DNC News

 

Helicobacter pylori: Nobel prize awarded to discoverers

October 4, 2005

Subject: Links to information on Helicobacter and a review of natural treatments that may be helpful

 

The Nobel Price in Medicine was awarded this week to the two doctors, Barry Marshall and Robin Warren, who discovered Helicobacter pylori and identified it as the cause of stomach ulcers.

 

A brief review of their work can be read at Science News:

 

http://www.nature.com/news/2005/051003/full/051003-2.html

 

The Center for Disease Control has a fact sheet on Helicobacter at:

http://www.cdc.gov/ulcer/md.htm

 

The idea that stomach ulcers were caused by an infectious agent rather than emotional stress was a new way of thinking for many doctors and it took years for a change in clinical treatment to occur. This delay in scientific knowledge being adopted into clinical practice was so pronounced that it became the subject of several studies [i] [ii] An excellent review article on this history can be found at:

Delayed Gratification: Why it Took Everybody So Long to Acknowledge that Bacteria Cause Ulcers

http://www.jyi.org/features/ft.php?id=101

 

Over the years I have paid a great deal of money to our favorite family therapist to teach me to think of and use the word, “and”. This is a perfect example where using that expensive little word pays off. Perhaps it is both infection ‘and' stress that causes stomach ulcers.

 

Helicobacter infections are transmitted during infancy, usually passed along from family members. The infections stay dormant causing little or now symptoms until later in life when they become active. Could it be that stress inhibits the protective mechanisms of the body allowing the dormant Helicobacter infection to become active? Stress typically lowers the production of hydrochloric acid in the stomach; does the acid keep Helicobacter at bay? Does stress set up the condition for the infection to erupt from its dormant state and cause ulcers? Sounds good, but I confess I haven't found a study that asks these questions directly.

 

Antibiotic therapy is not 100% effective against Helicobacter infections and this has been an impetus to investigate possible alternative therapies that inhibit Helicobacter growth.

 

Alan Gaby, MD has recently written a good article reviewing possible alternative therapies for treating Helicobacter. I am going to paste the full text below:

 

Note: Dr. Gaby mentions an older study which suggests vitamin C may be of benefit. A newer study published suggests that vitamin C provides no benefit. [iii]

 

 

Commentary by Alan R. Gaby, M.D.
Helicobacter pylori Eradication: Are There Alternatives to Antibiotics?


It is generally accepted that infection with Helicobacter pylori is an important cause of peptic ulcer disease and that eradication of this organism greatly reduces the recurrence rate of ulcers. H. pylori also can cause chronic gastritis and hypochlorhydria and is a risk factor for gastric cancer. Conventional eradication therapies, which consist of two antibiotics plus either a proton-pump inhibitor or a bismuth compound, are highly effective (cure rates are typically 85-90% or better). However, these treatments can cause significant side effects in some cases, such as pseudomembranous colitis (a potentially serious infection caused by Clostridium difficile ) or overgrowth of Candida albicans . Alternative methods of eradicating H. pylori are therefore being investigated, as are methods of reducing the side effects of conventional therapy. To date, the research in this area is still preliminary, and no treatment has emerged as a clear alternative to the conventional triple-therapy regimens. However, some natural substances may be useful, either in increasing the eradication rate from standard therapy, or in reducing its side effects.

It should be noted that in vitro activity against H. pylori does not necessarily imply an effect in vivo . In order for a compound to exert an antibacterial effect in vivo , it must achieve a bactericidal concentration in the gastric contents, penetrate the protective mucus layer of the gastroduodenal lining, and maintain its biological activity in the acidic environment of the stomach. Furthermore, the absence of detectable H. pylori at the end of a course of treatment is not sufficient evidence that the infection has been cured. H. pylori is relatively easy to suppress, but difficult to eradicate completely. Most researchers require a negative H. pylori test four weeks after the completion of treatment before concluding that the infection has been cured.

