H. pylori Protocol Updates, News, Articles...
Important Protocol Updates
PLEASE READ 24 July 2018 Update – Why Not To Use Proton Pump Inhibitors (PPIs) – A study published in the journal Gut identified an association between long-term PPI use and a 2.4 times higher risk of developing stomach cancer. Academics have previously identified a link between PPIs and a higher stomach cancer risk – but never in a study that first eliminates a type of bacteria suspected of fuelling the illness’s development. Research by the University of Hong Kong and University College London found that even after H. pylori was removed, the risk of developing the disease still rose in line with the dose and duration of PPI treatment.
Gastric cancer is the fifth most common cancer and the third most common cause of cancer-related death in the world. It is well-established that Helicobacter pylori infection predisposes individuals to gastric adenocarcinoma later in life. It has since been classified as a class I carcinogen by the World Health Organization. Research suggests that Helicobacter pylori’s oncogenic effects can occur through various mechanisms, including the indirect inflammatory impact of Helicobacter pylori on the gastric mucosa and the direct epigenetic effects of Helicobacter pylori on individual cells.
September 13, 2009, Update – I am taking Source Naturals – Broccoli Sprouts Extract, which provides 2,000mcg of sulforaphane daily. This is equivalent to eating more than a pound of fresh broccoli. Dietary Sulforaphane-Rich Broccoli Sprouts Reduce Colonization and Attenuate Gastritis in Helicobacter pylori–Infected Mice and Humans.
October 03, 2009, Update – H. pylori most likely will live in biofilm colonies, which make them even harder to kill or be identified by our host defenses. Read more about biofilms here and my procedure for removing them. BIOFILM
November 03, 2009, Update – I just came across this fascinating piece of data in my never-ending quest for knowledge. The H. pylori bacteria is thought to have been with us for around 58,000 years and migrated with modern man out of East Africa. Here is the link to this article. – An African origin for the intimate association between humans and Helicobacter pylori
November 18, 2009, Update – Here are two PubMed articles validating the effectiveness of Monolaurin for the prevention and/or eradication of H. pylori.
Int J Antimicrob Agents. 2002 Oct;20(4):258-62
Bactericidal effects of fatty acids and monoglycerides (Monolaurin) on Helicobacter pylori
Bergsson G, Steingrímsson O, Thormar H. Institute of Biology, University of Iceland, Grensasvegur 12, 108, Reykjavik, Iceland. bergsson@here.is
Salmonella spp., Escherichia coli, and Helicobacter pylori susceptibility to fatty acids and monoglycerides was studied. None of the lipids showed significant antibacterial activity against Salmonella spp. and E. coli. Still, eight of 12 lipids tested showed high activity against H. pylori, monocaprin and monolaurin being the most active. The high activity of monoglycerides against H. pylori suggests that they may be helpful as active ingredients in pharmaceutical formulations.
Mol Cell Biochem. 2005 Apr;272(1-2):29-34
Minimum inhibitory concentrations of herbal essential oils and monolaurin for gram-positive and gram-negative bacteria
Preuss HG, Echard B, Enig M, Brook I, Elliott TB. Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, DC 20057, USA. preusshg@georgetown.edu
New, safe antimicrobial agents are needed to prevent and overcome severe bacterial, viral, and fungal infections. Based on our previous experience and that of others, we postulated that herbal essential oils, such as those of origanum and monolaurin, offer such possibilities. We examined in vitro the cidal (def. killing, as in bactericidal) and/or static effects of oil of origanum, several other essential oils, and monolaurin on Staphylococcus aureus, Bacillus anthracis Sterne, Escherichia coli, Klebsiella pneumoniae, Helicobacter pylori, and Mycobacterium terrae. Origanum proved cidal to all tested organisms except B. anthracis Sterne, which was static. Monolaurin was cidal to S. aureus and M. terrae but not E. coli and K. pneumoniae. H. pylori was extremely sensitive to monolaurin, unlike the other two gram-negative organisms. Similar to origanum, monolaurin was static to B. anthracis Sterne. Because of their longstanding safety record, origanum and/or monolaurin, alone or combined with antibiotics, might prove helpful in the prevention and treatment of severe bacterial infections, especially those that are difficult to treat and/or are antibiotic resistant (also see biofilm, as a source of antibiotic resistance).
Note: Monolaurin has been shown to inactive many forms of bacteria and viruses protected by an outer lipid membrane, known as an envelope (H. pylori cell envelope). The mechanism is due to monolaurin’s ability to aid in the disintegration of this lipid membrane.
