Sugars and Blood Glucose Control"2: Thomas MS Wolever and Janette Brand Miller

Sugars and blood glucose control”2
Thomas MS Wolever and Janette Brand Miller
ABSTRACT The rise of blood glucose in normal and diabetic meal carbohydrate allowance if glycosylated hemoglobin con-
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subjects after meals varies markedly and depends on many factors, centrations are normal or near normal (5). The National Insti-
including the source of the carbohydrate, its method of prepara- tutes of Health concluded that added sugars intake up to 5% of
tion, and the composition of the total meal. Classification of carbohydrate energy is acceptable if used in mixed meals by
carbohydrates as simple or complex does not predict their effects lean subjects without carbohydrate-aggravated hyperlipidemia
on blood glucose or insulin. Rapidly absorbed carbohydrates, (6). The recommendation from the Dietitians Association of
which produce large blood glucose and insulin responses, may be Australia is also that added sugars intake should amount
in the form of both sugars and starches. Sugars added to foods have to 5% of total energy intake (7). Nevertheless, this value
no different effect on blood glucose from those of sugars alone. represents only about one-half of the average consumption
The natural sugars in fruit and fruit juices raise blood glucose by the general population (8). Thus, the implication still is
approximately as much as does sucrose and less than do most that individuals with diabetes should limit their sugars in-
refined starchy carbohydrate foods. The optimum amount of sug- take to amounts lower than those consumed by the rest of the
ars in the diet is not known. However, undue avoidance of sugars population.
is not necessary for blood glucose control and is not advised The use of glucose and glucose-containing simple sugars has
because it may result in increased intakes of fat and high- been restricted in the diets of most diabetic patients on the
glycemic-index starch. Am J C/in Nutr 1995;62(suppl):212S- premise that these sugars cause rapid rises in blood glucose
275. concentrations (9). This belief, however, stems largely from
Allen’s work on dogs in the 1920s (iO). Allen observed that
KEY WORDS Diet, sugars, glucose, glycemic index, in- pancreatectomized dogs showed greater glycosunia after glu-
sulin, sucrose, fructose, diabetes cose ingestion than after starch ingestion. On the basis of this
and other findings as well as his own clinical experience, Allen
concluded that glucose, compared with the complex carbohy-
drate stanch, caused a more rapid rise in blood glucose con-
INTRODUCTION
centrations and therefore greaten glycosunia. This poorly based
Two important aims in the dietary management of diabetes conclusion was subsequently expanded to include all simple
mellitus are to optimize blood glucose control and to minimize sugars, including common table sugar, or sucrose (iO).
the risk of hypoglycemia in people treated with insulin. The belief that meals containing sugars result in higher blood
Achieving these goals reduces the risk of acute and long-term glucose concentrations than do meals containing equivalent
complications (1). amounts of stanch has persisted in the minds of lay and scien-
In the late 1970s and early 1980s, the diabetes associations tifically trained people alike. Many of the studies that support
of many countries around the world reviewed their dietary the belief that simple sugars are more rapidly digested and
recommendations and began to advise a decrease in fat intake absorbed than complex carbohydrates have limitations. In
with a concomitant increase in carbohydrate intake (2, 3). In some studies, the lower glycemic response after starch inges-
contrast, advice regarding the restriction of sugars (glucose, tion can be explained by the use of uncooked starch (1 1).
fructose, sucrose, and lactose) was unchanged. However, the Uncooked stanch is not as readily hydrolyzed and is therefore
rationale behind the elimination of sugars was questioned and more slowly absorbed than cooked stanch (i2). Cooked
there was a general consensus that the harmful effects of sugars starches such as bread, rice, and potato cause glycemic re-
on people with diabetes had been exaggerated. Another con- sponses that are similar to or only slightly less than the glyce-
cern was that restricted sugars intake was often considered the mic response to glucose (ii, 13) and frequently the same or
only significant part of the diabetic diet, whereas other impon- greater than that observed with sucrose (i 1, 13, i4). Other
tant aspects of dietary therapy were ignored. In 1986 the investigators have drawn conclusions from comparisons
American Diabetes Association further revised its dietary nec-
ommendations. The consumption of a modest amount of sugars I From the Department of Nutritional Science, University of Toronto,
was considered to be acceptable, contingent on the mainte-
Ontario, and the Human Nutrition Unit, Department of Biochemistry,
nance of metabolic control (4). Other countries made similar University of Sydney, New South Wales, Australia.
cautious recommendations during the 1980s. The Canadian 2 Reprints not available. Address correspondence to TMS Wolever,
Diabetes Association suggests that < 3 g sucrose may be used Department of Nutritional Science, University of Toronto, 150 College
by people with diabetes without being counted as part of the Street, Toronto, Ontario, Canada M5S 1A8.
2125 Am J C/in Nuir l995;62(suppl):212S-27S. Printed in USA. © 1995 American Society for Clinical Nutrition
SUGARS AND BLOOD GLUCOSE CONTROL 2135
between test meals of unequal fat content (15) and between by the same subjects. The published GI value for a food was
liquid test meals containing simple sugars and solid test the mean value for six to eight individuals and the concept
meals containing starch (16). allowed comparisons of foods tested in different groups of
subjects. On the GI scale where 50 g glucose has a value of
100, sucrose was 60 and bread was 69. Many foods containing
ACUTE RESPONSES TO SUGARS COMPARED WITH
added sugars, such as ice cream and some chocolate bars,
STARCH IN HEALTHY SUBJECTS
produced lower GI values than did common starchy foods such
In 1976, Crapo et al (1 1) studied plasma glucose and insulin as white or whole-meal bread. For the past 10 y Jenkins’ group
responses to glucose, sucrose, and various starches given alone has advocated using white bread as the standard food for GI
in a drink and in combination with other nutrients (protein and calculations (white bread is ascribed a GI value of 100) (21),
fat) as a meal. For both drinks and meals, glucose and sucrose which yields greaten GI values than when glucose is used as the
produced significantly greater peak concentrations of plasma standard (when the GI of bread was used as the standard, the GI

glucose and insulin than did stanch. However, these findings of glucose was found to be a mean of 136 in five studies).
are confounded by the fact that the starch was raw and that 100 However, Woleven (22) showed that bread-based GI values can
g sucrose was compared with 50 g glucose and 50 g stanch to be adjusted proportionally to give the GI values that would
make the test carbohydrates glucose equivalent. have been obtained if glucose was used as the standard. For the
In a later study, Crapo et al (17) examined the acute effects purposes of this paper, the GI values quoted will be based on
of ingestion of 50-g loads of glucose, sucrose, and fructose 50 g glucose giving a GI of 100. The methods used to deter-
alone in a drink on in combination with protein and fat in a test mine the GI values of foods and the validity of the GI concept
meal. For both drinks and meals, fructose ingestion resulted in
and its implications were reviewed in detail elsewhere (21, 22).
significantly lower plasma glucose and insulin responses than
Pure solutions of different sugars were also compared using
did sucrose or glucose ingestion. Plasma glucose responses to
GI methodology (13). Although glucose had a score of iOO,
glucose were slightly (but not always so) greaten than the
fructose produced a mean score of only 23 in four studies. It
responses to sucrose. This finding, however, is contrary to the
became clear that the GI of a sugar could be predicted on the
glycemic index (GI) data published by Jenkins et al (13) and
basis of the molar ratio of glucose to other monosaccharides in
that of others as discussed below.
the sugar molecule. Hence, maltose, a disaccharide composed
of two glucose molecules, gave a scone of i05 ± 12 in one
EFFECT OF CHAIN LENGTH study (i ± SE, n 6) whereas sucrose, composed of glucose
and fructose, gave an average score of only 61 (the mean of the
In 1978, Wahlqvist et al (18) showed that the number of values for glucose, 100, and fructose, 23) in five studies.
glucose units in the polysacchanide molecule had no relation to
Honey, which is a mixture of fructose and glucose, has given
the glycemic effects of the carbohydrate. They compared glu-
variable results from as low as 58 to as high as 87, possibly
cose, maltose, and an oligosacchanide mixture (with an average
because of differences in monosaccharide composition (some
chain length of five glucose units) and a polysaccharide
manufacturers add glucose to their honey). Lactose, which is a
(starch) and found no significant differences with any of the
disaccharide of glucose and galactose, had a mean GI of 46 in
carbohydrate solutions in the rise and fall of blood glucose
two studies (22).
concentrations in healthy subjects.
The small hyperglycemic effect of fructose is explained
Jenkins et al (13), however, showed that the effects of starch
partly by the low rate of absorption of fructose compared with
on plasma glucose varied depending on food source and other
glucose (23) and partly by the very small effect of fructose on
factors. The starch in lentils produced very small glycemic
effects compared with equivalent amounts of stanch in bread. the overall rate of glucose appearance. Fructose is thought to be
They and others subsequently showed that the rate of digestion metabolized primarily in the liver, where it is converted to
of starch in the food in vitro was highly correlated with the fructose-i-phosphate, which, in turn, can be converted to glu-
glycemic effects of the food (19, 20). Until then it was corn- cose or lactate. Glucose can be released into circulation or
monly believed that starches were all digested and absorbed stored as glycogen, whereas lactate is released into circulation
slowly because of their long molecular structure. It is now and can ultimately be converted to glucose via the Con cycle
known that some starches such as that in instant potato are (24). There is evidence that “50% of a fructose load is con-
digested so rapidly that their glycemic effect is similar to that vented to glucose (25). However, the glucose synthesized from
of an equivalent glucose load (13). fructose is not additive to the endogenously produced glucose
present in the basal state but rather replaces an important part
of it. Thus, fructose has a sparing effect on endogenous glucose
GLYCEMIC INDEX OF FOODS
metabolism. The small hyperglycemic effect of lactose is partly
During the late i970s and early i980s, there was a swing explained by a slow rate of hydrolysis to its component sugars
away from the study of the effects of simple sugars alone in a (23). Galactose, like glucose, is actively absorbed in the small
drink or in a formula test meal to the examination of metabolic intestine. In the liver, galactose is converted by way of UDP-
responses to commonly eaten foods and meals. In 1981, Jen- glucose and USP-galactose to glucose, but very little glucose
kins et al (13) published the first comprehensive classification appears in blood after oral or intravenous galactose (26, 27).
of foods on the basis of their acute glycemic effect. Foods were The galactose rise in the blood is much lower in the presence
given in equicarbohydrate portions and the resulting area under of glucose, presumably because glucose and galactose compete
the glucose curve was compared with that for glucose ingested for active transport (28).
2145 WOLEVER AND BRAND MILLER
STUDIES IN INDIVIDUALS WITH NON-INSULIN- commonly eaten foods has no significant effect on either blood
DEPENDENT DIABETES MELLITUS glucose on plasma insulin concentrations in NIDDM.
Early on, the glycemic effects of four breakfast meals con-

