Glycaemic index in diabetes management
This paper was prepared by Robyn Perlstein, Jane Willcox, Carolyn Hines and Marianna Milosavljevic on behalf of the Dietitians Association of Australia.
Abstract The glycaemic index (GI) is a system of classifying foods which contain carbohydrate (CHO) based on their acute glycaemic response, with the view that the slower, flatter response may facilitate better glycaemic control and lipid profiles in people with diabetes. This paper examines the definition and methodology of GI, the factors affecting GI, the results of clinical studies incorporating GI, and the practical issues and recommendations for GI in diabetes management. Long-term studies provide justification for the incorporation of GI in diabetes nutrition management, through improvement in blood glucose control and lipid levels in people with diabetes. GI should not be used in isolation, but within the current macronutrient recommendations for people with diabetes. Future research and development are required in the areas of GI and diabetes prevention, GI and the food industry, resource materials and teaching methods, and health professional training. (Aust J Nutr Diet 1997;54:57-63). Keywords: glycaemic index, diabetes mellitus, nutrition, blood glucose, dietary carbohydrates.
Carbohydrate has been the main focus of diabetes nutrition management from as long ago as 1550 BC ( 1). As research has progressed, the physiological effects of various carbohydrates have become better understood.
The glycaemic index (GI) is a system of classifying foods which contain carbohydrate (CHO) based on their acute glycaemic response with the view that the slower flatter response may facilitate better glycaemic control and lipid profiles in people with diabetes ( 2, 3). Descriptions of the concept have ranged from 'a bucket of fluff' ( 4) to 'a functional measurement' ( 5) and the clinical applicability of GI has been widely debated. In Australia, GI has been incorporated into diabetes education to varying degrees.
This paper examines the definition and methodology of GI, the factors affecting GI, the results of clinical studies incorporating GI, and the practical issues and recommendations for GI in diabetes management.
Since the 1930s scientists have challenged the traditionally held view that the metabolic effects of carbohydrates can be predicted by the classifications as either 'simple' or 'complex' ( 6).
In the 1970s researchers such as Otto and Crapo ( 7-9) examined the glycaemic impact of a range of foods containing CHO. Studies, however, were not always directly comparable due to lack of standardisation of techniques employed ( 10).
To standardise the interpretation of glycaemic response data, Jenkins and colleagues proposed the glycaemic index (GI) in 1981 ( 11). This work disproved the assumption that equivalent amounts of carbohydrate from different foods elicit similar glycaemic responses. Furthermore, the researchers concluded that 'the carbohydrate exchange lists that have regulated the diets of many diabetics...may not reflect the physiological effect of foods' ( 11).
Since the early 1980s, research on the GI has proliferated, providing insight into the GI and its clinical applicability in diabetes management.
The GI of a food is determined by comparing the acute glycaemic response of a test food to a standard food in individual subjects. Subjects have included those with insulin dependent diabetes (IDDM), non-insulin dependent diabetes (NIDDM), and those without diabetes. Provided is a description of the most commonly employed method ( 12).
A 50 g available carbohydrate portion of the test food is administered to an individual after an overnight fast. Blood glucose levels are measured via capillary blood sampling every 15 to 30 minutes for two to three hours. Blood glucose results are plotted and the incremental area under the response curve, above baseline, is calculated. The same procedure is used to ascertain the individual's glycaemic response to a standard food such as white bread or glucose, and is generally repeated three times. Test and standard foods are administered in random order on different days with at least three days between tests. The area under the blood glucose response curve for the test food is expressed as a percentage of the mean response to the standard food. The GI value of a food is determined by repeating the procedure with a number of subjects. Five to fifteen subjects have been used ( 11, 13, 14, 15). The resulting values for each subject are averaged to obtain the GI value for the food.
The glycaemic index is defined as (11):
Incremental blood glucose area
Glycaemic after test food
index (GI) = Corresponding area after equi-- x 100
carbohydrate portion of standard
Initially glucose was used as the standard food ( 11). Because of the concerns of excessive sweetness and the osmotic effect of glucose solutions, it was suggested that white bread of known composition be utilised ( 12, 16). Consequently, different research groups use either standard. A conversion factor is used to compare results of the different standards ( 12). For example, if a food is tested using white bread as the standard, it can be multiplied by a conversion factor of 0.7 to compare it to a glucose standard; or if a food is tested using glucose as the standard, it can be multiplied by a conversion factor of 1.4 to compare it to a white bread standard.
GI values obtained from various centres can differ. This can be explained, in part, by the varied methods used in assessing the glycaemic response to foods and presentation of results. If these methods are standardised then they appear to have only a minimal influence on GI ( 12).
