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Food insulin index: Physiologic basis for predicting insulin demand evoked by
composite meals
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5 authors, including:
Jennie C Brand-Miller
The University of Sydney
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986 Am J Clin Nutr 2009;90:986–92. Printed in USA. Ó 2009 American Society for Nutrition
FOOD INSULIN INDEX 987
SUBJECTS AND METHODS low-fat meal the night before a test. On the test morning, subjects
reported to the laboratory after a 10–12-h fast. After warming the
Subjects hand in hot water, 2 baseline finger blood samples (’0.7 mL · 2)
Healthy subjects (n = 21, including 13 men), with a mean were obtained 5 min apart. Each meal was then consumed with
(6SD) age of 24 6 2.5 y and body mass index (BMI; in kg/m2) 250 mL water at a comfortable pace within 14 min. Additional
of 22.8 6 1.5, were recruited from the student population of the blood samples were taken 15, 30, 45, 60, 90, and 120 min after the
University of Sydney. All met the inclusion criteria: non- commencement of eating. Subjects remained seated throughout
smoking, aged 18–40 y, stable body weight, BMI of 19–25, and were not permitted to eat or drink until the end of session.
normal glucose tolerance, no prescription medication other than Blood samples were collected in anticoagulant-coated tubes
oral contraceptives, no known food allergy, regular physical (Eppendorf tubes, grade II; Sigma Chemical Company, Castle
activity, normal dietary habits, and no history of eating disorders. Hill, Australia) containing 10 IU heparin sodium salt and
The protocol was approved by the Human Research Ethics centrifuged immediately (1 min at 10,000 · g at room temper-
Committee of the University of Sydney, and subjects gave written ature). The plasma layer was pipetted into a labeled tube and
informed consent. Subject recruitment took place in 2 stages: stored at 220°C until analysis. Plasma insulin was measured by
from July to October 2005 and from July to October 2006. antibody-coated tube radioimmunoassay (Diagnostic Products
Corporation, Los Angeles, CA). The within- and between-assay
CVs were 3.0% and 3.5%, respectively. All samples in one
Test meals group study were analyzed within the same run.
In total, 13 isoenergetic mixed meals were tested in 2000-kJ
portions. Because of the large number of meals, 6 meals were Data analysis
g kJ % g g g g
White bread2 193 2000 100 19.4 4.8 3.8 93.4 70 65 100
Group 1 meals
Breakfast meals
M1
Grain bread3 77.7 786 39.3 12.0 5.4 4.2 23.2 36 — 71
Peanut butter4 25.0 668 33.4 5.8 13.4 2.9 4.4 14 — 15
Full-fat milk5 200 546 27.3 6.8 7.2 0.0 9.6 31 — 33
Total meal 302.7 2000 100 24.6 26.0 7.1 37.2 32 12 42
M2
Honeydew melon 100 140 7 0.7 0.3 1.0 6.5 62 — 127
Banana 98 353 17.7 1.7 0.1 2.2 19.6 52 — 81
Yogurt6 300 1167 58.3 15.9 2.7 0.0 44.1 31 — 115
Apple juice7 200 340 17 0.2 0.0 0.0 20.2 39 — 64
Total meal 698 2000 100 18.5 3.1 3.2 90.4 40 36 101
Snacks
M3
Walnuts8 44 1276 63.8 7.2 29.6 4.0 1.6 N/A9 — 7
Portion of
Food categories Serving size Energy energy Protein Fat Fiber AvCHO GI GL FII
g kJ % g g g g
Lunch meals
M11
Pizza21 90 1000 50 12.4 7.6 0.0 30.2 60 — 64
Coca-Cola22 583 1000 50 0.0 0.0 0.0 61.8 53 — 60
Total meal 673 2000 100 12.5 7.6 0.0 92.0 55 51 62
Dinner meals
M12
Pasta23 201 1000 50 7.8 8.0 3.5 45.6 44 — 40
Lentils24 253 1000 50 19.4 4.6 11.4 17.7 37 — 58
Total meal 454 2000 100 27.2 12.6 14.9 63.3 42 27 49
M13
Beef steak 158 1000 50 42.0 7.7 0.0 0.0 N/A — 51
Boiled potatoes25 368 1000 50 10.0 1.0 9.2 39.8 77 — 121
Total meal 526 2000 100 52.0 8.7 9.2 39.8 77 31 86
1
Glycemic index (GI) and GL values of the mixed meals were calculated with the use of GIs of individual food components and available carbohydrate
content. The FII value of each test meal in this table represented the predicted insulin response relative to white bread, which was calculated by the formula
a novel classification based on ranking the insulin responses to disease (15, 16). A system of ranking of foods based on relative
individual foods (ie, the FII). Surprisingly, in the current context, insulin demand could also have application in the clinical
carbohydrate, fiber, and protein content were found to be rela- management of diabetes.