May 02, 2010 Update – A recent review, just published, of available literature on the use of probiotics in the treatment or prevention of H. pylori infection validated that “Both in vitro and in vivo studies provide evidence that probiotics may represent a novel approach to the management of H. pylori infection.”
Helicobacter. 2010 Apr;15(2):79-87.
Role of probiotics in pediatric patients with Helicobacter pylori infection: a comprehensive literature review.
Lionetti E, Indrio F, Pavone L, Borrelli G, Cavallo L, Francavilla R. Department of Paediatrics, University of Catania, Catania, Italy. elenalionetti@inwind.it
March 28, 2011 Update – Helicobacter pylori infection has been associated with diverse extra-digestive morbidity, including insulin resistance (IR) syndrome (1), atherosclerosis, and cardiovascular diseases (2). Insulin resistance is the pathophysiologic background of the clinical features of atherosclerosis and cardiovascular diseases. Morbidity – The rate of incidence of a disease. (Medicine / Pathology). The morbidity rate is the relative incidence of a particular disease in a specific locality.
H. Pylori Articles
Helicobacter pylori Facts and More Facts…
Blog post – H. pylori-free, in just 34 days, without antibiotics.
H. pylori Treatment Testimonial – 03/2018
Lactobacillus gasseri For H. pylori Eradication
Natural H. pylori Treatment Worked Even After Antibiotics Failed
Herbs, Probiotics, and H. pylori
Dr. Ettinger’s Biofilm Protocol for Lyme and Gut Pathogens
Can H. pylori actually be good for us? An Endangered Species in the Stomach, by Martin J. Blaser
Probiotics May Represent a Novel Approach to The Management of H. pylori Infection.
Helicobacter Pylori and Alzheimer’s
Ulcer-Causing Helicobacter Pylori Survives In Our Acidic Gut By Turning It Neutral
H. pylori In The News
July 24, 2018 Update: H. pylori has several virulence factors that interact with specific cell targets and directly affect the severity of gastric disease. Vacuolating cytotoxin A (VacA) was previously the only main H. pylori factor that acts on mitochondria, causing cellular membrane and organelle dysfunction and ultimately leading to cell death.
Scientists from the Institut Pasteur and the CNRS have discovered that H. pylori uses at least two additional strategies to target mitochondria. These strategies do not lead to cell death but maintain an environment conducive to bacterial proliferation.
Their results show that H. pylori affects both mitochondrial transport systems (used to transfer proteins into mitochondria) and the machinery for replicating and maintaining the mitochondrial genome. The scientists also discovered that contrary to previously believed, VacA is not the only H. pylori component capable of affecting mitochondria. This suggests that the bacteria may produce other mitochondrial-interacting factors that have yet to be identified.
Co-author Miria Ricchetti of the Institut Pasteur says, “The damage to mitochondria caused by H. pylori bacteria is temporary and disappears once the infection has been eliminated. Despite remarkably high-stress levels, mitochondria, like cells, can remain functional and withstand infection longer than previously thought. We must consider this when looking for strategies to inhibit the bacterium’s pathogenic potential.”
For the first time, scientists have found that the binding of the bacteria to the stomach mucosal layer is acid-sensitive, allowing it to attach and detach when needed.
The bacteria bind to the stomach’s mildly acidic (pH 6) mucous layer. When the mucous is shed into the highly acidic (pH 2) stomach, the bacteria quickly unbind and move to a fresh mucous layer site.
Breakable binding: Previous studies have shown that the bacteria tightly attach to the epithelial cells and mucous of the stomach with the help of an adhesin called BabA. However, the researchers found that though tightly bound to the mucous, the binding affinity reduces once the bacteria sense more acidic pH (2-4 pH). The mucous lining of the stomach is constantly shed into the stomach, which is highly acidic compared with the mucous layer.
The scientists found 2—and 20-fold less binding at pH 4 and 2, respectively, compared to pH 6. When placed in a strong acid, 85% of the bacteria detached from the mucous layer within 30 seconds. They also saw that 95% recovered binding activity when shifted to a less acidic site.
“Such a pH-dependent, reciprocal attachment-detachment system should be a great advantage for long-term colonization in the stomach. Indeed, its importance is supported by the extensive microevolution of BabA,” Dr. Asish K. Mukhopadhyay from the National Institute of Cholera and Enteric Diseases (NICED), Kolkata, says in an e-mail to The Hindu.
