H. Pylori infection can cause, gastritis, ulcers, heartburn, SIBO, anemia, low stomach acid, Insulin resistance, rosacea, anxiety, depression, chronic fatigue, and more.
Dr. Marcus Ettinger B.Sc., D.C. “Since 2007 – The Original H. pylori Treatment Protocol™”
Disclaimer: This post is not a substitute for medical advice or treatment, and is for informational purposes only. Please consult with a physician before starting any nutritional protocol on your own.
December 13, 2016 – BREAKING NEWS – Help Eliminate H. pylori with Pylopass
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Important Note: In order to receive protocol information or help, you will need to become a distance patient – Distance Client Program. I truly do want to help any and all who are interested, but it’s finally gotten to the point where too many people want free advice, treatment plans, personalized protocols…. I’m a firm believer in fair exchange and I feel I have done that by providing the information in this post. I will help you and I can create a tailor-made protocol for your individual situation. Please fill out the distance patient application (link above) or if you have questions about the program, please call me at 714-639-4360
“Heartburn, chronic active gastritis, GERD, acid reflux, achlorhydria or H. Pylori – that is the question.” William Shakespeare. Is any of these conditions actually due to too much stomach acid (hyperchlorhydria)? Not necessarily. I have to admit here, I experienced a severe bout of gastritis – once when I started-up my first practice. And yes, it hurt. It felt exactly like someone poured a quart of battery acid down my throat, at the same time I was having a heart attack while licking a brand-new nine-volt battery. I think you get the picture.
Well, to make a long story short, my stress wasn’t going to go away in the next five minutes. I needed to apply my “medical detectiveness” and reverse engineer what was going on based on the pathophysiology of the condition, in order to figure out the cause. Knowing the cause and predisposing factors would allow me to apply the precise heartburn treatment, H. pylori treatment, chronic active gastritis treatment, GERD treatment, or low stomach HCl treatment. The cause and/or predisposing factors were:
My Predisposing Factors:
1. Chronic Dehydration – There are different types of mucous cells in the stomach, as well as the small and large intestine, and they are easy sources to supply the body with water when dehydrated. The thinning of the gastric mucosa or destruction of that mucous membrane layer makes the stomach vulnerable to acids – hydrochloric or those produced from fermentation of ingested sugars and purification of ingested proteins. Decreased stomach acid (HCl) also creates the perfect storm for the introduction and/or colonization of the dreaded H. pylori bacterium.
Phases of Digestion Series
Part 1 of the 5 Phases of Digestion – How Our Stress Level Affects Digestion And Assimilation
Parts 2 and 3 of the 5 Phases of Digestion – The Mouth and The Stomach
Part 4 of the 5 Phases of Digestion – The Small Intestine
Part 5 of the 5 Phases of Digestion – The Large Intestine/Colon
2. Zinc Deficiency – I picked up on this during a hair mineral analysis. Zinc deficiency as a single factor would, most likely, not cause anything overtly noticeable. When combined with a Helicobacter pylori (H. pylori) infection, the compounding effects created a more severe inflammatory reaction within the gastric lining.
3. One Bourbon, One Scotch, One Beer – Ethanol on its own can create painful erosion and inflammation of the gastric lining, but when combined with the zinc deficiency, it can compound the degree of inflammation and drastically delay healing.
4. H. pylori or Lack of HCl? – After testing, it was confirmed the H. pylori was present. Now was my lack of HCl the reason I got the H. pylori or was the H. pylori the cause of the reduced stomach acid? At this point, it didn’t matter because I couldn’t take HCl due to gastritis and further research showed that the H. pylori bacterium do indeed lower HCl levels (neutralize) in the stomach.
So, to make a long story short, not only was I up shit-creek without a paddle, I was missing the canoe too.
So What Was the True Cause of My Gastritis?
#1, #2, #3 and #4 all played their individual parts in my condition. A little more on #4 – Achlorhydria (lack of stomach HCl) or H. pylori bacteria: This is the, what came first, chicken or the egg dilemma. Did my lack of stomach acid allow the H. pylori a safe haven to take up residence or did the H. pylori infection cause the lack of stomach acid? Both are possible and both allow the other to exist and create a painful condition called atrophic gastritis. This is exactly what I had, and, I am sure, a little erosive gastritis as well.
After some diagnostic testing: allopathic (traditional medicine), which included BioHealth Diagnostics Laboratories 401H (GI Pathogen Screen w/ H. pylori Antigen $270.00) and energetic testing (Applied Kinesiology & Contact Reflex Analysis), I now knew what was going on, what caused it and what to do to get it completely under control. It was confirmed I did have Helicobacter pylori – H. pylori for short.
