Patients with irritable bowel syndrome (IBS) commonly report that food is a trigger of their symptoms. Studies have shown that 50% to 70% of patients make changes in their diet (1–4). Common dietary changes among patients with IBS include the following: avoidance of eating for some time (varying from 1 meal to 3 days) despite hunger; elimination of certain foods; or selection of foods that have been shown to alleviate either diarrhea or constipation (4,5). Despite these strategies, studies have not found evidence to support the role of diet in the development or exacerbation of IBS (6). The patients with IBS may be sensitive to some foods (7,8), but often cannot identify which ones affect their symptoms (9,10). As a result, they often exclude the wrong foods from their diet. Moreover, conflicting results have been reported for using exclusion diets to control symptoms of IBS (11). There is also no good evidence that adding foods such as fiber is helpful for the majority of patients (6,12–14). A recent Cochrane review concluded that there is no high-quality evidence for dietary interventions to treat chronic abdominal pain in children and adolescents (15).
Most of the existing literature on IBS focuses on the effect of diet as a trigger for symptoms; however, the discomfort a patient with IBS experiences may not be because of a specific food, but the response to eating itself (6,7). Eating stimulates the gut. The visceral nerves and muscles may overreact to this stimulation in patients with IBS, causing motility changes and visceral hypersensitivity, 2 findings associated with IBS. Eating has been found to precede symptoms of IBS approximately 50% of the time (16). Thus, patients may be sensitive to “normal” gastrointestinal processes associated with eating. Some patients will avoid eating altogether to avoid symptoms (5).
Disturbed eating patterns themselves can lead to changes in motility. Gastrointestinal disturbances such as delayed emptying and diminished gastric relaxation have been well described in anorexia nervosa and bulimia nervosa (17), 2 eating disorders that typically involve restricting food intake for a long time. These disturbances lead to symptoms such as early satiety, fullness, bloating, and constipation (17). With reestablishing a regular eating pattern, these gastrointestinal disturbances normalize (17). It is important to emphasize that motility impairment among patients with eating disorders may be a consequence of malnutrition. The studies, however, have shown motility disturbances can change without changes in nutrition status. For example, patients with bulimia nervosa within the normal weight range show disordered motility, and normalization of gastric emptying in patients with anorexia nervosa occurs while the body mass is still subnormal and amenorrhea present (17). These findings suggest that disordered eating by itself may be an important factor in driving motility changes.
Disturbed eating patterns affect gut motility, which may also be true for patients with IBS. The objective of the present study was to determine whether a relation exists between eating avoidance in patients with IBS and gut motility. We used objective measures including the electrogastrogram (EGG) and gut transit (Sitz markers) to make this comparison.
Subjects were recruited from patients at the University of North Carolina (UNC) pediatric gastroenterology and student health clinics. Patients were required to have a physician's diagnosis of IBS as well as to meet Rome III criteria for IBS (18) and to be between the ages of 15 and 21 years. Half of the subjects reported habitually avoiding eating, whereas the others did not. We termed this “eating restriction.” Eating restriction was defined as not eating ≥4 hours while hungry to control symptoms, at least 1 day/week, for 6 months or more. We chose these criteria based on a study in which 43.2% of adolescents with IBS attempted to control their IBS symptoms by not eating despite being hungry (4). Most adolescents will typically eat 5 times per day (19,20), which is on average every 3 hours, if allowing for 8 hours of sleep. Therefore, we believe that not eating for 4 hours while hungry likely captures a pattern of skipping meals to prevent IBS symptoms. The criterion “1 day per week for at least 6 months” was added to make sure that these dietary patterns were consistent and frequent. Patients who were trying to lose or had lost more than 5 lb in the past 6 months were excluded as well as patients with a current diagnosis of an eating disorder. All of the patients taking medication that can affect motility were excluded, with the exception of patients taking laxatives, enemas, or suppositories, which were requested to be discontinued during the study period.
We used whole-gut transit time and EGG as measures of gastrointestinal motility and gastric myoelectrical activity, respectively. Normative data on whole-gut transit time exist for patients with eating disorders (21) and patients with IBS (22,23). EGG data have also been described with evidence of gastric myoelectrical dysrhythmias in patients with anorexia (24) and in those with delayed gastric emptying such as unexplained nausea, diabetes, and dyspepsia (25).
