Glycemic index: overview of implications in health and disease1–4

David JA Jenkins, Cyril WC Kendall, Livia SA Augustin, Silvia Franceschi, Maryam Hamidi, Augustine Marchie,
Alexandra L Jenkins, and Mette Axelsen

ABSTRACT The glycemic index concept is an extension of of many of the issues that were raised after the formulation of both

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the fiber hypothesis, suggesting that fiber consumption reduces the concepts further defined possible preventive and therapeutic roles
rate of nutrient influx from the gut. The glycemic index has par- for the glycemic index classification of foods. The necessary
ticular relevance to those chronic Western diseases associated with research in this area was greatly facilitated by the compilation of
central obesity and insulin resistance. Early studies showed that comprehensive glycemic index food tables (6).
starchy carbohydrate foods have very different effects on post-
prandial blood glucose and insulin responses in healthy and dia-
betic subjects, depending on the rate of digestion. A range of GLYCEMIC INDEX AND GLYCEMIC LOAD
factors associated with food consumption was later shown to alter The glycemic index is the indexing of the glycemic response of
the rate of glucose absorption and subsequent glycemia and insu- a fixed amount of available carbohydrate from a test food to the
linemia. At this stage, systematic documentation of the differences same amount of available carbohydrate from a standard food con-
that exist among carbohydrate foods was considered essential. sumed by the same subject (initially, the standard “food” was glu-
The resulting glycemic index classification of foods provided a cose, but more recently it has been white bread; 7, 8). The blood
numeric physiologic classification of relevant carbohydrate foods glucose area after consumption of the test food was expressed as a
in the prevention and treatment of diseases such as diabetes. percentage of the standard. The glycemic load, which assesses the
Since then, low-glycemic-index diets have been shown to lower total glycemic effect of the diet and has proved very useful in epi-
urinary C-peptide excretion in healthy subjects, improve glycemic demiologic studies, is the product of the dietary glycemic index
control in diabetic subjects, and reduce serum lipids in hyper- and total dietary carbohydrate (9–11). In general, the insulin
lipidemic subjects. Furthermore, consumption of low-glycemic- responses, when measured, related well to glycemic responses
index diets has been associated with higher HDL-cholesterol (12, 13). It also appeared that the rate of digestion of the food was
concentrations and, in large cohort studies, with decreased risk an important determinant of glycemic response (14, 15). Thus, the
of developing diabetes and cardiovascular disease. Case-control rate of liberation of the carbohydrate products of digestion in vitro
studies have also shown positive associations between dietary over 3–5 h reflected the blood glucose area in vivo (14). Intrinsic
glycemic index and the risk of colon and breast cancers. Despite and extrinsic factors that alter the rate of gastrointestinal motility,
inconsistencies in the data, sufficient, positive findings have digestion and absorption, and the nature of the starch, cooking
emerged to suggest that the dietary glycemic index is of potential method, particle size, and the presence of fiber, fat, and proteins
importance in the treatment and prevention of chronic diseases. were all found to result in differences in the glycemic index (16, 17).
Am J Clin Nutr 2002;76(suppl):266S–73S. The starchy staples of traditional cultures were often foods that
had lower glycemic indexes, such as pasta, whole-grain pumper-
KEY WORDS Glycemic index, insulin, glucose, diabetes,
coronary heart disease, cancer
1
From the Clinical Nutrition and Risk Factor Modification Center,
St Michael’s Hospital, Toronto (DJAJ, CWCK, LSAA, MH, AM, and ALJ);
INTRODUCTION the Department of Nutritional Sciences, Faculty of Medicine, University of
The concept of a glycemic index was developed to provide a Toronto (DJAJ, CWCK, LSAA, MH, and AM); the Field and Intervention
numeric classification of carbohydrate foods on the assumption Studies Unit, International Agency for Research on Cancer, Lyon, France (SF);
that such data would be useful in situations in which glucose toler- and the Lundberg Laboratory for Diabetes Research, Department of Internal
ance is impaired. In many ways, the glycemic index concept was an Medicine, Sahlgrenska University Hospital, Göteborg, Sweden (MA).
2
Presented at a symposium held at Experimental Biology 2001, Orlando, FL,
extension of the dietary fiber hypothesis of Burkitt and Trowell (1),
1 April 2001.
who suggested that foods that are more slowly absorbed may have 3
Supported by the National Sciences and Engineering Research Council of
metabolic benefits in relation to diabetes and to the reduction of Canada, Ottawa. DJAJ is funded as a Canada Research Chair in Metabolism and
coronary heart disease (CHD) risk. At the same time the dietary Nutrition at the University of Toronto by the federal government of Canada.
fiber hypothesis was formed, the concept of a cluster of diseases 4
Reprints not available. Address correspondence to DJA Jenkins, Depart-
related to central adiposity and intraabdominal fat mass with atten- ment of Nutritional Sciences, Faculty of Medicine, University of Toronto,
dant insulin resistance was being developed (2–5). The similarity Toronto, Ontario, M5S 3E2, Canada. E-mail: cyril.kendall@utoronto.ca.