tively poor predictors of the overall insulin response, whereas GL The present study has both strengths and limitations. The
(the product of the available carbohydrate content and the GI of mixed meals were designed to represent typical Western diets,
the component foods) and fat content were significant predictors, and we selected component foods with a wide range of FIIs with
although less so than the FII. The findings suggest that if the the expectation that the range of insulin responses among the
database were sufficiently large, the FII classification could mixed meals would also be high. Although the predicted insulin
provide a more accurate alternative to carbohydrate content for demand varied over a 5-fold range (from 22 to 101), actual insulin
estimating insulin demand of different meals and diets. This responses ranged only 3-fold (from 35 to 116). The meal with the
classification may be useful in nutritional epidemiology because lowest predicted demand (M3: a snack of walnuts, raisins, and
diets associated with high-insulin demand have been hypothe- carrot juice) produced a somewhat higher than expected insulin
sized to increase the risk of diabetes, obesity, and cardiovascular response, although nonetheless the lowest of all 13 meals.
990 BAO ET AL
Similarly, the meal with the highest predicted demand (M2: subjects can be managed sufficiently to be able to show true
a breakfast of honeydew melon, banana, and yogurt) produced differences among foods and meals in their capacity to stimulate
a response a little higher than expected, but the highest response insulin secretion. However, our choice of subjects may also be
in practice. Our study also shows that some meals with widely a significant limitation because any ranking of foods according
disparate carbohydrate content had similar insulin responses to insulin demand in lean, young healthy subjects may not be
(both observed and predicted). For example, M12 and M1 had directly applicable to the diabetic population or the general
comparable FIIs (observed 45 and 44, predicted 49 and 42, re- population. Worsening insulin resistance in overweight subjects
spectively), yet their carbohydrate content varied markedly (63 and impairment in b cell function in diabetic individuals will
and 37 g, respectively). If carbohydrate counting was used to reduce the capacity to respond appropriately to everyday meals
predict the bolus insulin dose in type 1 diabetes, then the dose for and therefore reduce the range of responses seen. Nonetheless,
these meals would vary accordingly. In contrast, the FII suggests our findings could be applicable in the early stages of de-
the meals generate the same insulin demand. Nonetheless, the velopment of disease when b cell function is adequate.
study’s limitations should also be noted: the small number of Currently, carbohydrate counting is commonly recommended
meals, some with contrived portion sizes and relatively low fiber for matching insulin dosage to insulin demand in individuals with
content. The statistical power is therefore low, and it would not be type 1 diabetes, although the emphasis on carbohydrate counting
appropriate to dismiss available carbohydrates and fiber as related varies between clinics, and many dietitians consider that it is too
to insulin response. simplistic. In the present study, mixed meals with similar car-
The advantage of a classification system in which a reference bohydrate content produced widely disparate insulin responses.
food is used is that data can be derived from testing different For example, meal M13 (beef steak and potatoes) with ’40 g
groups of people. In the present study, the 2 groups of subjects carbohydrate produced twice the insulin response of meal M1
clearly show differences in insulin secretion, the first group (grain bread, peanut butter, and milk) despite a similar amount
showing an average insulin response to white bread which is of carbohydrate (’37 g). Although the addition of protein or fat
approximately half that of the second group (mean 6 SEM AUC: to a carbohydrate-rich meal is known to evoke additional or
14,350 6 2260 compared with 30,700 6 3100 pmol · min/L, synergistic insulin secretion and to contribute to the reduction in
respectively). However, this large between-subject variation was glycemia (8, 17, 18), these variables are often not considered in
diminished when the subjects’ individual responses were in- the day-to-day management of diabetes. Because the FII clas-
dexed to a reference food. Moreover, testing the reference food sification allows all the factors influencing insulin demand to be
twice reduces the effect of day-to-day variability within in- integrated into a single result, it may be an attractive component
dividuals. Hence, these sources of variation within and between in the very complex treatment of type 1 diabetes.
