Am J Clin Nutr 89: 97-105, 2009.
First published December 3, 2008; doi:10.3945/ajcn.2008.26354
American Journal of Clinical Nutrition, doi:10.3945/ajcn.2008.26354
Vol. 89, No. 1, 97-105, January 2009
© 2009 American Society for Clinical Nutrition
ORIGINAL RESEARCH COMMUNICATION |
Glycemic index, postprandial glycemia, and the shape of the curve in healthy subjects: analysis of a database of more than 1000 foods1,2
Jennie C Brand-Miller,
Karola Stockmann,
Fiona Atkinson,
Peter Petocz and
Gareth Denyer
1 From the Institute of Obesity, Nutrition and Exercise (JCB-M), and the School of Molecular and Microbial Biosciences (JCB-M, KS, FA, and GD), The University of Sydney, Sydney, Australia, and the Department of Statistics, Macquarie University, Sydney, Australia (PP).
2 Reprints not available. Address correspondence to JC Brand-Miller, Human Nutrition Unit, G08, The University of Sydney, Sydney, NSW, 2006. E-mail: j.brandmiller{at}mmb.usyd.edu.au.
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ABSTRACT
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Background: The glycemic index (GI) characterizes foods by using the incremental area under the glycemic response curve relative to a similar amount of oral glucose. Its ability to differentiate between curves of different shapes, the peak response, and other aspects of the glycemic response is debatable.
Objective: The objective was to explore the association between a food's GI and the shape of the curve in healthy individuals.
Design: A large database of 1126 foods tested by standardized GI methodology in 8–12 healthy subjects was analyzed systematically. Each food's absolute and incremental blood glucose concentrations were compared at individual time points with the GI. The average curve was generated for low-GI (
55), medium-GI (56–69), and high-GI (
70) foods within major food categories.
Results: The GI of individual foods was found to correlate strongly with the incremental and actual peak (Spearman's correlations of r = 0.76 and r = 0.73, respectively), incremental and actual glucose concentration at 60 min (r = 0.70 and r = 0.66, respectively), and maximum amplitude of glucose excursion (r = 0.68) (all P < 0.001). In contrast, there was only a weak correlation between the food's GI and the 120-min glucose concentration (incremental r = 0.20, P < 0.001; absolute r = 0.16, P < 0.001). Within food groups, the mean GI, 30- and 60-min glucose concentrations, and maximum amplitude of glucose excursion varied significantly for foods classified as having a low, medium, or high GI (P < 0.001).
Conclusions: The GI provides a good summary of postprandial glycemia. It predicts the peak (or near peak) response, the maximum glucose fluctuation, and other attributes of the response curve.
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INTRODUCTION
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In medical nutrition therapy, the American Diabetes Association emphasizes the amount of carbohydrate required to optimize glucose control and slow the development of complications (1). However, a large body of evidence indicates that the carbohydrate source is also an important consideration (2, 3). Changes in glycemia after the ingestion of equivalent carbohydrate exchanges vary widely, depending on food factors such as the final physical and chemical state of the starch (4), the viscosity and structural integrity of the fiber (5), and the nature of the monosaccharides and disaccharides present (6).
The glycemic index (GI) of foods was developed in an attempt to systematically classify the carbohydrates in different foods according to time-integrated effects on postprandial glycemia. Foods with high GI values have been shown to be more rapidly digested and absorbed, causing greater fluctuations in blood glucose per unit of carbohydrate than foods with lower GI values (7). Developments in food processing over the past 50 y, such as high-temperature, high-pressure extrusion technology, increase the degree of starch gelatinization, which results in easier enzymic accessibility and faster digestion (8, 9). As a consequence, the GI of many modern starchy foods falls within the high range. Even among whole-grain breads and breakfast cereals, GI values can vary widely (10).
The GI is defined methodologically as the incremental area under the curve (AUC) for the blood glucose response after consumption of a food relative to that produced by a reference food given in an equivalent carbohydrate amount (50 or 25 g) (11). Some investigators have expressed concern that use of the AUC, which integrates the entire blood glucose response over time, may not be appropriate because it fails to take into account the shape of the curve (12, 13). Theoretically, it is possible that the carbohydrates in some foods elicit a sharp glucose "spike" that disappears quickly and undershoots the baseline value and yet have the same AUC as the carbohydrates that provoke a more gradual rise and fall in blood glucose. The distinction is important because emerging data suggest that the postprandial glycemic spike and degree of blood glucose fluctuation per se may be more clinically adverse than sustained glycemia (14, 15).
