Diet plays an important role in the development and progression of inflammatory bowel disease (IBD, comprising Crohn’s disease (CD) and ulcerative colitis (UC)). However, little is known about the extent to which different diets reflect inflammation in IBD beyond measures such as faecal calprotectin or C-reactive protein. In this study, we aimed to unravel associations between dietary patterns and circulating inflammatory proteins in patients with IBD. Plasma concentrations of 73 different inflammation-related proteins were measured in 454 patients with IBD by proximity extension assay (PEA) technology. Food frequency questionnaires (FFQ) were used to assess habitual diet. Principal component analysis (PCA) was performed to extract data-driven dietary patterns. To identify associations between dietary patterns and plasma proteins, we used general linear models adjusting for age, sex, BMI, plasma storage time, smoking, surgical history and medication use. Stratified analyses were performed for IBD type, disease activity and protein intake. A high-sugar diet was strongly inversely associated with fibroblast growth factor-19 (FGF-19) independent of IBD type, disease activity, surgical history and deviance from recommended protein intake (false discovery rate (FDR) < 0.05). Conversely, a Mediterranean-style pattern was associated with higher FGF-19 levels (FDR < 0.05). A pattern characterised by high alcohol and coffee intake was positively associated with CCL11 (eotaxin-1) levels and with lower levels of IL-12B (FDR < 0.05). All results were replicated in CD, whereas only the association with FGF-19 was significant in UC. Our study suggests that dietary habits influence distinct circulating inflammatory proteins implicated in IBD and supports the pro-and anti-inflammatory role of diet. Longitudinal measurements of inflammatory markers, also postprandial, are needed to further elucidate the diet–inflammation relationship.
|Publication status||Published - 17 Jun 2022|
Bibliographical noteFunding Information:
Funding: This work was supported by the collaborative T cell driven Immune Mediated Inflammatory Diseases (TIMID) project (LSHM18057-SGF) financed by the PPP allowance made available by Top Sector Life Sciences & Health to Samenwerkende Gezondheidsfondsen (SGF) to stimulate public-private partnerships and co-financing by health foundations that are part of the SGF. L.A.B. and R.K.W. are supported by a research grant from the Seerave Foundation. This work was further supported by Takeda (no grant no., to L.M.S.) and the Junior Scientific Masterclass (JSM), University of Groningen, the Netherlands (grant no. 17-57, to A.R.B.). The funders had no role in the design of the study, collection, analysis or interpretation of data or in writing the manuscript.
Conflicts of Interest: G.D. received research grants from Royal DSM and speaker’s fees from Janssen Pharmaceuticals, Takeda, Pfizer and Abbvie (outside the submitted work). RKW acted as consultant for Takeda; received unrestricted research grants from Takeda, Johnson & Johnson, Tramedico and Ferring; and received speaker’s fees from MSD, Abbvie and Janssen Pharmaceuticals (outside the submitted work). MJEC-K received speaker’s fees from Takeda (outside the submitted work). All other authors have no conflict of interest to declare.
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