Nitin Shivappa1, Marialaura Bonaccio2, James R Hebert3, Augusto Di Castelnuovo2, Simona Costanzo2, Emilia Ruggiero2, George Pounis2, Maria Benedetta Donati2, Giovanni de Gaetano2, Licia Iacoviello4. 1. Cancer Prevention and Control Program, University of South Carolina, Columbia, South Carolina, USA; Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, South Carolina, USA; Connecting Health Innovations LLC, Columbia, South Carolina, USA. Electronic address: Shivappa@mailbox.sc.edu. 2. Department of Epidemiology and Prevention, IRCCS Istituto Neurologico Mediterraneo NEUROMED, Pozzilli (IS), Italy. 3. Cancer Prevention and Control Program, University of South Carolina, Columbia, South Carolina, USA; Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, South Carolina, USA; Connecting Health Innovations LLC, Columbia, South Carolina, USA. 4. Department of Epidemiology and Prevention, IRCCS Istituto Neurologico Mediterraneo NEUROMED, Pozzilli (IS), Italy; Department of Medicine and Surgery, Research Center in Epidemiology and Preventive Medicine (EPIMED), University of Insubria, Varese, Italy.
Abstract
OBJECTIVES: The association between diet and inflammation is well documented. Yet, no evidence exists on the relationship between the inflammatory potential of the diet and low-grade inflammation (LGI) as measured by a composite score of plasma and cellular biomarkers. The aim of this study was to assess the association between the Dietary Inflammatory Index (DII®) and LGI in a large population-based cohort. METHODS: Cross-sectional analyses were conducted on data from 20 823 adults (age ≥35 y; 48% male) without acute inflammation, who were recruited within the general population of the Moli-sani study from 2005 to 2010. LGI was measured by using a composite score (INFLA-score) including platelet and leukocyte counts, the granulocyte to lymphocyte ratio, and C-reactive protein. DII scores were computed based on dietary intake assessed by the EPIC food frequency questionnaire. Multivariable linear regression models were fit to produce adjusted regression coefficients and 95% confidence intervals (CIs). RESULTS: Higher DII scores were associated with increased LGI (β = 0.131; 95% CI, 0.089-0.174 for the highest versus lowest quintile of DII) after adjusting for age, sex, lifestyle, prevalence of chronic diseases, and health conditions. A higher DII score also was positively associated with each single biomarker of inflammation included in the INFLA-score, unhealthy behaviors (smoking, sedentary lifestyle), and insulin. CONCLUSIONS: Higher DII scores, indicating greater inflammatory potential of the diet, were directly associated with LGI, as measured by a composite score of plasma and cellular biomarkers of inflammation. These findings are consistent with the contributing role of diet-mediated inflammation in increasing risk for inflammation-related chronic diseases.
OBJECTIVES: The association between diet and inflammation is well documented. Yet, no evidence exists on the relationship between the inflammatory potential of the diet and low-grade inflammation (LGI) as measured by a composite score of plasma and cellular biomarkers. The aim of this study was to assess the association between the Dietary Inflammatory Index (DII®) and LGI in a large population-based cohort. METHODS: Cross-sectional analyses were conducted on data from 20 823 adults (age ≥35 y; 48% male) without acute inflammation, who were recruited within the general population of the Moli-sani study from 2005 to 2010. LGI was measured by using a composite score (INFLA-score) including platelet and leukocyte counts, the granulocyte to lymphocyte ratio, and C-reactive protein. DII scores were computed based on dietary intake assessed by the EPIC food frequency questionnaire. Multivariable linear regression models were fit to produce adjusted regression coefficients and 95% confidence intervals (CIs). RESULTS: Higher DII scores were associated with increased LGI (β = 0.131; 95% CI, 0.089-0.174 for the highest versus lowest quintile of DII) after adjusting for age, sex, lifestyle, prevalence of chronic diseases, and health conditions. A higher DII score also was positively associated with each single biomarker of inflammation included in the INFLA-score, unhealthy behaviors (smoking, sedentary lifestyle), and insulin. CONCLUSIONS: Higher DII scores, indicating greater inflammatory potential of the diet, were directly associated with LGI, as measured by a composite score of plasma and cellular biomarkers of inflammation. These findings are consistent with the contributing role of diet-mediated inflammation in increasing risk for inflammation-related chronic diseases.
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Authors: Nitin Shivappa; James R Hébert; Ernst R Rietzschel; Marc L De Buyzere; Michel Langlois; Evi Debruyne; Ascensión Marcos; Inge Huybrechts Journal: Br J Nutr Date: 2015-02-02 Impact factor: 3.718
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Authors: Nitin Shivappa; James R Hébert; Valentina Rosato; Marta Rossi; Massimo Libra; Maurizio Montella; Diego Serraino; Carlo La Vecchia Journal: Urology Date: 2016-09-29 Impact factor: 2.649
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Authors: Catherine M Phillips; Ling-Wei Chen; Barbara Heude; Jonathan Y Bernard; Nicholas C Harvey; Liesbeth Duijts; Sara M Mensink-Bout; Kinga Polanska; Giulia Mancano; Matthew Suderman; Nitin Shivappa; James R Hébert Journal: Nutrients Date: 2019-08-12 Impact factor: 5.717