Stool antigen Testing is the Prefered Method of Testing
The H. pylori Urea Breath Test (30C UBT) is a sensitive and specific method for the non-invasive detection of H pylori infection, but gastric bacterial overgrowth may lead to a false positive diagnosis. Patients with low to no hydrochloric stomach acid can present with many urease-positive bacteria other than H. pylori. The strong urease activity may be responsible for false positive results of an H. pylori Urea Breath Test in patients with suspected H. pylori infection.
Urease-positive bacteria other than Helicobacter pylori in human gastric juice and mucosa.
Gastric bacterial overgrowth is a cause of false positive diagnosis of Helicobacter pylori infection using 13C urea breath test
The True Cause – H. pylori:
One of our oldest companions is a microbe called Helicobacter pylori, or just H. pylori. It has been colonizing our stomachs and co-evolving with us, for the past 50,000 – 100,000 years. Helicobacter pylori (H. pylori) is a spiral-shaped gram-negative bacterium which was identified in 1979.
H. pylori, in those infected, can thrive in their gastric epithelium and in the very thin layer of overlying mucus that protects the stomach wall from the stomach’s hydrochloric acid, a special niche that is hostile to nearly all other microbes. One mechanism by which the bacterium does this is by producing urease in abundance. It is reported that urease functions in H. pylori infection to neutralize the gastric acid by producing ammonia (NH3). Enhanced production of NH3 also may facilitate the formation of NH3-derived compounds, such as monochloramine, which shows cytotoxic effects on host cells. Enhancement of bacterial motility and inhibition of phagocytic clearance of bacteria were also reported as functions of urease.
About half of the world’s population house H. pylori, in their stomach, and are unphased by it. But in about 10-15 percent of those infected, the microbes cause peptic ulcers and chronic active gastritis, and in an unluckier bunch, about 2%, the H. pylori is a causative agent for gastric (stomach) cancer and mucosa-associated lymphoid tissue lymphoma. It has also been shown to be associated with extra-gastric diseases, such as
It has also been shown to be associated with extra-gastric diseases, such as unexplained refractory iron deficiency anemia and idiopathic thrombocytopenic purpura[3-5].
“Everybody with Helicobacter does have inflammation or some irritation in the lining of the stomach and because it lasts your whole life it gradually builds up. This means Helicobacter needs to be treated in people, even if they do not feel unwell.” Professor Barry Marshall. Both Emeritus Professor Robin Warren and Professor Barry Marshall received the Nobel prize in 2005 for discovering the bacteria Helicobacter pylori (H. pylori).
1. Pajares JM, Gisbert JP. Helicobacter pylori: its discovery and relevance for medicine. Rev Esp Enferm Dig 2006; 98: 770-785
2. Sari YS, Sander E, Erkan E, Tunali V. Endoscopic diagnoses and CLO test results in 9239 cases, prevalence of Helicobacter pylori in Istanbul, Turkey. J Gastroenterol Hepatol 2007; 22:1706-1711
3. Bohr UR, Annibale B, Franceschi F, Roccarina D, Gasbarrini A. Extragastric manifestations of Helicobacter pylori infection — other Helicobacters. Helicobacter 2007; 12 Suppl 1: 45-53
4. Franceschi F, Roccarina D, Gasbarrini A. Extragastric manifestations of Helicobacter pylori infection. Minerva Med 2006;97: 39-45
5. Franceschi F, Gasbarrini A. Helicobacter pylori, and extragastric diseases. Best Pract Res Clin Gastroenterol 2007; 21: 325-334
6. Hideo Kuwahara, et. al., Helicobacter pylori Urease Suppresses Bactericidal Activity of Peroxynitrite via Carbon Dioxide Production. Infect Immun. 2000 Aug; 68(8): 4378–4383.
Flys – An Unexpected Route For H. pylori Infection
By Kristin Hugo: The flies in your home, at your picnic, and at the local food court may be even grosser than you thought. A new study finds that they are crawling with bacteria and even host diseases that could be harmful to humans.
Researchers at Penn State collected 116 blowflies and houseflies from different habitats in Brazil, Singapore, and the United States. They sampled from urban sites such as a food market and a hospital emergency entrance, rural sites including farms, and natural sites such as 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 is highly dependent on how susceptible you are to infection. Half of the world’s population already has this bacteria in their gut, but it’s not clear 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 do keep themselves clean enough. If you’ve ever seen a fly rubbing its legs together and scrubbing its face, that fly was actually cleaning itself, just as a cat or mouse would.
