Effect of cinnamon and turmeric on urinary oxalate excretion,
plasma lipids, and plasma glucose in healthy subjects1–3
Minghua Tang, D Enette Larson-Meyer, and Michael Liebman
ABSTRACT
Background: High oxalate intake resulting from consuming sup-
plemental doses of cinnamon and turmeric may increase risk of
hyperoxaluria, a significant risk factor for urolithiasis.
Objective: This study assessed urinary oxalate excretion from sup-
plemental doses of cinnamon and turmeric as well as changes in
fasting plasma glucose, cholesterol, and triacylglycerol concentra-
tions.
Design: Eleven healthy subjects, aged 21–38 y, participated in an
8-wk, randomly assigned, crossover study that involved the inges-
tion of supplemental doses of cinnamon and turmeric for 4-wk pe-
riods that provided 55 mg oxalate/d. Oxalate load tests, which en-
tailed the ingestion of a 63-mg dose of oxalate from the test spices,
were performed after each 4-wk experimental period and at the study
onset with water only (control treatment). Fasting plasma glucose
and lipid concentrations were also assessed at these time points.
Results: Compared with the cinnamon and control treatments, tur-
meric ingestion led to a significantly higher urinary oxalate excretion
during the oxalate load tests. There were no significant changes in
fasting plasma glucose or lipids in conjunction with the 4-wk periods
of either cinnamon or turmeric supplementation.
Conclusions: The percentage of oxalate that was water soluble
differed markedly between cinnamon (6%) and turmeric (91%),
which appeared to be the primary cause of the greater urinary oxalate
excretion/oxalate absorption from turmeric. The consumption of
supplemental doses of turmeric, but not cinnamon, can significantly
increase urinary oxalate levels, thereby increasing risk of kidney
stone formation in susceptible individuals. Am J Clin Nutr
2008;87:1262–7.
INTRODUCTION
About 75% of all kidney stones are composed primarily of
calcium oxalate (1), and hyperoxaluria is a primary risk factor for
this disorder (2). Urinary oxalate, derived from a combination of
exogenous and endogenously synthesized oxalate, is a primary
determinant of the level of calcium oxalate saturation (3). Al-
though it had been accepted that dietary oxalate contributes no
more than 10% to 20% of the oxalate excreted in the urine under
normal conditions (1, 4), recent work (5, 6) suggests that even in
the absence of gastrointestinal disorders, intestinal absorption of
dietary oxalate can make a more significant contribution to uri-
nary oxalate. Thus, high oxalate intake may increase risk of
hyperoxaluria, a significant risk factor for urolithiasis.
Oxalate is a common component in food, including nuts,
fruits, vegetables, grains, and legumes, and is a salt or ester of
1262 Am J Clin Nutr 2008;87:1262–7. Printed in USA. © 2008 American Society for Nutrition
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oxalic acid: (COO)2H2 (4). In food, oxalic acid is typically found
in its salt form, primarily as either sodium or potassium oxalate,
which are water soluble, or calcium oxalate, which is insoluble.
The propensity of a specific food to raise urinary oxalate is
dependent both on oxalate content and efficiency of absorption
because it is well established that little oxalate catabolism occurs
after absorption and 쏜90% of absorbed oxalate can be recovered
in the urine within 24 to 36 h (7).
Oxalate absorption in the small intestine occurs via active
transport, and there is passive absorption along the gastrointes-
tinal tract (8). Oxalate solubility within the small intestine ap-
pears to be a critical factor as evidenced by the propensity of
concomitant calcium ingestion to reduce oxalate absorption (5,
9), presumably by chelating with oxalic acid in the small intes-
tine. An unanswered question is whether the solubility of oxalate
in a specific food source is an important predictor of efficiency of
oxalate absorption. The assertion that the amount of soluble
oxalate in food is a major determinant of oxalate absorption is
supported by some (10, 11) but not all studies (12).
