Diet and gastrointestinal disease

CLINICAL NUTRITION

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DIET AND GASTROINTESTINAL DISEASE James J. Cerda, MD

More than three decades ago, Philip White stated, in a preface to a position paper by Weinstein and coworkers/6 that "Over the years, foods - What to eat and what not to eat - have enjoyed an almost revered position in the therapy of gastrointestinal disorders." In the three decades following that pronouncement, the mysticism and folklore surrounding dietotherapy have largely been replaced by scientific evidence which justifies its rational use. Much of this impetus for change can be attributed to the extraordinary amount of interest in nutritional therapy following the epochal observations on total parenteral nutrition (TPN) by Dudrick and associates. 6 This article reviews some of the more misunderstood areas related to nutritional management of patients with gastrointestinal disease. NUTRITIONAL ASSESSMENT

There is no substitute for a careful history and physical examination by the health care provider. A nutritional history by a registered dietitian is strongly recommended. In addition, the dietitian can assist the phYSician in providing anthropometric data (Table 1). This information, in conjunction with the clinical and biochemical assessment, provides a sensible and logical data base. This is an extremely important concept in the Western World, because blatant malnutrition as depicted by many standard textbooks of medicine and pediatrics is not commonly observed. Eating behavior disorders, biochemical changes, and subtle weight status changes are observed in the Western World. PEPTIC ULCER DISEASE

Dietotherapy of peptic ulcer disease is a prime example of diet misuse. It is now well established that peptic ulcer disease results from an imbalance of From the Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Florida, Gainesville, Florida MEDICAL CLINICS OF NORTH AMERICA VOLUME 77· NUMBER 4' JULY 1993

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Table 1. NECESSARY PARAMETERS FOR NUTRITION ASSESSMENT Anthropometric

Clinical

Weight Height Triceps skinfold thickness Mid-arm muscle circumference

Physical examination Usual daily intake (By history)

Biochemical Serum prealbumin Serum albumin Hemogram BUN Iron profile Serum carotene

acid secretion and protective mechanisms of gastrointestinal mucosa. Despite conclusive evidence, it is surprising how many health care providers dwell on the use of milk-based bland diets. Bland diets are of no use and may actually worsen the disease. For example, milk is not only a weak anti-acid but is also rich in calcium which contributes to the rebound hyperacidity clearly documented in patients with peptic ulcer disease. 9 Furthermore, bland diets decrease or eliminate dietary fiber. Although both caffeine and decaffeinated beverages have been shown to stimulate gastric acid production, there is probably little harm in one cup of coffee per day in patients with peptic ulcer disease. Therefore, patients with peptic ulcer disease should be strongly encouraged to eat a balanced diet eliminating only foods that may cause idiosyncratic reactions in individual cases. THE ROLE OF DIETARY FIBER

There has been an explosion of information on the role of dietary fiber since the 1970s when low-fiber diets became associated with gastrointestinal disorders including constipation, diverticulosis, and cancer. Despite the current craze for large quantities of fiber in the diet, it is important to note that there are several disorders associated with delayed gastric emptying in which dietary fiber is probably contraindicated. It is appropriate to decrease dietary fiber in the diet in the treatment of patients with postgastrectomy syndrome, intestinal pseudo-obstruction with delayed gastric emptying, and in patients with gastroparesis diabeticorum unresponsive to prokinetic agents. The probability of bezoar formation in this group of patients is high, making the use of abundant fiber questionable. Instead, the use of a synthetic fiber such as polycarbophil is recommended. In patients with milder diabetes, water-soluble fibers, if tolerated, are recommended because of more steady glucose absorption. 12, 17 The role of dietary fiber in the treatment of irritable bowel syndrome (IBS) and diverticulosis is better defined. The insoluble fibers such as cellulose, hemicellulose, and lignin add bulk to stools by increasing their water-holding capacity. The soluble fibers such as gums, pectins, and oat fiber tend to attract water and decrease serum cholesterol levels. 2,4 Patients with IBS are characterized primarily by alternating constipation and diarrhea and generally feel better with addition of fiber to the diet. The weight of the stool is increased, as is its frequency. Fiber, however, is certainly not the only factor in IBS. Controlled studies have shown personality is as important as dietary variables in determining stool production. IS, 25 Positive, outgoing, personality traits are associated with increased stool output as is dietary fiber intake. Persons with less-positive self-image may benefit most from a high-fiber diet. In some patients with IBS the increased flatulence sometimes associated with high-fiber diets may be disabling. In these patients, a gluten-free diet has been suggested. I

