Traditional stomach remedy attacks not just H. pylori but also the harmful S. mutans found in the mouth
By Richard P. Huemer, M.D.
In the beginning was the wad, and word was that the wad was mighty good. Wads of well-chewed resin have been dug up from early human dwelling sites in various parts of the world. It seems that people have found pleasure in chewing spruce sap, beeswax, chicle, or whatever for a great many millennia, and nothing is likely to change that.*
*Except, perhaps, in Singapore, where the importation and sale of chewing gum was banned in 1992 because of a litter problem on the otherwise squeaky clean streets. Cleanliness may be next to godliness, but fanaticism of this kind seems headed in the other direction.
The ancient Greeks enjoyed chewing the aromatic resin that exuded from the trunk of a certain tree indigenous to the Mediterranean region. Their name for the resin was mastikhe, which, like our word “masticate,” came from their word for “to chew.” Nowadays it’s usually called mastic gum. Greek women prized mastic gum for cleaning their teeth and sweetening their breath.
Mastic Targets Helicobacter pylori
According to traditional Mediterranean folk medicine, the shrublike mastic tree (Pistacia lentiscus) is good for healing a variety of stomach ailments. The principal source of this therapeutic power is the gum resin, which consists of a number of organic compounds called triterpenes, especially mastic acid and isomastic acid. A variety of volatile oils, collectively called mastic oil, can be extracted from the resin.
Many of the individual components of mastic gum show antimicrobial activity against a range of bacteria, and most likely they act synergistically.1 One susceptible germ of particular importance is a bacterium called Helicobacter pylori, which is largely responsible for gastritis and peptic ulcers. (See the sidebar on “The Last Laugh.”) Presumably mastic gum’s anti-pylori action explains its good track record against ulcers.2
The Last Laugh is Spelled N-O-B-E-L
Back in 1979, Australian pathologist J. Robin Warren noticed a hitherto unknown species of small, curved bacterium, associated with inflammation, when he performed stomach biopsies. He began to investigate. Soon Barry J. Marshall, a clinician, joined in the studies, and he succeeded in culturing the germ.
Five years later, Drs. Marshall and Warren told the world about the odd bacteria they had found in the stomachs of nearly everyone who had gastritis or peptic ulcers (ulcers of the stomach or duodenum), stating that the bacteria “may be an important factor in the etiology [cause] of these diseases.”1 But no one believed them. Everyone “knew” that stress and a bad lifestyle caused ulcers. Everyone “knew” that ulcers were a long-term illness that in extreme cases could be managed only with surgery. Marshall and Warren were widely ridiculed for their heretical theory.
Fast-forward to October 3, 2005. Scene: the renowned Karolinska Institute in Sweden. The Nobel Assembly meets and decides to award the 2005 Nobel Prize in Physiology or Medicine to Marshall and Warren “for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease.”2
It is now well known that H. pylori causes up to 80% of gastric ulcers and over 90% of duodenal ulcers, and it increases the risk for some kinds of gastric cancer. Fortunately, the infection can usually be eradicated with a relatively short course of antibiotics and acid-blocking drugs, and it may also yield to mastic gum (swallowed in capsule form), which kills H. pylori. Thus, peptic ulcer disease is no longer the chronic and often disabling condition it once was, before its true cause was discovered.
It often takes many years, even decades, for revolutionary medical concepts to become generally accepted—and for safety’s sake, that is probably as it should be. Who can guess what unorthodox ideas on the fringes of today’s medicine will become tomorrow’s conventional wisdom and mainline treatments?
Streptococcus mutans—The Enemy Within
Epic tales portray the women of ancient Greece as a comely lot. (Helen, said to be the daughter of Zeus and Leda, was so beautiful that a thousand warships were launched on her behalf when she was abducted to Troy.) We suspect that the women’s beauty came in part from an attractive smile and good teeth. Could the mastic gum they chewed deserve some of the credit for that?
Scientifically, the answer seems to be yes. As with peptic ulcers, we know that dental caries (cavities) and periodontal disease, with its attendant tooth loss, stem from bacterial action, which mastic combats. The chief culprit in the mouth is Streptococcus mutans, with Lactobacillus species also playing a role. These germs thrive on sugar, and every time we eat a meal or a snack, sugar levels in the mouth increase and nourish the resident bacteria. Within 20 minutes, sticky, destructive plaque begins to form on our teeth, and decay is underway.
Mastic Reduces Oral S. mutans Counts
Three years ago, Japanese researchers conducted a preliminary investigation with 20 healthy young dental students to evaluate mastic gum’s efficacy for plaque prevention.3They found that it significantly diminished the oral bacteria count, decreased the plaque index, and abated gum inflammation, when compared with a placebo gum that had no antimicrobial action. (In gum-chewing studies, a placebo is vital, because gum of any kind will improve some aspects of oral health by mechanical action alone—e.g., firming the gums, stimulating increased salivation, and removing food debris, including bacteria, from the mouth.)
More recently, a team of Turkish researchers purchased a quantity of mastic gum—at the Grand Bazaar in Istanbul, no less—and evaluated its ability to suppress the growth of S. mutans, both in petri dishes and in the mouths of 25 healthy young adults. The volunteers gave saliva samples, then chewed gum for 15 minutes, and then gave further saliva samples every half-hour for 2 hours. The reduction in salivary S. mutanscounts in those who chewed mastic gum versus those who chewed a placebo gum (paraffin) was statistically significant, even after that relatively short chewing period.4
In the laboratory, the researchers compared the effect of mastic on the growth of S. mutans with that of the antibiotic vancomycin and found their activities to be similar. That’s impressive, because vancomycin is such a powerful drug that it’s considered to be “the antibiotic of last resort—it’s usually used against serious infections only when all other drugs have failed. Because of vancomycin’s unique status in this regard, physicians have been reluctant to overuse it, lest such abuse lead to new, mutant strains of “supergerms” that are resistant to it. Unfortunately, however, that is already happening, with ominous implications for public health.
