Helicobacter pylori: The Bug That Beats the Acid Test

While most bacteria are doomed to extinction once they encounter the acidic environment of a normal
stomach, there is one, called Helicobacter pylori, that has found a way to live a long and happy life in the land of the low pH. Unfortunately, once established in the stomach, H. pylori becomes a serious threat to our health and longevity for a number of reasons:
*H. pylori is presently thought to be the leading cause of atrophic gastritis, accounting for 80 percent to 100 percent of cases.
*H. pylori also causes the vast majority of gastric (80 percent) and duodenal (95 percent) ulcers.
 *H. pylori has been linked to two forms of stomach cancer: adenocarcinoma and lymphoma. According to results of large epidemiologic studies from both Europe and the United States, H. pylori infection increases the risk of gastric carcinoma by 600 percent and is responsible for 50 percent of all cases of adenocarcinoma.
ponsible for 50 percent of all cases of adenocarcinoma.
*H. pyloriprotects itself from HCl in the stomach by a mechanism that mimics the way the stomach lining protects itself. The bacteria secrete an enzyme that results in the formation of ammonia and carbon dioxide, which in turn combine with water to produce ammonium bicarbonate. Bicarbonate molecules, of course, make excellent acid neutralizes. This means that H. pylori, bathing safely in its self-made neutralizing shield, is free to thrive and burrow its corkscrewlike body through the mucosal layer and into the gastric epithelium, where it is protected not just from stomach acid but from antibiotic drugs as well.
Exactly how H. pylori damages the stomach lining is still under investigation. Its damage can be diffuse (gastritis) or localized (ulcers). Depending on the location of the gastritis it causes, H. pylori infection can result in true hyperacidity (hyperchlorhydria) or a loss of stomach acid (hypochlorhydria or achlorhydria). When H. pylori infection is confined to the antrum of the stomach, the region where most of the gastrin-producing cells are located, it stimulates these G cells to work overtime making and secreting gastrin. The excess gastrin circulates in the blood, and when it reaches the parietal cells, located farther north in the body and fundus, it prods them to turn on the acid spigots full blast. All this extra acid, helped along by an H. pylori-mediated reduction in bicarbonate production in the duodenum, is the primary irritant (but not the cause) in duodenal ulcers. The acid degrades the gastric mucosal layer laid bare by H.
pylori. The resulting long-term irritation can lead to localized open sores called duodenal ulcers. Duodenal ulcers are one of the few GI disorders actually associated with excess stomach acid, or hyperacidity. (Notice we say “associated with” and not “caused by.” That’s because the causeof both the ulceration and the excess acidity is H. pylori itself.).
Do You Have “Bowel Breath”?

From time to time, I’m consulted at Tahoma Clinic by individuals who mention (usually reluctantly) that one of their symptoms is “very bad breath,” “incredibly bad breath,” or in one memorable instance, “bowel breath,” that won’t go away with brushing, flossing, or mouthwash. By now, chances are good that you’ve guessed where “bowel breath” comes from. That’s right: all those germs, uninhibited by stomach acid, making their happy home in the stomach and letting the world know by their odor!
Most of the time, H. pylori sets up shop in the centrally located body (corpus) of the stomach. When this happens, a whole different pattern of pathology emerges. The resulting inflammation—atrophic gastritis—inhibits normal acid secretion from the parietal cells located there. Localized irritation may develop into peptic ulcers, even as acid levels fall. Once an area is damaged by H. pylori, it doesn’t take much acid to make things worse. Prolonged atrophic gastritis and hypochlorhydria or achlorhydria can eventually develop into gastric cancer (see below). Thus, while acid suppression has long been a major treatment—sometimes the only treatment—for both duodenal and gastric ulcers, high acid levels are seen only with duodenal ulcers. Gastric ulcers occur despite low acid secretion. If this treatment doesn’t work very well, it’s not hard to see why.
Ulcers and Acid Suppression
This picture of peptic ulcers is actually a relatively recent discovery. Until the 1980s, conventional medicine considered ulcers to be a result of stress or other factors, which allowed “excess” stomach acid to cause the lesion. Although H. pylori was known to inhabit the stomach (called Campylobacter pylori at that time), few suspected that it had anything to do with ulcers.
In its time-(dis)honored fashion, though, the patent medicine industry took off after stomach acid as the “cause” of GI ulcers. Acid-suppressing drugs—from Tagamet to Prilosec—were initially developed to treat ulcers. Although they could often relieve some of the ulcer pain and discomfort and perhaps help slow their progression, the drugs could never “cure” ulcers, for the obvious reason that acid doesn’t cause them. People with ulcers who took these drugs needed to take them forever, because as soon as they stopped taking them, their ulcers would almost certainly flare up again. (Also in the 1980s, research in England demonstrated that an inexpensive licorice compound actually healed ulcers as well as Tagamet, and prevented ulcer recurrence even better … but it wasn’t patentable, so only people who visited natural food stores were ever informed about it.
The real breakthrough against ulcers came in the early 1980s when an Australian medical researcher, Barry Marshall, M.D., began presenting evidence that the actual cause of ulcers was H. 
pylori. With billions invested in acid-suppressing drugs, conventional medicine wanted nothing to do with Marshall’s discoveries, and for the better part of a decade, they ignored and ridiculed them. (Where have we heard that refrain before?) Eventually, though, the weight of the evidence became too much to ignore, and H. pylori infection was finally acknowledged as the primary cause of peptic ulcers.

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