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Diet can significantly affect insulin sensitivity and the risk of type 2

Apr 23, 2002

Diet can significantly affect insulin sensitivity and the risk of type 2 diabetes and CHD.44, 45

A high intake of rapidly absorbed carbohydrates can induce rapid postprandial glucose and insulin responses, leading to features of the metabolic syndrome or syndrome X—insulin resistance, hyperinsulinemia, and a characteristic dyslipidemia featuring high triglycerides and low HDL concentrations. 10, 46-48

The glycemic index (GI) is a measure of how quickly the rise in blood glucose occurs after eating a fixed amount of a particular source of carbohydrates 49 . The glycemic load takes into account the glycemic index as well as total amount of dietary carbohydrate, and it is a predictor of type 2 diabetes independent of total calories. 50, 51 Prospective studies of the glycemic load predicted who would develop type 2 diabetes after six years of follow-up. Those who ate a diet with higher glycemic load were at least 2 ½ times more likely to develop diabetes than those who ate a diet lower in glycemic load. 50, 51 These studies support the premise that diets with a high glycemic index or load predispose to hyperinsulinemia and type 2 diabetes. A similar large, prospective study shows that dietary glycemic load is directly associated with risk of CHD after adjustment for age, smoking status, total energy intake, and other coronary disease risk factors. 15 This is supported by two large studies in the US and Great Britain demonstrating that a low dietary glycemic index and glycemic load are associated with a higher HDL concentration. 10, 52 In a study of 244 apparently healthy, middle-aged women, a high dietary glycemic load was directly related to plasma concentrations of hs-CRP, independent of BMI, total energy intake, and other known risk factors of CHD. 53 While not proof of cause and effect, the data suggest that eating too many rapidly absorbed carbohydrates, i.e., a high glycemic load may worsen a proinflammatory state increasing the risk of CHD and diabetes, especially in overweight women, who are prone to insulin resistance.

A recent crossover study allocated 11 healthy men to 5 weeks of a low—or high—glycemic index (LGI or HGI) diet. The diets were essentially equal in total amount of carbohydrates, protein, fat, and total calories. The only difference was whether the carbohydrates were LGI or HGI. Five weeks on the LGI diet led to significant decreases in total body fat and a tendency to increase lean body mass or muscle without changing overall body weight, i.e., they lost fat and gained muscle. In addition, the LGI diet resulted in lower postprandial plasma glucose and insulin profiles and areas under the curve, and a lower plasma triacylglycerol excursion after lunch. The decreased total fat mass of approximately 700 g was associated with decreased plasma leptin as well as a decrease in lipoprotein lipase, and hormone sensitive lipase mRNA found in abdominal subcutaneous adipose tissue. 54 This supports the importance of glycemic index in selecting foods, and also demonstrates that although you can be eating the same numbers of calories, the types of foods providing those calories can make a tremendous difference in body composition and metabolism.

Although current American Diabetes Association recommendations allow for individual flexibility (specifically they suggest carbohydrate and monounsaturated fat should provide 60-70 percent of energy), 44, 55 the most commonly recommended diets are based on previous ADA guidelines and advocate at least 50 to 60 percent of calories as carbohydrates. 56 It is difficult to follow the logic in recommending a diet high in carbohydrates for a disease characterized by the inability to normally metabolize them.

The GI concept is supported and emphasized by the recent recommendations by the joint Food and Agriculture Organization (FAO/ World Health Organization Expert Consultation 57 as well as the European Association for the Study of Diabetes, 58 the Canadian Diabetes Association, 59 and Australian and New Zealand guidelines. 60 On the other hand, there is a lack of international consensus held up by the American Diabetes Association’s (ADA) refusal to recognize the importance of the glycemic index (GI) preferring that “first priority should be given to the total amount of carbohydrate consumed rather than the source of carbohydrate.” 61 In defending their position, the ADA’s committee cites studies showing that the single nutrient sucrose produces a similar GI to that of the starches bread, rice, and potatoes, and “moreover, fruits and milk consistently are reported to have lower glycemic responses than many starches.” 61 These findings are very much consistent with the more recent studies described above. Foods rich in soluble fiber and fructose, e.g., most fruits and vegetables, tend to have a lower glycemic index while starches and grains produce a higher insulin response and have a higher GI. Sucrose or table sugar is made up of fructose and glucose while white bread, potatoes, and other starches are almost entirely composed of glucose molecules strung together and once ingested quickly raise blood glucose levels.

