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Delayed effects of coffee, tea and sucrose on postprandial glycemia in lean, young, healthy adults

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In observational studies, habitual coffee consumption has been linked to a lower risk of type 2 diabetes. We hy- pothesized that the mechanism may be related to delayed effects on postprandial glycemia. The aim of this study is to investigate the glycemic and insulinemic effects of consumption of caffeinated and decaffeinated coffee, sweetened and unsweetened, tea and sucrose, 1 h prior to a high carbohydrate meal. On separate occasions in random order, lean young healthy subjects (n = 8) consumed a potato-based meal 1 hour after consumption of 250 mL of black coffee (COF), black coffee sweetened with 10 g of sucrose (COF+SUC), decaffeinated coffee (DECAF), black tea (TEA), 10 g sucrose (SUC) or hot water (CON). Fingerprick blood samples were taken at regular intervals over 2 h and the glucose and insulin responses quantified as area under the curve. Compared to CON, COF caused a 28% increase in postprandial glycemia (p = 0.022). In contrast, COF+SUC decreased gly- cemia compared with either COF (-38%, p < 0.001) or CON (-20%, p = 0.100) but had no effect on insulin re- sponses. DECAF, TEA and SUC had no significant effects on postprandial responses. SUC and DECAF reduced the absolute glucose concentration at the start of the meal (p < 0.01). In conclusion, only sweetened coffee sig- nificantly reduces postprandial glycemia. This observation may explain the paradoxical findings of observational and clinical studies relating coffee drinking to diabetes risk
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by Cat York on November 11th, 2010 at 12:50 pm
I am a 35 year old woman who suffers from chronic abdominal pain - especially during menses. My newest Doctor has instructed me to go on a restricted diet (not to lose weight as i am an average, healthy, relatively fit person) with careful attention to the glycemic index of the foods I eat. He said my severe intestinal pain may be a result of an insulin imbalance, especially during the hormonal days before and during menses. He said that the imbalance of insulin and adrenaline were affect the soft, smooth muscles of the intestines. I have never heard it explained that way to me. I feel better on this diet, and free of the pain that made me go days without eating ... I've been suffering though this for two years, many blood tests, CT scan, colonoscopy, medication. It's not an easy diet but as long as I can still have that cup of coffee in the morning - I'm ready. Thankful for Doctors and studies that help us understand how the body works. Thank you.
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Asia Pac J Clin Nutr 2008;17 (4):657-662
657
Original Article

Delayed effects of coffee, tea and sucrose on postprandial
glycemia in lean, young, healthy adults

Jimmy Chun Yu Louie MNutrDiet1, Fiona Atkinson MNutrDiet1, Peter Petocz PhD2,
Jennie C Brand-Miller PhD1

1Human Nutrition Unit, School of Molecular and Microbial Biosciences, The University of Sydney, Sydney,
Australia

2Department of Statistics, Macquarie University, Sydney, Australia


In observational studies, habitual coffee consumption has been linked to a lower risk of type 2 diabetes. We hy-
pothesized that the mechanism may be related to delayed effects on postprandial glycemia. The aim of this study
is to investigate the glycemic and insulinemic effects of consumption of caffeinated and decaffeinated coffee,
sweetened and unsweetened, tea and sucrose, 1 h prior to a high carbohydrate meal. On separate occasions in
random order, lean young healthy subjects (n = 8) consumed a potato-based meal 1 hour after consumption of
250 mL of black coffee (COF), black coffee sweetened with 10 g of sucrose (COF+SUC), decaffeinated coffee
(DECAF), black tea (TEA), 10 g sucrose (SUC) or hot water (CON). Fingerprick blood samples were taken at
regular intervals over 2 h and the glucose and insulin responses quantified as area under the curve. Compared to
CON, COF caused a 28% increase in postprandial glycemia (p = 0.022). In contrast, COF+SUC decreased gly-
cemia compared with either COF (-38%, p < 0.001) or CON (-20%, p = 0.100) but had no effect on insulin re-
sponses. DECAF, TEA and SUC had no significant effects on postprandial responses. SUC and DECAF reduced
the absolute glucose concentration at the start of the meal (p < 0.01). In conclusion, only sweetened coffee sig-
nificantly reduces postprandial glycemia. This observation may explain the paradoxical findings of observational
and clinical studies relating coffee drinking to diabetes risk.

