2 inhibitors mainly inhibit PGI2 while COX-1
inhibitors mainly inhibit TXA2 and TXB2.

Here is a good full text article on COX inhibititors:
http://www.asheducationbook.org/cgi/content/full/2005/1/445
It has a picture illustrating prostaglandin synthesis in the body:
http://www.asheducationbook.org/cgi/content/full/2005/1/445/F1
Also worth mentioning is that all selective COX-2 inhibitors also inhibit COX-1
to some degree and vice versa. This is because the COX-1 and COX-2 enzymes are
so structurally similar that it is hard to design an inhibitor that inhibits one
but not the other. -°Olafur]

[An important point to note is that all these "2"-type prostaglandins (also
called more generally prostanoids or still more generally eicosanoids) are made
from arachidonic acid (the end product of omega-6 metabolism. The "1" and "3"
series made from GLA and EPA, respectively (some of the same abbreviations as
above but ending instead with either 1 or 3), are less inflammatory. In
addition, the presence of GLA, EPA and their precursors, inhibits the generation
of arachidonic acid from its precursors (one of which is GLA) and thus reduces
the substrate available from which the COX enzymes make the pro-inflammatory and
pro-cloting prostanoids. --Paul]


PGI2 seems to be
counteract the clotting and vasoconstrictive effects of TXA2/TXB2,
which seems to indicate it might be a good idea to shoot for a low
TXB2/PGI2 ratio if you can.

[It is true that TXA2 and TXB2 have vasoconstrictive and platelet aggregation
effects and that PGI2 which is a vasodilator and a platelet anti-aggregator can
counteract some of the effects of TXA2 and TXB2. So it seems like a good idea
to have a low ratio of TXB2/PGI2 at least in regard to platelet function and
vasodilation. -°Olafur]


Curcumin doesn't seem to inhibit PGI2, but it does inhibit the other
bad prostaglandins like TXA2. Aspirin seems to inhibit both TXA2 and
PGI2 at even low doses like 80mg and especially at higher doses.

You seem to be getting a good amount of curcumin in your bloodstream
(especially with the piperine factored in). Maybe you should cut back
on the aspirin a bit.

[Aspirin inhibits both COX-1 and COX-2 and thus inhibits TXA2, TXB2 as well as
PGI2. And while traditional NSAIDs cause a reversible inhibition of COXs
aspirin irreversibly suppresses COXs, the result is that even very low doses of
aspirin largely inhibit TXA2, TXB2 and PGI2 particularly if taken on a regular
basis (PMID: 2126726, PMID: 1891022, PMID: 9923572). And as the abstract below
states TXA2 is formed in platelets while PGI2 is formed in endothelial cells.
Because platelets do not synthesize new protein [just like RBCs they do not
contain a nucleus and thus no nuclear DNA] while endothelial cells do it should
be possible to shift the balance between TXA2 and PGI2 in favor of the latter by
taking the appropriate dose of aspirin.

Scand J Clin Lab Invest Suppl. 1990;201:103-8.
Acetylsalicylic acid and the balance between prostacyclin and thromboxane A2.
Viinikka L.
Children's Hospital, University of Helsinki, Finland.

Arachidonic acid is metabolized in endothelial cells to antiaggregatory,
vasodilatory prostacyclin (PGI2), and in platelets to aggregatory,
vasoconstrictory thromboxane A2 (TxA2). The balance of these two prostanoids is
supposed to be involved with thrombogenesis and atherogenesis. Acetylsalicylic
acid (ASA) inhibits irreversibly the key enzyme of the synthesis of these
prostanoids, i.e. cyclo-oxygenase. Platelets do not synthetize new protein, but
endothelial cells do. Because of this, and certain pharmacokinetic
characteristics of ASA, it should be possible to shift the balance between PGI2
and TxA2 to the dominance of the former with the proper dose of this drug.
Altogether more than 50,000 subjects have volunteered for studies on the effect
of ASA in the primary or secondary prevention of myocardial infarction or
ischemic stroke. The results show that it is possible to reduce vascular attacks
by ASA. Furthermore, ASA has also found to prevent pre-eclampsia. Conclusions on
the effect of ASA on the PGI2/TxA2-balance are hampered by uncertainties
concerning the measurement PGI2 and TxA2 productions in vivo. It is, however,
evident that the doses of ASA used in most trials have been high enough to
inhibit partly also the production of PGI2. Whether smaller doses or less
frequent administration would be more efficient, remains to be studied.