The 2002 ADA expert consensus recommends that “sucrose and sucrose-containing foods should be eaten in the context of a healthy diet…As sucrose does not increase glycemia to a greater extent than isocaloric amounts of starch, sucrose and sucrose-containing foods do not need to be restricted…they should be substituted for other carbohydrate sources or, if added, covered with insulin or other glucose-lowering medication.” 44 In long-term care settings “it may often be preferable to make medication changes to control blood glucose than to implement food restrictions.” 55

To its credit the ADA now admits that “it is clear that carbohydrates do have differing glycemic responses,” 44, 55 and conclude that “although the use of low-glycemic index foods may reduce postprandial hyperglycemia, there is not sufficient evidence …to recommend general use of low-glycemic index diets in type 2 diabetes patients.” 55 Is there convincing evidence to suggest not encouraging low GI diets? The ADA encourages the use of fiber 44, 55 and recognizes the drug Acarbose which is designed to slow carbohydrate absorption which, in effect, lowers the glycemic index. 62, 63

The most recent ADA committee report (without negative criticism) details several studies supporting the benefits of lowering glycemic index and glycemic load. They readily acknowledge that “although studies in type 2 diabetes subjects have not consistently reported a relation between glycemic index and insulin levels, studies in other populations have reported an association between either lower glycemic index diets or lower glycemic loads with lipids, in particular HDL cholesterol, and insulin levels.”. 55 While some of these studies included patients with, or at risk for, CHD, perhaps it is best to consider type 2 diabetes as part of the ubiquitous metabolic/insulin resistance syndrome or syndrome X with generalized endothelial dysfunction, and not a uniquely isolated disease to which other logical principles do not apply.

In his recent review of the glycemic index, Ludwig points out that since 1988, 13 interventional studies have examined the possibility that a low-GI diet may improve management of diabetes. 64 Twelve studies found improvement in at least one measure of glycemic control with the low-vs high-GI diets, one study found no difference between diets, and none found improvement with the high—vs low—GI diet.

Jarvi et al, in a randomized crossover study of patients with type 2 diabetes, compared pre-weighed diets with different GIs during two consecutive 24-day periods 7 . The macronutrient composition (both were 55:16:28) and type and amount of dietary fiber were identical and throughout the study the patients were free living. The diets differed only in GI, which was modest (91 and 75). After 24 days plasminogen activator inhibitor-1 (PAI-1) activity was normalized on the low-GI diet, (-54%, P < 0.001), indicating an improved capacity for fibrinolysis, but remained unchanged on the high-GI diet. Both blood glucose and plasma insulin concentrations were lowered by 30 percent on the low-GI diet, and the extent of the total reduction of serum LDL-C was comparable to simvastatin and pravastatin (a decrease of 29%, p<0.001). HDL decreased slightly but similarly in both groups. The study shows that a diet characterized by low-GI foods lowers the glucose and insulin responses throughout the day and improves lipid profile and capacity for fibrinolysis, suggesting a therapeutic potential in diabetes.

A recent study compared a low glycemic diet to the American Heart Association (AHA) phase I diet in overweight but otherwise healthy men. Under ad libitum conditions, the AHA diet led to higher insulin levels, increased hunger, 25 percent greater total caloric consumption, and worsening of the cholesterol profiles, i.e., a 28% rise in TGs and a 10 percent lowering of HDL consistent with an increased risk for CHD. 65 In contrast, the low-glycemic diet (40% carbohydrates:30%protein: 30% fat) consumed ad libitum resulted in a spontaneous 25 % decrease (P<0.001) in total energy intake. As opposed to the AHA diet, the low-glycemic index-low-fat-high-protein diet produced a substantial decrease (-35 %) in plasma triglyceride levels, a significant increase (+1.6 %) in LDL peak particle diameter, and marked decreases in plasma insulin levels measured either in the fasting state, over daytime and following a 75 g oral glucose load. During a pair-fed session, in which subjects were exposed to a diet with the same macronutrient composition as the AHA diet but restricted to the same energy intake as during the low-GI diet, there was a trend for a decrease in plasma HDL-cholesterol levels which contributed to a significant increase in cholesterol:HDL-cholesterol ratio, and, again, subjects were hungry.

In a triple, crossover study of overweight teenage boys, Ludwig et al 66 found that a high GI meal compared to medium or low GI meals resulted in greater total plasma glucose response, higher serum insulin and lower plasma glucagon levels, a fall in blood glucose from baseline during the post-absorptive phase, and suppression of free fatty acids at 3.5 hours. In addition, voluntary food intake was greater after the high GI versus medium or low GI meals.

The investigators concluded that the rapid absorption of glucose following a high GI meal induces a sequence of hormonal and metabolic changes that may promote hunger, excessive food intake, and obesity. U.S. consumption of high GI carbohydrates has steadily increased especially in the form of highly processed low-fat foods. This has paralleled the epidemic rise in diabetes in the Western world.