Key Words: coffee, tea, postprandial glycemia, insulinemia, caffeine



INTRODUCTION
diabetes would be an ability to reduce postprandial gly-
There is good evidence that habitual coffee consumption
cemia. Although previous studies have found no demon-
reduces the risk of type II diabetes (T2DM). van Dam and
strable effect of 1-2 cups of coffee or tea when consumed
Feunekes1 found that individuals who drank at least 7
at the same time as the meal,23 it is possible that a lag-
cups of coffee a day had half the risk of developing
time exists between consumption and any effect on he-
T2DM compared to those who drank less than 2 cups.
patic or peripheral metabolism. Since coffee is often con-
Similarly, inverse relationships between coffee consump-
sumed between meals, any delayed effect on postprandial
tion and risk of developing T2DM,2-9 impaired glucose
glycemia would be physiologically relevant. The aim of
tolerance,10,11 fasting glucose concentration,11 2-hour in-
the present study was therefore to explore the postpran-
sulin glucose and insulin10,11 and insulin sensitivity,10 have
dial metabolic response to pre-feeding of normal and de-
been reported. Paradoxically, caffeine itself has been
caffeinated coffee, sweetened and unsweetened, 1 hour
found to reduce insulin sensitivity12 and impair glucose
prior to a starchy meal. Tea was also studied because it
tolerance.13,14 Arnlov et al,15 however, showed that the
represents a similarly popular caffeinated beverage that
effects of caffeine on insulin resistance diminished with
has not been linked to diabetes risk.
chronic consumption, while Battram et al16 found that

coffee had less effect than caffeine by itself. Hence other
MATERIALS AND METHODS
components in coffee may counteract the effects of caf-
Subjects
feine on glucose metabolism.16 Chlorogenic acid (CGA),
Eight (5 males, 3 females) healthy, non-smoking, regular
for example, the chief phenolic compound in coffee, can
coffee drinkers (? 1 cup/day) were recruited by adver-
inhibit glucose absorption from the small intestine17 and

down-regulate gluconeogenesis via the inhibition of glu-

cose-6-phosphatase.18,19 CGA supplements have been
Corresponding Author: Prof JC Brand-Miller, Human Nutri-
promulgated as an “alternative strategy” to a low glyce-
tion Unit, G 08, The University of Sydney, Sydney, NSW, 2006,
mic index (GI) diet.20 Tea also contains caffeine, but
Australia
unlike coffee, it contains no CGA, and tea drinking has
Tel: +61 2 9351 3759; Fax: +61 2 9351 6022
not been linked to reduced risk of diabetes.21, 22
Email: j.brandmiller@mmb.usyd.edu.au
We hypothesized that one mechanism which may ex-
Manuscript received 4 July 2008. Initial review completed 8
plain the effects of coffee drinking on the risk of type 2
December 2008. Revision accepted 12 December 2008.

658
JCY Louie, F Atkinson, P Petocz and JC Brand-Miller
tisement from the University of Sydney student popula-
Hitachi 912 Automatic Analyzer (Roche Diagnostics,
tion. The mean ± SEM age, weight and BMI of the sub-
Indianapolis, IN) employing the hexokinase/glucose-6-
jects were 26.3 ± 1.8 y (range 20 - 35 y), 62.2 ± 3.5 kg
phosphate dehydrogenase method (Unimate 5 Gluc HKTM,
(range 45.0 – 78.0 kg) and 20.8 ± 0.7 kg/m2 (range 17.6 –
Roche Diagnostic Systems, Frenchs Forest, Australia).
24.3 kg/m2) respectively. The study protocol was ap-
The intra-assay coefficient of variation is < 1.5% and the
proved by the Human Research Ethics Committee of the
mean ± SEM inter-assay coefficient of variation is 11 ±
University of Sydney and volunteers gave written, in-
4%. Insulin was quantified using a commercial radioim-
formed consent.
munoassay kit (Coat-a-Count, Diagnostic Products Cor-

