Letter: evidence of gut‐to‐brain and brain‐to‐gut pathways in the pathogenesis of functional gastrointestinal disorders – ‘first‐ever’ incidence would be needed to draw conclusions

SIRS, We read the article by Koloski et al. with interest. The authors aimed to evaluate if there are distinct groups of patients affected by functional gastrointestinal disorders (FGIDs): a group in which mood symptoms begin first (brain-to-gut patients) and another with gut symptoms as the starting condition (gut-to-brain patients). The existence of both groups would suggest that there are two independent pathways operating in the pathogenesis of irritable bowel syndrome (IBS) and functional dyspepsia (FD). To answer this question, a prospective population study was designed in which individuals responded to validated IBS and depression/anxiety questionnaires at two time points separated by an interval of 1 year. In their results, at baseline, the authors confirmed the existence of individuals who met criteria for mood disorders (but not for FGIDs) who later reported IBS or FD, and individuals who met criteria for FGIDs (but not for mood disorders) who later reported depression or anxiety. The authors argue that the study provides strong direct evidence that the gut and brain interacts bidirectionally in both IBS and FD. The authors have other publications with equivalent study designs addressing the same question. Similar longitudinal population studies have been performed in the past to shed a light on the natural history of FGIDs. 4 However, answering the question about the chronology of symptom development can be problematic. At baseline, these studies used the point prevalence or a very short period prevalence, instead of the lifetime prevalence to assess previous symptomatology. As Halder et al. stated in their prospective cohort study over a mean of 12 years, ‘this was not considered a true “firstever” incidence rate because subjects could have had symptoms (. . .) prior to the initial survey, which would not have been identified’. In another similar study, Ford et al. stated that ‘It should also be remembered that the incidence of new-onset IBS in this study is based on (. . .) only two points in time (. . .) and will therefore not include those that may have experienced (. . .) symptoms in the intervening years’. The use of point prevalence instead of lifetime prevalence is understandable since the latter can be strongly susceptible to recall bias, especially in the case of gastrointestinal or mood symptoms. Nevertheless, the natural order of appearance between FGIDs and mood disorders cannot be accurately assessed when a true ‘first-ever’ incidence is not collected. The paper by Koloski et al. had the same challenges related to the two-point symptom assessment. The lack of an in-depth discussion of these limitations was surprising. The authors concede that their results ‘do need to be interpreted with caution as FGIDs are not all stable over time and fluctuations can occur’. This fluctuation of symptoms complicates even more the interpretation of the results since the point prevalence assessed at the two time points will be a poor surrogate for the lifetime prevalence. New population studies with adequate study design will be needed to better elucidate the gut-to-brain and brain-to-gut pathways in FGIDs.