Eradicate H. pylori Infection and Protect Yourself from Ulcers Naturally!

Are you at risk for developing an ulcer?

Approximately 25 million Americans suffer from peptic ulcer disease (PUD) at some point in their life. And each year there are 500,000 to 850,000 new cases reported, and more than one million ulcer-related hospitalizations.1 Continue reading to find out if you are at risk … and what you can do to protect yourself—or heal yourself, if you already have an ulcer.

Not too long ago, the common belief was that excessive work and chronic stress caused stomach ulcers. Although it is true that stress can exacerbate an ulcer, we now know that H. pylori, a spiral-shaped bacterium, is the cause of more than 90% of duodenal ulcers and up to 80% of gastric ulcers.

Ulcers also tend to run in some families. But just because no one in your family has ever had an ulcer, it doesn’t mean that you’re immune. (More than 20% of patients who have a duodenal ulcer have a family history, compared with only 5-10% of control groups. In addition, weak associations have been observed between duodenal ulcer and blood type O. Also, patients who do not secrete ABO antigens in their saliva and gastric juice are known to be at higher risk. The reason for these apparent genetic associations is unclear.)3

What is Helicobacter pylori?

Helicobacter pylori (H. pylori) is a spiral-shaped bacterium that is found in the gastric mucous layer or epithelial lining of the stomach. It creates peptic ulcers by weakening the protective coating of the stomach and duodenum, which allows acid to irritate the sensitive stomach lining.

Approximately two-thirds of the world’s population is infected with H. pylori. However, the risk of developing a duodenal ulcer in an individual infected with H. pylori is only about 1% per year, and only 10-15% of individuals with H. pylori infection develop a duodenal ulcer at any point in their life.

In the United States, H. pylori is more prevalent among older adults, but people of all ages and backgrounds, including children and teens, can get infected. Studies also indicate that the infection is more prevalent in those who drink alcohol, smoke, or have cardiovascular disease.8

H. pylori is also believed to be a triggering factor for increasing the risk of acute ischemic stroke.9 A meta-analysis done by the Mayo Clinic found that patients with large vessel stroke had higher odds for H. pylori infection than patients with other types of stroke.10

Researchers have also found an interesting link between H. pylori and abnormal blood lipids. In one study, after eight weeks of treatment to eradicate H. pylori infection, high C-reactive protein levels decreased and low HDL (“good” cholesterol) levels increased in the 78 patients who were treated.11

H. pylori is implicated in these diseases, in addition to peptic ulcer disease:

  • stroke8910
  • atherosclerosis11
  • insulin resistance12
  • autoimmune diseases13
  • heart disease814
  • skin disorders, including rosacea and possibly chronic hives151617
  • some cancers, including MALT lymphoma and stomach cancer1819

How does H. pylori cause an ulcer?

The stomach secretes hydrochloric acid, mucus to protect the stomach walls from the acid, and proteolytic enzymes in order to break down protein into smaller peptide molecules. These enzymes require a fairly high acid environment with a pH level ranging between 1.0 and 2.0. This acid environment also helps kill bacteria, viruses, fungi and other microorganisms that enter the stomach with food.

At the Hiroshima University School of Medicine, Japan, researchers found that gastric acid decreases with age in older people who have H. pylori.20 But good acid production is necessary for killing microorganisms, and poor acid production or acid neutralization with antacids contributes to overgrowth. In fact, the use of antacids can contribute to the overgrowth of other organisms, including H. pylori, Lactobacillus, Enterobacter, Staphylococcus and Probionibacterium.

  • H. pylori is the only bacterial organism in the stomach that cannot be killed by hydrochloric acid. It has adapted to survive in the stomach mucosa, and produces substances that weaken the stomach’s protective mucus and make it more susceptible to the damaging effects of acid and pepsin.21
  • H. pylori can also grow in the small intestine, sticking to epithelial cells. This adherence leads to a variety of second-messenger signals, which invoke an immunologic response against those cells causing mucosal damage by host neutrophils and other inflammatory cells.21
  • H. pylori affects the gastric and duodenal mucous layer because this organism produces proteases that degrade the protective mucous layer. Moreover, H. pylori infection decreases the production of epidermal growth factor, which normally promotes healing of gastric and duodenal mucosa.21

Treating H. pylori—blocking acid secretion results in other problems

When it comes to calming down the burning pain of an inflamed stomach lining or ulcer, reducing the amount of acid in the stomach may seem like a good idea. But two new studies with laboratory mice, conducted by Howard Hughes Medical Institute scientists at the University of Michigan Medical School, indicate it could be exactly the wrong thing to do.