266S Am J Clin Nutr 2002;76(suppl):266S–73S. Printed in USA. © 2002 American Society for Clinical Nutrition
 GLYCEMIC INDEX: HISTORY AND OVERVIEW 267S

nickel breads, cracked wheat or barley, rice, dried peas, beans, and
lentils (18, 19). It appears that the traditional use of low-glycemic-
index carbohydrate foods in the diet was particularly prevalent
among cultures that are now experiencing high rates of diabetes, eg,
the Pima Indians and the Australian Aborigines, and where the
change to high-glycemic-index foods has been a more recent phe-
nomenon (20–22). Obviously, many other factors, such as obesity
and reduced physical activity, must play major roles in increasing
diabetes risk. Nevertheless, over time the desire for sweet foods, which
resulted from rapid carbohydrate breakdown of starch in the mouth,
may have resulted in the selection of rapidly digested (and hence
high-glycemic-index foods) as cultures became more affluent (18).
Thus, foods with high glycemic indexes are proposed further as a
dietary factor that favors the development of chronic disease.

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CONCERN OVER UTILITY OF THE GLYCEMIC INDEX
CLASSIFICATION
It is said that the glycemic index concept lacks clinical utility
because differences in glycemic indexes between foods are lost
once these foods are consumed in a mixed meal (23). Part of the rea-
son for this is that when a mixed meal consists of several carbohy-
drate sources, the effect of the lower glycemic index component is
diluted in proportion to the amount of carbohydrate from other
foods. Appropriate calculation of the mixed-meal glycemic index is
therefore required (8). Small amounts of fat added to the meal have
also been considered to greatly alter the glycemic response. How- FIGURE 1. Hypothetical effect of feeding diets with a low (A) or
ever, in studies in which 8–24 g fat was fed in mixed meals con- high (B) glycemic index on gastrointestinal glucose absorption and post-
taining 38–104 g carbohydrate, the added fat had little effect on pre- prandial blood glucose.
dicted glycemic response (24). Furthermore, although large
deviations in the dietary macronutrient profile will occur over time,
these differences by definition will also average out over time. Only same time achieving lower blood glucose concentrations (Figure 1).
in those subjects in whom there are substantial differentiations in Over time, with the reduction in FFA concentrations and the rise
daily macronutrient intake are changes in the dietary glycemic index in the respiratory quotient with tissue insulinization, glucose is
likely to be obscured, and in such individuals any meaningful withdrawn from the circulation at a faster rate. Consequently,
attempt at dietary modification is also likely to be difficult. blood glucose concentrations return toward baseline despite con-
It is said that the glycemic index concept adds further needless tinued glucose absorption from the small intestine. The rise in
complications and restrictions to the dietary management of dis- peak postprandial blood glucose is therefore reduced together with
eases and that such factors cannot be justified by the modest gains the incremental blood glucose area above baseline. Studies in
that might accrue (25). An alternative view might be that the healthy men have shown this effect after a glucose solution was
glycemic index is simply a tool for alerting the potential consumer sipped at an even rate over 180 min as opposed to being consumed
to new starchy foods they may not otherwise have considered eat- as a bolus at zero time (26). A marked economy in insulin secre-
ing. Over time, the introduction of new foods will expand the range tion with sipping the glucose solution was also seen (Figure 2),
of food choices available, providing foods to be selected not only together with improved glucose clearance (KG) for intravenous
for their glycemic index, but also for their range of health advan- glucose at 4 h. This was coincident with the lower serum FFA con-
tages. A certain amount of dietary understanding is certainly centrations compared with those after the bolus intravenous-
required, eg, carrots with a high glycemic index are not taboo. It is glucose-tolerance test. In part, this improvement, which was also
realized that there are other considerations relevant to the con- seen after consumption of low-glycemic-index meals, may be the
sumption of carrots, and that the glycemic index is not significant result of sustained tissue insulinization, suppression of FFA
in low-energy foods in which the ratio of other desirable factors release (26, 27), and the absence of a counterregulatory endocrine
(eg, minerals, vitamins, and fiber) to available carbohydrate is high. response (26, 28). Other studies that used low-glycemic-index
meals showed an improved second meal carbohydrate tolerance
that was reminiscent of the Staub-Traugott effect (ie, in which the
MECHANISMS OF ACTION first meal improves the glucose tolerance of the second meal) and
The hypothesized metabolic effects relate to the rate at which related the improved postprandial glycemia of the second standard
glucose is absorbed from the small intestine. A reduced rate of meal to lower FFA concentrations (27, 29).
glucose absorption after the consumption of low-glycemic-index In addition, increased food frequency, as a model for mimick-
carbohydrate foods will reduce the postprandial rise in gut hor- ing the slow digestion of low-glycemic-index foods, has been
mones (eg, incretins) and insulin. The prolonged absorption of shown to reduce glycemic and insulinemic responses over the
carbohydrate seen over time will maintain suppression of the free course of a day in diabetic subjects (30, 31). In the longer term,
fatty acids (FFA) and the counterregulatory responses, while at the increased food frequency has been associated with altered adi-
268S JENKINS ET AL

