From Dysbiosis to Distress: The Gut–Brain Connection in Trauma-Related Disorders

<b>Background</b>: Post-traumatic stress disorder (PTSD) and trauma-related disorders are increasingly recognized as complex conditions involving not only psychological and neurobiological factors but also systemic physiological alterations. Among these, growing evidence points to the crucial role of the gut-brain axis in modulating stress responses, emotional regulation, and neuroinflammation. <b>Objective</b>: This narrative review aims to synthesize the emerging literature on the interactions between the gut microbiota and the central nervous system in PTSD and trauma-related disorders, highlighting potential mechanisms and therapeutic implications. <b>Methods</b>: A comprehensive search of the literature was conducted across PubMed and Scopus and Web of Science as primary bibliographic databases, focusing on clinical, preclinical, and translational studies published in the last two decades. Emphasis was placed on studies exploring the microbiota's influence on neuroendocrine and immune pathways relevant to trauma, as well as intervention studies targeting the gut-brain axis. <b>Results</b>: Evidence suggests that dysbiosis and gut permeability alterations are associated with PTSD symptomatology, possibly via mechanisms involving hypothalamic-pituitary-adrenal (HPA) axis dysregulation, neuroinflammation, vagal signaling, and altered neurotransmitter production. Preclinical models support a bidirectional relationship between early-life stress, trauma, and gut microbiota alterations. Furthermore, preliminary clinical data indicate that interventions such as probiotics, diet modulation, and psychobiotics may exert beneficial effects on trauma-related psychopathology. <b>Conclusions</b>: The gut-brain axis represents a promising framework for understanding the pathophysiology of PTSD and related conditions. Although research is still in its early stages, targeting gut microbiota may offer novel preventive and therapeutic strategies. Further longitudinal and mechanistic studies are needed to validate these findings and guide clinical translation.