Inflammatory bowel disease (IBD) represents a growing public health challenge worldwide, and its prevalence is increasing year by year. A growing body of evidence suggests that diet plays a key role in shaping the gut microbiota, whose dysbiosis is a significant component of IBD pathogenesis. In response to the limitations of traditional, one-size-fits-all dietary recommendations, the concept of precision nutrition is emerging, which involves tailoring nutrition to a patient’s clinical, biological, and genetic characteristics. Of particular importance in this context is nutrigenomics, the science that studies the impact of dietary components on gene expression and the modulation of immune processes. Dietary components, such as polyphenols and certain vitamins, may influence gene expression and immune pathways. However, direct evidence that specific nutrients directly regulate genes associated with inflammatory bowel disease in humans remains limited. Nutrigenomic mechanisms reveal complex relationships between diet, gut microbiota, and genetic predispositions in IBD, encompassing transcriptome regulation, metabolomic changes, and epigenetic processes. A personalized nutritional approach, based on regular assessment of clinical and biological parameters and the close integration of dietary therapy with comprehensive treatment, appears to be a promising direction for the further development of IBD therapy.

Inflammatory bowel diseases, such as Crohn’s disease and ulcerative colitis, are chronic inflammatory conditions of the gastrointestinal tract characterized by periods of active disease and remission. Their pathogenesis is multifactorial and involves genetic predisposition, immune response, environmental factors, and alterations in gut microbiota composition and function. Growing evidence suggests that gut microbiota-associated metabolites not only reflect disease activity but also participate in regulating the immune response and maintaining the integrity of the intestinal barrier. The most important groups of metabolites associated with inflammatory bowel diseases include short-chain fatty acids, bile acids, and tryptophan derivatives. Reduced fecal butyrate and acetate concentrations have been reported in inflammatory bowel diseases, although the diagnostic value of fecal short-chain fatty acids remains uncertain. Potential therapeutic approaches include short-chain fatty acid supplementation, particularly sodium butyrate, and dietary interventions aimed at increasing short-chain fatty acid concentrations; however, the clinical efficacy of short-chain fatty acid supplementation remains inconclusive, and evidence for dietary interventions is limited. In the future, the use of gut microbiota metabolites may be based on personalized strategies grounded in multiomic data, enabling precise modulation of the microbiota–metabolite–immune system axis.