H. pylori ( helicobacter pylori) has been colonizing in human stomachs for at least 60,000 years! Studies of this commensal microbe have yet to understand it. It does dominate among all the other gastric microbes. Its colonization is associated with peptic ulcer disease and some gastric malignancies but only in a minority of people. In fact, H. Pylori appears to offer protection against esophageal disorders.
Until recently, microorganisms in the stomach were believed to be transient, coming from swallowed secretions or ingested food. In 1983 researchers published the first observation of the helicobacter pylori in the stomach’s epithelium in the setting of acute gastritis and pronounced it an infectious agent causing gastritis and peptic ulcer disease. H. Pylori has been linked subsequently with gastric carcinoma and lymphoma.
Despite the high prevalence of this bacterium, only a minority of colonized people develop disease. H. Pylori-associated disease is not sufficiently understood but becoming ill with it depends on factors such as the virulence of the strain, host age, genetic and environmental susceptibilities. The incidence of peptic ulcer disease is between 10 - 20%, and gastric cancers between 1-2%. It starts one thinking that an organism that has evolved with humans since the origin of the species must provide some benefit by its sharing its existence with us. What benefits are yet under debate. Treatment of H. pylori has dramatically declined its colonization rates offering the advantage of studying the effects of the bacterium.
There is evidence that as the prevalence of H. pylori colonization has diminished, gastroesophagel reflux and its complications such as inflammation of the esophagus and cancer of the esophagus has become more widespread. Allergies and autoimmune diseases are groups of disorders that have also increased; although highly controversial there may be associations and possible mechanisms of the ability of H. plori to increase T cell responses especially in childhood which may suppress excessive inflammatory responses. There is data supporting the protective role of high antibody titers to H. plori and the risk of developing multiple sclerosis, lupus and inflammatory bowel disease. Yet the current thinking is to test and treat the bacterium when detected.
Indiscriminant treatment of H. plori may not be in the patient’s best interest. A positive test should be seen in the setting of a full clinical scenario otherwise the benefits of treatment are unclear. Conventional treatment is antibiotic therapy but even with the most effective drugs only a limited success rate is achieved. Currently combinations of two , three, even four therapies such as three antibiotics plus proton pump inhibitor yield poor success rates. Low success rates are attributed to the bacterium’s ability to hide in the gastric mucus layer and also to the emergence of antibiotic resistance. Two additional factors are also likely to contribute to treatment failure - biofilm formation and replication evidence.
Biofilm is the gathering of bacteria
or fungi encased by a self-generated protein matrix attached to a surface. Bacteria
prefer this mode of existence because it provides protection from the host’s
immune responses and antibiotic resistance. H. pylori makes its own biofilm which
contributes to the low success rate of conventional therapy. H. pylori cells
were detected in the majority of antibiotic-treated cases months after treatment.
They were clustered within biofilm
Along with lactoferrin and antibiofilm enzymes, probiotics can improve treatment success rates and reduce side effects. Probiotics antagonize the bacterium with antimicrobial compounds, stimulate mucus production, inhibit bacterium adhesion to gastric epithelial cells and help with host immune response. Some strains of probiotics can damage the cellular structure of the bacterium. In addition probiotics prevent antibiotic-associated side effects. They can reduce the incidence of reinfection. In reviews of clinical trials probiotic bacteria administered along with standard therapy significantly increased eradication rates.
Oral N-acetyl-L-cysteine, a derivative of the amino acid L-cyteine can also disrupt H. pylori biofilm and mitigate antibiotic resistance. The addition of the supplement has shown potential in treatment particularly in patients who have failed prior sources of therapy.
Another equally important supplement is quercetin, a bioflavonoid antioxidant with anti-inflammatory properties. Quercetin in animal studies reduced H. pylori gastric mucosa infection and decreased inflammatory response. It can play a role in moderating inflammatory responses to colonization.
Complementary interventions such as probiotics, antibiofilm enzymes, lactoferrin, N-acetyl-L-cysteine and quercetin are adjunctive therapies offering the opportunity to improve conventional treatment success rates and reduce side effects. Until medicine knows more about this bacterium, the conventional treatment of multiple antibiotics is all that is offered. If you fall into the minority group with serious H. pylori infestation you may have to consider conventional treatment but at the same time consider complementary alternative treatment as well.
For supplies and further information consult Marie Cargill.