insulin infusion rates (42). However, in another study of healthy

men, 24-h urinary C-peptide output was found to be reduced with
low-glycemic-index diets (41). In addition, LDL-cholesterol con-
centrations were reduced with the low-glycemic-index diet as
was the serum C-peptide response to a standard breakfast after 2 wk.
Nevertheless, there were higher blood glucose concentrations at
45 and 60 min that were associated with the lower C-peptide
response. This apparent impairment in glucose tolerance may
have been related to gut adaptive responses with less incretin
secretion because the intravenous glucose tolerance test was sim-
ilar in both treatments (41). On the other hand, middle-aged,
insulin-resistant women, many of whom had already suffered
a myocardial infarction, showed improved insulin sensitivity
after an insulin tolerance test (43). In studies of persons with
type 1 and 2 diabetes, most studies (10 of 14) (Table 1; 44–57)

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showed improvement in glycated proteins, and in one study,
plasminogen activator inhibitor 1 concentrations were also
reduced (54). These effects occurred despite large variations in
the glycemic index difference between the test and control treat-
ments, the short duration of many studies, and the limited num-
bers of subjects in others. However, in an assessment of the
effects of monounsaturated fat compared with high-carbohydrate
diets and low- compared with high-glycemic-index diets in
patients with diabetes, the effects of both interventions on gly-
cated proteins were comparable (Figure 3; 59). After consuming
a low-glycemic-index diet for 1 mo, patients with hyperlipi-
demia showed reduced LDL-cholesterol and triacylglycerol con-
centrations (in those with higher triacylglycerol concentrations),
despite no significant difference in body weight (58). These data
are not definitive but suggest a potential therapeutic utility of the
glycemic index concept.

