AJCN 19th International Congress of Nutrition
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American Journal of Clinical Nutrition, Vol. 87, No. 1, 1-2, January 2008
© 2008 American Society for Nutrition


PERSPECTIVE

A role for the glycemic index in preventing or treating diabetes?1,2

John M Miles

1 From the Division of Endocrinology, Metabolism and Nutrition, Mayo Clinic, Rochester, MN

See corresponding articles on pages 114 and 126.

2 Reprints not available. Address correspondence to JM Miles, Endocrine Research Unit, Mayo Clinic, Rochester, MN 55905. E-mail: miles.john{at}mayo.edu.

Because of dramatic increases in prevalence that are related to modernization, type 2 diabetes is now considered a high-priority public health problem in nearly every country in the world (1). Views on the role of diet in the management of diabetes have undergone an evolution over the past 30 years. For many years, a high-fat, low-carbohydrate diet was recommended (2); then, in 1979, the American Diabetes Association (ADA) issued a consensus statement suggesting that a high-carbohydrate, low-fat diet was best for most patients (3). This official position was subsequently modified to emphasize glucose and lipid control rather than weight loss; this change allowed the inclusion of more fat (primarily monounsaturated) in the diet (4). However, just as it is a topic for avid discussion in popular culture, diet remains a subject of lively debate with respect to diabetes treatment.

An aspect of the debate about diet in diabetes treatment that has received much attention since its introduction nearly 30 y ago (5) is the role of the glycemic index (GI). The GI is a system for ranking carbohydrates according to their effects on postprandial glucose concentrations. Although low-GI foods are known to produce less postprandial hyperglycemia and hyperinsulinemia than are high-GI foods (6), the role of low-GI foods in the prevention and treatment of diabetes remains unclear. Elsewhere in this issue of the Journal, Wolever et al (7) report the results of the Canadian Trial of Carbohydrates in Diabetes (CCD). Patients with well-controlled type 2 diabetes who were treated with diet alone were randomly assigned to receive either a high-GI diet, a low-GI diet, or a low-carbohydrate, high-monounsaturated fat diet for 1 y.

The study was carefully conducted and of longer duration than many earlier trials. The investigators found no weight loss and a small increase in glycated hemoglobin (HbA1c) in all 3 groups. This increase in HbA1c is what one would expect with no intervention (8). The fact that glucose concentrations 2 h after an oral glucose challenge were significantly lower in persons who had followed the low-GI diet for 1 y than in those who followed the other 2 diets for 1 y suggests improvement in either insulin sensitivity or insulin secretion (or improvements in both). A small study in which euglycemic clamps were conducted in healthy subjects after 30 d of a low-GI or a high-GI diet actually showed greater insulin sensitivity in the subjects following the high-GI diet; this improved insulin sensitivity was associated with lower fasting and postprandial free fatty acid concentrations (9). It is possible that these differences in insulin sensitivity and free fatty acid metabolism are transient and that they disappear when the diet is followed for a longer time.

In the report of Wolever et al, there were several intriguing findings that warrant attention and, perhaps, further investigation. High-sensitivity C-reactive protein (hs-CRP) was 30% lower in the low-GI group than in the high-GI group, despite no significant weight difference between the groups. Decreases in hs-CRP are known to accompany weight loss (10). The mechanism by which hs-CRP is decreased by a low-GI diet is not understood, but it may involve less postprandial hyperglycemia or hyperinsulinemia (or both).

The CCD investigators also reported an interesting observation regarding blood pressure. Diastolic blood pressure was highest in the high-GI diet group, and the difference was greatest between the high-GI diet group and the low-carbohydrate diet group. The clinical implications of this observation are uncertain but of potential importance. Diastolic blood pressure is generally thought to be less important than systolic blood pressure with respect to cardiovascular disease risk (11), but increases in diastolic blood pressure may reflect activation of the sympathetic nervous system (12). Although no significant differences in fasting insulin concentrations were observed in the CCD study, it is likely that the subjects following the high-GI diet had greater postprandial hyperinsulinemia than did those following the other 2 diets (6). Insulin is known to activate the sympathetic nervous system (13), and it is an underappreciated mediator of sodium retention and volume expansion (14, 15). Additional studies of blood pressure control, sympathetic activity, and sodium balance in relation to the GI are needed to determine the importance of this observation.

If there is ambivalence in the literature concerning the role of GI in diabetes management, there is even less agreement as to whether GI could influence the risk of diabetes. In a separate study in this issue, Sahyoun et al (16) found no association in older adults between GI or glycemic load (GL) and the risk of developing type 2 diabetes. Although this study had a somewhat shorter duration and smaller sample size than several earlier studies that found an association between GI and diabetes risk, it strengthens the argument that high-GI diets per se do not increase the risk of diabetes.

