Helicobacter pylori infection: a review of current scientific research on the efficacy or potential of herbal medicine for the treatment of H. pylori infection of the gastric mucosa.
Objective: To conduct a review of the current scientific literature
on the efficacy of herbs in the treatment and eradication of
Helicobacter pylori infection in the gastric mucosa.
Methods: Research for scientific articles was obtained primarily through Medline and Google Scholar. A total of 53 scientific articles were examined, the vast majority of which were in vitro studies. Only one double blind randomised controlled study was identified involving the use of cranberry. Two controlled trials using garlic were also included.
Results: Helicobacter pylori infection of the gastric mucosa is prevalent throughout the world, especially in countries of poor socioeconomic background. Infection has been proven to be a risk factor for the development of peptic ulcers, gastritis and in some cases adenocarcinoma or lymphoma. Eradication of the bacterial infection and treatment of symptoms due to infection are primarily treated with two antibiotics and a proton pump inhibitor however bacterial resistance to antibiotic therapy is now becoming a problem. A safe and cheap alternative treatment for this widespread infection is being sought.
Current research shows that the use of herbs and herbal extracts for the treatment of Helicobacter pylori infection of the gastric mucosa has great potential. Unfortunately the majority of studies are in vitro with minimal in vivo studies currently being conducted. The most promising and most researched herbs for the treatment of H. pylori infection include cranberry and garlic. Garlic demonstrates strong antibacterial and antiadhesive actions against H. pylori and appears to have a synergistic action when used in conjunction with current orthodox antibiotic therapy. Cranberry inhibits H. pylori infection by preventing adhesion of the bacteria to the gastric mucosa and by acting as a bacteriostatic. Synergism between cranberry and antibiotic therapy with a proton pump inhibitor has been demonstrated. Licorice, green tea, cinnamon, chilli and numerous culinary herbs also demonstrate significant antibacterial or antiadhesive actions. Alcoholic extracts of herbs for the treatment of H. pylori infection appear to be most effective. With regard to herbal treatment, issues that need to be resolved with in vivo studies are herb extraction method, dosage, method of administration and length of time of treatment.
(Care and treatment)
Helicobacter infections (Research)
Medicine, Botanic (Usage)
Medicine, Botanic (Health aspects)
Medicine, Herbal (Usage)
Medicine, Herbal (Health aspects)
|Publication:||Name: Australian Journal of Medical Herbalism Publisher: National Herbalists Association of Australia Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2011 National Herbalists Association of Australia ISSN: 1033-8330|
|Issue:||Date: Fall, 2011 Source Volume: 23 Source Issue: 3|
|Topic:||Event Code: 310 Science & research|
|Geographic:||Geographic Scope: Australia Geographic Code: 8AUST Australia|
Helicobacter pylori is a common bacterium that infects the stomachs of approximately 50% of the world population (Go 2002). Australian physicians Warren and Marshall discovered the unidentified bacteria in the early 1980s in the gastric mucosa and duodenum of patients suffering from peptic ulceration (Gaby 2001). It is now accepted that Helicobacter pylori infection is a precursor to chronic gastritis, peptic and duodenal ulceration (Gaby 2001). Where gastric inflammation persists for decades, atrophic gastritis can evolve into adenocarcinoma or increase the person's risk of developing mucosa associated lymphoid tissue (MALT) lymphomas (Evans 2000, Guruge 1998). From 30-90% of gastric carcinomas are attributable to Helicobacter pylori infection (Guruge 1998). In countries such as Japan where the incidence of gastric cancer is high, the infection rate of Helicobacter pylori has also been found to be high (Go 2002). Helicobacter pylori infection is hypothesised to play a role in cardiovascular disease in some people however clear evidence is yet to be uncovered (Gasbarrini 1999, Martinez-Torres 2002).
Transmission of the bacterium is primarily through compromised water sources but also occurs through person to person transmission (Go 2002). A reduced incidence of infection has been observed in developed countries compared with underdeveloped nations where the carriage rates of infection are as high as 90% however the infection remains prevalent throughout the world (Go 2002, Sivam 1997).