EPIDEMIOLOGIC INSIGHTS
Two studies (one that used the third National Health and
Nutrition Examination Survey database and the other a British
study) showed a negative relation between glycemic index and
HDL cholesterol, suggesting that low-glycemic-index diets may
preserve HDL cholesterol and thus have a potentially positive
effect in reducing CHD risk (Table 2; 65, 66). In relation to
CHD, the Nurses’ Health Study showed a negative relation
FIGURE 2. Mean (± SE) blood glucose, serum free fatty acids (FFA), between fatal and nonfatal myocardial infarctions and glycemic
serum insulin, serum C-peptide, and plasma gastric inhibitory polypep-
index, as well as glycemic load (11). Of particular interest was
tide (GIP) concentrations after consuming a glucose solution (50 g in
the observation that there was no association of dietary glycemic
700 mL H2O) as a bolus over 5 min at time 0 () or after sipping the
same solution over 0–3.5 h at an even rate (). index with CHD in persons with a body mass index (in kg/m2)
< 23, suggesting that the effect of dietary glycemic index may be
increasingly important in those with a greater degree of insulin
pose tissue enzyme concentrations (32) and reduced fasting blood resistance (Table 2). On the other hand, no significant associa-
lipid concentrations, even though the same foods were eaten in tion of glycemic index or glycemic load and CHD was seen in
the same amount in any given 24-h period (33–38). For reasons older men in the Zutphen study (67). The relatively small num-
that are not clear, not all studies have shown these effects (39). ber of subjects in this study (< 1500) and their age at the start of
However, spreading the nutrient load does not appear to be the study (65–84 y) may be part of the explanation: large num-
advantageous in terms of increased thermogenic effects that bers of the original cohort had already died or were excluded
would favor weight reduction (40). because of diabetes or CHD (Table 2). The population left was
therefore preselected and may have been less vulnerable to envi-
ronmental factors.
EFFECTS IN HEALTH AND DISEASE In relation to diabetes outcome, both the Nurses’ Health Study
In healthy young men, low-glycemic-index diets have mini- (9) and the Health Professionals Studies (10) showed an inverse
mal effects in the short term (Table 1; 41, 42). In one euglycemic relation between glycemic index and the risk of developing dia-
hyperinsulinemic clamp study, glucose disposal was impaired betes by using a validated food-frequency questionnaire. In the
after 3 wk of a low-glycemic-index diet at high, but not low, case of the Health Professionals Study, both the association and
TABLE 1
Controlled studies of the effects of low-glycemic-index (GI) diets on carbohydrate and lipid metabolism in healthy, diabetic, and hyperlipidemic subjects1
Change Change in Type of Change
Dura- in dietary glycated glycated in blood First author, year,
Subjects tion GI2 proteins proteins lipids Comments and reference
wk % %
3,4
Healthy men aged 33 y (n = 6) 2 41 7 Fructosamine 15 TC3,5 32% urinary C-peptide excretion,3,5 12% 24-h creatine clearance3,5 Jenkins, 1987 (41)
Young men aged 24 y (n = 7) 3 24 NA NR NR Euglycemic hyperinsulinemic clamp showed no difference at low plasma Kiens, 1996 (42)
insulin but was reduced with low-GI diets at high plasma insulin
Insulin-resistant, middle-aged 3 18 NA NR No lipid With short insulin-tolerance test, in vivo insulin sensitivity improved Frost, 1998 (43)
women (post MI) (n = 28) changes after low-GI diet
Diabetic
Type 1, aged 12 y (n = 7 M) 6 12 193,4 Fructosamine 14 TC3,4 Reduced postprandial glucose response to a standard meal (90–180 mm) Collier, 1988 (44)
after low-GI diet
Type 1, aged 44 y (n = 4 M, 4 F) 3 14 183,4 Fructosamine 5.8 TG3,4 8.9% phospholipids,3,4 – 6.1% in daily insulin needs with low-GI diet3,4 Fontvieille, 1988 (45)
Type 1 (n = 7 M, 2 F) 2 27 6.55 Fructosamine NR Fasting blood glucose 23% lower with low-GI diet compared with Lafrance, 1998 (46)
control; no changes in insulin therapy
Type 1, aged 28 y (n = 54) 24 20 5.55 Hb A1c — Study design allowed for 35-g difference in fiber content between diets; Giacco, 2000 (47)
8.6 mmol/L daily blood glucose and less hypoglycemic events with
low-GI diet
Type 1, aged 8–13 y 52 1.2 6.53,5 Hb A1c NR 31% hyperglycemic events with low-GI diet; no changes in insulin Gilbertson, 2001 (48)
(n = 53 M, 51 F) therapy
Type 2, aged 65 y (n = 2 M, 6 F) 2 23 6.63,4 Hb A1c 5.8 TC3,4 30% fasting blood glucose with low-GI diet (8% NS with control)3,4 Jenkins, 1988 (49)
Type 2, aged 62 y (n = 10 M, 6 F) 12 14 113,4 Hb A1c — 75% 24-h urinary glucose output,3,5 used pasta and legumes to reduce GI Brand, 1991 (50)
Type 2, overweight (BMI = 32), 6 28 83,5 Fructosamine 6.8 TC3,5 22.4% TG for 5 subjects with TG < 2.2 mmol/L3,5 Wolever, 1992 (51)
aged 63 y (n = 3 M, 3 F)
Type 2, aged 67 y (n = 7 M, 8 F) 2 27 3.43,5 Fructosamine 73,5 TC 30% 24-h urinary C-peptide,3,5 29% postbreakfast blood glucose,3,5 Wolever, 1992 (52)
TG rose with control (P = 0.027) and fell with low-GI diet but the
2-wk treatment difference was NS
Type 2, BMI = 29, aged 56 y 12 5 163,4 Fructosamine 12.3 TC3,4 21% fasting blood glucose in low-GI group3,4 Frost, 1994 (53)
(n = 20 M, 6 F) 26 TG3,4
Type 2, BMI = 25.3, aged 65 y 3 31 5.93,4 Hb A1c 5 TC3,5 31% 9-h blood glucose profile,3,5 53% PA1-13,5; diet used same foods Järvi, 1999 (54)
(n = 15 M, 5 F) 8 LDL-C3,5 and relied on grinding (fine particle size) to raise GI
Type 2, BMI = 30.4, aged 57.4 y 4 20 1.85 Fructosamine +6 HDL3,5 Fasting plasma glucose 8% lower with low- compared with high-GI diet Luscombe, 1999 (55)
(n = 14 M, 7 F) (NS); diets did not contain legumes or pasta
GLYCEMIC INDEX: HISTORY AND OVERVIEW

