Pediatric Diabetes 2008: 9 (Part II): 50–56 doi: 10.1111/j.1399-5448.2007.00360.x All rights reserved # 2008 The Authors Journal compilation # 2008 Blackwell Munksgaard Pediatric Diabetes Original Article Type 1 diabetes: increased height and weight gains in early childhood Ljungkrantz M, Ludvigsson J, Samuelsson U. Type 1 diabetes: increased height and weight gains in early childhood. Pediatric Diabetes 2008: 9 (Part II): 50–56. Objective: The accelerator/beta-cell stress hypothesis regards insulin resistance as one common basis for type 1 and type 2 diabetes and weight increase as an important trigger of type 1 diabetes. To test this hypothesis, we examined children’s height and weight gain from birth to the time of diagnosis of type 1 diabetes. Method: Growth charts (n ¼ 316) from children 0–16 yr old up to the time of diagnosis of type 1 diabetes were compared with growth charts from age- and sex-matched controls. Results: Compared with their controls, children who developed diabetes had experienced more pronounced gain in both weight and height. In the year of diagnosis, they were taller [0.5 vs. 0.36 standard deviation score (SDS), p , 0.03] and heavier (0.7 vs. 0.45 SDS, p , 0.01). Children who developed diabetes aged 5 yr or less gained more weight during the period between their third month and third year of life (p , 0.01). Children who were diagnosed between 6 and 10 yr of age had gained more in height before they were 5 yr old (p , 0.05). Regression analysis showed that a high weight or a high body mass index (BMI) at 5 yr of age indicated, more than the other measurements, a high risk for diabetes later during childhood, while height and weight at ages less than 5 yr did not add any further information on diabetes risk. Conclusions: Rapid growth before 7 yr of age and increased BMI in childhood are risk factors for later type 1 diabetes. These findings support the accelerator/beta-cell stress hypothesis. Magnus Ljungkrantz a , Johnny Ludvigsson b and Ulf Samuelsson b a Department of Paediatrics, Blekingesjukhuset, Karlskrona, Sweden; and b Diabetes Research Centre and Division of Paediatrics, Department of Molecular and Clinical Medicine, Linko ¨ping University, Linko ¨ ping, Sweden Key words: age groups – BMI – growth – length – weight Corresponding author: Ulf Samuelsson MD, PhD Division of Paediatrics Department of Molecular and Clinical Medicine Linko ¨ ping University S-581 85 Linko ¨ ping Sweden. Tel: 146 13 22 20 00; fax: 146 13 14 82 65; e-mail: ulf.samuelsson@lio.se Submitted 24 November 2006. Accepted for publication 06 November 2007 There is a close connection between insulin secretion and growth in children (1). We have shown earlier, as also a study from Finland, that increased weight gain during infancy might be associated with increased risk of type 1 diabetes (2, 3). Some studies have also found a significant association between high birth weight and increased risk for type 1 diabetes (4, 5). While other studies have found no such association (2, 6). It is well known that during periods of rapid growth, demand for insulin production increases (7). This may explain the peak in the incidence of type 1 diabetes just before or during puberty when children have a growth spurt (8). Obesity is a well-known risk factor for type 2 diabetes, and a study from Finland has reported that it may also be a risk factor for type 1 diabetes (9). There have been several studies regarding child growth before, during and after clinical onset of type 1 diabetes (10–12). Some studies have reported that children with type 1 diabetes are taller than control children, even several years before clinical presentation (13, 14). However, one study that compared twins reported decreased growth before onset of diabetes (15). In fact, at diagnosis, diabetic children have been reported to be either taller (16), of the same height (17) or shorter (18) than non-diabetic control children. The accelerator hypothesis regards insulin resistance as a common basis for type 1 and type 2 diabetes and weight increase as the trigger of type 1 (19). Insulin resistance upregulates the beta cells metabolically and accelerates their loss through glucotoxicity (20). 50