To Your Stomach's Rescue

ne might think that no living thing could survive the brutal chemical assault of the stomach's hydrochloric acid and digestive enzymes. Indeed, most microorganisms that find their way into our stomachs (via our food, usually) are quickly killed. Some, however, are tough enough to survive, and some even thrive there - a testament to the almost miraculous ability of carbon-based life forms to flourish even in extremely hostile environments.


H. pylori bacteria above.
Peptic ulcer within stomach.

Of these survival champions, most are innocuous, but some are harmful and can make us sick (as many a world traveler can attest after a bout of diarrhea). Among the most prevalent and hardy of these is a nasty little creature called Helicobacter pylori (usually called H. pylori for short). This is a bacterium, typically helical, that is believed to infect about 40% of the human stomachs in the world. H. pylori is generally believed to be acquired through contaminated food or water, but its primary mode of transmission is unresolved. It is also thought to be transmitted from person to person by kissing, where there is typically contact with the other person's saliva.

WHAT H. PYLORI ACTUALLY DOES TO US
The pylori part of the name is due to the tendency of the bacteria to be most active near the pylorus. They survive in the stomach's acid bath by exuding urease, an enzyme that produces ammonia, which neutralizes the acid. Surrounded by this protective chemical "halo" of ammonia, they corkscrew themselves through the gastric and duodenal mucus layer and attach themselves to the surface of the underlying epithelial cells. There, it is believed, they cause gastritis and contribute to ulcer formation by thinning the protective mucous layer and by poisoning nearby cells with ammonia and other toxins.3 Infection with H. pylori is associated with virtually all cases of nonerosive gastritis and all cases of peptic ulcer, and it is believed to be the primary cause of these diseases.1

THE BEST REMEDY IS ERADICATION
The most effective remedy is to eradicate the organism from the stomach and duodenum. This will cure H. pylori-caused gastritis and peptic ulcers and prevent their recurrence. Furthermore, it will probably reduce the risk of stomach cancer, with which H. pylori is also strongly associated: persons infected with this organism are three to six times more likely to get stomach cancer than those who are not.1,3

The first evidence that H. pylori causes ulcers came to light only in 1982. The credit for this research belongs to Australian scientists Barry J. Marshall and J. R. Warner, who noted that nearly 100% of ulcer patients were infected with the bacterium. Their contention that H. pylori caused the ulcer was initially greeted with disbelief and derision, but by the mid-1990s, the evidence had become so compelling that it was widely accepted as fact.

Other factors that are often present with peptic ulcers are the use of aspirin or other NSAIDs, smoking, overconsumption of alcohol, and emotional stress, but it is not clear whether these can actually cause ulcers or whether they merely exacerbate them. Antacids are routinely used to alleviate the symptoms of ulcers, because anything that increases the stomach's acidity tends to aggravate them.

THE OLD REMEDIES NEVER DID WORK
Countless remedies for ulcers have been tried over the centuries, most of them worthless at best, and some of them downright harmful - including that old wives' tale about drinking milk. Not only does milk not promote ulcer healing, it actually promotes gastric acid secretion, thus making things worse, not better, after the brief soothing effect of the milk wears off. There is simply no evidence that changing a diet speeds ulcer healing or prevents recurrence, although it is generally recommended that one avoid foods that may cause stomach distress, such as fruit juices, highly spicy or fatty foods, and anything containing caffeine. Alcohol consumption should be limited to small amounts, and one should not smoke. Smoking is so harmful to the body in so many ways that it negates most health benefits acquired through beneficial lifestyle choices.

Some ulcer remedies of the past were downright bizarre, such as one, highly touted in the 1960s, in which an ice bag was passed into the patient's stomach to "freeze" (actually just chill) the ulcers temporarily. (Then what?) This "breakthrough" therapy was abandoned after only a few months, when people began to realize that it made no sense and didn't work.

MODERN MEDICINE MISSES THE POINT
Knowing what we do now about the pivotal role of H. pylori in peptic ulcers, the therapeutic focus has shifted to remedies that can eradicate it, because that, and that alone, solves the problem once and for all (except in rare cases of accidental reinfection). Modern medicine provides an impressive array of antibiotics and other drugs that, in combination, can kill H. pylori. The downside, however, is that: (1) they're expensive; (2) they cause side effects such as nausea, vomiting, diarrhea, and allergic reactions; and (3) they're primarily antibiotics - a class of drugs that is so consistently overused that they're becoming ever less effective, as microorganisms mutate into new, ever more resistant strains.

