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WGO Handbook on Diet and the Gut_2016_Final

World Digestive Health Day WDHD – May 29, 2016 THE GUT RESPONSE TO FOOD; A PHYSIOLOGICAL PERSPECTIVE ON FOOD-INDUCED GASTROINTESTINAL SYMPTOMS EAMONN M.M. QUIGLEY, MD, FRCP, FACP, MACG, FRCPI David M and Lynda K Underwood Center for Digestive Disorders, Division of Gastroenterology and Hepatology Houston Methodist Hospital and Weill Cornell Medical College Houston, Texas, USA Before launching into a discussion of the potential roles of food allergy or intolerance in gastrointestinal symptomatology, or even in the pathophysiology of a common functional gastrointestinal disorder, such as irritable bowel syndrome (IBS), one must first consider the potential role of a more fundamental factor in the precipitation of GI symptoms and gut distress on, or soon after, food ingestion; namely, the physiological response to food. All physiological processes in the gut, including motility, secretion and blood flow respond to food intake, or the anticipation thereof, in order to maximize digestion and absorption. Both neural (and the vagus, in particular) and hormonal elements contribute to these responses. Signals along the gut-brain axis, a bidirectional pathway between the GI tract and the brain, may initiate, perpetuate or modulate the food response. Other factors, including mucosal immune responses and even the gut microbiota may participate in this bidirectional interaction, the latter leading to the concept of the microbiota-gut-brain axis.1-3 The interplay between these factors in the genesis of gastrointestinal postprandial symptoms is nicely illustrated by IBS where these phenomena have been studied in some detail; food responses in IBS and their regulation will, therefore, be used as an illustrative example throughout this chapter. NEURAL REGULATION OF GUT RESPONSES The central nervous system (CNS) communicates with the enteric nervous system via the sympathetic and parasympathetic branches of the autonomic nervous system. The anticipation and/or ingestion of food stimulate the autonomic nervous system leading to such well-described physiological responses as the cephalic phase of gastric acid secretion, receptive relaxation of musculature in the upper gastrointestinal tract and the gastro-colonic response. Given the frequent localization by sufferers of their pain to the left lower quadrant and of the prominence of post-prandial urges to defecate in IBS, the gastro-colonic response, a neurally-mediated homeostatic reflex, was an early target of investigation in this disorder. Not only were IBS subjects shown to exhibit an exaggerated gastro-colonic response4-6 but exaggerated responses to food ingestion were also demonstrated in the small intestine and, even, in the gall bladder.7-11 That autonomic nervous dysfunction in response to a meal might contribute to symptom generation is nicely illustrated again by IBS; alterations in the autonomic nervous system have been reported in patients with IBS; the most consistent finding being increased sympathetic nervous system activity.12-16 In other words, IBS sufferers are more susceptible to, and experience more exaggerated manifestations of the “gut distress” that we all experience on occasion when extremely stressed. Such reactions are seen in perhaps their most florid form in the individual with a severe anxiety disorder. Changes in parasympathetic nervous system activity have been less consistent in IBS and, while responses have varied, decreased parasympathetic responses have been observed most frequently.12-16 ENDOCRINE REGULATION OF THE RESPONSE TO FOOD A number of gut hormones play an integral part in the responses to food17. Enteric endocrine cells populating the gut secrete an array of hormones, such as motilin, gastrin, cholecystokinin (CCK) and peptide YY and respond to the anticipation and/or arrival of food or the products of digestion, and, thereafter, modulate the fate of gut contents in either a paracrine or endocrine manner. Motilin is secreted in the inter-digestive period when it released on distension of the duodenum by intense contractile activity of phase III of the migrating motor complex and stimulates gastric motility. Ghrelin, thought to play a major role in satiety and also released on food ingestion, also stimulates motility. Interestingly, higher circulating ghrelin levels have been described in IBS patients and could contribute to associations between food ingestion, dysmotility and IBS symptoms in some affected individuals.18,19 Cholecystokinin release is stimulated by the arrival of fat and protein into the proximal gut and delays gastric emptying, increases gut motility and enhances rectal hypersensitivity.20 Both fasting and post-prandial levels of CCK are elevated in IBS and an exaggerated response or hypersensitivity to CCK can cause symptoms of constipation, bloating or abdominal pain.21 In disorders of maldigestion and/or malabsorption the arrival of unabsorbed nutrients in the distal ileum (and fat in particular) stimulates the release of peptide YY from ileal neuro-endocrine cells and leads to World Digestive Health Day WDHD May 29, 2016 WGO Handbook on DIET AND THE GUT 57


WGO Handbook on Diet and the Gut_2016_Final
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