We read the letter by Kountouras et al with interest. The authors comment on the findings presented in our recently published study, which provides evidence for the existence of bidirectional brain–gut interactions in patients with inflammatory bowel disease (IBD).1 Specifically, Kountouras et al provide a cogent overview of the putative pathophysiologic mechanisms that, when considered in combination, make up the brain–gut axis, dysfunction of which is the proposed mechanism underpinning our findings.