“…In our experience, an increasing prevalence of atrophic, metaplastic and even dysplastic changes was observed in patients with gastric ulcer, accompanied, from the pathophysiolog ical point of view, by a progressive reduction in acid-secretory capacity and pepsinogen re lease [9], But these patients were not 'normal subjects' and our findings could actually be restricted to the specific subset of gastric ulcer patients. Similarly, a number of trials have Age-group 3 been carried out on duodenal ulcer carriers: gastric acid output was found to be high and apparently unaffected by the patient's age [ 11,16] and parietal cell mass was consistently high even in elderly subjects [ 14], This kind of study has several major drawbacks: (1) to our knowledge, there are no studies considering the gastric pathophysiology of a sufficient number of patients observed at different times of their life; (2) most investigations have been carried out, as already mentioned, on patients with peptic ulcer disease; (3) large numbers of studies were performed in north ern countries, where chronic atrophic gastritis (particularly the fundic type) is quite frequent [17][18][19], It is therefore easy to speculate that the results of these earlier studies are bur dened by a high incidence of atrophic changes and achlorhydria. Repeating the study of gas tric acid secretory capacity during aging raises a difficult problem, mostly for ethical reasons, but studies which have attempted to solve the problem of studying normal subjects are somewhat scanty, contradictory or dated.…”