Crohn's DiseaseNCT02379117
Eating Behaviour in Crohn's Disease
An observational study of Crohn's Disease, run by University of Nottingham at 1 site in United Kingdom.
Trial summary
Food intake is mainly controlled through interactions between the gut and brain (the homeostatic control) and through our environment, with food exposure, mood and past experiences (the hedonic control) playing a major role. Read more about this study
- Who is it for?
- Ages 16 to 75 yearsHealthy volunteers can take part
- Conditions the study is for
- Crohn's Disease
- How many people
- 61 participants
- Where
- 1 siteUnited Kingdom
- Study dates
- Apr 2015to Jan 2018
- Phase
- Observational
- Are there results?
- Yes, posted in the registrySummary in the doctors' view
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 16 to 75 years
- All sexes
- Healthy volunteers accepted
- Child, Adult, Older adult
Study population: Recruitment The chief investigator is a specialist in Inflammatory Bowel disease and also an associate professor of gastroenterology at the University of Nottingham and Nottingham University Hospital which is a tertiary-level care academic institution covering a population of approximately 1 million people for secondary-level care and 4.5 million people for tertiary-level care. Collectively we manage approximately 4000 IBD patients. Participants shall be recruited from two sources: 1. Crohn's Disease patients from clinic. 2. Crohns Disease patients and Healthy Volunteers via the study flyer and social media.
Who may be able to join
- -
- We will study a cohort of CD patients with active disease as defined by:
- Age 16-75 years
- Ulceration seen at ileocolonoscopy, aiming for a simple endoscopic score for Crohn's disease (SES-CD) of 4-19, in the absence of stricturing disease or,
- Intestinal inflammation or deep ulceration seen on CT or MR enterography, with the disease activity quantified via the MaRIA score or
- Faecal calprotectin of >250µg/g or
Show all 10Show fewer
- C-Reactive protein >5mg/dl or,
- Harvey-Bradshaw index score of 5-16
- Body mass index (BMI) of 18-30.
- For HV participants, inclusion criteria's 1 and 7 apply.
Who cannot join
- Present or recent (within 12 weeks) corticosteroid usage
- Malignant disease
- BMI <18 or >30.
- Significant cardiovascular or respiratory disease
- Diabetes mellitus
- Current Infection
Show all 13Show fewer
- Neurological or cognitive impairment; significant physical disability
- Significant hepatic disease or renal failure
- Abnormal blood results other than those explained by CD including bleeding diatheses (apart from in the case of HV where all unexplained blood results are an exclusion criteria) ,
- Subjects currently participating in (or in the last three months) any other research project
- pregnancy or breastfeeding or
- Severe CD where a delay in a change in medical treatment for 1 weeks would not be clinically advisable
- For HV participants, all exclusion criteria apply with the exception of criteria no.12
Trial locations and contacts
1 site in 1 country.
United Kingdom1 site
Queens Medical Centre
Nottingham, Nottinghamshire, NG7 2UH
About this study
Food intake is mainly controlled through interactions between the gut and brain (the homeostatic control) and through our environment, with food exposure, mood and past experiences (the hedonic control) playing a major role. The link between the gut and the brain is mainly controlled through enteroendocrine cells (EC). These cells in the bowel sense nutrients in the food and link with the brain to control how much we eat. They make a number of hormones that link with the brain to control one's eating habits.
Crohn's disease (CD) is an inflammatory disease of the bowel which can present with a number of symptoms including weight loss and loss of appetite. We thought some time ago that an increase in the number and function of these EC could play a central role. Since then we have carried out work which has shown that in CD these EC increase in number and produce more hormones after a meal. This finding could have a negative effect on food intake. This would be one explanation to the symptoms so commonly experienced by these patients.
Read more
In CD we thus feel that there might be an imbalance in the appetite control. We expect an increasingly sensitive gut to food intake and a subdued mood and perception to food reward and that this imbalance will lead to a decrease in food reward and consequently a decrease in food intake.
This study will be carried out using Healthy Volunteers and CD patients. We plan to measure food intake though telephone interviews and plan to analyse eating behaviour through 5 questionnaires.This study will help us to improve our understanding of what it is that controls food intake. This will be particularly important to patients with CD who routinely lose weight and appetite.
