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Archive for the ‘H. pylori’ Category

Antiviral and Antibacterial Actions of Monolaurin and Lauric Acid

Monday, August 16th, 2010

Monolaurin - Monolauroylglycerin - Glycerol monolaurate

Lauric acid is a 12-carbon chain fatty acid found naturally in human breast milk (6.2% of total fat) and coconut oil (47.5% by weight). Lauric acid was originally discovered when microbiologists studied human breast milk to determine the protective (anti-viral and anti-bacterial) substances which protected infants from microbial infections. Other fatty acids were also found to have antimicrobial actions but lauric acid was found to be the most active.

The esterification of lauric acid, that naturally occurs in our body, yields an amazing compound known as monolaurin (glycerol monolaurate). Monolaurin is a non-ionic surfactant, which possesses an even greater anti-viral and anti-bacterial activity than its precursor, lauric acid. Monolaurin, when given orally, in therapeutic doses between 2,400 – 3,600 mg/day is generally well tolerated, with loose bowels as the only negative concern. Monolaurin has been studied at medical research centers, including the Center for Disease Control (CDC), because of its high antimicrobial (anti-viral, anti-bacterial, anti-fungal, anti-yeast and anti-protozoal) activity. These studies have provided information about the anti-viral and anti-bacterial mechanisms of monolaurin. Monolaurin was found to be effective against certain Lipid Coated Bacteria (LCBs) and Lipid Coated Viruses (LCVs) – enveloped DNA and RNA viruses.

Lipid Coated Virus

HIV-1, Influenza virus, paramyxoviruses, rubeola virus, bronchitis virus, and the herpes family of viruses (Epstein-Barr, cytomegalo, zoster, vericella-zoster and herpes type I and II). Sadly, monolaurin had no effect on diseases caused by non-enveloped viruses such as polio virus, coxsackie virus, encephalomyocarditis virus, rhinovirus, and rotaviruses.

Lipid Coated Bacteria

Helicobacter pylori (H. pylori),  Staphylococcus aureus and Streptococcus agalactiae.

The anti-viral and anti-bacterial action attributed to monolaurin is that of solubilizing the lipids and phospholipids in the protective envelope of these particular infective agents causing the disintegration of the lipid envelope. Recent publications have shown that monolaurin and lauric acid inhibit the replication of viruses by interrupting the communication and binding of virus to host cells and thus preventing the uncoating of viruses necessary for replication and infection. Other studies have shown that monolaurin is able to remove all measurable infectivity by directly disintegrating the protective bacterial and viral lipid envelop. Binding of monolaurin to the viral envelop also makes the virus more susceptible to degradation by host defenses, heat, or ultraviolet light.

Microorganisms Inactivated by Monolaurin

Ecological Formulas Monolaurin (600 mg’s – 90 caps) $34.00 Call to Purchase 714-639-4360

Surfactant: Surfactants are compounds that lower the surface tension of a liquid, allowing easier spreading, and lowering of the interfacial tension between two liquids, or between a liquid and a solid. Surfactants may act as: detergents, wetting agents, emulsifiers, foaming agents, and dispersants.

Biofilm and Microbubbles – A new way to identify bacterial infections?

Saturday, April 10th, 2010

microparticles "microbubbles" used for detection of bacterial biofilm

microparticles "microbubbles" used for detection of bacterial biofilm

Certain types of bacteria, such as: Borrelia burgdorferi, Escherichia coli, Candida albicans, Clostridium difficile, Helicobacter pylori, Klebsiella pneumoniae, Legionella pneumophila, Listeria monocytogenes, Pseudomonas aeruginosa, Salmonella typhimurium, Staphylococcus aureus, Staphylococcus epidermidis, and Vibrio cholerae, can join forces to form protective communities called biofilms.  These thin layers of bacteria, which grow on the surfaces of medical implants or directly on tissue in the body, can be difficult to treat because they are more resistant to drugs than the bacteria on their own.  Currently there is no established way to image biofilms in or out of the body.

Pavlos Anastasiadis and colleagues at the University of Hawaii at Manoa have developed a method to watch and measure growing biofilms with ultrasound.  The researchers used contrast agents, microparticles, more accurately, microbubbles, that are normally injected into the body to improve the quality of ultrasound images.  They modified the surface of bubbles in the agents to stick to two kinds of infectious bacteria that form biofilms (Staphylococcus aureus and Pseudomonas aeruginosa).   Acoustic pulses of ultrasound cause the bubbles to “ring” like a bell, revealing their location and the attached biofilm.

