Concerning the relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease (GORD), the debate is ongoing whether the infection confers protection, is harmful or whether both entities are independent. Epidemiological evidence is given for an increased prevalence of GORD and a decreased prevalence of H. pylori infection in the western world. The assumpton derived from it is that H. pylori protects from GORD. Pathophysiological aspects need to consider the type and expression of gastritis which is associated with varying changes of gastric function. Depending on the type of gastritis, acid secretion may either increase or decrease and thereby impact on acid exposure of the oesophagus. Other changes related to the role of H. pylori in pathophysiology of GORD are still hypothetical. Clinical data are controversial whether or not GORD increases after H. pylori eradication. Prospective studies including characterization of strains and gastric physiology will clarify this issue. An accelerated induction of gastric mucosal atrophy in patients on long-term proton pump inhibitors is reported in most available studies. An increase of inflammatory activity in fundic and corpus mucosa is a consistent phenomenon. Therefore, in the authors' opinion, eradication appears advisable.