Mice treated with prescription drugs called Proton Pump Inhibitors or PPIs, which block acid production, acquired more bacteria and developed more inflammatory changes in their stomach linings than untreated mice did. The study concluded that Proton Pump Inhibitors (including drugs marketed under the trade names Prilosec® and Prevacid®) dissipate stomach acid, which serves an important anti-microbial function and protects the body from ingested microorganisms.

And when acid suppression is removed, the majority of ulcers, particularly those caused by H. pylori, recur.2224

Are antibiotics a good idea?

Physicians typically prescribe a triple antibiotic regimen using metronidazole, clarithromycin, and amoxicillin to treat H. pylori-caused ulcers. The problem is, according to Dr. Manfred Kist, a leading German microbiologist, the bacterium is becoming resistant to the standard antibiotics used to treat the infection. Antibiotics can also upset the delicate balance of helpful bacteria in your gastrointestinal tract, paving the way for additional problems.

Kist, director of Germany’s National Reference Center for Helicobacter pylori, claimed in a Reuter’s article that many gastroenterologists don’t gather enough information before treating H. pylori infected patients with antibiotics. “This is a trend that will lead to increased drug resistance of H. pylori,” he said. Kist added that 40 to 50% of patients are now resistant to metronidazole, one of the three standard antibiotics used in Germany to treat H. pylori infection. This number rose from 30 percent in the 1980s.24

New sources of anti-H. pylori drugs are needed—which is why the new research showing that herbal extracts can eradicate the H. pylori bacteria is so exciting.

7 Herbs shown to kill H. pylori bacteria … and reduce risk of peptic ulcer disease

Ginger Extract

Most people are familiar with ginger as a seasoning, but it actually has been used for thousands of years as a medicinal herb. Interestingly, almost all of its benefits have been validated by modern science, and it is the pharmacopoeias of many countries.

Ginger is reported to help prevent cardiovascular disease by inhibiting platelet aggregation and promoting healthy cholesterol absorption.
It helps promote healthy digestion, and is particularly helpful as an anti-nausea and vomiting remedy, both prophylactically and acutely, from a variety of causes, including motion sickness, post-operative recovery, morning sickness, flu and even drug side effects. Ginger has also been shown to prevent ulcer formation.37

A study at the University of Illinois, Chicago, found that ginger root extracts inhibit the growth of H. pylori in vitro.38

Thyme Extract

A popular herbal remedy in ancient Egypt, Greece and Rome, thyme was mainly used for headaches, digestive problems, respiratory illness, and as a mood-enhancer.

Researchers who investigated the anti-microbial properties of 21 essential oils against five important food-borne pathogens, including E. coli, noted that thyme was among the top three at inhibiting the bacteria.25

Also, food and engineering researchers at Technion (the Israel Institute of Technology) found that when thyme extract was compared to several antibacterials, it had a significant inhibitory effect on H. pylori. They suggested that since thyme extract has significant therapeutic potential, it should be further studied in clinical trials.26

Terminalia Chebula Extract

Commonly called haritaki in Ayurvedic Medicine, this herb is from a tree that grows in India. The plant is used extensively in the preparation of many ayurvedic formulations for a variety of health concerns including chronic ulcers, fungal skin infections, digestive problems, constipation, heart disease, tumors, nervous disorders, asthma, and more.

Its principle constituents contain chebulagic, chebulinic acid and corilagin, and its fruit is used as an antiviral, coagulant, and laxative. Terminalia also has a wide antibacterial and antifungal spectrum, and is also known as an adaptogen and hepatoprotective (liver protectant).2728

More recently, in a study comparing with three other ayurvedic herbs, terminalia was found to be the best antioxidant among the four extracts.29

A study at the University of Tehran, Iran, tested extracts of terminalia chebula on H. pylori, which showed significant antibacterial activity on H. pylori and other bacterium.30

The H. pylori bacterium has been estimated to be present in 30-40% of the U.S. population, and is considered the world’s most common chronic infection.

Evodia Extract

Evodia is a seasonal tree, native to northern China and Korea. Its reddish-brown fruit has been used for thousands of years to treat gastrointestinal disorders such as nausea, vomiting, and diarrhea. Evodia has also been traditionally used as a painkiller to treat headaches that accompany nausea and vomiting, and relieve pain associated with abdominal hernias.34

Research done in Japan and Korea has found that evodia extracts strongly inhibit the growth of H. pylori, which reinforces its traditional use for digestive ailments.3536

Licorice Extract

Licorice has been used for thousands of years in Traditional Chinese Medicine as a tonic to rejuvenate the heart and spleen, and as a treatment for ulcers, cold symptoms, and skin disorders. It also has a long history throughout the world as a medicinal herb for numerous health complaints.