Methodological variables that can affect the GI result include:
the choice of the standard food and number of times tested in individual subjects ( 15, 17);
the variation in food portion size ( 11). For low concentration carbohydrate foods, such as peanuts, a 25 g available carbohydrate portion may be used due to the excessive volume of the foods needed to supply 50 g of carbohydrate. Dose response is linear up to 50 g of carbohydrate but flattens out between 50 and 100 g of carbohydrate (l 2);
the method, frequency and length of time of blood sampling ( 14, 15, 18);
the method of calculation of the area under the glycaemic response curve ( 15, 19);
the degree of individual glycaemic control of test subjects ( 14); and,
preprandial blood glucose levels ( 15, 17, 20, 21).
Variations exist in the glycaemic responses to foods due to differences that arise between individuals, and within the same individual. GI reduces the between-subject variation significantly, because rather than measuring the absolute glycaemic response to a food, it measures the relative glycaemic response by indexing a subject's response against his or her response to a standard ( 17, 22). Within-subject variation remains similar to that for absolute glycaemic response ( 22). NIDDM subjects are the least variable followed by normal and then IDDM subjects who are nearly twice as variable as NIDDM ( 15, 17). Glycaemic index has therefore been referred to as 'an effective way of standardising the glycaemic responses of different individuals' because it reduces total variability ( 22).
Wolever et al. report that between-subJect variability can be further reduced by using the mean of tests in each subject ( 17). Other research groups consider the use of the mean inadequate because it removes all individual variability ( 23). Wolever and colleagues have investigated the responses of individuals with diabetes to several low GI foods eaten at one sitting and found that each subject demonstrated a mean GI value for the foods tested that was similar to or below the predicted mean GI value for those foods ( 22). They concluded from this that 'the GI concept can be applied to individual diets composed of many foods'.
Glycaemic index values and factors affecting GI
There are now nearly 600 published GI values for various foods ( 24). This has enabled a ranking of foods according to their GI. The GI values of a selection of foods are listed in Table 1. When applying GI to diabetes patient management, it appears reasonable to classify carbohydrate foods using the following classification as suggested by Brand Miller ( 25): high GI (equal to or greater than 70); intermediate GI (56 to 69); or low GI (equal to or less than 55).
Many factors have been proposed to affect the glycaemic response to food including the nature of the carbohydrate, the physical form and processing, and the levels of fibre, antinutrients, fat and protein ( 5, 15). Each factor either influences the rate of absorption, or digestion or both, and in turn influences the glycaemic response. For these reasons, a GI range, rather than an absolute value, may be expected for each food, and differences of 10 to 15 units are within the error associated with the measurement of GI ( 12).
Nature of the carbohydrate
Determination of the GI of various monosaccharides, disaccharides and polysaccharides has challenged the historlcal categonsations of carbohydrates as simple and complex. The glycaemic indexes of the different sugars range from 20 for fructose to 105 for maltose ( 11). Fructose elicits a low GI, probably because of incomplete absorption ( 35) and only partial conversion to glucose. Sucrose, with a GI of 59, challenges the historical view that foods containing sugar cause an excessive rise in blood glucose levels and that sugars elicit a higher glycaemic response than starches ( 26).
Seasonal factors may also influence the nature of the carbohydrate. For example, ripening of bananas influences the starch content and hence the GI ( 36).
The type of starch present in a food influences the glycaemic response. A higher ratio of amylose to amylopectin produces a slower rate of digestion due to the extensive hydrogen bonding of amylose ( 27, 37). For example, Doongara rice, with a high amylose content, has a significantly lower GI than normal varieties of Australian rice, which are low in amylose ( 27). There is as yet no clear relationship between resistant starch and GI ( 14).
Physical form of food and processing
Processing such as milling, grinding, puffing, canning, flaking and dry heating of grains has been associated with increasing glycaemic responses ( 30). Processing may elevate GI by 40 to 50 units ( 38). Wolever showed that canning increased :the GI of dried beans by 17 units and hypothesised that the high pressure used in the canning process could alter the physical nature of the starch and antinutrient content ( 39).
The physical form of food also appears to influence the GI ( 40). The glycaemic response of food decreases with a higher proportion of whole intact grain ( 41, 42). The disruption to the grain increases the availability for enzymatic digestion and starch gelatinisation and hence elevates the GI ( 42, 43). For example, Brown et al. suggest that palatable low GI breads can be produced with up to 50% 'whole' grain ( 29).
