Kathy Vagianos1, Leigh Anne Shafer1,2, Kelcie Witges1, Laura E Targownik1,3, Clove Haviva1, Lesley A Graff1,4, Kathryn A Sexton1,4, Lisa M Lix1,5, Michael Sargent1,2, Charles N Bernstein1,2. 1. Inflammatory Bowel Disease Clinical and Research Centre, University of Manitoba, Winnipeg, Manitoba, Canada. 2. Department of Internal Medicine, University of Manitoba, Max Rady College of Medicine, Rady Faculty of Health Sciences, Winnipeg, Manitoba, Canada. 3. Department of Medicine, University of Toronto, Toronto, Ontario, Canada. 4. Department of Clinical Health Psychology, University of Manitoba, Max Rady College of Medicine, Rady Faculty of Health Sciences, Winnipeg, Manitoba, Canada. 5. Department of Community Health Sciences, University of Manitoba, Max Rady College of Medicine, Rady Faculty of Health Sciences, Winnipeg, Manitoba, Canada.
Abstract
BACKGROUND: We aimed to investigate (1) the stability of inflammatory aspects of diet over 1 year among persons with inflammatory bowel disease (IBD) and (2) the impact of change in diet on changes in inflammation and IBD symptoms over 1 year. METHODS: Participants were recruited to the Manitoba Living with IBD Study and completed the Harvard Food Frequency Questionnaire (FFQ). The Dietary Inflammatory Index (DII) and the Empirical Dietary Inflammatory Index (EDII) were used to calculate the inflammatory potential of the diet. Inflammation was measured by fecal calprotectin (≥250 µg/g). Symptoms were measured by the IBD Symptom Inventory (IBDSI). All measures were obtained at baseline and 1 year. Dietary Inflammatory Index and Empirical Dietary Inflammatory Index scores >0 and <0 reflect pro- and anti-inflammatory diet, respectively. Variance components analyses were used to describe diet stability. Associations between changes in diet and changes in active inflammation and symptoms were assessed using ordinal logistic regression and multilevel linear regression modeling. RESULTS: One hundred thirty-five participants (66% CD) were included. Approximately one third of the variance in EDII (36%) and DII (33%) scores was explained by changes in diet over time. Each unit increase in the change in EDII (baseline to follow-up) was associated with a greater odds of FCAL, indicating active inflammation (>250 µg/g; odds ratio, 3.1; 95% confidence interval [CI], 1.02-9.93; P = 0.04) and with a rise in IBDSI of 6.7 (95% CI, 1.0-12.4; P = 0.022; theoretical IBDSI range, 0-81). There was no association between changes in DII and changes in FCAL or IBDSI. CONCLUSION: The EDII, but not the DII, may have utility to identify the inflammatory potential of diet. This inflammatory potential can contribute to inflammation and/or disease symptoms in persons with IBD.
BACKGROUND: We aimed to investigate (1) the stability of inflammatory aspects of diet over 1 year among persons with inflammatory bowel disease (IBD) and (2) the impact of change in diet on changes in inflammation and IBD symptoms over 1 year. METHODS: Participants were recruited to the Manitoba Living with IBD Study and completed the Harvard Food Frequency Questionnaire (FFQ). The Dietary Inflammatory Index (DII) and the Empirical Dietary Inflammatory Index (EDII) were used to calculate the inflammatory potential of the diet. Inflammation was measured by fecal calprotectin (≥250 µg/g). Symptoms were measured by the IBD Symptom Inventory (IBDSI). All measures were obtained at baseline and 1 year. Dietary Inflammatory Index and Empirical Dietary Inflammatory Index scores >0 and <0 reflect pro- and anti-inflammatory diet, respectively. Variance components analyses were used to describe diet stability. Associations between changes in diet and changes in active inflammation and symptoms were assessed using ordinal logistic regression and multilevel linear regression modeling. RESULTS: One hundred thirty-five participants (66% CD) were included. Approximately one third of the variance in EDII (36%) and DII (33%) scores was explained by changes in diet over time. Each unit increase in the change in EDII (baseline to follow-up) was associated with a greater odds of FCAL, indicating active inflammation (>250 µg/g; odds ratio, 3.1; 95% confidence interval [CI], 1.02-9.93; P = 0.04) and with a rise in IBDSI of 6.7 (95% CI, 1.0-12.4; P = 0.022; theoretical IBDSI range, 0-81). There was no association between changes in DII and changes in FCAL or IBDSI. CONCLUSION: The EDII, but not the DII, may have utility to identify the inflammatory potential of diet. This inflammatory potential can contribute to inflammation and/or disease symptoms in persons with IBD.
Authors: Fred K Tabung; Stephanie A Smith-Warner; Jorge E Chavarro; Kana Wu; Charles S Fuchs; Frank B Hu; Andrew T Chan; Walter C Willett; Edward L Giovannucci Journal: J Nutr Date: 2016-06-29 Impact factor: 4.798
Authors: Fred K Tabung; Stephanie A Smith-Warner; Jorge E Chavarro; Teresa T Fung; Frank B Hu; Walter C Willett; Edward L Giovannucci Journal: J Nutr Date: 2017-06-28 Impact factor: 4.798
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Authors: Marcela Guevara; Elena Salamanca-Fernández; Estrella Miqueleiz; Diana Gavrila; Pilar Amiano; Catalina Bonet; Miguel Rodríguez-Barranco; José María Huerta; Luis Bujanda; María José Sánchez; María Dolores Chirlaque; Antonio Agudo; Eva Ardanaz; Jesús Castilla Journal: Nutrients Date: 2021-06-26 Impact factor: 5.717