Spices such as cinnamon and turmeric are currently being
consumed in supplemental doses because of their purported
health benefits (13, 14), which include improvements in glyce-
mic (15, 16) and lipid profiles (15, 17, 18). However, no studies
to date have reported the oxalate content and oxalate solubility of
these spices or assessed the efficiency of oxalate absorption.
Because previous unpublished work in our laboratory suggested
that cinnamon and turmeric are high-oxalate spices, their sup-
plementation could have a significant influence on total oxalate
absorption and urinary excretion, an important consideration for
individuals predisposed to the formation of calcium oxalate-
containing kidney stones. Thus, the primary objectives of this
study were to quantify the total and soluble oxalate content of
cinnamon and turmeric and to assess and compare the change in
urinary oxalate excretion from these 2 spices. A secondary ob-
jective was to assess fasting plasma glucose, cholesterol, and
triacylglycerol responses to 4-wk periods of cinnamon and tur-
meric supplementation in a healthy, nondiabetic population.
1
From the Department of Family and Consumer Sciences (Human Nutri-
tion), University of Wyoming, Laramie, WY.
2
Supported by funding from the University of Wyoming.
3
Reprints not available. Address correspondence to M Liebman, Depart-
ment 3354, 1000 E. University Avenue, Laramie, WY 82071. E-mail:
liebman@uwyo.edu.
Received August 21, 2007.
Accepted for publication December 13, 2007.
 OXALATE ABSORPTION FROM CINNAMON AND TURMERIC
SUBJECTS AND METHODS
Subjects
The study protocol was approved by the University of Wyo-
ming Institutional Review Board. Twelve healthy non–stone
formers (7 women and 5 men) were recruited from the university
community. Subjects were recruited without regard to sex be-
cause previous work had suggested no significant sex difference
in oxalate absorption from food sources (9). Written informed
consent was obtained from all participants. One participant
(man) dropped out of the study following the control test day for
personal reasons. Thus, all statistical analyses were based on an
n value of 11. Overall, subjects were judged to be healthy based
on a preexperimental screening questionnaire that assessed their
general health status. There were no reports of any intestinal or
renal problems that could have modified oxalate absorption or
excretion.
Study design
The study was a randomly assigned, crossover design with 6
subjects starting on the cinnamon treatment and the remaining 5
subjects starting on turmeric, each treatment of 4-wk duration.
Subjects were asked to maintain their normal dietary and exercise
patterns throughout the entire 8-wk experimental period with the
exception of consuming supplemental doses of cinnamon and
turmeric.
Subjects were given a supplemental dose of 3.0 g (6 capsules)
cinnamon or 2.8 g (7 capsules) turmeric (Puritan’s Pride, Oak-
dale, NY) for 4 wk. This provided 앒55 mg of oxalate per day.
The selected number of capsules approximated the doses used by
previous studies that assessed blood lipid or glucose responses to
cinnamon supplements (15, 16, 19). Subjects were directed to
take 2 capsules with breakfast, 2 with lunch, and the remaining
capsules with dinner. Subjects were given a 2-wk supply of the
assigned spice and asked to return any unconsumed capsules to
the researchers.
Oxalate load tests were performed and blood samples were
obtained at baseline, at 4 wk, and at 8 wk. The initial oxalate load
test entailed the ingestion of water only (control treatment). The
latter oxalate load tests were administered to coincide with the
completion of the 4-wk, randomly assigned cinnamon and tur-
meric treatments. The amount of cinnamon and turmeric used in
the oxalate load tests was adjusted to provide an 앒63-mg dose of
oxalate, which was either 7 capsules (3.5 g) of cinnamon or 8
capsules (3.2 g) of turmeric.
Subjects were provided with detailed lists of oxalate-rich
foods and were instructed to avoid these foods starting the day
before the oxalate load tests and for 24 h post– oxalate ingestion.
Subjects fasted overnight for a minimum of 12 h before each
data-collection day. Subjects were also given 360 mL of bottled
water to drink on the test days after their first urine voiding in the
morning to ensure adequate urine production. They were in-
structed to arrive at the lab within 2 h after their first urine voiding
at which time fasting blood samples were drawn into evacuated
tubes containing EDTA. Samples were centrifuged at 2500 ҂ g
for 10 min and plasma samples were frozen at –25 °C for sub-
sequent analyses. At the 2-h time point, subjects emptied their
bladders and the urine samples were collected. These initial urine
samples were designated as the baseline (B-2) urine samples.
