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      Dietary inflammatory potential and risk of mortality in metabolically healthy and unhealthy phenotypes among overweight and obese U.S. adults

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          Abstract

          Background and Aims

          This study was designed to investigate the association between the dietary inflammatory index (DII ®) scores, metabolic phenotypes, and risk of mortality risk in overweight/obese individuals from a representative sample of the U.S. population.

          Methods

          Data from 3733 overweight/obese adults (BMI≥25kg/m 2) aged 20–90 years from the National Health and Nutrition Examination Survey III, 1988–1994 were analyzed; these participants were followed for mortality through December 31, 2011. DII scores were computed based on baseline dietary intake using 24-hour dietary recalls. Metabolically unhealthy status was defined as having 2 or more of these metabolic abnormalities: high glucose, insulin resistance, elevated blood pressure, triglycerides, C-reactive protein levels, or low high-density lipoprotein-cholesterol values.

          Results

          In metabolically unhealthy overweight/obese (MUO) individuals, DII score was associated with increased risk of all-cause mortality (HR Tertile 3 vs Tertile 1 1.44; 95% CI 1.11–1.86 P trend=0.008; HR 1SD increase 1.08; 95% CI 0.99–1.18). Additionally, a stronger association with cardiovascular mortality was observed (HR T3 vs T1 3.29; 95% CI 2.01–5.37 P trend<0.001; HR 1SD increase 1.40; 95% CI 1.18–1.66), after adjusting for potential confounders. Furthermore, when analyses were restricted to obese individuals (BMI≥30 kg/m 2), the association was more pronounced, especially for cardiovascular mortality (HR T3 vs T1 5.55; 95% CI 2.11–14.57 P trend=0.006; HR 1SD increase 1.74; 95% CI 1.21–2.50). No association was observed between DII score and risk of mortality in individuals with metabolically healthy overweight/obese (MHO) phenotype, or for cancer mortality in either MHO or MUO phenotype.

          Conclusions

          A pro-inflammatory diet appears to increase risk of all-cause and cardiovascular mortality in the MUO phenotype, but not among the MHO phenotype.

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          Author and article information

          Journal
          8309603
          20838
          Clin Nutr
          Clin Nutr
          Clinical nutrition (Edinburgh, Scotland)
          0261-5614
          1532-1983
          29 May 2018
          16 April 2018
          April 2019
          01 April 2020
          : 38
          : 2
          : 682-688
          Affiliations
          [1 ]Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC
          [2 ]Department of Internal Medicine, Einstein Medical Center, Philadelphia, PA
          [3 ]Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea
          [4 ]Cancer Prevention and Control Program, University of South Carolina, Columbia, SC
          [5 ]Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC
          [6 ]Connecting Health Innovations, LLC, Columbia, SC
          [7 ]Department of Biostatistics, College of Medicine, The Catholic University of Korea, Seoul, Korea
          Author notes
          Corresponding Author: Seong-Su Lee, MD, PhD, Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Bucheon St. Mary's Hospital, The Catholic University of Korea, 327 Sosa-ro, Wonmi-gu, Bucheon-si, Gyeonggi-do, 420-717 Republic of Korea, Telephone: 82-32-340-2025; Fax: 82-32-340-2039; mddaniel@ 123456catholic.ac.kr
          Article
          PMC6389430 PMC6389430 6389430 nihpa967089
          10.1016/j.clnu.2018.04.002
          6389430
          29705061
          917e469c-7a91-4cd6-bef7-7027489dc532
          History
          Categories
          Article

          obesity,mortality,National Health and Nutrition Examination Survey III,metabolic health,overweight,Dietary Inflammatory Index

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