FOOD, MEDICINE, & HEALTH

Clinical Value of Glycemic Index Unclear
The concept that foods have different glycemic effects was advanced more than 20 years ago by Otto et al. (1981), and use of glycemic index as a possible tool for the management of type 1 diabetes and dyslipidemia was introduced nearly two decades ago by Jenkins (1985). Reports within the past several years suggest that an elevated glycemic index may be associated with increased risk of myocardial infarction, endometrial cancer, and insulin resistance and may be important in the treatment or prevention of chronic disease, including obesity.

On closer examination of the relationship between glycemic index and disease and a broad review of the scientific evidence of central pathways that regulate food intake and energy homeostasis, however, it becomes clear that it is premature to advise the general public and most patients to avoid foods with a high glycemic index.

Numerous factors affect the reproducibility of glycemic index (GI). For example, the GI of a food or meal in the morning following an overnight fast differs from that after lunch or dinner. The ripeness of fruit, the physical form and chemical nature of food, the type, processing, and preparation of the food, the combination of macronutrients within the food, including protein, fat, carbohydrate, and fiber, and even acidity influence GI (Pi-Sunyer, 2002).

Structural relationships, applied processing technologies (thermal and nonthermal), and the amount of water are among the many parameters that account for at least 25% variation in GI among carbohydrate-containing foods. For example, the amylose and amylopectin in potatoes and the D-glucose and mixture of 1-4 and 1-6 glucose linkages in different kinds of rice and pastas influence GI (Wolever et al., 2001).

Since it appears that GI is dependent on the processing, storing, ripening, curing, and cooking of a food, no one food has a single or definitive GI. In fact, a specific and standard GI value for a given food runs counter to our current understanding of these variations and misleads consumers and the food industry.

The popularization of GI as a potentially useful tool in reducing risks and preventing some chronic diseases such as obesity is confounded by the virtual absence of supporting clinical data. In general, some would suggest that high-GI foods increase food intake as a result of elevated glucose and possibly excessive post-prandial insulin response. The best long-term studies indicate no difference in weight gain between groups consuming high-GI and low-GI diets.

The preponderance of scientific literature supports the view that the use of GI as a biomarker and management tool in chronic disease states and obesity is limited and unique to individual responses. The best scientific evidence and clinical experience to date suggest that what is important in weight loss is the caloric content of food, not the source of its carbohydrate content or its impact on insulin response within a given individual. Other threats to the validity of any simplified construct involving GI and weight loss include the fact that GI has an enormously variable impact on metabolism, depending on many factors, including an individual’s weight, age, sex, physical activity level, general health, antecedent diet, the type of food and how it was processed and prepared, and variable rates at which aspects of digestion and gut motility occur.

There remain too many uncertainties regarding the validity of GI to label foods “good” or “bad.” Examination of the broad range of apparent GI quintiles in the Nurses’ Health Study and among men in the Health Professionals’ Follow Up Study suggests that it is both impractical and unreasonable to drive the GI down in the general population. In light of the current medical and scientific evidence, it seems irrational at this time to advocate GI as a prophylactic public health measure and to advise the avoidance of certain carbohydrates (Sievenpiper and Vuksan, 2004).

by ROGER CLEMENS, Dr. P.H.
Contributing Editor
Director, Analytical Research & Services
Adjunct Professor,
Molecular Pharmacology & Toxicology
USC School of Pharmacy, Los Angeles, Calif
[email protected]

by PETER PRESSMAN, M.D.
Contributing Editor
Assistant Professor of Clinical Medicine
USC Keck School of Medicine, Los Angeles, Calif.
[email protected]

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