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1263
Right after the initial 2-h urine collection period, subjects
ingested water (for the control oxalate load test) or the appropri-
ate oxalate-containing spice in capsule form at the 4- and 8-wk
time points. Each hour for 6 h post– oxalate ingestion, 150 –200
mL of distilled, deionized water was consumed to ensure ade-
quate urine production. Urine samples were collected at 2-h
intervals for 6 h, after which subjects were allowed to leave the
laboratory but continued to collect all urine samples to complete
a 24-h urine collection period. These urine samples were desig-
nated S-2, S-4, S-6, and S-22 to correspond to the urine collection
timing in hours post– oxalate/water ingestion. Forty-five minutes
after the ingestion of cinnamon or turmeric capsules or water
(control treatment), a standardized low-oxalate, low-calcium
meal was provided as subjects were allowed to choose from
sausage, scrambled eggs, a cold rice cereal with rice milk, apple,
grapes, and apple juice. Ten minutes after their third (S-4) urine
samples, subjects were given a low-oxalate snack that included
rice cakes, cheese, yogurt, apple, and grapes. Subjects kept a
detailed food record on the test day and were required to consume
the same type and amounts of food for the provided meal and
snack on all 3 test days to minimize any potential confounding
effects.
Diet records were started the day before the oxalate load tests
and continued through 24 h post– oxalate ingestion. Diet records
were reviewed for compliance to the low-oxalate diet and adher-
ence to the overall experimental protocol. Subjects were given a
written questionnaire on the last oxalate load test day to assess
whether there were any feelings of discomfort or gastrointestinal
symptoms in relation to taking the capsules either on a test day or
at any time during the 8-wk study.
Sample analyses
All urine volumes were recorded, samples were acidified with
HCl to a pH 쏝 2.0, and aliquots frozen for subsequent analysis.
Urine oxalate, as well as oxalate in cinnamon, turmeric, and the
foods provided for the breakfast and snack, was analyzed with
use of an oxalate kit purchased from Trinity Biotech (Berkeley
Heights, NJ). This method is based on the oxidation of oxalate by
oxalate oxidase followed by measurement of hydrogen peroxide
by a peroxidase-catalyzed reaction. Urinary creatinine was ana-
lyzed with use of the picric acid method (20). Urinary oxalate was
expressed in absolute values (mg) and relative to creatinine ex-
cretion (mg oxalate/g creatinine). Total oxalate and soluble ox-
alate from cinnamon and turmeric were extracted according to
the method described by Ross et al (21), which involved extract-
ing weighed amounts in a shaking water bath at 80 °C for 30 min
followed by centrifugation (10 min at 3000 ҂ g) and filtration.
The spices were extracted in 2 mol/L H3PO4 for total oxalate and
in distilled, deionized water for soluble oxalate. Plasma glucose,
total cholesterol, and triacylglycerol concentrations were ana-
lyzed in duplicate with use of a portable Micro-Stat Multi-Assay
Analyzer (Analox Instruments, Lunenburg, MA). The calcium
content of cinnamon and turmeric as well as the foods provided
for the breakfast and snack were obtained from the US Depart-
ment of Agriculture food composition database (22).
An estimation of net oxalate excretion is required to approx-
imate oxalate absorption. Net oxalate excretion represents the
difference between total urinary oxalate and that portion of total
urinary oxalate that can be attributed to endogenous oxalate
synthesis. The B-2 urinary oxalate excretion on the test days can
be considered an approximation of endogenous oxalate. Rate of
 1264 TANG ET AL
endogenous oxalate excretion was assumed to be constant
throughout the day. The 6- and 22-h endogenous oxalate was
computed by multiplying the B-2 urinary oxalate by 3 and 11 for
6 and 22 h, respectively. The original intent was to use the B-2
from each treatment to compute net oxalate over 6- and 22-h
postoxalate time periods. However, the mean CV across all sub-
jects for B-2 urinary oxalate on the 3 test days was high (17.6%).
