Although few would challenge the role of Helicobacter pylori as a major gastroduodenal pathogen, many paradoxes remain. Infection is mainly acquired in childhood, yet the major symptomatic diseases, peptic ulcer and gastric cancer, occur predominantly in adults or the elderly. Patterns of disease vary within and between different populations. In some countries, the incidence of duodenal ulcer is high whereas in others the progression of H pylori associated pathology is more towards gastric ulcer and adenocarcinoma. These patterns of disease are changing in certain countries and this seems to correlate with improvements in socioeconomic status. Thus in the United Kingdom and the United States, peptic ulcer and gastric cancer were rare before the 19th century.1 ,2 From the middle 1800s, gastric ulcer and cancer increased and by the early 1900s duodenal ulcers appeared and slowly started to surpass gastric ulcers in frequency. In more recent times, there has been a decline in the frequency of carcinoma, and both types of ulcer while reflux oesophagitis seems to be on the increase. In the less developed world, in countries such as Colombia and China, these changes have been delayed and gastric cancer remains a frequent cause of death.

Given that H pylori is an aetiological factor in both ulcer disease and gastric malignancy, how can these temporal and geographical trends be reconciled? One of us had postulated differences in acid output as the explanation.3 Higher acid restricts growth of H pylori and inflammation to the antrum while lower acid allows the bacterium to thrive in the body, inducing a pangastritis. We predicted that the mean local acid output in those populations with the gastric ulcer/gastric cancer profile would be less than in populations …