Each of the six different 14-day antiulcer regimens of today's mainstream medicine (per guidelines of the American College of Gastroenterology) is a triple-therapy regimen: it includes two antibiotics combined with one drug from either of two other classes of drugs - one designed to inhibit acid secretion and one designed to protect the mucous layer from chemical attack.4 These regimens must gladden the heart of the pharmaceutical industry, but not of Mother Nature, who prefers natural remedies without side effects. She has generously bestowed one such upon us.

MASTIC ERADICATES H. PYLORI
A natural remedy that has been in use for many centuries and for which modern science has provided solid evidence of efficacy and safety is mastic, the gum resin of the mastic tree, Pistacia lentiscus L. This evergreen tree grows primarily on Chios, a Greek island in the Aegean Sea that was noted in antiquity for its school of epic poetry.

Since ancient times, mastic gum has been used in Mediterranean cultures as an antiseptic, a food antioxidant, a chewing gum and breath sweetener, a flavoring additive in a variety of traditional foods and drinks, and a remedy for stomach pain, indigestion, and peptic ulcer.5 There is an extensive literature, going back many centuries, regarding its use for a variety of gastrointestinal ailments, including cancer.6 In recent years, laboratory experiments and clinical trials have shown conclusively that mastic kills H. pylori,5,7,8 as well as a variety of other harmful bacteria and fungi9,10 and may therefore be effective in helping to combat stomach distress, including gastritis and peptic ulcers.

TO THE RESCUE
Mastic is a safe, effective, natural agent with no side effects. Three more natural ingredients have also been shown in scientific studies to have antibacterial properties in the gastrointestinal tract. One is hyperforin, a compound extracted from the herb St. John's wort, which is widely used as an antidepressant.11,12 Even in low concentrations in laboratory studies, hyperforin is effective against a wide range of bacteria. The other two are cinnamon and thyme, both of which have a demonstrated ability to inhibit the growth of H. pylori.13 They are also effective against certain fungi.

It has been estimated that half the population of the United States has digestive complaints and that these account for about 20% of all illnesses. Furthermore, digestive ailments lead all other diseases as a cause of time lost from work and money spent for hospitalization, and tumors of the digestive organs account for one-third of all deaths from cancer.14 Considering that H. pylori is strongly implicated in several of these diseases, the modern rediscovery of a safe, effective, natural agent, mastic, for helping to eradicate this dreadful bacterium from our stomachs is a blessed alternative indeed.

References

  1. The Merck Manual of Diagnosis and Therapy, 17th ed. Merck Research Laboratories, Whitehouse Station, NJ, 1999, pp. 245-56.
  2. National Institutes of Health Consensus Statement, "Helicobacter pylori in Peptic Ulcer Disease," Feb 1994, Vol 12, No. 1.
  3. Komaroff AL, ed. Harvard Medical School Family Health Guide. Simon & Schuster, New York, 1999, pp. 754-7.
  4. Graber MA, Nugent A. Peptic ulcer disease: presentation, treatment, and prevention. Emerg Med 1999;31(11):66-78.
  5. Al-Said MS, Ageel AM, Parmar NS, Tariq M. Evaluation of mastic, a crude drug obtained from Pistacia lentiscus for gastric and duodenal anti-ulcer activity. J Ethnopharmacol 1986;15:271-8.
  6. Hartwell. Plants used against cancer. Lloydia 1967;30(4):379-436.
  7. Huwez FU, Al-Habbal MJ. Mastic in treatment of benign gastric ulcers. Gastroenterol Japon 1986;21(3):273-4.
  8. Huwez FU, Thirlwell D, Cockayne A, Ala'Aldeen DAA. Mastic gum kills Helicobacter pylori. NEJM 1998;339(26):1946.
  9. Tassou CC, Nychas GJE. Antimicrobial activity of the essential oil of mastic gum (Pistacia lentiscus var. chia) on Gram-positive and Gram-negative bacteria in broth and in model food system. Int Biodeterior Biodegrad 1995;411-20.
  10. 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(3):207-9.
  11. Gurevich AI, Dobrynin VN, Kolosov MN, Popravko SA, Riabova ID. Antibiotic hyperforin from Hypericum perforatum L. Antibiotiki 1971 Jun;16(6):510-3.
  12. Schempp CM, Pelz K, Wittmer A, Schopf E, Simon JC. Antibacterial activity of hyperforin from St. John's wort, against multiresistant Staphylococcus aureus and Gram-positive bacteria. Lancet 1999 Jun 19;353(9170):2129.
  13. Tabak M, Armon R, Potasman I, Neeman I. In vitro inhibition of Helicobacter pylori by extracts of thyme. J Appl Bacteriol 1996 Jun;80(6):667-72.
  14. Kraft SC. Digestion. Chapter 6 of The Trans\vision Book of Health. Encyclopedia Britannica, Inc., Chicago, 1974, pp. 73-93.

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