H. pylori Treatment Protocol
Original Pre-treatment – First, I took antacids (over the counter – Zantac OTC, an H2 blocker) to increase the susceptibility of the H. pylori to treatment (eradication), lessen the need of H. pylori to defend itself so vigorously, and to allow my gastric mucosa a chance to heal. At least that was my thinking at the time. Note: H. pylori forms protective bacterial colonies called biofilm, which is made up of a protective, extracellular polysaccharide shield. This protective shield is a defensive barrier against stomach hydrochloric acid and other substances, like antibiotics. Being a complex matrix of proteins and carbohydrates, which are probably interdependent, the H. pylori biofilm could possibly offer a protective haven for the survival of this gastric bacterial pathogen in the extra-gastric environments (Proteomannans in Biofilm of Helicobacter pylori ATCC 43504). As well as Candida albicans and other bacteria.
Current H. pylori pre-treatment consists of a personalized, 30-day BIOFILM PROTOCOL and Gut Restoration Protocol. Since H. pylori bacteria can produce a biofilm and is, day by day, becoming more immune to conventional antibiotics, I have found it quite helpful to weaken its outer defenses before the Marines (natural antimicrobial agents and antibiotics) are sent in.
The Original H. pylori Treatment – Second, my personal H. pylori bomb consisted of Monolaurin (lauric acid) or Lauricidin – also see coconut oil, which is 50% lauric acid by weight) and H-PLR (K-32) (Supports bacterial elimination) from Apex Energetics. I also juiced 1/4 cabbage every day (cabbage contains S-Methylmethionine known as Vitamin U; a great healer of ulcers and gastritis). After 4 weeks of my protocol, I was feeling like a new man! I re-checked myself, after 8 weeks (stool test), and was free of the foreign invaders, a breath test confirmed the same.
Current H. pylori Treatment consists of either the Prevpac, Omeclamox®-Pak or Pylera pharmaceutical regime minus the PPI (also, see August 2014 update below) and a personalized combination of natural antimicrobial agents. Below are the products I’m currently pulling from to create an individualized H. pylori protocol. Having the correct biofilm and H. pylori protocol IS just as important as having the correct therapeutic dosage of the products being used. To the degree that the balance of the three is off is to the degree that the entire protocol may fail. This is why is always best to have a qualified coach and to never self-treat.
- Black Seed Oil (Nigella Sativa)
- H-PLR and/or Bio-HPF and/or Berbemycin.
- Saccharomycin DF
- Bladderwrack and/or Cranberry Extract w/D-Mannose
- A More Streamlined Version Of Your Personalized Biofilm Protocol
- A Personalized Version Of My Health Restoration, Daily, Shake
Below are the products I don’t recommend as part of a natural H. pylori protocol. It’s not that these are bad products, in and of themselves, I’ve just found them to be weak or not effective.
- Mastic Gum
- Matula tea
- Manuka Honey
Note: As of September 2009, I’m also adding Klaire Labs – InterFase Plus, to my H. pylori treatment protocol. InterFase Plus is now an important and mandatory part of the protocol. InterFase Plus aids in the eradication of biofilm, especially H. pylori biofilm colonies. This is a major advancement in my protocol. Understanding what BIOFILM is is extremely important for a variety of reasons. Please follow any biofilm link to read more about it. Also, read about my biofilm protocol. Additional products that can be taken during the treatment phase: VSL#3 or Probiotic-10 (multi-strain probiotic and prebiotic formula), NAC by Now Foods, S. boulardii, and Psyllium Husk Fiber. My Biofilm Protocol is integrated into the H. pylori elimination Protocol.
Certain dietary restrictions and additions will need to be taken. These are determined on a case by case basis. The two that are required for everyone is: avoid all cow’s milk and gluten-containing products.
Prevention and Healing – Third, was to keep the H. pylori bacteria from coming back and keep the healing process moving forward. I took pancreatic enzymes w/HCl* and plant-based with each meal, zinc** and L-carnosine** Ulcetrol from Now Foods has both of these. Mastic gum***, TheraAloe****(No longer available), chlorella and/or spirulina, a daily broad-spectrum probiotic (VSL#3 or Probiotic-10 from Now Foods), NAC, psyllium husk fiber and tons of distilled water, for 6 weeks. I was now better than before my first symptom.
All-in-all, it was a learning experience and one that has made me a better doctor and a more diligent medical detective.
