MEETING SUMMARY

The 2019 James W. Freston Conference: at the Intersection of Gut Health and Disease Gerard E. Mullin,1 William D. Chey,2 Sheila E. Crowe,3 and the Freston Conference Faculty

1Division of Gastroenterology and Hepatology, Johns Hopkins University School of Medicine, Baltimore, Maryland; 2Division of Gastroenterology, Michigan Medicine, Ann Arbor, Michigan; and 3Division of Gastroenterology, Department of Medicine, University of California, San Diego, La Jolla, California

he American Gastroenterology Association’s James exacerbates GERD and losing weight, even small percentages T W. Freston Conference was held August 9-10, 2019 of body weight, can improve GERD symptoms.7 in Chicago, IL. The topic “Food at the Intersection of Gut Health and Disease” was chosen owing to the mounting Eosinophilic Esophagitis: Man vs Food evidence for the role of in modulating gastrointestinal Evan Dellon, presented on the role of in the disorders coupled with the paucity of formal training in pathophysiology and treatment of eosinophilic esophagitis nutrition for gastroenterologists. The conference faculty was (EoE). Given the exponential increase in incidence of EoE unique by including registered who provided over the last 2 decades, environmental factors have been insight into dietary management. An R13 grant was awar- hypothesized to trigger disease development. Likely culprits ded by the National Institutes of Health (NIDDK) for young that have become ubiquitous in food manufacturing over the faculty who moderated sessions and collaborated on this last several years include antibiotics, growth hormones, meeting summary. food additives and preservatives, and pesticides. Diet interventions diminish symptoms and improve Plenary Session 1. Food Intolerances endoscopic features. An empiric elimination diet is more from the Top effective than elimination diets based on allergy testing. However, it is often prudent to send the patient to the Keynote Lecture: Personalized Nutrition: The allergist to manage atopic diseases that affect this patient Hope, the Hype, the Reality population. Along with the use of proton pump inhibitors Bibiana Garcia-Bilao presented evidence that knowledge and topical steroids, the mainstay of EoE management rests of human genetic variation can be harnessed to “person- on dietary therapy, namely the 6-food elimination diet. Di- alize” individuals’ nutrition to improve health outcomes and eticians are best suited to provide teaching to EoE patients prevent disease. She described how human genetic variation given the complexity and difficulties with operationalizing in the form of single nucleotide polymorphisms, copy 6-food elimination diet.8 number variance, deletions, and mutations can influence the effect of nutrition on health outcomes and may explain the variation observed in health outcomes across different Plenary Session 2. Effect of Food on the populations. Different polymorphisms have been implicated Function and Sensation in the GI Tract in taste preference,1 appetite cravings,2 and nutrient meta- 3 Role of Nutrients and Other Food Components bolism, These genetic variations in taste preference, Interacting in the GI Tract nutrient metabolism, and appetite likely play a role in Jan Tack discussed the role of nutrient sensing in func- shaping our nutritional intake and how it affects health tional digestive disorders. Patients with functional outcomes. They can be applied to health setting and dyspepsia (FD) frequently experience symptoms that can manipulated to improved health outcomes. include postprandial fullness, early satiety, and epigastric Diet Therapies for Gastroesophageal Reflux pain and burning that are often triggered by inges- 9 Disease: Do They Work? tion. In the stomach, tension-sensitive mechanoreceptors primarily mediate nutrient sensing and chemoreceptors John Pandolfino discussed the use of diet therapy in the (including taste receptors and transient receptor potential management of gastroesophageal reflux disease (GERD). voltage channels primarily mediate nutrient sensing in the Avoiding triggers can reduce GERD symptoms, although results vary.4 Certain foods may also relieve GERD symptoms. In a small study, fiber supplementation decreased GERD symptoms.5 Additionally, adoption of the Most current article has been linked with improved GERD symptoms, but it is fi © 2020 by the AGA Institute unclear if it is due to the presence or absence of speci c food 0016-5085/$36.00 6 items or simply weight loss associated with the diet. https://doi.org/10.1053/j.gastro.2020.03.036

