Letter: Inflammatory Potential of the Diet and Risk of Crohn's Disease and Ulcerative Colitis

The study by Meyer et al. [1] based on the large EPIC cohort, employed rigorous statistical methods and utilised the Inflammatory Score of the Diet (ISD) to assess the impact of diet on the risk of inflammatory bowel disease (IBD). A key finding was that a high ISD score was significantly associated with an increased risk of Crohn's disease (CD), particularly among women, providing valuable dietary guidance for high-risk populations.

Despite the significance of this study, we would like to highlight some limitations.

First, the number of food items included in the Food Frequency Questionnaires (FFQs) across different centres ranged from 98 to 2059, indicating substantial variation in dietary diversity. However, the authors did not appear to have adjusted for region or centre as a covariate in subsequent analyses. This discrepancy may introduce systematic bias in ISD calculations across centres, potentially affecting the overall results. We suggest that future studies calculate ISD separately for each centre or standardise FFQ data across different regions to improve data comparability.

Second, the study examined the association between multiple dietary factors and IBD risk but did not appear to have applied false discovery rate correction or Bonferroni adjustment for multiple comparisons. This increases the risk of Type I errors, which may compromise the robustness of the conclusions. Future studies should employ appropriate statistical correction methods in multiple comparison analyses to reduce the likelihood of false positive results.

Third, a preliminary statistical power assessment suggested that the study's overall power, including both men and women, was low (~5%), with both groups falling below the recommended 80% threshold. Therefore, the lack of a significant association in men may be attributable to limited power rather than a true absence of a sex-specific effect. Furthermore, the non-significant interaction test between ISD and sex may be influenced by the overall low power rather than indicating the absence of a differential effect. Future studies should consider larger sample sizes, particularly in men, to enhance power and provide a more definitive evaluation of the impact of ISD on CD risk.

Finally, environmental factors like early antibiotic use, gastrointestinal infections, breastfeeding, diet, and smoking can alter gut microbiota and trigger immune activation in IBD-prone individuals [2]. Although the study adjusted for BMI, smoking, physical activity, and alcohol, it lacked adjustment for key confounders such as antibiotic use, breastfeeding history, and prior gastrointestinal infections.

Despite these limitations, this study remains a valuable contribution to the exploration of dietary influences on IBD. Future research may further enhance causal inference by integrating repeated dietary assessments and incorporating additional potential confounders. We appreciate the authors' contributions and look forward to future studies expanding on these findings.

Zhidong Zhou: writing – original draft, conceptualization. Nanren Sun: writing – original draft. Qiang Liu: writing – review and editing.

The authors have nothing to report.

The authors have nothing to report.

The authors declare no conflicts of interest.

This article is linked to Meyer et al. paper. To view these articles, visit https://doi.org/10.1111/apt.18497 and https://doi.org/10.1111/apt.70138.