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The dietary glycemic index concept supports a role for the rate of carbohydrate digestion in the prevention and treatment of chronic disease, including those diseases which have been highlighted in the dietary fiber and insulin-resistance syndrome hypotheses. This concept should not be seen as particularly radical at a time when pharmacological approaches to slowing absorption, notably the a-glycoside hydrolase inhibitors, are now accepted in the management of diabetes. Further longer term efficacy studies as well as effectiveness studies are required to better determine the importance of the glycemic index in the regulation of blood glucose and the prevention of diabetic complications, particularly in relations to CHD risk factors. The possible role of the glycemic index in decreasing postprandial oxidative stress and pro-inflammatory processes also merits further investigation.

References

1 Jenkins DJ, Leeds AR, Gassull MA, et al: Decrease in postprandial insulin and glucose concentrations by guar and pectin. Ann Intern Med 1977;86:20-23.

2 Crapo PA, Reaven G, Olefsky J: Plasma glucose and insulin response to orally administered simple and complex carbohydrates. Diabetes 1976;25:741-747.

3 Jenkins DJ, Wolever TM, Taylor RH, et al: Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981;34:362-366.

4 Wolever TM, Bolognesi C: Source and amount of carbohydrate affect postprandial glucose and insulin in normal subjects. J Nutr 1996;126:2798-2806.

5 Jenkins DJ, Ghafari H, Wolever TM, et al: Relationship between rate of digestion of foods and post-prandial glycaemia. Diabetologia 1982;22:450-455.

6 Thorne MJ, Thompson LU, Jenkins DJ: Factors affecting starch digestibility and the glycemic response with special reference to legumes. Am J Clin Nutr 1983;38:481-488.

7 Thorburn AW, Brand JC, Truswell AS: Slowly digested and absorbed carbohydrate in traditional bushfoods: a protective factor against diabetes? Am J Clin Nutr 1987;45:98-106.

8 Coulston, AM, Hollenbeck CB, Swislocki Al, Reaven GM: Effect of source of dietary carbohydrate on plasma glucose and insulin responses to mixed meals in subjects with NIDDM. Diabetes Care 1987;10:395-400.

9 Wolever TM, Nuttall FQ, Lee R, et al: Prediction of the relative blood glucose response of mixed meals using the white bread glycemic index. Diabetes Care 1985;8:418-428.

10 Wolever TM, Bolognesi C: Prediction of glucose and insulin responses of normal subjects after consuming mixed meals varying in energy, protein, fat, carbohydrate and glycemic index. J Nutr 1996;126:2807-2812.

11 Coulston AM, Reaven GM: Much ado about (almost) nothing. Diabetes Care 1997;20:241-243.

12 Jenkins DJ, Wolever TM, Ocana AM, et al: Metabolic effects of reducing rate of glucose ingestion by single bolus versus continuous sipping. Diabetes 1990;39:775-781.

13 Jenkins DJ, Wolever TM, Taylor RH, et al: Slow release dietary carbohydrate improves second meal tolerance. Am J Clin Nutr 1982;35:1339-1346.

14 Jenkins DJ, Wolever TM, Vuksan V, et al: Nibbling versus gorging: metabolic advantages of increased meal frequency. N Engl J Med 1989;321:929-934.

15 Jenkins DJ, Jenkins AL, Augustin LS, Kendall CW: Dietary therapy in type 2 diabetes mellitus: spreading the nutrient load; in LeRoith D, Taylor SI, Olefsky JM (eds): Diabetes Mellitus: A Fundatmental and Clinical Text, ed 3. Philadelphia, Lippincott Williams & Wilkins, 2004, pp 1085-1097.

16 Brand-Miller J, Hayne S, Petocz P, Colagiuri S: Low-glycemic index diets in the management of diabetes: a meta-analysis of randomized controlled trials. Diabetes Care 2003;26: 2261-2267.

17 Chiasson JL, Josse RG, Hunt JA, et al: Efficacy of acarbose in the treatment of patients with non-insulin-dependent diabetes mellitus. A multicenter controlled clinical trial. Ann Intern Med 1994;121:928-935.

18 Rodger NW, Chiasson JL, Josse RG, et al: Clinical experience with acarbose: results of a Canadian multicentre study. Clin Invest Med 1995;18:318-324.

19 Holman RR, Cull CA, Turner RC: A randomized double-blind trial of acarbose in type 2 diabetes shows improved glycemic control over 3 years (UK Prospective Diabetes Study 44). Diabetes Care 1999;22:960-964.

20 Chiasson JL, Josse RG, Gomis R, et al: Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial. Lancet 2002;359:2072-2077.