For these reasons, we explored the association between a food's GI and the shape of the curve in healthy individuals. Our working hypothesis was that the GI would reliably predict multiple attributes of the glycemic response. We considered the absolute and incremental peak glucose value (the "spike"); the 60-, 90-, and 120-min values; and the maximum excursion within 120 min (ie, maximum amplitude of the glucose excursion, or MAGE). We analyzed the absolute blood glucose responses recorded in a large database of foods that had been tested by our laboratory using the standard GI protocol. Average glucose curves were then generated for large numbers of foods classified as having a low, medium, or high GI within major food groups.
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SUBJECTS AND METHODS
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Since 1995, the University of Sydney has conducted contract GI testing for the food industry alongside research on the GI and its relevance to health. Between 2001 and June 2007, raw data were routinely entered into a specially developed database that permitted systematic analysis of all aspects of GI testing. During that period, 1126 individual food items were tested in healthy subjects according to the standard GI testing protocol; the responses to the test foods were compared with the responses to a reference food (16). In most cases, the reference food was 50 g glucose dissolved in 250 mL water and tested on 2 or 3 separate occasions within a 3-mo period for each subject. In a small minority of cases, 25-g carbohydrate portions were used to accommodate more dilute sources of carbohydrate. The protocol was approved by the University of Sydney Human Research Ethics Committee, and the subjects gave written informed consent.
For each test, 8–12 healthy subjects were recruited and presented to the metabolic kitchen in the morning after a 10–12-h fast. They consumed the food with 250 mL water within 10–15 min, and finger-prick capillary blood was collected at 0 (start of the meal), 15, 30, 45, 60, 90, and 120 min. Glucose was determined in duplicate either with HemoCue (HemoCue AB, Ängelholm, Sweden) (17) in whole blood or in plasma after 0.8 mL blood was collected into an Eppendorf tube containing 10 U heparin. In the latter case, plasma was separated after centrifugation and cooled on ice until same-day assay with the glucose hexokinase assay on a centrifugal analyzer. For each test, the incremental AUC was calculated according to the trapezoidal method and compared with the average AUC (n = 2 or 3) for the reference food in that particular subject (16). Any area under the baseline (fasting value) was ignored. The GI was determined as the mean ± SE in 8–12 different subjects and rounded to the nearest integer. In instances in which the value for any one individual was unusually large or small (>2 SD from the mean), the value was removed and the mean ± SE was recalculated. Thus, the GI of any one food was based on
480 separate glucose determinations (10 subjects, 8 time points, duplicate assays, 2 reference foods, and 1 test food). In the database, 51% of the foods were compared with 3 reference tests (glucose standard) and the remainder against 2. The within-subject CV for the 2–3 tests of the reference food was 17.4 ± 5.4%.
The database
A relational database was created by using FileMaker Pro 6 (FileMaker Inc, Santa Clara, CA) to link information regarding the subjects (eg, sex, ethnicity, height, and relevant medical information) and foods (eg, nutrient composition and food group classification) with test data (eg, age and weight of subjects and test conditions) and all assay results (ie, the glucose result at each time point). The database automatically calculated all of the variables investigated in this study (AUC, GI, CV, peaks and nadirs, MAGE, and all other relative and absolute glucose values for each test).
Analysis of the database
In the first analysis, all foods that had been GI-tested according to the standard protocol were considered (n = 1126). To determine the ability of the GI to predict postprandial glycemia at any one time point, the GI was correlated against both the absolute concentration and the incremental change in blood glucose at 30, 60, and 120 min. The degree of fluctuation, also called MAGE, was determined as the difference between the highest and lowest concentration over 120 min.
For the second analysis, all foods that could be categorized into discrete food groups were included (n = 780 foods). Twelve types of foods were identified: potatoes, breads (white and whole-wheat), breakfast cereals, rice, pasta, snack bars, potatoes, dairy products, fruit, fruit juices, and vegetables (other than potato). Within each category, foods were classified as high GI (
70), medium GI (56–69), or low GI (
55) according to recommendations of Standards Australia (16). The average curve was generated from the mean data at each time point. The peak responses and blood glucose concentrations at 60, 90, and 120 min for the high-, medium-, and low-GI foods within each category were then compared.