The research was done on isolated biofilms.  The next step will be to test it in living tissue.  Anastasiadis hopes to develop the technique to diagnose infective endocarditis, a disease in which bacterial biofilms form on the inner walls of damaged heart valves.

“Targeted ultrasound contrast agents for the imaging of biofilm infections” by Pavlos Anastasiadis  – Abstract: http://asa.aip.org/web2/asa/abstracts/search.may09/asa323.html

Quorum Sensing and Biofilm

Sunday, December 13th, 2009

What is Quorum Sensing and how do bacteria talk to each other?

The discovery that bacteria are able to communicate with each other changed our general perception of many single, simple organisms inhabiting our world. Instead of language, bacteria use signaling molecules which are released into the environment. As well as releasing the signaling molecules, bacteria are also able to measure the number (concentration) of the molecules within a population. Nowadays we use the term ‘Quorum Sensing’ (QS) to describe the phenomenon whereby the accumulation of signaling molecules enable a single cell to sense the number of bacteria (cell density). In the natural environment, there are many different bacteria living together which use various classes of signaling molecules. As they employ different languages they cannot necessarily talk to all other bacteria. Today, several quorum sensing systems are intensively studied in various organisms such as marine bacteria and several pathogenic bacteria.

Quorum Sensing & Biofilm Formation

Quorum Sensing & Biofilm Formation

Why do bacteria talk to each other?

(QS) enables bacteria to co-ordinate their behavior. As environmental conditions often change rapidly, bacteria need to respond quickly in order to survive. These responses include adaptation to availability of nutrients, defense against other microorganisms (biofilm formation) which may compete for the same nutrients and the avoidance of toxic compounds (biofilm formation) potentially dangerous for the bacteria. It is very important for pathogenic bacteria during infection of a host (e.g. humans, other animals or plants) to co-ordinate their virulence in order to escape the immune response of the host in order to be able to establish a successful infection. The University of Nottingham Quorum Sensing Research Group

From Dr. Ettinger’s Biofilm Protocol for Lyme and Gut Pathogens: Pathogenic bacteria known to reside in biofilms include: Borrelia burgdorferi, Escherichia coli, Candida albicans, Clostridium difficile, Clostridium perfringens, Helicobacter pylori, Klebsiella pneumoniae, Legionella pneumophila, Listeria monocytogenes, Pseudomonas aeruginosa, Salmonella typhimurium, Staphylococcus aureus, Staphylococcus epidermidis, and Vibrio cholerae. The number of human diseases shown to be associated with biofilms is expanding and includes chronic bacterial prostatitis, chronic rhinosinusitis, cystic fibrosis pneumonia, infective endocarditis, periodontitis, recurrent otitis media, and virtually all device and implant related infections. Strong evidence is also beginning to emerge for an etiologic role of pathogenic mucosal biofilms in gastrointestinal diseases, such as Irritable Bowel Disorders: Crohn’s disease and ulcerative colitis.

Biofilm Basics

Sunday, October 18th, 2009

Biofilm Formation

Biofilm Formation

What is a biofilm?

Most of you have never heard of the term “biofilm”, but you have certainly encountered “biofilm” on a routine basis. If you’ve ever been to the dentist and he’s scraped “plaque”, which causes tooth decay, off your teeth; that’s a type of bacterial biofilm. The “slim” that clogs your drains is also biofilm. The slippery coating on rocks, at the water’s edge of a stream or river, is just a  bacterial biofilm-coating. Pond-scum – a biofilm. If you’ve ever been diagnosed with Candida albicans, H. pylori or Lyme disease, chances are they’re living, hiding and replicating in a biofilm colony.

Biofilm Plaque

Iodine staining of biofilm plaque (upper right)

This is the best product for removing the bacterial biofilm that causes plaque – Biotene PBF Chewing Gum.

These microorganisms (biofilm colonies) are usually encased in an extracellular polysaccharide that they themselves synthesize, via the release of signaling molecules through quorum sensing (QS). This glue-like substance allows them to anchor to all kinds of surfaces – such as metals, plastics, soil particles, medical implant materials, and tissue. As long as sufficient moisture and nutrients are available, a bacterial biofilm can form just about anywhere. In your body that would be from your mouth, especially the teeth, through the stomach and GI tract, all the way down to the rectum. Biofilm in the environment can be found, most often, in ponds, streams, rivers, etc.  A biofilm can be formed by a single bacterial species, but more often than not, biofilms consist of many species of bacteria, as well as fungi/yeast, algae, protozoa, debris and corrosion products. Once anchored to a surface, biofilm microorganisms carry out a variety of detrimental or beneficial reactions, depending on the surrounding environmental or body conditions.