FYI: Gastritis is not a single condition, but several different conditions that all share inflammation of the stomach lining as a common symptom. Gastritis, most often, is caused by prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or aspirin, chronic dehydration, drinking too much alcohol or infection such as Helicobacter pylori bacteria (H. pylori). It may also occur after a major surgery, severe infections, trauma-injury-burns, or severe infections. Some diseases, such as pernicious (B12 deficiency) anemia, autoimmune diseases, and chronic bile reflux, can cause gastritis as well.
*Microscopy studies of the motility of H. pylori in gastric mucin at acidic and neutral pH in the absence of urea show that the bacteria swim freely at high (alkaline – achlorhydria) pH, and are strongly constrained at low (acidic) pH. Also, H. Pylori, through enzyme reactions promote increased ammonia production, which raises the pH of its environment – allowing it to move more freely.
(**)A combination of zinc and L-carnosine has been shown to prevent gross visible damage to gastric mucosa caused by ethanol ingestion. This combination also acts as a potent antioxidant, specifically benefiting the gastric mucosa. Polaprezinc, a mucosal protective agent, in combination with lansoprazole, amoxicillin and clarithromycin increases the cure rate of Helicobacter pylori infection
***There is conflicting data on whether mastic gum kills H. pylori effectively in vivo (live human trials). Killing it in a test tube or mice is one thing, but I am interested in living human beings. There is evidence that it aids in the healing of the gastric mucosa, possessing anti-inflammatory properties. I used it for healing rather than as an agent to kill the H. pylori bacteria. Note: there are studies that have shown that mastic gum kills H. pylori. The problem is that it is less than 30% of the trial groups. So it works in about 1 out of every 3 that try it as a primary treatment (at dosages of 500mg’s 3x/day).
****TherAloe is a high molecular weight polysaccharide containing aloe vera juice product. It’s healing capabilities, as far as I am concerned, are quite profound on the gastric mucosa.
H. Pylori Articles:
- Herbs, Probiotics and H. pylori
- Biofilm Basics
- Dr. Ettinger’s Biofilm Protocol for Lyme and Gut Pathogens
- Quorum Sensing and Biofilm
- 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.
- The H. pylori, Pseudomonas aeruginosa, and Antibiotic Connection
- Helicobacter Pylori and Alzheimer’s
- Ulcer-Causing Helicobacter Pylori Survives In Our Acidic Gut By Turning It Neutral
- Antibiotics Have Turned Our Bodies From Gardens Into Battlefields – an interview with microbiologist, Dr. Martin Blasser
- Helicobacter pylori and cardiovascular complications: a mechanism based review on role of Helicobacter pylori in cardiovascular diseases
- The bacterial virulence factor CagA induces microbial dysbiosis that contributes to excessive epithelial cell proliferation in the Drosophila gut.
Important Protocol Updates:
PLEASE READ 19 August 2014 Updated, Update – (Original: 08 Aug 2013): Why H. pylori Infections Are So Hard To Treat – I have been helping patients with H. pylori, a biofilm-producing bacteria, for almost 7 years now. In the beginning, eradicating this bug was very easy, in my opinion. As time progressed I noticed that the same protocol I had been using was becoming less and less effective – on first-timers, not re-treatments. There are now H. pylori strains that are now ‘multiple drug-resistant’. Medically there is no real explanation for this. Energetically there is a very good explanation, for me anyway, based on the research done by Rupert Sheldrake, Ph.D. on Morphic Fields and Morphic Resonance. Please read about his theory for further clarification.
Because of this new shift in loss of effectiveness, in some patients, I have had to use more than one round of products or add more products to the protocol. The end result has always been eradication but it’s now taking more to achieve this result. Also, there are many people contacting me and letting me know that they have undergone triple and quadruple therapies to no avail. This proves in my mind that biofilm and the bacteria that create them are learning to defend themselves more effectively. They are adapting and mutating, genetically, to survive. Good for them and bad for us.
My theory is that with the introduction of hundreds of blogs, chat-rooms, and websites devoted to H. pylori and biofilm, more and more people are self-treating. This self-treating is not killing the H. pylori or eliminating the biofilm but to the contrary, making them both stronger by building up the biofilm defense. Every time a bacteria that produces a biofilm is unsuccessfully treated it becomes more resistant to the next protocol. When this is combined with the theory of Morphic Fields, it’s no wonder that H. pylori and biofilm eradication is becoming harder and harder to achieve. The point of all of this is that there is still effective treatment options available, it may just take a little more time and/or more products, allopathic (Prevpac or Pylera) and/or natural to get to the desired end result – H. pylori and biofilm eradication.
