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© 2008 American Society for Nutrition J. Nutr. 138:139, January 2008


Letters to the Editor

Reply to Dr. White

Jukka Montonen*, Markku Heliövaara and Antti Reunanen

National Public Health Institute
Helsinki FIN 0300, Finland

Paul Knekt

National Public Health Institute
Helsinki FIN 0300, Finland
and
Social Insurance Institution
Helsinki FIN 00100 and Turku FIN 20720, Finland

Ritva Järvinen

Department of Clinical Nutrition
University of Kuopio
Kuopio FIN 70211, Finland

* To whom correspondence should be addressed. E-mail: jukka.montonen{at}ktl.fi.

Dear Editor,

The comments of Dr. John S. White concerning our article (1) raise two concerns. First, sucrose is composed of glucose and fructose and reaches the portal blood as monosaccharides in the same manner as fructose and glucose ingested separately. However, when the associations between dietary factors and health and disease are assessed, the components of foods are usually considered in the form that they are present in foods, not as the components that reach our body. The physical form of food and the presence of other foods can modify the associations observed for a given nutrient (2).

Second, Dr. White stated that a sucrose-sweetened caloric beverage cannot increase the risk of type 2 diabetes without sucrose posing the same risk. Nevertheless, our results suggest that consumption of berry juice, soft drinks, and intakes of fructose and glucose, unlike sucrose predict diabetes risk (1). It seems that the association between sugars and the development of diabetes differs according to the physical form of the foods consumed. For this reason it is important to focus not only on nutrients but on their dietary sources (2). In our data, approximately one-half of the sucrose was consumed as a sweetener at the table. Sugar was mainly added to coffee or tea or sprinkled on top of porridge. In nonexperimental epidemiological research, it cannot be excluded that nutrients or other components of foods under study may be indicators of something else associated with the outcome, such as disease.

Due to the explorative nature of our observational study, we did not conduct hypothesis testing. Our aim was to generate information on dietary risk indicators for type 2 diabetes. If replicated, our result that dietary fructose and glucose increase risk may prove useful. Type 2 diabetes develops as a result of a complex multifactor process. Dr. White pointed out that current hypotheses concerning fructose and caloric beverages have no credible scientific support. We agree that it is very difficult to form conclusions on this issue. The tangle of risk indicators and causal factors cannot be undone without epidemiological studies, although the verification of causality requires an experimental study design (3). Knowledge of the role of dietary factors of type 2 diabetes is increasing but is so scanty that it may be premature to speculate about the importance of any crucial nutrient in the etiology of the disease.

Manuscript received 2 November 2007.
    LITERATURE CITED
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 LITERATURE CITED
 

1. Montonen J, Järvinen R, Knekt P, Heliövaara M, Reunanen A. Consumption of sweetened beverages and intakes of fructose and glucose predict Type 2 diabetes occurrence. J Nutr. 2007;137:1447–54.[Abstract/Free Full Text]

2. Willett W. Nutritional epidemiology. New York: Oxford University Press;1998

3. Hennekens CH, Buring JE. Epidemiology in medicine. Boston: Little, Brown; 1987.





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