Diet Therapy: Gastrointestinal Disorders PDF 2023/2024

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Al-Balqa Applied University

2024

Al Balqa Applied University

Dr. Reem M. “Al Haj Ahmad"

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gastrointestinal disorders diet therapy digestive health nutrition

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This document is a set of lecture notes on diet therapy for gastrointestinal disorders, specifically prepared for the 2023/2024 academic year at Al Balqa Applied University. It covers various conditions like constipation, diarrhea, steatorrhea, gastritis, peptic ulcers, and hiatal hernia, alongside inflammatory bowel disease and celiac disease. Each disorder is presented with explanations, symptoms, potential causes, and dietary guidelines. The main keywords of the document are gastrointestinal disorders, diet therapy, digestive health, and nutrition.

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11/2/2024 Al Balqa Applied University Faculty of Agriculture and Technology Nutrition and Food Processing Diet Therapy Gastrointestinal Disorders (30402352)...

11/2/2024 Al Balqa Applied University Faculty of Agriculture and Technology Nutrition and Food Processing Diet Therapy Gastrointestinal Disorders (30402352) Dr. Reem M. “Al Haj Ahmad” 2023/2024 Diseases of Small Intestine: Celiac disease Inflammatory bowel disease Crohn's disease Intestinal obstruction Irritable bowel syndrome Ulcers, such as “peptic ulcer” 1 11/2/2024 Diseases of Large Intestine: Colorectal cancer Colonic polyps Ulcerative colitis - ulcers of the colon and rectum Diverticulitis - inflammation or infection of pouches in the colon Irritable bowel syndrome Common Intestinal Symptoms: Intestinal gas and flatulence Constipation Diarrhea Steatorrhea Gastrointestinal obstruction 2 11/2/2024 1. Constipation: It is defined as infrequent or difficult bowel movements. It is a symptom but NOT a disease. It is accompanied by abdominal discomfort, headaches, backaches, and production of gases (Flatulence). 1. Constipation: Causes: 1. Fluid and electrolyte imbalances 2. Hormonal imbalances 3. Chronic laxative abuse 4. Lack of physical activity 5. Use of some medications 6. Use of antacids 7. Use of anti-hypertensive drugs 8. Pregnancy and aging (Why??) 3 11/2/2024 1. Constipation: Causes: 1. Fluid and electrolyte imbalances 2. Hormonal imbalances 3. Chronic laxative abuse 4. Lack of physical activity 5. Use of some medications 6. Use of antacids 7. Use of anti-hypertensive drugs 8. Pregnancy and aging (Why??) 2. Diarrhea: Watery stool; increased frequency. It is a symptom but NOT a disease. Foul-smelling. Presence of blood. Abdominal pain & cramping. Dehydration and weight loss. Electrolyte and acid-base imbalances. 4 11/2/2024 2. Diarrhea: Medical Nutrition Intervention: Treat underlying disease  Antibiotics Restore fluid, electrolyte, acid-base balance  IV therapy, rehydration solutions Medications to treat symptoms Suggest prevention strategies 2. Diarrhea: Medical Nutrition Intervention: NPO or clear liquids for a long period– old recommendation Feed patient – stimulates recovery Oral rehydration solutions WHO (sodium, chloride, potassium, glucose) Low-residue diet, use of pectin Pro- and prebiotics 5 11/2/2024 3. Steatorrhea: Is the medical term for fat in stool. Fat in the stool can cause bulky stool that floats, has an oily or greasy appearance, and smells foul. Fat in the stool is fat that the digestive tract was unable to absorb. Temporary steatorrhea may result from dietary changes or intestinal infections. Steatorrhea that is persistent may result from diseases of the biliary tract, pancreas, or intestines. 3. Steatorrhea: Fat absorption is dependent upon bile (which is produced in the liver and stored in the gallbladder), pancreatic lipases (enzymes that break down fat), and normal intestine function. Absence of bile is often due to blockage of the biliary tract and can result in pale colored fatty stool and jaundice. Absence of pancreatic lipases is uncommon, but can occur as a result of a diseased pancreas, cystic fibrosis, or an abnormality that is present at birth. 6 11/2/2024 3. Steatorrhea: Normally, 90-98% fat is absorbed. In steatorrhea, about 20% of fat is excreted with the feces. Medium and short chain fatty acids are able to enter the portal venous blood for direct transport to the liver without being resynthesized into TG in the intestinal cells. 