P0759 The interplay between dietary intake and disease activity in Australian adults with and without Inflammatory Bowel Disease
Authors: Cosier D , Lambert K , Karen C , Batterham M , Little R D , Wu N , Tavakoli P , Ghaly S , Pipicella J L , Connor S , Leach S , Lemberg D , Houshyar Y , Jayawardana T , Koentgen S , Hold G 
Published: January 2025

Background

Diet has been considered as one driving factor in the onset and course of Inflammatory Bowel Disease (IBD[DT1] ) (1). However, the mechanisms of interplay between diet and disease activity are unclear. Given people living with IBD perceive diet to be an important modifiable factor in their disease management, ongoing research is needed to provide specific dietary recommendations (2). We explored dietary adequacy in people with IBD compared to healthy controls, and the association between dietary intake and disease activity.

Methods

We analysed cross-sectional baseline dietary and clinical data from the Australian IBD Microbiome (AIM) study, the largest longitudinal microbial cohort study in the Southern Hemisphere on people with Crohn’s disease (CD), Ulcerative colitis (UC), first-degree relatives and population healthy controls (both considered in the HC cohort). Nutrient intake, food groups, and the Dietary Inflammatory Index (DII) were calculated. Associations between dietary intake, clinical disease activity (remission or active) measured via the CDAI for CD participants or Partial Mayo for UC participants, and faecal calprotectin (FCP) were explored in adult participants.

Results

The analysis included 542 adults (CD = 155, UC = 144, HC = 243), with a median age of 46 years, and 58% female. Median partial Mayo (1 [0 – 2]) and CDAI (59 [29 – 146]) scores indicated clinical remission. Median FCP was higher in IBD (32.7 [0.0-179.0] μg/g) vs. HC (0.0 [0.0-0.0] μg/g), with no significant difference between UC and CD. Intake of grains, vegetable, dairy, and fruit was 25–50% below Australian Dietary Guideline recommended serves across all cohorts (3). Intake of dietary fibre, iodine and calcium was 25-40% lower than recommended intakes (4). There were no differences in intake of nutrients or food groups between IBD vs. HC or CD vs. UC cohorts. Within the UC cohort, kilojoule, iodine, iron, zinc, and grain intake were significantly lower in clinically active disease vs. remission. There was no difference in dietary intake based on clinical disease activity status in the CD cohort. The mean dietary inflammatory score was 0.17 ± 2.29, indicating a pro-inflammatory diet, with no differences between IBD and HC. No relationship was observed between dietary intake or DII score and FCP in IBD.

Conclusion

Dietary intake did not differ between the IBD cohort and HC cohorts. Both cohorts consumed pro-inflammatory diets with low adherence to Australian dietary guidelines. Further longitudinal studies will be beneficial to examine associations between baseline dietary intake and future disease activity.

References

1.Bischoff SC, Bager P, Escher J, Forbes A, Hébuterne X, Hvas CL, Joly F, Klek S, Krznaric Z, Ockenga J, Schneider S. ESPEN guideline on Clinical Nutrition in inflammatory bowel disease. Clinical Nutrition. 2023 Mar 1;42(3):352-79.

2.Limdi JK, Aggarwal D and McLaughlin JT. Dietary practices and beliefs in patients with inflammatory bowel disease. Inflammatory bowel diseases 2016; 22: 164-170.

3.National Health and Medical Research Council. Australian Dietary Guidelines Summary. Canberra: National Health and Medical Research Council [online],. 2013.

4.National Health and Medical Research Council, Australian Government Department of Health and Ageing, New Zealand Ministry of Health. Nutrient Reference Values for Australia and New Zealand. Canberra: National Health and Medical Research Council; 2006.