21 Augustin LS, Franceschi S, Jenkins DJ, et al: Glycemic index in chronic disease: a review. Eur J Clin Nutr 2003;56:1049-1071.

22 Frost G, Leeds AA, Doré CJ, et al: Glycaemic index as a determinant of serum HDL-cholesterol concentration. Lancet 1999;353:1045-1048.

23 Salmeron J, Manson JE, Stampfer MJ, et al: Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA 1997;277:472-477.

24 Knowler WC, Barrett-Connor E, Fowler SE, et al: Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393-403.

25 Hu FB, Manson JE, Stampfer MJ, et al: Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med 2001;345:790-797.

26 Tuomilehto J, Lindstrom J, Eriksson JG, et al: Prevention of type 2 diabetes meatus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 2001;344:1343-1350.

27 The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin treated diabetes mellitus. The Diabetes Control and Complications Trial Research Group. N Engl J Med 1993;329:977-986.

28 Franz MJ, Horton ES, Bantle JP, et al: Nutrition principles for the management of diabetes and related complications. Diabetes Care 1994;17:490-518.

29 Sheard NF, Clark NG, Brand-Miller JC, et al: Dietary carbohydrate (amount and type) in the prevention and management of diabetes: a statement by the American Diabetes Association. Diabetes Care 2004;27:2266-2271.

30 Ceriello A, Bortolotti N, Motz E, et al: Meal-generated oxidative stress in type 2 diabetic patients. Diabetes Care 1998;21:1529-1533.

Discussion

Dr. Knowler: You started your talk by showing the effects of frequent small meals compared to larger meals in saying that the glycemic index (GI) concept evolved from this. Doesn't that suggest that it might be just as easy to change meal frequency to frequent small meals rather than focusing on the GI for food? Might the same thing be accomplish more easily?

Dr. Kendall: I think that this could be a viable approach to try to decrease the postprandial rise in blood glucose. So you can sip your drinks or eat a number of small meals a day and that would be an effective strategy but obviously you want to have a healthy diet if you are doing this. We want to give people as many choices as possible. However, trying to get people to eat 3 meals a day is pretty tough, so trying to get them to eat 17 meals a day would probably be a bit tougher.

Dr. Mooradian: You started out defining the GI as essentially derived from the area under the curve of a test carbohydrate against a reference carbohydrate such as white bread or glucose, but you ended up focusing your discussion on the kinetics of glucose absorption and low GI of slowly absorbed food. How would this slow absorption change the area under the curve?

Dr. Kendall: When carbohydrate is slowly absorbed then the glucose rise is not going to be as large, the insulin will be secreted and will clear the glucose from the blood as well. Again it is the very high glucose peaks which appear to be most damaging. This is when the oxidative reactions are occurring.

Dr. Mooradian: Are you assuming that if the influx of glucose is slower then insulin will be more effective?

Dr. Kendall: The glucose peak just won't be the same and the level of insulin secretion won't be the same either. I think that was demonstrated in the slide shown where glucose was given either as a bolus or sipped throughout the day. Not only was the peak glucose reduced, peak insulin was reduced and serum C peptide was also reduced, as was C peptide excretion [1].

Dr. Mooradian: That is not a fair comparison. It is a quantitative effect; if you are taking less carbohydrate you are going to have less glucose.

Dr. Kendall: In that study the same amount of carbohydrate was provided, that was the point. So if the same amount of carbohydrate is given as a bolus or sipped throughout the day, the latter induces less insulin secretion [1].

Dr. Katsilambros: We know that acarbose also delays carbohydrate absorption. Do you know of any study comparing high GI with low acarbose versus low GI with placebo, or no acarbose?

Dr. Kendall: It would be nice to do the low acarbose plus low GI study. I don't believe it has been compared, at least not that I am aware of. But again if you reduce the rate of glucose absorption with acarbose, you get a similar effect that hopefully is achieved with a low GI diet.

Dr. Schiffrin: How do you assess the oxidative reaction after the hyperglycemic peak? What biomarkers are studied?

Dr. Kendall: It can be assessed in a number of different ways. The study presented was conducted in Italy, by Ceriello [2]. He has been looking at different measures of oxidative stress, so it could be as simple as looking at some antioxidant, vitamins or carotinoids. We know that diabetic subjects tend to have lower levels of antioxidants in their blood, so there are a number of different measures that can be looked at.

Dr. Halimi: How do you explain that despite a lower insulin response with low GI foods there is no benefit on body weight?

Dr. Kendall: We are actually talking about two different things. In tightly controlled studies of the GI we are trying to maintain body weight, as this would otherwise be a confounder by affecting insulin sensitivity and fasting glucose. To address your question we need free-living studies, where subjects are allowed to lose weight, comparing high GI diets with low GI diets. We have seen this in a weight loss study conducted by Raatz et al. [3]. However, when you are achieving significant weight loss by controlling energy intake, often both study groups achieve similar results and it becomes difficult to detect differences in insulin resistance and fasting glucose.