Statistical analysis
Spearman's correlation coefficients were calculated between the GI and MAGE and the glucose concentration at the 30-, 60-, 90-, and 120-min time points (absolute and incremental). Where relations appeared to be only approximately linear, loess curves were fitted to indicate the actual shape of the relation. Other relations were also explored, including quadratic and cubic equations. One-way analyses of variance were used to compare differences between foods classified as low GI, medium GI, and high GI with pairwise comparisons subject to Bonferroni corrections for multiple tests. All statistical analyses were carried out by using the SPSS statistical package (version 14.0; SPSS Inc, Chicago, IL), and tests used a significance level of 0.05.
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RESULTS
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A total of 546 different volunteers (58% female) participated in GI testing over the time frame of this study. Their mean ± SD age was 24.0 ± 4.8 y and body mass index (in kg/m2) was 22.2 ± 2.3. The mean (± SD) fasting glucose concentration was 5.11 ± 0.36 mmol/L in plasma (n = 8056) and 4.57 ± 0.47 mmol/L in whole blood (n = 3841). Most subjects were of European white origin (74%), and the largest minority group was Chinese (18%).
Within the total database (n = 1126 foods), the GI value was found to correlate strongly with the food's incremental peak (Spearman's r = 0.76), actual peak (r = 0.73), incremental glucose concentration at 60 min (r = 0.70), actual 60-min glucose concentration (r = 0.66), incremental 90-min glucose concentration (r = 0.43), actual 90-min glucose concentration (r = 0.34), and MAGE (r = 0.68); P < 0.001 for all (Figure 1). Actual peak concentration and MAGE were highly correlated (r = 0.83, P < 0.001). In contrast, only a weak correlation between the food's GI and the 120-min glucose concentration was found (incremental r = 0.20, P < 0.001; absolute r = 0.16, P < 0.001; Figure 2A); although weak, these correlations were significant because of the large amount of data.

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FIGURE 1. Scattergrams with fitted Loess curves that show the relation between (A) absolute peak glucose concentration compared with the glycemic index (GI) of each food (n = 1126; Spearman's r = 0.73, P < 0.001, (B) absolute 60-min glucose concentration compared with the GI of each food (n = 1126; r = 0.66, P < 0.001), and (C) the maximum amplitude of the glucose excursion (MAGE) compared with the GI of each food (n = 1126; r = 0.68, P < 0.001. Each food was tested in differing groups of 8–12 normal subjects.
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FIGURE 2. A: Scattergram with fitted Loess curve that shows absolute 120-min glucose concentration compared with the glycemic index (GI) of each food (n = 1126; Spearman's r = 0.14, P < 0.001. B: The rank order of 120-min incremental blood glucose concentration across 34 different food groups. Starchy foods generally gave higher values than foods rich in simple sugars, whether these were naturally occurring or added.
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We also explored nonlinear alternatives, but found little improvement. For example, for the 60-min time point versus GI, r2 was 0.40 for linear, 0.40 for quadratic, and 0.43 for cubic fits. Nonparametric loess curves were fitted to indicate the actual nature of the relation (Figures 1 and 2) and suggested a steeper relation between absolute peak versus GI when the GI was less than
55 (Figure 1A). For absolute glucose concentration at 60 min, the relation was steepest in the intermediate range (Figure 1B). For MAGE (Figure 1C), the relation was less steep for GI values above
40. No consistent pattern was apparent at the 120-min time point.
With one exception, starchy foods, irrespective of their GI, tended to remain above the baseline level at 120 min, whereas foods high in sugars (both naturally occurring and added) tended to undershoot the baseline (Figure 2B). The foods with the highest 120-min values were the high-GI rices (mean difference from baseline for 22 products = 0.4 mmol/L) and high-GI whole-grain breads (mean incremental level in 8 products = 0.4 mmol/L). The foods with the lowest 120-min values were soft drinks (mean difference from baseline for 7 products = –0.5 mmol/L) and fruit juices (mean difference from baseline for 29 products = –0.5 mmol/L). Potato products were the one exception and behaved like sugary foods, undershooting the baseline by 120 min (mean of 9 products = –0.4 mmol/L).