taming various amounts of starch and sugars (sucrose, fructose, STUDIES IN INDIVIDUALS WITH INSULIN-
and lactose) were studied in a group of subjects with non- DEPENDENT DIABETES MELLITUS
insulin-dependent diabetes mellitus (NIDDM) and good glu-
cose control; the sugars in the four meals contributed 5%, 30%, Forlani et al (37) studied the effect of substituting 28 g
45%, and 60% of total carbohydrate (29). Contrary to the sucrose for starch in a mixed meal given to subjects with
author’s expectations, the breakfasts that contained the highest insulin-dependent diabetes mellitus (IDDM) controlled by an
concentration of sugars produced significantly smaller blood artificial pancreas. Plasma glucose concentrations and insulin
glucose responses than did meals in which wheat starch infusion rates delivered by the artificial pancreas did not show

predominated. any significant differences with respect to basal and peak
When Crapo et al (30) examined the acute effects of the values, peak times, and areas under the curve. In the study by
ingestion of 50-g loads of glucose, sucrose, and fructose in Hassinger et al (38) starch was exchanged for 3 d at the
subjects with NIDDM, fructose ingestion resulted in signifi- breakfast meal by either 30 g xylitol (a nonabsorbable sugar) or
cantly lower plasma glucose and insulin responses than did 30 g sucrose (27% of total energy). Blood glucose concentra-
sucrose or glucose ingestion. However, compared with people tions and insulin requirements were measured by a glucose-
without diabetes, there were smaller differences between the controlled insulin infusion pump. Plasma glucose concentra-
tions after the sucrose breakfast were not statistically different
response to fructose and the responses to sucrose and dextrose.
from the other test carbohydrates. However, insulin require-
This was due principally to an increased response to fructose in
ments after sucrose significantly exceeded that after both xy-
NIDDM. Similarly, fructose-sweetened cakes and ice cream
litol and starch during the first 1 and 2 h, respectively.
produced lower glycemic responses than did sucrose-sweet-
Vaaler et al (39) studied blood glucose responses to sand-
ened cakes and ice cream, respectively (17). The differences
wiches with jam containing either 18 g sucrose on sorbitol
between the responses to fructose- and sucrose-sweetened
(19% of energy) in young subjects with IDDM. The sucrose
foods in persons with NIDDM were again smaller than that for
test meal produced a slightly faster postpnandial rise in blood
persons without diabetes.
glucose than did the sorbitol-sweetened meal, but this differ-
In subjects with NIDDM and poor glucose control, there
ence was not statistically significant at any time.
were no significant differences in plasma glucose or insulin
In a group of IDDM subjects with well-controlled blood
responses between test meals containing 24-25% sucrose, po-
glucose, Steel et al (40) measured the glycemic response to
tato, or wheat starch (31). However, a test meal containing
four different 20-g carbohydrate midmorning snacks of foods
24-25% fructose produced smaller plasma glucose responses
containing sucrose, fructose, or starch. There were no signifi-
than those of the sucrose, potato starch, wheat starch, and
cant differences between the glycemic effects of the four dif-
glucose meals.
ferent snacks. Bantle et al (31) reported findings in IDDM
In individuals with NIDDM and good glucose control, Slama
subjects similar to those found in both NIDDM and normal
et al (32) examined plasma glucose and insulin responses to a
subjects. Finally, adding 9% of energy as sucrose in exchange
sucrose-sweetened rice cake and a saccharin-sweetened rice
for stanch had no effect on blood glucose responses oven a 14-h
cake taken at the end of a regular mixed meal and Bornet et al
period in children with IDDM (41).
(33) examined the effect of exchanging sucrose or honey for
Overall, the evidence suggests that the isoenergetic exchange
stanch in a breakfast meal. In both studies there were no
of sucrose and starch at moderate intakes has no significant
significant differences between sucrose- and stanch-containing
effect on blood glucose responses in subjects with IDDM. In
meals with respect to plasma glucose and insulin responses,
some cases, however, insulin requirements may be higher if
whether in peak values, peaking times, or areas under the
sucrose replaces a low-GI carbohydrate.
curve.
There is some evidence that the effects of various sugars on
acute blood glucose responses in subjects with diabetes may
NATURALLY OCCURRING COMPARED WITH
depend on the severity of the diabetes. Wolever et al (34) and
REFINED SUGARS IN FOODS
Gannon et al (35) found that sucrose gave a glycemic response
intermediate between that of glucose and fructose in subjects Sugars in their natural state in plant foods are thought to
with NIDDM, as would be expected from the results of studies produce much flatter glycemic and insulinemic responses than
in nondiabetic subjects. However, Akgun and Ertel (36) found do their processed counterparts on foods containing added
that the expected difference between sucrose and fructose was sugars, although there is little scientific evidence to substanti-
only seen in subjects with NIDDM and with a fasting plasma ate this view. The results of one widely quoted study by Haben
glucose concentration < 7.7 rnmolfL (“ 140 mg/dL) and dis- et al (42) showed that apples in the form ofjuice on puree gave
appeared in those with a fasting glucose concentration > 7.7 rise to higher serum insulin responses and less satiety than did
mmolfL. whole apples. The differences in glycemic responses, however,
Hence, differences in blood glucose and insulin responses were not statistically significant. Jenkins et al (13) found
between sucrose- and fructose-sweetened foods and meals ap- that the GI of apple juice was similar to that of whole apples
pear to be smaller in individuals with NIDDM than in healthy and the GI of orange juice was similar to that of whole oranges
subjects. However, the isoenergetic exchange of sucrose and (Figure 1). Canned peaches in natural juice have the same GI
starch at moderate intakes and in a mixed meal composed of as do fresh peaches but those canned in sugar syrups have a
SUGARS AND BLOOD GLUCOSE CONTROL 215S
Bread
cherries
plum
grapefruit
peaches
Glycemic Index pear
(Glucose = 100) apples
oranges
grapes
mango
pawpaw
kiwifruit
banana,

rockmelon
pneapple
Armies Oranciea Pineapple Grapefruit watermelon
.--- ,. 1. .
FIGURE 1. Glycemic index (GI) of whole fruit compared with fruit 20 40 60 80
juice (GI of glucose = 100). Results are average values calculated from Glycemic index
published sources (13, 43-46). (Glucose = 100)
FIGURE 3. Glycemic index (GI) of fruit (GI of glucose 100). Results
are average values calculated from published sources (13, 43-47).
higher GI (Figure 2). This suggests that the disruption of cell
structure brought about by canning does not in itself alter the
rate of absorption of the sugars, although this may apply only were expressed on a scale on which glucose was 100. The
to peaches. median GI and insulin index of all the foods tested in eight
The GIs of fresh fruit vary over a threefold range from 22 for healthy subjects were 56 (range 14-102) and 56 (range 24-
cherries to 72 for watermelon (Figure 3). Tropical fruit have 124), respectively. The median GI of the foods containing
higher values than do temperate fruit. The differences among added sugars, 58, was similar to that of foods containing
the fruit may arise because of differences in monosaccharide naturally occurring sugars, 53 (Figure 4). Likewise, the me-
composition (particularly the ratio of glucose to fructose) and dian insulin index of the foods containing added sugars, 61,
the amount and nature of the fiber. Ha et al (43) found that was not significantly different from that of foods containing
contents of total and individual sugars correlated with the GI of naturally occurring sugars, 56.
kiwi fruit but not of apples and pears. Ripeness may also be Brand Miller and Lobbezoo (46) also studied breakfast cc-
relevant; undernipe bananas give a lower glycemic response reals and baked goods (muffins and banana cake) prepared with
than do overripe (48, 49). In subjects with NIDDM, glycemic and without added sugars and tested in equal carbohydrate
and insulinemic effects of foods rich in natural sugars such as portions. Products without added sugars gave similar if not
fruit and milk are similar to those in nondiabetic subjects both slightly higher responses than did those containing added sug-
in the context of single foods (35, 44) and mixed meals (50). ars (Figure 5 and Figure 6). Only with dairy products did
Brand Miller et al (45-47) studied glycemic and insulin incorporation of added sugars lead to higher glucose and insu-
responses in healthy subjects to more than 40 foods containing lin responses than for the counterpart without added sugar
sugar and compared foods with added sugars with those con-
taming naturally occurring sugars. The GI and insulin index
100#{149}
were determined according to standardized methodology and
0
0
80
0 S
60
. II
Glycemic Index CU)