In the human body, biofilm colonies are the main reason that certain conditions take so long to get handled. In my opinion, if it were not for “biofilm”, conditions caused by the microorganisms – Candida albicans, Candida sppH. pylori, Lyme’s bacteria (Borrelia burgdorferi) and many others, would be far easier to diagnose and/or treat. It is crucial in any treatment protocol to first handle the biofilm.  By doing so, it will make a significant difference in the amount of time, money and effort spent on treating many, so called, stubborn condition – like the above.

Related Posts: Biofilm Protocol, Quorum Sensing, Lactonase

Biofilm Research and Links/Resources

THE ROLE OF EXTRACELLULAR DNA IN MAINTENANCE OF BIOFILMS FORMED BY E. COLI, H. INFLUENZAE, K. PNEUMONIAE, P. AERUGINOSA, S. AUREUS, S. PYOGENES AND A. BAUMANNII George V. Tetz & Victor V. Tetz Dept. of Microbiology, Virology and Immunology; Saint-Petersburg State Pavlov Medical University, Russia Email: vtetzv@yahoo.com

It is known that bacteria within biofilms are much less susceptible to antibiotics particularly because of poor antimicrobial penetration through surface film that covers microbial community and inactivating role of extracellular matrix. Combined effects of DNase (Enzyme for digesting single and double-stranded DNA) and antibiotics on established biofilms of different unrelated bacteria were displayed. A Combination of antibiotics with DNase I resulted in significant decrease of established biofilm biomass compared to the reduction of biomass achieved when antibiotics or DNase I were used alone.

DETECTION OF HELICOBACTER PYLORI IN BIOFILMS BY USING REAL-TIME POLYMERASE CHAIN REACTION (PCR) Linke, S., Gebel, J., Büttgen, S., Exner, M. Institute for Hygiene and Public Health, University of Bonn

Our results confirmed a possible existence of H. pylori in drinking-water biofilms.

ANALYSIS AND IDENTIFICATION OF THE BIOFILM WOUND MICROFLORA IN HORSE WOUNDS Samantha J. Westgate1, Steven L Percival2*, Derek C. Knottenbelt1 and Christine A. Cochrane1 1University of Liverpool, Department of Veterinary Clinical Science, Division of Equine Studies, Leahurst, Neston, South Wirral, UK *2ConvaTec Wound Therapeutics, Deeside, Flintshire CH5 2NU, UK

Equine wound healing is notoriously problematic on the lower limb, specifically when biofilms are evident. Equine chronic wounds display similar characteristics to chronic wounds in humans thus these cases provide an effective model for human cases. Whether wounds are caused by trauma or surgery their high prevalence is of concern and treatment can be both challenging and costly. Biofilms are considered detrimental to normal healing in non-healing and infected chronic wounds because of their recalcitrant nature towards antimicrobial agents. Biofilms are also known to be resistant to the effects of the immune system. Because of this fact more research in the area of chronic wounds and biofilms is warranted.

Culturable analysis of the microflora revealed that the majority of bacteria isolated from the chronic wounds of horses were Staphylococcus spp, Pseudomonas spp, Micrococcus spp, Enterococcus spp, Corynebacterium spp, Streptococcus spp, Bacillus spp, Aerococcus spp and Clostridium spp. Further analysis of all isolates highlighted their biofilm forming potential and antibiotic resistance profiles. Biofilms were shown to be evident in a large percentage of the chronic wounds. In conclusion these studies provide evidence that biofilms exist in the chronic wounds of horse which may well provide an underlying reason as to why a large percentage of chronic wounds are recalcitrant to antimicrobial therapies, do not heal a timely manner and often become infected.

BACTERIAL BIOFILMS IN SURGICAL SPECIMENS OF PATIENTS WITH CHRONIC RHINOSINUSITIS (sinusitis).
Sanclement JA, Webster P, Thomas J, Ramadan HH. Department of Otolaryngology, West Virginia University, Morgantown, West Virginia 26506-9200, USA.

CONCLUSIONS: Biofilms were demonstrated to be present in 80% the 30 patients undergoing surgery for chronic rhinosinusitis (CRS); none of the (control) patients without CRS had any evidence of biofilms.

Heartburn/gastritis/GERD or achlorhydria or H. pylori?

Sunday, September 13th, 2009

gastritisMarcus Ettinger BSc, DC – H. pylori treatment – H. pylori protocol.