The average curve shapes for the high-, medium-, and low-GI foods within 10 major food categories are illustrated in Figure 3 and Figure 4. Universally, the peak glucose values occurred at 30 min, and, almost always, the lowest reading was recorded at 120 min. When dairy products were tested in 25-g carbohydrate portions, the nadir occurred at 60 min. Potatoes as a group had the highest GI (mean of 9 products = 90), followed by the high-GI breakfast cereals (mean of 29 products = 82; Table 1). The foods with the lowest GI values included legumes (mean of 11 products = 38), protein bars (mean GI of 59 products = 28), and plain milk (mean of 13 products = 25). Notably, no soft drinks, fruit juices, or dairy products fell into the high-GI category. Whole-grain breads and breakfast cereals were available in all 3 GI categories. Foods classified as high GI, medium GI, or low GI within each category usually differed significantly with respect to mean GI and 30-, 60-, and 90-min glucose concentrations (absolute and incremental) (Table 1).

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FIGURE 3. A–H: Incremental blood glucose profiles for high, medium, and low glycemic index (GI) foods within 8 different food categories. n = number of foods that were tested in each category in 8–12 subjects. All tests were 50-g portions of carbohydrate.
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FIGURE 4. Incremental blood glucose profiles for high, medium, and low glycemic index (GI) of dairy products (A and B) and vegetables (C). n = number of foods that were tested in each category in 8–12 subjects. Some dairy product tests were given with both 25- and 50-g portions of carbohydrate, as indicated.
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DISCUSSION
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The current analysis was the first attempt to systematically characterize the relation between a food's GI and other attributes of the postprandial glycemic response. It was shown that the GI, a number derived from the incremental AUC, was correlated with the absolute peak response (the glycemic spike), the glucose concentration at 60 and 90 min, and MAGE (the difference between the peak and the nadir). Although these relations were approximately linear, loess curves indicated that the steepness of the relation varied somewhat over the full GI range. In univariate analysis, each variable showed a positive correlation with GI and accounted for 50–60% of the variation. Consequently, the 2 food groups with the highest GI values (potatoes and breakfast cereals) also had among the highest glucose peaks (absolute peak: 8.7 and 7.7 mmol/L, respectively). The foods with the lowest GI values (plain milk and protein bars) were also the 2 categories that had among the lowest peak responses (absolute peak: 5.5 and 6.1 mmol/L, respectively). MAGE ranged from a high of 4 mmol/L for potatoes to only 1.3 mmol/L for legumes and 1.1 mmol/L for protein bars.
This analysis was also the first to explore differences in the shape of the curve of within- and between-food categories. As is evident in Figures 3 and 4, the general curve shape is similar within each food category even though the AUCs differ. The notion that low-GI foods produce a sustained rise in blood glucose was not supported. Moreover, high-GI foods all differed significantly from similar foods with a low GI at several time points (Table 1). Although there was also a positive relation between the GI and the 2-h glucose concentration, the correlation coefficient was weak (r = 0.16), and considerable heterogeneity was observed between the different types of foods. In general, sugary foods, including soft drinks and fruit juices, irrespective of GI, were more likely to return to baseline sooner (between 60 and 75 min) and to show an undershoot at the 120-min time point (Figure 2). In contrast, with the exception of potatoes, starchy foods tended to remain above baseline at 120 min. These findings can be explained by the fact that simple sugars such as sucrose, lactose, and fructose—whatever their source—contribute fewer glucose moieties than the same weight of starch. Fifty grams of sucrose, for example, contains only 25 g of glucose equivalents versus 50 g of glucose equivalents in starch. Compared with 50 g glucose, 25 g glucose produces a curve that returns to baseline earlier (Figure 4). Although the difference was subtle, the "undershoot" seen for fruit juices, soft drinks, and potatoes may have physiologic ramifications for appetite and weight control (18).
