Glycemic Index or Glycemic Load: Time to Inform Consumers About the Glycemic Impact of Their Diets?

Fred Brouns, Cerestar-Cargill R&D Centre, Vilvoorde, Belgium and Dept of Human Biology, Nutrition & Toxicology Research Institute, Maastricht University, Maastricht, Netherlands.

The glycemic index (GI) of carbohydrates has been the subject of studies for more than 30 years. Originally the GI concept was introduced to classify different sources of carbohydrate (CHO) in the diet, such as potatoes, rice, cereals etc, according to their effect on postprandial glycemia. Usually a 50g carbohydrates test load was used, which traditionally referred to available carbohydrates providing sugars for absorption. As such, low GI carbohydrates were classified as those that are digested and absorbed slowly and lead to a low glycemic response, whereas high GI carbohydrates are rapidly digested and absorbed and show a high glycemic response.

In some circumstances a high glycemic response is favourable, e.g. for recovery after intense performance. In other circumstances a low GI may have favourable effects on metabolism. In addition, epidemiological data, based on prospective cohorts, suggest a link between GI of the daily diet and some metabolic disease states. Based on such data some health professionals believe that a low GI of the daily diet may help reduce the risks of developing such diseases. Others, however, disagree with this and feel that the total amount of carbohydrates consumed may be more important. Based on these beliefs it has been proposed that food ingestion related glycemic response data could be used by consumers to make priorities for food selection within certain food groups. This development has lead to the measurement of the glycemic responses of many types of carbohydrate rich foods as well as of specific carbohydrates sources in controlled laboratory conditions¹.

Recently however, there is an ongoing debate^2,3,4,5 on the accuracy of certain aspects of the method for the measurement of GI, mainly because of observations that the GI of a carbohydrate may change during pre-meal food preparation, such as an effect of ripening, by influence of other components of the food matrix when added to mixed meals or the gastrointestinal function of the consuming individual^6,4. Another debate concentrates around the idea that there are alternative and possibly less difficult ways of describing the glycemic impact of foods or drinks. Some examples of the latter are:

1. glycemic load^7,8, being the product of the amount of carbohydrate in the diet and its glycemic index.
2. glycemic glucose equivalent ^9,10, being the theoretical weight of glucose that would induce a glycemic response equivalent to that of the given amount of food and
3. the concept of GI_food vs GI_carb ¹⁰, being the glycemic response value of a specified portion of food or of a specified portion of total carbohydrate compared to a control.

Fundamental to these developments are the questions:

1. do health professionals support the contention that GI is of such importance that food authorities should be advised to adapt food labelling legislation in such a way that GI becomes part of the food information panel on the product packaging?, and
2. is labelling possible in a way that the consumer understands what it is all about? With respect to the first question there is considerable controversy among scientists.

Partly this is caused by confounding factors that surround many studies performed so far. First of all, epidemiological studies indicate a relationship between the consumption of rapidly absorbable, high glycemic carbohydrates and overweight and Type 2 diabetes. However, it should be noted that these are observational data that do not allow for conclusions to be drawn about a cause-result relationship. Similarly, there may be a perfect correlation between getting grey hair and developing osteoporosis but causality requires other data.

Another example is that a range of animal studies has shown that chronic consumption of fructose or sucrose induces insulin resistance and or weight gain. However, the picture from available human intervention studies is less clear, some showing a positive relationship, some no effect at all and some a negative relationship^11,12. Basic to the latter is also the fact that the GI of fructose is as low as 27 and the GI of sucrose is only 65. Thus, even if there would be such an effect, it would be caused by a low and moderate GI carbohydrate response. This does not make it easy to differentiate between effects of certain carbohydrates based on GI alone.

Another aspect is that in many studies in which the effect of consuming high glycemic diets has been compared to low glycemic diets, substantial differences in the composition of the test meals/diets, in order to induce glycemic differences, could only be realised by making changes in the “carbohydrate: fat: protein” ratio. Accordingly, such experimental changes are often paralleled by an increased fat and/or protein content or by a substitution of viscous dietary fibres for available carbohydrates. Such changes will not only impact on glycemic response but also on other indices of carbohydrate-fat metabolism, for example blood lipid values or fermentation in the colon leading to the production of short chain fatty acids that may influence insulin action and nutrient partitioning¹³.

