Previous studies have demonstrated an increased gastroesophageal reflux after the ingestion of high-proof alcoholic beverages in normal subjects. Data on gastroesophageal reflux with usual amounts of low-proof alcoholic beverages are not available. The effect of white wine (7.5% v/v, pH 3.2) and beer (7.0% v/v, pH 4.5) was compared with water, a nonalcoholic beverage of pH 3.2, and an ethanol solution (7.5% v/v, pH 7.6) using ambulatory pH measurement in healthy volunteers. The fraction of time at pH < 4 in the first hour after ingestion of 300 ml white wine (median 13.2%) was significantly increased compared with beer (3.6%; P < 0.01), water (0.9%; P < 0.001), ethanol (1.3%; P < 0.001), and the nonalcoholic beverage (0.9%; P < 0.05). Beer provoked significantly more gastroesophageal reflux than water (P < 0.01). It is concluded that white wine and beer induce gastroesophageal reflux, which is neither related to their ethanol content nor to their pH. The mechanism for this effect remains to be identified.
Background: Patients with reflux disease often complain of heartburn after ingestion of coffee. Induction of gastro‐oesophageal reflux has been demonstrated by pH‐metry following the intake of coffee in healthy volunteers. The reflux was reduced when the coffee had undergone a decaffeination process. The aim of this study was to investigate the effect of decaffeination of coffee on reflux in patients with reflux disease. Methods: Seventeen reflux patients underwent two oesophageal 3‐h pH measurements. The patients received, in a double‐blind study design in a randomized order, 300 mL of either regular or decaffeinated coffee together with a standardized breakfast. The fraction time oesophageal pH < 4 was calculated during the three postprandial hours. Results: For regular coffee the fraction time was calculated to a median of 17.9% with a range of 0.7–56.6%. The fraction time was significantly reduced to 3.1% (0–49.9%) after ingestion of decaffeinated coffee. Conclusion: The amount of gastro‐oesophageal reflux induced by the intake of regular coffee in patients with reflux disease can be reduced by the decaffeination of coffee.
Background: Coffee and tea are believed to cause gastrooesophageal reflux : however, the effects of these beverages and of their major component, caffeine, have not been quantified. The aim of this study was to evaluate gastro-oesophageal reflux induced by coffee and tea before and after a decaffeination process, and to compare it with water and water-containing caffeine. Methods : Three-hour ambulatory pH-metry was performed on 16 healthy volunteers, who received 300 ml of (i) regular coffee, decaffeinated coffee or tap water ( n = 16), (ii) normal tea, decaffeinated tea, tap water, or coffee adapted to normal tea in caffeine concentration ( n = 6), and (iii) caffeine-free and caffeine-containing water ( n = 8) together with a standardized breakfast.Results: Regular coffee induced a significant ( P < 0.05) gastro-oesophageal reflux compared with tap water and normal tea, which were not different from each other. Decaffeination of coffee significantly ( P < 0.05) diminished gastro-oesophageal reflux, whereas decaffeination of tea or addition of caffeine to water had no effect. Coffee adapted to normal tea in caffeine concentration significantly ( P < 0.05) increased gastro-oesophageal reflux. Conclusions: Coffee, in contrast to tea, increases gastrooesophageal reflux, an effect that is less pronounced after decaffeination. Caffeine does not seem to be responsible for gastro-oesophageal reflux which must be attributed to other components of coffee.
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.
INTRODUCTIONIngestion of a meal decreases lower oesophageal sphincter pressure and induces gastro-oesophageal re¯ux in healthy volunteers and in patients with re¯ux disease. 1, 2 Because the high fat content of a meal and the ingestion of large meals were thought to be responsible for these meal effects, patients with re¯ux disease were advised to avoid high fat and large meals. 3±11 However, the amount of dietary fat necessary to reduce the lower oesophageal sphincter pressure seems to be rather low; whole milk (3.3±3.4% fat) but SUMMARY Background: Patients with gastro-oesophageal re¯ux disease are advised to avoid the ingestion of large meals. In healthy volunteers, a relationship between the amount of postprandial gastro-oesophageal re¯ux and the volume of a liquid meal has been demonstrated. Aim: To evaluate whether the amount of postprandial gastro-oesophageal re¯ux is also related to the calorie content of a meal, a second parameter that will be reduced by avoidance of the ingestion of large meals. Methods: Twelve healthy volunteers (six female, 19± 31 years) received two solid±liquid meals with either 842 kcal (solid 582 kcal, liquid 260 kcal) or 582 kcal (31% reduction) in a randomized order. The nutritional components (10% fat, 76% carbohydrates, 14% protein) and the volume of the meals were identical in both meals. The lower oesophageal sphincter pressure was measured continuously in the ®rst postprandial hour with a Dent sleeve, and pH-metry was performed for 3 h postprandially with a glass electrode in the distal oesophagus. Blinded to the type of ingested meal, we calculated the mean lower oesophageal sphincter pressure, the frequency of transient lower oesophageal
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