BACKGROUND: Obesity leads to increased risk of cardiovascular disease and glucose intolerance, which are phenomena of chronic inflammation. This study was performed to determine whether a higher body mass index (BMI) and central obesity are associated with low-grade inflammation. METHODS: An analysis of 8 453 adults aged > or =20 years was performed. Every subject completed a household interview and a questionnaire regarding personal health, and their BMI and serum C-reactive protein (CRP) level were measured. The BMI data were divided into quintiles, using multiple linear regression to estimate the relationship between CRP level and BMI quintiles. An extended-model approach was used for covariate adjustment. The association between central obesity and CRP level was examined by this method as well. RESULTS: After controlling for demographics, chronic diseases, health behaviours and levels of folate and vitamin B12, the beta coefficient (which represents the change of natural-log-transformed levels of CRP for each kg/m2 increase in BMI) was 0.078 (p < 0.001). The CRP levels also increased across increasing quintiles of BMI (p for trend <0.001). The beta coefficient, representing the change of natural-log-transformed levels of CRP comparing subjects with central obesity to those without, was 0.876 (p < 0.001). CONCLUSION: Higher BMIs as well as central obesity are independently associated with higher levels of CRP.
BACKGROUND:Obesity leads to increased risk of cardiovascular disease and glucose intolerance, which are phenomena of chronic inflammation. This study was performed to determine whether a higher body mass index (BMI) and central obesity are associated with low-grade inflammation. METHODS: An analysis of 8 453 adults aged > or =20 years was performed. Every subject completed a household interview and a questionnaire regarding personal health, and their BMI and serum C-reactive protein (CRP) level were measured. The BMI data were divided into quintiles, using multiple linear regression to estimate the relationship between CRP level and BMI quintiles. An extended-model approach was used for covariate adjustment. The association between central obesity and CRP level was examined by this method as well. RESULTS: After controlling for demographics, chronic diseases, health behaviours and levels of folate and vitamin B12, the beta coefficient (which represents the change of natural-log-transformed levels of CRP for each kg/m2 increase in BMI) was 0.078 (p < 0.001). The CRP levels also increased across increasing quintiles of BMI (p for trend <0.001). The beta coefficient, representing the change of natural-log-transformed levels of CRP comparing subjects with central obesity to those without, was 0.876 (p < 0.001). CONCLUSION: Higher BMIs as well as central obesity are independently associated with higher levels of CRP.
Authors: Mariusz Stępień; Anna Stępień; Rafał N Wlazeł; Marek Paradowski; Maciej Banach; Jacek Rysz Journal: Lipids Health Dis Date: 2014-02-08 Impact factor: 3.876
Authors: Liseth Siemons; Peter M Ten Klooster; Harald E Vonkeman; Piet L C M van Riel; Cees A W Glas; Mart A F J van de Laar Journal: BMC Musculoskelet Disord Date: 2014-11-06 Impact factor: 2.362
Authors: Anna J Stevenson; Daniel L McCartney; Robert F Hillary; Archie Campbell; Stewart W Morris; Mairead L Bermingham; Rosie M Walker; Kathryn L Evans; Thibaud S Boutin; Caroline Hayward; Allan F McRae; Barry W McColl; Tara L Spires-Jones; Andrew M McIntosh; Ian J Deary; Riccardo E Marioni Journal: Clin Epigenetics Date: 2020-07-27 Impact factor: 6.551