Vitamin C
Sixty patients with dyspepsia, chronic gastritis, and H. pylori infection were randomly assigned to receive antacids (control group) or 5 g/day of vitamin C, administered in 4 divided doses (2 g, 1 g, 1 g, 1 g), for 4 weeks.
1 At the end of the treatment period, H. pylori infection remained unchanged in all 24 patients in the control group, whereas there was no evidence of infection in 8 of 27 patients (30%) who completed vitamin C therapy (p = 0.01). Unfortunately, all of the patients in the study underwent conventional eradication therapy shortly after the trial was completed, so it was not possible to determine whether the effect of vitamin C on H. pylori infection was transient or long-lasting. However, even a suppressive effect of vitamin C against H. pylori might have clinical value, since most people can safely ingest moderate doses of vitamin C indefinitely.

Polyunsaturated Fatty Acids
Fifteen patients with mild non-ulcer dyspepsia and H. pylori infection were treated with 2 g/day of a 1:1 mixture of fish oil and black currant seed oil for 8 weeks.
2   This mixture contains several fatty acids (e.g., linoleic acid, alpha-linolenic acid, gamma-linolenic acid, and eicosapentaenoic acid) that have been shown to inhibit H. pylori in vitro . Six months after the end of treatment, 3 of the 15 patients (20%) had a negative urease test, indicating that the infection had been cured. A placebo-controlled study is needed to determine whether these results represent true H. pylori eradication or spontaneous remission, which is known to occur in some cases.

Lactobacilli
Lactobacilli have been shown to reduce the incidence of antibiotic-induced gastrointestinal side effects in several studies.
3,4 One effective dosage regimen was 6 x 10 9 Lactobacillus GG organisms, given twice a day, 2 hours after breakfast and dinner, for 14 days, during the week of eradication therapy and the following week. Other probiotic organisms, including Saccharomyces boulardii and Bifidobacteria have also been shown to reduce side effects in patients being treated for H. pylori infection. 5

In addition to reducing side effects, preliminary evidence suggests that lactobacilli might increase the effectiveness of antibiotic therapy. In vitro, L. acidophilus has been shown to inhibit the growth of H. pylori .
6 In a study in humans, the addition of L. acidophilus to triple therapy resulted in an eradication rate of 86.6%, as compared with 70% when triple therapy was given alone. 7

Mastic Gum
Mastic gum is a resinous exudate obtained from the stem and leaves of the mastic tree ( Pistacia lentiscus ), an evergreen shrub native to the Mediterranean Basin. In a double-blind trial, administration of mastic (1 g/day before breakfast) for 2 weeks resulted in an ulcer healing rate of 78%, compared with 22% in patients given a placebo (p < 0.01).
8 Mastic has also been shown to kill H. pylori in vitro , but it is not known whether it is capable of suppressing or eradicating H. pylori in humans.

Garlic
An aqueous extract of garlic cloves, standardized for its thiosulfinate concentration, was found to inhibit the growth of H. pylori in vitro , with a minimum inhibitory concentration of 40 mcg of thiosulfinate per ml.
9 To achieve that concentration of thiosulfinate using fresh garlic would require approximately 5 g of garlic (2 small cloves) in a 500-ml volume of stomach contents, which is considered a fairly modest dose of garlic. Despite this evidence of an antibacterial effect in vitro , clinical trials in patients with H. pylori infection have for the most part been disappointing. 10,11 In one study, however, supplementation with allicin (a compound present in garlic) resulted in an eradication rate of 23.3%, and the addition of allicin to conventional therapy increased the eradication rate from 66.7% to 90%. 12

Lactoferrin
Lactoferrin is a protein, present in human and bovine milk, that has bacteriostatic and bactericidal effects against various organisms. The antibiotic effect of lactoferrin has been attributed to its ability to bind iron, thereby preventing the utilization of iron by bacteria for growth. In addition, lactoferrin appears to cause changes in bacterial membrane permeability that might be expected to reduce the viability of the organisms. In a randomized trial, 50 patients with H. pylori infection received one week of triple therapy, with or without 200 mg of lactoferrin twice a day.
13 The eradication rate was 100% in the group receiving lactoferrin, compared with 76.9% in the group not receiving lactoferrin (p = 0.023).

