Mastic May Help To . . .

Protect Your Stomach
from Deadly Bacteria

n astounding 10% of the U.S. population has experienced peptic ulcer in their lifetime, and 500,000-850,000 new cases are diagnosed each year.1 Approximately 80% of these ulcers are associated with infection by a particularly unpleasant bacterium, Helicobacter pylori. Yet the public seems largely unaware of this relationship, as revealed by a 1997 survey conducted by the Centers for Disease Control and Prevention in Atlanta. The CDC found that only 27% of respondents were aware that H. pylori may cause ulcers; by contrast, 60% thought that stress was the leading cause, and 17% thought that ulcers were caused by eating spicy foods.2

Since the association between ulcers and H. pylori infection has been well established, it will probably not surprise you to learn that eradicating H. pylori from your stomach is an effective treatment for ulcers and other diseases associated with the digestive system. While a number of pharmaceutical approaches are available for H. pylori treatment, they can be complex, unpleasant, and expensive. Thankfully, a gentler method for removing H. pylori and treating peptic ulcers is also available. This method relies on mastic gum, which is extracted from the mastic tree, Pistacia lentiscus.

The digestive system is a marvelous feat of biological engineering. It is composed of discrete chambers (the mouth, esophagus, stomach, small intestine, and large intestine) that perform very distinct functions. Not surprisingly, the design of these organs relates specifically to their function. Take the stomach, for instance. Its main function is to "liquefy" food. Just like your blender, the stomach is capable of turning solid food into mush (although it takes a bit longer). Unlike the blender, however, it relies on chemical means to break down food particles, using hydrochloric acid and digestive enzymes to reduce solid food to a thick slurry that can be passed to the intestine.

Because the stomach walls enclose such a corrosive environment, the stomach protects itself by secreting a virtually impenetrable mucous layer. Epithelial cells on the surface of the muscle layer of the stomach continuously secrete this thick mucus to shield themselves from the acid and enzymes. These chemical compounds slowly degrade the mucus, but not as quickly as the epithelial cells secrete new mucus.

Eradicating H. pylori
from your stomach is
an effective treatment
for ulcers and other
diseases associated
with the digestive

On occasion, however, the mucous layer is partially destroyed, exposing the sensitive epithelial cells to the stomach acid and digestive enzymes; this gives rise to a peptic ulcer. So that burning pain that you feel when you have an ulcer is the result of stomach acid literally eating away at the cells it comes in contact with. The same is true of heartburn (esophageal reflux). Normally, the acid is kept securely in the stomach by a circular muscle that, much like a drawstring, closes the stomach off from the esophagus. When this muscle fails to contract completely, however, some acid may escape into the esophagus (a process called reflux) and inflame it, causing the sensation we describe as heartburn - because it occurs near the heart.

Your stomach's pH (its acidity, expressed on a logarithmic scale) is about 1.5, which makes it about 10,000 times more acidic than your mouth (pH about 5.5-6.0). In addition, it's full of protein-degrading enzymes such as pepsin. Given this harsh environment, it is surprising that any bacteria can actually survive in your stomach. But some bacteria do survive occasionally, and that's when problems can arise. The most dangerous of these bacteria is Helicobacter pylori, which employs an inventive approach to outwit the stomach's high acidity. H. pylori secretes a protective substance, the highly basic compound ammonia, which counteracts the acid. Surrounded by its protective ammonia "bubble," the bacterium attaches itself to the mucous layer of the stomach, burrows through it, and then attaches itself to the underlying epithelial cells. In this chemically snug environment, the bacteria proliferate and can damage the surrounding cells.

H. pylori bacteria produce a number of potent toxins, and they encourage the host's immune system to attack the epithelial cells.3 Together, these actions often result in the death of surrounding cells and prevent the stomach from performing its normal functions. Equally unsettling is the fact that H. pylori infection may cause cellular proliferation and thus heighten the risk of developing gastric (stomach) cancer.

Although H. pylori infection is associated with an increased risk of gastric cancer, such as adenocarcinoma, it is important not to become overly alarmed - the great majority of patients with this common infection will not develop gastric cancer. However, particularly intense H. pylori infections (those with a high density of bacteria) can lead to chronic gastritis, an inflammation of the stomach lining that may be marked by nausea, vomiting, bloating, and acute pain. Such infections are most associated with the development of diffuse-type gastric cancer.4

The abdominal pain and discomfort caused by H. pylori are not the end of this story, however, but just the beginning. Gastritis may progress through a series of stages, including intestinal metaplasia (conversion of stomach tissue to intestine-like tissue), glandular atrophy (loss of glandular tissue whose function is to produce crucial stomach enzymes for digestion), dysplasia (a potential precursor to cancer), and finally, sometimes, to stomach cancer itself. Needless to say, eradicating this nasty bacterium from your stomach decreases the possibility that any of these diseases will develop.

There are a couple of ways to eradicate H. pylori from your gastrointestinal tract. Pharmaceutical approaches rely mainly on drugs called proton pump inhibitors (PPIs), such as omeprazole (Prilosec®),which reduce the acid level of the stomach and curtail the growth of H. pylori. These are often coprescribed with antibiotics such as amoxicillin, penicillin, and clarithromycin to deal a final knockout punch to the bacteria. A recent clinical investigation suggests that this approach is an effective means for decreasing the development of precancerous growths.5

Researchers in Tokyo eradicated H. pylori in 115 patients using PPIs and antibiotics for one week, and assessed the development of glandular atrophy and intestinal metaplasia 12-15 months later. Of the patients who had glandular atrophy at the beginning of the study, 89% showed improvement at the study's end, and of those who had intestinal metaplasia, 61% showed improvement. These improvements were brought about by a successful eradication of H. pylori. By comparison, those patients in whom the bacteria were not successfully eradicated showed no significant improvement in either condition.5 The authors concluded that eradication of H. pylori from the stomach encourages the formation of a more normal mucosal lining and may help to protect against stomach cancer.

