pylori can easily penetrate the protective gastric mucosa, avoiding the acidic pH of the stomach and moving to a less acidic environment where it produces a significant amount of urease, an enzyme that converts urea in the stomach into carbon dioxide and ammonia which is the basis for the C13/C14 urea breath test: ammonia is then converted into ammonium, which leads to the neutralization of gastric acid (Kusters, van Vliet, Kuipers 2006). the bacteria also induce an inflammatory response, which weakens the stomach lining and allows stomach acid damage, ulcer formation, and gastric cancer, so if left untreated, H. pylori infections have a 10% to 15% risk of developing in peptic ulcers and a lifetime risk of between 1% and 2% of developing gastric tumors (Kusters, van Vliet, Kuipers 2006) In developed countries, perhaps for the first time in human experience, a large number of people are going through their lives without colonization by H pylori. This is a crucial observation with considerable relevance to understanding the changing pattern of gastrointestinal diseases (Falush, et al.