Ann R. McMeans

Randomised clinical trial: gut microbiome biomarkers are associated with clinical response to a low FODMAP diet in children with the irritable bowel syndrome.

A low fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) diet can ameliorate symptoms in adult irritable bowel syndrome (IBS) within 48 h.

Gut microbiota influences low fermentable substrate diet efficacy in children with irritable bowel syndrome

We sought to determine whether a low fermentable substrate diet (LFSD) decreases abdominal pain frequency in children with irritable bowel syndrome (IBS) and to identify potential microbial factors related to diet efficacy. Pain symptoms, stooling characteristics, breath hydrogen and methane, whole intestinal transit time, stool microbiome, and metabolite composition were collected and/or documented in eight children with IBS at baseline and during one week of an LFSD intervention. Pain frequency (P < 0.05), pain severity (P < 0.05), and pain-related interference with activities (P < 0.05) decreased in the subjects while on the LFSD. Responders vs. non-responders: four children (50%) were identified as responders (>50% decrease in abdominal pain frequency while on the LFSD). There were no differences between responders and non-responders with respect to hydrogen production, methane production, stooling characteristics, or gut transit time. Responders were characterized by increased pre-LFSD abundance of bacterial taxa belonging to the genera Sporobacter (P < 0.05) and Subdoligranulum (P < 0.02) and decreased abundance of taxa belonging to Bacteroides (P < 0.05) relative to non-responders. In parallel, stool metabolites differed between responders and non-responders and were associated with differences in microbiome composition. These pilot study results suggest that an LFSD may be effective in decreasing GI symptoms in children with IBS. Microbial factors such as gut microbiome composition and stool metabolites while on the diet may relate to LFSD efficacy.

Fructans Exacerbate Symptoms in a Subset of Children With Irritable Bowel Syndrome

BACKGROUND & AIMS: Dietary fructans exacerbate symptoms in some, but not all, adults with irritable bowel syndrome (IBS). We sought to determine whether fructans worsen symptoms in children with IBS and whether clinical and psychosocial factors, and/or gas production, can identify those who are fructan sensitive. METHODS: We performed a double‐blind placebo‐controlled (maltodextrin) cross‐over trial of 23 children with IBS, based on pediatric Rome III criteria, from September 2014 through December 2016. At baseline, participants completed 1‐week pain and stool diaries and a 3‐day food record and psychosocial factors (depression, anxiety, and somatization) were measured. Subjects were randomly assigned to groups that were provided meals for 72 hours containing either fructans or maltodextrin (0.5 g/kg; maximum, 19 g). Following a washout period of 10 days or more, the subjects received the meal they were not given during the first study period (crossed over). Gastrointestinal symptoms and breath hydrogen and methane production were captured during each meal period. Fructan sensitivity was defined as an increase of 30% or more in abdominal pain frequency following fructan ingestion. RESULTS: Subjects had more mean episodes of abdominal pain/day during the fructan‐containing diet (3.4 ± 2.6) vs the maltodextrin‐containing diet (2.4 ± 1.7) (P < .01), along with more severe bloating (P < .05) and flatulence (P = .01). Hydrogen (but not methane) production was greater while subjects were on the fructan‐containing diet (617 ± 305 ppm*h) than the maltodextrin‐containing diet (136 ± 78 ppm*h) (P < .001). Eighteen subjects (78.2%) had more frequent abdominal pain while on the fructan‐containing diet and 12 (52.2%) qualified as fructan sensitive. We found no difference between fructan‐sensitive and fructan‐insensitive subjects in baseline abdominal pain or bowel movement characteristics, dietary intake, psychosocial parameters, IBS subtype, or gas production. CONCLUSIONS: In a randomized controlled trial of children with IBS, we found fructans to exacerbate several symptoms. However, fructan sensitivity cannot be identified based on baseline gastrointestinal symptoms, dietary intake, psychosocial factors, or gas production. Clinicaltrials.gov no: NCT02842281.

Congenital sucrase-isomaltase deficiency: diet assessment and education guidelines.

C ongenital sucrase-isomaltase deficiency (CSID) is a genetic disorder that causes maldigestion of sucrose and starch due to a deficiency or absence of the enzymes sucrase and isomaltase in infants, children, and adults (1). Symptoms include chronic or intermittent osmotic diarrhea and abdominal pain. This disorder can include severe diarrhea with failure to thrive in infants (2), and be mistaken for chronic nonspecific diarrhea without growth failure in toddlers and irritable bowel syndrome in adolescents and adults before diagnosis (3,4). It is important that a nutrition assessment be done upon diagnosis of CSID to determine the extent, if any, of malnutrition and failure to thrive. Diet education is crucial for achieving optimum nutrition status and minimization of symptoms of CSID. A registered dietitian can provide nutrition support to patients and their families.

