WHO consultation

Carbohydrates and health—the FAO/WHO consultation Thomas Wolever Introduction Carbohydrates are the single most important source of energy for the wo...
Author: Wilfrid Lang
40 downloads 0 Views 85KB Size
Carbohydrates and health—the FAO/WHO consultation Thomas Wolever

Introduction Carbohydrates are the single most important source of energy for the world for human nutrition. Over the last 15 or 20 years there has been a lot of research conducted that has completely changed the way we think about dietary carbohydrates. For that reason the Food and Agriculture Organization (FAO) of the United Nations and the World Health Organization (WHO) convened an expert consultation on carbohydrates in human nutrition that was held in Rome in 1997, involving scientists from 13 countries (1). Many people feel that carbohydrates are unhealthy and we, as health professionals, need to correct that message. One of the most important recommendations that the consultation made was that the many health benefits of carbohydrate foods should be recognised and promoted. The health benefits of carbohydrates are many and include their roles in weight management and physical activity, in diabetes prevention and treatment, cardiovascular disease and cancer. One of the FAO/WHO recommendations was that an optimum diet of at least 55% of energy from carbohydrate is recommended for everybody over the age of two. For young children fat restriction may reduce their ability to obtain enough energy in the diet. Although a high carbohydrate diet is also appropriate for the elderly in general, this may need to be individualised because of concomitant medical or dental conditions or medication use.

Carbohydrates and energy balance It was recommended that energy balance should be maintained with a diet containing 55% of total energy from carbohydrate. How is energy balance promoted with a high carbohydrate diet? There is much evidence that a high carbohydrate diet promotes weight maintenance. In a study of healthy subjects who lived in a metabolic chamber for seven days, by the end of the period on a diet with 60% of energy from fat they had consumed over 16 700kJ (4000 cal) more energy than they had expended. Even on a typical Western diet containing 40% of energy from fat and 47% from carbohydrate, they were still in positive energy balance when given free access to foods. However, when their fat intake was reduced to 20% of total energy and carbohydrate intake increased to 67% of energy, they actually came into negative energy balance, consuming less than they expended (2) (Figure 1). This is probably because a high carbohydrate diet is very bulky and is difficult to overeat. Why then are high carbohydrate diets so unpopular? Why do the books promoting low carbohydrate diets become best-sellers (3)? It is because over the first few days of a high carbohydrate diet people actually gain weight so the diet does not appear to work. But this is because people are storing more muscle glycogen and body water is accumulating. If they persist with these diets then weight loss will indeed occur. Figure 1. Effect of varying proportions of dietary carbohydrate and fat on energy balance in human subjects (2)

Energy Balance (Kcal)

Abstract Carbohydrates are the single most important source of food energy in the world and have significant additional health influences. In April 1997, the Food and Agriculture Organization of the United Nations and the World Health Organization convened an expert consultation on carbohydrates in human nutrition in Rome that involved scientists from 13 countries. The consultation considered all aspects of carbohydrate nutrition and interpreted the current science on the health impact of dietary carbohydrates, especially where controversy existed. The ultimate aim was to promote a nutritious and safe food supply globally. Progress in carbohydrate chemistry and our growing understanding of the diverse physiological roles of carbohydrates in recent decades has led to new dietary approaches in which carbohydrates play a key role. Diet is one of the major risk factors in many modern diseases and dietary carbohydrates can beneficially influence obesity, type 2 diabetes, coronary heart disease and some cancers. The expert consultation released 22 recommendations to be passed to member countries to assist them to develop their own dietary guidelines. This paper focuses on the findings and recommendations related to the role of carbohydrates in the maintenance of health, including recommendations on the minimum content of carbohydrate in the diet, the most appropriate sources, the role of carbohydrates in body weight and endurance exercise, the practical applications of the glycaemic index and implications of carbohydrates for diabetes, cancer and cardiovascular disease. (Aust J Nutr Diet 2001;58 Suppl 1:S3–S8)

27:13:60

4000 3000

Carb:Pro:Fat (%energy)

