Reliable tables of glycemic indexes (GIs) and glycemic loads (GLs) are critical to research examining the relationship between glycemic qualities of carbohydrate in foods, diets, and health. In the 12 years since the last edition of the tables, a large amount of new data has become available. To systematically review and tabulate published and unpublished sources of reliable GI values, including an assessment of the reliability of the data. This edition of the tables lists over 4000 items, a 61% increase in the number of entries compared to the 2008 edition. The data have been separated into 2 lists. The first represents more precise values derived using the methodology recommended by the International Standards Organization (∼2100 items). The second list contains values determined using less robust methods, including using limited numbers of healthy subjects or with a large SEM (∼1900 food items). Dairy products, legumes, pasta, and fruits were usually low-GI foods (≤55 on the 100-point glucose scale) and had consistent values around the world. Cereals and cereal products, however, including whole-grain or whole-meal versions, showed wide variation in GI values, presumably arising from variations in manufacturing methods. Breads, breakfast cereals, rice, savory snack products, and regional foods were available in high-, medium-, and low-GI versions. Most varieties of potato were high-GI foods, but specific low-GI varieties have now been identified. The availability of new data on the GIs of foods will facilitate wider research and application of the twin concepts of GI and GL. Although the 2021 edition of the tables improves the quality and quantity of GI data available for research and clinical practice, GI testing of regional foods remains a priority. This systematic review was registered in PROSPERO as #171204.

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.

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.

It has been postulated that dietary sugar consumption contributes to increased inflammatory processes in humans, and that this may be specific to fructose (alone, in sucrose or in high-fructose corn syrup (HFCS)). Therefore, we conducted a meta-analysis and systematic literature review to evaluate the relevance of fructose, sucrose, HFCS, and glucose consumption for systemic levels of biomarkers of subclinical inflammation. MEDLINE, EMBASE, and Cochrane libraries were searched for controlled intervention studies that report the effects of dietary sugar intake on (hs)CRP, IL-6, IL-18, IL-1RA, TNF-α, MCP-1, sICAM-1, sE-selectin, or adiponectin. Included studies were conducted on adults or adolescents with ≥20 participants and ≥2 weeks duration. Thirteen studies investigating 1141 participants were included in the meta-analysis. Sufficient studies (≥3) to pool were only available for (hs)CRP. Using a random effects model, pooled effects of the interventions (investigated as mean difference (MD)) revealed no differences in (hs)CRP between fructose intervention and glucose control groups (MD: −0.03 mg/L (95% CI: −0.52, 0.46), I² = 44%). Similarly, no differences were observed between HFCS and sucrose interventions (MD: 0.21 mg/L (−0.11, 0.53), I² = 0%). The quality of evidence was evaluated using Nutrigrade, and was rated low for these two comparisons. The limited evidence available to date does not support the hypothesis that dietary fructose, as found alone or in HFCS, contributes more to subclinical inflammation than other dietary sugars.

Dietary fibre is a generic term describing non-absorbed plant carbohydrates and small amounts of associated non-carbohydrate components. The main contributors of fibre to the diet are the cell walls of plant tissues, which are supramolecular polymer networks containing variable proportions of cellulose, hemicelluloses, pectic substances, and non-carbohydrate components, such as lignin. Other contributors of fibre are the intracellular storage oligosaccharides, such as fructans. A distinction needs to be made between intrinsic sources of dietary fibre and purified forms of fibre, given that the three-dimensional matrix of the plant cell wall confers benefits beyond fibre isolates. Movement through the digestive tract modifies the cell wall structure and may affect the interactions with the colonic microbes (e.g., small intestinally non-absorbed carbohydrates are broken down by bacteria to short-chain fatty acids, absorbed by colonocytes). These aspects, combined with the fibre associated components (e.g., micronutrients, polyphenols, phytosterols, and phytoestrogens), may contribute to the health outcomes seen with the consumption of dietary fibre. Therefore, where possible, processing should minimise the degradation of the plant cell wall structures to preserve some of its benefits. Food labelling should include dietary fibre values and distinguish between intrinsic and added fibre. Labelling may also help achieve the recommended intake of 14 g/1000 kcal/day.