Modern herbalists commonly utilize licorice in treating adrenal insufficiencies such as hypoglycemia and Addison’s disease, counteracting stress, and in purifying the liver and bloodstream. In combination with other herbs, it is recommended as a demulcent to soothe mucous membranes, and as an expectorant useful in treating flu, colds, respiratory disorders, and bronchitis.

Licorice is commonly used in Europe to treat ulcers, and research is proving that it does, indeed, have very potent therapeutic effects. Licorice extracts protect the esophagus, stomach, and intestinal lining from stomach acids. In cases of heartburn, licorice also helps repair the stomach’s protective mucous lining. In the following studies, two of the standard anti-ulcer medications failed to perform as well as licorice extracts.

In a recent study at the Institute of Medical Microbiology and Virology, Kiel, Germany, researchers found that licorice extract produced a potent effect against strains of H. pylori that are resistant against clarithromycin, one of the antibiotics typically used in the three antibiotic treatment regimen. The authors concluded that this study provides hope that licorice extract can form the basis for an alternative therapeutic agent against H. pylori.32

A study at Toho University, Chiba, Japan, found that licorice extracts are also effective against H. pylori strains that are resistant to both amoxicillin and clarithromycin, making them viable as chemopreventive agents for peptic ulcer or gastric cancer in H. pylori-infected individuals.33


Berberine is a plant alkaloid isolated from the roots and bark of several plants including golden seal, barberry, coptis chinensis and Yerba mansa. Berberine-containing plants have been used medicinally in ayurvedic and Chinese medicine, and are known to have antimicrobial activity against a variety of organisms including bacteria, viruses, fungi, protozoans, helminths, and chlamydia. Currently, the predominant clinical uses of berberine include bacterial diarrhea, intestinal parasite infections, and ocular trachoma infections.

More recently, berberine has been demonstrated to be effective against H. pylori.42


Curcumin is the substance that gives the spice turmeric its yellow color. Curry powder, which is used extensively in Indian cuisine, is largely made of turmeric and other spices. Curcumin contains many powerful antioxidants and anti-inflammatory compounds, which have been shown to support colon health, a healthy cardiovascular system, and most recently brain health. Dozens of studies have shown that it is a chemopreventative, and more recently it has been shown to exert a strong antibacterial effect against H. pylori.

Studies carried out in the U.S.39, Italy40, and Germany41, produced results showing a significant in vitro effect of its extracts against H. pylori, leading researchers to conclude that curcumin could be considered a valuable support in the treatment of the infection.

Should you take these herbs without knowing for sure if you have H. pylori?

That’s a good question. Although you can get tested for H. pylori, the tests are very expensive. All of these herbs can be taken both therapeutically and prophylactically. In other words, they are perfectly safe to take whether you know you have H. pylori, or whether you just want to protect yourself from its devastating effects.

Thyme, licorice, evodia, terminalia chebula, berberine, curcumin and ginger have a long history of providing numerous health benefits without risk of side effects. And it’s important to remember that H. pylori has been implicated as a culprit in several diseases, not just peptic ulcer disease (PUD). It could be residing in your arteries or liver, in which case, you could end up with cardiovascular disease or worse.

So play it safe. If you know that you have an H. pylori infection, take these herbs at a high dose as a therapeutic treatment for 10 days, several times a year. And if you aren’t sure you have H. pylori but want to protect yourself, it’s perfectly safe to take these herbs year round at a low dose.

Caution: If you are pregnant or breastfeeding, you should consult with your health care professional before taking herbs.

Is there a test for H. pylori infection?

Yes, there are several noninvasive laboratory tests available, although the most common procedure is called endoscopy. This is an uncomfortable exam that requires a narrow tube to be inserted into the stomach through the mouth. Here are several simpler, non-invasive tests to detect H.pylori infection.21

  • Urea breath test is a highly accurate 15-minute test to detect H. pylori infection. The patient ingests radio-labeled urea, which, in the presence of urease produced by H. pylori, is metabolized to carbon dioxide and ammonia. A laboratory assay then is used to detect the radio-labeled carbon dioxide. The test detects very low levels of H. pylori colonization, assesses the entire gastric mucosa, and has a sensitivity of 90-95%. It can be used to diagnose infection, but it is more often used to evaluate the success of treatment of H. pylori infection.
  • Serology: Enzyme-linked immunoassay (ELISA) can detect both immunoglobulin G (IgG) and immunoglobulin A (IgA) antibodies directed against H. pylori. The sensitivity of most serologic tests is approximately 95%.
  • Fecal antigen test: The detection of H. pylori in feces is emerging as a noninvasive method of detection. This test is used mainly for children.