2000

47:13:40

1000 0

67:13:20 -1000 0

1

2

3

4

5

6

7

Days on Diet

Department of Nutritional Sciences, University of Toronto, Canada T. Wolever, DM, PhD, Professor of Nutritional Sciences and Medicine Correspondence: T. Wolever, Department of Nutritional Sciences, University of Toronto, Toronto, Ontaria, Canada M5S. Email: [email protected]

Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1

S3

Carbohydrates and physical activity The benefits of high carbohydrate intakes for physical activity have been known for a long time. In classic studies, Bergstrom et al. measured the time to exhaustion for cycling when subjects were fed three different kinds of diets (4). On a high carbohydrate diet the subjects cycled for three times longer than when they were on a high fat diet. This was related directly to the level of muscle glycogen that was accumulated before the exercise began. After exercise they had depleted their muscle glycogen to an equivalent extent on each diet.

Importance of dietary fibre A high carbohydrate diet is recommended, but does it matter what kinds of foods are consumed? The FAO/WHO recommended that the bulk of carbohydrates consumed should be rich in non-starch polysaccharides or dietary fibre and have a low glycaemic index. Recent research shows that dietary fibre can have a potentially positive effect in helping to maintain weight. Studies from Ludwig et al. of prospective ten-year weight gain in young adults found that fat intake did not affect weight gain. However, there was less weight gain for those with a higher fibre intake (5) (Figure 2). This suggests that having a high intake of dietary fibre may be an important way of helping to maintain a healthy body weight.

Glycaemic index The glycaemic index (GI) was one of the new aspects which was brought into the FAO/WHO recommendations. The GI is defined as the blood glucose response of a 50 g carbohydrate portion of food, expressed as a percentage for the same amount of carbohydrate from a reference food taken by the same subject (6). Both bread and glucose have been used as the reference food but, for international standardisation, it is recommended that GI values should be expressed relative to glucose. There is a large range of blood glucose responses to foods for the same amount of carbohydrate, both within and between various food groups (7). Very importantly, these differences in blood glucose response are reflected in similar differences in plasma insulin response (8). Foods with low blood glucose and insulin responses tend to be digested and absorbed slowly (9,10). Thus, the consultation recommended that for healthy food choices both Figure 2. Associations of dietary fibre and fat with ten-year weight gain in young adults (5)(a)

10-Year W eight Gain (lb)

White men and women (n=1602) Tertiles of Fiber Intake 9.0g/1000Kcal

30

Black men and women (n=1307) 30

20

20

10

10

0

39.1

0

39.1

the chemical composition and the physiological effects of food carbohydrate should be considered, because food composition alone does not predict what the physiological effects will be.

Effects of mixed meals on glucose and insulin responses It is often considered that fat and protein have a major effect on blood glucose and insulin responses. However, we proposed that variation in source and amount of carbohydrate was the primary determinant of blood glucose and insulin responses after normal mixed meals. To test this we fed healthy subjects test meals containing zero to 100 g carbohydrate from each of four single foods varying in GI so as to derive equations to predict glucose and insulin responses based on the amount and GI of the carbohydrate consumed (11). We then fed a different group of healthy subjects five mixed meals that were unmatched to each other with respect to their contents of energy [1670–2500 kj (400–600 kcal)], carbohydrate (38–104 g), protein (12–25 g), fat (8–24 g) and GI (43–99). If fat and protein were important in determining glucose and insulin responses, we would have expected that our equations based on carbohydrate alone would not be very accurate. However, we found that the predictions based on carbohydrate alone explained over 90% of the variation of the glucose and the insulin responses of the mixed meals (12). The large differences in protein and fat content of the mixed meals had negligible effects on glucose and insulin responses.

Glycaemic index and physical activity The kind of carbohydrate one eats also has relevance to physical activity. Studies done by Brand-Miller et al. demonstrate that if one has a snack of a low GI carbohydrate before exercise, then the endurance achieved is significantly greater than if one has a high GI carbohydrate snack (13). On the other hand, Burke et al. have shown that eating high GI foods aids recovery from strenuous activity. On a high GI diet significantly more muscle glycogen accumulated than after a low GI diet (14). So both high and low GI foods may be useful for athletes for various situations.