3. Steatorrhea: Medical Nutrition Intervention: Increase kcal to meet needs, especially protein and carbohydrate. Control fat level-Give only level tolerated. Use medium-chain triglycerides (MCT) oil to meet kcal needs with caution. Vitamin and mineral supplements.  Use fat-soluble vitamins; add extra Ca, Mg, Zn, Fe. 7 11/2/2024 3. Steatorrhea: What is MCT: MCT: used as medicine Man-made fat from coconut and palm kernel oil. MCFA being absorbed more efficiently than long chain fatty acids (LFCA). MCFA are transported in the portal blood directly to the liver, unlike LCFA which are incorporated into chylomicrons and transported through lymph. 5. Gastritis and Peptic Ulcers: Gastritis is a nonspecific term literally meaning inflammation of the stomach. It describes symptoms relating to the stomach, an endoscopic appearance of the gastric mucosa, or a histologic change. Acute gastritis refers to rapid onset of inflammation and symptoms. Chronic gastritis may occur over a period of months to decades, with reoccurring symptoms. 8 11/2/2024 5. Gastritis and Peptic Ulcers: Symptoms Nausea and vomiting Anorexia Hemorrhage Epigastric pain. Prolonged gastritis may result in atrophy and loss of stomach parietal cells, with a loss of HCl secretion and intrinsic factor, resulting in pernicious anemia. 5. Gastritis and Peptic Ulcers:  Peptic Ulcer Occurs at the end of the stomach and the upper part of the duodenum (around the pyloric sphincter)  Ulcer in the stomach is called a gastric ulcer.  Ulcer in the in the first part of the small intestine (duodenum) is called duodenal ulcer. More common in males than females. 9 11/2/2024 5. Gastritis and Peptic Ulcers: Normal gastric and duodenal mucosa is protected from the digestive actions of acid and pepsin by the secretion of mucus, the production of bicarbonate, the removal of excess acid by normal blood flow, and the rapid renewal and repair of epithelial cell injury. Symptomatic peptic ulcer disease occurs as a result of the breakdown of more than one of the normal defense and repair mechanisms. 5. Gastritis and Peptic Ulcers: 10 11/2/2024 5. Gastritis and Peptic Ulcers: Peptic ulcer is symptoms: Epigastric discomfort; burning or severe and continuous pain, which tends to be worse at night. Pain usually happens 1-3 h after eating, and may be followed by: – Nauseas, vomiting, discomfort in the GIT, flatulence, and significant loss of body weight. 5. Gastritis and Peptic Ulcers: Increase gastric contractions accompanied with hypersecretion of HCL (this is more associated with duodenal ulcer than gastric ulcer) Heart burn Bleeding in the later stages (occult blood in feces) Many nutrient deficiencies (B-vitamins, Fe). 11 11/2/2024 5. Gastritis and Peptic Ulcers: Risk factors of peptic ulcer: Helicobacter pylori is a gram-negative and resistant to the acidic environment in the stomach. H. pylori infection is responsible for most cases of chronic inflammation of the gastric mucosa and peptic ulcer, gastric cancer, and atrophic gastritis. 5. Gastritis and Peptic Ulcers: Other Risk factors: Genetics/Ethnicity (e.g. Hyperacidity (over secretion of HCL)) Age (30-60) but it may occur at any age. More prevalent in males. Environmental Risk factors:  Alcohol & smoking– can inhibit or reduce secretion of mucus and bicarbonate, increasing acid secretion.  Some medications– aspirin, steroids, and nonsteroidal-anti- inflammatory. 12 11/2/2024 5. Gastritis and Peptic Ulcers: Medical Nutrition Intervention (MNI): Vitamin B12 status should be evaluated because lack of intrinsic factor and gastric acid results in malabsorption of this vitamin. Low acid states may influence absorption of iron, calcium, and other nutrients because gastric acid enhances bioavailability. Protein foods temporarily buffer gastric secretions, but they also stimulate secretion of gastrin, acid, and pepsin. 5. Gastritis and Peptic Ulcers: Milk or cream, which in the early days of peptic ulcer management was considered important in coating the stomach, is no longer considered medicinal. The pH of a food has little therapeutic importance, except for patients with existing lesions of the mouth or the esophagus. Most foods are considerably less acidic than the normal gastric pH of 1 to 3.  