We now know that nine out of ten peptic ulcers are caused by an infection from the bacterium Helicobacter pylori and not by stress or spicy foods as previously thought. We also know that H. pylori may be a culprit in numerous other diseases, including cardiovascular and autoimmune, and various skin disorders and stroke.

Several H. pylori strains have become resistant to two of the three antibiotics used in the triple antibiotic drug therapy prescribed to eradicate it, and researchers are vigorously studying a number of herbal extracts to find an alternative treatment.

-Sponsored Ads-

Luckily, we now have an arsenal of natural herbs that have been proven to eradicate H. pylori in vitro, and more and more international laboratories are engaging in clinical studies to assess the efficacy of herbal extracts in treating H. pylori. Because of the growing resistance to antibiotics, it won’t be long before herbal extracts become the treatment of choice—and the key ingredients in pharmaceuticals—to eradicate H. pylori.

These gastric irritants can add fuel to the fire by contributing to the formation of an ulcer, or by exacerbating an existing one:

  • Alcohol has not been scientifically linked to peptic ulcers, but ulcers are more common in people who drink alcohol.8
  • H. pylori is more common in smokers.8 Smoking is also believed to slow down the healing process of an existing ulcer, and contribute to ulcer recurrence.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs), (aspirin, ibuprofen, and naproxen sodium) make your stomach susceptible to the harmful effects of acid and pepsin. They are believed to inhibit prostaglandins, substances that help maintain blood flow to the stomach, and protect the area from injury. And once injured, the stomach acid eats into the tissues. About 15% of people who take NSAIDs on a regular basis have gastric or duodenal ulcers. People who take NSAIDs and are infected with H. pylori are at least 61 times more likely to have ulcers of the stomach and/or duodenum than non-users and noninfected people.4
  • Corticosteroids (hydrocortisone, cortisone, prednisone, etc.) do not increase the risk of duodenal ulcers by themselves, but the risk of a duodenal ulcer is increased when corticosteroids are used in combination with NSAIDs compared to NSAID use alone.5
  • Caffeine seems to stimulate acid secretion in the stomach, which can aggravate the pain of an existing ulcer.
  • Stress is no longer considered a cause of ulcers, but people who already have ulcers frequently report that emotional stress increases their pain. Physical stress, however, can increase the risk of developing ulcers, particularly in the stomach. For example, people with severe burns and individuals undergoing major surgery often require special care to prevent ulcers and ulcer complications.
  • Acid and pepsin—Some health professionals believe that the stomach’s inability to defend itself against the powerful digestive fluids, hydrochloric acid and pepsin, contributes to ulcer formation. The acid pH of the stomach is very tricky, however. Taking antacids, the traditional method of treating ulcers, lowers stomach acid, which actually contributes to the formation of ulcers because of the body’s inability to protect itself against H. pylori. On the other hand, when stomach acid is too high, it can damage the stomach lining.
  • An Israeli study conducted in Kenya found that H. pylori was more prevalent in people who had dyspepsia (the medical term for indigestion) than those who did not (71% vs. 51%), particularly in people younger than 30 years old.6
  • Radiation therapy, burns, and physical injury that damage the stomach or duodenum wall, often set the stage for ulceration.
  • As surprising as it is, stomach acid production is actually increased after drinking milk, and does not relieve stomach ulcers.7


