Nutrition 31 (2015) 539–541

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Nutrition and food

A glance at. glycemic index Michael J. Glade Ph.D. a, *, Kyl Smith D.C. b a b

The Nutrition Doctor, Kailua-Kona, Hawaii, USA Progressive Laboratories Inc., Irving, Texas, USA

a r t i c l e i n f o Article history: Received 17 October 2014 Accepted 24 October 2014

Effective management of type 2 diabetes includes moderation of carbohydrate intake [1]. One tool that can be used to estimate the effect of a food or meal on glucoregulation is the glycemic index. The glycemic index of a food item represents a quantitative assessment of a chemical characteristic of the food item (its digestible carbohydrate [CHO] content) obtained through measurement of the cumulative effects of the consumption of the food item on the plasma glucose concentration [2,3]. Postconsumption changes in plasma glucose concentration reflect the net results of several physiological processes, including CHO hydrolysis and absorption in the small intestine, pancreatic insulin secretion in response to postabsorptive increase in plasma glucose concentration, and tissue glucose uptake in response to insulin [4,5]. These physiological processes are affected by the inherent chemical characteristics of the food item as well as by interindividual variability in alimentary canal, gastrointestinal and pancreatic efficiencies [4,6,7]. The outcome of such an analysis, the glycemic index, is determined from the measured postprandial excursions in plasma glucose concentrations that follow the consumption of a standardized amount (usually 100 g) of the food item of interest compared with the excursions after the consumption of 100 g of glucose (in both cases, measured during the first 120 min postconsumption) [8]:

 GIfood item ¼

For example, low glycemic index foods (such as chickpeas, lentils, barley) produce smaller postprandial increases in plasma glucose concentrations, while high glycemic index foods (such as honey, white bread) produce larger postprandial increases in plasma glucose concentrations [4,9]. The glycemic indices (GI) of more than 1000 individual food items have been determined and validated experimentally [2,3,10–14]. Adding glucose or sucrose (a source of 100% bioavailable glucose) to a food item increases the combination’s measured glycemic index to the extent predicted by the food item’s glycemic index and the amount of added glucose [15]. This observation suggests the glycemic index of a meal can be calculated from the tabulated GI of the individual food items of which the meal is composed: GImeal ¼ S{[GIfood item i][(g of CHOfood item i)/ (g of CHOtotal meal)]} [15]. In free-living adults, the GI of meals calculated using this formula are highly significantly correlated with, and predictive of, postprandial plasma glucose concentrations [16–20]. However, despite the correlation, the measured GI of mixed-food meals tend to be 20–50% lower than the corresponding values calculated from tables of the GI of individual food items [21]. It has been suggested that interactions among food items within the human gastrointestinal tract often slow the rate of glucose absorption (thereby reducing the measured glycemic index of

 area under the curve; plasma glucose concentration100 g food item ð100Þ   area under the curve; plasma glucose concentration100 g glucose

Support for this project was received from Progressive Laboratories, Inc., Irving, Texas, USA. * Corresponding author. Tel.:þ1-847-329-9818. E-mail address: [email protected] (M. J. Glade). http://dx.doi.org/10.1016/j.nut.2014.10.013 0899-9007/Ó 2015 Elsevier Inc. All rights reserved.

a mixed-food meal) [21]. Because the difference between predicted GImeal and measured GImeal is highly variable, no “correction factor” is available for general application and GImeal should be measured directly for the greatest accuracy.

