Helicobacter Pylori and Mastic Gum’s
Non-pharmaceutical Antimicrobial Aspects To It
Alfred W. Garbutt, D.C.,DACBN, DACRB, DAAPM, DABDA, FAFICC, FACCRB, CCSP
In 1982 the Australian researchers, Robin Warren and Barry Marshall proved
that the bacillus, Helicobacter pylori was responsible for most gastroduodenal
ulcers. For this discovery they were awarded the 2005 Nobel Prize for Physiology
(1) The organism they isolated in the antrum / pylorus of the stomach is a
gram-negative rod shaped helical bacterium. Prior to this the bacillus was
unknown and it was commonly believed that stress, smoking and certain dietary
habits were the cause of most ulcers.
There is usually a 6.0-6.5 pH in the oral cavity and a 10,000 time more
acidic environment of 1.5-2.5 pH in the stomach. There are about 35 million
parietal cell glands throughout the stomach secreting about 2-3 quarts
of hydrochloric acid per day for the purpose of digesting food and minimizing
pathogen infiltration to the intestinal system. Despite this highly acidic
level in the stomach, H.pylori can survive when most other bacteria will
not. Now the stomach itself is protected from its own hydrochloric acid
and pepsin by the gastric epithelial cells secreting a thick mucus coating,
which endures the low pH. If this mucus coating is breached then the
acid and protein digesting pepsin will irritate the gastric lining and
some level of gastritis or ulceration will develop. H.pylori survives
this highly acid environment by using the urease enzyme to catalyze urea
to ammonia thus creating an ammonia envelope around itself. (2) Ammonia
is an acid neutralizing alkaline compound, which protects the bacterium
for the acid.
Next using the mucolytic enzymes, bacterial protease and lipase, the
H.pylori degrades the mucus lining which exposes the epithelia lining
to acid and digestive enzyme damage then it can burrow into the epithelium.
In addition to this the cytokine response to resultant inflammation can
further oxidative stress damage to the mucosal layer, which can lead
to ulceration. (3) Once to the epithelial lining it uses two unique proteins
on its surface to adhere to the lining cells. One of these is, BabA (blood
group antigen binding adhesion), which mediates the adherence of the
bacteria to human blood group antigens located on gastric epithelium.
(4) (5) These proteins can also inhibit the immune system response to
them, thus keeping them safe from attack.
There are also several mechanisms by which H.pylori affects gastric
can change gastric regulatory physiology by causing a rise in plasma
gastrin levels and by decreasing gastric mucosal release of somatostatin,
a peptide, which has the capacity to inhibit the release of insulin and
somatrophin from the anterior pituitary. There may also be a gastric
mucosal atrophy with parietal cell loss. It has been observed that when
there is an infection with atrophy and with a low acid secretion there
is a greater occurrence of gastric cancer of the intestinal-type and
that duodenal ulcers are associated with an infection that has little
atrophy and a high acid secretion. (6)
H. pylori have a cytotoxin-associated gene (cag A) that causes a secretion
from the H. pylori cytoplasm into the host’s gastric epithelial cells.
(7) There can be cagA – and + genes in H. pylori. Patients with the cagA+
gene strain of H. pylori were four times more likely to have pyloric
area intestinal ulcers along with chronic gastric inflammation, polymorphic
activities, degeneration of the surface epithelium and metaplasia of
the intestines. (8) There is also a gene called vascuolating cytotoxin
gene that is responsible for creating vacuole lesions in the tissues.
Research suggests that the adherence of H. pylori due to BabA permits
an efficient delivery of vacA and cagA to the gastric cells. The strains
that do this are more virulent and often associated with the cases of
distal gastric adenocarcinoma. (9)
10-40 % of the people in western countries experience upper abdominal
pain or discomfort over the year. (10) According to the ASHP Commission
on Therapeutics, there are between 500,000 and 850,000 new cases of peptic
ulcers diagnosed each year and that 10% of the American population have
had peptic ulcers during their lifetime. (11) There are over one million
annual hospitalizations secondary to an ulcer related event. (12) Of
these peptic ulcers, approximately 80% are secondary to H.pylori infection.
