Economic and health-related quality of life impacts of posttraumatic stress disorder: a systematic review.

Disorders of gut‐brain interaction (DGBI) are highly prevalent conditions, with a global prevalence of 40.3% among adults []. These disorders are primarily characterized by gastrointestinal (GI) symptoms and can be categorized into anatomical groups based on the presumed origin of symptoms [, ]. Overlap between DGBI categories is frequently observed, with the number of affected gastrointestinal regions being related to greater symptom severity, psychological comorbidity, and reduced quality of life []. Many patients also report concomitant non‐GI complaints, underscoring the complex and multidimensional impact of DGBI [, ]. Fatigue is one such symptom, defined as a persistent feeling of mental or physical tiredness or weakness that is disproportionate to or independent of activity, and that is not alleviated by rest [, ]. It has been reported as one of the most bothersome non‐GI symptoms in patients with irritable bowel syndrome (IBS), a prototypical DGBI [, ]. In some cases, it is perceived as equally distressing as the GI symptoms themselves [, ]. Furthermore, fatigue has been shown to exert a multidimensional impact on patient outcomes, including increased symptom severity, impaired quality of life, reduced work productivity, and greater healthcare utilization and costs, underscoring the importance of recognizing and addressing this symptom [, , , ]. Importantly, although fatigue is recognized as a distressing and highly prevalent symptom in IBS, robust prevalence estimates for the broader DGBI population are lacking. Consequently, it remains unclear whether fatigue is underrecognized across DGBI as a whole and to what extent it contributes to overall patient burden. Efforts to effectively recognize and manage fatigue in DGBI are hindered by a limited understanding of its underlying mechanisms. The overlap with GI symptoms may be partially explained by shared pathophysiological pathways, including dysregulation of the hypothalamic–pituitary–adrenal axis, abnormalities in serotonin neurotransmission and alterations in immune activation with low‐grade inflammation [, , ]. Similar mechanisms have been implicated in fatigue among patients with inflammatory bowel disease (IBD) in remission, suggesting a role for altered gut‐brain signalling []. Multiple individual and health‐related factors may influence the occurrence of fatigue, including sex, BMI, sleep disturbance and psychological comorbidity [, , , ]. Furthermore, it remains uncertain whether fatigue represents a distinct non‐GI symptom or is secondary to comorbid conditions, such as depression, in which fatigue and loss of energy are central features []. Notably, many patients with IBS and functional dyspepsia (FD), another DGBI, meet the criteria for chronic fatigue syndrome, yet the mechanisms driving this overlap remain to be elucidated [, ].