EDITORIAL Atrophic Gastritis in the Arctic lmost 150 years after their first recorded use by Samuel Fenwick,1 the terms gastric atrophy and atrophic gastritis remain incompletely defined. Is metaplasia (intestinal, pyloric, or pseudopyloric) an essential part of gastric atrophy? Is gastric atrophy synonymous with atrophic gastritis? If not, what percentage of the gastric mucosa must be atrophic before it becomes atrophic gastritis? Do we need histologic confirmation, or is an endoscopic appearance sufficient to declare a stomach atrophic? Recently as a consensus on the morphology of atrophy has been reached, a number of histopathologic guidelines have made their way into the collective conscience of gastrointestinal clinicians and pathologists.2–4 In an article published in the current issue of Clinical Gastroenterology and Hepatology that might prompt a reconsideration of the established dynamics of atrophic gastritis, Song et al5 from the Karolinska Institut in Stockholm have not addressed the morphology of atrophy and have built their study on a purely functional definition. The authors evaluated the prevalence of low pepsinogen I (PG I) serologic levels, which they equate to atrophic corpus gastritis, in a well-characterized population from Norrebotten and Västerbotten, 2 large and sparsely inhabited provinces of arctic Sweden that include all of Swedish Lapland. In contrast to a reduction in the prevalence of atrophic gastritis in subjects aged 55 to 64 years, those between the ages of 35 and 44 years showed an unexpected substantial secular trend during the past 2 decades, which increased their prevalence from 22 to 64 per 1000. The significance of this increase in the prevalence of PG I-defined atrophic gastritis in a narrow age band of this population is difficult to fully appreciate without knowing some details of the pathology and physiology of these atrophic stomachs. Nevertheless, the surprising surge in atrophic gastritis in a segment of the population in which a decline would be expected is a departure from the conventional paradigm that deserves our full attention. Low serum PG I levels are the functional counterpart of parietal cell impairment. This may be due to diminishing function (that is, the cells are still there, but their ability to secrete pepsinogen is impaired) or to a reduced oxyntic cell mass. Several studies have established a reasonable correlation between PG I level