(13) The Centers for Disease Control and Prevention have estimated that
of all duodenal ulcers that 90% were linked to H. pylori infection. Even
though 50% of the world’s population is estimated to have an H.pylori
infection (14) only 10-20% of the carriers have or will develop gastric
diseases. These diseases can range from gastritis to ulcers to mucosa-associated
lymphoma or adenocarcinoma (15). There is a 4-to-6-fold risk increase
of developing stomach cancer with H. pylori infections. (16) Some key
factors, which increase virulence are, secretion of large quantities
of urease, amount of bacteria mobility, quality of adhesions to gastric
epithelium, presence of cagA and vacA. (16).
Gastritis is an inflammation of the stomach mucosal lining and depending
upon the amount of mucosal injury it is classified as erosive or nonerosive.
With acute gastritis the antrum and corpus of the stomach will show polymorphonuclear
cell infiltration. In chronic gastritis there is decreased mucosa functional
capacity associated with some degree of tissue atrophy or metaplasia.
The antrum region is usually the area of involvement and there becomes
a decrease of G cells and gastrin secretion. When the corpus is involved
there is a decrease of hydrochloric acid, pepsin and intrinsic factor
secondary to loss of oxyntic glands. (2) The decrease of intrinsic factor
will probably cause a vitamin B12 malabsorption problem along with other
nutritional deficiencies caused by less efficacious digestion. Health
care practitioners should bear this in mind when developing a clinical
nutrition program for a patient with gastritis. Even though some patients
may be asymptomatic, chronic gastritis may manifest as nausea, unexplained
vomiting, upper abdominal bloating and / or acute pain.
Meta-analysis (critical survey) has shown that indigestion or dyspepsia
is associated with H. pylori and that people with an infection are 60%
more likely to have non-ulcer related dyspepsia than people without an
H.pylori infection. (17)
Patients with gastro esophageal reflux disease (GERD) are more likely
to experience symptomatic relapse of GERD sooner if they have an H.pylori
infection than people that have had GERD but are not infected. (18)
Even though halitosis can stem from nasal passage or respiratory tract
infections, liver or kidney failure, uncontrolled diabetes and occasionally
acid reflux, the dental and medical experts feel that the majority
of the cases are from when certain oral bacteria break down amino acids,
such as, methionine, cysteine or lysine. Research performed in Turkey
in which patients with non-ulcer dyspepsia and were infected with H.
pylori were treated with the conventional “triple therapy” and 97.2%
of the subjects had their halitosis eradicated. (19) The “triple therapy”
is usually comprised of a seven day course of a stomach acid inhibiting
(omeprazole or lansoprazole) called a proton pump inhibitor and two different
antibiotics, usually clarithromycin and metronidazole or amoxicillin
or tetracycyline. (20) Why exactly this result occurred was not totally
clear but investigating the need for anti-H, pylori treatment may be
indicated in chronic halitosis.
There has been a case study that compared 111 coronary heart disease
(CHD) patients with 74 controls without CHD. Of the patients with CHD,
59% had evidence of H. pylori infection while the non-CHD controls had
a rate of 39% infection. (21) There have been additional studies demonstrating
a link with H.pylori and CHD. (22) (23) A study recently published in
The journal, Digestive disease and sciences reported “direct evidence
for an association between chronic H.pylori infection and insulin resistance.”
Research by Santamaria, et al. has shown an association with oral H.pylori
and the recurrent upper gastrointestinal bleeding and pain in children. (25)
Research in Japan showed that the “triple therapy” type regime was at least
91.6% effective when the bacteria were not measurably present in the mouth
and only about 52.1 % effective when oral H.pylori were detected. (26) German
researchers have shown that children can become infected with H.pylori if their
parents are infected. (27) The rate of infection for a child was approximately
3.9 times greater if the mother tested positive for H. pylori and 2.8 times
greater for a positive father as compared to children of non-infected parents.
