Dietary Glycemic Index and Load and the Risk of Type 2 Diabetes: Assessment of Causal Relations.

Geoffrey Livesey, Richard Taylor, Helen F Livesey, Anette E Buyken, David J A Jenkins, Livia S A Augustin, John L Sievenpiper, Alan W Barclay, Simin Liu, Thomas M S Wolever, Walter C Willett, Furio Brighenti, Jordi Salas-Salvadó, Inger Björck, Salwa W Rizkalla, Gabriele Riccardi, Carlo La Vecchia, Antonio Ceriello, Antonia Trichopoulou, Andrea Poli, Arne Astrup, Cyril W C Kendall, Marie-Ann Ha, Sara Baer-Sinnott, Jennie C Brand-Miller

Journal: Nutrients 2020;11(6):1436

PMID: 31242690

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Plain Language Summary

It is generally accepted that certain diet and lifestyle choices contribute to a person’s risk of developing type 2 diabetes (T2D). In this meta-analysis, researchers set out to review previous studies and assess whether there is any evidence that the amount and type of carbohydrate (measured by Glycaemic Index (GI) and Glycaemic Load (GL)) in a person’s diet has a direct influence on their risk of developing T2D. The authors concluded with a high level of confidence that eating high GI and GL foods can lead to a higher risk of developing T2D. They suggest that nutrition advice that favours low GI and GL foods could produce significant cost savings for public healthcare.

Abstract

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.

Address: Independent Nutrition Logic Ltd, 21 Bellrope Lane, Wymondham NR180QX, UK. [email protected].; Independent Nutrition Logic Ltd, 21 Bellrope Lane, Wymondham NR180QX, UK. [email protected].; Independent Nutrition Logic Ltd, 21 Bellrope Lane, Wymondham NR180QX, UK. [email protected].; Institute of Nutrition, Consumption and Health, Faculty of Natural Sciences, Paderborn University, 33098 Paderborn, Germany. [email protected].; Departments of Nutritional Science and Medicine, Faculty of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada. [email protected].; Clinical Nutrition and Risk Factor Modification Centre, St. Michael's Hospital, Toronto, ON M5C 2T2, Canada. [email protected].; Division of Endocrinology and Metabolism, Department of Medicine, St. Michael's Hospital, Toronto, ON M5C 2T2, Canada. [email protected].; Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON M5C 2T2, Canada. [email protected].; Clinical Nutrition and Risk Factor Modification Centre, St. Michael's Hospital, Toronto, ON M5C 2T2, Canada. [email protected].; Epidemiology, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", 80131 Napoli, Italy. [email protected].; Departments of Nutritional Science and Medicine, Faculty of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada. [email protected].; Clinical Nutrition and Risk Factor Modification Centre, St. Michael's Hospital, Toronto, ON M5C 2T2, Canada. [email protected].; Division of Endocrinology and Metabolism, Department of Medicine, St. Michael's Hospital, Toronto, ON M5C 2T2, Canada. [email protected].; Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON M5C 2T2, Canada. [email protected].; Glycemic Index Foundation, 26 Arundel St, Glebe, Sydney NSW 2037, Australia. [email protected].; Department of Epidemiology and Medicine, Brown University, Providence, RI 02912, USA. [email protected].; Departments of Nutritional Science and Medicine, Faculty of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada. [email protected].; Clinical Nutrition and Risk Factor Modification Centre, St. Michael's Hospital, Toronto, ON M5C 2T2, Canada. [email protected].; Departments of Nutrition and Epidemiology, Harvard T. H. Chan School of Public Health and Harvard Medical School, Boston, MA 02115, USA. [email protected].; Department of Food and Drug, University of Parma, 43120 Parma, Italy. [email protected].; Human Nutrition Unit, Department of Biochemistry and Biotechnology, Faculty of Medicine and Health Sciences, Institut d'Investigació Sanitària Pere Virgili (IISPV), Rovira i Virgili University, 43201 Reus, Spain. [email protected].; Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, 27400 Madrid, Spain. [email protected].; Retired from Food for Health Science Centre, Antidiabetic Food Centre, Lund University, S-221 00 Lund, Sweden. [email protected].; Institute of Cardiometabolism and Nutrition, ICAN, Pitié Salpêtrière Hospital, F75013 Paris, France. [email protected].; Department of Clinical Medicine and Surgery, Federico II University, 80147 Naples, Italy. [email protected].; Department of Clinical Sciences and Community Health, Università degli Studi di Milano, 201330 Milan, Italy. [email protected].; IRCCS MultiMedica, Diabetes Department, Sesto San Giovanni, 20099 Milan, Italy. [email protected].; Hellenic Health Foundation, Alexandroupoleos 23, 11527 Athens, Greece. [email protected].; Nutrition Foundation of Italy, Viale Tunisia 38, I-20124 Milan, Italy. [email protected].; Department of Nutrition, Exercise and Sports (NEXS) Faculty of Science, University of Copenhagen, 2200 Copenhagen, Denmark. [email protected].; Departments of Nutritional Science and Medicine, Faculty of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada. [email protected].; Clinical Nutrition and Risk Factor Modification Centre, St. Michael's Hospital, Toronto, ON M5C 2T2, Canada. [email protected].; College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, SK S7N 5B5, Canada. [email protected].; Spinney Nutrition, Shirwell, Barnstaple, Devon EX31 4JR, UK. [email protected].; Oldways, Boston, MA 02116, USA. [email protected].; Charles Perkins Centre and School of Life and Environmental Sciences, University of Sydney, Sydney NSW 2006, Australia. [email protected].

DOI: 10.3390/nu11061436

Patient Centred Factor

Triggers: High GI or GL diet

Clinical Imbalances

Hormonal

Modifiable Lifestyle Factors

Diet

Nutrition Evidence Keywords

Diabetes Insulin resistance GI GL Type 2 diabetes Glycaemic index Hyperglycaemia Blood glucose Glycaemic load Dysglycaemia

Bioactive Substances

Glucose

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MeSH Terms: Animals, Biomarkers, Blood Glucose, Diabetes Mellitus, Type 2, Diet, Glycemic Index, Glycemic Load, Humans, Incidence, Prognosis, Risk Assessment, Risk Factors