Type 1 (n = 10 M, 2 F) and 5 26 133,5 Fructosamine 20 TG3,5 11% fasting blood glucose,3,5 13% mean daily blood glucose3,5; beans Fontvieille, 1992
type 2 (n = 2 M, 4 F), and pasta, rye bread, and fruit used to lower GI; balanced for total and (56)
BMI = 24.8, aged 47.2 y soluble fiber
Type 1, BMI = 21, aged 26 y 4 5 35 Hb A1c No lipid No postprandial blood glucose differences found between high- and Calle-Pascual, 1988
(n = 12); type 2, BMI = 30, differences low-GI diets; rice, potatoes, pasta, carrots, and beetroot used in the (57)
aged 59 y (n = 12) high-GI diet; legumes used in the low-GI diet
Hyperlipidemic subjects, 4 17 1.3 Fructosamine When TG Changes in weight loss and fat intake did not explain the lipid effects; Jenkins, 1987 (58)
BMI = 24, aged 47.5–57 y (n = 6)5 > 2.0 mmol/L GI was lowered with pumpernickel bread, bulgur, pasta, barley, and
(n = 30) (n = 24); 8.8 TC,3,5 legumes; 5% reduction in 24-h urinary C-peptide (n = 10) (NS)
19.3 TG,3,5
9.1 LDL-C3,5
1
Hb A1c, glycated hemoglobin; MI, myocardial infarction; NR, not reported; PAI-1, plasminogen activator inhibitor 1; TC, total cholesterol; TG, triacylglycerol. BMI is in kg/m2.
2
The reference food was white bread.
3
P < 0.05.
4
Difference from baseline after treatment (within low-GI treatment).
5
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Endpoint difference (between treatments).

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270S JENKINS ET AL

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FIGURE 3. Mean (± SD) difference from the control diet in glycated proteins (hemoglobin A 1c or serum fructosamine) in diabetic subjects
consuming either low-glycemic-index (GI) or high-monounsaturated–fatty acid (MUFA) diets. The vertical line indicates no effect. Adapted
from reference 59.