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Although the quantitative individual responses to a given food or meal can be quite variable from day to day [22,23], the glycemic index provides useful relative estimates of an individual’s glycemic responses to consumed foods, and the GI of food items and of mixed-food meals are relatively good indicators of the effect of the consumption of food items and meals on postprandial insulin secretion. In free-living adults, the calculated GI of meals is highly significantly correlated with, and predictive of, postprandial plasma insulin concentrations [9,15, 16,24–29]. Fasting insulinemia is inversely correlated with insulin sensitivity [30–35]. Investigators performing a meta-analysis of the published results of 45 intervention studies concluded insulin sensitivity is inversely correlated with the glycemic index of an individual’s habitual diet and fasting glucose concentration and fasting insulinemia are directly correlated with the glycemic index of the habitual diet [36]. Furthermore, reducing the glycemic index of an individual’s diet for 4 d [37], 7 d [38], or 12 wk [39] produces an increase in the individual’s insulin sensitivity and a decrease in the fasting plasma insulin concentration. Consistent with these findings, the results of meta-analyses of the results of 37 [40] and 21 [41] previously published prospective observational epidemiologic studies indicated the risk for developing type 2 diabetes is significantly positively correlated with the average glycemic index of an individual’s habitual diet [40]. Reducing the glycemic index of the habitual diet also can reduce the level of chronic systemic oxidative stress. In a large cross-sectional study of healthy men and women ages 18–75 y, the plasma malondialdehyde concentration (a biomarker of the systemic rate of spontaneous nonenzymatic peroxidation of polyunsaturated fatty acids, and, therefore, a biomarker of the degree of oxidative damage throughout the body [42]) and the plasma F2-isoprostane concentration (a biomarker of the systemic rate of spontaneous nonenzymatic peroxidation of the arachidonic acid component of cell membranes, and, therefore, another biomarker of the degree of oxidative damage throughout the body [43]) were directly correlated with the calculated glycemic index of the habitual diet [44]. Among a cohort of children with and without type 1 diabetes, the 24-h urinary excretion of 8-iso-PGF2a, a product of the nonenzymatic oxidation of arachidonic acid in cell membranes [45], was highly correlated with the 24-h mean amplitude of glycemic excursions [46]. Mean amplitude of glycemic excursions is a measure of cumulative hyperglycemia over 24 h and in adults is highly correlated with 24-h urinary excretion of 8-isoPGF2a [47]. Conclusions The glycemic index of a food item represents the cumulative effects of its consumption on the plasma glucose concentration. Postconsumption changes in plasma glucose concentration reflect the net results of several physiological processes, including CHO hydrolysis and absorption in the small intestine, pancreatic insulin secretion in response to postabsorptive increase in plasma glucose concentration, and tissue glucose uptake in response to insulin. These physiological processes are affected by the inherent chemical characteristics of the food item as well as interindividual variability in alimentary canal, gastrointestinal and pancreatic efficiencies. Low glycemic index foods (such as chickpeas, lentils, barley) produce smaller postprandial increases in plasma glucose concentrations, while high glycemic index foods (such as honey,