Research has not elicited a clear relationship between dietary fibre and GI ( 38, 44). This may be due to the fact that many other factors related to fibre influence digestion, such as food form, particle size and antinutrients ( 45). Some studies show that insoluble and soluble fibre have no effect on glycaemic response ( 15, 45). In comparison, other studies show soluble and insoluble fibre are independent determinants of GI ( 44). Further research is required to elicit the relationship between types of fibre and GI.
The food content of antinutrients such as polyphenols (tannins), lectins and phytic acid correlates inversely with GI ( 46). High concentrations of antinutrients in legumes could partly explain the low GI of legumes.
Fat and protein
Fat and protein may significantly alter the GI of carbohydrate foods if present in relatively large quantities ( 47-49). Studies show that fat and protein generally alter the GI of foods containing carbohydrate if present in quantities greater than 25 g per 50 g carbohydrate serve ( 47, 48).
Fat is known to reduce gastric emptying, jejunal motility and postprandial flow rates in the intestine, and hence decrease the glycaemic response. This effect is also mediated by the potentiation of insulin secretion in the presence of fat ( 48).
Protein appears to reduce the glycaemic response through an increase in insulin secretion, and may also increase the osmolarity of stomach contents, thereby reducing the rate of gastric emptying ( 47, 49).
An insulin index can be calculated in the same way as GI, but using insulin curves ( 50). It measures the acute insulin response that foods invoke. It is defined as:
Incremental area under plasma
Insulin insulin curve for test food
= x 100
index (II) Incremental area under plasma
insulin curve for standard food
Most studies show a positive correlation between II and GI with a lower GI diet producing a lower insulin response( 26, 27, 51, 52). Protein foods, however, elicit an insulin response without a commensurate glycaemic response ( 53).
Insulin index may prove to be relevant as an indicator when assessing carbohydrate foods due to the correlation between GI and II. (This requires further research.) It may also be relevant in the study of the development of hyperlipidaemia and atherosclerosis due to the proposition that high insulin concentrations are associated with unfavourably high plasma levels of low density lipoprotein cholesterol, triglyceride and glucose, and also with central obesity ( 54). Prospective studies of insulin as a heart disease risk factor have given contradictory results, and therefore the role of insulin as a cardiovascular risk factor requires further investigation ( 55).
The relationship between satiety and glycaemic index has been well examined in recent years. In general, carbohydrate has been shown to have a greater satiety value than fat ( 56). Whilst there are some examples of foods with a high GI having a high effect on satiety (e.g. potato), foods with a low GI generally elicit the greater satiety effect ( 28, 57, 58).
Second meal effect
Low GI foods as part of a meal can improve the carbohydrate tolerance to subsequent meals. A study by Wolever and colleagues ( 59) showed that low GI carbohydrate foods eaten at an evening meal reduced the acute postprandial blood glucose response to the evening meal and to the subsequent standard breakfast.
Much work has been conducted in the examination of foods with a low GI in the context of a meal, referred to as 'mixed meals'. It is well accepted that substituting low GI foods for high GI foods in a meal will reduce the glycaemic response to the meal ( 50, 52, 60).
Wolever and colleagues described a method for predicting the blood glucose response to mixed meals as 'the sum of the GI contributions of each carbohydrate component of the meal' ( 60).
The issue of mixed meals is often raised as a criticism of GI, with a few studies showing contradictory results. Some researchers report that fat and protein, when eaten With a carbohydrate food as part of a mixed meal, abolishes any differences in GI that may have been obvious when the carbohydrate food was eaten alone ( 23). Others insist that there is no substantial evidence for this effect ( 15).
Incorporation of low GI foods--- fleet on glycaemic and lipaemic control
There have been 12 studies since 1984 that have examined the longer term effect of low GI foods on glycaemic and lipaernie control ( 2, 3, 31, 61-69). They have ranged from two weeks to 12 weeks in duration. All but one study showed improvements in metabolic control when measuring parameters including HbA1c, the ratio of HDL to LDL cholesterol, triglycerides and fructosamine. A meta-analysis was performed on 11 of these 12 studies ( 70). The results of the analysis showed modest improvements in glycaemic and lipid parameters with lower GI diets. For example, average reductions in HbAlc, serum cholesterol and triglycerides of 9%, 6% and 9% respectively were seen with an average reduction of 19 units in the GI of the diets.
A recent study in NIDDM patients at Hammersmith Hospital, London ( 3), compared standard dietary education based on the British Diabetic Association guidelines with standard dietary education that emphasised GI. The results showed a significant reduction in blood glucose and triglyceride levels by incorporating low GI foods at each meal. Although there was only an average difference of five units in GI between the two study groups, this study shows that a small reduction in total GI can have a positive metabolic effect.