Regional variation in glycaemic index The FAO/WHO recommended that the published glycaemic response data should be supplemented with tests of local foods normally prepared because of possible effects of food variety in cooking. For example, the ripeness of banana is very important. If a banana is under-ripe (slightly green at the tips) compared to one that is slightly over-ripe (yellow with a few brown spots), this makes a 50% difference in the blood glucose response (15). These are very subtle differences in ripeness. Another important example is potato. Brand Miller and colleagues tested several varieties of potatoes in Australia and have found that, regardless of how they are cooked, potatoes have a very high GI (16). We have found different results in tests on Canadian potatoes which tended to have intermediate GI values (17). We recently exchanged foods with Dr Brand Miller’s unit and when

Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1

we both tested exactly the same foods we obtained virtually identical results. This suggests that there are real differences in GI between Australian and Canadian potatoes.

Clinical use of glycaemic index The FAO/WHO recommended that the GI should be employed as a useful indicator of the impact of foods on blood glucose. It should be used to compare foods of similar macronutrient composition within food groups and for clinical applications including diabetes and impaired glucose tolerance. There is much evidence that low GI foods improve blood glucose control in diabetes. For example, we studied overweight subjects with type 2 diabetes for six weeks and found a significant improvement in glycosylated serum proteins with a low GI diet (18). In a recent review of nine studies in the literature on the use of low GI diets in the treatment of diabetes, eight of them show a statistically significant improvement in glycated serum proteins (19). The average improvement in all nine studies, 10%, is of similar magnitude to that achieved in the United Kingdom prospective diabetes study with oral hypoglycaemic agents or insulin (20).

Carbohydrates and insulin sensitivity Many diseases, such as obesity, heart disease and diabetes, are thought to be related to insulin sensitivity (21) (Figure 3). Insulin sensitivity is a concept that describes how sensitive the body is to the effects of insulin on whole body glucose uptake. An insulin-sensitive person needs a very small amount of insulin to dispose of glucose at a normal rate. An insulin-resistant person needs much more insulin to achieve a normal rate of glucose disposal. In some way we do not understand, the body senses that an individual is insulin-resistant and compensates by secreting a large amount of insulin. People that are insulinresistant with normal glucose levels have high blood insulin (22). Insulin resistance is partly due to genes, and is strongly inherited (23). However, insulin sensitivity also is affected by environmental factors. Physical activity promotes insulin sensitivity (24) and obesity promotes insulin resistance (25). There is now a view that the high blood insulin concentration related to insulin resistance might actually cause obesity because the high insulin levels may alter fat cell metabolism or the morphology of fat cells in some way. Hyperinsulinaemia may enhance the insulin resistance by down-regulating insulin receptors. This results in a vicious cycle whereby insulin resistance causes a high plasma insulin concentration which, in turn, promotes more insulin resistance (26). Insulin resistance is associated with heart disease because high blood insulin and insulin resistance lead to an increased rate of synthesis of very low density lipoproteins (VLDL) in the liver and a low rate of VLDL clearance from the blood (27). This, in turn, leads to the atherogenic blood lipid profile characterised by increased plasma triglyceride and low high density lipoprotein (HDL) cholesterol concentrations (28). These lipid abnormalities also raise plasma free fatty acids (29),

which not only feed-back and make insulin resistance worse (30) but also impair β-cell function (31). Insulin resistance is associated with the development of type 2 diabetes because, in the presence of insulin resistance, blood glucose can be maintained within the normal range only if the pancreatic β-cells can secrete large amounts of insulin. If the β-cells begin to fail, and are unable to maintain such high rates of insulin secretion, then blood glucose begins to rise, leading to type 2 diabetes (32). Dietary carbohydrates can affect this process in a number of ways. Although a high carbohydrate, low fat diet results in higher postprandial insulin responses, it is also associated with reduced postprandial plasma free fatty acids (33,34). The reduction in free fatty acids may help to improve insulin sensitivity and restore β-cell function. Use of low GI carbohydrates may have the added benefit of putting less strain on the pancreas because less insulin is required for their metabolism.