Read the detailed description
STUDY BACKGROUND INFORMATION AND RATIONALE
Crohn's disease (CD) patients can present with a variety of luminal and extra-luminal symptoms but nutritional abnormalities are a very common but poorly studied [1] problem in this disease [2]. Apart from disease burden and repeated surgery, reduced appetite [3] and associated symptoms such as nausea undoubtedly contribute, with a major impact on quality of life.
Appetite and satiation, the processes by which a meal is terminated, involve complex interactions of homeostatic and hedonic factors. While the hypothalamus is central in the homeostatic control of food intake, other neural circuits integrate environmental and emotional cues to constitute the hedonic drive of appetite regulation. The homeostatic control of food intake is governed by the enteroendocrine-gut brain axis. Enteroendocrine cells (EC) play a pivotal role in orchestrating physiological functions in the gastrointestinal (GI) tract. Sensing the nutrient content of the lumen, they secrete multiple peptides and amines that control gut secretory and motor functions. Gut hormones act on vagal afferents in the GI tract, directly relaying to key central nervous system (CNS) nuclei that interface within the hypothalamus and other cortical areas to regulate food intake. CD patients with active small bowel inflammation show significant up-regulation of EC cells with an increase in ileal expression of chromogranin A [4, 5], glucagon-like peptide-1 (GLP-1) [4], key transcription factors in the stem cell to EC differentiation pathway [4] , plasma polypeptide YY (PYY) [3], cholecystokinin (CCK) [6] levels and a reduction in the key enzyme dipeptidyl peptidase-4 expression [7]. This increase in plasma peptide levels is associated with the symptoms of nausea and anorexia, with both symptoms, and tissue and plasma EC-peptide expression decreasing to normality in remission [3].
An increase in EC expression at the tissue and plasma level might affect appetite regulation through an increase in CNS signalling.
Fatty-acids infused in the gut, lead to a CCK-dependent increase in CNS activity in areas related to homeostatic control of feeding such as the brainstem, the pons, hypothalamus, cerebellum and the motor cortical areas [8]. Glucose has been shown to decrease the response in the upper hypothalamus [9], possibly via a GLP-1-mediated pathway [10]. Ghrelin and PYY have known homeostatic CNS signalling properties but play a hedonic role in the control of food intake [11]. In effect, the increase in plasma PYY and GLP-1 seen after Roux-en-Y gastric bypass surgery in obese subjects or after parenteral administration [12] is associated with a lower activation in brain-hedonic food responses and a healthier eating behaviour [13]. In CD, we expect a subdued reward value of food, but postulate that this would be aversive, and inappropriately impairing appetite and food intake.
We hypothesize that in CD and small bowel inflammation we will observe a change in eating behaviour with loss of hedonic drives and food reward responses and an accentuated homeostatic response.
STUDY OBJECTIVES AND PURPOSE
PURPOSE The overall purpose of the study is to quantify food intake in patients with active Crohn's disease and compare it to when they are in remission and to healthy age, BMI and gender-matched healthy cohort of volunteers. We will quantify eating behaviour traits in the same patient cohort when in active disease and repeat when in remission. These data will be compared to that of healthy volunteers.
PRIMARY OBJECTIVE The primary objective is to quantify food intake in patients with active CD and compare this to HV.
SECONDARY OBJECTIVES The secondary objectives of this study are to a) quantify food intake in patients with active CD and compare that when in inactive disease. b) quantify changes in appetite and eating behaviour in patients with active CD and compare these to those in HV and inactive CD as measured by the appetite-related questionnaires
- Conditions
- Crohn's Disease
- Medical subject headings
- Crohn Disease
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Crohn's Disease Patients | Patients with a diagnosis of Crohn's disease fitting the studies inclusion \& exclusion criteria. | |
| Healthy Volunteers | For healthy volunteers the studies exclusion criteria apply. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Dietary Recalls (Calorific Intake)
The primary endpoints for this study will be food intake as measured by one telephone-administered 24-h dietary recall. Total calorific intake will be calculated.