0
(Glucose = 100, 40#{149}
20#{149}
n-40 n=34
0 . - . -
) Naturally Foods I
occurring containing
Apricots Peaches Peaches Peaches Pears sugars refined sugars
FIGURE 2. Glycemic index (GI) of fresh fruit vs canned fruit (GI of FIGURE 4. Distribution of the glycemic indexes (GIs) of foods con-
glucose = 100). Results are average values calculated from published taming naturally occurring sugars only and foods containing added sugars
(43-46) and unpublished sources. (GI of glucose = 100). Data from references 45-47.
2i6S WOLEVER AND BRAND MILLER
Sweetened breakfast cereals
Sustafn
Sultana Bran
Special K
Miniwheats
.‘-
.ll
Nutrirain
0
Natural muss) 0
#{149}0
0
Toasted muesli
.l-
o
20’

All Bran
0
, . ‘ Banana cake ,‘ . Muffins Bread
L’c’:L’ , ,t: , ,
FIGURE 6. Cornparisqnothe glycemic indexes (GIs) of baked goods
Unsweetened breakfast cereals
with and withou’add#{233}d’siigars (Glbfgl#{252}cose = 100). Data from references
‘,:A’i’.-k...r:,’ .. -.‘ #{149}.-s .. ‘
glucose curves but the insulin response to sucrose is higher

than the insulin response to glucose (1 1). This difference is
probably the result of the additional 50 g fructose equivalents
in the sucrose meal, which stimulates insulin with little effect
on plasma glucose (25). There is some evidence that fructose
increases plasma insulin responses; when fructose was con-
sumed 20 mm after an oral load of glucose on starch, plasma
insulin responses were increased (51). However, the amount
of fructose fed in this study was unphysiologically large
Glycemic index
(1.75 glkg).
(Glucose = 100)
Reiser et al (52) at the US Department of Agriculture re-
FIGURE 5. Comparison of the glycemic indexes (GIs) of breakfast ported the effects of a high-sucrose diet in individuals with an
cereals containing no added sugars and cereals in which sugars are incor- exaggerated insulin response to a carbohydrate load and there-
porated during manufacture (GI of glucose = 100). Results are average
fore at high risk of diabetes. The insulin response to sucrose
values calculated from published sources (13, 43-47). Sources of breakfast
loading was higher after 6 wk of consumption of the high-
cereals: Sustain, Sultana Bran, Special K, Miniwheats, Nutrigrain, Coco-
sucrose diet (30% by weight) than the stanch diet. Fasting
pops, All Bran, Rice Bubbles, and Cornflakes are from Kellogg Australia,
glucose and insulin were also elevated after the sucrose diet. A
Sydney; natural muesili, porridge, and Vits-Brits are from Uncle Toby’s,
Wahgunyah, Australia; toasted muesli is from Purina Foods, Wahgunyah, major confounding variable, however, was the gorging pattern
Australia; Weetabix is from Weetabix of Canada Ltd. Thornhill, Ontario; of consumption (iO% of energy at breakfast and 90% at sup-
shreaded wheat is from Nabisco Brands, Ltd, Toronto; and puffed wheat is
from Sanitarium, Sydney, Australia.
(Figure 7). This increase is predicted by the GI of the individ-

ual foods; unsweetened dairy products have a lower GI than
does sucrose itself. The effect of incorporating sucrose in a
food will therefore depend on the GI of the unsweetened food
(discussed below). In addition, we found no evidence of re-
bound hypoglycemia within 2 h of consumption of any of the .E II
foods containing added sugars, even after the confectionery .2 w
items that produced the highest responses (Figure 8). This EU)
0
study, which is distinguished by the large number of foods >1-
studied simultaneously, suggests that many foods containing

sugars, whether added or naturally occurring, probably affect
plasma glucose less than do most starchy foods in the Western
diet.
SUGAR AND INSULIN SECRETION

Chocolate
,
milk #{149} #{149}‘ Yogurt ‘ -
-‘.‘. .
Ice
‘-‘ -
confection
FIGURE 7. Comparison of the glycemic indexes (GI5) of dairy prod-

Glucose and sucrose, at a dose containing 50 g glucose (ie, ucts with and without added sugars (GI of glucose = 100). Data from
50 g glucose and 100 g sucrose), result in similar plasma references 45-47.
TABLE 1
Incremental area under the curve (LAUC) for plasma glucose and insulin
and calculated mixed-meal glycemic index (GI)’
Glucose Insulin 2
0 Meal GI
E IAUC IAUC
E
e mmo/’WL pmo/hIL
0)
C
(U Glucose 4.92 1125 79.8
‘C
0 Wheat starch 3.71 999 71.0
S
(I)
0 Potato starch 2.17 922 62.3
0
Sucrose 1.98 811 63.4
C.,
Fructose 1.10 704 42.3

I Data are for five different mixed meals of the same composition but
with one-half of the carbohydrate coming from glucose, wheat, potato,
sucrose, or fructose consumed by nondiabetic subjects (original data from
Time (mins) reference 31). Insulin areas under the curve calculated from mean values
FIGURE 8. Plasma glucose change after 50-g carbohydrate portions of given in Figure 2 of reference 31.
glucose, white bread, and two high sugar confectionery items (GI of 2 Meal GI calculated from GI values of the individual foods. GI of
glucose = 100). Data from references 45-47. Life savers is a form of glucose = 100. To adjust so that GI of bread 100, multiply by 1.36.
peppermint candy (Nabisco Foods, Lifesavers Division, Winston-Salem,
NC).
mixed meals containing sugars can be estimated from the GI
values of the individual foods provided that the nutrient com-
position of the meals is similar.
per), a pattern that also adversely affects glucose tolerance. The
Because sucrose alone has a glycemic response that is sim-
findings suggest that high-sucrose diets impair insulin sensi-
ilar to or less than that of starchy foods such as bread, potatoes,
tivity. However, there is no reason to believe that the effects
and rice, even large amounts of sucrose have no effect on
observed with sucrose would be restricted to sucrose per se and
would not also be produced by any diet with a high GI. overall glycemic responses. Indeed, sweetened breakfast cere-
als such as Golden Grahams (General Mills, Etobicoke, On-
In long-term experiments in rats fed moderate amounts of
tanio; GI = 75) often have a lower GI than do nonsweetened
sucrose (30% by wt), an increased insulin response to oral
glucose loading was seen in the presence of normal glucose cereals such as Rice Chex (Nabisco, Toronto, Ontario; GI =
93) (P < 0.05) (56). Sucrose will raise glycemic responses if

tolerance (53). These results also suggest that sucrose increases
insulin resistance, but again the effect may be related to the substituted for starchy foods such as beans that normally pro-
duce low blood glucose responses. Nevertheless, up to 20% of
overall GI of the diet rather than to sucrose pen se.
the starch from butter beans may be replaced by sucrose with
minimal increase in glucose and insulin responses but a large
PREDICTING THE ACUTE EFFECTS OF SUCROSE IN increase in palatability (57).
MIXED MEALS However, comparisons based on meals of equivalent carbo-
hydrate content may not be physiologic, because there is cvi-
The fact that mixed meals containing sucrose raise blood
glucose no more than a starchy meal with the same canbohy-
drate content has caused needless surprise and confusion. The 1200 Glucose
contribution of sucrose and other sugars to the overall blood
glucose response of mixed meals depends on the product of the
-J
GI of the sugar times the proportion of the total meal canbo-
-E: 900 Potato S
hydrate it contributes (54, 55). For meals of equivalent fat and
0
protein contents, plasma insulin responses are closely related to E
the meals’ blood glucose responses. Consider the results for
normal subjects from Bantle et al’s 1983 study (31). They fed 600
normal, NIDDM, and IDDM subjects five different mixed test
meals containing ‘#{176}‘2.93MJ (“700 kcal) with 84 g carbohy-
drate,
either
areas
under
31 g protein,
glucose,
under
the curve
the curve
fructose,
and
calculated
25 g fat. The
sucrose,
as reported
from graphs
potato,
carbohydrate
in the paper,
in the
on wheat.
the insulin
paper,
consisted
The glucose
areas
and the
of
I 300
meal GIs (54) are given in Table 1. Sucrose- and fructose-

