No-one doubts that acid and pepsin are the major factors responsible for symptoms and oesophageal mucosal damage which comprise the clinical spectrum of gastro-oesophageal reflux disease. Clinical and in vitro studies overwhelmingly support this view. However, the relations between both symptoms and increasing oesophageal injury on the one hand and increasing duration of acid reflux (assessed by oesophageal pH monitoring) on the other have not always been shown to be as close as one might expect.1 Symptom occurrence reflects changes in oesophageal mucosal sensitivity which do not always vary as expected with increases in oesophageal acid exposure.2 The production of mucosal damage is influenced by the ability to clear or neutralise the refluxate (primary and secondary peristalsis, saliva and possibly oesophageal bicarbonate production). Another factor which has been studied in this latter regard has been the role of refluxed duodenal contents, in particular bile acids and trypsin. The impetus for study came from clinical observations of both symptoms and oesophagitis in patients with achlorhydria (for example, pernicious anaemia) and following total gastrectomy.3 Animal models using surgical diversion of bile or duodenal contents into the oesophagus have clearly shown their ability to cause oesophagitis. During oesophageal perfusion …