Eric S. Freedland, MD graduated from University of Rochester School of Medicine in 1982, trained in internal medicine at Mt. Auburn Hospital in Cambridge, MA, and emergency medicine at Harbor-UCLA Medical Center in Torrance, CA, and has held faculty positions at Harvard Medical School (1990-1991) and Boston University School of Medicine (1992-1997). Dr. Freedland has developed a nutrition-centered model of disease with a special emphasis on diabetes. A staunch advocate for prescribing lifestyle changes before drugs, Dr. Freedland has written and lectured extensively on this subject.


43. Ruderman N, Chisholm D, Pi-Sunyer X, Schneider S. The metabolically obese, normal-weight individual revisited. Diabetes 1998; 47:699-713.

44. Association AD. Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications. Diabetes Care 2002; 25 Suppl 1:S50-63.

45. Krauss RM, Deckelbaum RJ, Ernst N, et al. Dietary guidelines for healthy American adults. A statement for health professionals from the Nutrition Committee, American Heart Association. Circulation 1996; 94:1795-800.

46. Miller JC. Importance of glycemic index in diabetes. Am J Clin Nutr 1994; 59:747S-752S.

47. Wolever TM, Jenkins DJ, Jenkins AL, Josse RG. The glycemic index: methodology and clinical implications. Am J Clin Nutr 1991; 54:846-54.

48. Jenkins DJ, Wolever TM, Collier GR, et al. Metabolic effects of a low-glycemic-index diet. Am J Clin Nutr 1987; 46:968-75.

49. Jenkins D, Wolever T, Talylor R, et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981; 34:362-366.

50. Salmeron JM, JoAnn; Stampfer, Meir; Colditz, Graham; Wing, Alvin; Willett, Walter. Dietary Fiber, Glycemic Load, and Risk of Non-insulin-dependent Diabetes Mellitus in Women. JAMA 1997; 277:472-477.

51. Salmeron JA, Alberto; Rimm, Eric; Colditz, Graham; Jenkins, David; Stampfer, Meir; Wing, Alvin; Willett, Walter. Dietary Fiber, Glycemic Load, and Risk of NIDDM in Men. Diabetes Care 1997; 20:545-549.

52. Frost G, Leeds AA, Dore CJ, Madeiros S, Brading S, Dornhorst A. Glycaemic index as a determinant of serum HDL-cholesterol concentration [see comments]. Lancet 1999; 353:1045-8.

53. Liu S, Manson JE, Buring JE, Stampfer MJ, Willett WC, Ridker PM. Relation between a diet with a high glycemic load and plasma concentrations of high-sensitivity C-reactive protein in middle-aged women. Am J Clin Nutr 2002; 75:492-8.

54. Bouche C, Rizkalla SW, Luo J, et al. Five-week, low-glycemic index diet decreases total fat mass and improves plasma lipid profile in moderately overweight nondiabetic men. Diabetes Care 2002; 25:822-8.

55. Franz MJ, Bantle JP, Beebe CA, et al. Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications. Diabetes Care 2002; 25:148-198.

56. Association AD. Nutritional recommendations and principles for individuals with diabetes mellitus. Diabetes Care 1987; 10:126-32.

57. Consultation CiHNroaJFWHOE. FAO Food Nutr Pap 1998; 66:1-140.

58. mellitus DaNSGotEAftSoDRftnmopwd. Diabetes Nutr Metab 1995; 8:1-4.

59. Statement) CDAGftnmodmitsP. Beta Release 1989; 13:8-17.

60. Health IDIDEf. Melbourne, International Diabetes Institute 1994.

61. Association AD. Nutrition recommendations and priciples for people with diabetes mellitus. (Position Statement). Diabetes care 1996; 19:s16-s19.

62. Hanefeld M, Fischer S, Schulze J, et al. Therapeutic potentials of acarbose as first -line drug in NIDDM insufficiently treated with diet alone. Diabetes Care 1991; 14:732-37.

63. Chiasson J-L, Josse R, Hunt J, et al. The 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.

64. Ludwig DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. Jama 2002; 287:2414-23.

65. Dumesnil JG, Turgeon J, Tremblay A, et al. Effect of a low-glycaemic index–low-fat–high protein diet on the atherogenic metabolic risk profile of abdominally obese men. Br J Nutr 2001; 86:557-68.

66. Ludwig D, Majzoub J, Dallal G, Roberts S. High glycemic index foods, overeating, and obesity (abst). Obesity Research 1997; 5 (suppl 1): O98.