H. pylori resources and links

Heartburn/gastritis/GERD/acid reflux.   Are any of these really due to too much stomach acid?  Not necessarily.  I have to admit, I experienced a bout of gastritis once, when I started my first practice;  and yes, it hurt.  It felt like someone poured battery acid down my throat, at the same time I was having a heart attack, while licking a nine volt battery.  I think you get the picture. (The Digestive System)

Well, to make a long story short, my stress wasn’t going to go away in the next five minutes, so I needed to apply my “medical detectiveness” and back-track the pathophysiology of the condition to figure out the cause.  Knowing the cause and the predisposing factors would allow me to apply the precise  heartburn treatment, H. pylori treatment, gastritis treatment, GERD treatment or low stomach HCl treatment.  The cause and predisposing factors were:

My predisposing factors:

1. Chronic Dehydration – There are different types of mucous cells in the stomach 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 HCl also creates the perfect storm for the introduction and colonization of the dreaded H. pylori bacterium.

2. Zinc deficiency - Picked-up on hair-mineral analysis.  Zinc deficiency as a single factor would, most likely, not cause anything overtly noticeable.  When combined w/H. pylori infection, the compounding effect created a more severe inflammatory reaction within the gastric lining.

3.  Wine and Beer - Ethanol on its own can create painful erosion and inflammation of the gastric lining, but when combined with the zinc deficiency, it compounds the degree of inflammation and drastically delays 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?

So, at this point, not only was I up the 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 part 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 condition called atrophic gastritis. This is exactly what I had, and, I am sure, a little erosive gastritis as well.  H. pylori is very bad news bacteria that secretes a potent exotoxin that can lead to gastric mucosal injury and ulcers, and may even predispose one to stomach cancer.

Hpylori

H. pylori bacteria

My H. pylori treatment protocol:

After some testing: allopathic (traditional medicine), which included BioHealth Diagnostics 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 under control.   I had Helicobacter pylori, H. pylori for short.

Pre-treatment – First, I took antacids (over the counter – Zantac OTC) to keep the H. pylori from excreting  it’s protective shield and allow the gastric mucosa to heal (H. pylori bacteria secrete a mucous layer in response to stomach hydrochloric acid, so an antacid will make the H. pylori more susceptible to treatment).

Treatment – Second, my personal H. pylori bomb consisted of: 1,200mg’s 2x/day of Monolaurin (600 mg’s lauric acid per cap – also see coconut oil, which is 50% lauric acid by weight) and 2 caps 2x/day of H-PLR (herbal antibacterial) from Apex Energetics.  I also juiced 1/4 cabbage every day (cabbage contains S-Methylmethionine also known as Vitamin U, a great healer of ulcers and gastritis).  After 4 weeks on my protocol I was feeling like a new man.  I rechecked myself, after 8 weeks, and was free of the foreign invaders, breath test confirmed the same.  As of September 2009,  I am now adding Klaire Labs – InterFase Plus, 2 caps 3x/day on an empty stomach 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 BIOFILM is extremely important for a variety of reasons.  Please follow any biofilm link to read more about it and also see my biofilm protocolAdditional products taken during this phase: Probiotic Defense Powder (multi-strain pro-biotic and pre-biotic formula) by Now Foods and Psyllium Husk Fiber.

Prevention – Third, was to keep the H. pylori bacteria from coming back and keep the healing process moving forward.  I took digestive enzymes w/HCl* – 1 w/ea. meal, plant based enzymes – 1 w/ea. meal, zinc** – 50mg’s 2x/day, L-carnosine** – 500mg’s 2x/day, mastic gum*** 1,000mg’s 2x/day, TheraAloe**** – 1 ounce 2x/day, chlorophyll – 100mg’s 2x/day, a daily broad-spectrum probiotic (Probiotic Defense Powder from Now Foods), psyllium husk fiber (1 heaping Tbsp 2-3x/day) 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, 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 deficient) 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.

***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 in less than 30% of the trial groups.  So it works in about 1 out of every 3 that try is as a primary treatment (at dosages of 500mg’s 3x/day).

****TherAloe is a high molecular weight polysaccharides containing aloe vera juice product. Its healing capabilities, as far as I am concerned, are quite profound on the gastric mucosa.

If you need to set-up a consultation to discuss diagnosing or handling H. pylori, please give me a call. I can also mail any of the products used in the protocol, anywhere in the United States. Call Rene at  (714)-639-4360 for assistance.

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. BIOFILMS

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. bergsson@here.is

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. 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 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. elenalionetti@inwind.it


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