containing meals did not produce high insulin responses in
1 2 3 4 5
relation to their glucose responses. Indeed, the best predictor of
the insulin response was the glucose response (r = 0.97, P < Glucose AUC (mmol’h/L)
0.01) (Figure 9). Interestingly, meal GI was a better predictor FIGURE 9. Relation between the area under the curve (AUC) for
of the insulin response (r = 0.94, P < 0.02) than of the glucose glucose and insulin for mixed meals of equal composition but with one-half
response (r = 0.93, P<0.05) (Figure 10). Thus, the relative of the carbohydrate consisting of fructose, sucrose, potato starch, wheat
size of acute blood glucose and insulin responses of different starch, or glucose. Data from reference 31 and Table 2.
TABLE 2
1200 5 Glucosei
GCucose Calculation of glycemic index (GI) of hypothetical breakfast cereal
..J -J meals with and without sucrose
‘Wheat ‘C
‘C 900 Potatoy
Wheat
0 0
/‘ . Sucrose a Meal and food amounts Food GI’ Carbohydrate Meal GI’
a fructose .5.3
600 Potato g
‘C ‘C
c S
In
I Sucrose
(proportion)
Oats without sucrose
U, 300
C Fructose Oatmeal (200 mL) 65 20 (0.77) 50.4
Milk (125 mL) 33 6 (0.23) 7.6
,J
0
-- 50 100
I.
0 50 100
Oats plus sucrose
Oatmeal (200 mL) 65 200 (0.56) 33.6
Glycemic Index Glycemic Index
Milk (125 mL) 33 6 (0.17) 5.5

FIGURE 10. Relation between the calculated meal GI (49) and the area Sucrose (2 tsp) 61 10 (0.28) 17.6
under the curve (AUC) for insulin and glucose for mixed meals of equal Larger oats portion, no sucrose
composition but with one-half of the carbohydrate consisting of fructose, Oatmeal (280 mL) 65 28 (0.78) 51.0
sucrose, potato starch, wheat starch, or glucose. Data from reference 31 and Milk (167 mL) 33 8 (0.22) 7.4
Table 2 (GI of glucose = 100). Cornflakes without sucrose
Cornflakes (250 mL) 89 20 (0.77) 68.5
Milk (125 mL) 33 6 (0.23) 7.6
dence that males and females of all ages who consume high Cornflakes plus sucrose
amounts of added sugars eat more total carbohydrate than do Comflakes (250 mL) 89 20 (0.56) 49.4
those who consume small amounts of added sugars (58-60). Milk (125 mL) 33 6 (0.17) 5.5
Thus, if sucrose is added to a meal with no reduction in the Sucrose (2 tsp) 61 10 (0.28) 17.1
Larger cornflakes portion, no sucrose
starch content of the meal, blood glucose and insulin responses
Cornflakes (350 mL) 89 28 (0.78) 69.2
would be expected to be increased compared with the same
Milk (167 mL) 33 8 (0.22) 7.4
meal without sucrose because the meal contains more carbo-
hydrate. In nondiabetic subjects consuming bread or glucose, ‘ GI of glucose = 100. To adjust so that GI of bread = 100, multiply by
1 .36. For meal totals see Table 3.
the incremental area under the blood glucose response curve
increases nearly linearly as the dose of oral carbohydrate is
increased from 0 to 50 g. However, the dose-response curve the glycemic response area by 16% if the cereal was oat-
flattens as the dose of oral carbohydrate increases from 50 to meal and only 7% if the cereal was corn flakes (Table 2 and
100 g (13) (Figure 11). Thus, the expected hyperglycemic Table 3). On the other hand, if sugar replaces cereal and milk
effect of adding sugar to a meal depends on the size of the meal carbohydrate such that total meal carbohydrate is kept constant,
and its GI. For example, adding 10 g sucrose to a bowl of cereal the glycemic response increases by only 2% for oats and
containing 20 g carbohydrate would be expected to increase the actually decreases by 6% if the cereal is corn flakes (see Tables
incremental glycemic response area by ‘#{176}‘26%
if the cereal was 3 and 4). Although the effects of replacing starch with sugar
oatmeal and = 16% if the cereal was corn flakes. Adding 20 g have been verified, it should be emphasized that the above
sucrose to 40 g carbohydrate from cereal would only increase estimates of the glycemic effect of adding sucrose to meals are
based on a mathematical model of glycemic responses and
have not been proven experimentally.
Co
a) SUGARS AND HYPOGLYCEMIA
0CO Hypoglycemia occurs when blood glucose concentrations

.
U)
a)
a) drop below normal and may occur with or without symptoms.
C.) In normal subjects, consumption of a solution containing 50 g
. L()
glucose is associated with a rapid rise in blood glucose and a

large insulin response. The latter stimulates peripheral glucose
uptake to such an extent the rate of glucose use exceeds the rate
of absorption and the blood glucose concentration falls below
0 40 80 120 the fasting level 2-4 h after the start of the drink. This is
Dose Oral Carbohydrate (g) accompanied by a modest counterregulatory response and a
rise in serum fatty acids, but there are usually no symptoms
FIGURE 1 1. Incremental blood glucose response areas ( ± SE) of (61). Reactive hypoglycemia is a rare syndrome in which the
normal subjects after they consumed different amounts of glucose, bread, symptoms of hypoglycemia occur 2-5 h after meals. It may be
and lentils. Data from reference 13. The curves represent the best fit for an caused by insulin-secreting tumors or gastric surgery but often
exponential association with the following equation: GR = GI X 1.73 X
the cause is unknown. In the absence of documented causes, it
(1 - e’o#{176}282><#{176}),
where GR = glycemic response expressed as a percent- is often difficult to prove that the symptoms occurred simulta-
age of that to 50 g carbohydrate from white bread, GI = GI of the food or
neously with the drop in glucose. The symptoms described
meal (GI of glucose = 100), and D = dose of oral carbohydrate in grams.
include tremor, lightheadedness, sweating, thirst, dizziness,
If the GI of bread = 100 the formula becomes: GR = GI X 1.27 X
mental lethargy, irritability, headache, and increased respira-
(1 - e#{176}’#{176}282><’).
TABLE 3
Predicted glycemic response of hypothetical breakfast cereal meals with and without sucrose expressed as a percent of the glycemic response to 50 g
carbohydrate from white bread
Relative glycemic
Meal (from Table 2) Carbohydrate Meal GI’
response
g
Oatmeal (200 mL) without sucrose 26 58.0 52.1
Oatmeal (200 mL) plus sucrose (10 g) 36 59.7 65.9
Oatmeal (400 mL) plus sucrose (20 g) 72 59.7 89.7
Cornflakes (250 mL) without sucrose 26 76.1 68.4

Cornflakes (250 mL) plus sucrose (10 g) 36 72.0 79.4
Cornflakes (500 mL) plus sucrose (20 g) 72 72.0 108.2
I Glycemic index of glucose = 100; to adjust so that the GI of bread = 100, multiply by 1.36.
2 Glycemic response relative to 50 g carbohydrate from white bread, calculated from the grams of carbohydrate in the meal (D) and the meal GI (GI
for glucose = 100) by using the following formula (see Figure 11): RGR = GI X 1.73 X (1 -e’ 0.0282 X D).
tion rate. Symptoms may occur when blood glucose concen- LONG-TERM EFFECTS OF SUCROSE AND FRUCTOSE
trations fall rapidly, as indicated by a hypoglycemic index IN DIABETES
> 1.0 (62). Treatment of reactive hypoglycemia involves
consumption of frequent, small, low-carbohydrate meals and As might be expected from the results of acute studies, isoen-
avoidance of sugars. However, when subjects with reactive ergetic replacement of starch with modest amounts of sucrose
hypoglycemia were given 100-g oral loads of glucose, su- (28-45 g/d) has no effect on blood glucose on insulin in patients
crose, on fructose, fructose resulted in flat blood glucose and with NIDDM (64, 65) or IDDM (66). Even as much as 220 g
insulin responses and did not cause hypoglycemic symptoms sucrose/d in NIDDM patients had no effect on blood glucose
in any subject (63). However, there was no indication in this control when compared with a diet containing < 3 g sucrose/d
paper that subjects were blinded to the treatment they re- (67). Adding 45 g sucrose/d (9% of energy) to the diet oven 6 wk
ceived, which may limit the validity of the conclusions had no effect on blood glucose in nine NIDDM subjects compared
about symptoms. Nevertheless, glucose caused a rapid and with 6-wk use of aspartame (68).
large increase followed by an undershooting of blood glu- Replacing sucrose in the diet (sucrose = 13% of total
cose and produced symptoms in all subjects. Sucrose die- energy) with fructose (range of fructose intake = 80-115
ited a flatter glycemic response than did glucose, with g/d) for 2 wk reduced postprandial blood glucose responses
symptoms in only 30% of the subjects. When 100 g sucrose without reducing insulin in seven subject with mild diabetes
or fructose was incorporated into cakes there were no hy- treated by diet alone (69). In a similar group of subjects,
poglycemic symptoms in any subject. when fructose replaced sucrose (76-124 g/d) for 3 mo there
was no effect on overall blood glucose control. However,
this study only had five subjects at the end so the power to
detect a difference was small (70). In a larger study, patients
with poorly controlled NIDDM were randomly assigned to
diets containing 60 g fructose/d or a nonenergetic sweetener
(saccharine on aspartame) for 6 mo and then crossed oven to
the other diet for another 6 mo (7i). After the subjects
= consumed the fructose diet for 6 mo, their fasting blood
0 glucose and glycosylated hemoglobin values decreased sig-
-J nificantly by 22% and 12%, respectively, whereas after 6 mo
0 of nonenergetic sweetener there were nonsignificant in-
E
E creases (Figure 12). There were no deleterious effects of
fructose on blood lipids.
CONCLUSIONS
Fasting
Blood Glucose Hemoglobin Sugars added to foods are no more likely to compromise
FIGURE 12. Long-term effect of fructose on blood glucose control in blood glucose control than are naturally occurring sugars or
patients with poorly controlled non-insulin-dependent diabetes. FBG, fast- most cooked starches. The natural sugar in fruit and fruit juices
ing blood glucose; Hb A1, glycosylated hemoglobin. Data from reference raises blood glucose concentrations approximately as much as
71. does table sugar (sucrose). This conclusion is based on the find-
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1:60-3.
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COMMENTARY peripheral insulin resistance. Is there evidence that patients