Thus, a more accurate estimate of 2-h endogenous oxalate could
be obtained through the use of the average B-2 across the 3
treatments for each subject. The average B-2 urinary oxalate was
used to approximate each subject’s 6- and 22-h endogenous
oxalate excretion, which in turn was used to compute net oxalate
excretion (ie, net oxalate ҃ total oxalate – endogenous oxalate).
Finally, net oxalate was used to approximate oxalate absorption
(ie, percentage absorbed ҃ net oxalate/63 mg, with 63 mg rep-
resenting the amount of oxalate provided by cinnamon and tur-
meric on the test days).
Statistical analysis
The initial statistical analysis made use of a crossover exper-
imental design to test the hypothesis that the cinnamon/turmeric
treatment order did not influence the results. When no treatment
order effect was detected, subsequent statistical analyses tested
for treatment effects without regard to treatment order. Treat-
ment differences in oxalate load urinary volume, oxalate, creat-
inine, and ratio of oxalate to creatinine were tested with use of a
repeated-measures analysis of variance in which both treatment
and time (with time representing the different time periods of
urine collection during the oxalate load tests) were entered into
the model. When a significant treatment effect, but no significant
treatment-by-time interaction, was observed, the interpretation
was that the treatment effect was essentially consistent over the
different time periods of urine collection during the oxalate load
tests. In this case, differences were not presented across treat-
ments at specific time points. In instances for which both signif-
icant treatment and treatment-by-time interactions were ob-
served, treatment differences at specific time points were
determined with use of the Tukey post hoc test. Treatment dif-
ferences in plasma glucose, cholesterol, and triacylglycerols
were tested with use of a repeated-measures analysis of variance.
Statistical calculations were based on the general linear model
procedure of SAS (version 8.1, SAS Institute Inc, Cary, NC).
Values of P 쏝 0.05 were considered to designate statistical sig-
nificance. Data are reported as means 앐 SD.
RESULTS
Eleven subjects (7 women, 4 men) completed the study. The
mean participant age was 27 앐 6 y (range: 21–38 y) and the mean
BMI was 24.7 앐 2.5 kg/m2 (range: 21.0 –28.2 kg/m2). Overall
compliance with taking the cinnamon and turmeric supplements
was judged to be excellent on the basis of the return of empty vials
that had contained the daily allotment of capsules. Two subjects
missed taking 9 capsules during the 8-wk supplementation pe-
riod, and 1 subject missed 5 complete days during the turmeric
supplementation period because of illness. The return of empty
vials suggested that the remaining subjects consumed all the
provided supplements.
Four subjects reported experiencing eructation in association
with taking cinnamon either on the oxalate load test day or during
the 4 wk of daily ingestion. One subject reported experiencing a
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headache in association with taking cinnamon on the test day.
Another subject reported an occasional burning stomach during
the 4 wk of cinnamon consumption. There were no other reported
symptoms with either cinnamon or turmeric consumption.
Total and soluble oxalate content of cinnamon and
turmeric
The total oxalate content of cinnamon and turmeric, analyzed
in duplicate on 4 occasions, was 1789 앐 54 and 1969 앐 56
mg/100 g, respectively. The percentage of oxalate that was water
soluble differed markedly between cinnamon (107 앐 8 mg/100
g, 6% of total) and turmeric (1788 앐 1 mg/100 g, 91% of total).
