title: The metabolic syndrome in relation with the glycemic index and the glycemic load.
abstract: The metabolic syndrome (MS) is a clustering of metabolic abnormalities that increases the risk to develop chronic diseases such as cardiovascular disease and type 2 diabetes mellitus. Although its precise aetiology is unknown, dietary habits play a major role. Nowadays, more and more attention is paid to the glycemic index (GI) and the glycemic load (GL) of a diet. The GI of a food is a value based on the average increase in blood glucose levels occurring when a 50 g carbohydrate portion of that food is consumed. The GL accounts for the amount of carbohydrate per serving. From reviewing the current literature, we conclude that for healthy and/or overweight subjects the importance of low GI or GL diets in relation to the metabolic syndrome has not been established. One of the reasons is that the diets used in the intervention studies frequently not only differed in GI or GL, but also in fibre, protein and/or fat content. In some of the prospective cohort studies, effects of GI or GL attenuated or even disappeared after correcting for fibre intake. This makes it impossible to ascribe the possible beneficial metabolic effects of low GI or GL diets unequivocally to the GI or GL. The question, therefore, remains open on to what components of the metabolic syndrome are specifically affected by the GI per se. To answer this question, controlled longer-term intervention studies are needed to monitor the effects of the GI on the various components of the metabolic syndrome.
authors.affiliation: Top Institute Food and Nutrition, 6700 AN Wageningen, The Netherlands.
authors.forename: R
authors.initials: R
authors.lastname: Vrolix
authors.forename: L E C
authors.initials: LE
authors.lastname: van Meijl
authors.forename: R P
authors.initials: RP
authors.lastname: Mensink
mesh_terms: D000818:Animals; D038321:Glycemic Index / Q000502:physiology*; D006801:Humans; D024821:Metabolic Syndrome / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology / Q000378:metabolism* / Q000628:therapy