Publication Types: Review
PMID: 2244178

When taking aspirin on a regular basis, endothelial cells can synthesize new
PGI2 in an attempt to bring levels of PGI2 back up while platelets which cannot
synthesize new protein cannot synthesize new TXA2. It follows logically from
this that low doses of aspirin taken regularly are likely to cause a more
favorable TXA2/PGI2 ratio. However even large doses of aspirin seem to have
favorable effects on this ratio. In PMID: 2126726 f.ex. aspirin in doses from
50-1300mg daily (ingested for one week) fully inhibited TXB2 and consequently
platelet function. So this certainly does not warrant decreasing their dose of
aspirin particularly since Paul and Kitty take plenty of supplements that
inhibit platelet function and increase vasodilation. -°Olafur]

[And even with our inhibition of platelet function and our always low levels of
platelets (particularly mine), we don't have any clotting problems whenever
either of us get cuts, scratches or prick our fingers for blood glucose
measurement. --Paul]


Biochem Pharmacol. 1999 Oct 1;58(7):1167-72.
Inhibitory effect of curcumin, a food spice from turmeric, on
platelet-activating factor- and arachidonic acid-mediated platelet
aggregation through inhibition of thromboxane formation and Ca2+
signaling.

Curcumin, a dietary spice from turmeric, is known to be
anti-inflammatory, anticarcinogenic, and antithrombotic. Here, we
studied the mechanism of the antiplatelet action of curcumin. We show
that curcumin inhibited platelet aggregation mediated by the platelet
agonists epinephrine (200 microM), ADP (4 microM), platelet-activating
factor (PAF; 800 nM), collagen (20 microg/mL), and arachidonic acid
(AA: 0.75 mM). Curcumin preferentially inhibited PAF- and AA-induced
aggregation (IC50; 25-20 microM), whereas much higher concentrations
of curcumin were required to inhibit aggregation induced by other
platelet agonists. Pretreatment of platelets with curcumin resulted in
inhibition of platelet aggregation induced by calcium ionophore
A-23187 (IC50; 100 microM), but curcumin up to 250 microM had no
inhibitory effect on aggregation induced by the protein kinase C (PKC)
activator phorbol myrsitate acetate (1 microM). Curcumin (100 microM)
inhibited the A-23187-induced mobilization of intracellular Ca2+ as
determined by using fura-2 acetoxymethyl ester. Curcumin also
inhibited the formation of thromboxane A2 (TXA2) by platelets (IC50;
70 microM). These results suggest that the curcumin-mediated
preferential inhibition of PAF- and AA-induced platelet aggregation
involves inhibitory effects on TXA2 synthesis and Ca2+ signaling, but
without the involvement of PKC.
PMID: 10484074


Prostaglandins Leukot Essent Fatty Acids. 1995 Apr;52(4):223-7.
Curcumin, a major component of food spice turmeric (Curcuma longa)
inhibits aggregation and alters eicosanoid metabolism in human blood
platelets.

In traditional medicine, Ayurveda, several spices and herbs are
held to possess medicinal properties. Earlier we have reported that
extracts from several spices, including turmeric, inhibit platelet
aggregation and modulate eicosanoid biosynthesis. Due to their
eicosanoid-modulating property, it was suggested that the spices may
serve to provide clues to drugs directed to arachidonic acid (AA)
pathway enzymes as pharmacological targets. Curcumin, a major
component of turmeric, inhibited platelet aggregation induced by
arachidonate, adrenaline and collagen. This compound inhibited
thromboxane B2 (TXB2) production from exogenous [14C] arachidonate in
washed platelets with a concomitant increase in the formation of
12-lipoxygenase products. Moreover, curcumin inhibited the
incorporation of [14C]AA into platelet phospholipids and inhibited the
deacylation of AA-labelled phospholipids (liberation of free AA) on
stimulation with calcium ionophore A23187. Curcumin's
anti-inflammatory property may, in part, be explained by its effects
on eicosanoid biosynthesis.
PMID: 7784468


Cancer Res. 1995 Jan 15;55(2):259-66.
Chemoprevention of colon carcinogenesis by dietary curcumin, a
naturally occurring plant phenolic compound.

