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Background: Crohn’s disease (CD) patients suffer from nutritional deficiencies when in active disease. We aim to examine calorific intake, macronutrient choice and disordered eating behaviour in patients with active CD. Methods: CD patients with matched healthy volunteers (HV) were recruited. Active disease was defined by faecal calprotectin >250ug/g, C-reactive protein >5mg/dl, or active disease seen on endoscopy or imaging. Symptoms were quantified by Harvey-Bradshaw Index (HBI). Calorific intake was assessed by 24-h dietary recall. Disordered eating was assessed using validated questionnaires [Binge Eating Scale (BES); Power of Food Scale (PFS); Control of Eating Questionnaire (CoEQ); Dutch Eating Behaviour Questionnaire (DEBQ); Three Factor Eating Questionnaire (TFEQ)]. Results: 30 CD (18M:12F, Age:32.3±2.19, BMI:24.9±0.8) and 31 matched HV (19M:12F, Age:32.8±2.0, BMI:24.7±0.5) were recruited. Mean faecal calprotectin was 1032.5±176µg/g,C-reactive protein 83.8±47.1mg/L and HBI 4.8±1. There were no significant differences in calorific intake between groups. Protein intake was lower in the CD cohort (p=0.03). Hospital Anxiety and Depression score was higher (p=0.01) and CoEQ-Positive Mood (p=0.001) lower in CD. CD were characterised by higher BES (p=0.01) and lower CoEQ Craving Control (p=0.027) with greater craving for Sweet (p=0.043), Savoury (p=0.021) foods. PFS food present (p=0.005), DEBQ Emotional (p=<0.001) and External Eating (p=0.022) were significantly higher than HV. Conclusions: Reduced protein consumption and more prevalent disordered eating behaviour traits were present in CD. Greater binge eating and decreased control of cravings may be attributed to lower mood and higher anxiety observed. Patients may benefit from stronger psychological support with firm dietetic advice for healthy eating.

Background: Crohn’s disease (CD) patients suffer from nutritional deficiencies when in active disease. We aim to examine calorific intake, macronutrient choice and disordered eating behaviour in patients with active CD. Methods: CD patients with matched healthy volunteers (HV) were recruited. Active disease was defined by faecal calprotectin >250ug/g, C-reactive protein >5mg/dl, or active disease seen on endoscopy or imaging. Symptoms were quantified by Harvey-Bradshaw Index (HBI). Calorific intake was assessed by 24-h dietary recall. Disordered eating was assessed using validated questionnaires [Binge Eating Scale (BES); Power of Food Scale (PFS); Control of Eating Questionnaire (CoEQ); Dutch Eating Behaviour Questionnaire (DEBQ); Three Factor Eating Questionnaire (TFEQ)]. Results: 30 CD (18M:12F, Age:32.3±2.19, BMI:24.9±0.8) and 31 matched HV (19M:12F, Age:32.8±2.0, BMI:24.7±0.5) were recruited. Mean faecal calprotectin was 1032.5±176µg/g,C-reactive protein 83.8±47.1mg/L and HBI 4.8±1. There were no significant differences in calorific intake between groups. Protein intake was lower in the CD cohort (p=0.03). Hospital Anxiety and Depression score was higher (p=0.01) and CoEQ-Positive Mood (p=0.001) lower in CD. CD were characterised by higher BES (p=0.01) and lower CoEQ Craving Control (p=0.027) with greater craving for Sweet (p=0.043), Savoury (p=0.021) foods. PFS food present (p=0.005), DEBQ Emotional (p=<0.001) and External Eating (p=0.022) were significantly higher than HV. Conclusions: Reduced protein consumption and more prevalent disordered eating behaviour traits were present in CD. Greater binge eating and decreased control of cravings may be attributed to lower mood and higher anxiety observed. Patients may benefit from stronger psychological support with firm dietetic advice for healthy eating.

Background: Crohn’s disease (CD) patients suffer from nutritional deficiencies when in active disease. We aim to examine calorific intake, macronutrient choice and disordered eating behaviour in patients with active CD. Methods: CD patients with matched healthy volunteers (HV) were recruited. Active disease was defined by faecal calprotectin >250ug/g, C-reactive protein >5mg/dl, or active disease seen on endoscopy or imaging. Symptoms were quantified by Harvey-Bradshaw Index (HBI). Calorific intake was assessed by 24-h dietary recall. Disordered eating was assessed using validated questionnaires [Binge Eating Scale (BES); Power of Food Scale (PFS); Control of Eating Questionnaire (CoEQ); Dutch Eating Behaviour Questionnaire (DEBQ); Three Factor Eating Questionnaire (TFEQ)]. Results: 30 CD (18M:12F, Age:32.3±2.19, BMI:24.9±0.8) and 31 matched HV (19M:12F, Age:32.8±2.0, BMI:24.7±0.5) were recruited. Mean faecal calprotectin was 1032.5±176µg/g,C-reactive protein 83.8±47.1mg/L and HBI 4.8±1. There were no significant differences in calorific intake between groups. Protein intake was lower in the CD cohort (p=0.03). Hospital Anxiety and Depression score was higher (p=0.01) and CoEQ-Positive Mood (p=0.001) lower in CD. CD were characterised by higher BES (p=0.01) and lower CoEQ Craving Control (p=0.027) with greater craving for Sweet (p=0.043), Savoury (p=0.021) foods. PFS food present (p=0.005), DEBQ Emotional (p=<0.001) and External Eating (p=0.022) were significantly higher than HV. Conclusions: Reduced protein consumption and more prevalent disordered eating behaviour traits were present in CD. Greater binge eating and decreased control of cravings may be attributed to lower mood and higher anxiety observed. Patients may benefit from stronger psychological support with firm dietetic advice for healthy eating.