Sugars The FAO/WHO consultation concluded that there was no evidence that sugars or starch are involved in lifestylerelated disorders, but that intakes of carbohydrates and sugars in excess of energy requirements should be avoided. Data from Scotland show that people who eat the largest amount of sugar have the lowest prevalence of obesity. This is exactly opposite to what most people believe and in fact, in this study, high fat intakes were related to obesity (35). Some people believe that sugar causes a special increase in insulin, but this is not true. We fed zero to 100 g doses of glucose, sucrose and fructose to healthy subjects and compared the resulting glucose and insulin responses to the same doses of starch from bread. In all cases the plasma insulin responses were directly proportional to the glucose responses elicited by the test meals. There was no additional secretion of insulin after the sugars in comparison to the starch (36). Another point is that sucrose (sugar) actually tends to produce lower glucose and insulin responses than an equal amount of carbohydrate from bread and many other refined starchy foods. Figure 3. Relationship between lifestyle factors (diet and exercise), obesity, insulin resistance, pancreatic βcell function, type 2 diabetes and atherosclerosis(a) ATHEROSCLEROSIS

! Plasma TG, " HDL Liver: ! VLDL synthesis Adipose: " VLDL clearance

Hyperinsulinaemia OBESITY Insulin Resistance Physical Inactivity

Diet

Plasma FFA

Hyperglycaemia

Beta-cell Function

Beta-cell Stimulation

Beta-cell Exhaustion Reduced Insulin Secretion TYPE 2 DIABETES

(a) TG, triglycerides; HDL, high density lipoprotein; VLDL, very low density lipoprotein; FFA, free fatty acids.

Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1

S5

This is counter-intuitive to many health professionals and people with diabetes who have been taught the opposite for so many years. However, it has been shown in normal (37) and diabetic (17) subjects that sugar-sweetened cereal produces a significantly lower blood glucose response than a cereal that is not sugar-sweetened. This does not mean that people with diabetes should eat an unlimited amount of sugar; but there is no need for undue avoidance of sugar. Sugar probably has a role in helping to make healthy foods more palatable and thus promoting their consumption.

Carbohydrates and cancer In terms of the role of carbohydrates for cancer, the data are not as strong as other areas. However colon and rectal cancer and breast and prostate cancers tend to be associated with high intakes of meat, protein and, to a lesser extent, fat. Low risk for these cancers is associated with high intakes of fruit and vegetables and, to a lesser extent, cereals. Butyrate produced by colonic bacterial fermentation of unabsorbed carbohydrates has a number of potential benefits for cancer prevention including increased cell differentiation and increased apoptosis or death of damaged cells. In established tumours, butyrate reduces cell proliferation rates. It is of interest, then, that starch fermentation yields a higher proportion of butyrate than the fermentation of dietary fibre. Finally, many carbohydrate foods are rich in phytochemicals and antioxidants that may have beneficial effects.

Carbohydrates and cardiovascular disease There is some controversy about the role of carbohydrates for cardiovascular disease. Few would argue with the contention that if we could reduce obesity this might help to reduce cardiovascular disease. It also is well established that a high carbohydrate diet lowers low density lipoprotein cholesterol by displacing saturated fat and that certain types of soluble fibre may lower serum cholesterol. Blood pressure is lowered by high intakes of vegetable and fruit, probably because of their high potassium and low sodium content. What is more controversial is the effect of carbohydrates on blood triglycerides and HDL-cholesterol. A number of studies, such as those from Reaven et al., have shown that high carbohydrate diets are associated with increased triglycerides, VLDL triglycerides and reduced HDL-cholesterol (38). This did not dissuade the FAO/WHO consultation from recommending a high carbohydrate diet for a number of reasons. Firstly, these were quite short-term studies—the longest ones being only about six weeks long. There is some evidence that the rise in triglycerides is only temporary and returns toward baseline after many months on the diet (39). Secondly, the rise in triglycerides and reduction in HDL does not occur with all kinds of carbohydrates. High carbohydrate diets with high fibre intakes or low GI foods will partly or completely mitigate these deleterious effects (40). Finally, studies showing the deleterious effects of high carbohydrate diets are designed with the subjects on both diets being forced to eat exactly the same amount of energy. However, it is known that people tend to eat a little less energy when on high carbohydrate diets. The S6

point is made very well by a study from Schaefer et al. which showed that when people on high carbohydrate diets were forced to maintain weight, their blood lipids deteriorated. But when they followed an ad libitum high carbohydrate diet, their weight fell and there was no deterioration of the blood lipids (41).