McDonald: Obesity and inactivity are consistently shown to with NIDDM who are not obese differ in their response to
be major risk factors for the development of glucose intol- sucrose compared with obese NIDDM individuals? That is,
erance and NIDDM (1-5). On the other hand, Wolever and have previous investigations suggesting a sucrose-induced
Brand Miller point out that Reisen et al (6-8) conclude that glucose intolerance adequately controlled for the effects of
insulin response is elevated after a sucrose diet and reflects obesity and/on inactivity?
The authors describe the symptoms of reactive hypoglyce- If a postprandial drop in blood glucose and insulin does
mia. These symptoms are similar to those described in the lay impair physical activity, which is suggested by the fact that
press for the perceived letdown after eating foods high in consuming a low-GI starchy food before exercise enhanced
sucrose. Some have suggested that consumption of sugary endurance compared with a high-GI starchy food (3), then
foods may attenuate physical performance (for example, see high-GI starchy foods would likely produce this effect just as
reference 9). Although it is well established that postconsump- well or better than sucrose. Wolever et al (4) have just com-
tion insulin concentrations can drop slightly below the concen- pleted a study comparing high-GI (GI 100) and low-GI (GI
trations before food ingestion (reflecting the lag period before = 62) breakfast test meals containing 2.10 MJ (500 kcal) and
initiation of glucagon release and liven gluconeogenesis), it is 84 g carbohydrate. The only sugars in the meals were standard
not clear that this drop in insulin concentrations should have amounts of milk on cereal, jam on bread, and juice; the GI of
any negative physiological consequences. Is there any evidence the meals were adjusted by using high- and low-GI starchy
to support the suggestion that ingestion of foods high in sucrose breakfast cereals (corn flakes and Oatloops, Kellogg, Battle

before exercise causes a decrement in physical performance? Creek, MI). After the high-GI meal, blood glucose at 2, 3, and
4 h after breakfast was, respectively, 4.8, 4.6, and 4.6 mmol/L
References compared with 5.3, 5.1, and 5.2 mmolfL after the low-GI
breakfast. Plasma insulin was also higher 4 h after the low-GI
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Gibney: Figure 7 shows that the GI of baked goods with added
7. Reiser S. Hallfrisch I. Insulin sensitivity and adipose tissue weight of
rats fed starch or sucrose diets ad libitum or in meals. J Nutr 1977;
sugar is not elevated relative to the unsweetened variety. How-
107:147-55. ever, for dairy products (Figure 8), this is not the case. For each
S. Reiser S. Handler HB, Gardner LB. et al. Isocaloric exchange of category of dairy products, the test meal containing added
dietary starch and sucrose in humans. II. Effect on fasting blood sugar led to a markedly increased GI relative to the unsweet-
insulin, glucose, and glucagon and on insulin and glucose response to ened variety. Have the authors any explanation why baked
sucrose load. Am J Clin Nutr 1979;32:2206-16. goods should behave differently from dairy products? Is it
9. Clark N. Sports nutrition guidebook. Champaign, IL: Leisure Press, related to fat content? Does lactose play a role? Are the
1990.
differences explicable by the argument under the heading “Pre-
dieting the acute effects of sucrose on mixed meals”? If so, the
Authors’ reply: We agree, obesity and probably physical
text that refers to Figure 7 might be altered to attune the reader
inactivity are risk factors for developing glucose intolerance,
to the possible explanation as to why baked goods differ from
but few subjects with NIDDM are not obese (perhaps 10-20%
dairy products.
of all NIDDM subjects). However, the primary metabolic de-
feet is the same, ie, insulin resistance, which leads to hypenin- Author’s reply: I believe the reason why sucrose increases the
sulinemia and glucose intolerance. NIDDM develops when the glycemic response of dairy products but not baked goods is
pancreas can no longer keep producing enough insulin to because the GI of sucrose is similar or less than that of baked
compensate for insulin resistance. The pathogenesis of the goods but is considerably greater than that of lactose. Thus,
/3-cell failure is thought to be due to increasing insulin nesis- replacing lactose with sucrose will increase the glycemic ne-
tance caused by hypeninsulinemia and effects of glucose tox- sponse according, as you say, to the articulated argument. I feel
icity (1, 2). Insulin resistance can be genetically determined the effect of fat on glycemic responses is overrated, and adding
(hence, thin subjects with NIDDM) or can be due to environ- fat to reduce glycemic responses is certainly not concordant
mental factors such as obesity or physical inactivity. We know with current nutritional guidelines to reduce fat intake. One has
of no evidence for, non reason why, thin on obese NIDDM to add a lot of fat to a meal to reduce gastric emptying enough
subjects with a comparable degree of severity of diabetes to reduce the overall glycemic response-something approxi-
would differ in their responses to sucrose. However, this has mate to 40-50 g fat added to 50 g carbohydrate, that is, tripling
not been studied specifically. We do not believe that sucrose energy intake. Even so, fat has nothing to do with the low
promotes glucose intolerance. High postprandial blood glu- glycemic responses of dairy products. A 50-g carbohydrate
cose and insulin responses may promote development of portion of whole milk (3.9% fat) is 1.04 L, which contains 41
glucose intolerance, but most common refined starchy foods g fat, 40 g more fat than in skimmed milk (0.1% fat). Never-
produce higher blood glucose and insulin responses than theless, the GI (GI of 50 g glucose = 100) of whole milk is 34,
does sucrose. which is no different from that of skimmed milk, which has a
GI of 32 (1). Gannon et al (2) showed in subjects with NIDDM trying to analyze our foods before feeding them (2). One
that a 50-g carbohydrate portion of skimmed milk (0.951) had problem with using one’s own analysis is that the public is
the same glycemic response as did 50 g lactose even though the advised about food portions from food tables, and if our results
insulin response to the milk was about four times that of the are very different from food tables then our results may not
lactose. apply for the public or may be used incorrectly. Patients
consuming therapeutic diets are advised by dietitians using
food plans that are even more of an estimate of food compo-
References
sition than is found in food tables. We believe that authors
1. Jenkins DJA, Wolever TMS, Taylor RH, et al. Glycemic index of should state how much food was considered to contain 50 g
foods: a physiological basis for carbohydrate exchange. Am I Clin available carbohydrate and the basis for that estimate.
Nutr 1981;34:362-6. The weight of a food, such as potato, that different investi-
2. Gannon MC, Nuttall FQ, Krezowski PA, Billington Ci, Parker S. The
gators consider to contain 50 g carbohydrate varies markedly