Results to date support the inclusion of GI in diabetes nutrition management.
Practical applications of GI
The use of GI
The use of GI in improving blood glucose control and lipid levels has now been validated through longer term studies. In addition the satiating effect of lower GI foods may be useful in the weight management of people with diabetes. Health professionals are therefore seeking information about its practical use. Limited work has been done in this area but recent publications have provided some insight by recommending the inclusion of two low GI foods daily ( 70) or the inclusion of one low GI food at each meal ( 71) or the replacement of 50% of carbohydrate with low GI choices ( 70).
It is essential that GI not be used in isolation (see 'The misuse of GI', below). Instead, it should be incorporated along with current macronutrient and carbohydrate distribution recommendations.
Various studies have suggested different ways of incorporating low GI foods into the diet( 2, 3, 31, 61-69). Examples include:
Brand Miller asked subjects in her study to emphasise certain foods at the expense of others, for example, oatmeal, porridge and All Bran instead of Weetbix and other higher GI cereals; and inclusion of pasta or legumes once per day while restricting intake of potatoes and other high GI fruits and vegetables ( 2).
Frost especially encouraged subjects to use wholegrain rye bread, oats, barley and pasta, and to increase intakes of beans, pulse vegetables and fruit ( 3).
Incorporation into client education
Incorporating GI into the current macronutrient recommendations, and therefore into client education material, is the challenge for dietitians. There are several hurdles which must first be overcome.
• Re-examination of old beliefs
GI may be an unfamiliar concept to both health professionals and to people with diabetes, and its use may be complicated by old beliefs. An example is the earlier theories of carbohydrate digestion and absorption, which led to the recommendation of complete abstinence from any sugar. It is now known that not all sugars have a high GI. Studies support the incorporation of sucrose in place of some carbohydrate, as it does not appear to be associated with poorer glycaemic control ( 72, 73). Restrictions on sucrose intake could be relaxed to correspond with recommendations on sugar intake for the normal, healthy population.
• Descriptions and terminology
The concept of GI may be difficult to explain, particularly as there is no rule of thumb to determine GI except scientifically. Also, not all foods have been tested, and not all factors affecting GI have yet been established. Creating a link with past descriptions of carbohydrate may prove helpful. For example, although the former separation of carbohydrate into 'simple' and complex' is no longer applicable, similar terminology can be used such as 'quick acting' and 'slow acting'. In addition, other descriptions have been proposed such as a 'small rise in blood glucose levels (BGLs)' or a 'large rise in BGLs' ( 71), 'high' or 'low' GI ( 25), 'fast' or 'slow' digestion ( 71), and 'slow' versus 'moderate' and 'fast' acting ( 74).
• Carbohydrate measurement GI should not be confused with the issue of carbohydrate measurement and exchanges. Research into GI does not really give answers as to whether or not carbohydrate foods should be measured, but it challenges the concept that equal 'exchanges' of carbohydrate will elicit similar glycaemic responses. Current exchange lists of carbohydrate foods do not give a true comparison of the blood glucose effects of different carbohydrate foods, and this is required. There is work currently being undertaken by Colagiuri and Brand Miller ( 75) to formulate a listing of quantities of foods which have equivalent glycaemic impact, which will be an improvement over currently available exchange lists.
Once the hurdles have been overcome the incorporation of GI into client education will be made easier and can be enhanced by the availability of resource material. Whilst this is an area in need of expansion, several key resources are available which provide practical advice, and may assist in the incorporation of GI into client education ( 25, 71, 74).
Other areas of application
There are some key areas in which GI may have a specific application in diabetes management.
While GI may help explain some of the variations in postprandial blood glucose, it may also be used to optimise the treatment of hypoglycaemia. GI values suggest the more appropriate choices for the treatment of hypoglycaemia. Traditional lower GI choices included fruit juice and chocolate, while better choices may be glucose-containing foods such as glucose tablets, Lucozade[TM] and glucose confectionery. Incorporation of lower GI foods into the general diet has been shown to reduce episodes of nocturnal hypoglycaemia ( 76). Further research is required to validate the use of GI in the treatment of hypoglycaemia.
The application of GI in sports nutrition has been examined ( 77, 78). Lower GI foods may have a role prior to exorcise and higher GI foods after exercise. Information from work done in this area may be useful for individuals with diabetes who exercise. Further work in the area of diabetes, exercise and carbohydrate intake needs to be undertaken to substantiate its application in diabetes nutrition management.