poration, LA, USA) in a single batch, with a mean ± SEM
Study design
inter-assay CV of 15 ± 6%. Cumulative changes in
Subjects undertook a total of 7 separate sessions in ran-
plasma glucose and insulin response were expressed as
dom order after an overnight fast. The test beverages rep-
the area under the 120 minute response curves (AUC)
resented 250 mL of the following solutions: black coffee
calculated according to the trapezoidal rule, truncated at
(COF, made with 4g Nestlé® NESCAFÉ® Blend43TM
the 0 minute reading (baseline concentration).24 Areas
instant coffee powder containing ~150 mg of caffeine),
below the baseline were ignored. A ‘glucose score’ was
black coffee sweetened with 10 g of sucrose (COF+SUC),
calculated for each subject using the following equation:
black decaffeinated coffee (DECAF, made with 4 g
Nestlé® NESCAFÉ® Decaf® instant coffee powder),
Area under the 120 min glucose response curve produced by prefeedingof the test drink
Glucose Score =
x 100
black tea (TEA, made by brewing 1 Tetley® black tea
Area under the 120 min glucose response curve produced by control (water)
bag for 3 minutes), 10 g sucrose (SUC) and hot water
Insulin scores were calculated in similar fashion. Results
(CON, tested on 2 occasions). All beverages were made
were expressed as mean ± SEM glucose or insulin score.
with just boiled water and consumed within 10 min. Arti-
Two-way ANOVA with drinks as fixed factor and sub-
ficial sweetener (Equal® Tablets) was used to sweeten
jects as random factor was used to determine statistical
the test drinks if desired, remaining constant within sub-
differences among the test drinks (Statistical Packages for
jects. After 55 min, 2 fingerprick blood samples (~1 mL)
Social Sciences version 15). A p value < 0.05 was con-
were taken 5 min apart (-5 and 0 min, baseline concentra-
sidered marginally significant and p < 0.01 was consid-
tion) and subjects consumed 586 g of instant mashed po-
ered statistically significant. No adjustment was made for
tato (Edgell® Instant Mash, prepared according to in-
multiple comparisons because only specific comparisons
structions, providing 75 g of available carbohydrate).
were of a Priori interest.
Subjects were permitted to drink 250 mL water with the

meal, remaining constant within subjects. A further 6
RESULTS
blood samples were collected at 15, 30, 45, 60, 90 and
Changes in plasma glucose and insulin concentrations are
120 min after the start of the meal using an automated
shown in Figure 1 and 2 respectively. Compared with
lancet device (Accu-Chek® Safe-T-Pro Plus, Roche Di-
CON (hot water), COF consumed 1 h before a meal in-
agnostics Australia, Castle Hill, Australia). Samples were
creased postprandial glycemia (+28%, p = 0.022). In con-
collected into previously heparinized (10 IU heparin so-
trast, sweetened coffee (COF+SUC) decreased glycemia
dium salt, Sigma Chemical Co., St Louis, USA) Eppen-
compared with either COF (-38%, p < 0.001) or CON (-
dorf micro-centrifuge tubes and centrifuged at 12,500 g
20%, p = 0.100). DECAF, TEA and SUC produced simi-
for 1 min. Plasma was collected into chilled tubes and
lar postprandial glucose responses to CON. Apart from
stored at -20oC until analysed (< 1 month). Plasma glu-
COF vs. DECAF (insulin scores 122 ± 13 vs. 98 ± 6, p =
cose concentration was measured in duplicate using a
0.036), there were no significant differences in insulin