Carbohydrates and diabetes Diabetes is a very important condition which is reaching worldwide epidemic proportions. In virtually every country of the world, it is estimated that within 25 years the number of people with diabetes will nearly double (42). In developed countries this increase in diabetes largely will take place in people over the age of 65 years, reflecting our aging population and the fact that diabetes is more prevalent in the older age groups. The tragedy, however, is that in developing countries the increase largely will occur in middle-aged subjects at the peak of their productive lives. This is likely due to the increased Westernisation and rising rates of obesity in these countries. So the FAO/WHO consultation recommended that populations in transition from traditional diets to diets more like those in developed countries should be provided with dietary recommendations to ensure nutritional adequacy and an appropriate balance of micronutrients. What kind of a diet should be recommended for populations at high risk for diabetes? One school of thought is that a high carbohydrate diet should not be used by people with insulin resistance because it is associated with an increase in plasma insulin which not only has deleterious effects on blood lipids and cardiovascular risk, but also may make insulin sensitivity worse. Again, the FAO/WHO was not persuaded by this argument because it is known from other studies that high carbohydrate diets are associated with improvements in fasting blood glucose and improvements in oral glucose tolerance, measures that are used to define diabetes. A high carbohydrate diet is also associated with lower plasma insulin response to a standard carbohydrate challenge (43). Indeed, it is not just the amount of total carbohydrate that is important, but also its quality, including the amount of dietary fibre and its GI. Data from the nurses health (44) and health professionals (45) studies, conducted at Harvard University, show that the amount of total carbohydrate in the diet was not related to the risk of developing diabetes in either men or women (Figure 4). However, in an almost identical fashion, higher fibre intakes were associated with reduced risk of diabetes and a high GI diet with increased risk of diabetes. This protective effect of low GI diets potentially could be due to improved insulin sensitivity.There is at least one study showing that there was an improvement in insulin sensitivity when women with a family history of cardiovascular disease ate a low GI diet (46). Thus, in considering the role of carbohydrates on the risk of developing diabetes, it is possible to speculate that a high carbohydrate diet may be beneficial by improving β-cell function, perhaps by reducing plasma free fatty acids, and that high fibre, low GI foods may be beneficial by improving insulin sensitivity.

Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1

Figure 4. Association of total carbohydrate and dietary fibre intakes and diet glycaemic index (GI) with risk of developing diabetes in males (45) and females (44)

Total Carbohydrate Men - ns Women - ns

1.5 Relative Risk

Cereal Fibre

Glycaemic Index

Men - p=0.007 Women - p=0.001

Men - p=0.03 Women - p=0.005

1.0

0.5

0.0

1

2

3

4

5

1

2

3

4

5

1

2

3

4

5

Quintiles of Intake (adjusted for energy; GI also adjusted for cereal fibre)

Environmental impact of human diets

9.

The health of the individual ultimately is related to the health of the environment. The world population has increased rapidly from about one billion after the end of World War II, to about four billion now, and estimated to reach six billion in the next 25 years. This increase in population, if not caused by, has certainly been sustained by, the increased availability of carbohydrate foods as a result of the green revolution. Some argue that the human diet should be low in carbohydrate and high in protein, similar to that consumed by our hunter-gatherer ancestors. However, a hunter-gatherer diet is expensive both from the economic and ecological points of view; it sustained a world population of only a few hundred million human beings. We now have ten times as many mouths to feed, and perhaps the only sustainable way to do so is with carbohydrate foods. Therefore we must strive to ensure the best quality of carbohydrates for human health.

Jenkins DJA, Ghafari H, Wolever TMS, Taylor RH, Barker HM, Fielden H, et al. Relationship between the rate of digestion of foods and postprandial glycaemia. Diabetologia 1982;22:450–5.

10. Wolever TMS, Jenkins DJA, Collier GR, Lee R, Wong GS, Josse RG. Metabolic response to test meals containing different carbohydrate foods: 1. Relationship between rate of digestion and plasma insulin response. Nutr Res 1988;8:573–81. 11. Wolever TMS, Bolognesi C. Source and amount of carbohydrate affect postprandial glucose and insulin in normal subjects. J Nutr 1996;126:2798–806. 12. Wolever TMS, 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;126:2807–12. 13. Thomas DE, Brotherhood JR, Brand JC. Carbohydrate feeding before exercise: effect of glycemic index. Int J Sports Med 1991;12:180–6. 14. 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. 15. Wolever TMS, Jenkins DJA, Jenkins AL, Vuksan V, Wong GS, Josse RG. Effect of ripeness on the glycaemic response to banana. J Clin Nutr Gastroenterol 1988;3:85–8.