e.g. The pH of orange juice and grapefruit is 3.2 to 3.6, and the pH of commonly used soft drinks ranges from approximately 2.8 to 3.5. 13 11/2/2024 5. Gastritis and Peptic Ulcers: On the basis of their intrinsic acidity and the amount consumed, fruit juices and soft drinks are not likely to cause peptic ulcers or appreciably interfere with healing. Coffee, even decaffeinated coffee, should be avoided because it raises gastric acid production, resulting in mucosal irritations. Omit alcohol, tobacco, pepper, chili powder, and mustard seeds. Supply nutrients needed for healing (protein, vitamin C, Zinc). 6. Hiatal Hernia: Normally the lower end of the esophagus enters the chest cavity through an opening in the diaphragm membrane called the hiatus. A hiatal hernia occur when a portion of the upper stomach: swells through this opening also. Clinical symptoms: 1. Reflux of acid gastric contents leading it: heartburn which is the most common symptom. 14 11/2/2024 6. Hiatal Hernia: 6. Hiatal Hernia:  It is frequently sever, occurring 30 to 60 minutes after eating.  Pernicious vomiting.  The acid reflux may be caused by: pregnancy, obesity, aging, or congenital weakness of the diaphragm. 2. Iron-deficiency anemia. 3. Complication: food may easily be captured in the herniated area of the stomach , mixed with acid and pepsin , may be vomited back up into the lower portion of the esophagus. 15 11/2/2024 6. Hiatal Hernia: 4. Gastritis may occur in the herniated portion of the stomach and cause bleeding and anemia. Medical treatment: Ingestion of antacids and surgery is sometime necessary. Dietary modification: Since obesity is associated with hiatal hernia, weight reduction is a primary consideration. 6. Hiatal Hernia: Small, frequent meals consisting of a normal balanced diet are recommended. Known food intolerances are avoided, especially those that may irritate the mucous membranes (e.g. orange juice, tomato juice). No food is allowed for approximately 3 hour before bed time and the person should remain in the upright position after eating. 16 11/2/2024 7. Inflammatory Bowel Disease (IBD): Inflammatory bowel disease (IBD) is a chronic disorder of the gastrointestinal tract (GIT) that involved intestinal inflammation and mucosal injury associated with increased expression of cytokines. Crohn’s disease (CD) and ulcerative colitis (UC) are the two forms of IBD. The mucosa is the lining of the tubes, like a kind of skin. 7. Inflammatory Bowel Disease (IBD): 17 11/2/2024 7. Inflammatory Bowel Disease (IBD): 7. Inflammatory Bowel Disease (IBD): 18 11/2/2024 7. Inflammatory Bowel Disease (IBD): 7. Inflammatory Bowel Disease (IBD): 1. The place and the pattern of occurrence: CD (often but not always ) is found in the ileum and may extend to the colon. UC is usually found in the colon but sometimes may extend to the whole intestine. 19 11/2/2024 7. Inflammatory Bowel Disease (IBD): CD: Any part of the GIT, transmural, and discontinuous pattern. UC: Restricted to the colon, affect only the mucosa and superficial submucosa, and continuous pattern. 7. Inflammatory Bowel Disease (IBD): 2. The nature of the inflammation: UC: Mucosal inflammation CD: Submucosal inflammation 20 11/2/2024 7. Inflammatory Bowel Disease (IBD): 7. Inflammatory Bowel Disease (IBD): Etiology and Pathogenesis: Environmental Triggers Genetic Immune Susceptibility Response 21 11/2/2024 7. Inflammatory Bowel Disease (IBD): Risk factors of the disease: a. Race: CD more common in certain races (western). UC more distributed (high incidence) in western Europe and US. Whites are more likely to develop IBD than non-whites. b. Age: Both diseases are young adulthood diseases. 7. Inflammatory Bowel Disease (IBD): c. Gender Both gender are equally affected. d. Smoking: Smokers are more likely to develop CD and have more aggressive form than non-smokers. Smokers are less likely to develop UC and tend to have a less severe course than non-smokers. 22 11/2/2024 7. Inflammatory Bowel Disease (IBD): e. Genetics: 10-20% of IBD patients have one or more other family members affected with IBD. Both diseases can also exist in the same family 7. Inflammatory Bowel Disease (IBD): 1 1 Phase I: Pre-disease stage. Genetic and Environmental Factors. Impaired Barrier Function of Intestinal Mucosa Bacterial Translocation. 23 11/2/2024 7. Inflammatory Bowel Disease (IBD): 12 Phase II: Acute Intestinal Inflammation. Immune Cell Activation. Cytokine Production. 