Helicobacter pylori is a gram negative curved rod bacterium (Nostro 2005). H. pylori survives in the acid environment of the stomach by releasing the enzyme urease. Urease converts urea to ammonia, a strong base, which neutralises the acidity of the stomach, protecting the bacteria. The reduction in stomach acidity results in hypochlorhydria which may lead to a variety of gut disorders especially digestive disorders (Lin 2005). Ammonia generated by H. pylori causes damage to the gastric mucosa inducing gastritis and potentially leading to ulceration (Lin 2005).
The bacterium takes hold through adhesin host cell interactions between gastric epithelial cells and erythrocytes (Burger 2002, Evans 200). As of 2002 approximately 10 different types of adhesins have been described however it is accepted that many other mechanisms of adhesion may be involved (Burger 2002). Upon infection, rapid reproduction of the bacterium occurs in the stomach causing gastritis and a reduction in gastric acid production (Guruge 1998). In the majority of people this gastric inflammation associated with Helicobacter pylori infection will settle causing asymptomatic gastritis and normal acid production. This condition will persist indefinitely unless treated.
Helicobacter pylori infection is primarily treated with two antibiotics such as clarithromycin and amoxicillin or metronidazole in conjunction with a proton pump inhibitor such as omeprazole (O'Mahony 2005). This regimen is called triple therapy. However the prevalence of antibiotic resistance has increased over the years resulting in a decrease in effectiveness of triple therapy (O'Mahony 2005). As a consequence new therapy regimes have been designed where four or five drugs are prescribed to combat the infection (O'Mahony 2005). Eradication of the bacterial infection is conclusive when there is no evidence of infection 4 weeks after treatment however reinfection is not uncommon occurring in approximately 20-40% of patients who have undergone triple therapy. Reinfection typically occurs 3-6 months after initial treatment (Gaby 2001, Wittschier 2009). At the present time orthodox treatment is the only therapy that has a proven record for eradicating H. pylori with a cure rate of up to 95% (where triple therapy is used) (Mahady 2005).
There is currently no viable, proven alternative to antibiotic therapy (Gaby 2001). Due to the rising incidence of antibiotic resistance, research into alternative solutions including plant based therapies, are now being investigated. Research on the effectiveness of herbal medicine in treating H. pylori infection has been primarily in vivo thus far. Positive in vitro results unfortunately do not necessarily mean that the herb will be successful in vivo and this is where current research information is severely deficient. The current focus of treatment, whether orthodox or herbal, is based on the antibiotic or antimicrobial properties of a herb or drug and its ability to prevent bacterial adhesion to gastric cells (O'Mahony 2005).
The medical database Medline (1950 to present) and Google Scholar were used to identify research involving Helicobacter pylori and herbal medicine. Key words included Helicobacter pylori, herbal medicine, herbs, phytotherapy in combination. Specific herbs were also targeted including garlic, turmeric, cranberry, chilli, tea and licorice.
Relevant articles included in the review included in vivo and in vitro research involving herb or plant products effect against Helicobacter pylori specifically. References from recent research were investigated to obtain first hand information and results.
Results: specific herbal therapies
Cranberry, Vaccinium macroparpon
As described, the primary method of infection by Helicobacter pylori is through the bacterium adherence to the gastric mucous cells and gastric epithelial cells underlying the mucous layer in the stomach. One of the primary directions of research is to find ways of preventing adhesion of the bacterium to the epithelial cells thus reducing infection rates. The consumption of cranberry (Vaccinium macrocarpon) juice daily has been proven to be effective in preventing adhesion of E. coli to the bladder wall, preventing or reducing the incidence of cystitis (Burger 2000). Howell et al (2005) suspect that A-type proanthocyanidins found in cranberry (as well as other berries), are the primary cause of anti-adhesion activity. A small in vitro study examining the effects of a proanthocyanidin isolated cranberry juice cocktail on adhesion of E. coli to the bladder wall demonstrated significant anti-adhesion activity. It is this mechanism of anti-adhesion that has been applied to H. pylori.