(a)
(b)
p < 0.01
160%
4.5
CON
)
COF
*
126%
4
l
/
L

DECAF
140%
o
3.5
TEA
m
SUC
120%
#
+
(
m

3
98%
100%
100%
COF+SUC
e
100%
2.5
r
e
100%
**
c
os

o
79%
l
u

2
80%

G

e
Sc

a
1.5
os
m
60%
l
uc

1
l
as

G

P

0.5
n
40%
i
0
ge
20%
an -0.5 0
15
30
45
60
75
90
105
120
Ch
0%
-1
Time (mins)
CON
COF
DECAF
TEA
SUC
COF+SUC



Figure 1. (a) Changes in postprandial plasma glucose concentration over time and (b) ‘glucose scores’ (AUC expressed as % of control) pro-
duced by the different test beverages. Values are expressed as mean and mean + SEM respectively (n = 8). p values were calculated by two-
way ANOVA comparing CON with different test beverages. *COF vs CON, p = 0.022; #COF vs DECAF, p = 0.019; +COF vs TEA, p = 0.011;
**COF vs COF+SUC, p < 0.001.


Coffee and postprandial glycemia
659

(a)
(b)
400
CON
160%
p = 0.272
COF
)
L
350
DECAF
l/
140%
122%
o
TEA
113%
m 300
SUC
*
108%
120%
100%

(
p

COF+SUC
99%
lin 250
100%
r
e
100%
s
u

o
n
I
200
a
80%
m
lin Sc
150
s
u

l
as

60%

P

I
n

100
in
40%
ge
50
an
h

20%
C
0
0
15
30
45
60
75
90
105
120
0%
Time (mins)
CON
COF
DECAF
TEA
SUC
COF+SUC



Figure 2. (a) Changes in postprandial plasma insulin concentration and (b) ‘insulin scores’ (AUC expressed as % of control) produced by
different test beverages. Values are expressed as mean and mean + SEM respectively (n = 8). p values were calculated by two-way
ANOVA comparing CON with different test beverages. *COF vs DECAF, p = 0.036.

responses among the beverages.
mia. Using a realistic 1-hour pre-meal study design, one
Absolute glucose and insulin concentrations also var-
cup of normal coffee, but not decaffeinated coffee or tea,
ied significantly according to treatment (Table 1). Com-
had adverse effects on carbohydrate metabolism, increas-
pared to CON, there was a significantly lower plasma
ing postprandial glycemia (+28%) and insulin (+20%) to
glucose concentration at the start of the meal preceded by
a delayed high-carbohydrate meal. Battram et al16 found
DECAF (p = 0.007) and SUC (p < 0.001). Compared to
that caffeine, either in its pure form or in roasted coffee,
CON, COF+SUC tended to produce a lower 2-h glucose
reduces insulin sensitivity. In their double-blinded ran-
concentration (p = 0.023) but significantly higher plasma
domized trial, 11 healthy men consumed pure caffeine
insulin concentration at the start of the meal (p = 0.010).
(4.46 mg/kg body weight), roasted coffee (providing the
Glucose and insulin scores were correlated within the
same amount of caffeine as the capsules), placebo or de-
COF, TEA and SUC trials (Pearson correlation coeffi-
caffeinate coffee on separate occasions, and underwent a
cient = 0.66, 0.66 and 0.74 respectively), but not
2-h oral glucose tolerance test (OGTT) one hour after that.
COF+SUC or DECAF (Pearson correlation coefficient <
They found pure caffeine produced a significantly higher
0.05).
blood glucose response and significantly lower insulin

sensitivity index (ISI) during the 2-h OGTT compared to
DISCUSSION
the same amount of caffeine in roasted coffee. This is
On the basis of observational studies linking coffee drink-
consistent with our findings which showed caffeinated
ing with reduced risk of type 2 diabetes, we hypothesized
coffee impaired glucose metabolism and produced higher
that coffee drinking might attenuate postprandial glyce-
insulin response. Remarkably, the addition of a small


Table 1. The effect of pre-feeding different test drinks 1 hour before consumption of a starchy meal on plasma glu-
cose concentrations.

