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Letters to the Editor |
Italian State Railways Via Savonarola 144 35137 Padua Italy
Dear Sir:
Daly et al (1) state that animal work has clearly shown the capacity of high-sucrose diets to reduce insulin sensitivity, but that "the evidence from human studies is often inconclusive or conflicting." Their study, unfortunately, does not help to clarify this issue because they did not specify the form in which sucrose was consumed, as others also have not (2–7). This specification, however, is so important that only the results of studies in which is it provided can be usefully compared to extend the knowledge in this area (7). For example, sucrose consumed in solid form has been reported to increase both fasting and postprandial serum insulin and glucose concentrations (8), whereas no adverse effects were observed when "virtually all sucrose contained in the high-sucrose diet was added to fruits, milk, beverages, and coffee" (9). That sugars are innocuous and even beneficial only in the form of diluted solutions is also suggested by the improved glucose tolerance with a liquid-formula diet containing 85% of energy as dextrose or a mixture of dextrins and maltose (10).
Daly et al (1) state that in further work they are exploring the effects of alterations in the type of carbohydrate in the diet. In view of the central role played by the form in which simple carbohydrates are consumed (7), they should also take the energy density of sugars into account.
REFERENCES
Human Nutrition Research Centre Department of Biological and Nutritional Sciences University of Newcastle Newcastle on Tyne NE1 7RU United Kingdom
Dear Sir:
In a recent review article, we concluded that there is good evidence from animal studies that high intakes of sucrose or fructose have detrimental effects on insulin sensitivity, particularly in association with the induction of hypertriglyceridemia (1). The more limited studies in humans have produced conflicting results, partly because of heterogeneity in study design. We thus undertook a series of controlled feeding studies in healthy human volunteers to examine the influence of type and amount of dietary carbohydrate on insulin sensitivity. In the study to which Baschetti refers, major alterations in the intake of starch compared with sucrose, in the absence of changes in fat or energy intake, had no detectable effect on insulin sensitivity in healthy young adults (2). Baschetti argues that this study does not help to clarify the issue of the conflicting results because we did not specify the form in which the sucrose was consumed. In Table 1 of our paper we gave the quantitative composition of each of our experimental diets. For the high-sucrose diet, most of the sucrose was provided as an admixture with cream (at breakfast and dinner) or as a butter icing (sucrose blended with polyunsaturated margarine; provided at lunch and supper). In each case, the sucrose was consumed as part of a main meal.
Baschetti appears to suggest that the physical form in which sucrose is consumed has a critical role in determining whether this sugar has an effect on glucose tolerance or insulin sensitivity. Given that sucrose is readily soluble in aqueous solutions, we find it hard to imagine the physiologic mechanism that might underlie such a phenomenon. One would expect sucrose, regardless of the form in which it is ingested, to be in solution within a short time of reaching the stomach (except possibly in conditions of severe dehydration). In this context, the report by Brunzell et al (3) is not relevant because they compared a very-high-carbohydrate, low-fat diet (containing sucrose) with a diet of conventional macronutrient composition. Given the design of their study, inferring causality is difficult because of the impossibility of separating effects of the high carbohydrate intake from those of the low fat intake.
REFERENCES
This article has been cited by other articles:
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  R. Baschetti Concentrations of sugars in high-carbohydrate diets Am. J. Clinical Nutrition, January 1, 2001; 73(1): 129 - 129. [Full Text] [PDF]
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