Can Mastic Improve Your Breath?
Mastic gum might also clear up bad breath, although the evidence for this is only suggestive. Most (but not all) halitosis originates from bacteria and fungi in the mouth. In one study, people whose H. pylori infections had been eradicated had almost no halitosis afterward. Whether that had anything to do with H. pylori is debatable, because the treatment kills other germs as well. Since mastic gum suppresses several kinds of bacteria, we might expect it to have a relatively nonspecific effect on bad breath. (For more on this subject, see “Halitosis May Be Linked to Dyspepsia” in the April 2003 issue.)
If mastic accomplished nothing more than preserving your smile and sweetening your breath, that would be reason enough to chew some every day. But there’s more. The pathogenic S. mutans bacteria can travel through the bloodstream and infect the interior linings of the heart, causing infectious endocarditis, a very serious disease. In the worst-case scenario, this can lead to damaged heart valves and congestive heart failure. Concern over the possibility of endocarditis is one reason why dentists usually administer antibiotics before performing invasive procedures on susceptible individuals, such as those with periodontal disease.
Besides brushing and flossing, chewing mastic gum is a good way to keep your teeth relatively plaque-free and your oral bacteria count low—which, in turn, should minimize your risk of acquiring infectious endocarditis from S. mutans. Thus, maintaining healthy teeth and gums can lead, in a roundabout way, to a healthier heart and better circulation. There is even some suggestive evidence that angina due to diseased coronary arteries might be forestalled by controlling H. pylori infections.5
Xylitol Is Both Sweet and Potent
Mastic gum is nontoxic and harmless. The only problem with it, as with many other healthful things, is that it doesn’t taste very good. Neither does chicle, the base used in most commercial chewing gum—which is why gum manufacturers add sugar to their products. Bad idea—sugar feeds bacteria. S. mutans thrives on it, so ordinary gum will promote cavities.
The effect of mastic on the growth of
S. mutans was comparable with that
of vancomycin, a drug so powerful
that it is considered to be
“the antibiotic of last resort.”
There is one kind of sugar, though, that tastes sweet yet can’t be metabolized by S. mutans. It’s xylitol, a sugar alcohol produced from plant sources and also made naturally in our bodies. Several companies have come out with xylitol-sweetened gum, which they claim will help prevent caries. Improving on artificial sweeteners, such as aspartame, xylitol goes beyond just tasting sweet and depriving oral bacteria of nutrition—it actually inhibits the growth of S. mutans, thereby actively diminishing plaque and tooth decay.6 It’s so good at this that it has been endorsed by the professional dental associations of Finland, Sweden, England, and Ireland.
Researchers in Finland and Estonia recently reconfirmed xylitol’s value in oral hygiene.7For 6 months they gave a group of 136 teenagers either a placebo or one of three different sugar alcohols (xylitol, erythritol, or sorbitol) in the form of chewable tablets and a dentifrice that they were instructed to use. Xylitol and erythritol (but not sorbitol) significantly reduced the kids’ plaque and the levels of S. mutans in their saliva.
More Potential Benefits of Mastic
The benefits of mastic, which start in the mouth and extend to the stomach and duodenum, don’t stop there. Keep going … it now turns out that mastic also kills colon cancer cells (although this has not been demonstrated in an actual colon). Researchers in Florida and Greece reported on laboratory experiments involving a human colon cancer cell line to which they added varying concentrations of a mastic gum extract. The mastic killed the cells in a dose-dependent and time-dependent manner. Whether this will work in real life, however, remains to be seen. (For further information, see “Mastic Kills Colon Cancer Cells” in the September 2005 issue.)
There may be still other potential benefits to be found in the use of mastic, for such conditions as heartburn, glaucoma, viral (as opposed to bacterial) infections, atherosclerosis, and heart disease.* There may even be a link between mastic’s best known target, H. pylori, and insulin resistance (see the sidebar on this topic). While we await further research to clarify these matters, maintaining sparkling, healthy teeth and fresh breath is reason enough for anyone to make regular use of mastic.
Does H. pylori Increase Insulin Resistance?
The hallmark of type 2 (adult-onset) diabetes is insulin resistance—the inability of cells to respond to the insulin signals that allow our cells to utilize glucose (blood sugar). This condition, in its earlier stages, is the precursor to overt diabetes. Surprisingly, it may be related to H. pylori infection, according to researchers in Turkey.1 They assessed both H. pylori status and insulin resistance in 63 middle-aged men and women (average age 47) who were generally healthy; 27 of them were H. pylori-negative, and 36 were H. pylori-positive.The results were intriguing: insulin resistance in the H. pylori-positive group was found to be 48% stronger than in the H. pylori-negative group. This, according to the authors, is the first direct evidence of an association between chronic H. pylori infection and insulin resistance. They speculated that H. pylori may increase insulin resistance by leading to a chronic inflammatory state that affects hormones acting on insulin regulation. It’s also possible, however, that there is no cause and effect at all. More studies will be needed to settle this provocative question.
If H. pylori does turn out to increase insulin resistance in some way, the implications are huge. We can speculate that someday, antibacterial substances (including mastic) might have a role in managing this pernicious condition. It’s too soon to tell, but stay tuned.
About those Neolithic gum wads dug up by archaeologists: the people who discarded them could not have known about gum’s health benefits, but they knew that chewing gum was pleasurable. From the tooth marks left in one sample, we can deduce something about the chewer: about adult size, but with teeth showing no signs of wear from the clan’s primitive diet. A teenager, wouldn’t you know?