Gastroenterology 2020;159:20–25 MEETING SUMMARY intestine.10 Differences in nutrient sensing via gastric Plenary Session 4. Role of Foods in mechanoreceptors, and intestinal chemoreceptors play a contributing role in development of symptoms in FD and Irritable Bowel Syndrome and Other understanding these interactions will assist in developing Functional GI Disorders 10,11 therapeutic options for these patients. Natural products Functional Foods and Dietary Supplements: The seem to modulate the pathophysiology and symptoms of FD Good, The Bad, and The Ugly by acting through transient receptor potential voltage Gerard Mullin presented on functional foods and dietary channels (ie, capsaicin, eucalyptol, camphor, etc). supplements. Approximately 80% of gastroenterologists – reported familiarity with complementary and alternative Gastroparesis and FD The Same or Different? medicine therapies, but rarely recommend their use.18 To Linda Nguyen reviewed the similarities and differences date, most complementary and alternative medicine studies between FD and gastroparesis. The symptoms and patho- for treatment of irritable bowel syndrome (IBS) symptoms physiology of both FD and gastroparesis have significant fi 9 have focused on ber/psyllium, probiotics, and peppermint overlap. Additionally, there are several types of gastric oil.19 Certain probiotics may be beneficial in reducing IBS neuromuscular dysfunction that can lead to the symptoms of symptoms; however, the quality of evidence is low. Meta- either FD or gastroparesis, including impaired gastric accom- analyses have demonstrated fiber and peppermint oil are modation, antral hypomotility, pylorspasm, gastric arrhyth- 20 12 effective at reducing IBS symptoms. Iberogast and herbal mias, and visceral hypersensitivity. These abnormalities may preparations with caraway improve IBS and FD symptoms. fi give rise to speci c GI symptoms, but may or may not affect Capsaicin supplementation as part of a desensitization gastric emptying as currently measured. Although the overlap protocol has been shown to decrease heartburn and FD in symptoms and pathophysiology can result in some degree symptoms. Rikkunshito (TJ-43) is an herbal supplement that of complexity when managing patients, there are similarities in is widely used in Japan and has been shown to promote treatment for both disorders, including diet modification, 12 gastric emptying and decrease FD symptoms. Mullin high- neuromodulators, and prokinetics. lighted the difference between dietary supplements (no US Food and Drug Administration [FDA] regulation), FDA Plenary Session 3. Food Allergy and regulated medical foods (FDA regulated and require clinical study evidence), and FDA-approved drugs (FDA regulated Pseudoallergy 21 and require phase I–III studies). Many Tests for Food Allergies, But Many Are Not Helpful Sheila Crowe reviewed food allergies, celiac disease, food Evidence-Based Diet Therapies for IBS: Which 13,14 intolerance, and sensitivity. This has led to more Ones for Which Patients? fi research to nd biomarkers for nonceliac gluten sensitivity, William Chey discussed evidence-based diet therapies fi health screening, gut health pro ling, intestinal antigen for IBS. Chey highlighted that >70% of patients report permeability screening, and various stool panels. These tests changing their diet owing to bowel symptoms. Despite are often directly marketed to the consumers without frequent implementation of a gluten-free diet (GFD) by pa- proper clinical validation and can be overwhelming and tients with IBS, a meta-analysis including 2 randomized, misleading for patients. When a patient presents to a controlled trials did not provide sufficient evidence to gastroenterologist for a consultation, they often have recommend a GFD for IBS.22 Despite gluten being self- already undergone one of these tests and seek advice on identified by patients as a trigger, fructan consumption what to do about the results. GI physicians will increasingly has been shown to cause increased IBS symptoms more fi need to understand the scienti c validity of these tests and than gluten in patients with nonceliac wheat intolerance. help patients to identify the best path forward. There is also growing evidence regarding the pathophysi- ology of food-associated symptoms. For example, confocal Mast Cell Activation Syndrome laser endomicroscopy of the duodenum in patients with IBS Matthew Hamilton presented a state-of-the-art lecture on has identified changes in intraepithelial gaps and compro- mast cell activation syndrome, a condition in which overly mised enterocyte integrity after exposure to food antigen reactive mast cells can trigger anaphylaxis like attacks.15 Afew challenges.23 known triggers for exacerbation of mast cell activation were There is growing evidence for use of the low described as well as key physical findings including derma- diet for the treatment of IBS symptoms. A meta-analysis of tographism, flushing, abdominal pain, and tachycardia.16 Lab- 7 randomized, controlled trials evaluating the low FOD- oratory diagnosis includes serum tryptase and 24-hour urine MAPs diet for the treatment of IBS symptoms demonstrate metabolites.17 Dr Hamilton discussed the different mecha- decreased overall symptoms; however, the quality of the nisms of food-induced symptoms and compared them with datawasverylow.DrCheyemphasizedthatthelow that of mast cell activation syndrome. He pointed out that food FODMAPs diet consists of 3 phases: elimination, reintro- diaries, elimination diets trials, and minimizing eating out or duction of foods containing individual FODMAPs to exposure to high histamine foods may aid in the management determine sensitivities, and using that information to of mast cell activation syndrome. personalize each patient’s diet. Given the complexity and