The misuse of GI
The most prominent misuse of GI has been in relation to its numerical figures. Unfortunately many health professionals and people with diabetes view these figures as the sole factor in determining a food's suitability. For example, they may consider a food with a low GI, such as chocolate, to be suitable and one with a high GI, such as potato, to be unsuitable. Additionally people focus on individual values rather than whether foods have a high or a low GI or its macronutrient composition.
It is essential that GI be incorporated with the current macronutrient recommendations, which must always take the highest priority. In the example above, chocolate is not recommended due to its high saturated fat content, despite its low GI. Potato, however, is recommended because it is low in fat and high in carbohydrate, despite the fact that its carbohydrate is quick acting.
Future research and recommendations
The practical application of GI to diabetes management still a relatively new area. Further research is required to determine other factors affecting GI and, although difficult, long-term studies conducted in a realistic free living situation, as in the Frost study ( 3), would be useful.
The use of GI in diabetes prevention is an area growing interest ( 52). The effects of lower GI diets on the incidence of diabetes in genetically susceptible group would be of interest. The importance of the insulin index and its relevance to cardiovascular disease also need to be further examined( 55). If the differences in insulin responses to foods are clinically significant, then this may mean that the insulin index of all foods is needed to supplement tables of GI values ( 24).
Health professional education needs to be expanded in order for consistent messages to be relayed to people wit diabetes and the general public. This would be enhance by the development and evaluation of a wider range of resource material and teaching methods. In addition, greater involvement by the food industry through the development of low GI foods and the testing of a wide range of foods is required. Food labelling issues also need to be debated. Inroads into these areas have already begun ( 25).
Longer term studies provide justification for the incorporation of GI in diabetes nutrition management but the macronutrient recommendations remain the primary con sideration. Within the carbohydrate component of these recommendations, GI is a useful tool in providing a: understanding of the acute glycaemic response of food which contain carbohydrate. It should not be used in isolation, and consideration of the numerical figures alone can lead to its misuse.
Future research and development should further enhance the understanding and use of GI in diabetes nutrition management.
Table 1. Glycaemic index values of a selection of foods
using glucose as the standard (11,16, 26-34)
Pumpernickel 46 Lentils 29
Wholemeal 67 Soya beans 15
White 71 Soya beans, tinned 14
Wholegrain 47 Baked beans, tinned 40
Milk, skim 32 Fructose 20
Milk, whole 34 Sucrose 59
Ice cream 62 Glucose 100
Yoghurt 33 Maltose 105
Other grain products Fruit, vegetables
Rice, white 83 Orange 40
Rice, brown 66 Orange juice 57
Rice, Doongara 64 Banana 58
Spaghetti, white 42 Apple 39
Spaghetti, wholemeal 42 Dried apricots 30
Barley, rolled 66 Potato, new, boiled 70
Barley 22 Sweet potato 48
Buckwheat 51 Carrots 92
Sweet corn 48
Rolled oats 42 Plain sweet 69
Allbran(a) 50 Ryvita 63
Cornflakes(a) 80 Digestives 62
Sultana bran(a) 52
Rice bran 19
1. Powers MA. A review of recent events in the history of diabetes nutritional care. Diab Educator 1992;18:393-400.
2. Brand JC, Colagiuri S, Allen A, Roberts DCK, Trustwell AS. Low-glyceamic control in NIDDM. Diad Care 1991;14:95-101
3. Frost G. Wilding J. Dietary advice based on the glycemic index improves dietayr profile and metabolic control in type 2 diabetic paitents. Diabet Med 1994;11:397-401.
4. Kolata G. Diabetics should lose weight, avoid diet fads. Science 1987;235:163-4.
5. Nathan DM. The glycemic index: meat and potatoes of just gravy? Diab care 1987;10:524-5.
6. Moskowitz E. Der Einfluss vegetabiler Nahrugsmittel auf den Blutzucker bei Diabetikern. Z Klin Med 1937;131:648-59
7. Otto H, Bleyer G, Pennartz M, Sabin G, Schauberger G, Spathe K. Kohlenhydrataustaush nach biologischen aquivalenten. In: Otto H, Spehte R, editors. Diatetik bei Diabetes Mellitus. Bern: Huber, 1973.
8. Crapo PA; Reaven G, Olefsky J. plasma glucose and insulin responses to orrally administered simple and complex carbohydrates. Diabetes 1976;25:741-7.
9. Crapo PA; Reaven G, Olefsky J. Post-prandial plasma glucose and insulin responses to different complex carbohydrates. Diabetes 1977;26:1178-83.
10. Jenkins DJA, Wolever TMS, Jenkins AL. Starchy foods and glycemic index. Diab Care 1988;11: 149-59.
11. Jenkins DJA, Wolever TMS, Taylor RH, Barker H, Fielden H, Baldwin JM, et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981 ;34:362-6.