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The case for a high-fiber diet in the prevention of colon cancer remains speculative. There is some evidence that increasing fiber content while decreasing fat content may have a beneficial effect.l3 It is also possible that the increase in other protective agents such as plant phenols, dithiones, thioethers, terpenes, carotene terpenes, and selenium may be responsible for this effect. Fat and vegetables may be the more important elements. In addition, the breakdown products of some water-soluble fibers such as butyrate may provide important energy substrates for colonic epithelium. 3 Wheat bran may normalize elevated rectal cell proliferation. 7 This and other evidence have prompted the Food and Drug Administration to cautiously recommend, with reservations, a low-fat, high-fiber diet in the prevention of colon cancer.21 ACUTE AND CHRONIC PANCREATITIS

Regardless of the cause, patients with acute pancreatitis are usually given nothing by mouth until the clinical course indicates that oral feedings can be resumed. Initially, TPN is frequently used. No evidence exists suggesting that judicious use of intravenous fat is contraindicated in acute pancreatitis. If enteral feedings are indicated, an elemental diet is recommended. When pancreatitis becomes chronic, the search for a cause becomes more important in regard to nutritional management. Examples would include alcohol-related pancreatitis and hypertriglyceridemic pancreatitis. Regardless of the cause, chronic pancreatitis is characterized by chronic abdominal pain with further complications including steatorrhea, diabetes mellitus, and malnutrition. Clinical recognition of pancreatitis associated with hypertriglyceridemia is important because dietary management is a cornerstone of its treatment. Pain is generally related to serum triglyceride levels greater than 500 mg/dL. To keep triglyceride levels as normal as possible, a low-carbohydrate diet is recommended. Compliance can be a problem because of nausea and abdominal pain. Large doses of pancreatic enzymes administered orally have been proven extremely useful in this regard. 23 Unless there is concomitant steatorrhea, pancreatic enzyme therapy is discontinued after triglyceride levels fall below 500 mg/dL. When steatorrhea and weight loss occur, the term pancreatic insufficiency more clearly describes the disease process. A high-protein, moderately low-carbohydrate, low-fat diet is recommended. Supplements such as medium chain triglycerides (MCT) can be quite useful in adding calories. There are several nutritionally complete products specially designed for patients who require medium chain triglycerides. These products contain upwards of 85% MCT oil and have been well accepted by patients. 1O MALABSORPTION

Malabsorption can be defined as a syndrome in which there is failure of the normal products of digestion to traverse the intestinal mucosal and enter the lymphatic or portal venous branches. Symptoms of malabsorptive disorders may range from only subtle clinical and biochemical changes, to a dramatic presentation of steatorrhea, weight loss, and malnutrition. There are many disorders likely to induce malabsorption (Table 2).'6 Postgastrectomy Dumping Syndrome

Since the need for gastric surgery has decreased concomitant with the increased use of H2 blockers for peptic ulcer disease, postgastrectomy dumping

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Table 2. PATHOPHYSIOLOGY OF MALABSORPTION Pathologic Condition' (Anatomical or Functional) Gastric surgery Billroth I Billroth 11 Roux-en-Y Zollinger-Ellison syndrome Small-bowel bacterial overgrowth Chronic pancreatitis Pancreatic carcinoma Chronic cholestasis Biliary tract disease Endocrine disorders Hormonally active tumors Jejunoileal bypass Ileal resection Short-bowel syndrome Infectious enteritis Crohn's disease Celiac sprue Giardiasis Whipple's disease Eosinophilic enteritis Small-bowel lymphoma Radiation enteritis Lymphangiectasia Abetalipoproteinemia

Mechanism of Malabsorption* No feedback control of chyme release Improper mixing of chyme with digestive enzymes Duodenal bypass Duodenal bypass Inactivation of enzymes due to low duodenal pH Bile acid deconjugation Mucosal damage Insufficient digestive enzymes or bile Insufficient digestive enzymes or bile Insufficient digestive enzymes or bile Insufficient digestive enzymes or bile Rapid transit, decreased contact time Rapid transit, decreased contact time Bypass of absorbing sites Loss of absorbing sites Loss of surface area Mucosal damage Transmural inflammation and mucosal atrophy Transmural inflammation and mucosal atrophy Unknown Infiltration of lamina propria by bacteria Inflammation Loss of brush border enzymes . Submucosal fibrosis Blocked lymphatic drainage Blocked transport from bowel target issues

*A particular condition may be operative on different levels. Adapted from Meyer S, Cerda JJ: Malabsorption: Pathophysiologic considerations and diagnosis. Compr Ther 11 :49-54, 1985; with permission.

syndrome is now less common. Nevertheless, to prevent the postprandial osmotic diarrhea associated with dumping syndrome, a diet relatively high in complex carbohydrates, high in fat and protein, and as low as possible in simple sugars is used. Eating should be divided into six small meals with lowcarbohydrate beverages between feedings. Wheat, oats, corn, rice, potatoes, and other starches are generally well tolerated. Not so for sugars such as sucrose and fructose. Fat should be maintained at about 35% of total daily kilocalories. Lactose Intolerance

