A Natural Approach to a
Healthy Digestive Tract -- New Research on H.
Pylori
by Jim English and
Ward Dean, MD -- reprinted by permission from Vitamin Research
Helicobacter pylori (H.
pylori) is a tiny bacterium that was completely unheard of twenty years
ago. Today, H. pylori is known to afflict almost two-thirds of all
humans and is recognized as the most prevalent form of bacterial infection in
the world.(1) Residing in the stomach and duodenum of infected
individuals, H. pylori is a spiral-shaped bacterium that has been strongly
implicated in the development of gastrointestinal inflammation (gastritis) and
gastric and duodenal ulcers. Now, new research strongly implicates H.
pylori as the primary agent for development of gastric (stomach) cancer.
Mastic gum is a natural substance from the sap of the Mediterranean evergreen
tree, Pistacia lentiscus. Mastic gum has been shown to be effective in
helping the digestive system and supporting health issues associated with H.
pylori. Although it has not been clinically tested for this purpose,
mastic gum may be a possible agent to effectively protect the stomach.
A Brand New Bug
Gastric (stomach) and duodenal problems were once thought to be caused by
spicy foods, stomach acid, and stress. This view was radically altered
in 1982, when researchers in Australia discovered a new form of gram-negative
bacteria in the stomachs of patients.(2) Dr. Robin Warren, a pathologist
at the Royal Perth Hospital in Western Australia, first reported the unique
spiral-shaped bacterium in biopsy specimens from patients with
gastritis. Later, Warren and fellow Perth researcher Barry Marshall
reported the presence of the new bacterium in virtually every biopsy specimen
of 100 patients with duodenal ulcers.
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)
Widespread Infection
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.
Stomach Cancer
Gastric cancer is the second most common cancer worldwide. In certain
countries, such as Colombia and China, where H. pylori infects over half the
population in early childhood, gastric cancer is the most prevalent form of
cancer.(8) According to the National Institutes of Health (NIH) about
24,000 people in the United States are diagnosed with stomach cancer 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 cancer, 4) pancreatic cancer, 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 cancer.
Japanese Study
H. pylori infection rates are much higher in Japan than in the US. Each
year gastric cancer 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 cancer, 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 cancer. Gastric cancer 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 cancer. 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 cancer 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 bolsters evidence of the association between
H. pylori and gastric cancer, and suggest that in the future, physicians may
need to view H. pylori ... as something akin to tobacco.(12)
Gum Mastic
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 support 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 antisecretory 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 that,
"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 that mastic gum was
supportive in 99.9 percent of H. pylori when tested against seven different
strains—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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