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Intestinal dysbiosis as a common denominator in Crohn’s disease and colorectal cancer: (Master thesis)

Έρτσου, Δήμητρα–Μαρία/ Ertsou, Dimitra-Maria/ Τρόφιμα, Διατροφή και Μικροβίωμα

This paper reviews the critical role of gut dysbiosis as a common denominator in the pathophysiology of Crohn's disease and both colorectal and small intestinal cancers, focusing on the impact of diet and specific nutritional interventions. Under eubiotic conditions, the gut microbiome maintains immunological homeostasis and mucosal barrier integrity. However, its disruption triggers dysbiosis, increased intestinal permeability ("leaky gut"), and metabolic endotoxemia, driving the chronic low-grade inflammation that supports carcinogenesis. In Crohn's disease, there is a pronounced depletion of beneficial bacteria, such as Faecalibacterium prausnitzii and Roseburia intestinalis, which produce anti-inflammatory short-chain fatty acids (SCFAs), alongside an expansion of pathogenic families like Enterobacteriaceae. In colorectal cancer, specific microorganisms, including Fusobacterium nucleatum, E. coli (pks+), and enterotoxigenic Bacteroides fragilis (ETBF), promote oncogenesis by activating pro-tumorigenic pathways (such as beta-catenin), producing genotoxins (colibactin), and disrupting epithelial tight junctions. While the small intestine normally exhibits a relative "immunity" to neoplasia, the onset of Small Intestinal Bacterial Overgrowth (SIBO) collapses these protective mechanisms. SIBO induces the deconjugation of bile salts into cytotoxic free bile acids, leading to reactive hyperplasia, reactive oxygen species (ROS) accumulation, and severe DNA damage, while simultaneously causing vitamin B12 and folate deficiencies that impair genomic repair pathways. Diet serves as the primary modifiable factor governing this microbial balance. While the Western dietary pattern (high in saturated fats and simple sugars) exacerbates dysbiosis, the Mediterranean Diet provides strong anti-inflammatory protection. Targeted strategies, such as Exclusive Enteral Nutrition (EEN) and the Crohn's Disease Exclusion Diet (CDED) combined with PEN, effectively promote mucosal healing and induce clinical remission in Crohn's disease. For colorectal cancer prevention, key recommendations include adequate dietary fiber intake (which ferments into butyrate to induce cancer cell apoptosis), restricting red and processed meat (avoiding genotoxic HCAs, PAHs, and NOCs), and ensuring optimal calcium and vitamin D levels. For SIBO and small intestinal cancer management, the Low-FODMAP diet and Elemental Diets reduce bacterial load, while omega-3 fatty acids attenuate the inflammatory cascade. Despite the limitations of current human studies, future clinical perspectives point toward personalized precision nutrition driven by metagenomic profiling and artificial intelligence.