In a study involving 198 adults participants, better diet quality was linked to lower inflammation in those with inflammatory bowel disease.
However, the analysis showed that the gut microbiome played different roles in Crohn’s disease (CD) compared with ulcerative colitis (UC).
In the study, 49 patients with CD, 49 with UC and 100 healthy controls completed a validated 58-item food frequency questionnaire and provided stool samples at baseline and 6 months. Researchers used shotgun metagenomic sequencing to identify which microbes were present and what functions they could perform. To assess clinical activity, they used the Harvey-Bradshaw Index (HBI) for CD and the Colitis Activity Index (CAI) for UC as well as measured C-reactive protein (CRP) and fecal calprotectin in both groups. Causal mediation analyses adjusted for age, sex, body mass index, smoking, infliximab, mesalazine, and recent antibiotic use.
Dietary profiles differed significantly between inflammatory bowel disease (IBD) and controls at the level of food items, food groups, and macronutrients (Permutational Multivariate Analysis of Variance [PERMANOVA]), with CD and UC clustering more tightly compared with controls. In addition, both IBD groups reported a lower intake of vegetables, fruits, nuts, seeds, and fiber, alongside lower scores on the Alternative Mediterranean Diet (aMED), Healthy Eating Index–2015 (HEI-2015), Índice de Alimentación Saludable, the Healthy Food Diversity Index, Mean Adequacy Ratio (MAR), and healthful Plant-Based Diet Index (hPDI). The participants with CD also had reduced carbohydrate and protein intake.
Microbial diversity followed a disease gradient, in which dviersity was lowest in the participants with CD, intermediate in those with UC, and highest in controls (Chao1 and Shannon indices. Microbial dysbiosis scores were highest in the participants with CD. Alpha diversity correlated inversely with CRP and bowel frequency, while dysbiosis correlated positively. Higher aMED, HEI-2015, hPDI, and MAR scores were associated with greater diversity and lower dysbiosis.
Overall, the researchers found that the participants' usual fiber intake wasn't linked to levels of CRP, calprotectin, or overall disease activity. The only exception was a small link in those with CD, where higher fiber intake was related to slightly lower HBI scores. They also found no statistically significant differences in diet between the participants in relapse and those in remission. Alterations in diet over the 6-month study period weren't linked to changes in inflammatory markers.
In CD, healthier dietary indices, coffee, and whole-wheat bread were associated with lower HBI scores but not via global diversity metrics. Instead, taxon-specific mediation was observed. Higher HEI-2015 and MAR scores and coffee intake were linked to lower HBI scores through the increased relative abundance of Bacteroides caccae, B faecis, and B thetaiotaomicron, relative to B fragilis. Whole-wheat bread intake was mediated by increased Butyricimonas paravirosa, B faecihominis, and Odoribacter splanchnicus as well as decreased Coprobacter fastidiosus. Coffee intake was also associated with lower calprotectin via increased Lawsonibacter asaccharolyticus and reduced Clostridiales bacterium.
Functional mediation analyses showed that short-chain fatty acid pathways play an important role. In CD, nearly one-third of coffee’s overall effect on the HBI was explained by a pathway that ferments hexitols into acetate. Soft drink intake was linked to higher HBI scores, and more than 80% of this effect was explained by a mixed-acid fermentation pathway.
In UC, most of the effects were explained by overall changes in the gut microbiome. Higher unhealthy Plant-Based Diet Index scores were linked to higher levels of CRP and calprotectin. This was partly because these diets were associated with lower microbial diversity and greater dysbiosis. Higher aMED scores were linked to lower CRP and calprotectin levels, mainly through reduced dysbiosis. About 60% of aMED’s anti-inflammatory effects on CRP were explained by an acetate-related pathway called acetylene degradation. Fruit, coffee, and olive oil intake showed similar patterns, with their effects linked to greater microbial diversity and less dysbiosis.
The researchers acknowledged limitations of their study, including reliance on self-reported diet and treatment of repeated measures as independent observations. “In UC, diet appears to modulate inflammation primarily through restoration of microbial diversity and functional balance, whereas in CD, selective modulation of specific taxa and metabolic pathways may play a dominant role,” wrote lead study author Luis Mayorga, of the Microbiome Lab at Vall d'Hebron Institut de Recerca at Vall d'Hebron Hospital Campus in Spain, and colleagues. “These findings underscore the potential of personalized, microbiome-informed dietary strategies as complementary tools for precision management of IBD.”
The study was funded by the Instituto de Salud Carlos III and co-funded by the European Union and the Spanish Ministry of Economy and Competitiveness. Additional support came from the Fondo Europeo de Desarrollo Regionaland the Agency for Management of University and Research Grants. THe study authors reported no competing interests.
Source: Gut