12. Wolever TMS, Jenkins DJA, Jenkins AL, Josse RG. The glycemic index: methodology and clinical implications. Am J Clin Nutr 1991 ;54:846-54.
13. Wolever TMS, Jenkins DJA, Collier GR, Ehrlich RM, Josse RG, Wong GS, et al. The glycemic index: effect of age in insulin dependent diabetes mellitus. Diab Res 1988;7:71-4.
14. Truswell AS. Glycaemic index of foods. Eur J Clin Nutr 1992;46 (Suppl 2):S9 1-S 101.
15. Wolever TMS. The glycemic index. In: Bourne GH, editor. Aspects of some vitamins, minerals and enzymes in health and disease. World Rev Nutr Diet 1990;62:120-85.
16. Jenkins DJA, Wolever TMS, Jenkins AL, Thorne M J, Lee R, Kalmusky J, et al. The glycemic index of foods tested in diabetic patients: a new basis for carbohydrate exchange favouring the use of legumes. Diabetologia 1983;24:257-64.
17. Wolever TMS, Nuttall FQ, Lee R, Wong GS, Josse RG, Csima A, Jenkins DJA. Prediction of the relative blood glucose response of mixed meals using the white bread glycemic index. Diab Care 1985;8:418-28.
18. Gannon MC, Nuttall FQ. Factors affecting interpretation of post-prandial glucose and insulin areas. Diab Care 1987;10:759-63.
19. Coulston AM, Hollenbeck CB, Swislocki ALM, Reaven GM. Effect of source of dietary carbohydrate on plasma glucose and insulin responses to mixed meals in subjects with NIDDM. Diab Care 1987;10:395-400.
20. Nielsen PH, Nielsen GL. Preprandial blood glucose values: influence on glycemic response studies. Am J Clin Nutr 1989;49:1243-6.
21. Hermansen K, Rasmussen O, Arnfred J, Winther E, Schmitz O. Differential glycemic effects of potato, rice and spaghetti in type 1 (insulin dependent) diabetic patients at constant insulinemia. Diabetologia 1986;29:358--61.
22. Wolever TMS, Csima A, Jenkins DJA, Wong GS, Josse RG. The glyceamic index: variation between subjects and predictive differcate. J Am Coil Nutr 1989;8:235-47.
23. Hollenbeck CB, Couiston AM, Reaven GM. Glycemic effects of carbohydrates: a different perspective. Diab Care 1986;9:641-7.
24. Foster-Powell K, Brand Miller J. International tables of glycemic index. Am J Clin Nutr 1995;62 (Suppl):871S-93S.
25. Brand Miller J, Foster-Powell, K, Colagiuri S. The GI factor--the glycaemic index solution. Sydney: Hodder and Stoughton, 1996.
26. Brand Miller J, Pang E, Broomhead L. The glycaemic index of foods containing sugars: comparison of foods with naturally-occurring v added sugars. Br J Nutr 1995 ;73:613-23.
27. Brand Miller J, Pang E, Brainall L. Rice: a high or low glycemic index food? Am J Clin Nutr 1992;56:1034-6.
28. Jenkins DJA, Wolever TMS, Jenkins AL, Giordano C, Giudici S, Thompson LU, et al. Low glycemic response to traditionally processed wheat and rye products: bulghur and pumpernickel bread. Am J Clin Nutr 1986;43:516-20.
29. Brown D, Tomlinson D, Brand Miller JC. The development of low glycaemic index breads [abstract]. Proc Nutr Soc Aust 1992;17:62.
30. Brand JC, Nicholson PL, Thorburn AW, Truswell AS. Food Processing and the glycemic index. Am J Clin Nutr 1985;42:1192-6.
31. Jenkins DJA, Wolever TMS, Kalmusky J, Giudici S, Giordana C, Wong GS, et al. Low glycemic index carbohydrate foods in the management of hyperlipidemia. Am J Clin Nutr 1985;42:604-17.
32. Oannon MC, Nuttall FQ, Krezowski PA, Billington CJ, Parker S. The serum insulin and plasma glucose responses to milk and fruit products in type 2 (non-insulin-dependent) diabetic patients. Diabetologia 1986;29:784-91.
33. Holt S, Brand J, Soveny C, Hansky J. Relationship of satiety to postprandial glycaemic, insulin, and cholecystokinin responses. Appetite 1992; 18:129--41.
34. Wolever TMS, Katzman-Relle L, Jenkins AL, Vuksan V, Josse RG, Jenkins DJA, et al. Glycemic index of 102 complex carbohydrate foods in patients with diabetes. Nutr Res 1994; 14:651-69.