2 7. Inflammatory Bowel Disease (IBD): 13 Phase III: Chronic Inflammation. Failure of Regulation Mechanisms 2 3 24 11/2/2024 7. Inflammatory Bowel Disease (IBD): 413 Phase IV: Tissue Destruction and Manifestations. 2 4 7. Inflammatory Bowel Disease (IBD): Symptoms: 1. CD: a. Fistula- an abnormal connection between the intestine and other organs. b. Abscess- collection of pus. c. Stricture- an area of narrowing that can lead to intestinal blockage. 25 11/2/2024 7. Inflammatory Bowel Disease (IBD): 2. UC: The inflammation occurs only in the innermost layer of the lining of the intestine. It usually begins in the rectum and lower colon, but may also spread continuously to involve the entire colon. Bleeding is more common in UC. 7. Inflammatory Bowel Disease (IBD): Organs other than the intestinal tract can be involved by IBD: – The eyes ( red eye or blurred vision) – The mouth (sores in the mouth) – Joints (joint pain with or without joint swelling and redness) – Skin (rashes or skin ulcers most involving the lower legs) 26 11/2/2024 7. Inflammatory Bowel Disease (IBD): Nutritional problems: 1. Weight loss and anemia:  Due to diarrhea and bleeding 2. Poor growth in children due to malnutrition associated with the disease and medications (corticosteroids) 3. Decreased bone mineral density is common in children, adolescents and adults with IBD. 7. Inflammatory Bowel Disease (IBD):  Inadequate intake and absorption of calcium  Vitamin D deficiency 4. Macro/Micro-nutrient deficiency  Inadequate intake → Protein energy malnutrition.  Low iron, B-12 and folate → Anemia  Low vitamin D, vitamin K → Osteomalacia and osteoporosis  Low vitamin E → Peripheral neuropathy 27 11/2/2024 7. Inflammatory Bowel Disease (IBD):  Low vitamin A → Night blindness  Low thiamine and B vitamins → Beriberi, stomatitis, or glossitis 7. Inflammatory Bowel Disease (IBD): Medical Nutrition Intervention Major objectives: to restore and maintain the nutrition status of the individual.  To promote immunity and healing  To control signs and symptoms  To prevent nutritional deficiencies (e.g. anemia and osteoporosis)  To maintain normal growth (children) 28 11/2/2024 7. Inflammatory Bowel Disease (IBD): Nutritional Assessment  Detailed assessment including dietary intake, anthropometric evaluation and biochemical measurement of vitamins and trace elements is needed. 7. Inflammatory Bowel Disease (IBD): Dietary intervention may change during remissions and flares of the disease. Flares of the disease characterized by partial obstructions, nausea, abdominal pain, bloating, or diarrhea. Foods that are responsible for some GI symptoms (i.e. gas, bloating, diarrhea) are likely to be triggers. NO single dietary treatment for reducing symptoms or decreasing flares has been found to be conclusively effective. 29 11/2/2024 7. Inflammatory Bowel Disease (IBD): A. Calories and macronutrients:  Energy needs of patients with IBD are not increased (unless weight gain is desired).  Protein requirements may be increased, depending on the severity and stage of the disease and the restoration requirements.  Inflammation and treatment with corticosteroids induce a negative nitrogen balance and cause a loss of lean muscle mass. 7. Inflammatory Bowel Disease (IBD):  Protein losses also occur in areas of inflamed and ulcerated intestinal mucosa via defects in epithelial tight junctions.  To maintain positive nitrogen balance, 1.3 to 1.5 g/kg/day of protein is recommended.  Supplemental vitamins and minerals: folate, B6, B12, iron and trace elements because of maldigestion, malabsorption, drug-nutrient interactions, or inadequate intake. 30 11/2/2024 7. Inflammatory Bowel Disease (IBD):  Diarrhea can aggravate losses of zinc, potassium, and selenium.  Corticosteroids may need supplemental calcium and vitamin D.  Omega-3 fatty acid supplements in CD significantly reduce disease activity.  Use of foods and supplements containing prebiotics and probiotic supplements may alter the gut microbiota. 7. Inflammatory Bowel Disease (IBD): B. Route of delivery:  In adults: Enteral nutrition (EN) is NOT as effective as corticosteroid therapy to induce remission in adults with CD.  In children: EN is far more effective and should be considered as a primary therapy.  Complete bowel rest using parenteral nutrition (PN) is may be used in those with inadequate functioning bowel. 