A common cause of abdominal cramping and diarrhea is lactose intolerance. Lactose is composed of glucose and galactose and is present in human and cow milk, as well as in infant formulas and dairy products, such as ice cream and cheese. Lactose is often used as a filler for foods and medications. Patients themselves generally learn to avoid milk products. It is also of interest that most patients who are lactase deficient tolerate yogurt. Digestion of yogurt is apparently pH dependent, allowing the enzyme to be liberated in the stomach and reactivated in the duodenum. \1 Other cultured dairy products such as buttermilk and hard cheeses are usually better tolerated and provide essential

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calcium and riboflavin. Dark leafy green vegetables and enriched breads and cereal products also contribute these two nutrients whose intake may be marginal in lactose intolerant patients. It is now possible to purchase lactasetreated milk. Lactase tablets may also be purchased individually and can be added to fluid milk. It is noteworthy that it is the amount of lactose ingestion and not whether or not one can tolerate any lactose that leads to symptoms. Malabsorption Resulting From Inflammatory Bowel Disease

In both acute as well as chronic stages, malabsorption can result from inflammatory bowel disease (!BD). A matched control study has recently reported that TPN is clinically beneficial in both early management of patients with acute attacks of !BD and later in recovery.5 Nutritional deficiency in chronic !BD is multifactorial and can occur as a result of (1) dietary lack (self-induced or iatrogenic dietary lack), (2) increased loss due to malabsorption or diarrhea, (3) enteric losses, (4) absorption interference by drugs used in therapy such as corticosteroids, sulfasalazine, and cholestyramine, or (5) increased requirements secondary to inflammation and cell proliferation. 20 There is no universally accepted diet for Crohn's disease. Some investigators 18 have not been able to demonstrate any clear difference in the clinical course of patients who are randomly allocated to a low-fiber diet, unrestricted sugar diet, or to a diet with little or no sugar and high in unrefined carbohydrate. Controversy also exists regarding the use of defined formula diets with or without corticosteroids in active Crohn's disease. It has been proposed that elemental diets affect intestinal permeability and inflammation in Crohn's disease. 22 On the other hand, recently randomized prospective trials comparing a defined formula diet, plus corticosteroids in active Crohn's disease suggested that defined formula diets were not beneficial in the treatment of active Crohn's disease. 14 Short Bowel Syndrome

Patients with short bowel syndrome require intravenous fluids, electrolytes, and TPN during the acute phases. H 2-receptor antagonists should also be included because peptic ulcer disease is common in these patients secondary to gastric acid hypersecretion. Once stabilized, enteral support is recommended. Enteral nutrients are important for small bowel maturation. TPN is tapered as the enteral feedings are advanced and medium chain triglycerides should be instituted if steatorrhea is present. 8 As the patient adapts, repeated nutritional assessments will assist in recognizing what will be necessary for long-term maintenance. There are several special situations. For example, patients with ileal resection and jejunocolic anastomosis should be watched for oxaluria. In addition, patients with ileal resection may develop bile salt diarrhea and vitamin B12 deficiency. 19 This would necessitate monthly vitamin B12 injections and therapy with cholestyramine. Caution should be exercised with cholestyramine in that it binds fat-soluble vitamins. Celiac Sprue

Celiac sprue is characterized by a nonspecific mucosal lesion of the small intestine caused by certain cereal-derived proteins, resulting in impaired nu-

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trient absorption. Improvement of the mucosal lesion occurs on withdrawal of these certain proteins which are found in wheat, rye, barley, and oats. The patient must maintain a gluten-free diet throughout life. It is of interest that the disease occurs almost solely in whites and Asians from India and Pakistan. It is nonexistent in native Africans, Japanese, and Chinese. 24 A gluten-free diet generally initiates a prompt remission. A small number of patients do not appear to respond to the gluten-free diet. Most of these patients, upon careful questioning, have not complied with the dietary restrictions. If dietary indiscretion can be ruled out, a trial of corticosteroids may be initiated in addition to the gluten-free diet. The clinician must always be alert to the evolution of lymphoma or to collagenous sprue in these patients. Therefore, lifelong adherence to the diet, as well as careful follow-up, is recommended. SUMMARY

Diet therapy in the treatment of gastrointestinal disease has become better defined. Because maldigestion or malabsorption frequently occurs, malnutrition is a common complication. Careful assessment of nutritional status by the health care providers is mandatory. Diet therapy, by eliminating offending foods such as lactose or gluten or by addition of specialized enteral formulas containing MCT, or elemental diets can be instituted with marked relief in symptoms. The role of dietary fiber is now better defined in the treatment and prevention of many diseases. Further refinement and rational uses of diet therapy can be expected in future years. ACKNOWLEDGMENTS The author thanks Alex Burgin and Elizabeth Patrick for expert technical assistance.

