Letter: The Persistence of Anxiety and Depression in Inflammatory Bowel Disease: A Core Phenotype Beyond Inflammatory Activity

We read with great interest the longitudinal study by Riggott et al., who evaluated in a large IBD cohort trajectories of anxiety and depression using HADS scores collected quarterly over 1 year and then annually for 2 further years. They showed that fluctuating and persistently abnormal or worsening trajectories strongly predicted ongoing anxiety and depression symptoms, indicating that poor psychological health often remains stable over extended follow-up. Although disease outcomes such as flares, need for gluco-corticosteroids, treatment escalation, hospitalisation and intestinal resection were systematically recorded, these events were not more frequent according to anxiety or depression trajectories, suggesting no clear effect of mood trajectories on these adverse outcomes in this cohort [1]. These observations are consistent with epidemiological data on psychological comorbidity in IBD. A large systematic review and meta-analysis including more than 30,000 adults with IBD showed that about one-third of patients report anxiety symptoms and one-quarter report depressive symptoms, with higher prevalence during active disease. Female sex and Crohn's disease were associated with increased risk of both conditions, indicating that psychological distress is a core component of the IBD phenotype rather than a marginal feature [2]. Psychological comorbidity also appears to influence the clinical course of IBD. In a systematic review and meta-analysis of longitudinal studies, baseline anxiety and depression were associated with higher risks of treatment escalation, hospitalisation, surgery and composite adverse outcomes, even after adjustment for conventional predictors [3]. In this context, the lack of association between mood trajectories and adverse outcomes in the study by Riggott et al. contrasts with prior pooled evidence and may reflect differences in outcome definitions, follow-up duration and assessment of inflammatory burden. These discrepant findings underline the need for further longitudinal studies with rigorous phenotyping of psychological status and objective disease activity. Overall, available data support a bidirectional brain–gut axis, whereby psychological distress and intestinal inflammation can mutually influence each other over time, even if the magnitude and consistency of effects on specific clinical outcomes remain to be fully clarified [3, 4]. Clinically, these findings should prompt reconsideration of how psychological health is integrated into routine IBD care. Systematic screening with brief, validated instruments such as the HADS, used alongside biomarkers of inflammation, could identify patients with persistently abnormal or worsening scores who may benefit from psychological interventions, optimisation of anti-inflammatory therapy or closer multidisciplinary follow-up. At the same time, the therapeutic armamentarium for moderate-to-severe IBD is expanding, with several novel agents for Crohn's disease and ulcerative colitis in development [5, 6]. In this evolving context, incorporating patient-reported outcomes and robust assessment of psychological status into routine practice and clinical trials is essential to ensure that therapeutic choices reflect not only inflammatory control, but also the broader mental health and quality-of-life burden experienced by patients. In summary, the study by Riggott et al. reinforces the notion that anxiety and depression represent a persistent and clinically meaningful dimension of the IBD phenotype, even if their exact impact on specific clinical outcomes remains debated [1]. Future research should include interventional trials of integrated care models that combine advanced pharmacological strategies with structured psychological assessment and treatment, to test whether modifying adverse psychological trajectories can improve long-term outcomes in IBD. Brigida Barberio: conceptualization, writing – review and editing, writing – original draft. Edoardo Vincenzo Savarino: writing – review and editing, conceptualization. The authors have nothing to report. Brigida Barberio has served as speaker for Abbvie, Agave, Alfasigma, AGPharma, Eli Lilly, Ferring, Johnson & Johnson, MSD, Pfizer, Sofar, Takeda, Unifarco. Sha has served as consultant for Abbvie, Eli Lilly, Johnson & Johnson. Edoardo Vincenzo Savarino has served as speaker for Abbvie, Agave, AGPharma, Alfasigma, Aurora Pharma, CaDiGroup, Celltrion, Dr. Falk, EG Stada Group, Fenix Pharma, Fresenius Kabi, Galapagos, Janssen, JB Pharmaceuticals, Innovamedica/Adacyte, Malesci, MayolyBiohealth, Omega Pharma, Pfizer, Reckitt Benckiser, Sandoz, SILA, Sofar, Takeda, Tillots, Unifarco; has served as consultant for Abbvie, Agave, Alfasigma, Biogen, Bristol-Myers Squibb, Celltrion, DiademaFarmaceutici, Dr. Falk, Fenix Pharma, Fresenius Kabi, Janssen, JB Pharmaceuticals, Merck & Co, Nestle, Reckitt Benckiser, Regeneron, Sanofi, SILA, Sofar, Synformulas GmbH, Takeda, Unifarco; he received research support from Pfizer, Reckitt Benckiser, SILA, Sofar, Unifarco, Zeta Farmaceutici. This article is linked to Riggott et al. paper. To view this article, visit https://doi.org/10.1111/apt.70431. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.