Measured: Participants will be included in this study for 1 week
Secondary outcomes (5)
Three Factor Eating Questionnaire (TFEQ) Restraint, Disinhibition and Hunger Subscales
The TFEQ contains 51 items and measures three dimensions of human eating behaviour: Cognitive Restraint of Eating [I], Disinhibition [II], and Hunger [III]. Each item scores either 0 or 1 point. The minimum score for factors I, II. and III is therefore 0, with the pos- sible maximum scores being 21, 16, and 14 respectively. High scores mean worse outcome.
Measured: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
The Binge Eating Scale
The BES is a 16-item questionnaire that assesses the severity of binge eating tendencies. Eight questions describe the behavioural mani- festations of binge eating behaviour and eight describe the feelings and cognitions associated with binge eating. Scores are summed to produce a total score ranging from 0 to 46. Cut-off points have previously been reported denoting mild [≤17], moderate [18-26], and severe [≥27] binge eating behaviours. High score means worse outcome
Measured: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
The Power of Food Scale
The PFS is a 15-item questionnaire reflecting the psychological influence of the food environment. It measures appetite for, rather than consumption of, palatable foods and may be a useful measure of the hedonic impact of food environments replete with highly palatable foods. Items are grouped into three domains according to food proximity; food available but not physically present; food present but not tasted; and food tasted but not consumed. High scores mean worse outcome
Measured: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
The Dutch Eating Behaviour Questionnaire
The 33-item DEBQ assesses different eating styles that may contribute to weight gain: emotional eating, external eating, and restraint. 'Emotional eating' occurs in response to emotional arousal states such as fear, anger, or anxiety; 'external eating' occurs in response to external food cues such as sight and smell of food; and 'restraint eating' is overeating after a period of slimming when the cognitive resolve to diet is abandoned. High score means worse outcome
Measured: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
The Control of Eating Questionnaire
The CoEQ is a 21-item questionnaire designed to assess the severity and type of food cravings experienced over the previous 7 days. The CoEQ has four subscales: Craving Control, Craving for Savoury, Craving for Sweet, and Positive Mood. Items on the CoEQ are assessed by 100-mm visual analogue scales [VAS], with items relating to each subscale being averaged to create a final score. High positive mood is better outcome
Measured: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted4 Mar 2015 (estimated)
- Study startApr 2015
- Primary completionJan 2018
- Study completionJan 2018
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Posted resultsParticipant flow, outcome measures and adverse events reported by the sponsor.
- Publications (13)Papers the sponsor has linked to this study.
- Other trials for Crohn's DiseaseStudies of the same condition, open and under way.
- More trials run by University of NottinghamThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 61 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Nottingham
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Gordon W Moran, Principal investigator, University of Nottingham
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02379117
- Sponsor's protocol ID
- 15005
- Status last verified
- Apr 2019
- First submitted
- 26 Feb 2015
- Last updated
- 15 Jul 2019
- Results posted
- Yes, on ClinicalTrials.gov
- Data monitoring committee
- Yes
Publications
Bryant RV, Trott MJ, Bartholomeusz FD, Andrews JM. Systematic review: body composition in adults with inflammatory bowel disease. Aliment Pharmacol Ther. 2013 Aug;38(3):213-25. doi: 10.1111/apt.12372. Epub 2013 Jun 14.
PubMed 23763279Lochs H, Dejong C, Hammarqvist F, Hebuterne X, Leon-Sanz M, Schutz T, van Gemert W, van Gossum A, Valentini L; DGEM (German Society for Nutritional Medicine); Lubke H, Bischoff S, Engelmann N, Thul P; ESPEN (European Society for Parenteral and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Gastroenterology. Clin Nutr. 2006 Apr;25(2):260-74. doi: 10.1016/j.clnu.2006.01.007. Epub 2006 May 15.
PubMed 16698129Moran GW, Leslie FC, McLaughlin JT. Crohn's disease affecting the small bowel is associated with reduced appetite and elevated levels of circulating gut peptides. Clin Nutr. 2013 Jun;32(3):404-11. doi: 10.1016/j.clnu.2012.08.024. Epub 2012 Sep 3.