white bread) produce larger postprandial increases in plasma glucose concentrations. The glycemic index of a meal can be calculated from the tabulated GI of the individual food items of which the meal is composed. The calculated GI of meals is highly correlated with and predictive of postprandial glucose and insulin concentrations. In addition, the average glycemic index of the habitual diet is predictive of the degree of insulin sensitivity. Reducing the average glycemic index of the habitual diet can decrease fasting glucose concentrations, increase insulin sensitivity, reduce the cumulative effects of hyperglycemic episodes, and reduce the average level of chronic systemic oxidative stress. References [1] American Diabetes Association, Bantle JP, Wylie-Rosett J, Albright AL, Apovian CM, Clark NG, et al. Nutrition recommendations and interventions for diabetes: A position statement of the American Diabetes Association. Diabetes Care 2008;31:S61–78. [2] Galgani J, Aguirre C, Dıaz E. Acute effect of meal glycemic index and glycemic load on blood glucose and insulin responses in humans. Nutr J 2006;5:22. [3] Brand-Miller JC, Stockmann K, Atkinson F, Petocz P, Denyer G. Glycemic index, postprandial glycemia, and the shape of the curve in healthy subjects: Analysis of a database of more than 1,000 foods. Am J Clin Nutr 2009;89:97–105. [4] Esfahani A, Wong JM, Mirrahimi A, Srichaikul K, Jenkins DJ, Kendall CW. The glycemic index: Physiological significance. J Am Coll Nutr 2009;28: 439S–45S. [5] Schenk S, Davidson CJ, Zderic TW, Byerley LO, Coyle EF. Different glycemic indexes of breakfast cereals are not due to glucose entry into blood but to glucose removal by tissue. Am J Clin Nutr 2003;78:742–8. [6] Fajkusova Z, Jadviscokova T, Pallayova M, Matuskova V, Luza J, Kuzmina G. Glycaemic index of selected foodstuffs in healthy persons. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2007;151:257–61. [7] Venn BJ, Williams SM, Perry T, Richardson S, Cannon A, Mann JI. Agerelated differences in postprandial glycaemia and glycaemic index. Age Ageing 2011;40:755–8. [8] Jenkins DJ, Srichaikul K, Kendall CW, Sievenpiper JL, Abdulnour S, Mirrahimi A, et al. The relation of low glycaemic index fruit consumption to glycaemic control and risk factors for coronary heart disease in type 2 diabetes. Diabetologia 2011;54:271–9. [9] Jamurtas AZ, Tofas T, Fatouros I, Nikolaidis MG, Paschalis V, Yfanti C, et al. The effects of low and high glycemic index foods on exercise performance and beta-endorphin responses. J Int Soc Sports Nutr 2011;8:15. [10] Atkinson FS, Foster-Powell K, Brand-Miller JC. International tables of glycemic index and glycemic load values: 2008. Diabetes Care 2008;31: 2281–3. [11] Atkinson FS, Foster-Powell K, Brand-Miller JC. International tables of glycemic index and glycemic load values: 2008. Supplemental Table 1. Diabetes Care 2008;31:2281–3. [12] Atkinson FS, Foster-Powell K, Brand-Miller JC. International tables of glycemic index and glycemic load values: 2008. Supplemental Table 2. Diabetes Care 2008;31:2281–3. [13] Atkinson FS, Foster-Powell K, Brand-Miller JC. International tables of glycemic index and glycemic load values: 2008. References for supplemental Tables 1 and 2. Diabetes Care 2008;31:2281–3. [14] Foster-Powell K, Holt SH, Brand-Miller JC. International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr 2002;76:5–56. [15] Brand-Miller J, Atkinson F, Rowan A. Effect of added carbohydrates on glycemic and insulin responses to children’s milk products. Nutrients 2013;5:23–31. [16] Fabricatore AN, Ebbeling CB, Wadden TA, Ludwig DS. Continuous glucose monitoring to assess the ecologic validity of dietary glycemic index and glycemic load. Am J Clin Nutr 2011;94:1519–24. [17] Kochan AM, Wolever TM, Chetty VT, Anand SS, Gerstein HC, Sharma AM. Glycemic index predicts individual glucose responses after self-selected breakfasts in free-living, abdominally obese adults. J Nutr 2012;142:27–32. [18] Febbraio MA, Keenan J, Angus DJ, Campbell SE, Garnham AP. Preexercise carbohydrate ingestion, glucose kinetics, and muscle glycogen use: Effect of the glycemic index. J Appl Phys 2000;89:1845–51. [19] Mondazzi L, Arcelli E. Glycemic index in sport nutrition. J Am Coll Nutr 2009;28:455S–63S. [20] Papanikolaou Y, Palmer H, Binns MA, Jenkins DJ, Greenwood CE. Better cognitive performance following a low-glycaemic-index compared with a high-glycaemic-index carbohydrate meal in adults with type 2 diabetes. Diabetologia 2006;49:855–62. [21] Dodd H, Williams S, Brown R, Venn B. Calculating meal glycemic index by using measured and published food values compared with directly measured meal glycemic index. Am J Clin Nutr 2011;94:992–6.

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