Fundamental to the current debate about the value of GI is also the increased knowledge in the area of insulin insensitivity, insulin resistance and the development of Type 2 diabetes^14,15. Insights have changed considerably over time. Decades ago it was thought that regularly elevated blood glucose responses after the consumption of sugars was the cause of diabetes. Later this was changed and the early advice not to consume sugars was changed to “moderation of sugar consumption”. With regard to recommendations for people suffering from diabetes, international organisations have also made recommendations concerning the value of GI. The Canadian Diabetes Association advocates a focus on using GI as a useful tool to help manage glucose control, as does the European Association for the Study of Diabetes, Diabetes UK and Diabetes Australia. Yet the American Diabetes Association (ADA) has, based on the same set of available data, the opinion that GI is not useful3. Consensus is lacking! Yet, carefully designed studies show that children suffering from diabetes have significantly less episodes of hypoglycemia, sleep better and experience an overall improved quality of life when using GI information as a guideline for meal composition¹⁶, and a recent meta-analysis showed a clinically significant reduction in glycated haemoglobin, a cardiovascular risk factor related to persistent hyperglycemia¹⁷, when using low GI diets¹⁸. The ADA has made a recommendation to reduce the amount saturated fat in the diet, while increasing mono-unsaturated and poly-unsaturated fats and dietary fibre intake. This recommendation fits with an increased focus on a key role of fatty acids and fat related metabolites, rather than carbohydrates, in the development of insulin insensitivity and resistance^19,20,21,22. Moreover, the fact that overweight and obesity are so closely related to developing insulin resistance has lead to the understanding that having central adiposity in combination with insulin resistance results in a continuous flux of fatty acids into the circulation further promoting insulin resistance and finally causing Type 2 diabetes in the obese subject. Essential to the understanding of the role of overweight is also the observation that enlarged adipocytes change their production of inflammatory markers and adipocytokines^23,24,25, inducing chronic inflammation and changes in appetite/hunger perceptions. Losing weight generally results in rapidly improved insulin sensitivity and a reduction of inflammatory markers; much more rapidly than when the development of these took place.

Yet, the question of whether intentionally dieting to lose weight or the following of a low GI diet should be recommended to reduce morbidity and mortality in the overweight population has recently been challenged and resulted in both YES and NO opinions pointing to the fact that overweight and Type 2 diabetes are multi-factorial disease states that do not depend significantly on food intake and ^26,27,28,29. Illustrative of this aspect is a recent statement by Sievenpiper et al³⁰ “although insulin resistance affects carbohydrate metabolism, it is not a carbohydrate consumption disease”. Inherent to this statement is also the observation that healthy subjects can accurately regulate their glucose homeostasis despite very high intakes of high glycemic carbohydrates or fructose containing sugars. This is evident from carefully performed studies in children, adolescents³¹ as well as from elite endurance athletes who are known to be very lean and highly insulin sensitive but may ingest rapidly available carbohydrates in quantities of >15g/kg body weight /day during periods of intense competition^32,33. Thus, it seems that factors other than carbohydrates and their GIs are required to develop overweight and insulin resistance. The effects on indices of overweight and diabetes of a chronic imbalance between daily energy intake and energy expenditure needs to be addressed ^thoroughly34. Striking in this respect is the title from a recent publication “Too much Sugar, too much carbohydrate or just too much?”³⁵. There is a clear need for long term intervention studies in humans with an experimental set-up that allows in one respect the avoidance of body weight changes by dietary interventions, while studying the effect of diets with differing levels of GI on insulin action. To do this properly, diets should be similar in macronutrient and fibre content and should also be similar in the supply of saturated, mono-unsaturated and polyunsaturated fatty acids. Apart from this, the effect of such interventions on bodyweight change itself should be addressed as well, both with ad libitum food intake allowing for effects of satiety³⁶ and with standardised eucaloric meals.

In this regard the use of alternative ways of expressing glycemic impact of foods and drinks such as glycemic load or GGE for informing consumers and food labelling is awaiting foundation. At present most promising seems to be a combination of lifestyle counselling leading to regular exercise, a high fibre intake and a low fat intake. Such an approach has shown to reduce overall glycemic load of the diet as well as diabetes risk factors by more than 40%^37,38 and may also significantly reduce the chance to become overweight³⁴. Based on the currently available data it may be concluded that:

1. GI may be a useful tool for the study of the effects of specific glucose supplying carbohydrate sources on metabolism.
2. GI should not be used in isolation⁶.
3. Overall glycemic load of the diet may be more relevant that GI itself.
4. Recommendation for use of GI to inform consumers requires solid data as well as international consensus on its value. Especially the latter which has not been obtained at present.

Currently working on this are international working groups of ILSI Europe, ILSI North America as well research Consortia supported by EU governmental grants.

Article reviewed by Prof Wim Saris (Maastricht Univ) and Prof Robbert Jan Brummer (Wageningen University)

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BIOGRAPHY

Dr Brouns obtained a PhD in Nutritional Physiology at the Maatricht University in the Netherlands on the Topic “Food and Fluid related aspects in Highly trained athletes” with a special focus on macronutrient metabolism. For this work he was awarded the Netherlands Sports Medicine Award. He achieved fellowships of the American College of Sports Medicine and the European College of Sports Sciences. He is an active member of the UK Nutrition Society and is world wide speaker in the field of Life Sciences and Nutrition. He has published extensively, both scientifically and in popular journals. In 1999 he joined the Health & Nutrition Group of Eridania Beghin Say and currently the Cerestar-Cargill Research & Development Center, Vilvoorde, Belgium as Research fellow and Manager Nutritional Sciences Europe. He has a guest research position at the Nutrition and Toxicology Research Institute, Dept of Human Biology, Maastricht University, The Netherlands.