PubMed 22999064Moran GW, Pennock J, McLaughlin JT. Enteroendocrine cells in terminal ileal Crohn's disease. J Crohns Colitis. 2012 Oct;6(9):871-80. doi: 10.1016/j.crohns.2012.01.013. Epub 2012 Mar 3.
PubMed 22398079Moran GW, McLaughlin JT. Plasma chromogranin A in patients with inflammatory bowel disease: a possible explanation. Inflamm Bowel Dis. 2010 Jun;16(6):914-5. doi: 10.1002/ibd.21096. No abstract available.
PubMed 19760780Keller J, Beglinger C, Holst JJ, Andresen V, Layer P. Mechanisms of gastric emptying disturbances in chronic and acute inflammation of the distal gastrointestinal tract. Am J Physiol Gastrointest Liver Physiol. 2009 Nov;297(5):G861-8. doi: 10.1152/ajpgi.00145.2009.
PubMed 20501434Moran GW, O'Neill C, Padfield P, McLaughlin JT. Dipeptidyl peptidase-4 expression is reduced in Crohn's disease. Regul Pept. 2012 Aug 20;177(1-3):40-5. doi: 10.1016/j.regpep.2012.04.006. Epub 2012 May 2.
PubMed 22561447Lassman DJ, McKie S, Gregory LJ, Lal S, D'Amato M, Steele I, Varro A, Dockray GJ, Williams SC, Thompson DG. Defining the role of cholecystokinin in the lipid-induced human brain activation matrix. Gastroenterology. 2010 Apr;138(4):1514-24. doi: 10.1053/j.gastro.2009.12.060. Epub 2010 Jan 18.
PubMed 20080096Smeets PA, de Graaf C, Stafleu A, van Osch MJ, van der Grond J. Functional magnetic resonance imaging of human hypothalamic responses to sweet taste and calories. Am J Clin Nutr. 2005 Nov;82(5):1011-6. doi: 10.1093/ajcn/82.5.1011.
PubMed 16280432Pannacciulli N, Le DS, Salbe AD, Chen K, Reiman EM, Tataranni PA, Krakoff J. Postprandial glucagon-like peptide-1 (GLP-1) response is positively associated with changes in neuronal activity of brain areas implicated in satiety and food intake regulation in humans. Neuroimage. 2007 Apr 1;35(2):511-7. doi: 10.1016/j.neuroimage.2006.12.035. Epub 2007 Jan 18.
PubMed 17317222Batterham RL, ffytche DH, Rosenthal JM, Zelaya FO, Barker GJ, Withers DJ, Williams SC. PYY modulation of cortical and hypothalamic brain areas predicts feeding behaviour in humans. Nature. 2007 Nov 1;450(7166):106-9. doi: 10.1038/nature06212. Epub 2007 Oct 14.
PubMed 17934448De Silva A, Salem V, Long CJ, Makwana A, Newbould RD, Rabiner EA, Ghatei MA, Bloom SR, Matthews PM, Beaver JD, Dhillo WS. The gut hormones PYY 3-36 and GLP-1 7-36 amide reduce food intake and modulate brain activity in appetite centers in humans. Cell Metab. 2011 Nov 2;14(5):700-6. doi: 10.1016/j.cmet.2011.09.010. Epub 2011 Oct 13.
PubMed 22000927Scholtz S, Miras AD, Chhina N, Prechtl CG, Sleeth ML, Daud NM, Ismail NA, Durighel G, Ahmed AR, Olbers T, Vincent RP, Alaghband-Zadeh J, Ghatei MA, Waldman AD, Frost GS, Bell JD, le Roux CW, Goldstone AP. Obese patients after gastric bypass surgery have lower brain-hedonic responses to food than after gastric banding. Gut. 2014 Jun;63(6):891-902. doi: 10.1136/gutjnl-2013-305008. Epub 2013 Aug 20.