Whole-gut transit time was measured by the Sitzmark technique. We followed a method of measuring whole-gut transit time by the Sitzmark technique adapted by Abrahamsson et al (26), in which subjects swallow a gelatin capsule containing 24 barium-impregnated rubber rings daily for 5 days followed by an abdominal radiograph on the sixth day. All subjects discontinued laxatives, enemas, and suppositories for the duration of the Sitzmark study. The number of radiopaque markers remaining in the colon on the sixth day is counted and used as an estimate of whole-gut transit time in hours. Two assumptions are made. First, when the markers are ingested daily, the number excreted through defecation will come into equilibrium with the number ingested, so that the number remaining in the colon on a given day is a function of transit time. Second, because 24 rings are ingested each day and there are 24 hours in a day, it is possible to equate hours of transit with numbers of rings. This measure shows good test-retest reliability (27,28) and correlates with stool consistency (29). Stool burden was also determined from the abdominal radiograph by a pediatric gastroenterologist blinded to the study condition.
Gastric myoelectrical activity was measured by EGG in combination with the water load test. The water load test provides additional information on possible gastric hyperalgesia and/or gastric compliance. These may be factors in eating restriction because both children and adults with IBS have been found to tolerate less volume, which is associated with symptom reports (30,31). After a night of fasting, subjects were asked to eat a 200-kcal meal (consisting of 8 ounces of apple juice and 2 slices of toast) in the morning, 2 hours before testing. EGG recordings were obtained as described by Koch and Stern (32). Subjects reclined in a comfortable chair throughout the study. EGG recordings included a 15-minute baseline tracing, after which patients ingested noncarbonated water for 5 minutes or until they perceived their stomach to be full. EGG recording continued for 30 minutes after water ingestion. A custom software program for EGG data analysis was used (3CPM Co, Towson, MD). Frequencies were defined as bradygastria (1.0–2.5 cpm), normal (2.5–3.75 cpm), and tachygastria (3.75–10 cpm), and duodenal or respiratory frequencies (10–15 cpm) based on the raw EGG recording, the running spectral plot, and the percentage distribution of EGG power. The EGGs were interpreted as normal or abnormal (tachygastria, bradygastria, or mixed dysrhythmia—a combination of tachygastria and bradygastria).
The t test was used to compare whole-gut transit times and ingested water volume between the groups with and without eating restriction. The χ2 tests were used to compare the percentage of subjects with abnormal EGG recordings in the groups with and without eating restriction.
Subjects visited UNC research clinics twice. During the first visit, subjects were screened and consented. Subjects also received the Sitzmark capsules together with an explanation of how to take the capsules at home. All of the subjects were asked to discontinue laxatives, enemas, and suppositories starting the day of their first visit and were requested to do so for the duration of the Sitzmark study (until the radiography 6 days later). A diary was kept to record date/time of capsule ingestion. A second visit was scheduled for exactly 6 days later. During the second visit, all female subjects were administered a urine test to exclude pregnancy (no test was found to be positive). EGG testing and an abdominal radiograph were obtained. The study was approved by the UNC biomedical institutional review board, and all of the subjects (and their parents in case of minors) gave informed consent before starting the study.
A total of 17 subjects between the ages of 15 and 21 years (mean age 19.2) were enrolled, predominantly girls (64.7%) and white (82.4%) or African American (11.8%), and all had normal body mass indices (20–25). The majority of patients were IBS-mixed subtype (64.7%), followed by IBS-diarrhea predominant (17.6%), and IBS-constipation predominant (5.9%). No differences between restrictors (N = 8) and nonrestrictors (N = 9) were found in the IBS subtype. Only 2 subjects regularly used laxatives. Because the majority of subjects were IBS mixed and this may be associated with constipation (hard stool) and overflow stool (soft stool), we decided to examine the stool burden. Two restrictors and 3 nonrestrictors had at least mild stool burden, which was not significantly different between the 2 groups. In addition, there were no differences between subjects who restricted and those who not restricted eating in age (mean 19.1 vs 19.2; P = 0.9), sex (N = 6 vs N = 5 girls; P = 0.8), and race (N = 7 whites in both groups, P = 0.6)
No differences were found in the number of patients with gastric dysrhythmias between those who habitually restricted eating and those who did not (62.5% of restrictors vs 77.8% of nonrestrictors, P = 0.5). Restrictors consumed significantly less water (mean 464.4; standard deviation [SD] 106.9) than nonrestrictors (mean 613.3, SD 118.8, P = 0.02). We found that whole-gut transit time as well as distribution of Sitzmarkers was not different between restrictors and nonrestrictors. Whole-gut transit time was on average, however, 13.5 hours slower in restrictors (mean 51.0, SD 23.2) than nonrestrictors (mean 37.5, SD 16.2, P = 0.18). This difference may not have reached significance because of the small sample size. Power analysis revealed that at α = 0.05 and power of 80%, each group needs N = 35 for this difference to become statistically significant.
