Objectives:The low FODMAPs diet has emerged as an option for the treatment of irritable bowel syndrome (IBS). One major challenge of this diet is that it is very restrictive, and compliance is usually low. Preliminary findings suggest an association between eating disorder (ED) and the risk of developing IBS. The primary aim of the study is to assess the correlation between compliance to low FODMAPs diet and risk of eating disorder behaviours among an irritable bowel syndrome cohort.
Methods:We report a single centre study in the IBS patient population at University College London Hospital (UCLH). 233 patients (186 female) who commenced a low FODMAPs group programme for IBS (Rome III or IV). Self-reported diet adherence at the end of the 6week programme was measured. At baseline, participants completed the SCOFF questionnaire (a validated 5-item screening tool for EDs), the validated HADS questionnaire and the validated IBS-symptom severity score (IBS-SSS).
Results:The SCOFF questionnaire identified 54 (23%) patients at an increased risk of ED behaviour. Overall, 95 (41%) participants were diet-adherent at 6 weeks, with significantly greater adherence in identified ED individuals (57%). The highest adherence rate (51%) was in the IBS-D subtype and the lowest rate (10%) in IBS-C. There was no significant relationship between IBS symptom severity and either adherence or ED severity.
Conclusion:In our IBS patient cohort greater adherence to a low FODMAPs diet is associated with eating disorder behaviour. The implications of our study are for clinicians to have a high index of suspicion of EDs in IBS patients, but also that low FODMAPs dietary advice to the general IBS population should be couched alongside psychological support.
Reduced contractile effectiveness persisted in BE with the more representative esophageal challenge of swallowing solids and free drinking; while in ENRD and FHC peristalsis usually improved, demonstrating peristaltic reserve. Furthermore, symptom association and refluxate clearance were reduced in BE. These factors may underlie BE pathogenesis.
Introduction: Despite clinical relevance and potential role on the disease pathogenesis, underlying mechanisms of constipation in Parkinson's disease (PD) remain poorly understood. A systematic assessment using complementary physiological investigations was performed to elucidate constipation pathophysiology in order to improve its symptomatic management. Methods: PD patients with constipation were evaluated with clinical questionnaires, colonic transit, high-resolution anorectal manometry and MRI defecography. Results were compared and correlated with clinical features. Results: A total of 42 patients (69% male; age 68 ± 8 years; disease duration 10.5 ± 6.1 years) were included, of whom 33 (78.6%) had objective constipation defined by < 3 bowel movements per week or straining. Severity of constipation measured by self-administered questionnaires correlated with disease severity, burden of motor and non-motor symptoms but not with age, disease duration or Parkinson's medications. Colonic transit and anorectal function (high-resolution anorectal manometry and/or MRI defecography) was assessed in 15 patients. A combination of both delayed colonic transit and anorectal dysfunction was the pattern most commonly found (60% of patients) and overall anorectal dysfunction was more prevalent than isolated slow transit constipation. Physiological findings were heterogeneous including reduced colonic motility, rectal hyposensitivity, defecatory dyssynergia and poor motor rectal function. Conclusion: Subjective constipation in PD is poorly correlated with commonly used definition, assessment questionnaires and physiological results. Multiple complex overlapping pathophysiological mechanisms are responsible including slow transit and anorectal dysfunction. Complementary investigations to assess colonic transit and anorectal function are required in those with refractory symptoms for a systematic assessment and appropriate symptomatic management.
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