There are three main factors involved in the pathogenesis of gastroesophageal (GE) disease.

        1) Abnormalities of GE junction. Degenerative changes cause weakening of the extrinsic sphincter and phreno-esophageal ligament causing proximal migration of proximal stomach forming hiatus hernia and loss of flap valve. This allows reflux and impaired clearance.

        2) The second is central obesity and associated increase in abdomino-thoracix pressure gradient.  Increasing intra-abdominal pressure experimentally by even 5mmHg causes an eight-fold increase in reflux after meals in patients with reflux disease. ( Mitchell et al. Gatroenterology 2017;152:1881-88 ).  Central obesity therefore promotes reflux in subjects with dysfunction of the GE sphincter.

        3) The third factor is the acidity and peptic activity of the gastric juice and this is mainly related to H.pylori gastritis. We recently studied the intragastric pH along with measuring the density of parietal and chief cells in healthy middle aged volunteers with and without H.pylori infection ( Mitchell et al. Gut 2017;66:1555-62 ). Those with H.pylori had substantially reduced acidity most marked close to the GE junction. The density of parietal cells was also reduced by more than 50% in the H.pylori positive volunteers. This explains the protective effect of H.pylori in the aetiology of reflux. 

         In conclusion, Abnormality of the of GE junction is an essential factor in pathogenesis of reflux but the promoting effect of central obesity and protective effect of H.pylori gastritis are important co-factors