35. Truswell AS, Seach JM, Thorburn AW. Incomplete absorption of pure fructose in healthy subjects and the facilitating effect of glucose. Am J Clin Nutr 1988;48:1424-30.
36. Hermansen K, Rasmussen O, Gregersen S, Larsen S. Influence of ripeness of banana on the blood glucose and insulin response in type 2 diabetic subjects. Diabet Med 1992;9:739-43.
37. van Ameisvoort JMM, Weststrate JA. Amylose-amylopectin ratio in a meal affects postprandial variables in male volunteers. Am J Clin Nutr 1992;55:712-8.
38. Trout DL, Behall KM, Osilesi O. Prediction of glycemic index for starchy foods. Am J Clin Nutr 1993;58:873-8.
39. Wolever TMS, Jenkins DJA, Thompson LU, Wong GS, Josse RG. Effect of canning on the blood glucose response to beans in patients with type 2 diabetes. Hum Nutr Clin Nutr 1987;41C: 135-40.
40. Crapo PA, Henry RR. Postprandial metabolic responses to the influence of food form. Am J Clin Nutr 1988;48:560-4.
41. Jenkins DJA, Wesson V, Wolever TMS, Jenkins AL, Kalmusky J, Guidici S, et al. Wholemeal versus wholegrain breads: proportion of whole or cracked grain and the glycaemic response. B M J 1988 ;297:958--60.
42. Granfeldt Y, Liljeberg H, Drews A, Newman R, Bjorck I. Glucose and insulin responses to barley products: influence of food structure and amylose-amylopectin ratio. Am J Clin Nutr 1994;59:1075-82.
43. O'Dea K, Nestel PJ, Antonoff L. Physical factors influencing postprandial glucose and insulin responses to starch. Am J Clin Nutr 1980;33:760-5.
44. Nishimune T, Yakushiji T, Sumimoto T, Taguchi S, Konishi Y, Nakahara S, et al. Glycaemic response and fibre content of some foods. Am J Clin Nutr 1991 ;54:414-9.
45. Wolever TMS. Relationship between dietary fibre content and composition in foods and the glycemic index. Am J Clin Nutr 1990;51:72-5.
46. Thompson LU, Yoon JH, Jenkins DJA, Wolever TMS, Jenkins AL. Relationship between polyphenol intake and blood glucose response of normal and diabetic individuals. Am J Clin Nutr 1984;39:745-51.
47. Nuttall FQ, Mooradian AD, Gannon MC, Billington C, Krezowski P. Effect of protein ingestion on the glucose and insulin response to a standardized oral glucose load. Diab Care 1984;7:465-70.
48. Collier G, O'Dea K. The effect of coingestion of fat on the glucose, insulin and gastric inhibitory polypeptide responses to carbohydrate and protein. Am J Clin Nutr 1983;37:941-4.
49. Gulliford MC, Bicknell EJ, Scarpclio JH. Differential effect of protein and fat ingestion on blood glucose responses to high and low glycemic index carbohydrates in noninsulin dependent diabetic subjects. Am J Clin Nutr 1989;50:773-7.
50. Bornet FRJ, Costagliola D, Rizka!la SW, Blayo A, Fontvieille AM, Haardt MJ, et al. Insulinemic and glycemic indexes of six starch rich foods taken alone and in a mixed meal by type 2 diabetics. Am J Clin Nutr 1987;45:588-95.
51. Crapo PA, Henry RR. Postprandial metabolic responses to the influence of food form. Am J Clin Nutr 1988;48:560-4.
52. Chew I, Brand JC, Thorburn AW, Truswell AS. Application of glycaemic index to mixod meals. Am J Clin Nutr 1988;47:53-6.
53. Krezowski PA, Nuttall FQ, Gannon MC, Bartosh NH. The effect of protein ingestion on the metabolic response to oral glucose in normal individuals. Am J Clin Nutr 1:986;44:847-56.
54. De Fronzo RA, Ferrannini E. Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemla, and atherosclerotlc cardiovascular disease. Diab Care 1991;14:173-94.
55. Ferrara A, Barrett-Connor EL, Edelstein SL. Hyperinsulinemia does not increase the risk of fatal cardiovascular disease in elderly men or women without diabetes: the Rancho Bernardo Study, 1984-1991. Am J Epidemiol 1994;140:857-69.
56. Lawton CL, Burley VJ, Wales JK, Blundell JE. Dietary fat and appetite control in obese subjects: weak effects on satiation and satiety. Int J Obesity t 993; 17:409-16.
