| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Letter to the Editor |
1 Unit for Nutrition Research, Eiriksgata 29, Landspitali-University Hospital, 101 Reykjavik, Iceland, E-mail: bryndise{at}landspitali.is
2 Icelandic Heart Association, Holtasmara 1, 201 Kopavogur, Iceland
Dear Sir:
"High Birth Weight Does Not Guarantee Protection from Type 2 Diabetes" is the title of the letter by Willows and Gray-Donald that comments on our article (1), which was published in the August issue of the Journal. We totally agree that high birth weight does not guarantee protection from type 2 diabetes, and we are sorry that Willows and Gray-Donald interpreted the results of our study in this way. Epidemiologic methods can measure trends and relative risks among a group of people, but they cannot measure cause. High birth weight, therefore, can no better guarantee the prevention of type 2 diabetes than can normal weight in an adult. The lower risk of glucose intolerance among populations with a high birth weight is not unique to the Icelandic population, because this association has been observed in epidemiologic studies around the world (2–5). However, as stated in our article (1), some studies also observed an increased prevalence of type 2 diabetes in populations with very high birth weights (5, 6), such as the Pima Indians (6). This finding was attributed in part to gestational diabetes, which resulted in the births of large infants who were prone to diabetes later in life (5, 6). It would therefore be interesting to study the relation between size at birth and type 2 diabetes among the aboriginal peoples living in Canada. High birth weight due to gestational diabetes represents a state of overnutrition, a clinical disorder that should be treated and cannot be equated to high birth weight after a normal pregnancy.
In explaining the epidemiologic association between birth size and risk of adult diseases, studies indicate the importance of fetal nutrition and fetal adaptations (invoked when the maternoplacental nutrient supply fails to match the nutrient demand) (7, 8) as well as the importance of childhood nutrition and growth (3). As pointed out by Willows and Gray-Donald, tall women seem to have a lower risk of type 2 diabetes than do shorter women, which further indicates the importance of fetal nutrition because of the relation between length at birth and adult length. Sudden affluence may adversely affect nations in which the food supply has been inadequate for generations (contributing to low birth weight), resulting in overnutrition and an increased prevalence of gestational diabetes and type 2 diabetes. This, however, is not the case in Iceland, where birth size has been high for at least the past 100 y (1). Examination of fetal nutrition and of other potential in utero determinants of both birth size and type 2 diabetes may therefore yield new means to prevent this disease (5).
Prevention of impaired growth and development in utero is a laudible goal for all nations and international organizations and might, apart from decreasing the rates of mortality and morbidity, lower the risk of type 2 diabetes and other adult diseases (7). Therefore, our conclusion about the importance of decreasing the prevalence of low-birth-weight in children worldwide relates to the goal that every fetus should be allowed to fulfill its genetic growth potential.
REFERENCES
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
