The Glycemic Index

I t is essential that clinicians be aware of expected outcomes from possible nutrition therapy interventions so that they can assist people with diabetes using the best approaches to achieve metabolic goals. Outcomes can be predicted from evidence-based technical reviews or from meta-analyses. Both are now available: the American Diabetes Association (ADA) 2002, Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications, technical review (1) and position statement (2), and in this issue of Diabetes Care, Brand-Miller et al. (3) report on a performed meta-analysis of low–glycemic index (GI) diets. The ADA technical review and position statement reviewed the role of the GI in medical nutrition therapy for diabetes. The reports acknowledge that differing food sources of carbohydrates have differing glycemic responses when the food is studied independently, in 50-g portions, and compared with 50 g of either glucose or bread (1). However, after reviewing the evidence, it was concluded that the total amount of available carbohydrate in meals or snacks is more important than the source (starch or sugar) or type (low or high GI) (A-level evidence), and although low-GI foods may reduce postprandial hyperglycemia, there was not sufficient evidence to recommend use of low-GI diets as a primary strategy in food/ meal planning (B-level evidence) (2). These statements were based on a review of over 20 studies in which subjects with type 1 or type 2 diabetes ingested a variety of starches or sucrose, both acutely and for up to 6 weeks, with no significant differences in glycemic response if the amount of carbohydrate was similar. This recommendation was questioned in a letter to Diabetes Care by Irwin (4) with a reply to the letter by Franz and Bantle (5). In the reply to Irwin, it was noted that in subjects with type 1 diabetes, four studies compared a lowto a high-GI diet with none reporting statistically significant improvements in HbA1c from the low-GI diet; three reported significant improvements in fructosamine, one did not, and none reported improvements in fasting plasma glucose. Two studies included in the Brand-Miller meta-analysis were not included in the reply to Irwin. In the Gilbertson et al. (6) study, although the children in the low-GI group did have significantly better HbA1c levels than the group using a carbohydrate exchange diet, the study reported no differences in mean GI between the two groups at study end, and the authors stated, “it is difficult to attribute the lower HbA1c levels solely to differences in diet, particularly when there was no apparent difference in mean GI.” Also not included was the study by Giacco et al. (7), in which the low-GI diet contained 50 g/day of fiber compared with 15 g/day in the high-GI diet. It cannot accurately be determined whether the better glycemic outcome was related to the high fiber content or the low-GI diet because dietary fiber content is not consistently related to the GI. The authors stated, “the results obtained can be ascribed only to the different consumption of high fiber foods.” In subjects with type 2 diabetes, nine studies compared a lowto a high-GI diet. One reported a statistically significant improvement of HbA1c, four did not, and three reported statistically significant improvement in fructosamine, while three did not; none reported improvements in fasting plasma glucose. Included in the reply to Irwin was the Heilbronn et al. (8) study (not included in the Brand-Miller et al. meta-analysis) in which there were no significant differences in glycemic control or weight loss between lowand high-GI diets. Brand-Miller also includes the study by Komindr et al. (9) in which ingestion of mungbean noodles (a low-GI diet) produced a nonsignificant lower glycated hemoglobin compared with glutinous rice (a high-GI diet). Based on the above reviews, the ADA position is that there is not strong supporting evidence for the use of a low-GI diet as a primary nutrition therapy strategy. The meta-analysis by Brand-Miller et al. provides support for this recommendation. They report that implementing a low-GI diet will have a small effect on overall glycemic control in diabetes; low-GI diets reduce overall HbA1c by 0.43% units compared with high-GI diets (representing a 7.4% reduction in HbA1c/fructosamine). In patients with type 1 diabetes, HbA1c was reduced by 0.4% units and in subjects with type 2 diabetes by 0.2% units. This latter result is surprising, as one would expect a greater response in subjects with type 2 diabetes who, because of loss of first-phase insulin response, might be expected to benefit more from a low-GI diet than subjects with type 1 diabetes in whom mealtime insulin can be adjusted to control postprandial glycemic responses. Actual GI of the usual diet is also controversial. Brand-Miller suggests that the high-GI diet (83) in their meta-analysis represents usual GI. However, the GI quintiles for women in the Nurses’ Health Study and for men in the Health Professionals’ study range from 64 to 77 and 65 to 79, respectively (10). The highest number would be less than the high GI (83), and the lower number would be similar to the low GI (65). This is also a relatively small range, suggesting that it may be difficult to move the GI down a few units in individuals with diabetes. In their article, Brand-Miller et al. compare the low-GI diet’s effect to that of the effect of pharmacological agents that also target postprandial hyperglycemia. However, it may be more appropriate to compare the outcomes of the low-GI diet to the outcomes from other nutrition interventions. Doing this allows clinicians to select an approach that is likely to result in the most beneficial outcomes for the individual with diabetes. Therefore, the question becomes, what primary nutrition therapy interventions lead to better outcomes? E D I T O R I A L ( S E E B R A N D M I L L E R E T A L . , P . 2 2 6 1 )