(27) These odds ratios are important and a child of an infected parent should
also be evaluated. According to a study published in the Lancet, young children
(4-9 years of age) are at a greater risk of acquiring an H.pylori infection
than young adults (21-23 years of age). Once infected there is a tendency to
remain infected at a rate of 84%? (28) Even though these infections in children
may cause gastritis with these children they may persist into adulthood where
they contribute to lifelong diseases, such as, ulcers or stomach cancer.
H.pylori can be spread through oral infection. Activities, such as, sharing
drinking or eating utensils, kissing and the consumption of water, meat, sea
food or vegetables (Schorr M. H.pylori “ulcer bug” can be found in store-bought
food. Reuters Health, May 23, 2002.) that are contaminated with the bacterium
can infect a person. Of these, the person-to-person route is the most common.
Therefore, safe food preparation and good personal hygiene are an essential
defense mechanism to minimize acquiring H.pylori infection or further spreading
of it to others.
The CDC estimates that there are over 3 million Americans and 67 million people
world wide with glaucoma, which is the second leading cause of blindness. (CDC
Fact Sheet for Health Care Providers. Helicobacter pylori. July 1998.) Greek
physicians conducted a study that showed 88% of the glaucoma patients tested
had an H.pylori infection while the control group had a 47% infection rate,
which would be about the average for infection in the general population. (29)
This research further showed a statistical improvement in their glaucoma when
the positive subjects were treated for H.pylori.
Despite the “triple therapy” proving itself to be effective against
H. pylori, 42% of the patients have experienced side effects. (30) The
side effects make it difficult for some patients to comply while another
concern by the medical community is the issue of drug resistant strains
of H.pylori. (31) There has been research in Iran that also showed a
20% rate of resistance of Helicobacter pylori to the antibiotic tested.
A non-pharmaceutical alternative for killing H. pylori is substance
that has been used as an antimicrobial for thousands of years. This substance
is mastic gum.
(33) (34) Mastic gum is a natural whitish resin from the Pistacia lentiscus
tree, which is an evergreen shrub from the pistachio family. This tree
is only found on the Greek island of Chios or Hios in the Aegean Sea.
In addition to its medicinal uses it is used in the paint industry, cosmetics,
paint varnish, artist color oils, the food industry for flavoring liqueurs,
ice cream, chewing gum and in Greek and Arabic breads, cheeses, milk,
cookies and candies.
The famous Roman physician, Galen, Aristotle and the Turkish born Greek
surgeon and botanist, Dioscorides, who created the pharmacological treatise
De Materia Medica, all wrote of the medicinal uses of mastic gum. British
researchers in 1998 published an article about mastic gum’s 99.9% kill
rate of H.pylori in an overnight incubation. (35) As little as one gram
per day for two weeks has shown to relieve the symptoms of gastric ulcers.
A common therapeutic dose is one gram in the morning and one before sleep
for 2-4 weeks. A maintenance dose for dyspepsia is 500 mg. per day. In
addition to its ability to kill H.pylori mastic gum has shown that it
also has antimicrobial properties against Staphylococcus aureus, Escherichia
coli, Sarcina lutea, Candida albicans, Candida parapsilosis, Torullopsis
glabrata and Cryptococcus neoformans. (36) Chewing gum and toothpaste
with mastic gum can be used to assist with controlling oral H. pylori
in addition to the ingestion of capsules of it.
Even though a significant amount of research has been performed world
wide on H.pylori, the average doctor does not pay adequate attention
to this bacteria’s involvement in human dis-ease. One should consider
H.pylori as a potential stressor with any oral and / or gastrointestinal
complaint. Since mastic gum has no reported side effects, it should be
consider as an effective antimicrobial against it.
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