Human epidemiological and laboratory animal model studies have
suggested that nonsteroidal antiinflammatory drugs reduce the risk of
development of colon cancer and that the inhibition of colon
carcinogenesis is mediated through the alteration in cyclooxygenase
metabolism of arachidonic acid. Curcumin, which is a naturally
occurring compound, is present in turmeric, possesses both
antiinflammatory and antioxidant properties, and has been tested for
its chemopreventive properties in skin and forestomach carcinogenesis.
The present study was designed to investigate the chemopreventive
action of dietary curcumin on azoxymethane-induced colon
carcinogenesis and also the modulating effect of this agent on the
colonic mucosal and tumor phospholipase A2, phospholipase C gamma 1,
lipoxygenase, and cyclooxygenase activities in male F344 rats. At 5
weeks of age, groups of animals were fed the control (modified
AIN-76A) diet or a diet containing 2000 ppm of curcumin. At 7 weeks of
age, all animals, except those in the vehicle (normal saline)-treated
groups, were given two weekly s.c. injections of azoxymethane at a
dose rate of 15 mg/kg body weight. All groups were continued on their
respective dietary regimen until the termination of the experiment at
52 weeks after the carcinogen treatment. Colonic tumors were evaluated
histopathologically. Colonic mucosa and tumors were analyzed for
phospholipase A2, phospholipase C gamma 1, ex vivo prostaglandin (PG)
E2, cyclooxygenase, and lipoxygenase activities. The results indicate
that dietary administration of curcumin significantly inhibited
incidence of colon adenocarcinomas (P < 0.004) and the multiplicity of
invasive (P < 0.015), noninvasive (P < 0.01), and total (invasive plus
noninvasive) adenocarcinomas (P < 0.001). Dietary curcumin also
significantly suppressed the colon tumor volume by > 57% compared to
the control diet. Animals fed the curcumin diet showed decreased
activities of colonic mucosal and tumor phospholipase A2 (50%) and
phospholipase C gamma 1 (40%) and levels of PGE2 (> 38%). The
formation of prostaglandins such as PGE2, PGF2 alpha, PGD2, 6-keto
PGF1 alpha, and thromboxane B2 through the cyclooxygenase system and
production of 5(S)-, 8(S)-, 12(S)-, and 15(S)-hydroxyeicosatetraenoic
acids via the lipoxygenase pathway from arachidonic acid were reduced
in colonic mucosa and tumors of animals fed the curcumin diet as
compared to control diet. Although the precise mechanism by which
curcumin inhibits colon tumorigenesis remains to be elucidated, it is
likely that the chemopreventive action, at least in part, may be
related to the modulation of arachidonic acid metabolism.
PMID: 7812955


Carcinogenesis. 1993 Nov;14(11):2219-25.
Inhibition by dietary curcumin of azoxymethane-induced ornithine
decarboxylase, tyrosine protein kinase, arachidonic acid metabolism
and aberrant crypt foci formation in the rat colon.