PubMed 23964100
Study at a glance
From the registry record, last updated by the sponsor on 15 Jul 2019. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Eating Behaviour in Crohn's Disease
- ClinicalTrials.gov ID
- NCT02379117
- Acronym / sponsor ID
- 15005
- Conditions
- Crohn's Disease
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 61 participants (actual)
- Lead sponsor
- University of NottinghamUniversity, hospital or other
- Study start
- Apr 2015
- Primary completion
- Jan 2018 (actual)
- Study completion
- Jan 2018 (actual)
- First posted
- 4 Mar 2015 (estimated)
- Results
- Posted 15 Jul 2019
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Food intake is mainly controlled through interactions between the gut and brain (the homeostatic control) and through our environment, with food exposure, mood and past experiences (the hedonic control) playing a major role. The link between the gut and the brain is mainly controlled through enteroendocrine cells (EC). These cells in the bowel sense nutrients in the food and link with the brain to control how much we eat. They make a number of hormones that link with the brain to control one's eating habits.
Crohn's disease (CD) is an inflammatory disease of the bowel which can present with a number of symptoms including weight loss and loss of appetite. We thought some time ago that an increase in the number and function of these EC could play a central role. Since then we have carried out work which has shown that in CD these EC increase in number and produce more hormones after a meal. This finding could have a negative effect on food intake. This would be one explanation to the symptoms so commonly experienced by these patients.
In CD we thus feel that there might be an imbalance in the appetite control. We expect an increasingly sensitive gut to food intake and a subdued mood and perception to food reward and that this imbalance will lead to a decrease in food reward and consequently a decrease in food intake.
This study will be carried out using Healthy Volunteers and CD patients. We plan to measure food intake though telephone interviews and plan to analyse eating behaviour through 5 questionnaires.This study will help us to improve our understanding of what it is that controls food intake. This will be particularly important to patients with CD who routinely lose weight and appetite.
Detailed description
STUDY BACKGROUND INFORMATION AND RATIONALE
Crohn's disease (CD) patients can present with a variety of luminal and extra-luminal symptoms but nutritional abnormalities are a very common but poorly studied [1] problem in this disease [2]. Apart from disease burden and repeated surgery, reduced appetite [3] and associated symptoms such as nausea undoubtedly contribute, with a major impact on quality of life.
Appetite and satiation, the processes by which a meal is terminated, involve complex interactions of homeostatic and hedonic factors. While the hypothalamus is central in the homeostatic control of food intake, other neural circuits integrate environmental and emotional cues to constitute the hedonic drive of appetite regulation. The homeostatic control of food intake is governed by the enteroendocrine-gut brain axis. Enteroendocrine cells (EC) play a pivotal role in orchestrating physiological functions in the gastrointestinal (GI) tract. Sensing the nutrient content of the lumen, they secrete multiple peptides and amines that control gut secretory and motor functions. Gut hormones act on vagal afferents in the GI tract, directly relaying to key central nervous system (CNS) nuclei that interface within the hypothalamus and other cortical areas to regulate food intake. CD patients with active small bowel inflammation show significant up-regulation of EC cells with an increase in ileal expression of chromogranin A [4, 5], glucagon-like peptide-1 (GLP-1) [4], key transcription factors in the stem cell to EC differentiation pathway [4] , plasma polypeptide YY (PYY) [3], cholecystokinin (CCK) [6] levels and a reduction in the key enzyme dipeptidyl peptidase-4 expression [7]. This increase in plasma peptide levels is associated with the symptoms of nausea and anorexia, with both symptoms, and tissue and plasma EC-peptide expression decreasing to normality in remission [3].
An increase in EC expression at the tissue and plasma level might affect appetite regulation through an increase in CNS signalling.
Fatty-acids infused in the gut, lead to a CCK-dependent increase in CNS activity in areas related to homeostatic control of feeding such as the brainstem, the pons, hypothalamus, cerebellum and the motor cortical areas [8]. Glucose has been shown to decrease the response in the upper hypothalamus [9], possibly via a GLP-1-mediated pathway [10]. Ghrelin and PYY have known homeostatic CNS signalling properties but play a hedonic role in the control of food intake [11]. In effect, the increase in plasma PYY and GLP-1 seen after Roux-en-Y gastric bypass surgery in obese subjects or after parenteral administration [12] is associated with a lower activation in brain-hedonic food responses and a healthier eating behaviour [13]. In CD, we expect a subdued reward value of food, but postulate that this would be aversive, and inappropriately impairing appetite and food intake.