serum insulin and plasma glucose responses to milk and fruit products
from 240 g (3) to 317 g (4); this corresponds to a 5% difference
in type 2 (non-insulin-dependent) diabetic patients. Diabetologia 1986;
in carbohydrate content: 21% or 16%. This may be due partly
29:784-91.
to whether fiber is included in the carbohydrate. Fortunately,
because of biological variability, the effect on blood glucose
Southgate: The evidence from comparison of monosacchar- responses of even such large errors in food analysis are not
ides with sucrose and starch suggests that the small intestine readily detected.
has developed mechanisms for the absorption of disaccharides We discuss, among other things, the glycemic responses of
that are more effective than those for monosaccharides. How- fruit. I have very little idea as to why different fruit produce
ever, the situation is more complex because blood glucose different blood glucose responses; some of the variability could
concentrations are the end result of a number of successive be experimental. There is only a weak correlation between the
stages in absorption and metabolism and direct interpretation in observed blood glucose response and what would be expected
terms of absorption is difficult (1). from the content of sugars in fruit (ie, fructose, glucose, and
Many of the studies of the GIs of foods rely on carbohydrate sucrose) (5). It may be possible to define the cellular and
values taken from nutritional databases or food composition molecular characteristics of stanch or dietary fiber in ways that
tables. It would be useful to identify studies for which direct reliably predict their biological effects but I am not aware that
analytical data on the food tested were available. Databases this has been achieved. Those interested in food chemistry and
have limited predictive value and may not be adequate for these those interested in metabolism will need to work together on
precise metabolic studies. For example potatoes of the same this problem.
variety grown in the same season may differ in starch content
by as much as 5% by weight. Is it possible to distinguish those
food matrices that produce lower GIs in more detail and to References
suggest mechanisms?
1. Ha M-A, Mann II, Melton LD, Lewis-Barned NI. Relationship be-
tween the glycemic index and sugar content of fruits. Diabetes Nutr
Reference Metab 1992;5:199-203.
2. Wolever TMS, Katzman-Relle L, Jenkins AL, Vuksan V, losse RC,
1. Marks V. Glycemic responses to sugars and starches. In: Dobbing I, Jenkins DIA. Glycemic index of 102 complex carbohydrate foods in
ed. Dietary starches and sugars in man: a comparison. London: patients with diabetes. Nutr Res 1994:14:651-69.
Springer Verlag, 1989:151-67. 3. Hermansen K, Rasmussen 0, Arnfred I, Winther E, Schmitz 0.
Differential glycemic effects of potato, rice and spaghetti in type 1
(insulin-dependent) diabetic patients at constant insulinaemia. Diabe-
Authors’ reply: We agree that the relative glycemic response
tologia 1986;29:358-61.
of various sugars is more complex than merely considering
4. Crapo PA, Kolterman OG, Waldeck N, Reaven GM, Olefsky IM.
differences in rates of absorption, although this does play a Postprandial hormonal responses to different types of complex carbo-
role. This is a drawback of using the GI for foods rich in sugars. hydrate in individuals with impaired glucose tolerance. Am I Clin Nutr
The GI concept was developed primarily for starchy foods and 1980;33: 1723-8.
works well when the absorbed carbohydrate is primarily glu- 5. Wolever TMS, Vuksan V, Katzman-Relle L, et al. Glycemic index of
cose. However, for foods rich in simple sugars, the interpretation some fruits and fruit products in patients with diabetes. Int I Food Sci
of the GI is different and more complex than for starchy foods Nutr 1993;43:205-12.
because of the different metabolism of fructose and galactose.

We agree that variability in food composition is a source of
Schneeman: Can information on glucose response be accu-
variation of blood glucose responses. Ideally, food composition
rately interpreted without the corresponding data on insulin
would always be analyzed before blood glucose responses are
response? Current research indicates that cholecystokinin re-
tested. However, people do not analyze all the foods they study
lease is also important for maintenance of glycemia.
because it is difficult and expensive. If a subtle difference in
food composition, such as the sugar content of fruit (1), is Authors’ reply: There is good evidence (1) that the insulin
found to influence glycemic responses, the results may be of responses of starchy foods are closely related to their glycemic
little use if the information is not generally available in food responses in nondiabetic subjects although this is not always
tables or the difference in composition is highly dependent on seen. As indicated in Figure 9, the same holds for mixed meals
things that are hard to quantify, such as ripeness, growing containing sugars. In subjects with NIDDM, insulin responses
conditions, and storage for example. Recently we have been are sluggish and do not always show the differences expected.
Nevertheless, where it has been measured, reducing diet GI by bananas (1). This difference suggests that underripe bananas
using starchy foods has resulted in reduced 24-h urinary C- would have a response #{176}#{176}30%
less than that of ripe bananas,
peptide as a measure of insulin secretion in both normal and and this is quite close to the difference in glycemic response
diabetic subjects (2, 3). This is most likely due to the effect that actually observed: Woleven et al (2) found that underripe
slowing absorption or spreading the nutrient load has on re- bananas had a glycemic response #{176}#{176}35%
less than ripe bananas,
ducing insulin secretion (4-7). However, I am not sure the whereas Henmansen et al (3) more recently found a difference
same can be said for sugars, because the mechanisms by of 42%. We agree that these results cannot be extrapolated
which fructose and galactose reduce blood glucose re- precisely to all fruit; nevertheless, according to our understand-
sponses are different. I am not familiar with the work on ing, the composition of fruit does change as they ripen and so
cholecystokinin and blood glucose and cannot comment. My their glycemic responses may very well change. Therefore, we
question about it would be if this is simply a relation, could cannot be sure until more comparisons are made.
it be that slow absorption both reduces glucose and chole- This is heresy, but we see no particularly good reason to

cystokinin, rather than the cholecystokinin reducing blood restrict sugars use in persons with diabetes except in those
glucose? individuals (and there are some) for whom sucrose or fructose
is deleterious to their metabolic control because of increased
blood lipids or inability to lose weight. We would feel com-
References
fortable if people with diabetes used the same amount of added
1. Wolever TMS, Jenkins DJA, Collier GR, Lee R, Wong GS, Josse RG. sucrose as the general population, that is, 10-12% of energy.
Metabolic response to test meals containing different carbohydrate We would not mention sugar restriction in advice to patients.
foods: 1. Relationship between rate of digestion and plasma insulin
response. Nutr Res 1988;8:573-81.
References
2. Jenkins DJA, Wolever TMS, Collier GR, et al. The metabolic effects
of a low glycemic index diet. Am I Clin Nutr 1987;46:968-75.
1. Englyst HN, Cummings JH. Digestion of the carbohydrates of banana
3. Wolever TMS, Jenkins DJA, Vuksan V, et al. Beneficial effect of a
(Musa paradisiaca sapientum) in the human small intestine. Am I Clin
low-glycemic index diet in type 2 diabetes. Diabetic Med 1992;9:
Nutr 1986;44:42-50.
451-8.
2. Wolever TMS, Jenkins DJA, Jenkins AL, Vuksan V, Wong GS, Josse
4. Jenkins DJA, Wolever TMS, Vuksan V. et al. “Nibbling versus gorg-
RG. Effect of ripeness on the glycemic response to banana. I Clin Nutr
ing”: metabolic advantages of increased meal frequency. N Engl I Med
Gastroenterol 1988;3:85-8.
1989;321 :929-34.
3. Hermansen K, Rasmussen 0, Gregersen 5, Larsen S. Influence of
5. Jenkins DJA, Wolever TMS, Ocana AM, et al. Metabolic effects of
ripeness of banana on the blood glucose and insulin response in type
reducing rate of glucose ingestion by single bolus versus continuous
2 diabetic subjects. Diabetic Med 1992;9:739-43.
sipping. Diabetes 1990;39:775-81.
6. Wolever TMS. Metabolic effects of continuous feeding. Metabolism
1990;39:947-51. Anderson: The glycemic index in the Wolever lab centers
7. Jenkins DJA, Ocana A, Jenkins AL, cC al. Metabolic advantages of around a test dose of 50 g carbohydrate and all conclusions
spreading the nutrient load: effects of increased meal frequency in appear to be derived from this fixed dose. Others have ques-
non-insulin-dependent diabetes. Am I Clin Nutr 1992;55:461-7. tioned whether body size and obesity should be considered, but
I also wonder about the role of habitual diet in determining the
Kingman: Wolever and Brand Miller mention that underripe index and whether the index holds over a range of doses from,
bananas give a lower glycemic response than do overripe for example, 50 to 250 g. Wolever and Brand Miller point to a
bananas. This is to be expected because the ripening process in flattening of the response as carbohydrate load increases in
bananas involves breakdown of a large amount of highly amy- diabetic subjects, but what about in normal subjects? Does the
lase-resistant stanch into readily digestible sugars (1). However, GI hold on even matter if a large bolus of carbohydrate is
the degradation of resistant starch is not typical of the ripening consumed? What has been the purpose of developing the GI
of most fruit, so the principle may not be generally applicable and in selecting the dose of 50 g? Has it had any application to
to the GI values of fruit at different stages of maturity. On the normal individuals or diseases other than diabetes? Although it
basis of our knowledge of sugars and their effects on glycemic may serve the purpose of the point of this document as dis-
control in subjects with diabetes, what level of sucrose and cussed, I think a bit more background for the reader on the
fructose in the diet would you feel happy to recommend to such strength and weakness of the concept of the GI is needed. As
people for everyday use? presented here, its quantitative value seems to be emphasized.
Is this the main point?
Reference Authors’ reply: The validity of the GI concept has been

