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

Disclaimer: This post is not a substitute for medical advise or treatment and is for informational purposes only. Please consult with a physician before starting any nutritional protocol on your own.

Blog post – H. pylori free, in just 34 days, without antibiotics on Dr. Ettinger’s protocol! Lab tests to prove it.

H. pylori – Resources and Links

“Heartburn, chronic active gastritis, GERD, acid reflux, achlorhydria or H. Pylori - that is the question.” William Shakespeare. Are 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. (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 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 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 acid (HCl) also creates the perfect storm for the introduction and/or colonization of the dreaded H. pylori bacterium.

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.  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 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?

So, at this point, 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.

H. pylori bacteria

Diagnostic Testing:

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. I confirmed that I did have Helicobacter pylori - H. pylori for short.

The True Cause – H. pylori:

Helicobacter pylori (H. pylori) is a spiral-shaped gram-negative bacterium which was identified in 1979[1]. It produces urease in abundance, the activity of which, through the production of   ammonia, together with the bacterium’s motility and ability to adhere to the gastric mucosa, enables its survival in the acid environment of the stomach. About half of the worlds population house H. pylori, in their stomach, and are unphased by it. But in about 15 percent of those infected, the microbes cause peptic ulcers and chronic active gastritis, and in an unluckier bunch the H. pylori is a causative agent for gastric cancer and mucosa associated lymphoid tissue lymphoma[2]. It has also been shown to be associated with extragastric diseases, such as iron deficiency anemia and idiopathic thrombocytopenic purpura[3-5].

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

My H. pylori Treatment Protocol

Pre-treatment – First, I took antacids (over the counter – Zantac OTC) to increase the susceptibility of the H. pylori to treatment/eradication (lesson the need of  H. pylori to defend itself so vigorously) and allow my gastric mucosa a chance to heal.  Note: The H. pylori form protective bacterial colonies called biofilm, which are made up of a protective, extracellular polysaccharide shield. This protective shield is a defensive barrier against stomach hydrochloric acid and other factors, 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 extragastric environments (Proteomannans in Biofilm of Helicobacter pylori ATCC 43504).

Treatment – Second, my personal H. pylori bomb consisted of: x,xxx mg’s 2x/day of Monolaurin (xxx mg’s lauric acid per cap – also see coconut oil, which is 50% lauric acid by weight) and x caps x times per day of H-PLR (Supports bacterial elimination) 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.

Note: As of September 2009, I’m also adding Klaire Labs – InterFase Plus, x caps x per 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 protocol. Additional products taken during the treatment phase: Probiotic Defense Powder (multi-strain pro-biotic and pre-biotic formula), NAC by Now Foods and Psyllium Husk Fiber.

Certain dietary restrictions and additions will need to be taken. These are determined on a case by case basis.

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* – x w/ea. meal, plant based enzymes – x w/ea. meal, zinc** – xx mg’s x per day, L-carnosine** – xxx mg’s x times per day, mastic gum*** x,xxx mg’s x times per day, TheraAloe**** – x ounce x times per day, chlorophyll – xxx mg’s x per day (chlorella or spirulina can be substituted for chlorophyll), a daily broad-spectrum probiotic (Probiotic Defense Powder or Probiotic-10 from Now Foods), psyllium husk fiber (x heaping Tbsp x-x times per 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 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.

***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 it 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.

Important Note on Purchasing Products:

All dosages will be provided if you purchase some or all of your products through my office. I truly do want to help all who are interested, but it’s finally gotten to the point where too many people want free advice and an increasing amount of my time, and then buy all of their products elsewhere. I am a firm believer in fair exchange and I feel I have done that by providing the information in this post.

I also offer tailor made protocols for your individual situation, please contact our office for product prices and distance patient information (714) 639-4360

H. Pylori Articles:

Updates:

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

March 28, 1011 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.

1. Gunji T. Helicobacter pylori infection significantly increases insulin resistance in the asymptomatic Japanese population. Helicobacter. 2009 Oct;14(5):144-50.
2. Polyzos SA. The Association Between Helicobacter pylori Infection and Insulin Resistance: A Systematic Review. Helicobacter. 2011 Apr;16(2):79-88. doi: 10.1111/j.1523-5378.2011.00822.x.