21 MEETING SUMMARY time necessary to provide proper education, the low as RYGB result in decreased energy intake and decreased FODMAP diet is best administered with the aid of a net calorie absorption 5 months postoperatively as trained registered . compared with preoperatively. The nutrients at greatest risk of malabsorption include iron, calcium, B, and fi Educational Tools for Your Practice: Best in Class , with highest risk of de ciencies in patients un- dergoing biliopancreatic diversion with a switch.7 Suggested Kate Scarlata spoke about the role of the dietitian and nutritional evaluations after bariatric surgery include bone other resources available to aid in the management of pa- density every 2 years; urine calcium every 6 months; and tients with FGIDs. The involvement of a dietitian and shared serum iron, folate, and parathyroid hormone, and vitamin decision between provider and patients showed improved B levels every quarter. outcomes.24 Although online resources have the advantage 12 of being readily available and easily accessible, they can be erroneous and even potentially cause health risk. MONASH Session 6. Celiac Disease and Other University’s low FODMAP diet mobile app (paid) is a good educational resource. There are also other free mobile apps Wheat-Related Disorders and websites that can help with symptom tracking. Cook Gut-related disorders associated with wheat consump- books for low FODMAP diets are readily available in the tion can be divided into 3 categories: celiac disease, non- electronic marketplace and websites/blogs that are great celiac gluten sensitivity, and wheat allergy. Alessio Fasano resources for providers as well as patients. and Benjamin Lebwohl discussed these disorders and pro- vided their insight into the GFD as well as the future for managing these conditions. Session 5. Delivering Nutrition When Celiac disease is an autoimmune disease triggered by ingestion of gluten from wheat, barley, and rye. The prev- Gut Anatomy Is Altered alence of celiac disease in the general population is Short Bowel approximately 1%. Additional factors, including quality and Carol Rees Parrish discussed the nutritional manifes- quantity of gluten, timing of gluten introduction, breast- tations of short bowel syndrome, which is characterized feeding, history of gastrointestinal infections, and variability fl by a physical or functional loss of bowel, leaving the pa- in the gut microbiome, may in uence celiac disease devel- tient unable to maintain or balance their nutrition, hy- opment and explain why it can develop at any age and affect 28 dration, and electrolytes. Whole nutrients in the gut can almost any race. Elimination of the trigger, gluten, often fl help with the growth and adaption of the intestine after leads to improvement in gut in ammation and its conse- resection. Complex carbohydrates are often well- quences. Nonceliac gluten sensitivity is described as having tolerated, whereas simple sugars and sugar alcohols, intestinal and/or extraintestinal symptoms upon ingestion which tend to induce osmotic effects and dumping, should of gluten-containing foods without a diagnosis of celiac be reduced. Adjusting fat intake to approximately 30% of disease or wheat allergy; it is a diagnosis of exclusion 28 the total calorie needs of the patient is advised, to mini- (Figure 1). mize the consequences of fat maldigestion, such as steat- Currently, the only available treatment for celiac disease orrhea. To help meet essential fatty acids requirements, is a GFD; however, new concepts and techniques are being oils rich in essential fatty acids are recommended, such as investigated for the management of celiac disease. Dr Leb- ’ walnut,soybean,orsunflower oils.25 Key nutrient labo- wohl s talk also covered emerging do-it-yourself techniques ratory tests to monitor in short bowel syndrome include such as the Nima sensor, which is purported to detect the presence of gluten at >20 ppm; however, its role as a tool to iron, vitamin D, and vitamin B12. Monitoring urine volume is important in patients with short bowel syndrome to check gluten-free foods for contamination is controversial. assess for fluid intake deficit, a good range of urine output Moving forward, the do-it-yourself approach may have a is 1200–1500 mL/d, the larger amount preferred in those role in self-monitoring, but should not be employed for 29 prone to nephrolithiasis. diagnosis of celiac disease. The second part of the session was a panel discussion on how to incorporate a dietitian into a physician practice when Nutrition Management in Bariatric Surgery caring for