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Chapter 27 : Coevolution of Helicobacter pylori and Humans
By the early 1990s, it was becoming clear that carriage of H. pylori increased risk for peptic ulcer disease and for gastric cancer, where both are consequences of the Helicobacter pylori induced gastric inflammation, although in separate ways. In recent years, using more sophisticated analytical techniques, there has come greater support for the notion that H. pylori has colonized humans since before the out-of-Africa migrations of about 58,000 years ago, and that as humans migrated to all parts of the world, they brought their H. pylori strains with them. It has been hypothesized that for H. pylori and humans, there are actually a series of equilibria, nested in one another, that create the governing boundaries at each level. Postulated benefits for humans for early-life carriage of H. pylori include resistance to colonization by exogenous pathogens (through manipulation of gastric pH and gastric immunity, as well as direct competition), as well as close regulation of metabolism, through gastric leptin (5 to 10% of body total) and ghrelin (60 to 80% of body total). In summary, H. pylori has evolved over a long period of time as a highly interactive member of the human gastrointestinal microbiota. There is extensive evidence that H. pylori coevolved with its human hosts, enabling its nearly universal gastric persistence. The interaction had little or no cost (and possible some benefit) to its early-in-life hosts, but also conferred certain late-in-life disease costs, including gastric cancer.