Background: Crohn’s disease (CD) patients suffer from nutritional deficiencies when in active disease. We aim to examine calorific intake, macronutrient choice and disordered eating behaviour in patients with active CD. Methods: CD patients with matched healthy volunteers (HV) were recruited. Active disease was defined by faecal calprotectin >250ug/g, C-reactive protein >5mg/dl, or active disease seen on endoscopy or imaging. Symptoms were quantified by Harvey-Bradshaw Index (HBI). Calorific intake was assessed by 24-h dietary recall. Disordered eating was assessed using validated questionnaires [Binge Eating Scale (BES); Power of Food Scale (PFS); Control of Eating Questionnaire (CoEQ); Dutch Eating Behaviour Questionnaire (DEBQ); Three Factor Eating Questionnaire (TFEQ)]. Results: 30 CD (18M:12F, Age:32.3±2.19, BMI:24.9±0.8) and 31 matched HV (19M:12F, Age:32.8±2.0, BMI:24.7±0.5) were recruited. Mean faecal calprotectin was 1032.5±176µg/g,C-reactive protein 83.8±47.1mg/L and HBI 4.8±1. There were no significant differences in calorific intake between groups. Protein intake was lower in the CD cohort (p=0.03). Hospital Anxiety and Depression score was higher (p=0.01) and CoEQ-Positive Mood (p=0.001) lower in CD. CD were characterised by higher BES (p=0.01) and lower CoEQ Craving Control (p=0.027) with greater craving for Sweet (p=0.043), Savoury (p=0.021) foods. PFS food present (p=0.005), DEBQ Emotional (p=<0.001) and External Eating (p=0.022) were significantly higher than HV. Conclusions: Reduced protein consumption and more prevalent disordered eating behaviour traits were present in CD. Greater binge eating and decreased control of cravings may be attributed to lower mood and higher anxiety observed. Patients may benefit from stronger psychological support with firm dietetic advice for healthy eating.

Reduced appetite has been observed in patients with ileal Crohn’s disease, which has been attributed to the upregulation of enteroendocrine cells and the consequent increase of satiety hormones secretion, therefore possibly negatively affecting appetite signalling to the central nervous system. The specific hypotheses to be tested in this thesis were that Crohn’s disease patients with ileal inflammation, when compared with Crohn’s disease patients with colonic inflammation and healthy controls, will show A) an alteration in brain-gut stimulation, B) an increase in the postprandial plasma enteroendocrine peptides response (CCK, GLP-1 and PYY) with associated alteration in appetite scores, C) a change in eating behaviour, and D) an alteration in brain structure and resting-state functional connectivity. Ileal Crohn’s disease patients showed greater fasting GLP-1 concentrations compared with healthy controls. No difference was found between ileal and colonic Crohn’s disease patients in the fasting and postprandial concentrations of GLP-1, CCK and PYY. The ileal Crohn’s disease patients showed a greater postprandial decrease in neuronal activity in the right superior frontal gyrus in the default mode network in response to saline compared with the fat meal. The mechanism underlying this phenomenon is unclear and requires further investigation. Greater neuronal activity was found in areas including the cerebellum, hippocampus, posterior cingulate gyrus, middle temporal gyrus, thalamus and medulla in response to fat, which is in line with the previous literature. The fat induced greater activity of the posterior cingulate gyrus, was driven by Crohn’s disease patients, with colonic Crohn’s disease patients showing stronger activation in this region compared with the ileal Crohn’s disease patients. This finding may be linked with abdominal pain or GLP-1 elevations, which remains to be investigated. Stronger hedonic control of food intake was observed in the ileal CD patient

Background: Crohn’s disease (CD) patients suffer from nutritional deficiencies when in active disease. We aim to examine calorific intake, macronutrient choice and disordered eating behaviour in patients with active CD. Methods: CD patients with matched healthy volunteers (HV) were recruited. Active disease was defined by faecal calprotectin >250ug/g, C-reactive protein >5mg/dl, or active disease seen on endoscopy or imaging. Symptoms were quantified by Harvey-Bradshaw Index (HBI). Calorific intake was assessed by 24-h dietary recall. Disordered eating was assessed using validated questionnaires [Binge Eating Scale (BES); Power of Food Scale (PFS); Control of Eating Questionnaire (CoEQ); Dutch Eating Behaviour Questionnaire (DEBQ); Three Factor Eating Questionnaire (TFEQ)]. Results: 30 CD (18M:12F, Age:32.3±2.19, BMI:24.9±0.8) and 31 matched HV (19M:12F, Age:32.8±2.0, BMI:24.7±0.5) were recruited. Mean faecal calprotectin was 1032.5±176µg/g,C-reactive protein 83.8±47.1mg/L and HBI 4.8±1. There were no significant differences in calorific intake between groups. Protein intake was lower in the CD cohort (p=0.03). Hospital Anxiety and Depression score was higher (p=0.01) and CoEQ-Positive Mood (p=0.001) lower in CD. CD were characterised by higher BES (p=0.01) and lower CoEQ Craving Control (p=0.027) with greater craving for Sweet (p=0.043), Savoury (p=0.021) foods. PFS food present (p=0.005), DEBQ Emotional (p=<0.001) and External Eating (p=0.022) were significantly higher than HV. Conclusions: Reduced protein consumption and more prevalent disordered eating behaviour traits were present in CD. Greater binge eating and decreased control of cravings may be attributed to lower mood and higher anxiety observed. Patients may benefit from stronger psychological support with firm dietetic advice for healthy eating.