patients with celiac disease and other GI disorders. Samuel Klein discussed the commonly performed bar- William Chey and Ms Emily Haller enumerated the benefits of iatric surgical procedures: Roux-en-Y gastric bariatric partnering with a dietitian to enhance patient care. (RYGB), laparoscopic adjustable gastric band, vertical sleeve gastrectomy, biliopancreatic diversion with or without duodenal switch. Several large studies have suggested that Session 7. Role of Nutrition in there are fewer complications postoperatively in subjects Inflammatory Bowel Disease who had preoperative weight loss.26,27 The effects of RYGB on glucose metabolism after meal ingestion are most drastic Does Food Cause Symptoms and/or as compared to LAGB and vertical sleeve gastrectomy.5,6 Inflammation in IBD There was a significant spiking of glucose and insulin in Ashwin Ananthakrishnan noted that nearly two-thirds of patients who underwent RYGB.5 Bariatric procedures such patients with inflammatory bowel diseases (IBD; Crohn’s

22 MEETING SUMMARY

Figure 1. Proposed mechanisms of nonceliac wheat sensitivity (NCWS). In patients with NCWS, removal of gluten from the diet leads to symptomatic improvement, but the lack of specific biomarkers for NCWS makes diagnosis challenging. Wheat allergy is an IgE-mediated phenomenon characterized by an adverse immunologic reaction to wheat and other related cereal proteins which leads to inflammatory responses.37 Fructans in wheat can also cause fermentation related gas and bloating and alter the gut microbiome. Wheat gluten can also alter intestinal permeability. The treatment for wheat allergy, NCWS and celiac disease is a strict gluten-free diet (GFD). disease, ulcerative colitis) report that diet plays a role in diets to achieve mucosal healing is lacking.35 The Crohn’s triggering either onset or relapse of established disease.30 Disease Exclusion Diet combines partial enteral nutrition Several layers of evidence also support that in addition to with other dietary recommendations including exclusion of food-induced symptoms, diet plays an important role in foods thought to be proinflammatory, such as emulsifiers, inciting and propagating intestinal inflammation.31,32 Over the saturated fats, and red meats while emphasizing potentially past decade, prospective cohort studies from North America beneficial components such as dietary fiber.36 In a ran- and Europe have provided evidence linking reduced dietary domized controlled trial for 12 weeks, the Crohn’s Disease fiber, particularly from fruits and vegetables, to increased Exclusion Diet þ partial enteral nutrition diet was more incidence of Crohn’s disease, while higher n-3 polyunsaturated effective and better tolerated when compared with exclu- fatty acid intake and lower n-6 PUFA intake is associated with sive enteral nutrition followed by an unrestricted diet. With a decreased risk of ulcerative colitis. emerging high-quality evidence, dietary therapy will In addition to macronutrient components, micro- increasingly become part of the care plan for IBD patients. nutrients such as dietary and vitamin D may play a role At present, patients should be encouraged to follow a in modifying disease. Constituents of food such as emulsi- Mediterranean-style diet prepared from fresh ingredients fiers may also enable intestinal inflammation by altering the that may have beneficial effects beyond IBD. microbiome and disrupting intestinal mucin.33 Experimental evidence suggests that diet may lead to intestinal inflam- Conclusions mation through several mechanisms involving the gut The 2019 Freston Conference was the first to provide a microbiome and through direct interaction between dietary gut-nutrition bootcamp for physicians in practice, fellows, ligands and the intestinal immune response. and nutritionists. The conferences highlighted the evidence for dietary manipulation to improve gastrointestinal out- Diet Therapies for IBD (Where’s the Beef?) comes in digestive disorders. James Lewis divided the dietary approaches to IBD into 3 categories. First, one could add beneficial components of References food to the diet. Second are exclusion diets, where a broad 1. Hayes JE, Feeney EL, Allen AL. Do polymorphisms in range of dietary components are excluded. The third way is chemosensory genes matter for human ingestive through modification of the diet without wholesale restric- behavior? Food Qual Prefer 2013;30:202–216. tion of all foods. The strongest evidence in support of di- 2. de Luis DA, Aller R, Izaola O, et al. Effects of a high- 34 etary treatment is through exclusive enteral nutrition. protein/low-carbohydrate diet versus a standard hypo- Observational case series support a benefit with reduction caloric diet on weight and cardiovascular risk factors: of symptoms with exclusion diets such as the specific car- role of a genetic variation in the rs9939609 FTO gene bohydrate diet, but evidence supporting the ability of such variant. J Nutrigenet Nutrigenomics 2015;8:128–136.

