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  • Pundziute-Lyckå, Auste, et al. (författare)
  • Diet, growth, and the risk for type 1 diabetes in childhood : a matched case-referent study.
  • 2004
  • Ingår i: Diabetes Care. - : American Diabetes Association. - 0149-5992 .- 1935-5548. ; 27:12, s. 2784-9
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To study the association between type 1 diabetes risk and previous intake of energy, accounting for body size and previous intake of nutrients and foods, accounting for the energy intake. RESEARCH DESIGN AND METHODS: We conducted an incident population-based case-referent study in Stockholm, Sweden, including 99 of 100 eligible 7- to 14-year-old diabetic children and 180 of 200 age-, sex-, and area-matched referent children identified through the Swedish population register. Average daily energy and nutrient intake 1 year before diabetes diagnosis/interview was estimated using the food frequency questionnaire with assessment of consumed food amounts. Mean SD scores of growth measurements taken during the last 4 years before the diagnosis were used. Odds ratios (ORs) were calculated by conditional logistic regression. RESULTS: Average intake of energy, carbohydrate, fat, and protein was significantly higher among the case subjects as well as mean weight-for-age SD score. Higher energy intake and weight-for-age were both associated with increased diabetes risk after adjustment for each other: OR (95% CI) for medium and high levels of energy intake were 1.33 (0.52-3.42) and 5.23 (1.67-16.38), respectively, and for weight-for-age were 3.20 (1.30-7.88) and 3.09 (1.16-8.22), respectively. High intake of carbohydrates, especially disaccharides and sucrose, increased diabetes risk. CONCLUSIONS: Higher energy intake and larger body size were independently associated with increased diabetes risk. Of the different nutrients, higher intake of carbohydrates, particularly disaccharides and sucrose, increased the risk. Lifestyle habits leading to higher energy intake and more rapid growth in childhood may contribute to the increase of childhood-onset type 1 diabetes by different mechanisms.
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