To know the exact pH at which bacteria lose binding, they tested 21 Swedish bacteria isolates. They found that the bacteria detached at pH ranging from 2.3 to 4.9, which shows that they can adapt to individual acid secretion patterns. Dr. Asish Kumar Mukhopadhyay, in an article for The Hindu
Research shows how H. pylori bacteria can cause neutrophils, a type of white blood cell, to morph.
“The concept of neutrophil plasticity is new and, to our knowledge, these data are the first evidence that neutrophils can undergo subtype differentiation in vitro in response to bacterial pathogen infection. We hypothesize that these changes favor H. pylori persistence and disease.” March 1, 2017, in the Journal of Immunology
Antibiotic resistance among Helicobacter pylori clinical isolates in Lima, Peru
Results: Seventy-six isolates were recovered from gastric biopsies. Clinical isolates showed evidence of antibiotic resistance to 1 (27.6%, n=21/76), 2 (28.9%, n=22/76), or ≥3 antibiotics (40.8%). Of 76 isolates, eight (10.5%) were resistant to amoxicillin and clarithromycin, part of the standard triple therapy for H. pylori infection. No trends were seen in the presence of cagA, vacA m1, or vacA m2 and antibiotic resistance.
Conclusion: The rate of antibiotic resistance among H. pylori isolates in Lima, Peru, is higher than expected and presents cause for concern. To develop more targeted eradication therapies for H. pylori in Peru, more research is needed to better characterize antibiotic resistance among a more significant number of clinical isolates prospectively. Infection and Drug Resistance, March 10, 2017
Helicobacter pylori Adapts to Chronic Infection and Gastric Disease via pH-Responsive Protein Adhesion Molecule.
For H. pylori to thrive in the stomach’s acidic environment, the gastric pathogen uses a specific protein to attach to the protective pH-neutral mucous lining. New research shows how a specific adhesin protein has a pH-responsive mechanism, allowing H. pylori to rapidly detach from old cells before they reach the brunt of the gastric acid. The release mechanism lets the bacteria return to the pH-neutral mucous lining and recycle the chronic infection. The Umeå University-led research findings are published today in Cell Host & Microbe Cell Host & Microbe, March 08, 2017
Helicobacter pylori infection significantly increases insulin resistance in the asymptomatic Japanese population.
Helicobacter pylori infection has been shown to contribute to atherosclerosis and cardiovascular diseases. Insulin resistance is the pathophysiologic background of the clinical features of atherosclerosis and cardiovascular diseases. Helicobacter, October 14, 2009
The Association Between Helicobacter pylori Infection and Insulin Resistance: A Systematic Review. Although data indicates a potential association between H. pylori infection and IR, further studies are needed to strengthen this association and clarify whether there is a causative link between them. Suppose a causal link is confirmed in the future. In that case, this may have a significant impact on the pathophysiology and management of IR syndrome, including type 2 diabetes mellitus and nonalcoholic fatty liver disease. Helicobacter. April 16, 2011
Flys - An Unexpected Route For H. pylori Infection
By Kristin Hugo: The flies in your home, at your picnic, and the local food court may be even grosser than you thought. A new study finds they are crawling with bacteria and even host diseases that could harm humans.
Researchers at Penn State collected 116 blowflies and houseflies from different habitats in Brazil, Singapore, and the United States. They sampled urban sites, such as a food market and hospital emergency entrance, rural sites, farms, and natural sites like the Amazon Rainforest. In addition to the wild-caught flies, they also sampled control flies from a colony of blowflies that had been captive-bred for 20 generations. They found that the bodies of the animals, especially the wild-caught ones, were covered in bacteria—including bacteria that can be harmful to humans.
Most bacteria found on the flies wouldn’t be able to infect a human host, but Helicobacter pylori can live in your gut for years and then form ulcers and could, according to some research, increase the risk of stomach cancer. The researchers found virulent strains of the bacteria on several blowflies. However, they also noted that the chance that you could be adversely affected by this microbe highly depends on how susceptible you are to infection. Half of the world’s population already has this bacteria in their gut, but it’s unclear how many people got the infection from flies.
After collecting the wild-caught flies, the researchers sequenced the genomes of the life found on their respective bodies. They found that the wings and legs of the animals had the most microbial diversity or different types of microbes living on them. Surprisingly, the flies collected from urban environments were covered with even more pathogens than those collected from stables. The research was published in the journal Scientific Reports.
It shouldn’t be too surprising that flies might carry pathogens. Flies aren’t known for their attraction to cleanliness and prefer to lay their eggs on rotting carcasses and in feces. However, they keep themselves clean enough. If you’ve ever seen a fly rubbing its legs together and scrubbing its face, it was cleaning itself, just as a cat or mouse would.