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3. Cornelis MC, El-Sohemy A, Kabagambe EK, et al. Cof- analysis of the pooled clinical data. BMC Complement fee, CYP1A2 genotype, and risk of myocardial infarction. Altern Med 2019;19:21. JAMA 2006;295:1135–1141. 20. Ford AC, Harris LA, Lacy BE, et al. Systematic review 4. Newberry C, Lynch K. Can we use diet to effectively treat with meta-analysis: the efficacy of prebiotics, probiotics, esophageal disease? A review of the current literature. synbiotics and antibiotics in irritable bowel syndrome. Curr Gastroenterol Rep 2017;19:38. Aliment Pharmacol Ther 2018;48:1044–1060. 5. Morozov S, Isakov V, Konovalova M. Fiber-enriched diet 21. Burnett BP, Mullin G. Therapeutic food claims: a global helps to control symptoms and improves esophageal perspective. Curr Opin Clin Nutr Metab Care 2017; motility in patients with non-erosive gastroesophageal 20:522–528. reflux disease. World J Gastroenterol 2018;24:2291–2299. 22. Dionne J, Ford AC, Yuan Y, et al. A systematic review 6. Mone I, Kraja B, Bregu A, et al. Adherence to a pre- and meta-analysis evaluating the efficacy of a gluten-free dominantly Mediterranean diet decreases the risk of diet and a low FODMAPs diet in treating symptoms of gastroesophageal reflux disease: a cross-sectional study irritable bowel syndrome. Am J Gastroenterol 2018; in a South Eastern European population. Dis Esophagus 113:1290–1300. 2016;29:794–800. 23. Fritscher-Ravens A, Schuppan D, Ellrichmann M, et al. 7. Yadlapati R, Pandolfino JE, Alexeeva O, et al. The reflux Confocal endomicroscopy shows food-associated improvement and monitoring (TRIM) program is associ- changes in the intestinal mucosa of patients with irrita- ated with symptom improvement and weight reduction ble bowel syndrome. Gastroenterology 2014; for patients with obesity and gastroesophageal reflux 147:1012–2020 e4. disease. Am J Gastroenterol 2018;113:23–30. 24. Tuck CJ, Reed DE, Muir JG, et al. Implementation of the 8. Dellon ES, Gonsalves N, Hirano I, et al. ACG clinical low FODMAP diet in functional gastrointestinal symp- guideline: evidenced based approach to the diagnosis toms: a real-world experience. Neurogastroenterol Motil and management of esophageal eosinophilia and 2019:e13730. eosinophilic esophagitis (EoE). Am J Gastroenterol 2013; 25. Parrish CR, DiBaise JK. Managing the adult patient with 108:679–692; quiz 693. short bowel syndrome. Gastroenterol Hepatol (N Y) 9. Stanghellini V, Chan FK, Hasler WL, et al. Gastroduo- 2017;13:600–608. denal disorders. Gastroenterology 2016;150:1380–1392. 26. Anderin C, Gustafsson UO, Heijbel N, et al. Weight loss 10. Farre R, Tack J. Food and symptom generation in before bariatric surgery and postoperative complica- functional gastrointestinal disorders: physiological as- tions: data from the Scandinavian Obesity Registry pects. Am J Gastroenterol 2013;108:698–706. (SOReg). Ann Surg 2015;261:909–913. 11. Carbone F, Verschueren S, Rotondo A, et al. Duodenal 27. Holderbaum M, Casagrande DS, Sussenbach S, et al. nutrient exposure contributes to enhancing gastric ac- Effects of very low calorie diets on liver size and weight commodation. Neurogastroenterol Motil 2019:e13697. loss in the preoperative period of bariatric surgery: a 12. Kim BJ, Kuo B. Gastroparesis and functional dyspepsia: systematic review. Surg Obes Relat Dis 2018; a blurring distinction of pathophysiology and treatment. 14:237–244. J Neurogastroenterol Motil 2019;25:27–35. 28. Leonard MM, Sapone A, Catassi C, et al. Celiac disease 13. Bischoff S, Crowe SE. Gastrointestinal food allergy: new and nonceliac gluten sensitivity: a review. JAMA 2017; insights into pathophysiology and clinical perspectives. 318:647–656. Gastroenterology 2005;128:1089–1113. 