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LETTER TO THE EDITOR |
Human Nutrition Unit
University of Sydney
Sydney, NSW 2006
Australia
E-mail: j.brandmiller{at}mmb.usyd.edu.au
Dear Sir:
Tuomainen et al have suggested that our meta-analysis draws bold conclusions on the basis of inadequate evidence, implying that only 1–2 studies were considered (1). In fact, our conclusions were based on the aggregated findings of 37 prospective studies of various diseases, all of them linked by the hypothesis that glucose and insulin metabolism played a role in the pathogenesis of the diseases. Furthermore, we described the relation as "a modest effect overall" (page 634), but similar in magnitude to that of dietary fiber and whole grains. The effect was most pronounced in type 2 diabetes, for which there were 8 studies altogether and 5 valid studies (correlation coefficients 
0.5 between total carbohydrate intakes from food-frequency questionnaires and other dietary assessment methods), and the rate ratio was 1.40 (95% CI: 1.23, 1.59) for glycemic index (GI) and 1.27 (1.12, 1.45) for glycemic load (GL).
Tuomainen et al correctly state, "[D]iseases are not equal, and not all of them necessarily have a common background." However, the multiple authors of all 37 studies must have considered the possibility that the combined metabolic effect of postprandial glycemia, insulin resistance, and compensatory hyperinsulinemia may be a mitigating factor, or they would not have bothered to undertake their analyses. Similarly, most nutritionists consider it valid to examine the relation between dietary fiber and whole-grain foods and a wide range of different diseases. If so, then it is equally valid to consider other measures of carbohydrate quality, such as GI and GL. There are recognized limitations to estimating the true GI and GL of a diet, but there are similar uncertainties surrounding the estimation of fiber and whole-grain intake (both, for example, are subject to methodologic variation and problems of definition). Indeed, the assumption that fiber and whole grains are linked to many diseases is based partly on the underlying assumption that they are surrogate measures of the rate of digestion and absorption. In this respect, GI and GL are more likely to reflect the relative extent of postprandial glycemia and insulin response than is a food's fiber or whole-grain content (2)
A variety of mechanisms may link GI and GL to the risk of certain chronic diseases. With respect to diabetes, postprandial hyperinsulinemia can lead to progressive loss of insulin sensitivity in the muscles, liver, and other organs. In susceptible persons, insulin resistance and defects in insulin secretion eventually lead to the development of type 2 diabetes (3, 4). With respect to coronary heart disease, high blood glucose and insulin concentrations lead to increased protein glycosylation and oxidative stress, chronic low-grade inflammation, impaired fibrinolysis, and poor endothelial function, which combine to produce damage to endothelium of the blood vessels and an increase in the risk of thrombosis (3-5). Finally, high-GI and high-GL diets have been independently associated with higher LDL and C-reactive protein concentrations and lower concentrations of HDL cholesterol (3, 4, 6, 7). The net effect is greater transport of potentially atherogenic cholesterol particles to peripheral tissues and organs and the decreased removal of those particles.
With respect to certain cancers, glucose is a powerful stimulant for insulin release, and insulin itself stimulates an increase in insulin-like growth factor-1 (IGF-1) in target organs. IGF-1 is a structural homologue of insulin; many tissues types have been shown to have receptors for both IGF-1 and insulin, some of which have the capacity to cross-bind insulin and IFG-1 to their mutual receptors (8). Both insulin and IGF-1 are known mitogens, which are necessary for the cell to progress from G1 to the S phase of the cell cycle, then stimulating cell proliferation and inhibiting cell death (apoptosis) (8). In addition, both insulin and IGF-1 stimulate the synthesis of the sex hormones and regulate their bioavailability through the inhibition of the synthesis of sex hormone–binding globulin (SHBG) (8). Elevated insulin, IGF-1, sex hormones, or decreased concentrations of SHBG (or all 4) have been associated with a greater risk of a range of cancers, including premenopausal breast (9) and colorectal (8, 10) cancer.
Therefore, dietary patterns that stimulate postprandial elevations in blood glucose and insulin concentrations, such as those with a high GI and GL, may potentially increase the risk of a range of diseases, including type 2 diabetes, cardiovascular disease, and some cancers.
ACKNOWLEDGMENTS
JCB-M is a coauthor of The New Glucose Revolution book series, the director of a not-for-profit glycemic index–based food endorsement program in Australia, and manager of the University of Sydney glycemic index testing service. AWB is a coauthor of Diabetes and Pre-diabetes Handbook, one of the books in The New Glucose Revolution series, and is a consultant to a not-for-profit glycemic index–based food endorsement program in Australia.
REFERENCES
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