Low FODMAP Dietary Food Lists are Often Discordant

more lists either agreeing to allow the food in some capacity (no restriction or partial restriction) or agreeing to fully restrict the food. Disagreement was defi ned as one list fully restricting a food, whereas another list recommended only partial restriction or no restriction. Combined together, the three lists provided recommendations for 332 unique foods. List A provided guidance on 207 foods, recommending full restriction of 71 (34.3%), partial restriction of 24 (11.6%), and no restriction of 112 (54.1%). List B provided guidance on 203 foods, recommending full restriction of 85 (41.7%), partial restriction of 8 (2.2%), and no restriction on 110 (53.9%). List C provided guidance on 156 foods, recommending full restriction of 62 (39.7%), partial restriction of 20 (12.8%), and no restriction of 74 (47.4%). With respect to overlap among lists, we found 170 (50.9%) foods were only listed on one of the lists: List A had 67 unique foods; List B had 83 unique foods; and List C had 20 unique foods. With respect to the 162 foods contained on more than one list in which agreement could be assessed, 54 (32.7%) foods had general agreement among all three lists, 73 (45.7%) foods had general agreement on two lists (without a recommendation from a third list), and 35 (21.3%) foods had disagreement among the lists ( Table 1 ). In summary, we found that three readily available US-based low FODMAP food lists are oft en discordant with respect to the foods that are listed (lack of overlap in >50%). When the same foods are listed on more than one list, there is generally good agreement, though there are a sizable number of foods (>20%) with recommendations that are in disagreement. It should be To the Editor: A low fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) diet ameliorates gastrointestinal symptoms in adults and children with irritable bowel syndrome ( 1,2 ). To follow a low FODMAP diet, dietary education is required as subjects are oft en asked to restrict fermentable substrates for several weeks with gradual reintroduction challenges ( 3,4 ). Th e most ideal way to educate subjects regarding the low FODMAP diet is still being actively studied ( 5 ). Currently the education process oft en includes providing FODMAP food lists that both recommend foods (and amounts), which may be consumed, and those that should be restricted. Th e education process is made more diffi cult by the fact the FODMAP content of foods may diff er according to the country of origin and may require tailoring recommendations to the patient’s cultural dietary preferences ( 6 ). Whether readily available US-based low FODMAP diet food lists provide consistent guidance is unknown. We evaluated three low FODMAP dietary guidance food lists from sources affi liated with US academic institutions. Th ese lists were readily available (all obtained from the internet in May 2015), contained >150 specifi c food items, and provided specifi c recommendations regarding each listed food. Dietary recommendations for each listed food item was classifi ed into one of three categories: full restriction (food not allowed to be consumed at all); partial restriction (small amount allowed to be consumed), or no restriction. Where two or more lists provided information on the same food, agreement was assessed. General agreement was defi ned as two or case of high-risk individuals. Although oral calcium carbonate is an eff ective antacid, it has been shown to increase gastric acid secretion and serum gastrin levels ( 4 ); hence, presence of calcium carbonate should be duly noted, especially in combination with aspirin. OTC aspirin-antacid products are sold under various trade names in various countries; they are also available as generic products. Usage of this combination is alarmingly increasing in both the developing and the developed world. We recommend all the physicians and healthcare people to be cautious about the potential complications of OTC antacids in combination with aspirin.

Evaluation of FODMAP Carbohydrates Content in Selected Foods in the United States

&NA; We analyzed the fermentable oligosaccharide, disaccharide, monosaccharide, and polyols (FODMAP) content of several foods potentially low in FODMAP which are commonly consumed by children. We determined that several processed foods (eg, gluten‐free baked products) had unlabeled FODMAP content. Determining FODMAP content within foods distributed in the US may support educational and dietary interventions.

946 Low Fermentable Substrate Diet (LFSD) in Children With Irritable Bowel Syndrome (IBS): Pilot Efficacy and Microbiological Predictors of Response