Research involving cranberry's effects on preventing H. pylori adhesion are primarily in vivo. Burger et al (2002) demonstrated that there is significant inhibition of Helicobacter pylori adhesion to human gastric mucous when exposed to high molecular weight constituents of cranberry at 37[degrees]C. Cranberry juice also appears to inhibit sialic acid specific adhesion to gastric mucous, the mechanism of which is yet to be identified. Specific glycoprotein receptors known as fimbriae or lectins are found on the H. pylori wall surface that have the ability to specifically bind to sugars that are present on mucosal cell or epithelial cell walls. Large molecular weight sugars, such as those found in cranberry juice, have been shown to block these receptors preventing bacterium and cell adhesion (Vattem 2005).
The bacteriostatic actions of cranberry were identified by Matsushima et al (2008). The in vivo study using cranberry extract showed complete inhibition of H. pylori growth and proliferation. Inhibition of the bacterium was dose dependent. The researchers then focused on which constituent of cranberry was responsible for this bacteriostatic action and found that the polyphenol content was the primary inhibitor. Morphological analysis of the bacterium after exposure to cranberry identified a shape change in the bacterium from a curved rod to a coccoid form, thereby preventing its proliferation and normal function.
A double blind randomised placebo controlled trial conducted in China by Zhang et al (2005), assessing the efficacy of cranberry juice in suppressing H. pylori infection in 189 patients, found that the consumption of 250 mL of cranberry juice twice daily for 90 days was effective in treating 14% of the patients when compared with the placebo group (p=<0.05). Interestingly this data found that suppression of H. pylori was clearly evident after 35 days of cranberry consumption with very little statistical difference beyond this time frame (i.e. between day 35 and day 90).
As well as presenting with bacteriostatic and anti-adhesive abilities, cranberry has also been found to be useful as an adjunct treatment for eradicating H. pylori infection. Cranberry was found to improve the effectiveness of antibiotic triple therapy that includes the use of a proton pump inhibitor (Shmuely 2004, Shmuely 2007). Interestingly the benefits of using cranberry in conjunction with triple therapy appeared to be most effective in female patients. The reason why this should occur could not be explained. It was suggested that the interaction of the bacteria to female versus male epithelia may be different (Shmuely 2007).
As well as an adjunct to orthodox therapies, cranberry may be effective when used in conjunction with probiotics such as Lactobacillus johnsonii La. A study by Gotteland et al (2008) suggested that cranberry when used in conjunction with the probiotic L. johnsonii may be useful in treating asymptomatic H. pylori infection by inhibiting the growth and proliferation of the bacteria. The researchers conducted their study using a pediatric population (ages 6-16 years). Minimal synergistic effects were observed when compared with the efficacy of each product individually. It is worth noting that cranberry did not appear to have a detrimental effect on the probiotic. The effect of cranberry on commensal gastric and gut bacteria has not been fully researched.
Synergy between cranberry and oregano (Origanum vulgare) was demonstrated in an in vivo study conducted by Lin et al (2005). Researchers focused on urease inhibition of H. pylori in agar diffusion. Significant inhibition of urease production was demonstrated when the two substances were used in conjunction. The mechanism of inhibition was not clearly identified however the combination of phenolics (found in both oregano and cranberry) at the bacteria cellular membrane were suspected to be strongly involved. When the inhibitory actions of each substance were examined individually, the extent of inhibition was significantly less. The most effective combination was found to be 25% oregano to 75% cranberry.
Garlic (Allium sativum)
Garlic has been used in the treatment of ailments for centuries. It has proven antimicrobial, antibiotic, antibacterial and immunostimulating properties (Braun 2005). Researchers investigated the efficacy of garlic as an antimicrobial in the eradication of H. pylori. Difficulties with studying the role of garlic have arisen due to the different varieties of garlic that are available, the composition of the garlic used, the form in which it is utilised and the amounts or dosages used for consumption or investigation being all so variable that evaluation and reproducibility of research results is difficult (Sivam 2001). Despite these issues some interesting facts have already been identified. Firstly the incidence of stomach cancer (which is now known to be primarily due to H. pylori infection) is low in populations with a high consumption of garlic and other Allium vegetables such as onions (Sivam 2001). Secondly the antibiotic action of garlic (suspected to be due to its thiosulfinate content) has not resulted in the development of bacterial resistance which is not the case with current antibiotic therapies (Sivam 2001).