References 1. Anderson IH, Levine AS, Levitt MD: Incomplete absorption of the carbohydrate in all-purpose wheat flour. N Engl J Med 304:891-892, 1981 2. Anderson JW, Story L, Sebring B, et al: Hypocholesterolemic effects of oat bran or bean intake for hypercholesterolemic men. Am J Clin Nutr 40:1146-1155, 1984 3. Bergman EN: Energy contributions of volatile fatty acids from the gastrointestinal tract in various species. Physiol Rev 70:567-590, 1990 4. Cerda JJ, Robbins FL, Burgin CW, et al: The effects of grapefruit pectin on patients at risk for coronary heart disease without altering diet or lifestyle. Clin Cardiol 11:589-594, 1988 5. Christie PM, Hill L, Graham L: Effect of intravenous nutrition on nutrition and function in acute attacks of inflammatory bowel disease. Gastroenterology 99:730736, 1990 6. Dudrick SJ, Wilmore DW, Vars HM, et al: Long term total parenteral nutrition with growth development and positive nitrogen balance. Surgery 64:134-142, 1968 7. Gelter-Allinger V, Bresmar B, Reinholt FP, et al: Soluble fecal acidic lipids and colorectal epithelial cell proliferation in normal subjects and in patients with colon cancer. Scand J Gastroenterol 10:1069-1074, 1991 8. Greenberger NJ: The management of the patient with short bowel syndrome. Am J Gastroenterol 70:528-540, 1978 9. Ippoliti AF, Maxwell V, Isenberg JI: The effect of various forms of milk on gastricacid secretion. Ann Intern Med 84:286-289, 1970

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10. Johnson RC, Cotter R: Metabolism of medium chain triglycerides lipid emulsion. Nutrition International 2:150-158, 1986 11. Kolars JC, Levitt MD, Aouju M, et al: Metal yogurt-an auto digesting source of lactose. N Engl J Med 310:1-3, 1984 12. Levitt NS, Vinik AI, Sive AA, et al: The effect of dietary fiber on glucose and hormone responses to a mixed meal in normal subjects and in diabetic subjects with and without autonomic neuropathy. Diabetes Care 3:515-519, 1980 13. Lewin MR: Is there a fibre-depleted aetiology for colorectal cancer? Experimental evidence. Rev Environ Health 9:17-30, 1991 14. Lindor KD, Fleming CR, Burnes JV, et al: A randomized prospective trial comparing a defined formula diet, corticosteroids, and a defined formula diet plus corticosteroids in active Crohn's disease. Mayo Clin Proc 67:328-333, 1992 15. Longstreth GF, Fox DP, Youkiles L, et al: Psyllium therapy in the irritable bowel syndrome. Ann Intern Med 95:53-56, 1981 16. Meyer B, Cerda JJ: Malabsorption: Pathophysiologic considerations and diagnosis. Compr Ther 11:49-54, 1985 17. Miranda PM, Horwitz DL: High fiber diets in the treatment of diabetes mellitus. Ann Intern Med 88:482-486, 1978 18. Ritchie J, Wadsworth J, Lennard-Jones JE, et al: Controlled multicentre therapeutic trial of an unrefined carbohydrate fibre-rich diet in Crohn's disease. Br Med J 295:517520, 1987 19. Rowell WG, Cerda JJ: The short bowel syndrome. Practical Gastroenterology 14:1016, 1990 20. Sitrin M, Rosenberg IH, Chawla K, et al: Nutritional and metabolic complications in a patient with Crohn's disease and ileal resection. Gastroenterology 78:1069-1079, 1980 21. Taylor E, Smigel K: Late-breaking news: FDA proposes fat, cancer health claim; hesitates on fiber. J Natl Cancer Inst 83:1618-1619, 1991 22. Teachon K, Smithurst P, Pearson M, et al: The effect of elemental diet on intestinal permeability and inflammation in Crohn's disease. Gastroenterology 101:84-89, 1991 23. Toskes PP: Hyperlipidemic pancreatitis. Gastroenterol Clin North Am 19:783-791, 1990 24. Trier JS: Celiac Sprue. N Engl J Med 325:1709-1719, 1991 25. Tucker DM, Sand stead HH, Logan Jr G, et al: Dietary fiber and personality factors as determinants of stool output. Gastroenterology 81:879-883, 1981 26. Weinstein L, Olson RE, Van Itallie TB, et al: Diet as related to gastrointestinal function. JAMA 176:935-941, 1961

Address reprint requests to James J. Cerda, MD Department of Medicine University of Florida Box 100214, JHMHC Gainesville, FL 32610-0214