57. Leathwood P, Pollet P. Effects of slow release carbohydrates in the form of bean flakes on the evolution of hunger and satiety in man. Appetite 1988; 10:1-11.
58. Holt SHA, Brand Miller J. Particle size, satiety and the glycaemic response. Eur J Clin Nutr 1994;48:496-502.
59. Wolever TMS, Jenkins DJA, Ocana AM, Rao VA, Collier GR. Second meal effect: low glycemic index foods eaten at dinner improve subsequent breakfast glycemic response. Am J Clin Nutr 1988;48:1041-7.
60. Wolever TMS, Jenkins DJA. The use of the glycemic index in predicting the blood glucose response to mixed meals. Am J Clin Nutr 1986;43:167-72.
61. Jenkins DJA, Wolever TMS, Collier GR, Ocana A, Rao AV, Buckley G, et al. Metabolic effects of a low glycemic index diet. Am J Clin Nutr 1987;46:968-75.
62. Jenkins DJA, Wolever TMS, Buckley G, Lam KY, Giudici S, Kalmusky J, et al. Low glycemic index starchy foods in the diabetic diet. Am J C!in Nutr 1988;48:248-54.
63. Wolever TMS, Jenkins DJA, Vuksan V, Jenkins AL, Buckley GC, Wong GS, et al. Beneficial effect of a low glycemic index diet in type 2 diabetes. Diabet Med 1992;9:451-8.
64. Wolever TMS, Jenkins DJA, Vuksan V, Jenkins AL, Wong GS, Josse RG. Beneficial effect of low glycemic index diet in overweight NIDDM subjects. Diabetes Care 1992;15:562-4.
65. Fontvieille AM, Rizkalla SW, Penfornis A, Acosta M, Bornet FRJ, Slama G. The use of low glycemic index foods improves metabolic control of diabetic patients over 5 weeks. Diabet Med 1992;9:444-50.
66. Calle-Pascual AL, Gomez V, Leon E, Bordiu E. Foods with a low glycemic index do not improve glycemic control of both type I and type 2 diabetic patients after one month of therapy. Diabete Metab 1988; 14:629-33.
67. Collier GR, Giudici S, Kalmusky J, Wolever TMS, Helman G, Wesson V, et al. Low glycemic index starchy foods improve glucose control and lower serum cholesterol in diabetic children. Diab Nutr Metab 1988;1:11-9.
68. Fontvieille AM, Acosta M, Rizkalla SW, Bornet F, David P, Letanoux M, et al. A moderate switch from high to low glycemic index foods for 3 weeks improves the metabolic control of type 1 (IDDM) diabetic subjects. Diab Nutr Metab 1988; 1:139-43.
69. Jenkins DJA, Wolever TMS, Kalmusky J, Guidici S, Giordano C, Patten R, et al. Low glycemic index diet in hyperlipidemia: use of traditional starchy foods. Am J Clin Nutr 1987;46:66-71.
70. Brand Miller JC. Importance of glycemic index in diabetes. Am J Clin Nutr 1994;59(Suppl):747S-52S.
71. International Diabetes Institute. Diabetes---eating for health. Melbourne: International Diabetes Institute, 1994.
72. Shimakwa T, Warram JH, Herrera-Acena MG, Krolewski AS. Usual dietary intake and hemoglobin A1 level in patients with insulin-dependent diabetes. J Am Diet Assoc 1993;93:1409-12.
73. Wolever TMS, Nguyen PM, Chiasson JL, Hunt JA, Josse RG, Palmason C, et al. Determinants of diet glycemic index calculated retrospectively from diet records of 342 individuals with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 1994;59:1265-9.
74. Nutrition Department, Central Coast Area Health Service. Putting GI into practice--reviewing diabetes education in light of the glycaemic index--an area health perspective. Gosford, NSW: Central Coast Area Health Service, 1996.
75. Colagiuri S, Brand Miller JC. Developing a new carbohydrate exchange diet based on the glycemic index [abstract]. Proc Nutr Soc Aust 1996; 20:174.
76. Kaufman FR, Dergan S. Use of uncooked cornstarch to avert nocturnal hypoglycemia in children and adolescents with type I diabetes. J Diab Comp 1996; 10:84-7.
77. Burke LM, Collier GR, Hargreaves M. Muscle glycogen storage after prolonged exercise: effect of the glycemic index of carbohydrate feedings. J Appl Physiol 1993 ;75:1019-23.
78. Thomas DE, Brotherhood JR, Brand JC. Carbohydrate feeding before exercise: effect of glycemic index. Int J Sports Med 1991;12:180-6.