Our pilot study aimed to study the association of frequent eating restriction with motility disturbances in adolescent patients with IBS. The basis of this comparison is predicated on evidence that eating restriction is associated with slower gastric and overall motility changes among patients with eating disorders.17 Our findings suggest that repeated eating restriction may be associated with some changes in patients with IBS as well, although much more data are needed before any definitive conclusions can be drawn.
We found gastric abnormalities in sensation as measured by the water load test: patients with IBS who regularly restrict their eating were able to tolerate less water on an empty stomach. It is unclear whether this is because of gastric allodynia or discomfort from reduced gastric accommodation. The water load test has been shown to effectively test for both causes (33,34). Compared with nonrestrictors, patients who restricted their eating did report less change in hunger and fullness after the water load test, suggesting that they may not have drunk until completely full. This may be either because of gastric discomfort or because of fear of discomfort, which may indicate that sensation is a reason for reduced consumption.
We also found a decrease in transit time of almost 14 hours in those who restricted their eating, but this difference did not meet statistical significance. This could indicate that there is no difference between restrictors and nonrestrictors in whole-gut transit time. The lack of significance is possibly also the result of the lack of power from such a smaller sample size. Furthermore, we defined eating restriction as skipping a meal per day once per week to control IBS symptoms. Skipping meals is common in adolescence and, therefore, future studies may want to consider using more restrictive definitions (eg, those who restrict meals on 3 days or more per week), because there may be a dose-response association between more eating restriction and motility.
Other limitations to our study are as follows: inclusion of only adolescent patients with IBS, which limits the generalizability of the results, the cross-sectional nature of the present study, limiting our ability to determine whether gastric sensation is a cause or consequence of eating restriction, and the limited number of motility measures. Diagnostic measures such as gastric emptying and gastric accommodation were not performed. These parameters have been found to be affected in patients with eating disorders and in children with functional abdominal pain (17,35) and will need to be incorporated in future studies to better define the functional effects of eating restriction in various parts of the gut.
Despite these limitations, this is the first study to investigate the association between eating behaviors and motility in adolescent patients with IBS. The data from this pilot study underscore the need for larger, prospective trials to determine whether a relation between eating restriction and motility dysfunction exists.
1. Halpert A, Dalton CB, Palsson O, et al. What patients know about irritable bowel syndrome (IBS) and what they would like to know. National Survey on Patient Educational Needs in IBS and development and validation of the Patient Educational Needs Questionnaire (PEQ). Am J Gastroenterol
2. Rees GA, Davies GJ, Parker M, et al. Gastrointestinal symptoms and diet of members of an irritable bowel self-help group. J R Soc Health
3. Nanda R, James R, Smith H, et al. Food intolerance and the irritable bowel syndrome. Gut
4. van Tilburg MAL, Squires M, Blois-Martin N, et al. Diet and eating associated symptoms in adolescents with IBS. Gastroenterology
5. Jarrett M, Visser R, Heitkemper M. Diet triggers symptoms in women with irritable bowel syndrome. The patient's perspective. Gastroenterol Nurs
6. van Tilburg MAL, Felix CT. Diet and functional abdominal pain in children and adolescents. J Pediatr Gastroenterol Nutr
7. Lea R, Whorwell PJ. The role of food intolerance in irritable bowel syndrome. Gastroenterol Clin North Am
8. Park MI, Camilleri M. Is there a role of food allergy in irritable bowel syndrome and functional dyspepsia? A systematic review. Neurogastroenterol Motil
