Angela D Liese1, Xiaonan Ma2, Xiaoguang Ma3, Murray A Mittleman4, Natalie S The5, Debra A Standiford6, Jean M Lawrence7, Catherine Pihoker8, Santica M Marcovina9, Elizabeth J Mayer-Davis10, Robin C Puett11. 1. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. Electronic address: liese@sc.edu. 2. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. 3. Department of Nutrition and Food Hygiene, School of Public Health, Zhejiang University, Zhejiang, China. 4. Department of Epidemiology, TH Chan Harvard School of Public Health, Boston, MA, USA. 5. Department of Health Sciences, Furman University, SC, USA. 6. Division of Pediatric Endocrinology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. 7. Department of Research & Evaluation, Kaiser Permanente Southern California, Pasadena, CA, USA. 8. Department of Pediatrics, University of Washington, Seattle, USA. 9. Department of Medicine, University of Washington, Seattle, WA, USA. 10. Departments of Nutrition and Medicine, University of North Carolina, Chapel Hill, NC, USA. 11. Maryland Institute for Applied Environmental Health, School of Public Health, University of Maryland, MD, USA.
Abstract
BACKGROUND: Systemic inflammation is a key process underlying cardiovascular disease (CVD) development, and CVD risk is significantly elevated in persons with type 1 diabetes (T1D). Youth with T1D exhibit increased levels of inflammation. Studies in persons without diabetes suggest that dietary quality influences inflammation, yet little is known about dietary influences on inflammation in youth with T1D. METHODS: This study evaluated the association of four distinct dietary quality indices (Dietary Approaches to Stop Hypertension (DASH), Healthy Eating Index 2010 (HEI2010), modified KIDMED and Total Antioxidant Capacity (TAC)) with biomarkers of inflammation (C-reactive protein (CRP), fibrinogen and interleukin-6 (IL-6)) in a sample of 2520 youth with T1D participating in the SEARCH for Diabetes in Youth Study. RESULTS: Average diet quality was moderate to poor, with mean scores of 43 (DASH, range 0-80), 55 (HEI2010, range 0-100), 3.7 (mKIDMED, range 3-12) and 7237 (TAC). None of the four diet quality scores was associated with the selected biomarkers of inflammation in any analyses. Evaluation of a non-linear relationship or interactions with BMI or levels of glycemic control did not alter the findings. Replication of analyses using longitudinal data yielded consistent findings with our cross-sectional results. CONCLUSIONS: Biomarkers of inflammation in youth with T1D may not be directly influenced by dietary intake, at least at the levels of dietary quality observed here. More work is needed to understand what physiologic mechanisms specific to persons with T1D might inhibit the generally beneficial influence of high dietary quality on systemic inflammation observed in populations without diabetes.
BACKGROUND:Systemic inflammation is a key process underlying cardiovascular disease (CVD) development, and CVD risk is significantly elevated in persons with type 1 diabetes (T1D). Youth with T1D exhibit increased levels of inflammation. Studies in persons without diabetes suggest that dietary quality influences inflammation, yet little is known about dietary influences on inflammation in youth with T1D. METHODS: This study evaluated the association of four distinct dietary quality indices (Dietary Approaches to Stop Hypertension (DASH), Healthy Eating Index 2010 (HEI2010), modified KIDMED and Total Antioxidant Capacity (TAC)) with biomarkers of inflammation (C-reactive protein (CRP), fibrinogen and interleukin-6 (IL-6)) in a sample of 2520 youth with T1D participating in the SEARCH for Diabetes in Youth Study. RESULTS: Average diet quality was moderate to poor, with mean scores of 43 (DASH, range 0-80), 55 (HEI2010, range 0-100), 3.7 (mKIDMED, range 3-12) and 7237 (TAC). None of the four diet quality scores was associated with the selected biomarkers of inflammation in any analyses. Evaluation of a non-linear relationship or interactions with BMI or levels of glycemic control did not alter the findings. Replication of analyses using longitudinal data yielded consistent findings with our cross-sectional results. CONCLUSIONS: Biomarkers of inflammation in youth with T1D may not be directly influenced by dietary intake, at least at the levels of dietary quality observed here. More work is needed to understand what physiologic mechanisms specific to persons with T1D might inhibit the generally beneficial influence of high dietary quality on systemic inflammation observed in populations without diabetes.
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