the trend became significant only after adjustment for fiber insulin resistance and insulin-like growth factors have also been
intake (10). The Iowa Women’s Health Study, although it also implicated (72, 77). Therefore, the greater part of the epidemio-
showed a negative association between cereal fiber intake and logic literature provides additional support for a role of dietary
the risk of diabetes, showed no significant association between glycemic index in disease.
glycemic index or load and diabetes incidence (69). This dis-
crepancy may relate to the frequency of application of the food-
frequency questionnaire during the study, the glycemic index NEWER ASPECTS OF GLYCEMIC INDEX RESEARCH
database used, and the age range of the subjects studied. Older There is considerable interest in the relations between insulin
cohorts selected as free of disease at the outset of a study may resistance, the generation of reactive oxygen species, tissue dam-
already have excluded a significant proportion of vulnerable sub- age, and the liberation of proinflammatory cytokines and acute
jects. In this respect, the Iowa Women’s Health Study subjects phase proteins, the latter appearing to be powerful markers of
were generally older than the subjects in the Nurses’ Health chronic diseases, notably CHD (78). The dietary glycemic index
Study (Table 2). may play a role in this sequence of events.
The glycemic index may have relevance to cancer prevention. Studies have shown that the postprandial rise in glucose is
In addition, insulin resistance and insulin-like growth factors consistent with depression of serum antioxidants, including lyco-
have been implicated in the so-called diet-related cancers: colon, pene and vitamin E (79, 80). Presumably, the higher the glycemia,
breast, and prostate (73, 74). Preliminary data support this asso- the greater the postprandial depression of serum antioxidants (80).
ciation for colon cancer (75). A case-control study showed a Finally, supplementing subjects’ diets with the antioxidant vita-
direct association between dietary glycemic index and colon min E has been shown to improve glycemic control (81). Studies
cancer risk. A sedentary lifestyle in conjunction with a high- such as these suggest a possible beneficial role for low-
glycemic-index diet increased risk relative to a sedentary lifestyle glycemic-index diets by reducing oxidative damage.
with a low dietary glycemic index or relative to an active It has been suggested that obesity is related to glycemic index
lifestyle with a high dietary glycemic index (76). An Italian case- or glycemic load (28, 82, 83). Studies on altering glycemic index
control study reported that the dietary glycemic index was related and load have indicated that the lower the glycemic index and
to colorectal cancer risk, ie, the higher the glycemic index, the load of the first meal, the less food is consumed in the subse-
greater the risk of colorectal cancer (71). The same relation of quent meal (28). Longer-term studies are required to define the
glycemic index and disease was also shown for breast cancer (72). relevance of these interesting findings.
Prostate and ovarian cancers, among other forms of cancer, may Finally, more studies are required to assess the relation of
be influenced by the dietary glycemic index. In these cases, glycemic index to chronic diseases, including cancer, CHD, and
TABLE 2
Cross-sectional and cohort studies of the relation of glycemic index (GI) to the risk of cardiovascular disease, diabetes, and cancer and its association with HDL and glycated hemoglobin (Hb A1c)1
Difference First author, year,
Subjects Study type Duration in GI Main effect Comments and reference
HDL
NHANES III 20-y survey, Cross-sectional NR Quintiles, For HDL with increasing quintile of HDL effect in men and women with Ford, 2001 (65)
BMI = 26.5 (n = 6825 M, 7052 F) survey, FFQ GI ≤ 75 to ≥ 88 GI 1.38–1.27, P for trend < 0.001 both high (> 25) and low BMI (< 25),
after age adjustment
British Adults (1986–1987 survey) Cross-sectional NR Quintiles, mean P for trend (univariate analysis) HDL related to total carbohydrate and Frost, 1999 (66)
aged 16–64 y (x– = 39.9 y) survey, 7-d DH GI: 86 for HDL (negative) < 0.001 starch P < 0.001 (negative); 93 subjects
(n = 699 M, 721 F) excluded from analysis because DH
and estimated energy needs discrepant
by ≥ 1000 kcal (4187 kJ)
CHD
US Nurses’ Health Study, aged Cohort, FFQ 10 y Quintiles, 72–80 CHD risk; GL, P for trend < 0.0001; The relative risk of CHD was seen to Liu, 2000 (11)
38–63 y, BMI = 25 (n = 75 521) (by GL) GI, P for trend < 0.008; increase with GL when BMI > 23
multivariate analysis
Elderly Dutch men (Zutphen Study) Cohort and 10 y Quintiles, 74–85 CHD risk, no GI association Earlier analysis of Zutphen data show van Dam, 2000 (67)
aged 65–84 y in 1955, BMI = 25.5 cross-sectional (1985–1995) disease-diet relations (1993–1995)
(555 of 1088 men still alive dietary recall but none reported in current assessment
from original survey plus 711 new at interview
men of same age)
Hb A1c
Type 1 diabetic subjects aged 33 y Survey, 3-d DH NR Quartiles, Hb A1c: 6.05–6.66 for quartile of For HDL (negative) and TG (positive), Buyken, 2001 (68)
(51% M), BMI = 26.7 (n = 2810) GI: 74.9–88.55 GI 1–4, P for trend = 0.0001 P for trend in biovariate model
= 0001 and 0.01, respectively
Diabetes
Nurses’ Health Study, aged 40–65 y Cohort FFQ 6y Quintiles, Diabetes RR: 1.37 (1.09, 1.71) for P for trend = 0.005 after adjustment Salmeron, 1997 (9)
(n = 65 173 F) GI: 64–79 5th quintile of GI, 1.47 (1.16, 1.86) for load for diabetes for GI fiber
for 5th quintile of GL (P = 0.04 unadjusted for fiber);
P for trend = 0.003 for diabetes and
GL after adjustment for cereal fiber
Health Professionals Study, Cohort FFQ 6y Quintiles, Diabetes RR: 1.37 (1.02, 1.83) for GI: P for trend = 0.03 after adjustment Salmeron, 1997 (10)
aged 40–75 y (n = 42 759 M) GI: 65–79 5th quintile of GI after fiber for fiber; no significance for load; for
adjustment high glycemic level and low cereal
fiber, the RR for diabetes was 2.17
(1.04, 4.54)
Older women aged 55–69 y Cohort FFQ 6y Quintiles, Diabetes RR for GI in 3rd quintile: RR of diabetes increased and then Meyer, 2000 (69)
(n = 35 988) GI: < 58 to > 80 1.22 (1.02, 1.47) but negative decreased with increasing quintiles
P for trend; no effect for GL of GI
GLYCEMIC INDEX: HISTORY AND OVERVIEW