31 11/2/2024 7. Inflammatory Bowel Disease (IBD):  EN has the potential to feed the intestinal epithelium and alter GI flora and is the preferred route of nutrition support in patients with adequate bowel length. 7. Inflammatory Bowel Disease (IBD): C. During flares:  During exacerbations of the disease, the diet is tailored to the individual but usually includes reduced fiber intake and decaffeinated, low-sugar beverages for adequate hydration.  In people e with rapid intestinal transit, excessive intake of lactose, fructose, or sorbitol may contribute to abdominal cramping, gas, and diarrhea; and high fat intake may result in steatorrhea  Small, frequent feedings may be tolerated better than large meals. 32 11/2/2024 8. Celiac Disease: Celiac disease (or nontropical sprue or gluten sensitivity) is a disorder characterized by malabsorption of virtually all nutrients. It is thought to be due to heredity. The onset and first occurrence of symptoms may appear any time from infancy to adulthood. The disease may become apparent when an infant begins eating gluten- containing cereals. 8. Celiac Disease: It may not appear until adulthood, when it may be triggered or unmasked during GI surgery, stress, pregnancy, or viral infection. It may be discovered as a result of evaluation for another suspected problem (such as constipation, abdominal pain, unexplained anemia). It is a malabsorption disease in which the primary cause is malabsorption because of the atrophy of villi and microvilli resulting in low surface area. 33 11/2/2024 8. Celiac Disease: It is given different names: - Malabsorption syndrome. - Gluten – induced enteropathy. - Non – tropical sprue (in children). If occurs in adult, it is called adult celiac. 8. Celiac Disease: Etiology and Pathogenesis: Genetic Environmental susceptibility trigger Exposure to Autoimmune gluten response 34 11/2/2024 8. Celiac Disease: What is gluten? Gluten refers to specific peptide fractions of proteins found in wheat, rye, and barley. These peptides are generally more resistant to complete digestion by GI enzymes and may reach the small intestine intact. In a normal, healthy intestine, these peptides are harmless, as the intestinal barrier is intact and prevents translocation from the intestine. 8. Celiac Disease: In persons with CD these peptides:  Travel from the intestinal lumen → the lamina propria → trigger an inflammatory response → flattening of intestinal villi and elongation of secretory cells → more general systemic immune response. The “triggers” that cause a genetically predisposed individual to develop CD are not well understood, but stressors (e.g., illness, inflammation) are thought to play a role. 35 11/2/2024 8. Celiac Disease: Atrophy and flattening of villi consequences: 1. Damage of the intestinal mucosa. 2. Compromise normal secretory, digestive, and absorptive functions. 3. Impaired micronutrient and macronutrient absorption. 4. Cells of the villi become deficient in the disaccharidases and peptidases needed for digestion and also in the carriers needed to transport nutrients into the bloodstream. 8. Celiac Disease: Gluten sensitivity is used commonly to describe persons with nonspecific symptoms, without the immune response characteristic of CD or the consequential intestinal damage. Gluten intolerance, also called nonceliac gluten sensitivity, describes individuals who have symptoms after ingesting gluten-containing foods. 36 11/2/2024 8. Celiac Disease: Symptoms: Nausea that might be accompanied with vomiting, Abdominal cramps and distention of the stomach, Diarrhea and steatorrhea , Brain fog, Stool become bulky, watery, greasy, and foamy with foul smell, Growth failure, and Many micronutrient deficiencies. 8. Celiac Disease: Complication/Nutritional Problems: Mal-absorption of fat, protein and carbohydrate (sever malnutrition, delayed growth, underweight). – Folate, B12, Iron deficiency (Anemia). – Vitamin K deficiency (Coagulopathies/ bleeding disorders) – Inadequate Calcium absorption (bone disease). 37 11/2/2024 8. Celiac Disease: 8. Celiac Disease: MNI (See Attachment): Remove gluten from the diet: —Wheat —Rye —Buckwheat —Barley 38 11/2/2024 8. Celiac Disease: Gluten-Free food: — Fruits — Vegetables — Meat and poultry — Fish and seafood — Dairy — Beans, legumes, and nuts 9. Diverticular Disease: Pressure inside the colon →→ pushes out the mucosa and the submucosa layer → → a blood vessel penetrates the muscle layer of the intestine→→ 1. Gastrointestinal bleeding. 