FOOD INSULIN INDEX 991
Interestingly, in the present study, the fat content of the mixed database currently has 120 single foods, including the most
meal showed a significant inverse relation (r = 20.60) with common sources of energy in Western diets (12) (J Bao, F
observed insulin responses and was a more reliable predictor of Atkinson, JC Brand-Miller, unpublished data, 2007), further ex-
insulin demand than the amount of carbohydrate. This finding pansion is required. Dose-response and day-long investigations
is consistent with our previous study of 38 single foods (12). extending from breakfast to the evening meal are needed. To
The explanation may be the reciprocal relation between fat and confirm the food rankings in a broader population, studies in
the sum of the other 2 macronutrients, protein and carbohy- overweight and obese subjects and in individuals with impaired
drate. Although carbohydrate is the primary stimulus for in- glucose tolerance and impaired insulin secretion, including type 2
sulin secretion, insulinotropic amino acids and bioactive diabetes, should be undertaken. Although it is possible that
peptides are also potent stimulators of insulin release (11, 19, worsening defects in insulin secretion may obviate the ability to
20). Because protein stimulates insulin secretion, particularly detect differences among foods, the concept itself may still be
when combined with carbohydrate (8, 20), the meals with the relevant in the management of those conditions.
highest protein and carbohydrate content (and hence lowest fat In summary, the relative insulin demand evoked by mixed
content) produce the highest insulin responses. meals consumed by lean young healthy subjects is best predicted
Further research is needed to validate the FII concept and to by a physiologic index based on integrating insulin responses to
show its usefulness. The ability of FII to predict the diet-disease isoenergetic portions of single foods. In the context of composite
relation in epidemiologic research vis-á-vis other nutrients, GI, meals of similar energy value but varying macronutrient content,
and GL will be a major test of its usefulness. Although the carbohydrate counting had limited value.
992 BAO ET AL
The authors’ responsibilities were as follows—JCB-M: conceived the study versus measured carbohydrate exchange diets on glycemic control in
and interpreted the data; JB and VdJ: conducted the study, prepared the meals, children with type 1 diabetes. Diabetes Care 2001;24:1137–43.
and collected the data; JB and JCB-M: wrote the manuscript; FA: designed the 8. Gannon MC, Nuttall FQ, Neil BJ, Westphal SA. The insulin and glucose
experiment, adjusted the composition of the meals, and assisted with the writ- responses to meals of glucose plus various proteins in type II diabetic
subjects. Metabolism 1988;37:1081–8.
ing of the manuscript; and JCB-M, JB, and PP: analyzed the data.
9. Gannon MC, Nuttall FQ, Westphal SA, Seaquist ER. The effect of fat
JCB-M is a co-author of The New Glucose Revolution book series (Hodder
and carbohydrate on plasma glucose, insulin, C-peptide, and triglyc-
and Stoughton, London; Marlowe and Co, New York; Hodder Headline, erides in normal male subjects. J Am Coll Nutr 1993;12:36–41.
Sydney and elsewhere) and director of a nonprofit, glycemic index (GI)– 10. Collier GR, Greenberg GR, Wolever TM, Jenkins DJ. The acute effect of
based, food endorsement program in Australia. JCB-M and FA manage the fat on insulin secretion. J Clin Endocrinol Metab 1988;66:323–6.
University of Sydney GI testing service. None of the other authors had 11. Frid AH, Nilsson M, Holst JJ, Bjorck IME. Effect of whey on blood
a conflict of interest. glucose and insulin responses to composite breakfast and lunch meals in
type 2 diabetic subjects. Am J Clin Nutr 2005;82:69–75.
12. Holt SH, Brand-Miller JC, Petocz P. An insulin index of foods: the in-
sulin demand generated by 1000-kJ portions of common foods. Am J
REFERENCES Clin Nutr 1997;66:1264–76.
1. Porte D Jr. Clinical importance of insulin secretion and its interaction 13. Foster-Powell K, Holt SHA, Brand-Miller JC. International table of
with insulin resistance in the treatment of type 2 diabetes mellitus and its glycemic index and glycemic load values: 2002. Am J Clin Nutr 2002;
complications. Diabetes Metab Res Rev 2001;17:181–8. 76:5–56.
2. Garg A, Bantle JP, Henry RR, et al. Effects of varying carbohydrate 14. Wolever TM, Jenkins DJ, Jenkins AL, Josse RG. The glycemic index:
content of diet in patients with non-insulin-dependent diabetes mellitus. methodology and clinical implications. Am J Clin Nutr 1991;54:846–54.
JAMA 1994;271:1421–8. 15. Liu S, Willett WC, Stampfer MJ, et al. A prospective study of dietary
3. Barclay AW, Petocz P, McMillan-Price J, et al. Glycemic index, gly- glycemic load, carbohydrate intake, and risk of coronary heart disease in
cemic load, and chronic disease risk a meta-analysis of observational US women. Am J Clin Nutr 2000;71:1455–61.
studies. Am J Clin Nutr 2008;87:627–37. 16. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett