BACKGROUND: The postprandial increase of gastroesophageal reflux (GER) results largely from an increase in the rate of transient lower esophageal sphincter relaxations (TLESRs). Gastric distension is believed to be the most important contributing factor. The aim of this study was to determine the impact of rapid food intake on GER in healthy volunteers using combined multichannel intraluminal impedance and pH (MII-pH) testing to record both acid and nonacid reflux. Our hypothesis was that rapid food intake overstresses the gastric pressure-volume response and contributes to increased postprandial GER. METHODS:Twenty healthy volunteers were included in the study. On two separate days the participants were asked to eat the same standard meal within 5 or 30 min in random order. Acid and nonacid reflux episodes were recorded over a 2-h postprandial period. RESULTS: Intake of a standard meal within 5 min was associated with more reflux episodes (median = 14) than an intake within 30 min (median = 10, p= 0.021). The increase was confined to the first postprandial hour and was caused predominantly by an increase of nonacid reflux. During the entire 2-h postprandial period, 469 reflux episodes were noted in the 40 studies. During the first postprandial hour 45% (135/303) of reflux events were nonacid as opposed to 22% (37/166) noted during the second hour (p < 0.0001). CONCLUSION: Since rapid food intake produces more GER in healthy volunteers, studies in GERD patients are warranted to evaluate if eating slowly may represent another "life-style modification" aimed at reducing GER.
RCT Entities:
BACKGROUND: The postprandial increase of gastroesophageal reflux (GER) results largely from an increase in the rate of transient lower esophageal sphincter relaxations (TLESRs). Gastric distension is believed to be the most important contributing factor. The aim of this study was to determine the impact of rapid food intake on GER in healthy volunteers using combined multichannel intraluminal impedance and pH (MII-pH) testing to record both acid and nonacid reflux. Our hypothesis was that rapid food intake overstresses the gastric pressure-volume response and contributes to increased postprandial GER. METHODS: Twenty healthy volunteers were included in the study. On two separate days the participants were asked to eat the same standard meal within 5 or 30 min in random order. Acid and nonacid reflux episodes were recorded over a 2-h postprandial period. RESULTS: Intake of a standard meal within 5 min was associated with more reflux episodes (median = 14) than an intake within 30 min (median = 10, p= 0.021). The increase was confined to the first postprandial hour and was caused predominantly by an increase of nonacid reflux. During the entire 2-h postprandial period, 469 reflux episodes were noted in the 40 studies. During the first postprandial hour 45% (135/303) of reflux events were nonacid as opposed to 22% (37/166) noted during the second hour (p < 0.0001). CONCLUSION: Since rapid food intake produces more GER in healthy volunteers, studies in GERDpatients are warranted to evaluate if eating slowly may represent another "life-style modification" aimed at reducing GER.
Authors: Georg R Linke; Andreas Zerz; Radu Tutuian; Francesco Marra; Rene Warschkow; Beat P Müller-Stich; Jan Borovicka Journal: J Gastrointest Surg Date: 2008-01-23 Impact factor: 3.452
Authors: F Cremonini; M Camilleri; M M Clark; T J Beebe; G R Locke; A R Zinsmeister; L M Herrick; N J Talley Journal: Int J Obes (Lond) Date: 2009-01-13 Impact factor: 5.095