Oxalate and calcium content of the provided breakfast
and snack
An attempt was made to provide similar breakfasts and snacks
for each subject for the 3 treatments to minimize the potentially
confounding effect of differing nutrient intakes, especially ox-
alate and calcium. The breakfast was designed to be low in both
oxalate and calcium. Computed oxalate intakes (x៮ 앐 SD) for this
meal were 8.3 앐 4.1, 6.4 앐 3.8, and 6.8 앐 5.0 mg for the control,
cinnamon, and turmeric treatments, respectively; the corre-
sponding calcium intakes from breakfast for the same order of
treatments were 77 앐 25, 67 앐 21, and 60 앐 29 mg. Mean oxalate
intakes from the snack ranged from 21.2 to 22.8 mg for the 3
treatments. Because the snack was provided 쏜4 h after the ox-
alate loads were ingested, calcium consumed at this time would
not be expected to interfere with oxalate absorption from the
oxalate loads. Thus, these calcium intakes were not strictly con-
trolled with mean intakes for the 3 treatments ranging from 380
to 420 mg.
Oxalate absorption from cinnamon and turmeric
Baseline as well as postoxalate load urine volumes and oxalate
and creatinine levels are presented in Table 1. There were no
significant treatment differences for either urine volumes or cre-
atinine levels. The statistical analysis indicated a significant
main effect of treatment but no significant treatment-by-time
interaction for postload urinary oxalate levels. The Tukey sepa-
ration test of treatment means, averaged over the 5 separate time
points, indicated a significantly higher mean urinary oxalate for
the turmeric compared with the control treatment, whereas the
control and cinnamon treatments were not significantly different.
The total 6- and 22-h urinary oxalate parameters represent the
total oxalate excretion accumulated after B-2 for 6 and 22 h. The
significantly higher urinary oxalate for turmeric, compared with
both the control and cinnamon treatments, for the total 6-h pa-
rameter appeared to largely account for the similar finding for the
total 22 h parameter. There were no significant differences be-
tween the cinnamon and control treatments for either total 6-h or
total 22-h urinary oxalate levels.
Baseline as well as postoxalate load urine ratios of oxalate to
creatinine are presented in Table 2. The statistical analysis in-
dicated a significant treatment effect as well as a significant
treatment-by-time interaction. There were no significant treat-
ment differences for B-2 and S-22. The ratio of oxalate to creat-
inine for the turmeric treatment was significantly higher than the
corresponding ratios for the control and cinnamon treatments for
S-2, S-4, and S-6.
 OXALATE ABSORPTION FROM CINNAMON AND TURMERIC 1265
TABLE 1 TABLE 2
Baseline and oxalate load urine volumes and oxalate and creatinine Baseline and postoxalate load urine oxalate/creatinine (mg/g) ratios1
concentrations1
Treatment
Treatment
Parameter and Sample no. Control Cinnamon Turmeric
sample no. Control Cinnamon Turmeric
B-2 14.3 앐 3.9 14.7 앐 4.4 14.6 앐 2.8
Volume (mL) S-2 17.9 앐 6.8a 25.1 앐 14.2a 36.8 앐 12.2b
B-2 221 앐 157 151 앐 104 201 앐 165 S-4 21.9 앐 8.1a 22.7 앐 9.8a 38.5 앐 15.1b
S-2 404 앐 241 428 앐 155 444 앐 186 S-6 18.6 앐 5.2a 18.1 앐 7.5a 23.9 앐 7.9b
S-4 486 앐 299 421 앐 204 467 앐 200 S-22 17.7 앐 5.9 16.0 앐 4.7 17.8 앐 9.4
S-6 265 앐 171 375 앐 178 323 앐 169
x៮ 앐 SD; n ҃ 11. B-2 refers to the 2-h baseline urine sample collected
1
S-22 1398 앐 836 1289 앐 562 1276 앐 693
before initiation of the oxalate load test; S-2, S-4, and S-6 refer to the 2-h urine
Oxalate (mg)
samples sequentially collected after oxalate ingestion (cinnamon and tur-
B-2 1.6 앐 0.5 1.5 앐 0.5 1.6 앐 0.6
meric treatment) or water ingestion (control treatment); S-22 refers to the
S-2 1.6 앐 0.5 2.1 앐 0.9 3.4 앐 1.3
pooled urine sample that represented the approximately 16-h period initiated
S-4 2.1 앐 1.2 2.3 앐 1.0 3.8 앐 1.5
after S-6 up through the first urine voiding the following morning. There was
S-6 2.1 앐 0.6 1.9 앐 0.8 2.7 앐 1.7
a significant treatment by time interaction. Means within a row with different
S-22 12.6 앐 4.9 13.0 앐 3.0 12.3 앐 3.6
superscript letters are significantly different, P 쏝 0.05 (repeated- measures
Total 6 h 5.7 앐 1.9a 6.4 앐 2.1a 9.9 앐 3.2b
analysis of variance and Tukey post hoc test); there are no significant differ-
Total 22 h 18.3 앐 6.6a 19.3 앐 4.3a,b 22.3 앐 6.4b
ences within a row in cases in which no superscript letters appear.
