Glycemic Index

Myth: sugar has a high glycemic index

Sugar has a moderate glycemic index (GI). By comparison, wheat bread and brown rice have similar glycemic indexes. The popular belief that sugar should be avoided because it’s perceived to have a high glycemic index misleads diabetics and non-diabetics alike.

The body must convert the starches and sugars in foods into blood glucose to meet basic energy needs. Glycemic index is the term coined by scientists to describe how fast the body breaks down starches and sugars after a particular food or beverage is consumed.

Both the U.S. Institute of Medicine and the 2005 Dietary Guidelines for Americans reject the concept of glycemic index as a useful measure of diet quality.

The reality is this: Blood glucose levels depend not only on how much and what types of carbohydrates are eaten but also on how much fat or protein is eaten with the carbohydrates.

The chart below shows that sugar/sucrose is at the low end of the medium GI range and has a low GI load.

Comparison of glycemic index and glycemic load of certain foods
Food Glycemic index Glycemic load
Apple 40 6
Baked potato 85 26
Brown rice 50 16
Carrots 92 5
Corn flakes 92 24
Orange juice 50 13
Plain bagel 72 25
Potato chips 54 11
Pound cake 54 15
Wheat bread 53 11
Table sugar (sucrose) 58 6
Ranges for glycemic index (GI) and glycemic load (GL)
  GI GL
High 70 or more 20 or more
Medium 56 to 69 11 to 19
Low 55 or less 10 or less

From International Table of Glycemic Index and Glycemic Load Values by K.F. Powell et al (2002, Am J Clin Nutr 2002; 76:5-56)

Myth: sugar high

The premise of a “sugar high” is that white table sugar uniquely causes a rapid, abnormally high rise in blood glucose or glycemic response which then triggers an excess production of insulin. The premise continues by alleging that the excess insulin induces an equally unnatural release followed by a drop in blood glucose to an unusually low level. The chart above shows clearly that the glycemic response sugar is moderate, not a high glycemic food.

The myth that sugar initiates a rapid, unnatural rise in blood glucose is not a physiological or scientific reality.


A recently published study questions the usefulness of applying glycemic index as a measure of overall diet quality. The abstract of the British Journal of Nutrition article is provided below.

Abstract

Towards understanding of glycaemic index and glycaemic load in habitual diet: associations with measures of glycaemia in the Insulin Resistance Atherosclerosis Study.

Mayer-Davis EJ, Dhawan A, Liese AD, Teff K, Schulz M.

Center for Research in Nutrition and Health Disparities and Department of Epidemiology and Biostatistics, University of South Carolina Arnold School of Public Health, 2718 Middleburg Drive, Columbia, SC 29 208, USA.

Epidemiologic studies have applied the glycaemic index (GI) and glycaemic load (GL) to assessments of usual dietary intake. Results have been inconsistent particularly for the association of GI or GL with diabetes incidence. We aimed to advance understanding of the GI and GL as applied to food frequency questionnaires (FFQ) by evaluating GI and GL in relation to plasma measures of glycaemia. Included were 1255 adults at a baseline examination (1994-6) and 813 who returned for the 5-year follow-up examination. Usual diet, at both examinations, was assessed by a validated FFQ. GI and GL were evaluated in relation to average fasting glucose (two measures at each examination) and 2 h post-75 g glucose load plasma glucose (baseline and follow-up), and glycated haemoglobin (A1c; follow-up only); using generalized linear models. Correlation coefficients (r) for GI and GL related to measures of glycaemia, adjusted for total energy intake, ranged from -0.004 to 0.04 (all NS) for both examinations. Adjustment for potential confounders, for fasting glucose in models for 2 h glucose (to model incremental glucose) and for average fasting glucose in models for A1c (to account, in part, for overnight endogenous glucose production) also did not materially alter findings, nor did inclusion of data from both examinations together in linear mixed models. The present results call into question the utility of GI and GL to reflect glycaemic response to food adequately, when used in the context of usual diet. Further work is needed to quantify usual dietary exposures relative to glucose excursion and associated chronic glycaemia and other metabolic parameters.

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