We hypothesize that in CD and small bowel inflammation we will observe a change in eating behaviour with loss of hedonic drives and food reward responses and an accentuated homeostatic response.
STUDY OBJECTIVES AND PURPOSE
PURPOSE The overall purpose of the study is to quantify food intake in patients with active Crohn's disease and compare it to when they are in remission and to healthy age, BMI and gender-matched healthy cohort of volunteers. We will quantify eating behaviour traits in the same patient cohort when in active disease and repeat when in remission. These data will be compared to that of healthy volunteers.
PRIMARY OBJECTIVE The primary objective is to quantify food intake in patients with active CD and compare this to HV.
SECONDARY OBJECTIVES The secondary objectives of this study are to a) quantify food intake in patients with active CD and compare that when in inactive disease. b) quantify changes in appetite and eating behaviour in patients with active CD and compare these to those in HV and inactive CD as measured by the appetite-related questionnaires
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Crohn's Disease Patients | – | –Patients with a diagnosis of Crohn's disease fitting the studies inclusion \& exclusion criteria. |
| Healthy Volunteers | – | –For healthy volunteers the studies exclusion criteria apply. |
Who may qualify
- Ages
- 16 to 75 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Child, Adult, Older adult
- Study population
- Recruitment The chief investigator is a specialist in Inflammatory Bowel disease and also an associate professor of gastroenterology at the University of Nottingham and Nottingham University Hospital which is a tertiary-level care academic institution covering a population of approximately 1 million people for secondary-level care and 4.5 million people for tertiary-level care. Collectively we manage approximately 4000 IBD patients. Participants shall be recruited from two sources: 1. Crohn's Disease patients from clinic. 2. Crohns Disease patients and Healthy Volunteers via the study flyer and social media.
Key inclusion criteria (10 listed)
- -
- Age 16-75 years
- Ulceration seen at ileocolonoscopy, aiming for a simple endoscopic score for Crohn's disease (SES-CD) of 4-19, in the absence of stricturing disease or,
- Intestinal inflammation or deep ulceration seen on CT or MR enterography, with the disease activity quantified via the MaRIA score or
- Faecal calprotectin of >250µg/g or
Key exclusion criteria (13 listed)
- Present or recent (within 12 weeks) corticosteroid usage
- Malignant disease
- BMI <18 or >30.
- Significant cardiovascular or respiratory disease
- Diabetes mellitus
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Dietary Recalls (Calorific Intake)
Time frame: Participants will be included in this study for 1 week
The primary endpoints for this study will be food intake as measured by one telephone-administered 24-h dietary recall. Total calorific intake will be calculated.
5 secondary outcomes
Three Factor Eating Questionnaire (TFEQ) Restraint, Disinhibition and Hunger Subscales
Time frame: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
The Binge Eating Scale
Time frame: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
The Power of Food Scale
Time frame: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
The Dutch Eating Behaviour Questionnaire
Time frame: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
The Control of Eating Questionnaire
Time frame: Healthy volunteer participants will be included in this study for 1 week. Crohn's Disease participants will be included in the study until they are re-assessed in remission. A time limit of 12 months will be given.
Results and safety
Loading the posted results from ClinicalTrials.gov…
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 15 Jul 2019.
- Posted resultsParticipant flow, baseline, all outcome measures and adverse events.
- Results publication: PubMed 23763279Bryant RV, Trott MJ, Bartholomeusz FD, Andrews JM. Systematic review: body composition in adults with inflammatory bowel disease. Aliment Pharmacol Ther. 2013 Aug;38(3):213-25. doi: 10.1111/apt.12372. Epub 2013 Jun 14.
- Results publication: PubMed 16698129Lochs H, Dejong C, Hammarqvist F, Hebuterne X, Leon-Sanz M, Schutz T, van Gemert W, van Gossum A, Valentini L; DGEM (German Society for Nutritional Medicine); Lubke H, Bischoff S, Engelmann N, Thul P; ESPEN (European Society for Parenteral and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Gastroenterology. Clin Nutr. 2006 Apr;25(2):260-74. doi: 10.1016/j.clnu.2006.01.007. Epub 2006 May 15.