Creatinine (mg)
B-2 121 앐 46 107 앐 42 114 앐 42
S-2 98 앐 46 99 앐 51 102 앐 51 There were no significant treatment differences for fasting
S-4 101 앐 47 109 앐 41 103 앐 38 plasma glucose or lipid concentrations.
S-6 116 앐 40 115 앐 45 118 앐 42
S-22 777 앐 336 851 앐 275 812 앐 374
Total 22 h 1092 앐 448 1173 앐 400 1135 앐 482 DISCUSSION
1
x៮ 앐 SD; n ҃ 11. B-2 refers to the 2-h baseline urine sample collected Supplemental doses of cinnamon and turmeric have been
before initiation of the oxalate load test; S-2, S-4, and S-6 refer to the 2-h urine shown to be beneficial in decreasing blood lipids in patients with
samples sequentially collected after oxalate ingestion (cinnamon and tur-
hyperlipidemia and in improving glycemic control in diabetic
meric treatment) or water ingestion (control treatment); S-22 refers to the
patients (15–17). Because these supplements are widely avail-
pooled urine sample that represented the approximately 16-h period initiated
after S-6 up through the first urine voiding the following morning. Means able, their very high oxalate content should be taken into con-
within a row with different superscript letters are significantly different, P 쏝 sideration. The primary purpose of the current study was to
0.05 (repeated-measures analysis of variance and Tukey post hoc test). There determine whether ingestion of high doses could increase the risk
were no significant treatment differences for either urine volumes or creat- of kidney stone formation in susceptible individuals. The cinna-
inine levels; because no significant treatment by time interaction was ob- mon and turmeric supplements used in this study had oxalate
served for urinary oxalate, differences are not presented across treatments at contents of 1798 and 1969 mg/100 g, respectively. It has been
specific time points. recommended that kidney stone patients limit dietary oxalate
intake to no more than 50 mg of oxalate per day (23), a level
which would likely be exceeded with cinnamon or turmeric sup-
plementation. For example, cinnamon supplementation at a level
An estimation of net oxalate, the difference between total of 3 g/d would provide an additional 51 mg of oxalate.
urinary oxalate and that portion of total urinary oxalate that can The amount of urinary oxalate is dependent on both the oxalate
be attributed to endogenous oxalate synthesis, is required to content of the diet and oxalate bioavailability. Oxalate absorp-
approximate oxalate absorption. The computed estimate of en- tion rates from different foods have been estimated to range from
dogenous oxalate excretion was used to compute net oxalate 2% to 15% (24, 25). Oxalate absorption appears to depend on a
excretion (ie, net oxalate ҃ total oxalate – endogenous oxalate), number of factors, including absorptive properties of the intes-
which in turn was used to approximate oxalate absorption (ie, tine, gut transit time, presence of divalent cations such as calcium
percentage absorbed ҃ net oxalate/63 mg, with 63 mg represent-
ing the amount of oxalate provided by cinnamon and turmeric
TABLE 3
on the test days). The estimates of net oxalate excretion and
Computed net oxalate excretion and oxalate absorption from cinnamon
absorption were significantly higher for the turmeric com- and turmeric1
pared with the cinnamon treatment for both the 6- and 22-h
time periods (Table 3). Treatment

Fasting glucose and lipids Parameter Cinnamon Turmeric

Fasting plasma glucose, total cholesterol, and triacylglycerols Net 6 h (mg) 1.7 앐 2.0 a
5.2 앐 2.6b
for the control, cinnamon, and turmeric treatments are summa- 6 h absorption (%) 2.6 앐 3.2a 8.2 앐 4.2b
rized in Table 4. At the initial (control) time point, all subjects Net 22 h (mg) 1.9 앐 3.3a 4.8 앐 4.6b
had normal fasting blood glucose (쏝100 mg/dL) and total cho- 22 h absorption (%) 3.0 앐 5.3a 7.7 앐 7.4b
lesterol (쏝200 mg/dL) concentrations. Four subjects had ele- 1
x៮ 앐 SD; n ҃ 11. Means within a row with different superscript letters are
vated fasting triacylglycerol concentrations (쏜150 mg/dL). significantly different, P 쏝 0.05 (repeated-measures analysis of variance).

