Predictably, traditional gastroenterologists initially rejected these new findings. In response to his critics, Warren swallowed a liquid culture of the bacteria, hoping to prove that H. pylori was the cause of peptic ulcers. Within weeks, he was diagnosed with a full-blown case of self-induced gastritis, proving his hypothesis was correct. In October, 1989, the new bacterium (previously called Campylobacter pylori) was officially recognized as a new genus and, due to its ability to occasionally take on the shape of a helix, given the new name Helicobacter.
Mechanism of Action
Prior to the discovery of H. pylori, the stomach was thought to be a sterile environment. Indeed, a constant flood of digestive enzymes and concentrated hydrochloric acid makes the gut an extremely hostile environment for most pathogens. But research has revealed that H. pylori is uniquely adapted to take advantage of the hellish digestive brew. First, H. pylori uses its spiral shape and several whip-like tails (flagellae) to drill into the gastric mucosa -- the mucus lining that protects the stomach and keeps it from being dissolved by its own gastric juices. Simultaneously, H. pylori produces a potent enzyme on its outer surface called urease. Urease protects H. pylori from being destroyed by gastric juices. Urease also disrupts the gastric mucus lining, making it easier for the bacteria to penetrate the layer and attach to the stomach and duodenum. Urease also protects H. pylori by converting urea (which is abundant in saliva and gastric juices) into a pair of strong bases -- ammonia and bicarbonate. These, in turn, neutralize gastric acids in effect, creating a protective antacid barrier around H. pylori.
H. pylori also defends itself from another threat -- the human immune system. The immune inflammatory response involves the production of vast numbers of neutrophils that are mobilized to destroy invading pathogens. Safely ensconced behind its mucus and antacid barriers, H. pylori is protected from attack by the immune system which cannot penetrate the mucus lining. Additionally, H. pylori produces another enzyme called catalase that further protects the bacteria from neutrophils. The result is that instead of repelling H. pylori, the immune inflammatory response causes severe damage to the stomach lining, thus contributing to gastritis and ulcer formation.(3)
While it is known that humans serve as the natural host of H. pylori, the exact mechanism of transmission is still unclear. Most researchers believe that infection occurs via oral-oral (kissing) or fecal-oral (food or water contamination) transmission.(4) In the United States only 20 percent of the population under 40 years of age is infected. But since infection continues to spread with time, the rate grows with each passing year until 50 percent of all US citizens over the age of 60 are infected. The infection problem is even greater outside of the US, with infection beginning early in childhood, leading to adult rates of infection approaching 90 percent in some parts of Asia and Africa.(5)
While many infected people may never show any symptoms, H. pylori is strongly associated with a number of gastrointestinal diseases, including chronic active, chronic persistent, and atrophic gastritis. Additionally, H. pylori infection is established to be a major cause of gastric ulcers, 6) and up to 80% of all duodenal ulcers are blamed on H. pylori infection.(7) Since the immune system is helpless to control H. pylori, unless eradicated by other means, infection generally lasts a lifetime.
Gastric canc is the second most common canc worldwide. In certain countries, such as Colombia and China, where H. pylori infects over half the population in early childhood, gastric canc is the most prevalent form of canc.(8) According to the National Institutes of Health (NIH) about 24,000 people in the United States are diagnosed with stomach canc each year.(9) Of these, about 14,000 will die from the disease.
Data gathered from population studies had previously found an association between H. pylori infection and later development of a number of diseases, including 1) gastric mucosa-associated lymphoid tissue (MALT), 2) MALT lymphoma, 3) gastric canc, 4) pancreatic canc, 5) ischemic heart disease, 6) ischemic cerebrovascular disease, 7) atherosclerosis, 8) periodontal disease, and 9) skin diseases such as rosacea.(10)
Now, research published in the September 13, 2001 issue of the New England Journal of Medicine confirms the hypothesis that H. pylori is the primary agent for the development of stomach canc.
H. pylori infection rates are much higher in Japan than in the US. Each year gastric canc develops in 300,000 (0.5 percent) of the estimated 60 million infected with H. pylori. To study the link between H. pylori and stomach canc, Japanese researchers enrolled 1,526 patients who suffered from ulcers, gastric hyperplasia, or non-ulcer dyspepsia (ulcer-like pain, but no ulcer). The study included 869 men and 657 women with an average age of 52 years. Patients underwent endoscopic biopsy at the time of enrollment, and at three years to assess H. pylori infection. They were monitored for an average of 7.8 years. Of the 1526 enrolled patients, a total of 1,246 (82%) were found to be infected with H. pylori.(11)
Over the course of the study 36 patients (2.9 percent) from the infected group developed stomach canc. Gastric canc did not develop in any of the uninfected patients. The researchers report that certain forms of gastric disturbance were associated with a higher risk of gastric canc. Those patients most at risk were those with severe gastric atrophy (shrinkage and weakening of the stomach), gastritis (stomach inflammation), and abnormal intestinal tissue changes.
The researchers concluded that gastric canc develops in persons infected with H. pylori, but not in uninfected persons. An accompanying editorial published in the September 13, 2001 New England Journal of Medicine stated that the findings substantially bolster evidence of the association between H. pylori and gastric canc. Concurrently, physicians may need to view H. pylori as something akin to tobacco.(12)
For centuries, mastic gum has been used by traditional healers to support stomach health. Modern research supports the use of mastic to aid proper gastrointestinal and digestive function. In addition, research has shown that mastic gum may help with issues associated with benign gastric ulcers (14) and duodenal ulcers. In one double-blind clinical trial, researchers found that oral doses of one gram per day of mastic over a period of two weeks helped with pain in 80 percent of patients with duodenal ulcers. The study also found endoscopic evidence that mastic assisted the healing of gastric mucosal tissues. Animal studies have found that mastic possesses cytoprotective (cell protective) and anti-secretion properties and that it can reduce gastric mucosal damage.(16)
Mastic and H. pylori
Researchers writing in the December 24, 1998 issue of the New England Journal of Medicine reported that mastic has strong implications associated with the treatment of H. pylori. In the report the authors stated, "Even low doses of mastic gum -- one gram per day for two weeks may be helpful."(17)
The researchers conducted in vitro tests that revealed mastic gum was helpful in 99.9 percent of H. pylori when tested against seven different strains of NCTC 11637 (a standard reference strain) and six clinical isolates, including three others. Of note was the finding that mastic was equally supportive even at very low concentrations. These results suggest that mastic has definite activity when involved with H. pylori.
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