Low-GI and/or low-GL diets are independently associated with a reduced risk of certain chronic diseases. In diabetes and heart disease, the protection is comparable with that seen for whole grain and high fiber intakes. The findings support the hypothesis that higher postprandial glycemia is a universal mechanism for disease progression.

Given the high prevalence of diabetes and pre-diabetes worldwide and the consistency of the scientific evidence reviewed, the expert panel confirmed an urgent need to communicate information on GI and GL to the general public and health professionals, through channels such as national dietary guidelines, food composition tables and food labels.

Published meta-analyses indicate significant but inconsistent incident type-2 diabetes (T2D)-dietary glycemic index (GI) and glycemic load (GL) risk ratios or risk relations (RR). It is now over a decade ago that a published meta-analysis used a predefined standard to identify valid studies. Considering valid studies only, and using random effects dose–response meta-analysis (DRM) while withdrawing spurious results (p < 0.05), we ascertained whether these relations would support nutrition guidance, specifically for an RR > 1.20 with a lower 95% confidence limit >1.10 across typical intakes (approximately 10th to 90th percentiles of population intakes). The combined T2D–GI RR was 1.27 (1.15–1.40) (p < 0.001, n = 10 studies) per 10 units GI, while that for the T2D–GL RR was 1.26 (1.15–1.37) (p < 0.001, n = 15) per 80 g/d GL in a 2000 kcal (8400 kJ) diet. The corresponding global DRM using restricted cubic splines were 1.87 (1.56–2.25) (p < 0.001, n = 10) and 1.89 (1.66–2.16) (p < 0.001, n = 15) from 47.6 to 76.1 units GI and 73 to 257 g/d GL in a 2000 kcal diet, respectively. In conclusion, among adults initially in good health, diets higher in GI or GL were robustly associated with incident T2D. Together with mechanistic and other data, this supports that consideration should be given to these dietary risk factors in nutrition advice. Concerning the public health relevance at the global level, our evidence indicates that GI and GL are substantial food markers predicting the development of T2D worldwide, for persons of European ancestry and of East Asian ancestry.

We propose that this method can be considered as a standardised approach for the estimation of added sugar content of foods to improve cross-study comparison.

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Background and Purpose-It is unclear whether diets with high glycemic index (GI) and low cereal fiber (CF) are associated with greater risk of stroke. We aimed to assess the relationship between dietary GI and CF content, retinal microvasculature changes, and stroke-related mortality. Methods-The study consisted of a population-based cohort, 49ϩ years, examined at baseline (1992 to 1994). At baseline, participants completed validated food frequency questionnaires. Mean GI was calculated using an Australian database.Retinal arteriolar and venular diameters were measured from photographs. Mortality data were derived using the Australian National Death Index. Results-Over 13 years, 95 of 2897 participants (3.5%) died from stroke. Increasing GI (hazard ratio, 1.91; 95% CI, 1.01 to 3.47, highest versus lowest tertile) and decreasing CF (hazard ratio, 2.13; 95% CI, 1.19 to 3.80, lowest versus highest tertile) predicted greater risk of stroke death adjusting for multiple stroke risk factors. Persons consuming food in the highest GI tertile and lowest CF tertile had a 5-fold increased risk of stroke death (hazard ratio, 5.06; 95% CI, 1.67 to 15.22). Increasing GI and decreasing CF were also associated with retinal venular caliber widening (P trend Ͻ0.01). Adjustment for retinal venular caliber attenuated stroke death risk associated with high GI by 50% but did not affect the risk associated with low CF consumption. Conclusions-High-GI and low-CF diets predict greater stroke mortality and wider retinal venular caliber. The association between a high-GI diet and stroke death was partly explained by GI effects on retinal venular caliber, suggesting that a high-GI diet may produce deleterious anatomic changes in the microvasculature.

While dietary factors are important modifiable risk factors for type 2 diabetes (T2D), the causal role of carbohydrate quality in nutrition remains controversial. Dietary glycemic index (GI) and glycemic load (GL) have been examined in relation to the risk of T2D in multiple prospective cohort studies. Previous meta-analyses indicate significant relations but consideration of causality has been minimal. Here, the results of our recent meta-analyses of prospective cohort studies of 4 to 26-y follow-up are interpreted in the context of the nine Bradford-Hill criteria for causality, that is: (1) Strength of Association, (2) Consistency, (3) Specificity, (4) Temporality, (5) Biological Gradient, (6) Plausibility, (7) Experimental evidence, (8) Analogy, and (9) Coherence. These criteria necessitated referral to a body of literature wider than prospective cohort studies alone, especially in criteria 6 to 9. In this analysis, all nine of the Hill’s criteria were met for GI and GL indicating that we can be confident of a role for GI and GL as causal factors contributing to incident T2D. In addition, neither dietary fiber nor cereal fiber nor wholegrain were found to be reliable or effective surrogate measures of GI or GL. Finally, our cost–benefit analysis suggests food and nutrition advice favors lower GI or GL and would produce significant potential cost savings in national healthcare budgets. The high confidence in causal associations for incident T2D is sufficient to consider inclusion of GI and GL in food and nutrient-based recommendations.

These data provide new epidemiologic evidence of a potentially important link between GI and inflammatory disease mortality among older women.