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Letter to the Editor |
1 Human Nutrition Unit, School of Molecular and Microbial Biosciences, University of Sydney, New South Wales 2006, Australia. E-mail: j.brandmiller{at}biochem.usyd.edu.
2 Department of Mathematical Sciences, University of Technology, New South Wales 2007, Australia.
Dear Sir:
Recently, the American Diabetes Association published the following statement: "with regard to the glycemic effects of carbohydrates, the total amount of carbohydrate in meals and snacks is more important than the source or type" (1). However, the revised glycemic index (GI) table published in the July 2002 issue of the Journal (2) indicates that even when foods contain the same amount of carbohydrate (ie, carbohydrate exchanges), there are up to 10-fold differences in the glycemic effect among them. Moreover, prospective observational studies found that the risk of developing diseases of affluence (eg, type 2 diabetes, cardiovascular disease, and some cancers) is independently related to the overall dietary GI and glycemic load (GL), but not to the total carbohydrate content (3). GL—the product of the carbohydrate content of a serving of food and its GI—is a measure of both the quantity and quality of carbohydrate and the interaction between them. Thus, in the 2002 table (2), we included not only the GI values of the foods but the carbohydrate content per nominal serving and its calculated GL value. In the table, each unit of GL is the glycemic equivalent of 1 g of pure glucose.
The question remains, however, which is the stronger determinant of GL: the amount of carbohydrate per serving or the GI? At Mendosa’s suggestion, we used the data published in the revised tables to explore the statistical relations between GI, GL, and carbohydrate content.
As the first step, we excluded data for foods in which carbohydrate was either a very minor component (high-protein meal-replacement shakes) or was only partially absorbed (sugar alcohols and bulking agents), producing a final data set with a total of 1058 entries. Among these, the amount of carbohydrate per serving varied from 3 to 75 g (
± SD: 25 ± 12 g) and the GI values ranged from 5 to 139 (54 ± 19). Subsequently, we performed a regression analysis to determine how much of the variation in GL values was explained by the amount of carbohydrate in nominal portions of foods versus the corresponding GI values. Obviously, both factors will be directly related to GL, because the values were calculated by using the following formula: GL = (amount of carbohydrate in the portion of food x GI value for the food)/100 (3).
The data were transformed onto a log scale, because GL values are a product of the multiplication and not the addition of the carbohydrate content and the GI. Linear regression analysis with the use of the log scale indicated that the carbohydrate content alone explained 68% of the variance in GL values, whereas the GI value alone explained 49% of the variance in GL values. The results were similar when the data were analyzed on the ordinary scale, as shown in Figure1
. Hence, although carbohydrate is indeed the greater determinant of GL, it makes no sense to ignore a factor that accounts for almost 50% of the variation in GL on its own and an additional 32% of the variation when carbohydrate is also included in the linear regression analysis
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10 for a low GL and 
20 for a high GL. Hence, a GL between 11 and 19 represents a medium GI. These cutoffs should be reevaluated in the future. It remains to be shown, of course, that the concept of GL makes physiologic sense. Currently, 2 assumptions need to be tested in vivo: 1) that food portions calculated to have the same GL produce similar glycemic responses and 2) that stepwise increases in GL produce proportionate increases in glycemia and insulinemia. Such relations need to be proven in a variety of subjects (eg, lean and obese and insulin-sensitive and insulin-resistant). Until then, it makes sense to consider both the carbohydrate content and the GI of foods in the research and management of postprandial glycemia.
REFERENCES
This article has been cited by other articles:
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  A. W. Barclay, J. C. Brand-Miller, and T. M.S. Wolever Glycemic Index, Glycemic Load, and Glycemic Response Are Not the Same Diabetes Care, July 1, 2005; 28(7): 1839 - 1840. [Full Text] [PDF]
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N. F. Sheard, N. G. Clark, J. C. Brand-Miller, M. J. Franz, F. X. Pi-Sunyer, E. Mayer-Davis, K. Kulkarni, and P. Geil Dietary Carbohydrate (Amount and Type) in the Prevention and Management of Diabetes: A statement by the American Diabetes Association Diabetes Care, September 1, 2004; 27(9): 2266 - 2271. [Full Text] [PDF]
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 S. Scaglioni, G. Stival, and M. Giovannini Dietary glycemic load, overall glycemic index, and serum insulin concentrations in healthy schoolchildren Am. J. Clinical Nutrition, February 1, 2004; 79(2): 339 - 340. [Full Text]
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N. M. McKeown, J. B. Meigs, S. Liu, E. Saltzman, P. W.F. Wilson, and P. F. Jacques Carbohydrate Nutrition, Insulin Resistance, and the Prevalence of the Metabolic Syndrome in the Framingham Offspring Cohort Diabetes Care, February 1, 2004; 27(2): 538 - 546. [Abstract] [Full Text] [PDF]
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