Helicobacter (formerly known as Campylobacter) pylori, a recently discovered gastrointestinal bacterial pathogen, has been shown to be etiologic for Type B or antral gastritis, and usually has chronic active pathological changes associated with its presence. Acute Helicobacter infection in most cases induces reduced stomach acid secretion which usually returns to normal levels of secretion after a few months. Yet Helicobacter gastritis has never been known to spontaneously remit after it has been established, and there is evidence suggesting that it often progresses to cause atrophic changes in the gastric mucosa. Since chronic gastritis has been shown in past studies to lead to chronic persistent hypochlorhydria from atrophic damage to secretory tissue, and Helicobacter has been shown to cause most chronic gastritis, the reasonable conclusion is that Helicobacter infection is etiologic for most chronic persistent hypochlorhydria. The apparent exception of the hyperchlorhydria in duodenal ulcer disease associated with Helicobacter infection is explained. The possible clinical relevance of hypochlorhydria will be the subject of a subsequent paper.