29. Lerner BA, Phan Vo LT, Yates S, et al. Detection of gluten 14. Leung J, Crowe SE. Food allergy and food intolerance. in gluten-free labeled restaurant food: analysis of crowd- In: Matarese LE, Mullin GE, Raymond J, eds. The health sourced data. Am J Gastroenterol 2019;114:792–797. professional’s guide to gastrointestinal nutrition. Chi- 30. Limdi JK, Aggarwal D, McLaughlin JT. Dietary practices cago, IL: Academy of Nutrition and Dietetics, and beliefs in patients with inflammatory bowel disease. 2014:222–234. Inflamm Bowel Dis 2016;22:164–170. 15. Valent P, Akin C. Doctor, I think I am suffering from 31. Lee D, Albenberg L, Compher C, et al. Diet in the path- MCAS: differential diagnosis and separating facts from ogenesis and treatment of inflammatory bowel diseases. fi – ction. J Allergy Clin Immunol Pract 2019;7:1109 1114. Gastroenterology 2015;148:1087–1106. 16. Qureshi AA, Friedman AJ. A review of the dermatologic 32. Levine A, Sigall Boneh R, Wine E. Evolving role of diet in symptoms of idiopathic mast cell activation syndrome. the pathogenesis and treatment of inflammatory bowel J Drugs Dermatol 2019;18:162–168. diseases. Gut 2018;67:1726–1738. 17. Weiler CR. Mast cell activation syndrome: tools for 33. Chassaing B, Koren O, Goodrich JK, et al. Dietary diagnosis and differential diagnosis. J Allergy Clin emulsifiers impact the mouse gut microbiota promoting Immunol Pract 2019;8:498–506. colitis and metabolic syndrome. Nature 2015;519:92–96. 18. Gallinger ZR, Nguyen GC. Practices and attitudes toward 34. Swaminath A, Feathers A, Ananthakrishnan AN, et al. complementary and alternative medicine in inflammatory Systematic review with meta-analysis: enteral nutrition bowel disease: a survey of gastroenterologists. therapy for the induction of remission in paediatric Crohn’s J Complement Integr Med 2014;11:297–303. disease. Aliment Pharmacol Ther 2017;46:645–656. 19. Alammar N, Wang L, Saberi B, et al. The impact of 35. Limketkai BN, Iheozor-Ejiofor Z, Gjuladin-Hellon T, et al. peppermint oil on the irritable bowel syndrome: a meta- Dietary interventions for induction and maintenance of

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remission in inflammatory bowel disease. Cochrane QOL Medical, and Ritter; and has received research grants from Biomerica, Commonwealth Diagnostics, Nestle, QOL Medical, and Zespri. Ashwin Database Syst Rev 2019;2:CD012839. Ananthakrishan reports research support from Pfizer. Bibiana Garcia-Bailo 36. Levine A, Wine E, Assa A, et al. Crohn’s disease exclu- is an employee of Nutrigenomix, Inc. Evan Dellon is a consultant for Adare, sion diet plus partial enteral nutrition induces sustained Alivio, Allakos, AstraZeneca, Banner, Calypso, Celgene/Receptos, Enumeral, EsoCap, Gossamer Bio, GSK, Regeneron, Robarts, and Shire; has received remission in a randomized controlled trial. Gastroenter- research support from Adare, Allakos, Celgene/Receptos, GSK, Regeneron, ology 2019;157:440–450 e8. and Shire; and has received educational grants from Banner and Holoclara. John DiBaise is a consultant for Allena Pharmaceuticals; an advisory board 37. Elli L, Branchi F, Tomba C, et al. Diagnosis of gluten member for Zealand Pharmaceuticals, as well as Coram/CVS; and receives related disorders: celiac disease, wheat allergy and non- book royalties from McGraw-Hill, Springer, and CRC Press. Alessio Fasano celiac gluten sensitivity. World J Gastroenterol 2015; is a consultant for Inova Diagnostics, Innovate Biopharma, and uBiome; is an advisory board member for Axial Biotherapeutics; receives research 21:7110–7119. support from Takeda; has a speaking agreement with Mead Johnson Nutrition; and is a stockholder of Alba Therapeutics. Matthew J. Hamilton is a consultant for Takeda, Pfizer, Allakos and AbbVie. Sam Klein is a Correspondence consultant for Pfizer and NovoNordisk; receives