Lastly, I am not against self-treating per se. The issue is that the information, out on the web, on biofilm and H. pylori, is not comprehensive or clear enough for the layperson to be their own doctor or to successfully self-treat. I have always advocated and promoted that if you want to get better with or at something, you need a coach who is an expert in that field or subject. There are times and places where self-help is good, but biofilm and H. pylori treatment are not one of them. This is just my opinion.
PLEASE READ 24 July 2018 Update – Why Not To Use Proton Pump Inhibitors (PPI’s) – A study published in the journal Gut identified an association between long-term use of PPI’s and a 2.4 times higher risk of developing stomach cancer. A link between PPIs and a higher stomach cancer risk has previously been identified by academics – 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 the 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 now well-established that Helicobacter pylori infection predispose individuals toward gastric adenocarcinoma later in life. It has since been classified as a class I carcinogen by the World Health Organization. Research suggests that the oncogenic effects of Helicobacter pylori can occur through a variety of mechanisms, including the indirect inflammatory effects of Helicobacter pylori on the gastric mucosa and the direct epigenetic effects of Helicobacter pylori on individual cells.
H. pylori In The News – Updated Regularly
July 24, 2018 Update – H. pylori has several virulence factors that interact with specific targets in the cell and directly affect the severity of gastric disease. Vacuolating cytotoxin A (VacA) was previously the only main H. pylori factor known to act on mitochondria, causing cellular membrane and organelle dysfunction, ultimately leading to cell death.
Scientists from the Institut Pasteur and the CNRS have discovered that H. pylori use at least two additional strategies to target mitochondria. These strategies do not lead to cell death but maintain an environment that is conducive to bacterial proliferation.
Their results show that H. pylori affect both mitochondrial transport systems (used to transfer proteins into mitochondria) and the machinery for the replication and maintenance of the mitochondrial genome. The scientists also discovered that, contrary to what was previously believed, VacA is not the only H. pylori component capable of affecting mitochondria. This suggests that the bacteria may produce other mitochondria-interacting factors that have not been yet 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 levels of stress, mitochondria, like cells, can remain functional and withstand infection for longer than previously thought. It is important for us to bear this in mind 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 mildly acidic (pH 6) mucous layer of the stomach and when the mucous is shed into the highly acidic (pH 2) stomach, the bacteria quickly unbinds and moves 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. But now 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 a 2- and 20-fold less binding at pH 4 and 2, respectively, compared to pH 6. Within 30 seconds, 85% of the bacteria detached from the mucous layer when placed in a strong acid. They also saw that 95% of them recovered binding activity when shifted to 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.
In order to know the exact pH at which bacteria loses binding, they tested 21 Swedish bacteria isolates. They found that that the bacteria detached at pH ranging from 2.3 to 4.9 showing 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, which are 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 larger 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 acidic environment of the stomach, 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. Healthcanal.com-Digestive System and 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 seem to indicate a potential association between H. pylori infection and IR, further studies are needed to strengthen this association and to clarify whether there is a causative link between them. If a causal link is confirmed in the future, this may have a major impact on the pathophysiology and management of IR syndrome, including type 2 diabetes mellitus and nonalcoholic fatty liver disease. Helicobacter. April 16, 2011
September 13, 2009, Update – I am now taking, Source Naturals – Broccoli Sprouts Extract, which provides 2,000mcg’s 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 protocol to remove them. BIOFILM
November 03, 2009, Update – In my never-ending quest for knowledge, I just came across this interesting piece of data. 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. email@example.com
The susceptibility of Salmonella spp., Escherichia coli and Helicobacter pylori to fatty acids and monoglycerides was studied. None of the lipids showed significant antibacterial activity against Salmonella spp. and E. coli but 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 useful 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. firstname.lastname@example.org
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 with the exception of B. anthracis Sterne in which it was static. Monolaurin was cidal to S. aureus and M. terrae but not to E. coli and K. pneumoniae. Unlike the other two gram-negative organisms, H. pylori were extremely sensitive to monolaurin. 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 useful 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 virus’ that are protected by an outer lipid membrane, known as an envelope (H. pylori cell envelope). The mechanism is due to monolaurin’s ability 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 review of the literature.
Lionetti E, Indrio F, Pavone L, Borrelli G, Cavallo L, Francavilla R. Department of Paediatrics, University of Catania, Catania, Italy. email@example.com
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) Also called morbidity rate the relative incidence of a particular disease in a specific locality.
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