S Carlsson1, A Ahlbom, P Lichtenstein, T Andersson. 1. Department of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden. sofia.carlsson@ki.se
Abstract
AIMS/HYPOTHESIS: The aim of this study was to examine the long-term associations of BMI and physical activity with type 2 diabetes, and to estimate shared genetic components of these traits. METHODS: We used data from the Swedish Twin Registry on 23,539 twins born 1886-1958 who answered questionnaires between 1967 and 1972 and were followed up until 1998. The risk of type 2 diabetes in relation to BMI and physical activity was assessed by Cox regression. Structural equation models were used to estimate genetic and environmental variance components and genetic correlations. RESULTS: The risk of type 2 diabetes increased with BMI (HR 1.32 [95% CI 1.29, 1.35] per kg/m²) and decreased with physical activity (HR 0.56 [95% CI 0.39, 0.80] for high vs low). Heritability was estimated to be 77% (95% CI 54%, 83%) for type 2 diabetes, 65% (95% CI 58%, 73%) for BMI, and 57% (95% CI 47%, 67%) for physical activity. The genetic correlation with type 2 diabetes was 0.43 (95% CI 0.31, 0.58) for BMI and -0.23 (95% CI -0.46, 0.02) for physical activity, implying that 18% (95% CI 9%, 34%) of the genetic influence on type 2 diabetes is shared with BMI and 5% (95% CI 0%, 20%) with physical activity. CONCLUSIONS/ INTERPRETATION: Indications of shared genetic effects are found for BMI and type 2 diabetes, which suggests that these traits are partly influenced by the same genetic factors. In contrast, our findings suggest that the genes related to physical activity are essentially different from those associated with type 2 diabetes.
AIMS/HYPOTHESIS: The aim of this study was to examine the long-term associations of BMI and physical activity with type 2 diabetes, and to estimate shared genetic components of these traits. METHODS: We used data from the Swedish Twin Registry on 23,539 twins born 1886-1958 who answered questionnaires between 1967 and 1972 and were followed up until 1998. The risk of type 2 diabetes in relation to BMI and physical activity was assessed by Cox regression. Structural equation models were used to estimate genetic and environmental variance components and genetic correlations. RESULTS: The risk of type 2 diabetes increased with BMI (HR 1.32 [95% CI 1.29, 1.35] per kg/m²) and decreased with physical activity (HR 0.56 [95% CI 0.39, 0.80] for high vs low). Heritability was estimated to be 77% (95% CI 54%, 83%) for type 2 diabetes, 65% (95% CI 58%, 73%) for BMI, and 57% (95% CI 47%, 67%) for physical activity. The genetic correlation with type 2 diabetes was 0.43 (95% CI 0.31, 0.58) for BMI and -0.23 (95% CI -0.46, 0.02) for physical activity, implying that 18% (95% CI 9%, 34%) of the genetic influence on type 2 diabetes is shared with BMI and 5% (95% CI 0%, 20%) with physical activity. CONCLUSIONS/ INTERPRETATION: Indications of shared genetic effects are found for BMI and type 2 diabetes, which suggests that these traits are partly influenced by the same genetic factors. In contrast, our findings suggest that the genes related to physical activity are essentially different from those associated with type 2 diabetes.
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