research support from Address correspondence to: Gerard Mullin, Department of Medicine, Johns Merck and Janssen; is on the Scientific Advisory Board for Dannon/Yakult Hopkins University School of Medicine, 600 N Wolfe Street, Baltimore, and Merck; and is a stockholder of Aspire Bariatrics. Benjamin Lebwohl is Maryland 21205. e-mail: [email protected]. a consultant for Takeda and Innovate Biopharmaceuticals. John Leung is a consultant for Shire. James Lewis is a consultant for Crohn’s & Colitis Acknowledgments Foundation, IBD Plexus, Samsung Bioepis, Pfizer, Gilead, UCB, Bridge An R13 travel grant was awarded by the National Institutes of Health (NIDDK) Biotherapeutics, Bristol-Myers Squibb, Arena Pharmaceuticals; and receives for the junior faculty who moderated sessions and collaborated on this meeting research support from Takeda, Janssen, Nestle Health Science and summary. AbbVie. Linda Nguyen is a consultant for Allergan, Ironwood, and Nevro, Members of the Freston Conference Faculty: Ashwin Ananthakrishan,4 and receives research support from Vanda. John Pandolfino is a consultant Bibiana Garcia-Bailo,5 Evan S. Dellon,6 John DiBaise,7 Alessio Fasano,8 Emily for Medtronic, Diversatek, Ironwood, and Tora-Ethicon; receives research Haller,2 Matthew J. Hamilton,9 Sam Klein,10 Benjamin Lebwohl,11 John support from Impleo; receives a salary and speaking honorarium from Leung,12,13 James Lewis,14 Linda Nguyen,15 John Pandolfino,16 Carol Rees Medtronic/Crospon for EndoFLIP; and holds stocks in Cropon and Parrish,17 Kate Scarlata,18 Jan Tack,19 Jeanetta Frye,17 Kimberely Harer,20 Trmedyne Laser. Carol Rees Parrish receives honoraria from Shire and Victor Zevallos,21 Sachin Srinivasan,22 Sandeep Verma,23 Claire Jansson- Takeda for paid publications as well as from Shire for speaking. Kate Knodell,24 Vermont Dia,25 Samara Rifkin,20 and Laura Pace26 Scarlata consults for FODY Food Company (a low FODMAP Company), 4Massachusetts General Hospital; 5University of Toronto and Campbell Soup, Rachel Pauls Food, Casa de Sante Foods; and Nestle; Nutrigenomix Inc; 6University of North Carolina School of Medicine; 7Mayo and conducts sponsored talks at Nutrition Events. Jan Tack is a consultant Clinic; 8Massachusetts General Hospital for Children; 9Brigham and for AlfaSigma, AlfaWassermann, Allergan, Alnylam, Arena, Christian Hansen, Women’s Hospital; 10Washington University School of Medicine; 11Columbia Danone, EA Pharma, Grünenthal, Ironwood, Kyowa Kirin, Menarini, Mylan, University Medical Center; 12Tufts University; 13New England Medical Center; Neurogastrx, Neutec, Novartis, Noventure, Nutricia, Shionogi, Shire, 14University of Pennsylvania; 15Stanford University School of Medicine; Takeda, Theravance, Tramedico, Truvion, Tsumura, Zealand, and Zeria; 16Northwestern University; 17University of Virginia Health System; 18Boston receives research support from Shire, Tsumura, Abbott, Allergan, Ironwood, University; 19KU Leuven; 20University of Michigan; 21St. Mary’s University, Kyowa Kirin, Menarini, Mylan, Novartis, Shire, Takeda, Truvion, and Zeria. UK; 22Kansas University School of Medicine; 23Sinai Hospital; 24Indiana Jeanetta Frye is a consultant to Isothrive. Claire Jansson-Knodell owns University; 25University of Tennessee, Knoxville; and 26University of Utah. stocks in Exact Sciences, Bristol-Myers Squibb, Johnson & Johnson, and Eli Lilly. Laura Pace reports research from Vanda Pharmaceuticals. Sheila Conflicts of interest Crowe receives honoraria from UpToDate, New England Journal of The authors have made the following disclosures: William Chey is a Medicine, and Annals of Internal Medicine. All other authors report no consultant for Biomerica, Commonwealth Diagnostics, IM Health Sciences, conflicts of interest.

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