Background: The cardioprotective diet was reported to be associated with several chronic cardiometabolic diseases through an anti-inflammation effect. However, the association between the cardioprotective diet and the risk of inflammatory bowel disease (IBD) was unclear and deserved to be further explored. Methods: We calculated the cardioprotective diet score based on the consumptions of seven common food groups using the validated food frequency questionnaire data in the UK Biobank. Incident IBD was ascertained from primary care data, inpatient data, and the death registry. Cox proportional hazard models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between the cardioprotective diet score and the risk of IBD. Results: During a mean follow-up of 12.1 years, we documented 2717 incident IBD cases, including 851 cases of Crohn’s disease and 1866 cases of ulcerative colitis. Compared to participants with a cardioprotective diet score of 0–1, we observed a decreased risk of IBD among participants with cardioprotective diet scores of 3 (HR 0.85, 95% CI 0.73–0.99), 4 (HR 0.84, 95% CI 0.72–0.98), and 5–7 (HR 0.77, 95% CI 0.66–0.89) (p-trend < 0.001). Conclusions: A greater adherence to the cardioprotective diet was associated with a lower risk of IBD. Our finding highlighted the importance of focusing on the cardioprotective diet to prevent IBD.

Background: The Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet is emerging as a promising candidate for preventive measures against inflammatory bowel disease (IBD), though there is currently no direct evidence from population-based studies. This study aims to bridge the gap in understanding of the association of the MIND diet with IBD risk. Methods: We utilized data from 187 490 participants in the UK Biobank who provided dietary information and were free of IBD at baseline. Dietary information was obtained using a validated web-based 24-hour dietary recall questionnaire. A MIND diet score was evaluated based on the intake of ten beneficial and five unhealthy food groups and the scores were further grouped into tertiles. The outcome of interest was incident IBD, Crohn's disease (CD), and ulcerative colitis (UC). Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazard models adjusted for demographic characteristics, lifestyle factors, cancer history, and other dietary factors. Mediation analyses were performed to evaluate the role of systemic inflammation and metabolic disorders represented by the integrated biomarkers in the MIND diet–IBD association. Results: After a mean follow-up of 10.7 years, we documented 825 incident IBD cases (250 CD and 575 UC). The average age of the participants was 56.2 years, of which 55.0% were females. We found that greater adherence to the MIND diet, represented by a higher diet score, was associated with a lower risk of IBD (HR_{comparing extreme tertiles} 0.74, 95% CI 0.62–0.90, p = 0.002; p for trend = 0.005), CD (HR 0.66, 95% CI 0.47–0.94, p = 0.022; p for trend = 0.023), and UC (HR 0.78, 95% CI 0.62–0.98, p = 0.031; p for trend = 0.022). The associations were partially mediated by metabolic and inflammation status (mediation proportion: 5.5–15.9%). Conclusion: We found higher adherence to the MIND diet was associated with a lower risk of IBD, and that inflammatory and metabolic conditions may play an important role in the underlying mechanistic pathways.

Background: The effect of alcohol consumption on IBD remains inconclusive, potentially due to the overlooked role of alcohol metabolism. Objective: We aimed to investigate the potential modifying role of alcohol metabolic capacity in the associations. Design: A prospective cohort study (n=455 417) was used for association analysis between alcohol consumption and IBD risk using Cox proportional hazards regression. An acetaldehyde burden score, using genetic variants of alcohol dehydrogenase and aldehyde dehydrogenase validated by expression quantitative trait loci and proteomic data, was constructed to test effect modification. Genetic and metabolomic analyses, along with mice and human-derived colonic organoid experiments, were conducted to strengthen causal inference. Results: The inverse association between alcohol and IBD risk was mainly attributable to red wine. Among individuals with low burden, reflecting low acetaldehyde generation and high acetaldehyde metabolism, per SD increase in red wine consumption (equivalent to 59.4 g/week of pure alcohol intake) was associated with a 20% (95% CI 7% to 31%) reduced Crohn’s disease risk, whereas a 38% (95% CI 13% to 70%) increased risk among those with high burden. Genetic and metabolomic analyses further revealed harmful effects of acetaldehyde and protective effects of acetate. In vivo and in vitro experiments further confirmed these effects and showed that modulation of aldehyde dehydrogenase activity significantly altered colitis outcomes. Conclusion: Acetaldehyde metabolism burden modifies susceptibility to alcohol-related IBD and emphasises the importance of considering individual differences in alcohol metabolism when developing precision prevention strategies for IBD.

Background and Aims: Total carbohydrate intake has been inconsistently associated with inflammatory bowel disease (IBD) risk in previous epidemiological studies. We aimed to evaluate the effects of glycemic index and glycemic load, 2 main indicators for measuring the quality and quantity of carbohydrates, on the risk of IBD subtypes (ie, Crohn’s disease [CD] and ulcerative colitis [UC]). Methods: We included 121 148 UK Biobank participants without IBD at baseline, and collected dietary information from a validated web-based 24-hour dietary recall questionnaire. Overall dietary glycemic index and glycemic load were estimated. Cox proportional hazard models were used to calculate multivariable-adjusted hazard ratios (HRs) and 95% CIs. Substitution analyses were conducted to test associations after replacing medium- or high-glycemic-index foods with low-glycemic-index foods. Results: During a median follow-up of 10.6 years, 133 incident CD and 335 incident UC cases were identified. Dietary glycemic index was associated with UC but not CD. The HR of UC was 1.13 (95% CI, 1.01–1.27) per 1-SD increment and 1.46 (95% CI, 1.07–1.99) for the highest versus lowest quartile of glycemic index. Replacing medium or medium- and high-glycemic-index foods with low-glycemic-index foods was associated with a lower risk of UC. No significant associations were found between dietary glycemic load with risk of CD and UC. Conclusions: A higher dietary glycemic index, but not glycemic load, is associated with an increased risk of UC, underscoring the importance of considering glycemic index in dietary recommendations for UC prevention.