Conclusion
To date, no alternative therapy has been proven to be reliably effective for eradicating H. pylori infection. Some treatments, however, have been shown to reduce the side effects, or to enhance the effectiveness, of conventional therapy. With additional research, using different combinations and doses of some of the substances mentioned in this review, perhaps a safe and effective alternative to triple therapy will be found.

References for Gaby Article:
1 Jarosz M, Dzieniszewski J, Dabrowska-Ufniarz E, et al. Effects of high dose vitamin C treatment on Helicobacter pylori infection and total vitamin C concentration in gastric juice. Eur J Cancer Prev 1998;7:449-454.
2 Frieri G,
Pimpo MT , Palombieri A, et al. Polyunsaturated fatty acid dietary supplementation: an adjuvant approach to treatment of Helicobacter pylori infection. Nutr Res 2000;20:907-916.
3 Gotz V, Romankiewicz JA, Moss J,
Murray HW. Prophylaxis against ampicillin-associated diarrhea with a lactobacillus preparation. Am J Hosp Pharm 1979;36:754-757.
4 Armuzzi A, Cremonini F, Ojetti V, et al. Effect of Lactobacillus GG supplementation on antibiotic-associated gastrointestinal side effects during Helicobacter pylori eradication therapy: a pilot study. Digestion 2001;63:1-7.
5 Cremonini F, Di Caro S, Covino M, et al. Effect of different probiotic preparations on anti- Helicobacter pylori therapy-related side effects: a parallel group, triple blind, placebo-controlled study. Am J Gastroenterol 2002;97:2744-2749.
6 Bhatia SJ, Kochar N, Abraham P, et al. Lactobacillus acidophilus inhibits growth of Campylobacter pylori in vitro . J Clin Microbiol 1989;27:2328-2330.
7 Canducci F, Armuzzi A, Cremonini F, et al. A lyophilized and inactivated culture of Lactobacillus acidophilus increases Helicobacter pylori eradication rate. Gut 2000;47(Suppl 1):A101.
8 Al-Habbal MJ, Al-Habbal Z, Huwez FU. A double-blind controlled clinical trial of mastic and placebo in the treatment of duodenal ulcer. Clin Exp Pharmacol Physiol 1984;11:541-544.
9 Sivam GP, Lampe JW, Ulness B, et al. Helicobacter pylori - in vitro susceptibility to garlic ( Allium sativum ) extract. Nutr Cancer 1997;27:118-121.
10 Ernst E. Is garlic an effective treatment for Helicobacter pylori infection? Arch Intern Med 1999;159:2484-2485.
11 Aydin A, Ersoz G, Tekesin O, et al. Garlic oil and Helicobacter pylori infection. Am J Gastroenterol 2000;95:563-564.
12 Kockar C, Ozturk M, Bavbek N. Helicobacter pylori eradication with beta carotene, ascorbic acid and allicin. Acta Medica 2001;44:97-100.
13 Di Mario F, Aragona G, Bo ND, et al. Use of lactoferrin for Helicobacter pylori eradication. Preliminary results. J Clin Gastroenterol 2003;36:396-398.

 

 

[i] Dan Med Bull. 1995 Sep;42(4):374-7The Helicobacter pylori theory and duodenal ulcer disease. A case study of the research process.

Christensen AH, Gjorup T.

 

[ii] http://cogsci.uwaterloo.ca/Articles/Pages/Ulcers.one.html

 

[iii] Arq Gastroenterol. 2005 Jul-Sep;42(3):167-72. Epub 2005 Sep 22.

[Effect of vitamin C administration on gastric colonization by Helicobacter pylori.]

Kamiji MM, Oliveira RB.

 


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