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 1266 TANG ET AL
TABLE 4
Fasting plasma glucose and lipid concentrations following control,
cinnamon, and turmeric treatments1
Treatment
Parameter Control Cinnamon Turmeric
Glucose (mg/dL) 90 앐 8 88 앐 11 90 앐 9
Total cholesterol (mg/dL) 155 앐 19 145 앐 19 151 앐 31
Triacylglycerols (mg/dL) 139 앐 93 166 앐 64 175 앐 115
1
x៮ 앐 SD; n ҃ 11. There were no significant treatment differences
(repeated-measures analysis of variance).
and magnesium that can bind oxalate within the gastrointestinal
tract, and presence of oxalate-degrading bacteria (26, 27). There
is a lack of consensus as to whether oxalate absorption is depen-
dent on the amount of soluble compared with insoluble oxalate in
food (27, 28). Our data support the contention that the relative
amount of soluble and insoluble oxalate plays a role in determin-
ing efficiency of oxalate absorption. There was a significantly
higher computed 6-h oxalate absorption rate from turmeric in-
gestion (8.2%) than from cinnamon ingestion (2.6%), which was
most likely explained by the 91% soluble oxalate content of
turmeric compared with 6% for cinnamon. This difference in
oxalate solubility could likely be attributed to the higher calcium
content of cinnamon than turmeric (1002 compared with 183
mg/100 g), which resulted in computed calcium/oxalate molar
ratios of 1.3 and 0.2 for cinnamon and turmeric, respectively. A
previous study by Chai and Liebman (11) also suggested that the
relative amount of soluble and insoluble oxalate in food has an
important role in the determination of oxalate absorption. Ox-
alate absorption from almonds (5.9%) was significantly higher
than that from black beans (1.8%). Soluble oxalate accounted for
앒31% of total oxalate from almonds whereas black beans had a
soluble content of 5%.
There was no significant change from baseline in urine oxalate
excretion after cinnamon consumption, possibly because of the
low soluble oxalate content (6%). For those predisposed to kid-
ney stones, cinnamon can be considered a low-oxalate food in
terms of absorption, and its ingestion would not be expected to
increase risk for kidney stone formation.
Hyperoxaluria has been defined as urine oxalate excretion that
exceeds 40 mg/24 h (26). Twenty-four-hour oxalate excretion
increased from 19.9 mg (control treatment) to 24.9 mg (turmeric
treatment). Thus, even with the computed 6-h oxalate absorption
rate of 8.2% from turmeric, total 24-h oxalate excretion remained
well below the cutoff that designates increased risk. There is
some evidence that kidney stone formers have an increased rate
of endogenous oxalate synthesis (29) and may absorb a higher
percentage of dietary oxalate (30). Most kidney stone formers are
also likely to have higher oxalate intakes than those imposed in
the present study on test days. For these reasons, the ingestion of
supplemental doses of turmeric by some stone formers may raise
24-h urinary oxalate levels close to or above the 40-mg threshold.