References 1.

FAO/WHO. Carbohydrates in human nutrition: report of a joint FAO/WHO expert consultation, Rome, 14–18 April 1997. FAO Food and Nutrition Paper 66. Rome: FAO; 1998.

16. Soh NL, Brand Miller J. The glycaemic index of potatoes: the effect of variety, cooking method and maturity. Eur J Clin Nutr 1999;53:249–54.

2.

Stubbs RJ, Harbron CG, Murgatroyd PR, Prentice AM. Covert manipulation of dietary fat and energy density: effect on substrate flux and food intake in men eating ad libitum. Am J Clin Nutr 1995;62:316–29.

17. Wolever TMS, Katzman-Relle L, Jenkins AL, Vuksan V, Josse RG, Jenkins DJA. Glycaemic index of 102 complex carbohydrate foods in patients with diabetes. Nutr Res 1994;14:651–69.

3.

Atkins RC. Dr Atkins’ new diet revolution. New York: Harper Collins; 1998.

4.

Bergstrom J, Hermansen L, Hultman E, Saltin B. Diet, muscle glycogen and physical performance. Acta Physiol Scand 1967;71:140–50.

5.

Ludwig DS, Pereira MA, Kroenke CH, Hilner JE, Van Horn L, Slattery ML, et al. Dietary fiber, weight gain, and cardiovascular disease risk factors in young adults. JAMA 1999;282:1539–46.

6.

Wolever TMS, Jenkins DJA, Jenkins AL, Josse RG. The glycemic index: methodology and clinical implications. Am J Clin Nutr 1991;54:846–54.

7.

Foster-Powell K, Brand Miller J. International tables of glycemic index. Am J Clin Nutr 1995;62:871S–93S.

8.

Holt SHA, Brand Miller JC, Petocz P. Interrelationships among postprandial satiety, glucose and insulin responses and changes in subsequent food intake. Eur J Clin Nutr 1996;50:788–97.

18. 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;15:562–6. 19. Wolever TMS. The glycemic index: flogging a dead horse? Diabetes Care 1997;20:452–6. 20. UK Prospective Diabetes Study Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998;352:827–53. 21. DeFronzo RA, Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia and atherosclerotic cardiovascular disease. Diabetes Care 1991;14:173–94. 22. Kahn SE, Prigeon RL, McCulloch DK, Boyko EJ, Bergmen RN, Schwartz MW, et al. Quantification of the relationship between insulin sensitivity and ß-cell function in human subjects: evidence for a hyperbolic function. Diabetes 1993;42:1663–72. 23. Martin BC, Warram JH, Krolewski AS, Bergman RN, Soeldner JS, Kahn CR. Role of glucose and insulin resistance in development of

Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1

S7

type 2 diabetes mellitus: results of a 25-year follow-up study. Lancet 1992;340:925–9.

saturated fat in the long-term dietary management of type 2 diabetes. Am J Clin Nutr 2000;72:439–49.

24. Henriksson J. Influence of exercise on insulin sensitivity. J Cardiovasc Risk 1995;2:303–9.

35. Hill JO, Prentice AM. Sugar and body weight regulation. Am J Clin Nutr 1995;62 Suppl 1:264S–74S.

25. Su HY, Sheu WH, Chin HM, Jeng CY, Chen YD, Reaven GM. Effect of weight loss on blood pressure and insulin resistance in normotensive and hypertensive obese individuals. Am J Hypertens 1995;8:1067–71.

36. Lee BM, Wolever TMS. Effect of glucose, sucrose and fructose on plasma glucose and insulin responses in normal humans: comparison with white bread. Eur J Clin Nutr 1998;52:924–8.