- Results publication: PubMed 22999064Moran GW, Leslie FC, McLaughlin JT. Crohn's disease affecting the small bowel is associated with reduced appetite and elevated levels of circulating gut peptides. Clin Nutr. 2013 Jun;32(3):404-11. doi: 10.1016/j.clnu.2012.08.024. Epub 2012 Sep 3.
- Results publication: PubMed 22398079Moran GW, Pennock J, McLaughlin JT. Enteroendocrine cells in terminal ileal Crohn's disease. J Crohns Colitis. 2012 Oct;6(9):871-80. doi: 10.1016/j.crohns.2012.01.013. Epub 2012 Mar 3.
- Results publication: PubMed 19760780Moran GW, McLaughlin JT. Plasma chromogranin A in patients with inflammatory bowel disease: a possible explanation. Inflamm Bowel Dis. 2010 Jun;16(6):914-5. doi: 10.1002/ibd.21096. No abstract available.
- Results publication: PubMed 20501434Keller J, Beglinger C, Holst JJ, Andresen V, Layer P. Mechanisms of gastric emptying disturbances in chronic and acute inflammation of the distal gastrointestinal tract. Am J Physiol Gastrointest Liver Physiol. 2009 Nov;297(5):G861-8. doi: 10.1152/ajpgi.00145.2009.
- Results publication: PubMed 22561447Moran GW, O'Neill C, Padfield P, McLaughlin JT. Dipeptidyl peptidase-4 expression is reduced in Crohn's disease. Regul Pept. 2012 Aug 20;177(1-3):40-5. doi: 10.1016/j.regpep.2012.04.006. Epub 2012 May 2.
- Results publication: PubMed 20080096Lassman DJ, McKie S, Gregory LJ, Lal S, D'Amato M, Steele I, Varro A, Dockray GJ, Williams SC, Thompson DG. Defining the role of cholecystokinin in the lipid-induced human brain activation matrix. Gastroenterology. 2010 Apr;138(4):1514-24. doi: 10.1053/j.gastro.2009.12.060. Epub 2010 Jan 18.
- Results publication: PubMed 16280432Smeets PA, de Graaf C, Stafleu A, van Osch MJ, van der Grond J. Functional magnetic resonance imaging of human hypothalamic responses to sweet taste and calories. Am J Clin Nutr. 2005 Nov;82(5):1011-6. doi: 10.1093/ajcn/82.5.1011.
- Results publication: PubMed 17317222Pannacciulli N, Le DS, Salbe AD, Chen K, Reiman EM, Tataranni PA, Krakoff J. Postprandial glucagon-like peptide-1 (GLP-1) response is positively associated with changes in neuronal activity of brain areas implicated in satiety and food intake regulation in humans. Neuroimage. 2007 Apr 1;35(2):511-7. doi: 10.1016/j.neuroimage.2006.12.035. Epub 2007 Jan 18.
- Results publication: PubMed 17934448Batterham RL, ffytche DH, Rosenthal JM, Zelaya FO, Barker GJ, Withers DJ, Williams SC. PYY modulation of cortical and hypothalamic brain areas predicts feeding behaviour in humans. Nature. 2007 Nov 1;450(7166):106-9. doi: 10.1038/nature06212. Epub 2007 Oct 14.
- Results publication: PubMed 22000927De Silva A, Salem V, Long CJ, Makwana A, Newbould RD, Rabiner EA, Ghatei MA, Bloom SR, Matthews PM, Beaver JD, Dhillo WS. The gut hormones PYY 3-36 and GLP-1 7-36 amide reduce food intake and modulate brain activity in appetite centers in humans. Cell Metab. 2011 Nov 2;14(5):700-6. doi: 10.1016/j.cmet.2011.09.010. Epub 2011 Oct 13.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Gordon W Moran principal investigator
University of Nottingham
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Crohn's Disease, run by University of Nottingham at 1 site in United Kingdom.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 10 inclusion and 13 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 15 Jul 2019. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United Kingdom. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Yes. Results are posted in the registry (first posted 15 Jul 2019). A summary is in the For doctors view, and the full results are on ClinicalTrials.gov.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Dietary Recalls (Calorific Intake) (time frame: Participants will be included in this study for 1 week). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02379117, which also lists 13 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 15 Jul 2019.