Background: A LFSD has demonstrated efficacy in reducing gastrointestinal (GI) symptoms in adults with IBS, though not all respond. The efficacy of a LFSD in children with IBS is unknown. We sought to determine whether a LFSD decreases abdominal pain frequency in children with IBS and factors determining efficacy of the diet. Methods: Children with Pediatric Rome III-defined IBS completed a 1-wk baseline period on their habitual diet followed by a 1-wk LFSD intervention. Participants were informed they would be taught one of two potential diets, although all participants were taught the same LFSD by a dietitian. Measurements during baseline and LFSD intervention included: A Pain/Stool Diary (capturing the number of pain episodes, stool frequency, and stool form using the modified Bristol Stool Form Scale for children), breath hydrogen/methane production, whole intestinal transit time, and stool microbiome composition analysis. Responders were defined as having ≥ 50% decrease in abdominal pain frequency. Results: Eight children (4 girls), mean age 9.0 ± 3.6 yrs were enrolled and completed the LFSD. Baseline vs LFSD Diet: As a group, overall pain frequency, pain severity, and pain related interference with activities decreased, with a trend toward fewer bowel movements but no differences in stool form (Table). There were no changes in breath hydrogen or methane production, or intestinal transit time. Trends toward increased abundances of Clostridiales and decreased abundance of Bacteroidetes were observed during the LFSD. Responders vs Non-responders: Four children (50%) were identified as responders. There were no differences between responders and non-responders with respect to baseline pain frequency, stool frequency, stool form, hydrogen, or methane production. During the LFSD, responders produced less hydrogen than non-responders (P,0.05), without differences between the groups in stooling characteristics or methane production. Responders (n=3) and non-responders (n=3) with constipation-predominant IBS could be separated by principal components analysis based on the relative species abundance of their baseline gut microbiota. Responders were characterized by increased abundance of taxa belonging to the genera Sporobacter (P ,0.05) and Subdoligranulum (P,0.02) and decreased abundance of taxa belonging to Bacteroides (P,0.05) relative to nonresponders. In addition, other differences in microbiome composition between responders vs. non-responders were identified during the LFSD. Conclusions: A LFSD was effective in decreasing abdominal pain frequency in children with IBS. Those children who had ≥ 50% reduction in pain frequency had less hydrogen production and a different stool microbiome composition vs. those who did not respond to the LFSD suggesting that gut microbiome makeup may predict LFSD efficacy in childhood IBS. Pain and stool characteristics (baseline vs. LFSD*)

Research progress reported at the 50th Anniversary of the Discovery of Congenital Sucrase-Isomaltase Deficiency Workshop.

C ongenital sucrase-isomaltase deficiency (CSID) is a rare autosomal intestinal disease caused by mutations of the sucrase-isomaltase gene. Patients with CSID have different phenotypes and enzymatic activities associated with sucrase-isomaltase ranging from mild reduction of sucrase activity to complete absence. Low sucrase activity leads to maldigestion of sucrose, resulting in dyspepsia-like symptoms such as chronic diarrhea, abdominal pain, and bloating. The severity of the symptom is related to the amount of sucrase activity and quantity of sucrose ingested. Reduced maltase activity is expected to occur in patients with CSID because both subunits of the SI complex contribute to the total mucosal maltose activity. Indeed, low maltase activity can also lead to maldigestion of starches contributing to the symptoms of dyspepsia. When children are assessed for this gene mutation, duodenal mucosal histology is invariably normal. Because there are no noninvasive methods for specific confirmation of sucrase-isomaltase deficiency, a novel noninvasive C-sucrose labeled substrate has been developed and validated as a sucrase activity breath test for screening and confirmation of CSID. It has been shown that primary sucrase deficiency can be confirmed using this new C breath test, as well as the effectiveness of sucrase replacement therapy. On December 21 and 22, 2011, the 8th Workshop of the Starch Digestion Consortium (SDC) was held at the Children’s Nutrition Research Center at the Baylor College of Medicine and Texas Children’s Hospital. The theme of the workshop was ‘‘50 Years of Progress Since Congenital Sucrase-Isomaltase Deficiency (CSID) Recognition.’’ This was a multidisciplinary workshop that blended clinical medicine with nutritional and food science. The purpose of this workshop was to review progress toward clinical diagnosis and management of sucrase-isomaltase enzyme deficiency during the past 50 years. The nutritional and food technological objectives of the conference were 2-fold: first, to define the role of sucrase-isomaltase enzyme complex in human starch digestion to glucose (a-glucogenesis), and second, by studying sucrase-isomaltase–deficient patients with CSID, envision approaches to botanical and technological alterations in food that will benefit all populations. More than 50 authors and attendees participated in this workshop from 12 different countries. Eighteen original communications were presented. Special thanks go to QOL Medical, the supplier of Sucraid oral enzyme supplement, for sponsoring this event. This supplement to the Journal of Pediatric Gastroenterology and Nutrition reports the proceedings of this workshop. E. Roseland Klein served as the technical editor of the workshop publication. Beth Mays was responsible for all travel arrangements and the workshop organization. Adam Gillum was responsible for graphic and audio arrangements. The group of participants standing among the lobby statuary at the SDC/CSID workshop held at the Children’s Nutrition Research Center, December 21–22, 2011 is shown in Figure 1. Statues are identified by italics; Borden is by Joseph Paderewski (1914–2000) and the others are copies of the work of Elizabet Ney (1833–1907). Research Progress Reported at the 50th Anniversary of the Discovery of Congenital Sucrase-Isomaltase Deficiency Workshop