The etiopathogenesis of complex disorders affecting the gut–brain axis is based on a multifactorial model driven by the interaction between genetic susceptibility, environmental stimuli, and impairment of biological barriers. The intestinal epithelium and tight junction complexes regulate paracellular permeability; loss of barrier integrity allows macromolecules, luminal antigens, and dysbiotic metabolites to enter the bloodstream, contributing to a state of low-grade systemic inflammation capable of reaching and influencing the blood–brain barrier.

Within this framework, the first 1,000 days of life represent a critical developmental window: neonatal microbial colonisation and barrier maturation shape neuroimmune programming, hypothalamic–pituitary–adrenal (HPA) axis stress reactivity, and vagal function. In neurodevelopmental conditions such as autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), as well as in paediatric disorders of gut–brain interaction (DGBI), cohort data and metabolomic profiles require rigorous control of confounding factors, particularly to distinguish microbiological alterations secondary to food selectivity from primary causal relationships.

Throughout adolescence and into adulthood, this biological vulnerability may persist and manifest clinically through visceral pain and altered bowel habits, as observed in irritable bowel syndrome (IBS), as well as an increased susceptibility to mood disorders. It may also represent a potential pathway for enteric involvement in the prodromal stages of neurodegenerative diseases such as Parkinson’s disease and cognitive decline.

The congress aims to establish a key methodological framework by comparing preclinical research data with clinical trial outcomes, in order to define validated diagnostic and therapeutic pathways—including targeted dietary modulation, support for barrier integrity, specific probiotic strains, and vagal stimulation—across the entire life course.