The present study was designed to investigate the modulatory role
of dietary curcumin on (i) azoxymethane (AOM)-induced ornithine
decarboxylase (ODC), tyrosine protein kinase (TPK) and arachidonic
acid metabolism in liver and colonic mucosa of male F344 rats, (ii) in
vitro arachidonic acid metabolism in the liver and colonic mucosa and
(iii) AOM-induced aberrant crypt foci (ACF) formation in the colon of
F344 rats. At 5 weeks of age groups of animals were fed one of the
experimental diets containing 0 or 2000 p.p.m. curcumin. Two weeks
later all the animals except the vehicle-treated groups were given
s.c. injections of AOM, 15 mg/kg body wt, once weekly for 2 weeks. The
animals intended for biochemical study were killed 5 days later and
the colonic mucosa and liver were analyzed for ODC, TPK, lipoxygenase
and cyclo-oxygenase metabolites. The animals intended for ACF study
were killed 9 weeks later and analyzed for ACF in the colon. The
results indicated that in saline-treated animals dietary curcumin
significantly inhibited the ODC (P < 0.001) and TPK (P < 0.05)
activities in the liver and colonic mucosa. Dietary curcumin
significantly decreased the levels of AOM-induced ODC activity in the
liver and colon (P < 0.0001) and TPK activity in the liver and colon
(P < 0.01-0.0001) and the formation of 5(S)-, 8(S)-, 12(S)- and
15(S)-hydroxyeicosatetraenoic acids (HETEs) in the liver and colon (P
< 0.0001). Also, curcumin suppressed AOM-induced prostaglandin (PG)
and thromboxane (Tx) formation in the liver (PGE2, PGF2 alpha, PGD2,
6-keto-PGF1 alpha and TxB2 to 40, 59, 55, 53 and 39% respectively) and
in the colon (PGE2 and PGF2 alpha to 39 and 41% respectively).
Further, dietary curcumin reduced the in vitro formation of HETEs, PGs
and Tx in a dose-dependent manner. AOM-induced colonic ACF were
significantly (P < 0.001) inhibited in the animals fed the curcumin
diet. The results of the present study indicate that curcumin, present
in turmeric, inhibits AOM-induced colonic preneoplastic lesions and
other cellular events relevant to colon carcinogenesis.
PMID: 8242846


J Cardiovasc Pharmacol. 1980 Jul-Aug;2(4):387-97.
Effect of oral aspirin dose on platelet aggregation and vascular
prostacyclin (PGI2) synthesis in humans and rabbits.

Large doses of oral aspirin inhibit platelet aggregation and
vascular synthesis of the antiaggregatory vasodilator prostaglandin I2
(PGI2) by irreversibly acetylating the cyclooxygenase enzyme. In order
to determine if one can achieve selective inactivation of platelet
cyclooxygenase using oral doses of aspirin, we studied human and
rabbit platelet aggregation and rabbit aortic synthesis of PGI2 before
and 3 hr after various doses of aspirin. In rabbits, lower doses of
aspirin produced a major inhibition of platelet aggregation and a
minor inhibition of PGI2 synthesis, while higher doses of aspirin
inhibited both platelet aggregation and vascular PGI2 synthesis. In
humans, we found that a dose equivalent to approximately 1/4 of one
300 mg aspirin tablet consistently produced a major inhibition of
cyclooxygenase-dependent platelet aggregation in a pattern similar to
the inhibition of rabbit platelet aggregation where the majority of
rabbit PGI2 synthetic capacity was not inhibited. In another rabbit
study, we found that it takes the vasculature over 24 hr to return to
control PGI2 synthetic capacity following a single, high dose of oral
aspirin. In conclusion, we speculate that approximately 1/4 of an
aspirin tablet, which inhibits a major portion of
cyclooxygenase-dependent human platelet aggregation, may not inhibit a
major portion of vascular cyclooxygenase-dependent PGI2 synthesis and
may be more efficacious as an antithrombotic agent in man than are
higher doses of aspirin.
PMID: 6156337

[This abstract states basically what I said above that low doses of aspirin
would have more favorible effects on platelet aggregation than high doses.
-°Olafur]


Arzneimittelforschung. 1986 Apr;36(4):715-7.
Effect of curcumin on platelet aggregation and vascular
prostacyclin synthesis.
Srivastava R, Puri V, Srimal RC, Dhawan BN.