reviewed elsewhere (1). Indexing against a standard food is
1. Englyst HN, Cummings JH. Digestion of the carbohydrates of banana perhaps the only practical way to express the results of blood
(Musa paradisiaca sapientum) in the human small intestine. Am J Clin
glucose and insulin responses of many different foods and to
Nutr l986;44:42-50.
compare their results, because it would be almost impossible to
test 40-50 foods in a single group of subjects. Our aim is not
Authors’ reply: Yes, we agree underripe banana contains less to prove or discuss the validity of the quantitative aspects of the
available carbohydrate than does overripe banana. The work of GI; we believe it is valid and quantitative and it is taken for
Englyst and Cummings (1) showing this prompted Wolever et granted as being so for the purposes of this paper. Whether the
al (2) to test the glycemic responses of bananas. Overripe concept is valid or not is not really important for the main
bananas contain 3% starch compared with ‘37% for undennipe points being made: sucrose produces acute blood glucose and
insulin responses that are similar to or less than the responses wt 24 h evenly distributed at 0, 4, 8, and 21 h after
of many starchy foods, whether taken alone or in a mixed meal. glycogen-depleting exercise) with a high GI (GI = 108) pro-
There is no evidence that sucrose causes a deterioration of duced a significantly greater rate of muscle glycogen synthesis
blood glucose control in the long term, nor is there any evi- than did consumption of a carbohydrate with low GI (GI = 71)
dence that sucrose causes insulin secretion in excess of that (106 ± 12 compared with 72 = 7 mmol kg 24 h ‘) . .
from a starchy food of the same GI. Reisen et al’s (2, 3) results
suggest that sucrose causes hypeninsulinemia, but they use very
References
large amounts of sucrose and fructose and abnormal eating
patterns on both, so we are uncertain whether their results can 1. Coyle EF, Coyle E. Carbohydrates that speed recovery from training.
be extrapolated to normal sucrose use (whatever that is!). Physician Sports Med 1993;21 :111-3.
Body size and obesity influence the absolute glycemic effect 2. Burke LM, Collier GR, Hargreaves M. Muscle glycogen storage after
of foods but do not have any influence on relative effects, at prolonged exercise: effect of the glycemic index of carbohydrate

feedings. I AppI Physiol 1993;75:1019-23.
least of starchy foods. The GI of lentils in children with
insulin-dependent diabetes, 44, was virtually identical to the
value obtained in adults with insulin dependent diabetes, 43 Authors’ reply: The effect of fiber on GI depends on whether
(4). The effect of obesity has not been published, but we have you are adding purified fibers to foods on considering the fiber
never noticed any correlation between GI and body mass index. naturally present in foods. For the addition of purified fiber
A low-carbohydrate diet influences the absolute glycemic re- there is fairly consistent evidence that viscous (soluble) types
sponse to a standard oral carbohydrate load, but we presume of fiber reduce blood glucose (1). However, the mechanism is
that the relative effects of foods would not be influenced as still not agreed on; delayed gastric emptying and slow absorp-
long as the diet was kept constant; this has not been tested. As tion from the intestinal lumen due to viscosity are the major
fan as the dose of carbohydrate goes, our Figure 1 1 suggests contenders. Purified nonviscous (insoluble) fibers have little or
that the GIs of foods hold across any range of carbohydrate no effect on postprandial blood glucose. When one looks at the
intake. The curves on the graph seem to fit the data fairly well fiber naturally occurring in foods, a completely different pie-
and are derived from a nonlinear regression analysis (by using tune emerges: the relation between soluble fiber and GI is
an exponential equation) with the different curves derived by weaken than that between GI and insoluble fiber (2, 3). The
multiplying the term by the food GI. We are currently doing a reasons for this are not known but indicate that many factors in
study that will allow us to see if the GI of four foods holds foods influence glycemic responses.
across a range of carbohydrate intakes from 25 to 100 g.
Jenkins et al (5) used 50 g as the standard originally because
References
when studies began in the United Kingdom, a 50-g load of
glucose was commonly used in that country as the standard 1. Wolever TMS, Jenkins DJA. Effect of dietary fiber and foods on
glucose tolerance test for diagnosing diabetes. carbohydrate metabolism. In: Spiller G, ed. A CRC handbook of
dietary fiber in human nutrition. 2nd ed. Boca Raton, FL: CRC Press,
References 1993:111-52.
2. Wolever TMS. Relationship between dietary fiber content and corn-
1. Wolever TMS, Jenkins DJA, Jenkins AL, Josse RG. The glycemic position in foods and the glycemic index. Am I Clin Nutr l990;51:
index: methodology and clinical implications. Am I Clin Nutr 1991; 72-5.
54:846-54. 3. Wolever TMS. In vitro and in vivo models for predicting the effects of
2. Reiser 5, Handler HB, Gardner LB. Hallfrisch JG, Michaelis OE, dietary fiber and starchy foods on carbohydrate metabolism. In:
Prather ES. Isocaloric exchange of dietary starch and sucrose in Anderson 1W, Kritchevsky D, Bonfield C, eds. Dietary fiber. Proceed-
humans II. Effect on fasting blood insulin, glucose and glucagon and ings of the 4th Washington Symposium on Dietary Fiber and the
on insulin and glucose response to a sucrose load. Am I Clin Nutr Vahouny Fiber Symposium. St Paul, MN: Eagan Press, 1995:360-77.
1979;32:2206-16.
3. Reiser 5, Powell AS, Yang GY, Canary II. An insulinogenic effect of
oral fructose in humans during postprandial hyperglycemia. Am I Clin K#{246}nig:What is the individual (intersubject) variation of the GI
Nutr 1987;45:580-7. for a food (range and SD)?
4. Wolever TMS, Jenkins DJA, Collier GR, et al. The glycemic index:
Authors’ reply: Typical CVs for GI values (ie, 100 X SD!
effect of age in insulin dependent diabetes mellitus. Diabetes Res
1988;7:71-4.
mean) would be somewhere in the region of 30-50%. Because
5. Jenkins DJA, Wolever TMS, Taylor RH, et al. Glycemic index of these values are based on single tests of foods with 5-10
foods: a physiological basis for carbohydrate exchange. Am I Clin subjects, this variation includes both between- and within-
Nutr 1981;34:362-6. subject variability. The total variation and portioning between
the various sources depends on several factors.
Sherman: It is interesting to note that Coyle and Coyle (1) The first consideration is that the GI is the ratio of two
advocate the use of the 01 for athletes to choose foods that will independently variable measurements, ie, the glycemic re-
produce a rapid synthesis of muscle glycogen after prolonged sponse to the food and the glycemic response to the standard in
exercise. They recommend that athletes consume at least 50 g the same subject. The within-individual variability of glycemic
high- (GI 85) or moderate- (GI = 60-84) GI foods imme- responses depends on the glucose tolerance status of the sub-
diately after exercise and every 2 h thereafter for two or three ject. For repeated tests of 50 g glucose in 1 1 normal subjects
additional feedings. (mean of eight tests in each subject) the mean within-subject
Also, Burke et al (2) reported that consuming the same CV of glycemic responses was 25% (between-subject CV =
amount of carbohydrate (10 g carbohydrate kg body . 26%); for repeated tests of 50 g carbohydrate from white bread
in 22 subjects with NIDDM (mean of nine tests each), mean References

within-subject CV was 15% (between-subject CV 32%), and
1. Wolever TMS, Nuttall FQ, Lee R, et al. Prediction of the relative blood
for 14 IDDM subjects (mean of nine tests of bread each) the
glucose response of mixed meals using the white bread glycemic
mean within-subject CV was 29% (between-subject CV =
index. Diabetes Care 1985;8:418-28.
34%) (1). The variability of a ratio is greater than the vaniabil- 2. Wolever TMS, Jenkins DJA, Jenkins AL, Josse RG. The glycemic
ity of the numerator and denominator; if the variability of the index: methodology and clinical implications. Am I Clin Nutr 1991;
numerator and denominator is large, this results in a skewed 54:846-54.
distribution of the ratios and actually increases the mean of the 3. Wolever TMS, Jenkins DJA, Josse RG, Wong GS, Lee R. The glyce-
ratios (2). The variability of the denominator, ie, the glycemic mic index: similarity of values derived in insulin-dependent and non-
response of the standard food, can be reduced by taking the insulin-dependent diabetic patients. I Am Coil Nutr 1987;6:295-305.
4. Wolever TMS, Jenkins DJA, Vuksan V, Josse RG, Wong GS, Jenkins
mean of several measurements of the glycemic response; this
AL. Glycernic index of foods in individual subjects. Diabetes Care
has the effect both theoretically (1, 3) and actually (2) of

