The bacterium Helicobacter pylori was first described in 1983 and currently represents one of the most active research topics in medicine. Our knowledge of its mechanisms and how to treat it has come a long way. Yet, while it is entirely possibly to wipe out H. pylori with prescription drugs - the so-called triple therapy of antibiotic, antisecretory, and anti-inflammatory drugs - there are shortcomings with this regimen, to say the least.

Antibiotic Jeopardy: Not only can the overuse of antibiotics result in increased vulnerability to systemic yeast infections, but each successive use increases the likelihood that other, antibiotic-resistant bacteria will colonize the body. This is indeed what has happened with H. pylori. A recent study conducted in Italy with 210 H. pylori-positive dyspeptic patients found that there was widespread resistance to one or more antibiotics - including metronidazole, tetracycline, and amoxycillin - and that the eradication of the bacteria was significantly reduced.1

In another study, Chinese researchers at the Shanghai Second Medical University collected bacterial samples from the stomachs of 81 women and 72 men. The investigators found that 78% were resistant to metronidazole, 59% to tetracycline, and 72% to amoxycillin. Surprisingly, 39% of the H. pylori isolates were resistant to all three antibiotics tested.2 The researchers thought that the reason that so many multiresistant strains were identified may reflect extensive use of these three antibiotics in that area.

Antisecretory Complications: The antisecretory omeprazole may increase cancer risk when used to treat H. pylori-infected patients, according to a recent paper published in Gastroenterology.3 In this study, Dr. Craig Mowat and colleagues, from Western Infirmary in Glasgow, Scotland, analyzed various H. pylori samples from the gastrointestinal (GI) tracts of healthy volunteers before, during, and after omeprazole treatment.

During treatment, the stomach pH increased (acidity decreased) in both groups, but to a significantly greater degree in those with H. pylori infections than in those without. Apparently, the drug's mechanism of action can lead to profound, long-term suppression of acid production. The accompanying changes in the gastric environment subsequently render the GI tract at increased risk for mutagenesis and carcinogenesis. This is not a good tradeoff, to say the least.

Anti-inflammatory Morass: Anti-inflammatory drugs as a class, but especially nonsteroidal anti-inflammatory drugs (NSAIDs), are a major risk factor for the formation of ulcers. While the development of a new generation of NSAIDs has held out the promise of a marked reduction in gastrointestinal side effects, the fulfillment of this promise is still apparently a long way off.

In a study conducted in 1996, patients with upper-GI bleeding or dyspepsia and H. pylori-related ulcers were found to have their risk of bleeding associated with the use of NSAIDs.4 Other studies have shown that the eradication of H. pylori helps prevent the recurrence of bleeding duodenal ulcers,5 provided that those infected with the bacterium are not NSAID users.

Curiously, it has been reported that gastroesophageal reflux disease (GERD) symptoms are more prevalent in successfully treated H. pylori patients (those in whom the bacteria have been eradicated) than in unsuccessfully treated ones.6 This has led some researchers to conclude that eradication may be of marginal benefit. If this view is valid, however, it is valid only in terms of eradication efforts conducted with drugs, whose use often entails forcing square pegs into round holes. There are frequently unintended consequences that, in effect, replace one disease by another. This type of problem is far less likely to occur when nutritional supplements are used.

A recent Gallup survey found that in about 75% of individuals with GERD, the condition interferes with their sleep and sometimes wakes them up. Another four out of ten respondents said that sleep loss due to reflux symptoms made it difficult for them to function the next day. According to Dr. William Orr, a member of the board of directors of the National Sleep Foundation, as many as 100,000 traffic accidents and 1500 deaths each year in the United States are attributed to drowsy drivers who presumably slept poorly.

As mentioned earlier, ulcer drugs often create more problems, such as that of the antisecretories disrupting the acid balance in the GI tract, in a way that continues long after treatment. Therefore, an agent that did not affect pH, regardless of H. pylori status, would be highly beneficial in the treatment of GERD (as well as ulcers) and might also lower treatment costs. Is there such an agent?