Garlic oil has been researched as a treatment for H. pylori and appears to be promising in the in vivo setting (O'Gara 2000, 2008, Ohta 1999). However garlic oil was found to be most effective in a high acid environment, a condition that may be lacking in the stomachs of infected persons (O'Gara 2008). Reduced acidity is apparent when food and drink is in the stomach, hence the effectiveness of garlic oil was found to be reduced in an in vitro experiment where the efficacy of garlic oil was tested in a replicated, non fasted environment (O'Gara 2008). Therefore in vivo investigation of the efficacy of garlic oil needs to be performed in both the fasting and non fasting patient. The dosage of garlic oil also needs to be defined.
A small study containing 5 patients examined the effectiveness of steam distilled garlic oil in the suppression of H. pylori. The patients were given 4 mg of garlic oil with each meal over a 14 day period. No beneficial effect was identified (McNulty 2001). An additional study using 15 female patients found no benefit when using garlic oil standardised to 800 [micro]g of allicin over a two week period (Aydin 2000).
A randomised factorial controlled trial using aqueous ethanol garlic extract (400 mg) and steam distilled garlic oil (2 mg twice daily) over a 7.3 year period yielded negative results where there was no evidence of H. pylori suppression or eradication. The results were compared with a 2 week course of antibiotics which produced positive results. The study did not identify any synergistic action between garlic and the antibiotics prescribed (Gail 2007).
Inhibition of H. pylori by garlic appears to relate to its thiosulfinate content. Approximately 40 [micro]g/mL of thiosulfinate has been shown to exert significant inhibitory effects upon H. pylori which equates to approximately 5 g (2 small cloves) of fresh garlic (Sivam 1997). The researchers of this study suggest that this is effective in a non fasted stomach and that for efficacy, the consumption of garlic needs to be maintained for long periods (not specified). This may explain why in populations which have a high and constant intake of garlic in their diets there is a lower incidence of H. pylori infection (Sivam 1997). Additional research has demonstrated a lack of synergy or antagonism between garlic and antibiotics however the study did uncover a synergistic action between omeprazole (proton pump inhibitor) and garlic (Cellini 1996, Jonkers 1999). The researchers recommended further investigation.
Chilli, cayenne (Capsicum frutescens)
Capsaicin is the active ingredient in chilli which is responsible for the inhibition of pro-inflammatory cytokines and chilli's cytoprotective actions (Lee 2007). Capsaicin has been found to be effective in inhibiting H. pylori induced inflammation by inhibiting the release of interleukin-8 which is produced by infected gastric cells (Lee 2007). Capsaicin inhibits the growth of H. pylori (in vitro) in a time and concentration dependent manner with maximum bactericidal activity occurring in less than 4 hours (Jones 1997). The maximum inhibitory concentration (MIC) was found to be approximately 1 mg/mL which is easily achievable in a population that consumes a high volume of chilli (Jones 1997). It is recognised however that increased chilli consumption is potentially detrimental to the gastric mucosa due to the promotion of gastric epithelial cell exfoliation following chilli consumption. High chilli consumption is considered a causative factor in gastric cancer development and is independent of H. pylori infection (Lopez-Carillo 2003).
Tea (Camellia sinensis)
The consumption of tea on a regular basis has also been assessed as a protective factor against H. pylori infection. Yee et al (2002) found a significant inverse relationship between H. pylori infection and tea consumption. The active constituents were considered to be the catechin components of tea such as epigallocatechin (EGC), epicatechin (EC), epitechin gallate (ECG) and epigallocatechin gallate (EGCG). Catechins act on bacterial membranes and inhibit urease activity of H. pylori in vitro (Matsubara 2003, Yee 2000, Yee 2002). The type of tea could not be defined as the study was retrospective and many types of Chinese tea were consumed by the test subjects on a random basis. In vitro studies of tea on H. pylori failed to conclude whether or not tea can eradicate H. pylori or only induce suppression (Yee 2000). Research conducted by Lee et al (2006) suggests that tea may act as a bacterial anti-adhesion agent against H. pylori.