The authors concluded that eradication
of H. pylori from the stomach
encourages the formation of a more
normal mucosal lining and may help to
protect against stomach cancer.

Supporting evidence for this view comes from a study in Germany. Researchers in the Department of Medicine of Erlangen-Nuremberg University report that two proteins thought to promote tumor growth occur with higher frequency in individuals infected with H. pylori. In patients in whom the bacteria were eradicated, the amount of these proteins was significantly reduced, suggesting that the risk of stomach cancer decreases in these individuals as well.6

In some studies, acid suppression via the proton pump inhibitor omeprazole appears to increase the risk of atrophic gastritis in certain regions of the stomach.7 In addition, an increased risk of gastritis may lead to an increase in the risk of cancerous events in the stomach.8 Thus, although the profound acid suppression that results from the use of PPIs may rid the stomach of harmful H. pylori, it may increase the risk of other diseases, such as gastritis and stomach cancer.

These results suggest that the eradication of H. pylori by some other mechanism may be preferable to the PPI/antibiotic treatment. Fortunately, less invasive alternatives are available.

Nature has a way of curing most of our ills. Thus, it is not surprising that a natural remedy has been passed down through the centuries to address stomach problems that stem from H. pylori infection. One of these natural substances is mastic gum, which comes from the stem and leaves of an evergreen tree (Pistacia lentiscus) that grows in the Mediterranean region. This gummy resin is a potent antibacterial and has been shown not only to kill H. pylori but also to inhibit the growth of other bacteria, such as Staphylococcus aureus, Escherichia coli, and Sarcina lutea.9 The specific ingredient in mastic gum that wreaks havoc on these bacteria has not yet been identified, but it is known that small amounts (about 1 gram) of mastic are sufficient, when taken on a daily basis for two weeks, to treat peptic ulcers effectively.10

Thyme and cinnamon have been found to inhibit H. pylori growth as well,11. Finally, another antibacterial agent that kills many gram-positive bacteria that lurk in the gut is added for good measure. This compound, hyperforin, is purified from St. John's wort; it inhibits the growth of stubborn bacteria that are resistant to heavily used antibiotics such as penicillin.12

It is known that small
amounts (about 1
gram) of mastic are
taken on a daily basis
for two weeks, to
treat peptic ulcers

As you can see, a colony of H. pylori is not something that you want hanging out in your stomach. In addition to the discomfort of gastritis and ulcers, this bacterial infection can lead to even more sinister complications, such as gastric cancer. Do yourself a favor and eradicate H. pylori from your digestive system. Your stomach will thank you for it.


  1. ASHP Commission on Therapeutics. ASHP therapeutic position statement on the identification and treatment of Helicobacter pylori-associated peptic ulcer disease in adults. Am J Health Syst Pharm 2001;58:331-7.
  2. Centers for Disease Control and Prevention. Knowledge about causes of peptic ulcer disease in the United States: March-April 1997. MMWR 1997;46:985-7.
  3. Xia HH, Talley NJ. Apoptosis in gastric epithelium induced by Helicobacter pylori infection: implications in gastric carcinogenesis. Gastroenterol 2001;96:16-26.
  4. Fukuda S, Tanaka M, Soma Y, et al. Histological analysis of gastritis and Helicobacter pylori infection in patients with early gastric cancer: a case-control study. J Gastroenterol Hepatol 2000;15:1370-6.
  5. Okhusa T, Fujiki K, Takashimizu I, et al. Improvement in atrophic gastritis and intestinal metaplasia in patients in whom Helicobacter pylori was eradicated. Ann Int Med 2001;134:380-6.
  6. Konturek PC, Hatwich A, Zuchowicz M. Helicobacter pylori, gastrin and cyclooxygenases in gastric cancer. J Physiol Pharmacol 2000;51:737-49.
  7. Kuipers EJ, Lundell L, Klinkenberg-Knol EC, et al. Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N Eng J Med 1996;334:1018-22.
  8. Stolte M, Meining A, Schmitz JM, Alexandridis T, Seifert E. Changes in Helicobacter pylori-induced gastritis in the antrum and corpus during 12 months of treatment with omeprazole and lansoprazole in patients with gastro-oesophageal reflux disease. Aliment Pharmacol Ther 1998;12:247-53.
  9. Iauk L, Ragusa S, Rapisarda A, Franco S, Nicolosi VM. In vitro antimicrobial activity of Pistacia lentiscus L. extracts: preliminary report. J Chemother 1996;8:207-9.
  10. Huwez FA, Thirlwell D, Cockayne A, Ala'Aldeen DAA. Mastic gum kills Helicobacter pylori. New Eng J Med 1998;339:1946.
  11. Tabak M, Armon R, Potasman I, Neeman I. In vitro inhibition of Helicobacter pylori by extracts of thyme. J Appl Bacteriol 1996;80:667-72.
  12. Schempp CM, Pelz K, Wittmer A, Schöpf E, Simon JC. Antibacterial activity of hyperforin from St. John's wort, against multiresistant Staphylococcus aureus and gram-negative bacteria. Lancet 1999;353:2129.

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