Cancer
US colon cancer patients Case-control 1991–1994 NR Colorectal cancer risk for GI in 5th Being sedentary plus a high GI resulted Slattery, 1997 (70)
(n = 1099 M, 894 F) and FFQ quintile: 1.37 for M (1.04, 1.82), and in a higher risk than being active plus
controls (n = 1290 M, 1120 F) 1.34 for F (1.00, 1.81) (after a high GI or sedentary plus a low GI;
multiple adjustments, eg, age, the daily average GI was calculated
BMI, physical activity, NSAIDs, differently from other epidemiologic
and fiber) studies; GL was not calculated
Italian colorectal cancer patients Case-control 1992–1996 Quintiles Colorectal cancer risk for GI in 5th Similar findings for GL Franceschi, 2001
(n = 1125 M, 828 F) and hospital FFQ (upper limit), quintile: 1.7 (1.4, 2.0), P for trend (71)
controls (n = 2073 M, 208 F); GI: 70.7–79.6 < 0.001 (after multiple adjustments,
BMI = 26 (mean of middle tertile) (4th quintile) eg, age, sex, physical activity,
alcohol, and fiber)
Italian breast cancer patients Case-control 1991–1994 Quintiles Breast cancer risk for GI in 5th Similar findings for GL Augustin, 2001 (72)
(n = 2569) and hospital controls FFQ (upper limit), quintile: 1.4 (1.1, 1.6), P for trend
(n = 2588) GI: 69.6–78.9 < 0.01 (after multiple adjustments,
(4th quintile) eg, age, physical activity, alcohol,
271S

fiber, and parity)

1
CHD, coronary heart disease; DH, diet history; FFQ, food-frequency questionnaire; GL, glycemic load; NHANES III, third National Health and Nutrition Examination Survey; NSAIDS, nonsteroidal
antiinflammatory drugs; RR, relative risk; NR, not reported.

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272S JENKINS ET AL

diabetes. In addition, large-scale intervention studies are under- 19. Jenkins DJ, Wolever TM, Jenkins AL, et al. Low glycemic response
way and more are required to define the theraputive utility of the to traditionally processed wheat and rye products: bulgur and
glycemic index concept. pumpernickel bread. Am J Clin Nutr 1986;43:516–20.
20. Boyce VL, Swimburn, BA. The traditional Pima Indian diet. Com-
position and adaptation for use in a dietary intervention study. Dia-
CONCLUSION betes Care 1993;16:369–71.
21. O’Dea K. Westernisation, insulin resistance and diabetes in Aus-
The dietary glycemic index concept suggests a possible role tralian aborigines. Med J Aust 1991;155:258–64.
for the rate of carbohydrate digestion in the prevention and treat- 22. Thorburn AW, Brand JC, Truswell AS. Slowly digested and
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We thank Thomas Wolever for his help and provision of Figure 3. responses of normal subjects after consuming mixed meals varying
in energy, protein, fat, carbohydrate and glycemic index. J Nutr
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