National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands  Department of Human Biology, Nutrition and Toxicology Research Institute of Maastricht (NUTRIM), University of Maastricht, Maastricht, The Netherlands.
Objectives:To investigate whether dietary glycaemic index (GI) and glycaemic load (GL) were associated with subsequent weight and waist circumference change.Design:Population-based prospective cohort study.Setting:Five European countries, which are Denmark, Germany, Italy, The Netherlands and the United Kingdom.Participants:A total of 89 432 participants, aged 20-78 years (mean =53 years) at baseline and followed for 1.9-12.5 years (mean=6.5 years). All participants were free of self-reported cancer, cardiovascular diseases and diabetes at baseline.Methods:Glycaemic index and GL were calculated on the basis of dietary intake assessed by food frequency questionnaires and by using a GI table developed for this study with published GI values as the main sources. Anthropometric data were collected both at baseline and at the end of follow-up. Multiple linear regression analyses were conducted in each centre and random-effect meta-analyses were used to combine the effects. Adjustment was made for baseline anthropometrics, demographic and lifestyle factors, follow-up duration and other dietary factors.Results:Mean GI and GL were 57 and 134, respectively. Associations of GI and GL with subsequent changes of weight and waist circumference were heterogeneous across centres. Overall, with every 10-unit higher in GI, weight increased by 34 g per year (95% confidence interval (CI): -47, 115) and waist circumference increased by 0.19 cm per year (95% CI: 0.11, 0.27). With every 50-unit higher in GL, weight increased by 10 g per year (95% CI: -65, 85) and waist circumference increased by 0.06 cm per year (95% CI: -0.01, 0.13).Conclusions:Our findings do not support an effect of GI or GL on weight change. The positively significant association between GI, not GL, and subsequent gain in waist circumference may imply a beneficial role of lower GI diets in the prevention of abdominal obesity. However, further studies are needed to confirm this finding given the small effect observed in this study.International Journal of Obesity advance online publication, 25 August 2009; doi:10.1038/ijo.2009.163.
AIMS/HYPOTHESIS: Mutations at the gene encoding wolframin (WFS1) cause Wolfram syndrome, a rare neurological condition. Associations between single nucleotide polymorphisms (SNPs) at WFS1 and type 2 diabetes have recently been reported. Thus, our aim was to replicate those associations in a northern Swedish case-control study of type 2 diabetes. We also performed a meta-analysis of published and previously unpublished data from Sweden, Finland and France, to obtain updated summary effect estimates. METHODS: Four WFS1 SNPs (rs10010131, rs6446482, rs752854 and rs734312 [H611R]) were genotyped in a type 2 diabetes case-control study (n = 1,296/1,412) of Swedish adults. Logistic regression was used to assess the association between each WFS1 SNP and type 2 diabetes, following adjustment for age, sex and BMI. We then performed a meta-analysis of 11 studies of type 2 diabetes, comprising up to 14,139 patients and 16,109 controls, to obtain a summary effect estimate for the WFS1 variants. RESULTS: In the northern Swedish study, the minor allele at rs752854 was associated with reduced type 2 diabetes risk [odds ratio (OR) 0.85, 95% CI 0.75-0.96, p = 0.010]. Borderline statistical associations were observed for the remaining SNPs. The meta-analysis of the four independent replication studies for SNP rs10010131 and correlated variants showed evidence for statistical association (OR 0.87, 95% CI 0.82-0.93, p = 4.5 x 10(-5)). In an updated meta-analysis of all 11 studies, strong evidence of statistical association was also observed (OR 0.89, 95% CI 0.86-0.92; p = 4.9 x 10(-11)). CONCLUSIONS/INTERPRETATION: In this study of WFS1 variants and type 2 diabetes risk, we have replicated the previously reported associations between SNPs at this locus and the risk of type 2 diabetes.