AUC

Start of meal
p
Peak response
p
2-hour glucose
p
p
(mmol/L·120
(mmol/L)
value†
(mmol/L)
value†
(mmol/L)
value†
value††
min)
CON
5.49 ± 0.09
-
9.06 ± 0.15
-
5.12 ± 0.28
-
197 ± 19
-
COF
5.27 ± 0.12
0.077
9.41 ± 0.37
0.325
4.90 ± 0.28
0.304
248 ± 31
0.022
DECAF
5.13 ± 0.13
0.007
8.80 ± 0.42
0.482
4.78 ± 0.16
0.115
193 ± 23
0.948
0.294‡
0.096‡
0.572‡
0.019‡
TEA
5.28 ± 0.13
0.087
8.79 ± 0.27
0.463
4.92 ± 0.38
0.346
196 ± 32
0.782
0.952§
0.091§
0.931§
0.011§
SUC
4.97 ± 0.12
< 0.001
8.53 ± 0.18
0.143
4.86 ± 0.16
0.227
198 ± 21
0.917
COF+SUC
5.54 ± 0.19
0.690
8.72 ± 0.25
0.346
4.61 ± 0.24
0.023
155 ± 19
0.100
0.021¶
0.059¶
0.191¶
< 0.001¶

Values are presented as mean ± SEM (n = 8).
p values were calculated by two-way ANOVA comparing CON with different test beverages
p values were calculated by two-way ANOVA comparing DECAF with COF
§p values were calculated by two-way ANOVA comparing TEA vs COF
p values were calculated by two-way ANOVA comparing COF+SUC vs COF
††p values were calculated after the AUC were converted to glucose scores (see text)


660
JCY Louie, F Atkinson, P Petocz and JC Brand-Miller
amount (10 g) of sucrose to the coffee reversed this effect,
A particular strength of our study was the deliberate
and reduced the postprandial glycemic response by ~40%
use of fingertip blood sampling. The site of sampling has
(COF vs. COF+SUC, p < 0.001). This could be explained
an important effect of blood glucose variability and on the
by a significantly higher plasma insulin level at the start
ability to detect rapid changes in blood glucose as occurs
of meal (22.2 ± 3.2 vs. 29.5 ± 4.7, p = 0.021) which sug-
after a carbohydrate-containing meal. Ellison et al29 re-
gests a ‘priming’ effect of COF+SUC, resulting in an
ported that finger tip blood samples may identify changes
earlier peak insulin response to the test meal. Together,
in blood glucose immediately after a meal more readily
these observations might explain the conflicting literature
than that from forearm and thigh sites. In recent research
whereby coffee drinking has been linked to reduced risk
employing fingertip sampling, we were able to document
of diabetes6,9,10 despite adverse effects on insulin sensitiv-
clinically useful effects of alcoholic beverages on post-
ity.12,14 The common habit of sweetening coffee to mask
prandial glycemia,30 differences that were probably unde-
bitterness, but not hot tea, may account for why coffee is
tectable in earlier studies employing venous sampling. In
more consistently associated with reduced risk.
the present study, we recruited normal healthy young sub-
The novel observation that 2 teaspoons of sucrose
jects using a pre-meal design that represented realistic
could not only neutralize the effect of coffee, but also
food patterns, i.e., consuming coffee between meals. One
have additional beneficial effects, was unexpected. A
cup of coffee or tea followed by 75 g carbohydrate por-
small amount of fructose, one of the products of sucrose
tion is a physiological amount, an average person con-
digestion, is known to inhibit gluconeogenesis.25 How-
suming 240 g carbohydrate per day. These attributes in-
ever, in the present study, sucrose alone (in hot water) did
crease the generalisability of the findings but the small
not produce separate beneficial effects. This suggests the
number of subjects (n = 8) and the fact that most were of
possibility of an interaction between the components of
Chinese ethnicity suggests caution. Young lean healthy
coffee and sugar. Unfortunately, most of the epidemiol-
subjects of Asian origin display higher postprandial gly-
ogical studies on the subject of coffee1,3-5,9,26 did not ex-
cemic and insulinemia than their Caucasian counterparts31
amine the separate effect of consuming unsweetened cof-
and there may be differences in insulin sensitivity and
fee vs. sweetened coffee. Indeed, most studies adjusted
postprandial glycemia between the two groups. Thus the
for differences in macronutrient intake, so that any poten-
findings should be confirmed in other groups.
tial effect of consuming extra sucrose among coffee
In summary, the hypothesis that coffee consumption 1-
drinkers was removed. A study by van Dam et al10 on the
hour before meal would reduce postprandial glycemia and
other hand, showed consistent protective effect of habit-
insulinemia was not supported by the current findings.
ual coffee drinking on 2 hour postprandial blood glucose
Indeed, prior coffee consumption increased postprandial
level regardless of sugar use, but the association was
glycemia by 28%. However, the observation that addition
slightly attenuated (from -8.8% to -8.4%) with adjustment
of a small amount of sucrose (10 g) to coffee reverses this
on added sugar intake, suggesting possible contribution of
effect is novel and noteworthy, suggesting that greater
the use of sugar in the risk reduction.
attention be given to food combinations and interactions
In a systematic review, van Dam et al26 showed that
in clinical and epidemiological research.
habitual coffee consumption, particularly of decaffeinated