Dr. Slama: Can I add something to this question? First of all I don't see any reason why people exhibiting less hyperglycemia and less hyperinsulinemia should lose weight because all the calories which are ingested are metabolized and the net energy balance is exactly the same whatever the blood glucose excursion. We have just finished a study done on a Weightwatcher population and we tried to see if people eating low GI food lose weight. In fact there was exactly the same weight loss in the two populations with high and with low GI; the only difference was satiety. The people on low GI said that it was much easier to follow the diet rather than the high GI because of satiety. So there is no reason to lose weight more than to equal the energy intake but it is an easier way to follow the diet.

Dr. Kendall: I think that is a good point. Many low GI foods are whole foods, the energy density would tend to be lower. If you look at low GI food you actually do get an increased excretion or malabsorption of starch as well. There is a correlation between low GI foods and increased starch excretion.

Dr. Jianqin Sun: I have a question regarding the low GI for the lower body mass index. I would like to know what the mechanism for the weight loss is. My second question is with regard to the GI classification in terms of low, median and high; it seems a little different from the reference described in the literature.

Dr. Kendall: The second question first. I was using the bead index, so to use the glucose index you have to multiply those numbers by 0.7. The reason for weight loss with low GI? Again low GI diets tend to contain many whole foods; they tend to be higher in fiber as well, so this may be responsible for the increased weight loss.

Dr. Jianqin Sun: Is there any evidence for the energy expenditure difference between the low GI diet and the high GI diet?

Dr. Kendall: I don't think it has been looked at very carefully. There have been some studies looking at postprandial association with appetite. If you look at a lunch intake after a low versus a high GI breakfast, the amount of food consumed after the low GI breakfast tends to be lower [4].

Dr. Katsilambros: I would like to come back to Dr. Slama's comment about the same weight loss between low and high GI diets in humans. I recall a study published 3 years ago in rats fed high and low GI diets. These animals are a good model because exactly the same amount of energy can be given to them, and we are not sure what happens in humans. All the experimental animals on a low GI diet lost more weight.

We shouldn't ignore these studies. Certainly with humans it does not seem to happen but again we don't know how strictly humans adhere to the given instructions.

Dr. Kendall: Again we tend to think that all carbohydrates are available or that all protein and fat are absorbed and I don't think we are that efficient in absorbing all the nutrients that we take in. We have recently run a study looking at nut intake at 3 different doses and on the highest nut intake there is an excretion of about 60 kcal/day with the high nuts and approximately 15-20% of the energy from nuts was not absorbed [5]. This represents a significant proportion of the diet. This may be one of the reasons why whole foods, intact particles, are extremely healthy. Not only is there reduced absorption of some nutrients but they are then reaching the large intestine. What happens to that food system in the large intestine? We know it is quite good for the bacteria and it may have a myriad of other biochemical and physiological effects that are extremely healthy.

Dr. Katsilambros: It might be a good explanation. Are there any observations concerning physical activity and energy and movements, automatic movements of the muscles on the one diet and on the other diet? This could at least explain the animal findings.

Dr. Kendall: That is a good point. The GI has been looked at in terms of energy performance and with the low GI diet at least in some studies there seems to be increased performance [6]. I think this is an area that has not really been looked at very carefully.

Dr. Slama: I would like to add something to what Dr. Katsilambros said, and later I will show some results from an animal study. You are right that rats gained less weight during the first weeks and then caught up, and at 5 weeks finished up with exactly the same body weight.

Mr. Wuersch: This was one of our concerns 20 years ago when we started this project on the GI: What role does the availability of the nutrients play? When we take two extremes, for example potato or pulses, which have a GI ratio of roughly 1-2 or 1-2.5, we find that 10% of the carbohydrate is not absorbed in the pulses, which is confirmed by the resistant starch analysis. This means that on the diet side, it represents a maximum of 5% of the energy intake, so it comes back to your 80 calories roughly for a daily intake. Consequently this difference is probably not so significant and it has nothing to do or only marginally to do with the GI measured [7].

Dr. Kendall: I think that is also an important point. So while there is a loss of carbohydrate in some low GI foods, this does not account for the dramatic reduction in GI in the food. However that 5% loss in calories in terms of weight maintenance could be extremely important. We tend to gain 0.45 kg a year, 0.9 kg a year, it is a very slow progression in terms of weight gain. The balance between weight maintenance and weight gain is very finely tuned, so anything that can help us to excrete some energy could be extremely important.

