Although there is no doubt that gastric acidity is directly involved in GERD pathogenesis, relationships between gastric and esophageal acidity are not clear. Lack of focus on gastric acid may relate to the general belief that gastric acid secretion is usually normal in GERD. Distinct patterns of esophageal acidity in GERD have been previously reported. There is a clear relationship between these descriptors and the present findings of integrated esophageal acidity. Previous pH-based analyses have nicely correlated esophagitis grade with acid exposure, but gastric acidity has been somewhat neglected as the major determinant of esophageal acid exposure in GERD aside from observations that acid inhibition could diminish esophageal acid exposure. Hirschowitz reported basal and pentagastrin-stimulated gastric acid secretion in esophagitis comparable to unspecified medical conditions without esophagitis. Others, however, have reported increased basal, peak, or maximal gastric acid secretion in GERD compared to healthy subjects. In studies of gastro-esophageal reflux, the esophageal pH electrode is traditionally positioned above the proximal limit of the lower esophageal sphincter (LES). This convention was adopted early on to avoid the electrode slipping into the stomach during swallowing when the esophagus shortens by 2-3 cm. As consequence, a conventionally placed electrode will only detect acid refluxing into the distal esophagus if it reaches this point 5 cm above the LES. If acid exposure of the most distal esophagus and proximal stomach is greater than that of the conventional measuring point proximal to the LES, it could have significance clinically. This reflux in the distal esophagus and proximal stomach may explain the high incidence of metaplasia and neoplasia of the most distal esophagus that occurs in the general population.