The results of these studies will be disappointing to some advocates of low-GI diets. The ADA's position statement on nutrition concluded that the use of GI and GL may have a modestly greater benefit in controlling diabetes than is observed when total carbohydrate is considered alone (17). The ADA further stated that information is not sufficient to allow a conclusion that low-GL diets reduce diabetes risk; nevertheless, the consumption of low-GI foods that are rich in fiber is to be encouraged (17). The 2 studies reported in this issue of the Journal provide no compelling reason to modify those recommendations.

ACKNOWLEDGMENTS

The author had no personal or financial conflict of interest.

REFERENCES

  1. Sorensen TI. The changing lifestyle in the world. Body weight and what else? Diabetes Care 2000;23(suppl):B1–4.
  2. Arky RA. Nutritional management of the diabetic. In: Ellenberg M, Rifkin H, eds. Diabetes mellitus: theory and practice. 3rd ed. New Hyde Park, NY: Medical Examination Publishing Company, 1983:539–66.
  3. Nuttall FQ, Brunzell DJ. Principles of nutrition and dietary recommendations for individuals with diabetes mellitus: 1979. American Diabetes Association. Diabetes 1979;28:1027–30.
  4. Nutrition recommendations and principles for people with diabetes mellitus. Diabetes Care 1994;17:519–22.[Abstract]
  5. Jenkins DJ, Wolever TM, Taylor RH, et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981;34:362–6.[Abstract/Free Full Text]
  6. Diaz EO, Galgani JE, Aguirre CA. Glycaemic index effects on fuel partitioning in humans. Obes Rev 2006;7:219–26.[Medline]
  7. Wolever TMS, Gibbs AL, Mehling C, et al. The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein. Am J Clin Nutr 2008;87:114–25.
  8. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:837–53.[Medline]
  9. Kiens B, Richter EA. Types of carbohydrate in an ordinary diet affect insulin action and muscle substrates in humans. Am J Clin Nutr 1996;63:47–53.[Abstract/Free Full Text]
  10. Selvin E, Paynter NP, Erlinger TP. The effect of weight loss on C-reactive protein: a systematic review. Arch Intern Med 2007;167:31–9.[Abstract/Free Full Text]
  11. Strandberg TE, Pitkala K. What is the most important component of blood pressure: systolic, diastolic or pulse pressure? Curr Opin Nephrol Hypertens 2003;12:293–7.[Medline]
  12. Baguet JP, Hammer L, Levy P, et al. Night-time and diastolic hypertension are common and underestimated conditions in newly diagnosed apnoeic patients. J Hypertens 2005;23:521–7.[Medline]
  13. Kern W, Peters A, Born J, Fehm HL, Schultes B. Changes in blood pressure and plasma catecholamine levels during prolonged hyperinsulinemia. Metabolism 2005;54:391–6.[Medline]
  14. DeFronzo RA, Cooke CR, Andres R, Faloona GR, Davis PJ. The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man. J Clin Invest 1975;55:845–55.[Medline]
  15. Sarafidis PA, Bakris GL. The antinatriuretic effect of insulin: an unappreciated mechanism for hypertension associated with insulin resistance? Am J Nephrol 2007;27:44–54.[Medline]
  16. Sahyoun NR, Anderson AL, Tylavsky FA, et al. Dietary glycemic index and glycemic load and the risk of type 2 diabetes in older adults. Am J Clin Nutr 2008;87:126–31.
  17. Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association. Diabetes Care 2007;30(suppl):S48–65.[Free Full Text]
Received for publication October 2, 2007. Accepted for publication October 3, 2007.


Related articles in AJCN:

The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein
Thomas MS Wolever, Alison L Gibbs, Christine Mehling, Jean-Louis Chiasson, Philip W Connelly, Robert G Josse, Lawrence A Leiter, Pierre Maheux, Remi Rabasa-Lhoret, N Wilson Rodger, and Edmond A Ryan
AJCN 2008 87: 114-125. [Abstract] [Full Text]  

Dietary glycemic index and glycemic load and the risk of type 2 diabetes in older adults
Nadine R Sahyoun, Amy L Anderson, Frances A Tylavsky, Jung Sun Lee, Deborah E Sellmeyer, Tamara B Harris, and for the Health, Aging, and Body Composition Study
AJCN 2008 87: 126-131. [Abstract] [Full Text]  



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