2. Blood vessels can get weaker. 3. Bacteria and undigested food may get stuck inside and cause infection. 4. Bowel obstruction. 5. Formulation of abscess (pocket of infected pus). 6. Some patient diverticula can rapture and cause peritonitis. 39 11/2/2024 9. Diverticular Disease: Pressure inside the colon →→ pushes out the mucosa and the submucosa layer → → a blood vessel penetrates the muscle layer of the intestine→→ 1. Gastrointestinal bleeding. 2. Blood vessels can get weaker. 3. Bacteria and undigested food may get stuck inside and cause infection. 4. Bowel obstruction. 5. Formulation of abscess (pocket of infected pus). 6. Some patient diverticula can rapture and cause peritonitis. 9. Diverticular Disease: Pressure inside the colon →→ pushes out the mucosa and the submucosa layer → → a blood vessel penetrates the muscle layer of the intestine→→ 1. Gastrointestinal bleeding. 2. Blood vessels can get weaker. 3. Bacteria and undigested food may get stuck inside and cause infection. 4. Bowel obstruction. 5. Formulation of abscess (pocket of infected pus). 6. Some patient diverticula can rapture and cause peritonitis. 40 11/2/2024 9. Diverticular Disease: Pressure inside the colon →→ pushes out the mucosa and the submucosa layer → → a blood vessel penetrates the muscle layer of the intestine→→ 1. Gastrointestinal bleeding. 2. Blood vessels can get weaker. 3. Bacteria and undigested food may get stuck inside and cause infection. 4. Bowel obstruction. 5. Formulation of abscess (pocket of infected pus). 6. Some patient diverticula can rapture and cause peritonitis. 9. Diverticular Disease: Symptoms: Diverticulitis - when these pouches become inflamed.  Symptoms: fever, abdominal pain, GI bleeding, elevated WBC. Diverticulosis – asymptomatic 41 11/2/2024 9. Diverticular Disease: Risk Factors: A. Modifiable: Low fiber intake, hx of constipation, increased colonic pressure Increases inflammatory response Other risks: obesity, sedentary, steroids, alcohol and caffeine intake, cigarette smoking, certain medications (e.g. NSAID) B. Non-modifiable: Genetic factor Age >40 Y/O 9. Diverticular Disease: MNT: A. Diverticulosis  High-fiber diet: fruits, vegetables, whole grains (2 tsp bran daily).  The bulk provided by the high-fiber diet will: 1) increase stool volume, 2) reduce the pressure in the colon, 3) shorten the time the food is in the intestine → giving bacteria less time to grow. 42 11/2/2024 9. Diverticular Disease: B. Diverticulitis  A clear liquid diet, followed by a low-residue diet that allows the bowel to rest and heal.  Residue: refers to undigested food, including fiber, that make up stool. The goal of the diet is to have fewer, smaller bowel movements each day, in order to ease symptoms such as diarrhea, bloating, gas, and stomach cramping. 10. Irritable Bowel Syndrome (IBS): Another name: the buzzle disease (syndrome). It is a disease affect the digestive system. More common in females than males. It can start at early adulthood, but it can occur at any age. Common syndrome involving altered intestinal motility, increased sensitivity of the GI tract, and increased awareness and responsiveness of the viscera to internal and external stimuli. Alternating constipation and diarrhea, abdominal pain, and bloating. 43 11/2/2024 10. Irritable Bowel Syndrome (IBS): Risk Factors: The exact causative agent is unknown, but risk factors include: 1) Low fiber consumption 2) Psychological stress 3) Infection (gastroenteritis) 4) Certain medications 10. Irritable Bowel Syndrome (IBS): MNT: 1. Resting and reduce stress. 2. Avoid a group of food items given the acronym FODMAP (fermentable, oligosaccharide, disaccharides, monosaccharides and polyols), which can trigger the symptoms of IBS. 3. High fiber diet. 4. Avoid gas formers (ex. cruciferous vegetables, legumes). 5. Avoid any irritating agents (intolerances). 44 11/2/2024 10. Irritable Bowel Syndrome (IBS): MNT: 6. Reduce total fat in the diet. 7. Avoid large meal (eat more frequent meals). 8. Avoid air swallowing habits (due to eating large amount of food, eating rapidly, carbonated beverages, smoking and chewing gums). 45

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