Markus Juonala1, Gurmeet R Singh2, Belinda Davison3, Katherine van Schilfgaarde4, Michael R Skilton5, Matthew A Sabin6, Michael Cheung6, Susan Sayers3, David P Burgner7. 1. Department of Medicine, University of Turku, Turku, Finland; Division of Medicine, Turku University Hospital, Turku, Finland; Murdoch Childrens Research Institute, Melbourne, Australia. Electronic address: markus.juonala@utu.fi. 2. Northern Territory Medical Program, Flinders University, Darwin, Australia; Menzies School of Health Research, Charles Darwin University, Darwin, Australia. 3. Northern Territory Medical Program, Flinders University, Darwin, Australia. 4. The Royal Children's Hospital, Melbourne, Australia. 5. Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders, University of Sydney, Sydney, Australia. 6. Murdoch Childrens Research Institute, Melbourne, Australia; The Royal Children's Hospital, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia. 7. Murdoch Childrens Research Institute, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia; Department of Paediatrics, Monash University, Melbourne, Australia.
Abstract
BACKGROUND/ OBJECTIVES: We evaluated whether atherosclerotic changes associated with MetS in Australian Aboriginals are reversible in childhood. In addition, we investigated whether heightened inflammation is mediating the adverse effects of MetS. METHODS: The study cohort comprised of 351 children from the Aboriginal Birth Cohort Study (a longitudinal study based in the Northern Territory of Australia) aged 9-13 years at baseline examination who were followed up 6 years later. MetS was defined by at least three of the following parameters within the extreme sex- and age-specific quartile: highest quartile for waist circumference, blood pressure, triglycerides, and glucose, and lowest quartile for HDL-cholesterol. Carotid intima-media thickness (IMT) and C-reactive protein (CRP) were assessed at follow-up. RESULTS: Individuals with MetS at baseline or follow-up had increased carotid IMT at follow-up (mean ± SEM 539 ± 3 vs. 561 ± 8 μm, P=0.007; and 537 ± 3 vs. 567 ± 8 μm, P<0.0001 respectively). In combined analyses from baseline and follow-up studies, those individuals with MetS only at baseline had partially improved vascular status; their IMT was not significantly increased compared to those without MetS at both time-points (534 ± 3 vs. 550 ± 10 μm, P=0.09). At the follow-up examination, MetS status was associated with increased IMT levels only among individuals with CRP levels above the median (≥ 2.1mg/l) (536 ± 5 vs. 573 ± 9 μm, P<0.0001, P for interaction 0.01). CONCLUSIONS: MetS in childhood is associated with subclinical atherosclerosis in an Australian Aboriginal population and the effects appear to be mediated by increased inflammation. The extent of atherosclerosis was partially reduced if metabolic status improved during the follow-up.
BACKGROUND/ OBJECTIVES: We evaluated whether atherosclerotic changes associated with MetS in Australian Aboriginals are reversible in childhood. In addition, we investigated whether heightened inflammation is mediating the adverse effects of MetS. METHODS: The study cohort comprised of 351 children from the Aboriginal Birth Cohort Study (a longitudinal study based in the Northern Territory of Australia) aged 9-13 years at baseline examination who were followed up 6 years later. MetS was defined by at least three of the following parameters within the extreme sex- and age-specific quartile: highest quartile for waist circumference, blood pressure, triglycerides, and glucose, and lowest quartile for HDL-cholesterol. Carotid intima-media thickness (IMT) and C-reactive protein (CRP) were assessed at follow-up. RESULTS: Individuals with MetS at baseline or follow-up had increased carotid IMT at follow-up (mean ± SEM 539 ± 3 vs. 561 ± 8 μm, P=0.007; and 537 ± 3 vs. 567 ± 8 μm, P<0.0001 respectively). In combined analyses from baseline and follow-up studies, those individuals with MetS only at baseline had partially improved vascular status; their IMT was not significantly increased compared to those without MetS at both time-points (534 ± 3 vs. 550 ± 10 μm, P=0.09). At the follow-up examination, MetS status was associated with increased IMT levels only among individuals with CRP levels above the median (≥ 2.1mg/l) (536 ± 5 vs. 573 ± 9 μm, P<0.0001, P for interaction 0.01). CONCLUSIONS: MetS in childhood is associated with subclinical atherosclerosis in an Australian Aboriginal population and the effects appear to be mediated by increased inflammation. The extent of atherosclerosis was partially reduced if metabolic status improved during the follow-up.
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