For many decades the dictum ‘no acid, no ulcer’ dominated thinking on the pathogenesis of peptic ulcer. When I was a medical student, not surprisingly, the standard therapy for a peptic ulcer was an antacid possibly combined with carbenoxolone. As a medical registrar, I was involved in the early studies with H 2 -receptor antagonists which, at the time, many of us believed would lead to the removal of peptic ulceration as a clinically important disease. It was soon evident, however, that ulcers returned rapidly when the H 2 -receptor antagonist was withdrawn and the concept of maintenance therapy was born. Within about 5 years of the launch of the first H 2 -receptor antagonist, cimetidine, two major developments occurred namely the discovery of Helicobacter pylori and the characterisation of the proton pump with the development of drugs to inhibit its action. The dicovery of H. pylori not only turned the aetiopathogenesis of peptic ulceration on its head but soon emerged as a major factor in the causation of gastric cancer and mucosa associated lymphocytic tissue (MALT) gastric lymphoma. The potential clinical impact of this organism continues to expand, with suggestions that it might be involved in growth retardation in children and possibly a factor in the development of ischaemic heart disease. The high prevalence of this organism worldwide presents clinicians and other healthcare workers with a formidable challenge with regard to its control at a population level.