Effect of low and high fat meals on lower esophageal sphincter motility and gastroesophageal reflux in healthy subjects
The reported effects of fatty meals on lower esophageal sphincter pressure (LESP) and gastroesophageal reflux (GER) are controversial. Therefore, the aim of the present study was to reevaluate the effect of isocaloric and isovolumetric low and high fat meals on LESP and GER.
Twelve healthy volunteers (six women, six men, 19 to 31 yr) received an isocaloric (842 kcal) solid-liquid (310 ml with 260 kcal) meal with either a low (10% fat, 14% proteins, 76% carbohydrates) or a high fat content (50% fat, 18% proteins, 32% carbohydrates) in a randomized, double-blinded fashion. The nutritional composition was identical for the solid and liquid part of the meals. In the first post-prandial hour LESP was recorded continuously using a Dent sleeve, and esophageal pH measurement was performed for 3 h postprandially with a glass electrode. We calculated the mean LESP, the frequency of transient LES relaxations (TLESR) and of reflux episodes (RE), the percentage of TLESR with GER, and the fraction time pH <4.
For all parameters measured no difference was observed between the low and the high fat meal. Mean LESP amounted to a median of 10.7 mm Hg (range, 7.3 to 15.1 mm Hg) after the low fat meal and to 11.1 mm Hg (5.2 to 16.3 mm Hg) after the high fat meal. The frequency of TLESR (n/1 h) rated to 9 (5 to 13) and 8 (4 to 14), and of RE (n/3 h) to 12 (3 to 22) and 11 (1 to 30). The percentage of TLESR with GER were 37% (0 to 100) and 30% (0 to 78). The fraction time pH <4 amounted to 2.3% (0.2 to 23.7) and 1.8% (0.1 to 28.8) after the low and high fat meal, respectively.
In healthy volunteers no difference in post-prandial LESP and GER was seen after a high fat meal compared with an isocaloric and isovolumetric low fat meal. Our results suggest that it is inappropriate to advise GER patients to reduce the fat content of their meals for symptom relief.
Available from: Henry I. Jacoby
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ABSTRACT: Geoffrey C. Wall is an Associate Professor of Pharmacy Practice in the College of Pharmacy and Health Sciences. He can be contacted at email@example.com PROLOGUE: Gastroesophageal reflux disease (GERD) is a pathologic condition of injury to the esophagus caused by regurgitation of gastric or gastroduodenal contents into the lumen of the esophagus. Histopathology of the esophageal mucosa may or may not be present. Gastroesophageal reflux of acid and gastric contents often causes a condition commonly referred to as heartburn. This is characterized as a retro-sternal burning sensation that radiates to the throat and interscapular region. It may be confused, even in the emergency room, with anginal pain or the onset of myocardial infarction; therefore its rapid diagnosis is important. In many patients GERD should be considered a chronic and lifelong illness and maintenance therapy is often needed. Repeated exposure of the esophagus to stomach contents leads to esophagitis. In severe cases, this can actually erode esophageal tissue (erosive esophagitis). In the last five to seven years several new treatment options for GERD have become available. These include antise-cretory agents such as the proton pump inhibitors, and new surgical techniques that have improved Nissen fundoplication safety and efficacy rates(3-4). Clinicians caring for patients with this common disorder need to understand the pathology behind GERD, its common (and uncommon) clinical manifestations, and current treatment options as recommended by the American College of Gastroenterology.
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ABSTRACT: INTRODUCTION: Symptomatic esophageal reflux affects a large number of individuals. Many find relief by avoiding trigger substances such as coffee or sweets; in other cases, lifestyle modifications do not suffice and drug treatment is necessary for symptom control. An adequate classification of gastroesophageal reflux disease (GERD) is currently lacking; esophagitis can be graded according to Savary and Miller or the more recent metaplasia ulcer stricture erosions (MUSE) classification. TREATMENT AIMS: The control of symptoms should be achieved in all patients: in addition, if esophagitis is present, the healing of erosions/ulcers as well as the prevention of further complications, such as strictures, hemorrhage, Barrett's esophagus or ulceration, must be accomplished. SHORT-TERM TREATMENT: In the case of rare symptoms, control might be achieved by lifestyle modifications and by antacids or mucosal protectants taken on demand. In the case of continuous symptoms or signs of esophagitis, effective inhibition of gastric acid secretion with proton pump inhibitors (PPIs) is necessary in many patients. PREVENTION OF RELAPSE: After discontinuation of medical therapy, almost all patients with esophagitis will experience a relapse within 30 weeks. The regimen offering the highest rate of remission in these patients is the one that induced remission in the first place. Reduction of PPI dose or a switch to H2 receptor antagonists increases the rate of relapse. RISKS OF LONG-TERM TREATMENT: Long-term acid suppressive therapy, as with the use of PPIs, may lead to hypergastrinemia, a situation in which the endocrine cells of the stomach may proliferate. In the presence of Helicobacter pylori infection, PPIs are more efficient in healing esophagitis; however, the occurrence of gastric mucosal atrophy, a potentially pre-cancerous condition, has been described. To date, however, no case of gastric cancer or endocrine neoplasia associated with PPI treatment has been documented; gastric mucosal atrophy is more likely to result from H. pylori infection and gastric carcinoid formation needs a genetic predisposition, such as multiple endocrine neoplasia (MEN) type I. CONCLUSIONS: Most cases of GERD can be effectively treated by non-surgical measures; in patients presenting with warning symptoms or persistent heartburn, endoscopy of the upper gastrointestinal tract is mandatory. Long-term use of PPIs seems to be a safe and efficient treatment for GERD. For the prevention of relapse, similar doses are needed as for the induction of remission in reflux esophagitis.
Available from: Alexander Meining
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ABSTRACT: Gastroesophageal reflux disease (GERD) and the complications associated with it are very common in the Western world. There has been speculation for many years that certain dietary and lifestyle factors may play a role in the pathogenesis or course of GERD. However, a wide-ranging review of the available data reveals conflicting findings regarding the impact of most of these factors. In addition, the majority of the studies concerned have been based on small numbers of patients, and in most cases these studies do not meet the criteria for evidence-based medicine. Consequently, any advice given on modifying diet and/or lifestyle in the management of GERD represents a form of empirical therapy. A general consensus on the control of GERD through alterations in diet and lifestyle factors could hardly be based on the results of clinical or outcome studies. In practice, however, the treatment of GERD is oriented toward the individual patient's symptoms, and includes offering reasonable advice on how to adapt to personal dietary intolerance and lifestyle factors.
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