9. Dainese R, Galliani EA, De Lazzari F, et al. Discrepancies between reported food intolerance and sensitization test findings in irritable bowel syndrome patients. Am J Gastroenterol
10. Young E, Stoneham MD, Petruckevitch A, et al. A population study of food intolerance. Lancet
11. Karamanolis G, Tack J. Nutrition and motility disorders. Best Pract Res Clin Gastroenterol
12. Ford AC, Talley NJ, Spiegel BM, et al. Effect of fibre, antispasmodics, and peppermint oil in the treatment of irritable bowel syndrome: systematic review and meta-analysis. BMJ
13. Bijkerk CJ, Muris JW, Knottnerus JA, et al. Systematic review: the role of different types of fibre in the treatment of irritable bowel syndrome. Aliment Pharmacol Ther
14. Zuckerman MJ. The role of fiber in the treatment of irritable bowel syndrome: therapeutic recommendations. J Clin Gastroenterol
15. Huertas-Ceballos AA, Logan S, Bennett C, et al. Dietary interventions for recurrent abdominal pain (RAP) and irritable bowel syndrome (IBS) in childhood. Cochrane Database Syst Rev
16. Ragnarsson G, Bodemar G. Pain is temporally related to eating but not to defaecation in the irritable bowel syndrome (IBS). Patients’ description of diarrhea, constipation and symptom variation during a prospective 6-week study. Eur J Gastroenterol Hepatol
17. Hadley SJ, Walsh BT. Gastrointestinal disturbances in anorexia nervosa and bulimia nervosa. Curr Drug Targets CNS Neurol Disord
18. Drossman DA, Corazziari E, Delvaux M, et al. Rome III: The Functional Gastrointestinal Disorders. McLean, VA:Degnon Associates; 2006.
19. Anderson AS, Macintyre S, West P. Dietary patterns among adolescents in the west of Scotland. Br J Nutr
20. Kerver JM, Yang EJ, Obayashi S, et al. Meal and snack patterns are associated with dietary intake of energy and nutrients in US adults. J Am Diet Assoc
21. Kamal N, Chami T, Andersen A, et al. Delayed gastrointestinal transit times in anorexia nervosa and bulimia nervosa. Gastroenterology
22. Cann PA, Read NW, Brown C, et al. Irritable bowel syndrome: relationship of disorders in the transit of a single solid meal to symptom patterns. Gut
23. Sadik R, Stotzer PO, Simren M, et al. Gastrointestinal transit abnormalities are frequently detected in patients with unexplained GI symptoms at a tertiary centre. Neurogastroenterol Motil
24. Abell TL, Malagelada JR, Lucas AR, et al. Gastric electromechanical and neurohormonal function in anorexia nervosa. Gastroenterology
25. Parkman HP, Hasler WL, Barnett JL, et al. Electrogastrography: a document prepared by the gastric section of the American Motility Society Clinical GI Motility Testing Task Force. Neurogastroenterol Motil
26. Abrahamsson H, Antov S, Bosaeus I. Gastrointestinal and colonic segmental transit time evaluated by a single abdominal X-ray in healthy subjects and constipated patients. Scand J Gastroenterol Suppl
27. Knowles JD, Whitehead WE, Meyer KB. Reliability of a modified Sitzmark study of whole gut transit time. Gastroenterology
28. Lewis SJ, Heaton KW. Stool form scale as a useful guide to intestinal transit time. Scand J Gastroenterol
29. Whitehead WE, Palsson O, Gangarosa LM, et al. Lubiprostone does not influence visceral pain thresholds in patients with irritable bowel syndrome. Neurogastroenterol Motil
30. Koch KL, Hong SP, Xu L. Reproducibility of gastric myoelectrical activity and the water load test in patients with dysmotility-like dyspepsia symptoms and in control subjects. J Clin Gastroenterol
31. Walker LS, Williams SE, Smith CA, et al. Validation of a symptom provocation test for laboratory studies of abdominal pain and discomfort in children and adolescents. J Pediatr Psychol
32. Koch KL, Stern RM. Kumar D, Wingate DL. Electrogastrography. Illustrated Guide to Gastrointestinal Motility
. London:Churchill Livingston; 1993. 290–307.
33. Anderson JL, Acra S, Bruehl S, et al. Relation between clinical symptoms and experimental visceral hypersensitivity in pediatric patients with functional abdominal pain. J Pediatr Gastroenterol Nutr
34. De Schepper HU, Cremonini F, Chitkara D, et al. Assessment of gastric accommodation: overview and evaluation of current methods. Neurogastroenterol Motil
35. Devanarayana NM, Rajindrajith S, Rathnamalala N, et al. Delayed gastric emptying rates and impaired antral motility in children fulfilling Rome III criteria for functional abdominal pain. Neurogastroenterol Motil