1990;13:126-32.
reducing the variability and the mean of GI values. For exam-
5. Wolever TMS. Glycemic index versus glycemic response: nonsynony-
ple, mathematical modeling suggested that increasing the with- mous terms. Diabetes Care 1992;15:1436-7.
in-individual variability of glycemic responses from 15% (as in
NIDDM) to 29% (as in IDDM) would increase the mean value
of the GI by =5, which was similar to the actual difference Hill: Does the fat content (ie, amount and type) of foods
seen between the mean of the GI values of 20 foods tested in influence GI via modification of glucose absorption and
IDDM and NIDDM subjects (3). Thus, Wolever et al (2) metabolism?
recommend that when GI values are determined for foods, the The last paragraph of the conclusions is not exactly clear to
mean of three tests of the standard food in each subject should me. Specifically, why would a low sucrose intake be associated
be used for the calculations. with difficulty in limiting dietary fat? It seems that at least in
The next question is whether different subjects really have some people, there is a preference for a sweet-fat taste.
consistently different GI values for the same foods. To test this,
Authors’ reply: There has been much to-do made over the fact
three different foods were fed four times each to 12 different
that fat reduces upper gastrointestinal tract motility and thus
diabetic subjects chosen to be heterogenous with respect to
their glycemic responses (4). The results of this study showed slows gastric emptying and can reduce glycemic responses.
However, the amount of fat required is quite large, certainly
that mean glycemic response areas for the different subjects
more than would be compatible with current dietary recom-
varied over a fourfold range but mean GI values were not
mendations. For example, the fat in peanuts may have some-
significantly different in the different subjects. The sources of
thing to do with why they have a low glycemic response, but
the variance of glycemic responses and GI values for the data
the fat is > 70% of energy. In practical terms, fat has little or
from this study wereAnalysis of variance
published later (5).
no effect on glycemic responses. Wolever et al (1) recently
was used to determine the variation due to the different foods
tested > 100 different complex carbohydrate foods in diabetic
(bread, rice, and spaghetti) and due to between- and within-
subjects and the range of fat content in the 50-g carbohydrate
subject variation. Expressed as CVs, the variance of the gly-
portions of the foods was from 0 to =25 g, or up to 50% of
cemic response areas due to food, within-subject variation, and
energy (examples of high-fat foods are French-fried potatoes
between-subject variation were 31%, 25%, and 49%, respec-
and corn chips). There was no correlation between GI and fat
tively. Between-subject variation was large because the sub-
content across this range of fat. When we added 22 g fat to
jects were chosen to be heterogenous. Expressing the results as
cornmeal to simulate the composition of corn chips, the rate of
the GI, the variance due to food and within-subject variation
rise of blood glucose was slightly slower but the hyperglycemia
were virtually identical to those for the areas, 30% and 21%,
was more prolonged, so the mean GI values of cornmeal with
respectively, but the between-subject variation was reduced
and without margarine were virtually identical. In our view, the
from 49% to only 8%, which is almost negligible.
effect of fat is overemphasized.
Thus, paradoxically, most of the variance of GI values for a
In practice it appears that low sucrose intake is associated
food comes from within-subject variation; there is little van-
with high fat. Although people may like sweet-fat foods,
ance between subjects. Thus, GI does what it is supposed to do,
Gibney et al (2) show that these do not contribute more than
ie, normalize the glycemic responses of different subjects with-
=10-15% of energy.
out affecting the variation between the foods.
Having said all this, we want to emphasize that what has
been said above applies to starchy foods only. There may be References
true differences between subjects for sugars. For example,
subjects with lactose deficiency will have no glycemic re- 1. Wolever TMS, Katzman-Relle L, Jenkins AL, Vuksan V, Josse RG,
Jenkins DJA. Glycemic index of 102 complex carbohydrate foods in
sponse to lactose because they do not absorb the sugar. There
patient with diabetes. Nutr Res 1994;14:651-69.
are only minimal data to suggest it, but it is possible that the
2. Gibney M, Sigman-Grant M, Stanton IL Jr, Keast D. Consumption of
GIs of sucrose and fructose may, at least theoretically, be sugars. Am I Clin Nutr 1995;62(suppl):178S-94S.
different in subjects with various degrees of insulin resistance
or glucose intolerance due to differences in the way the liver
metabolizes fructose. More work needs to be done in this area. Harland: Reactive hypoglycemia is the name given to a poorly
The implications of a low GI may be different for fructose- and defined set of systems and a poorly defined condition. The
galactose-containing foods compared with starchy foods. validity of this concept is challenged (1).
Reference ideal, but it is better than nothing. In addition, measurement

of insulin was not the original goal of the GI. When Jenkins
1. Marks V. Biologist 1986;33(4).
et al (1) started their GI work, they knew from work on
dietary fiber that slowing absorption reduced both glucose
Authors’ reply: We agree that hypoglycemia is probably
and insulin responses (1). Jenkins et al (2) showed that
overdiagnosed. Many people may have quite low blood glu-
starchy foods were digested at different rates and so there
cose concentrations without symptoms or have symptoms with-
was a close analogy with fiber. Thus GI was really a
out low blood glucose. What is clear is that sucrose is no more
measure of digestibility. Jenkins and Wolever have tested
prone to producing low blood glucose than are high-GI starchy
the glycemic responses of > 200 different foods over the
foods such as bread or potato.
past 10 y, have had very many surprises, and have learned a
Schneeman: Current research indicates that cholecystokinin great amount. If we had tried to measure insulin as well as
(CCK) release is also important for maintenance of glycemia.

glucose, we would not have been able to test one-tenth this
many. It was only 15 y ago that technology became available
Authors’ reply: Brand Miller’s data suggest that there is a
close correlation between glucose and insulin responses. In for finger-prick blood sampling and for measurement of
general there is an inverse relation between GI and CCK and an glucose in 0.1 mL samples of whole blood, which allowed
inverse relation between insulinemic index and CCK. It would rapid testing of foods. Jenkins et al (3) and Wolever et al (4)
take a whole chapter to review the effects of the various gut have done some insulin tests and found that glucose and
hormones that may play a role in blood glucose regulation, insulin responses correlate very well. In the literature this is
such as gastric inhibitory polypeptide, glucagon-like peptide-1, generally true as well, even for meals containing large
and CCK. amounts of simple sugars. More recently, Brand Miller has
tested glucose and insulin responses to many foods and finds
Khan: It is generally agreed that weight control is a critical
that they correlate very well (unpublished). It may be valu-
factor in the successful dietary management of NIDDM. Al-
able to look at glycemic response of foods as a preliminary
though I agree in principle with the notion that “sugar is not
step to doing other investigations, because then it would be
just a source of empty calories . . . ,“ it should be noted that
possible to make a reasonable hypothesis and design a study
energy-dense foods containing both fat and sugar (ie, ice
with a good chance of obtaining positive results.
cream) may not contribute to immediate blood glucose re-
sponse (because fat delays gastric emptying) but may contnib-
ute to increased insulin resistance and weight gain. This may be
References
a potential problem in studying effects of sugars on blood
glucose responses in isolation from plasma insulin responses. 1 . Jenkins DJA. Wolever TMS, Leeds AR, et al. Dietary fibres, fibre
analogues and glucose tolerance: importance of viscosity. Br Med I
Authors’ reply: We agree that weight control is critical for the
1978; 1:1392-4.
management of NIDDM. Thus, we would not recommend that
2. Jenkins DJA, Ghafari H, Wolever TMS, et al. Relationship between
diabetic people eat a lot of ice cream because it is fattening. If
the rate of digestion of foods and postprandial glycaemia. Diabetologia
they want ice cream, we would recommend use of low-fat ice
l982;22:450-5.
milk or other lower-fat ice cream substitutes. It is probably the
3. Jenkins DJA, Wolever TMS, Taylor RH, et al. Slow release carbohy-
fat in ice cream that has all the deleterious effects you mention, drate improves second meal tolerance. Am I Clin Nutr 1982;35:
not the sugar. GI need not be the only judge of the desirability 1339-46.
of a food; not all foods with a low GI are desirable and not all 4. Wolever TMS, Jenkins DIA, Collier GR, Lee R, Wong GS, Josse RG.
foods with a high GI are undesirable. Metabolic response to test meals containing different carbohydrate
We agree that studying the effects of foods (including sug- foods: 1. Relationship between rate of digestion and plasma insulin
ars) on blood glucose without also measuring insulin is not response. Nutr Res 1988;8:573-81.

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Thomas MS Wolever and Janette Brand Miller

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Early on, the glycemic effects of four breakfast meals con-

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FIGURE 1. Glycemic index (GI) of whole fruit compared with fruit 20 40 60 80

Glycemic Index CU)

Sweetened breakfast cereals

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glucose curves but the insulin response to sucrose is higher

(Figure 7). This increase is predicted by the GI of the individ-

studied simultaneously, suggests that many foods containing

SUGAR AND INSULIN SECRETION

FIGURE 7. Comparison of the glycemic indexes (GI5) of dairy prod-

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93) (P < 0.05) (56). Sucrose will raise glycemic responses if

meal GIs (54) are given in Table 1. Sucrose- and fructose-

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0CO Hypoglycemia occurs when blood glucose concentrations

glucose is associated with a rapid rise in blood glucose and a

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390-3. of starch in well-controlled diabetics. Lancet 1984;2:122-5.

197-207. honey at breakfast have no additional acute hyperglycaemic effect over

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COMMENTARY peripheral insulin resistance. Is there evidence that patients

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because of the different metabolism of fructose and galactose.

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Reference Authors’ reply: The validity of the GI concept has been

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in 22 subjects with NIDDM (mean of nine tests each), mean References

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Reference ideal, but it is better than nothing. In addition, measurement

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