coffee, was linked to a substantially lower risk of devel-
ACKNOWLEDGEMENTS
oping type 2 diabetes with a RR in the highest vs. lowest
We would like to thank Kai Lin Ek, and Karola Stockmann for
quintile of consumption of coffee = 0.65. The authors
their technical assistance in the testing kitchen and laboratory.
suggested that components of coffee such as CGA17,18,27

and quinides28 improved either the postprandial glycemic
AUTHOR DISCLOSURES
response and/or insulin sensitivity, contributing to the
Professor Jennie Brand-Miller serves on the board of directors
of Glycemic Index Ltd, a non-profit company that administers a
lower risk of T2DM.19 In the present study, we demon-
food labeling program in Australia (www.gisymbol.com.au), as
strated a significantly lower baseline plasma glucose con-
director of a not-for-profit GI testing service at the University of
centration (p = 0.007) in DECAF vs. CON, supporting the
Sydney www.glycemicindex.com and is the co-author of a se-
view that compounds in coffee may be producing benefi-
ries of books under the title ‘The New Glucose Revolution’
cial effects. However, this did not extend to the whole
(Marlowe and Co., USA). Jimmy Chun-Yu Louie, Fiona Atkin-
postprandial period, there being no difference between
son and Peter Petocz, no conflict of interests.
the glucose and insulin scores of DECAF vs. CON. This

is in contrast to the findings of Battram et al,16 who
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662
JCY Louie, F Atkinson, P Petocz and JC Brand-Miller
Original Article

Delayed effects of coffee, tea and sucrose on postprandial
glycemia in lean, young, healthy adults

Jimmy Chun Yu Louie MNutrDiet1, Fiona Atkinson MNutrDiet1, Peter Petocz PhD2,
Jennie C Brand-Miller PhD1

1Human Nutrition Unit, School of Molecular and Microbial Biosciences, The University of Sydney, Sydney,
Australia

2Department of Statistics, Macquarie University, Sydney, Australia

????????????????????????
??

??????????????????? 2 ???????????????
???????????????????????????????????
?????????? 1 ????????(??????)?????????
???????????????????????????8 ???????
????? 250 ?????(COF)???? 10 ???(COF+SUC)??????
?(DECAF)???(TEA)???(? 10 ????SUC)???(CON)? 1 ????
??????????????? 2 ???????????????????
??????????????????????????????(CON)?
??COF ?????????? 28% (p=0.022)?????COF+SUC ???
COF (-38%?p<0.001)????(-20%?p=0.100)??????????????
???????????????????????????????????
??????????????????????????(p<0.01)????
????????(COF+SUC)?????????????????????
????????????????????????????????

??????????????????????????


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