26. Del Prato S, Leonitti F, Simonson DC, Sheehan P, Matsuda M, DeFronzo RA. Effect of sustained physiologic hyperinsulinaemia and hyperglycaemic on insulin secretion and insulin sensitivity in man. Diabetologia 1994;37:1025–35. 27. Maheux P, Azhar S, Kern PA, Chen YD, Reaven GM. Relationship between insulin-mediated glucose disposal and regulation of plasma and adipose tissue lipoprotein lipase. Diabetologia. 1997;40:850–8. 28. Haffner SM, D’Agostino R Jr, Mykkanen L, Tracy R, Howard B, Rewers M, et al. Insulin sensitivity in subjects with type 2 diabetes. Relationship to cardiovascular risk factors: the insulin resistance atherosclerosis study. Diabetes Care 1999;22:562–8. 29. Laws A, Hoen HM, Selby JV, Saad MF, Haffner SM, Howard BV. Differences in insulin suppression of free fatty acid levels by gender and glucose tolerance status. Relation to plasma triglyceride and apolipoprotein B concentrations. Insulin resistance atherosclerosis study (IRAS) investigators. Arterioscler Thromb Vasc Biol 1997;17:64–71. 30. Boden G, Chen X, Ruiz J, White JV, Rossetti L. Mechanisms of fatty acid-induced inhibition of glucose uptake. J Clin Invest 1994;93:2438–46. 31. Zhou Y-P, Grill VE. Long-term exposure of rat pancreatic islets to fatty acids inhibits glucose-induced insulin secretion and biosynthesis through a glucose fatty acid cycle. J Clin Invest 1994;93:870–6. 32. DeFronzo RA. Lilly Lecture 1987: the triumvirate: ß-cell, muscle, liver: a collusion responsible for NIDDM. Diabetes 1987;37:667–87. 33. Wolever TMS, Bentum-Williams A, Jenkins DJA. Physiologic modulation of plasma FFA concentrations by diet: metabolic implications in non-diabetic subjects. Diabetes Care 1995;18:962–70. 34. Tsihlias EB, Gibbs AL, McBurney MI, Wolever TMS. Comparison of high- and low-glycemic index breakfast cereals versus monoun-

S8

37. Brand Miller JC, Lobbezoo I. Replacing starch with sucrose in a high glycaemic index breakfast cereal lowers glycaemic and insulin responses. Eur J Clin Nutr 1994;48:749–52. 38. Jeppesen J, Schaaf P, Jones C, Zhou M-Y, Chen I, Reaven GM. Effects of low-fat, high carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women. Am J Clin Nutr 1997;65:1027–33. 39. Antonis A, Bersohn I. The influence of diet on serum-triglycerides in South African White and Bantu prisoners. Lancet 1961;i:3–9. 40. Wolever TMS, Jenkins DJA. Effect of dietary fiber and foods on carbohydrate metabolism. In: Spiller GA, editor. CRC handbook of dietary fiber in human nutrition. 2nd Edition. Boca Raton, Florida: CRC Press; 1993. p. 111–52. 41. Schaefer EJ, Lichtenstein AH, Lamon-Fava S, McNamara JR, Schaefer MM, Rasmussen H, et al. Body weight and low-density lipoprotein cholesterol changes after consumption of a low-fat ad libitum diet. JAMA 1995;274:1450–5. 42. King H, Aubert RE, Herman WH. Global burden of diabetes, 1995–2025. Prevalence, numerical estimates, and projections. Diabetes Care 1998;21:1414–31. 43. Swinburn BA, Boyce VL, Bergman RN, Howard BV, Bogardus C. Deterioration in carbohydrate metabolism and lipoprotein changes induced by modern, high fat diet in Pima Indians and Caucasians. J Clin Endocrinol Metab 1991;73:156–65. 44. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC. Dietary fiber, glycemic load, and risk of non-insulindependent diabetes mellitus in women. JAMA 1997; 277:472–7. 45. Salmeron J, Ascherio A, Rimm EB, Colditz GA, Spiegelman D, Jenkins DJ, et al. Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care 1997;20:545–50. 46. Frost G, Leeds A, Trew G, Margara R, Dornhorst A. Insulin sensitivity in women at risk of coronary heart disease and the effect of a low glycemic diet. Metabolism 1998;47:1245–51.

Australian Journal of Nutrition and Dietetics (2001) 58 Suppl 1

Suggest Documents