Issue:
106
Page: 38-40
Cinnamon Extract Reduces Postprandial Blood Sugar Levels in Humans and Rats
by Amy C. Keller
HerbalGram.
2015; American Botanical Council
Reviewed: Beejmohun V, Peytavy-Izard M, Mignon C, et al.
Acute effect of Ceylon cinnamon extract on postprandial glycemia: alpha-amylase
inhibition, starch tolerance test in rats, and randomized crossover clinical
trial in healthy volunteers. BMC Complement Altern Med. 2014;14(1):351. doi: 10.1186/1472-6882-14-351.
Hyperglycemia, or
high blood sugar, is central to the etiology of type 2 diabetes. Controlling
postprandial (after-meal) hyperglycemia is important to maintaining overall
health and reducing the risk of both type 2 diabetes and cardiovascular
diseases. “Ceylon” or “true” cinnamon
(Cinnamomum verum syn. C. zeylanicum, Lauraceae) has been used
traditionally for gastrointestinal problems and continues to be used for
respiratory infections. Although clinical trials have addressed the potential
hypoglycemic activity of various types and preparations of cinnamon, studies
conflict as to its efficacy. This in vitro, in vivo, and randomized,
placebo-controlled, crossover human clinical trial investigated the starch
tolerance of rats and healthy humans supplemented with Ceylon cinnamon bark
extract.
Ceylon cinnamon bark extract (CCE; MealShape™;
Dialpha; Montferrier sur Lez, France) is a 10:1 concentrate extracted with
water and ethanol (50:50), which is then filtered and dried. [Note: Four of the
seven study authors are Dialpha employees.] The resultant powder is
standardized to contain at least 40% polyphenols, primarily oligomeric
procyanidins composed of catechin and epicatechin. As a comparison for using the
alcoholic solvent, an aqueous extract also was made. An enzymatic plate assay
was used to gauge the inhibition of α-amylase
(an enzyme that breaks down starches into sugars) activity, with acarbose (an
anti-diabetic drug sold as Precose®
in North America; Bayer; Whippany, New Jersey) as a positive control.
Animal studies
The authors used
male Wistar rats for the in vivo experiments. Various groups comprising eight
to 20 animals were tested to determine effects of CCE on glucose and insulin at
50 mg/kg body weight; dose-effects of CCE on glucose response at 6.25, 12.5,
25, 50, or 100 mg/kg body weight; and comparative responses between CCE and
aqueous extracts at 50 mg/kg body weight. Fasted rats underwent a starch
tolerance test (STT) and were fed wheat (Triticum aestivum, Poaceae)
starch alone at 1.5 g/kg body weight as a control, or wheat starch with
cinnamon extract at 20 mL/kg body weight. Blood glucose levels were measured at
baseline, 15, 30, 60, 90, and 120 minutes.
During the STT,
rats administered CCE and starch at 50 mg/kg body weight experienced a
significant 20.4% decrease in glucose area under the curve (AUC; a calculation
used to estimate a compound’s
bioavailability and clearance from the body) from 0-120 minutes, as compared to
the control group (P<0.05). At the same dose, insulin AUC was significantly
less after 60 minutes compared to control (P<0.05), with an insulin peak
reduction of 40.6%. Glucose AUC from 0-120 minutes also was significantly less
in rats given CCE at 12.5, 25, 50, and 100 mg/kg body weight (P<0.05 for
all). Compared to the aqueous cinnamon extract, CCE consumption in rats
resulted in a significantly greater reduction in glucose AUC from 0-15
(P<0.05), 0-30 (P<0.01), and 0-60 minutes (P<0.05).
In vitro analysis
In the pancreatic α-amylase
activity assay, CCE had an inhibitory concentration of 50% (IC50; a
measure of how much a substance inhibits a biological process) of 25 µg/mL,
while the acarbose control had an IC50 of 18 µg/mL.
When comparing the aqueous and alcoholic cinnamon extracts, the CCE had an IC50
of 30 µg/mL while the water extract had an IC50 of 40 µg/mL.
Human study
The clinical trial
took place at the Clinic Nutrition Center at Hôpital
Saint Vincent de Paul in Lille, France, and was administered by Naturalpha, a
contract research company based in Lille, France. The study’s primary endpoint was glucose AUC
from 0-120 minutes following consumption of a standard white bread meal.
Secondary endpoints included glucose AUC from 0-60 minutes, insulin AUC from
0-60 and 0-120 minutes, maximum concentrations of glucose and insulin, and
concentrations of both at each time point. Adverse side effects (ASEs) were
recorded and classified as mild, moderate, or severe.
Included subjects
(aged 18 to 45 years) had a body mass index between 18.5 and 25 kg/m2
and less than a 5% variation in body weight for the three months prior to the
study. Those with fasting glucose concentrations greater than 110 mg/dL, a
history of diabetes, a smoking habit, or who took any supplements or
pharmaceuticals that could impact glucose or insulin were excluded. Subjects
who had two-hour postprandial capillary blood glucose concentrations greater
than 140 mg/dl were excluded as well.
Subjects were
instructed to maintain their current lifestyle and were randomly assigned to
receive either CCE followed by placebo or placebo followed by CCE. Treatment
consisted of two capsules of CCE (500 mg each) or placebo (500 mg; containing
20% microcrystalline cellulose and 80% dicalcium phosphate). After an overnight
fast, participants had blood drawn 35 minutes prior to the test and were given
CCE or placebo five minutes later with 125 mL water. At baseline, a
standardized meal was consumed with 250 mL water within eight minutes (103 g of
white bread containing 52.2% carbohydrates [3.6% of which were sugars], 7.4%
protein, 0.1% lipids, and 3.3% fiber). Fasting glucose concentrations were
calculated as an average of measurements taken five and 10 minutes before the
meal; fasting insulin was determined five minutes before the meal; and glucose
and insulin were measured at 15, 30, 45, 60, 90, and 120 minutes following the
meal.
Of the 22 subjects
initially screened, 18 were randomly assigned to CCE (n=9) or placebo (n=9).
Two subjects were not included in the per-protocol analysis due to protocol
deviations, leaving 16 subjects in the final analysis. Upon supplementation
with CCE, there was a significantly lower glucose AUC from 0-60 minutes
compared to placebo (P<0.05). No other significant effects were noted, and
no ASEs were observed.
Conclusions
In summary, CCE
consumption in rats decreased both glucose and insulin concentrations during a
starch tolerance test, and doses of 12.5 mg/kg body weight and above resulted
in decreased glucose concentrations. Comparable IC50 levels for CCE
and acarbose in the α-amylase activity
assay suggest that enzyme inhibition is a likely mechanism of action for the
alcoholic cinnamon extract. Although CCE significantly lowered glucose
concentrations in healthy subjects, no effects were seen on insulin
concentrations, which points to mechanisms independent of increased insulin in
humans.
The authors mention
that Ceylon cinnamon contains much less coumarin (a potentially toxic compound)
than cassia (Cinnamomum aromaticum syn. C. cassia), although
alcohol extraction can increase an extract’s coumarin content due to its
solubility. The CCE used in the study exposed participants to less than 0.2 mg
coumarin per day (per one gram dose), well below the European Food Safety
Authority’s
tolerable daily intake guideline of seven mg/day for a 70-kg (154-lb) person.
This study reports more robust bioactivity with the alcoholic extract than the
aqueous extract, which deserves further investigation. Future clinical trials
of hyperglycemic individuals should continue to examine the use of Ceylon
cinnamon extract in managing this condition.
—Amy C. Keller, PhD
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