Dr. T. Wilkin: I am not sure this question is a sensible one. You are obliged to use the GI because of the individual variation you would otherwise get. So what you are left with are relative, comparative data. How big is the range in absolute terms that you get between different foods? Is that a meaningful question? There could be relative differences but they could be very narrow differences in absolute terms.

Dr. Kendall: No, the absolute difference can be quite large. Nuts have an extremely low GI of around 20 or so, and pasta will have a GI of around 60, mash potatoes are around 100, boiled potatoes may be slightly less than 100.

Dr. T. Wilkin: That tells me there is a ratio of 6 or 7 to 1 across the range, but is that what is that meant in absolute terms?

Dr. Kendall: Yes, a range of about 6- to 7-fold which is quite large. So there is variation from day to day in someone's response to particular foods. We are still dealing with a black box, and if you look at some of the studies in saturated fat reduction, the majority of subjects reduce their low-density lipoprotein (LDL) cholesterol but there are still some subjects who raise their LDL. So I don't think you would interpret those data as saturated fat is good for the majority but not for those two individuals. You expect differences in response between individuals at particular times. The person who had an increase in LDL with decreased saturated fat on one occasion will most likely have a decrease in LDL with decreased saturated fat on most occasions.

Dr. Gerasimidi-Vazeou: I would like to ask you whether there are any long-term studies regarding the effect of GI diets on HbA1c in type-1 diabetic patients?

Dr. Kendall: I don't believe any very long-term studies have been undertaken in type-1 diabetic subjects. Most of the studies have been conducted in type-2 diabetes and most have not been of great length, typically around 12 weeks. I know with the increased interest in carbohydrates and GI, more longer-term studies are in progress. So I think we will begin to see data from these longer-term studies in the next year or two.

Dr. Bantle: I think the GI is largely predictable based on three main determinants which are fiber, fat and fructose. I ask you to comment on whether you think that is true. I would also like to ask you about the effect on the GI when you combine nutrients in a meal. In fact, does this not substantially diminish the difference among foods of different GIs?

Dr. Kendall: If there are large amounts of fat in a meal and large amounts of protein, that can affect the glycemic response, but typically these are not at a level that will have a significant effect. We have looked at the glycemic responses to nuts, which are high in fat. A standard white bread control was provided with 0, 28, 56, or 85 g of nuts, and there was always a significant reduction at the 56- and 85-gram level. But this is a dramatic level of nuts, 56 and 85 g [8]. So although you can see an effect, it is not typically seen for most meals. In terms of a fiber effect, foods that have high levels of soluble fiber will have a reduced glycemic response. Although the same is not true for non-viscous fiber. For example whole wheat bread, brown bread or grains that have been finely ground will have the same GI as white bread. So food form is important as is the nature of starch. Pasta, which is also made from wheat flour, has a much lower glycemic response than does brown or white bread.

References

1 Jenkins DJ, Wolever TM, Ocana AM, et al: Metabolic effects of reducing rate of glucose ingestion by single bolus versus continuous sipping. Diabetes 1990;39:775-781.

2 Ceriello A: Postprandial hyperglycemia and diabetes complications: is it time to treat? Diabetes 2005;54:1-7.

3 Raatz SK, Torkelson CJ, Redmon JB, et al: Reduced glycemic index and glycemic load diets do not increase the effects of energy restriction on weight loss and insulin sensitivity in obese men and women. J Nutr 2005;135:2387-2391.

4 Anderson GH, Woodend D: Effect of glycemic carbohydrates on short-term satiety and food intake. Nutr Rev 2003;61:S17-S26.

5 Kendall CW, Ellis PR, Marchie A, et al: Lipid bioavailability from almonds: implications for cardiovascular health and weight loss - a randomized controlled dose-response study (abstract). Ann Nutr Metab 2003;47:617.

6 Kirwan JP, Cyr-Campbell D, Campbell WW, et al: Effects of moderate and high glycemic index meals on metabolism and exercise performance. Metabolism 2001;50:849-855.

7 Schweizer TF, Andersson H, Langkilde AM, et al: Nutrients excreted in ileostomy effluents after consumption of mixed diets with beans or potatoes. II. Starch, dietary fibre and sugars. Eur J Clin Nutr 1990;44:567-575.

8 Kendall CW, Marchie A, Parker TL, et al: Effect of nut consumption on postprandial starch digestion - a dose-response study (abstract). Ann Nut Metab 2003;47:636.

Bantle JP, Slama G (eds): Nutritional Management of Diabetes Mellitus and Dysmetabolic Syndrome. Nestlé Nutr Workshop Ser Clin Perform Program, vol 11, pp 57-72, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2006.

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  • Makda
    What is insulin resistance research paper?
    10 months ago

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