  1. H. pylori Fact Sheet for Health Care Providers, Centers for Disease Control and Prevention.
  2. H. pylori Myth Sheet. University of Maryland Medical Center, Digestive Disorders, Stomach and Duodenal Ulcers (Peptic Ulcers)
  3. Devlin, Shane, Meddings, Jon. “Duodenal Ulcers”. E-Medicine: Instant Access to the Minds of Medicine.
  4. Pounder R. Helicobacter pylori and NSAIDs – the end of the debate? Lancet 358:3-4, 2002.
  5. Larkai EN.Gastroduodenal mucosa and dyspeptic symptoms in arthritic patients during chronic nonsteroidal anti-inflammatory drug use. Am J Gastroenterol. 1987 Nov;82(11):1153-8.
  6. Shmuely H, Obure S, Passaro DJ, Abuksis G, Yahav J, Fraser G, et al. Association between dyspeptic symptoms and Helicobacter pylori infection in Nakuru, Kenya. Emerg Infect Dis [serial online] 2003 Sept [date cited].
  7. Ippoliti AF. The effect of various forms of milk on gastric-acid secretion. Studies in patients with duodenal ulcer and normal subjects.Ann Intern Med 1976 Mar;84(3):286-9.
  8. Andreica V, Sandica-Andreica B, Draghici A, Chiorean E, Georoceanu A, Rusu M. The prevalence of anti-Helicobacter pylori antibodies in the patients with ischemic heart disease. Rom J Intern Med. 2004;42(1):183-9.
  9. Sawayama Y, Ariyama I, Hamada M, Otaguro S, Machi T, Taira Y, Hayashi J. Association between chronic Helicobacter pylori infection and acute ischemic stroke: Fukuoka Harasanshin Atherosclerosis Trial (FHAT). Atherosclerosis. 2005 Feb;178(2):303-9.
  10. Cremonini F, Gabrielli M, Gasbarrini G, Pola P, Gasbarrini A. The relationship between chronic H. pylori infection, CagA seropositivity and stroke: meta-analysis. Atherosclerosis. 2004 Apr;173(2):253-9.
  11. Kanbay M, Gur G, Yucel M, Yilmaz U, Boyacioglu S. Does eradication of Helicobacter pylori infection help normalize serum lipid and CRP levels? Dig Dis Sci. 2005 Jul;50(7):1228-31.
  12. Aydemir S, Bayraktaroglu T, Sert M, Sokmen C, Atmaca H, Mungan G, Gun BD, Borazan A, Ustundag Y. The Effect of Helicobacter pylori on insulin resistance. Dig Dis Sci. 2005 Nov;50(11):2090-3.
  13. Gasbarrini A, Franceschi F. Does H. pylori infection play a role in idiopathic thrombocytopenic purpura and in other autoimmune diseases? Am J Gastroenterol. 2005 Jun;100(6):1271-3.
  14. Aceti A, Are R, Sabino G, Fenu L, Pasquazzi C, Quaranta G, Zechini B, Terrosu P. Helicobacter pylori active infection in patients with acute coronary heart disease. J Infect. 2004 Jul;49(1):8-12.
  15. Zandi S, Shamsadini S, Zahedi MJ, Hyatbaksh M. Helicobacter pylori and rosacea. East Mediterr Health J. 2003 Jan-Mar;9(1-2):167-71.
  16. Vazquez Romero M, et. al[Chronic urticaria and Helicobacter pylori] [Article in Spanish] Med Clin (Barc). 2004 Apr 24;122(15):573-5.
  17. Federman DG, Kirsner RS, Moriarty JP, Concato J. The effect of antibiotic therapy for patients infected with Helicobacter pylori who have chronic urticaria. J Am Acad Dermatol. 2003 Nov;49(5):861-4.
  18. Kawahara Y, Mizuno M, Yoshino T, Yokota K, Oguma K, Okada H, Fujiki S, Shiratori Y. HLA-DQA1*0103-DQB1*0601 haplotype and Helicobacter pylori-positive gastric mucosa-associated lymphoid tissue lymphoma. Clin Gastroenterol Hepatol. 2005 Sep;3(9):865-8.
  19. Morgner A, Bayerdorffer E, Neubauer A, Stolte M. Malignant tumors of the stomach. Gastric mucosa-associated lymphoid tissue lymphoma and Helicobacter pylori. Gastroenterol Clin North Am. 2000 Sep;29(3):593-607.
  20. Haruma K, Kamada T, Kawaguchi H, Okamoto S, Yoshihara M, Sumii K, Inoue M, Kishimoto S, Kajiyama G, Miyoshi A. Effect of age and Helicobacter pylori infection on gastric acid secretion. J Gastroenterol Hepatol. 2000 Mar;15(3):277-83.
  21. Devlin, Shane M., Meddings, Jon. “Duodenal Ulcers.”