Licorice (Glycyrrhiza glabra)
Licorice is another herb traditionally used for the treatment of peptic ulcers (Braun 2005). Strong anti-adhesive and mild cytotoxic effects against H. pylori were demonstrated using an aqueous extract of licorice (Wittschier 2009). Specific flavonoids extracted from Glycyrrhiza species such as glycyrrhetinic acid were found to exhibit significant antibacterial properties against H. pylori as well as clarithromycin and amoxicillin resistant strains of H. pylori (Fukai 2002, Krausse 2004). These results have prompted the proposition that licorice extracts may be useful in preventing reinfection after prior triple therapy (Fukai 2002).
Many herbal extracts have been researched for their in vitro antimicrobial and antibacterial properties against bacteria such as H. pylori. Unfortunately very few in vivo studies have been conducted. Well designed clinical trials involving large numbers of patients are required to provide proof of efficacy which, despite promising in vivo results, have not been conducted (Martin 2003).
Nostro et al (2005) conducted an in vitro study on the efficacy of 17 herbs for their antibacterial activity against Helicobacter pylori. Ethanolic and aqueous extracts of each herb were obtained and examined against the bacterium. The results concluded that the aqueous extracts of globe artichoke (Cynara scolymus) and oregano (Origanum vulgare) demonstrated the most potent inhibition of H. pylori. Of the ethanol extracted herbs, Cynara scolymus and ginger (Zingiber officinalis) were the most effective at inhibiting H. pylori. Overall the ethanol extracts exhibited stronger antibacterial properties compared with the aqueous extracts. The authors presumed this to be due to the higher amounts of bioactive compounds extracted by ethanol compared with water. This information may have implications for future in vivo study designs.
O'Mahony et al (2005) evaluated common culinary herbs such as garlic, turmeric, chilli, ginger, cumin, cinnamon, borage, oregano, black caraway, sage, tarragon, nutmeg, dill, black pepper, coriander, fenugreek, tea, Bengal quince and nightshade for their ability to inhibit adhesion or inhibit growth of H. pylori. The herbs were boiled in water to simulate the cooking process and these individual extracts were assessed against the H. pylori bacterium. The extracts of turmeric (Curcuma longa), borage (Borago officinalis) and parsley (Petroselinum crispum) were found to be the most effective inhibitors of H. pylori. As for effective antibacterial properties, cumin (Cuminum cyminum), ginger (Zingiber officinalis), chilli (Capsicum frutescens) and turmeric (Curcuma longa) were found to be the most efficient. It was suspected that heat associated with the boiling of garlic reduced its antibiotic qualities.
Previous research has proven that the thiosulfinate content of garlic is negatively affected by high heat and it is the thiosulfinate content that is responsible for the antibacterial properties of garlic (Canizares 2004, Cellini 1996, Jonkers 1999).
By using a methanolic extraction of herbs, Mahady et al (2005) found that fennel (Foeniculum vulgare), ginger (Zingiber officinalis), marjoram (Origanum majorana), nutmeg (Myristica fragrans), passionflower (Passiflora incarnata), rosemary (Rosmarinus officinalis), turmeric (Curcuma longa) and yarrow (Achillea millefolium) were all effective in inhibiting the growth of H. pylori. These herbs as well as others were chosen for their traditional use in treating gastrointestinal conditions. Turmeric is used traditionally in Asia for the treatment of peptic ulcers (Mahady 2005) and it has been confirmed that the curcumin content of turmeric is responsible for its antibacterial action against H. pylori (Mahady 2002). It is interesting to note that two different studies using different extraction methods both found turmeric effective as an inhibitor and anti-adhesive of H. pylori.