All subjects maintained a low-oxalate diet starting the day
before a data collection day by avoiding a detailed list of oxalate-
containing foods during this period. This allowed the supple-
mental doses of either cinnamon or turmeric given on an oxalate
load day to be the major source of exogenous oxalate. It also
allowed an approximation of the subjects’ endogenous 2-h base-
line oxalate excretion. Although it was assumed that endogenous
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oxalate synthesis occurred at a constant rate throughout the 22-h
postoxalate load periods, there is the possibility that a component
of the cinnamon or turmeric supplement could have altered en-
dogenous oxalate synthesis. Another study limitation relates to
the possible effect of chronic oxalate feeding on adaptation by
colonic oxalate-degrading bacteria, a phenomenon that has been
well established (31). However, this factor was thought to be of
only minor significance because the 4-wk cinnamon and tur-
meric supplementation periods added only an additional 55 mg
of oxalate to the subjects’ normal daily diets. Providing the test
oxalate loads (63 mg) as a single dose rather than having the
cinnamon and turmeric supplements spread throughout the day,
as was done during the 4-wk experimental periods, could have
altered the efficiency of oxalate absorption. Previous work doc-
umented a marked decrease in absorptive efficiency as dietary
oxalate was increased from very low levels up to 앒50 mg (6). All
of these considerations highlight the inherent assumptions that
should be acknowledged with respect to the presently reported
estimates of oxalate absorption.
The finding that the increase in urinary oxalate occurred pri-
marily during the initial 6 h after oxalate ingestion is in agreement
with previous studies (5, 11) and suggested only a small colonic
contribution to overall oxalate absorption. After 6 h of consump-
tion, there was a similar oxalate excretion for the 3 treatments.
The ratio of oxalate to creatinine was also computed to com-
pare the 3 treatments. Expressing urinary oxalate relative to cre-
atinine helps normalize the data for irregularities in urine flow
and for any urine which was inadvertently not collected. Thus,
the ratio of oxalate to creatinine can be more accurate than the
absolute amount of oxalate, especially when a subject fails to
collect all the 24-h urine. Only turmeric ingestion led to a marked
increase in the ratio of oxalate to creatinine for the S-2, S-4, and
S-6 samples, thus further supporting the finding of a significantly
higher oxalate absorption from turmeric than from cinnamon.
The secondary objective of the study was to determine whether
4 wk of supplementation with cinnamon or turmeric would affect
fasting glucose and lipid concentrations. Previous studies (15,
16) have found that supplementation with 1 to 6 g cinnamon/d for
40 to 앑120 d modestly improved both blood glucose and lipids
in individuals with type 2 diabetes, although this finding has not
been universally reported (19). A recent study (32) in nondiabetic
subjects also found that 6 g of cinnamon added to rice pudding
significantly reduced the postprandial blood glucose response.
Supplementation with turmeric has also been shown (17, 18) to
improve the lipid profile in experimental animals with hyperlip-
idemia. Our findings extend previous research and show that
supplementation with 앑3 g of cinnamon or turmeric does not
alter blood glucose or plasma lipid concentrations in healthy,
young nondiabetic men and women. Whereas it is not surprising
that the hypolipidemic benefit of these spices is experienced only
in those with elevated lipid levels, it is important to note that
hypoglycemia is not a potential side effect of supplementation in
healthy subjects who may supplement with these spices to gain
other health benefits (13, 14).
In summary, the estimated 6-h oxalate absorption from tur-
meric (8.2%) was significantly higher than the corresponding
value for cinnamon (2.6%). The difference in soluble oxalate
content appeared to be the primary cause of the significantly
greater urinary oxalate excretion/oxalate absorption from tur-
meric. Neither cinnamon nor turmeric supplementation affected
fasting blood glucose or lipid concentrations.
 OXALATE ABSORPTION FROM CINNAMON AND TURMERIC
We thank Kentz Willis for his help with the plasma glucose and plasma
lipid analyses. We also thank all the volunteers who participated in the study.
The authors’ contributions were as follows—MT and ML: design; MT, 17.
ML and DEL: data collection, analysis, and article preparation; ML: principal
investigator. None of the authors had any financial or personal conflicts of
interest. 18.
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