In vitro and ex vivo effects of
1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione
(diferuloylmethane, curcumin) and acetylsalicylic acid (ASA) on the
synthesis of prostacyclin (PGI2) and on platelet aggregation has been
studied in rat. Both drugs inhibited adenosine diphosphate (ADP)-,
epinephrine (adrenaline)- and collagen-induced platelet aggregation in
monkey plasma. Pretreatment with ASA (25-100 mg/kg), but not curcumin
(100-300 mg/kg), inhibited PGI2 synthesis in rat aorta. In the in
vitro system, too, curcumin caused a slight increase in the synthesis
of PGI2, while ASA inhibited it. Curcumin may, therefore, be
preferable in patients prone to vascular thrombosis and requiring
antiarthritic therapy.
PMID: 3521617

http://www.bioperine.com/BioWithCur.htm looks like 2g of curcumin
with 20mg bioperine can get you up into the 0.2microg/ml range

[This is not a peer reviewed source of information and therefore cannot be
considered as any kind of evidence. The abstract which the site is referring to
is below. It does not state the concentration of curcumin reached after
supplementation and since the full text article is not freely available the
numbers given on this site cannot be verified. However the abstract does state
that the increase in bioavailability was 2000% when 20mg of piperine was
administered along with 2g of curcumin in humans.

Planta Med. 1998 May;64(4):353-6.
Influence of piperine on the pharmacokinetics of curcumin in animals
and human volunteers.
Shoba G, Joy D, Joseph T, Majeed M, Rajendran R, Srinivas PS.
Department of Pharmacology, St. John's Medical College, Bangalore, India.

The medicinal properties of curcumin obtained from Curcuma longa L. cannot be
utilised because of poor bioavailability due to its rapid metabolism in the
liver and intestinal wall. In this study, the effect of combining piperine, a
known inhibitor of hepatic and intestinal glucuronidation, was evaluated on the
bioavailability of curcumin in rats and healthy human volunteers. When curcumin
was given alone, in the dose 2 g/kg to rats, moderate serum concentrations were
achieved over a period of 4 h. Concomitant administration of piperine 20 mg/kg
increased the serum concentration of curcumin for a short period of 1-2 h post
drug. Time to maximum was significantly increased (P < 0.02) while elimination
half life and clearance significantly decreased (P < 0.02), and the
bioavailability was increased by 154%. On the other hand in humans after a dose
of 2 g curcumin alone, serum levels were either undetectable or very low.
Concomitant administration of piperine 20 mg produced much higher concentrations
from 0.25 to 1 h post drug (P < 0.01 at 0.25 and 0.5 h; P < 0.001 at 1 h), the
increase in bioavailability was 2000%. The study shows that in the dosages used,
piperine enhances the serum concentration, extent of absorption and
bioavailability of curcumin in both rats and humans with no adverse effects.

Publication Types: Clinical Trial
PMID: 9619120

-°Olafur]


which is about equal to http://en.wikipedia.org/wiki/Curcumin Molar mass 368.38
g/mol >>>> 0.2mg/L = 0.54microM, so maybe you're not getting high enough to
get to the 70microM IC50.

[Again this is not a peer reviewed source of information. Since anyone can
write whatever he wants on Wikipedia.org there is no way to make sure the
information contained there is correct. However the molar mass you gave for
curcumin is correct and so are your computations; the only problem is that the
0,2mg/L figure cannot be verified. -°Olafur]

[A major reason why the information at the bioperine.com site is useless without
access to the full paper text, is that the dosage of 2g/kg for rats is not
identified with respect to whether it was by weight of rat or by weight of food.
Clearly, the information at the site is meant for the promotion of the value of
bioperine rather than for any value toward scientific dosage computation. Thus,
although Robert's calculations are correct, the end effect is another example of
the old adage "garbage in, garbage out". --Paul]


