Editorial: Cumulative Impact of Clinical Disease Activity, Biochemical Activity and Psychological Health on the Natural History of Inflammatory Bowel Disease During 8 Years of Longitudinal Follow-Up. Authors' Reply

Abstract

We would like to thank Drs Massouridis and Swaminathan for their editorial dealing with our article and welcome this opportunity for further discussion [1, 2]. Bi-directionality of gut–brain axis communications has been highlighted consistently in inflammatory bowel disease (IBD), with both a high prevalence of symptoms of common mental disorders (CMD) and an association between the presence of these symptoms and future adverse disease outcomes [3]. Although poor psychological health is most apparent during periods of disease activity, the prevalence of symptoms compatible with a CMD remains twice that of the general population even in quiescent disease, suggesting factors beyond inflammatory burden contribute to their development [1, 3]. Furthermore, a recently published longitudinal follow-up study examining trajectories of these symptoms in patients with IBD demonstrates that abnormal anxiety and depression scores persist in almost half of patients, suggesting poor psychological health is a constant for many patients [4]. Psychological health may, therefore, be an important therapeutic target in IBD.

A biopsychosocial model of care is advocated for patients with irritable bowel syndrome (IBS), including access to brain–gut behavioural therapies and gut–brain neuromodulators to manage the associated symptoms [5, 6]. With the current lack of focus on psychological health in IBD management guidelines, holistic care models are yet to translate to routine IBD care. A substantial barrier to the implementation of such models is a lack of informative research. Few randomised controlled trials (RCTs) have assessed the effects of brain–gut behavioural therapies or gut–brain neuromodulators in patients with IBD with pre-existing psychological co-morbidity, who are the patient group most likely to benefit from the addition of such therapies [7]. In addition, identifying patients with symptoms of a CMD may be difficult given the time-sensitive nature of routine IBD care, where the focus is on managing inflammatory burden. Model-based clustering techniques incorporating measures of psychological and gastrointestinal symptom severity have identified clusters of patients with IBD and high psychological symptom burden, and could serve in clinical practice to identify subgroups of patients who may experience a benefit from brain–gut behavioural therapies or gut–brain neuromodulators [8]. Furthermore, one quarter of patients with IBD with endoscopically quiescent disease also report symptoms that are compatible with IBS [9]. Such patients, if identified in clinical practice, may also be best managed with brain–gut behavioural therapies or gut–brain neuromodulators, similar to the paradigm in IBS.

Finally, as suggested, replication of this research is required in ethnically and socioeconomically diverse cohorts [2]. In fact, the underrepresentation of ethnic minorities in all aspects of research is a significant issue, and this lack of inclusivity may, ultimately, result in healthcare inequality for these communities. This is true not only in observational research, but also in RCTs of IBD therapies, where ethnic minority representation is clearly diminished [10]. Strategies to ensure inclusivity of ethnic minority groups and participants from diverse socioeconomic backgrounds in research are essential. Qualitative research studying the barriers to participation among these groups is necessary and should be a priority.