The strengths of this analysis include the size of the database, the large number of food categories examined, the use of standardized GI protocols with 2–3 reference foods tested for each test food, and the use of finger-prick capillary sampling. It is not yet widely recognized that changes in blood glucose immediately after a meal may be identified more readily at finger sites than at the forearm (19). The use of finger-prick blood sampling is also associated with less variability in resulting GI values (20). Our subjects also showed low intraindividual (within-subject) variability for repeat tests of the reference food (
17%), which is substantially lower than that recorded by others; for example, Vega-Lopez et al (21) reported a variability of
43%. The limitations, however, included the fact that the database was built on the testing of single foods in healthy individuals. This may make the findings less generalizable to mixed meals and to individuals with diabetes, although there is abundant evidence of support (22–25). The findings are also derived from the average of many foods, and the scattergrams clearly suggest wide prediction intervals. These data should therefore not be used to predict responses to individual foods or groups of foods.
A potential limitation of this analysis was the assumption that one large group of subjects has approximately the same degree of glucose tolerance as another large group. This assumption is not appropriate when small numbers of subjects (n
10) are involved; however, in the present context, the mean glycemic response within each food category (eg, high-GI white breads) was often the average of
200 or more individuals. As a group, glucose tolerance in these
200 subjects was no different from that of any other group of
200 lean young healthy subjects (data not shown). Significant heterogeneity among subjects would work against the chance of detecting differences at various time points of the glycemic response.
Our study was unique from the standpoint of defining "normal" postprandial glycemia. The results indicate that the normal response depends on the choice of carbohydrate food. For example, MAGE varied over a 4-fold range and the peak varied >3-fold. The threshold for unacceptable postprandial glycemia defined by the American Diabetes Association and World Health Organization is 8.89 mmol/L (>160 mg/dL) at any time after the meal (25); however, in the present analysis, potatoes gave an average absolute peak of 8.67 mmol/L in healthy individuals consuming 50 g carbohydrate. Realistically, meals often contain larger quantities of carbohydrate. Postmeal glycemia. as elicited by modern carbohydrate foods, can therefore contribute to the dysglycemic "iceberg" or hidden glycemia that may be more important over the longer term than an increase in fasting glucose.
Mounting evidence suggests that the postprandial state contributes to the development of chronic disease, particularly atherosclerosis (26). In individuals with diabetes or prediabetes, the postprandial phase is characterized by a large and more prolonged increase in blood glucose concentrations. Observational studies have shown that postchallenge or postmeal glucose peaks are an independent risk factor for cardiovascular disease (14, 27, 28). Many cardiovascular disease risk factors, including coagulatory proteins, are modified in the postprandial phase in diabetic subjects and are directly affected by an acute increase in glycemia (29). Postmeal glycemic spikes within the normal range can also act directly to increase oxidative stress and inflammatory responses (30). Recently, we reported that increases in nuclear transcription factor-
B activation (an inflammatory marker) in mononuclear cells of healthy individuals were 3-fold higher after a high-GI carbohydrate meal or glucose challenge than after a low-GI carbohydrate meal (31).
In summary, this analysis supports the hypothesis that the GI reliably predicts multiple attributes of the glycemic response. We found that the overall shape of postprandial glycemia is similar for foods categorized as having a low, medium, or high GI according to Standards Australia criteria (16). The notion that a low-GI food has a uniquely long tail or extended glucose profile is not correct. Although a slowly digested starch or sugar may represent a slow-release form of energy, this does not imply that a low-GI food produces a sustained glucose response. The message to eat whole grains can result in the intake of carbohydrates with a GI no different from that in response to the consumption of white bread. Finally, if a reduction in postprandial glycemia is to be part of the strategy for preventing and managing diabetes and cardiovascular disease, the GI is as relevant as the amount of carbohydrate.
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ACKNOWLEDGMENTS
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The authors' responsibilities were as follows—JCB-M and GD: conceived the study; GD and FA: created the database; and JCB-M, KS, and PP: analyzed the data. All authors contributed to the interpretation of the findings and the writing of the manuscript. JBM is a co-author of The New Glucose Revolution book series (Hodder and Stoughton, London, United Kingdom), director of a nonprofit GI-based food-endorsement program in Australia, and director of the University of Sydney GI testing service. FA and KS were employed by the University of Sydney for the purposes of commercial GI testing. PP and GD had no conflicts of interest to declare.
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Received for publication May 1, 2008.
Accepted for publication September 18, 2008.