http://www.findarticles.com/p/articles/mi_m0FDN/is_1_7/ai_83582834
Phase I clinical trial of curcumin, a chemopreventive agent, in
patients with high-risk or pre-malignant lesions - Abstracts
Alternative Medicine Review, Feb, 2002
Curcumin (diferuloylmethane), a yellow substance from the root of the
plant Curcuma longa Linn., has been demonstrated to inhibit
carcinogenesis of murine skin, stomach, intestine and liver. However,
the toxicology, pharmacokinetics and biologically effective dose of
curcumin in humans have not been reported. This prospective phase-I
study evaluated these issues of curcumin in patients with one of the
following five high-risk conditions: 1) recently resected urinary
bladder cancer; 2) arsenic Bowen's disease of the skin; 3) uterine
cervical intraepithelial neoplasm (CIN); 4) oral leucoplakia; and 5)
intestinal metaplasia of the stomach. Curcumin was taken orally for 3
months. Biopsy of the lesion sites was done immediately before and 3
months after starting curcumin treament. The starting dose was 500 mg/
day. If no toxicity > or = grade II was noted in at least 3 successive
patients, the dose was then escalated to another level in the order of
1,000, 2,000, 4,000, 8,000, and 12,000 mg/day. The concentration of
curcumin in serum and urine was determined by high pressure liquid
chromatography (HPLC). A total of 25 patients were enrolled in this
study. There was no treatment-related toxicity up to 8,000 mg/day.
Beyond 8,000 mg/day, the bulky volume of the drug was unacceptable to
the patients. The serum concentration of curcumin usually peaked at 1
to 2 hours after oral intake of crucumin and gradually declined within
12 hours. The average peak serum concentrations after taking 4,000 mg,
6,000 mg and 8,000 mg of curcumin were 0.51 +/- 0.11 microM, 0.63 +/-
0.06 microM and 1.77 +/- 1.87 microM, respectively. Urinary excretion
of curcumin was undetectable. One of 4 patients with CIN and 1 of 7
patients with oral leucoplakia proceeded to develop frank malignancies
in spite of curcumin treatment. In contrast, histologic improvement of
precancerous lesions was seen in 1 out of 2 patients with recently
resected bladder cancer, 2 out of 7 patients of oral leucoplakia, 1
out of 6 patients of intestinal metaplasia of the stomach, 1 out of 4
patients with CIN and 2 out of 6 patients with Bowen's disease. In
conclusion, this study demonstrated that curcumin is not toxic to
humans up to 8,000 mg/day when taken by mouth for 3 months. Our
results also suggest a biologic effect of curcumin in the
chemoprevention of cancer.

Maybe bioperine would have significantly increased these levels.

[It probably would have. The above study is PMID: 11712783 and the
concentrations reached for the 4000 mg, 6000 mg and 8000 mg doses were 0,51
microM, 0,63 microM and 1,77 microM. What is strange about this is that these
numbers are similar to the 0,54microM you calculated above using the 0,2mg/L
figure which apparently was reached when taking piperine along with curcumin.
Since in that study curcumin was taken along with piperine, one would expect the
concentration reached to be much higher than in the study above since pirerine
increases the bioavailability of curcumin by about 2000%. This tells me that
either the 0,2mg/L figure is incorrect or that these studies are for some reason
not comparable. It is clear though that without piperine you will not reach
anywhere close to the 70microM IC50 value for inhibition of TXA2 by curcumin.
Whether taking piperine along with curcumin will get you close to the 70microM
concentration cannot be determined by these abstracts. Obviously more research
is needed in this area.

[Actually, I think Robert got the 0.54 microM from simply using my personal
dosage of curcumin with bioperine and the rat data at the bioperine.com website.
However, since the real meaning of rat data is unknown without the full text of
the paper, if I use the data from the paper above, assume a linear increase of
serum concentration with dosage and that the amount of bioperine I take (11 mg
each meal) is sufficient to increse the biolavailability by 2000%, then my 3250
mg daily dosage should give me a serum amount of (very roughly) 3250 x 2000% x
1.77 / 8000 = 14 microM. I would not want to increase it any more since my
polyphenol load is already quite high (polyphenols raise homocysteine levels)
and any prothrombotic potential because of blood clotting is already taken care
of by multiple other of my supplement, dietary and lifestyle factors. --Paul]

BTW curcumin is derived from the spice turmeric and I decided to check how much
curcumin is contained in turmeric. When searching pubmed I didn't find any
abstract which stated the percentage of curcumin in turmeric. However the full
text article of PMID: 16081279 states the following: "Curcumin
(diferuloylmethane) is a low molecular weight polyphenol, first chemically
characterised in 1910, that is generally regarded as the most active constituent
of and comprises 2–8% of most turmeric preparations 3 and 4." According to this
quote turmeric contains about 2-8% curcumin. -°Olafur]