Panax ginseng has been shown to act as a gastro-protective agent by inhibiting release of interleukin-8 and the COX-2 pathway in infected gastric mucosa (Park 2005, 2007). Panax also demonstrated anti-adhesion properties due to its polysaccharide content (Lee 2004).
Cladosiphon fucoidan is a type of edible seaweed common in the Japanese diet. The seaweed contains long chain polysaccharides that block adhesion of H. pylori to gastric cells (Shibata 1999, Shibata 2003).
The fresh juice of okra (Abelmoschus esculentus), due to its high mucilaginous content, has been traditionally used for the treatment of gastritis. In vitro analysis demonstrated that pretreated H. pylori inhibits adhesion ability completely (Lengsfeld 2004). Broccoli sprouts (Brassica oleracea italica) was found to eradicate H. pylori in 7 out of 9 patients involved in a small trial where they consumed fresh broccoli sprouts for a period of 7 days (Galan 2004). An optimal dose was not described. Researchers are hypothesising that broccoli sprouts may be a useful adjunct to triple therapy (Galan 2004).
Cinnamon (Cinnamomum verum/cassia) alcoholic extracts have been found to be an effective antibacterial against H. pylori inhibiting both its growth and urease production in vitro (Tabak 1999). The most potent antibacterial constituents were cinnamaldehyde followed by eugenol (obtained from Eugenia caryophillis, clove) and carvacrole (Ali 2005, Tabak 1999). It was noted that an acidic environment did not have an adverse effect upon the action of the cinnamon extract.
A small study conducted by Nir et al (2000) involved 15 H. pylori infected patients given 80 mg of cinnamon extract twice daily for four weeks. The researchers found that cinnamon was ineffective in eradicating the infection in these test cases however they did concede that a higher concentration of the extract may be required.
Other herbs that have proven effective against H. pylori in vivo through either antibacterial or anti-adhesive abilities include thyme (Thymus vulgaris), Plumbago zeylanica, Scutellaria baicalensis, the bark of a Brazilian tree Calophyllum brasiliense, Nigella sativa seeds, fenugreek sprouts (Trigonella foenum-graecum) and blackcurrent (Ribes nigrum) seeds (Lengsfeld 2004, Randhir 2004, Salem 2010, Souza 2009, Tabak 1996, Wang 2005, Wu 2008).
Comments and conclusion
There have been numerous in vitro studies examining the effect of herbs and herbal extracts on Helicobacter pylori, many of which have proven antibacterial, anti-adhesive and gastroprotective effects. There has been a paucity of in vitro studies and those that have been conducted often contain very small numbers. Overall the most researched and at this time the most promising herbs that could be used for the treatment of Helicobacter pylori infection include garlic, cranberry and oregano in combination with cranberry, chilli, Chinese tea, turmeric and licorice. Many culinary herbs also appear to be beneficial which interestingly have been used traditionally for the treatment of gastric and gut disorders for thousands of years.
There are many factors that need to be decided before an effective in vivo study can be conducted on a herb, some of which have been addressed in several of the presented research papers. Probably the most important factor is the preparation of the herb. As noted by several authors, ethanolic or alcoholic extracts appear to be the most potent in inhibiting or eradicating H. pylori compared with aqueous extracts however both often displayed effectiveness against the bacteria. Heat may be detrimental to some of the active constituents of other herbs. Identification of the active constituent and ensuring it has been extracted sufficiently may be another factor in study design. Other obvious issues include dosage, the part of the plant used, the duration of use, fasting versus non fasting before ingestion of the herb or supplement and frequency of dosage.
At this point in time current research has proven the bactericidal nature of many herbs in an in vitro setting as well as other actions against H. pylori such as anti-adhesive abilities and the inhibition of bacterial urease production. What is now required are substantial, large scale, well designed in vivo studies to confirm the efficacy of herbal medicines against Helicobacter pylori infection.
A summary of research for the treatment of H. pylori infection using herbal preparations can be found on www.nhaa.org.au under Publications/AJMH/downloads.
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Currently completing an Advanced Diploma of Western Herbal Medicine at Nature Care College Sydney
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