  22. Zavros Y, Rieder G, Ferguson A, Samuelson LC, Merchant JL. Genetic or chemical hypochlorhydria is associated with inflammation that modulates parietal and G-cell populations in mice.Gastroenterology. 2002 Jan;122(1):119-33.
  23. Zavros Y, Rieder G, Ferguson A, Samuelson LC, Merchant JL.Hypergastrinemia in response to gastric inflammation suppresses somatostatin.Am J Physiol Gastrointest Liver Physiol. 2002 Jan;282(1):G175-83.
  24. Reuters. Frankfurt. March 6, 2002.
  25. Smith-Palmer, A., et al., “Antimicrobial properties of plant essential oils and essences against five important food-borne pathogens,” Lett Appl Microbiol (1998), 26(2):118-22.
  26. 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.
  27. Akhtar, H. et. al., Edrs., Dictionary of Indian Medicinal Plants, CIMAP, Lucknow, 1992, 458.
  28. Inamdar, M.C. and Rajarama Rao, M.R., Studies on the pharmacology of Terminalia chebula., J. Sci. Ind. Res., 1962, 21C, 345.
  29. Naik GH, Priyadarsini KI, Satav JG, Banavalikar MM, Sohoni DP, Biyani MK, Mohan H. Comparative antioxidant activity of individual herbal components used in Ayurvedic medicine. Phytochemistry. 2003 May;63(1):97-104
  30. Malekzadeh F, Ehsanifar H, Shahamat M, Levin M, Colwell RR. Antibacterial activity of black myrobalan (Terminalia chebula Retz) against Helicobacter pylori. Int J Antimicrob Agents. 2001 Jul;18(1):85-8.
  31. Fabry W, Okemo P, Mwatha WE, Chhabra SC, Ansorg R. Susceptibility of Helicobacter pylori and Candida spp. to the east African plant Terminalia spinosa. Arzneimittelforschung.1996 May;46(5):539-40.
  32. Krausse R, Bielenberg J, Blaschek W, Ullmann U. In vitro anti-Helicobacter pylori activity of Extractum liquiritiae, glycyrrhizin and its metabolites. J Antimicrob Chemother. 2004 Jul;54(1):243-6. Epub 2004 Jun 9.
  33. Fukai T, Marumo A, Kaitou K, Kanda T, Terada S, Nomura T. Anti-Helicobacter pylori flavonoids from licorice extract. Life Sci. 2002 Aug 9;71(12):1449-6
  34. Molony D. Complete Guide to Chinese Herbal Medicine. New York: Berkeley Books,1998.
  35. Hamasaki N, Ishii E, Tominaga K, Tezuka Y, Nagaoka T, Kadota S, Kuroki T, Yano I. Highly selective antibacterial activity of novel alkyl quinolone alkaloids from a Chinese herbal medicine, Gosyuyu (Wu-Chu-Yu), against Helicobacter pylori in vitro. Microbiol Immunol. 2000;44(1):9-15.
  36. Rho TC, Bae EA, Kim DH, Oh WK, Kim BY, Ahn JS, Lee HS. Anti-Helicobacter pylori activity of quinolone alkaloids from Evodiae fructus. Biol Pharm Bull. 1999 Oct;22(10):1141-3.
  37. Presser, Arthur M. Pharmacists’s Guide to Medicinal Herbs. Smart Publications, 2000, Petaluma, CA.
  38. Mahady GB, Pendland SL, Yun GS, Lu ZZ, Stoia A. Ginger (Zingiber officinale Roscoe) and the gingerols inhibit the growth of Cag A+ strains of Helicobacter pylori. Anticancer Res. 2003 Sep-Oct;23(5A):3699-702.
  39. Mahady GB, Pendland SL, Yun G, Lu ZZ. Turmeric (Curcuma longa) and curcumin inhibit the growth of Helicobacter pylori, a group 1 carcinogen. Anticancer Res. 2002 Nov-Dec;22(6C):4179-81.
  40. Nostro A, Cellini L, Di Bartolomeo S, Di Campli E, Grande R, Cannatelli MA, Marzio L, Alonzo V. Antibacterial effect of plant extracts against Helicobacter pylori. Phytother Res. 2005 Mar;19(3):198-202.
  41. Foryst-Ludwig A, Neumann M, Schneider-Brachert W, Naumann M. Curcumin blocks NF-kappaB and the motogenic response in Helicobacter pylori-infected epithelial cells. Biochem Biophys Res Commun. 2004 Apr 16;316(4):1065-72.
  42. Mahady GB, Pendland SL, Stoia A, Chadwick LR. In vitro susceptibility of Helicobacter pylori to isoquinoline alkaloids from Sanguinaria canadensis and Hydrastis canadensis. Phytother Res.2003 Mar;17(3):217 21.