Yes. The phytonutrient gum mastic eradicates H. pylori without affecting acid balance, increasing vulnerability to antibiotic-resistant bacteria, or increasing inflammation - and it does a lot more. See back issues of Life Enhancement or see our Web site at

Goodbye Pylori Mar. 1999
Discovering Antibacterial Mastic Apr. 1999
Explorer Columbus Apr. 1999
Publisher's Commentary May 1999
Mastic Toothpaste for the New Millennium Sept. 1999
Letters from Readers Oct. 1999
Mastic Plus Phytochemicals for Improved GI Health Nov. 1999
Biomedical Tidbits: Bye-Lori Applications Widen Dec. 1999
Antibacterial Bye-Lori Jan. 2000
Celebrating the Future Jan. 2000
The Human Stomach Feb. 2000
Bye-Lori to Your Stomach's Rescue Feb. 2000
Stomach Distress: What People Are Saying Mar. 2000
Reducing Oral Bacteria Benefits the Stomach Apr. 2000
Bye-Lori and MASTICdent Work Better Together May 2000
Bye-Lori as Preventive June 2000
H. Pylori Spreading Worldwide July 2000
Helps Stomach Distress and Lifts Mood Sept. 2000

Why hasn't the world at large known about mastic until now? According to materia medica historian John Riddle, Ph.D., professor of history at North Carolina State University and the author of a splendid book about the first-century Hellenic physician Dioscorides,

Mastic disappeared from medicine for many centuries because when universities were established, pharmacological knowledge was not included. Learned men of the time did not trust folk cures based on herbs.

The discovery that H. pylori causes most ulcers in the stomach and duodenum led to a search for new treatments, and in the Middle East, doctors who remembered the ancient remedy decided to test mastic scientifically. While there have been only a few double-blind studies, the results have been clear. And although the mechanisms are still not well understood, the results are clearer still when one hears the accolades of those who have effortlessly discovered the benefits of mastic for themselves.

Mastic offers relief even to the relatively poor. Throughout much of the world, ulcers are a major problem, yet even now, conventional triple therapy is very expensive, costing the equivalent of several months' income for many families in some Third World nations. Mastic, however, is considerably less expensive and is well within the reach of many more people.

Concerning the revival of mastic as a treatment - Life Enhancement was the first company to market it worldwide - Professor Riddle believes there is an important lesson to be learned. That lesson is the study of the past: "If today's pharmaceutical firms would read more of the ancient Greek, Roman, and Egyptian medical texts, they might not have to constantly reinvent the wheel,” he says. "We could have had mastic much sooner."*

*And perhaps more . . . see lead article with a Greek theme in this issue.


  1. Savarino V, Zentilin P, Pivari M, Bisso G, Mele MR, Bilardi C, Borro P, Dulbecco P, Tessieri L, Mansi C, Borgonovo G, De Salvo L, Vigneri S. The impact of antibiotic resistance on the efficacy of three 7-day regimens against Helicobacter pylori. Aliment Pharmacol Ther 2000 Jul;14(7):893-900.
  2. Wu H, Shi XD, Wang HT, Liu JX. Resistance of Helicobacter pylori to metronidazole, tetracycline and amoxycillin. J Antimicrob Chemother 2000;46:121-3.
  3. Mowat C, Williams C, Gillen D, Hossack M, Gilmour D, Carswell A, Wirz A, Preston T, McColl KE. Omeprazole, Helicobacter pylori status, and alterations in the intragastric milieu facilitating bacterial N-nitrosation. Gastroenterology 2000 Aug;119(2):339-47.
  4. Hsu PI, Lai KH, Tseng HH, Lin CK, Lo GH, Cheng JS, Chan HH, Chen GC, Jou HS, Peng NJ, Ger LP, Chen W, Hsu PN. Risk factors for presentation with bleeding in patients with Helicobacter pylori-related peptic ulcer diseases. J Clin Gastroenterol 2000 Jun;30(4):386-91.
  5. Vergara M, Casellas F, Saperas E, de Torres I, Lopez J, Borruel N, Armengol JR, Malagelada JR. Helicobacter pylori eradication prevents recurrence from peptic ulcer haemorrhage. Eur J Gastroenterol Hepatol 2000;12:733-7.
  6. Fallone CA, Barkun AN, Friedman G, Mayrand S, Loo V, Beech R, Best L, Joseph L. Is Helicobacter pylori eradication associated with gastroesophageal reflux disease? Am J Gastroenterol 2000 Apr;95(4):914-20.

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