“Abdominal pain – you most sour and unpleasant thing. Your many faces are so plain to see but I still don’t know your name. Heartburn, chronic active gastritis, GERD, acid reflux, achlorhydria, H. Pylori or SIBO – that is the question.” William Shakespeare, 1602, after a night of strong ale and under-cooked guinea fowl.
My H. pylori Story – It was the Summer of 1992 and I was just opening up my solo practice. It was a time of excitement for my new journey and a time of stress caused by the three most influential stressors in life: all that is money, all that is love and all that is me. I remember the exact second the pain hit me. I was having a Coors light with some friends. The first few sips were fine. Then another sip and boom, the bomb went off. It felt exactly as if 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. This pain was not relieved by antacids, eating or not eating. I just sucked-it-up, for the time being and decided I had to get this figured out NOW. The stress of opening up my practice wasn’t going to go away in the next five minutes, so I needed to apply my “medical detectiveness” and reverse engineer the pathophysiology of the condition, to figure out the cause. Knowing the cause and predisposing factors would help me to apply the precise treatment.
My First Clue – Differential Diagnosis
Applying ‘differential diagnosis’ I knew there had to be one or more of these going on: Heartburn, H. pylori, Chronic Active Gastritis, GERD, hyperchlorhydria, hypochlorhydria and/or SIBO. The question at hand: Are the conditions above actually caused by too much stomach acid (hyperchlorhydria) or by the lack of stomach acid (achlorhydria)? They can be caused by both, but more likely they are due to the latter. Each needed to be worked-up.
Second Clue – My Predisposing Factors
1. Chronic Dehydration and Electrolyte Imbalance – based on a blood chem panel and the fact that I was not consuming much water and drinking too much coffee (diuretic). 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 (HCl) 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, which as we all know can cause low HCl and gastric inflammation all by itself.
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 Helicobacter pylori (H. pylori) infection and/or low calcium, sodium and chloride, 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 and H2O 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.
Third Clue – Diagnostic Testing
After some diagnostic testing: allopathic (traditional medicine), which included CBC, chem panel, Doctor’s Data mineral hair analysis, 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 and an electrolyte imbalance.
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.
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 . 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 world’s 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 . It has also been shown to be associated with extra-gastric 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 First H. pylori Treatment Protocol
(Make sure to read the 19 August 2014 update below)
Pre-treatment: I took antacids (over the counter – Zantac OTC, an H2 blocker – NO PPI) to reduce HCl levels, increasing the susceptibility of the H. pylori to treatment/eradication by reducing H. pylori’s need to defend itself so vigorously) and allow my gastric mucosa a chance to heal.
Note: H. pylori and other gram-negative bacteria form 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 (HCl) and other substances, like antibiotics. Being a complex matrix of proteins and carbohydrates, which are probably interdependent, the H. pylori biofilm offers 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.
Treatment: My personal H. pylori bomb consisted of Monolaurin (lauric acid) or Lauricidin (Antiviral and Antibacterial Actions of Monolaurin, Lauricidin, and Lauric Acid) – also see coconut oil, which is 50% lauric acid by weight) and H-PLR (K-32) (a bactericidal agent) 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 (stool test), and was free of the foreign invaders, breath test confirmed the same.
Treatment update September 2009: I’m now adding in Klaire Labs – InterFase Plus, to my all future H. pylori protocols. 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 its attributes. Also, read about my biofilm protocol. Additional products that were taken during this 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 now integrated into the H. pylori elimination Protocol in every case.
Certain dietary restrictions and supplement additions will be added in. These are determined on a case by case basis and based on many factors. The two that are required for everyone is: avoid all cow’s milk and gluten containing products.
Prevention and Healing: Now it’s time 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.
*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 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. Its healing capabilities, as far as I am concerned, are quite profound on the gastric mucosa.
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.
Important Treatment Protocol Updates:
IMPORTANT! PLEASE READ! Updated, Update – 19 August 2014 (Original: 08 Aug 2013): I have been helping patients with H. pylori, a biofilm-producing, gram-negative, bacteria, since late 2007. In the beginning, eradicating this bug, in my opinion, was very easy. 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 H. pylori strains that are now multiple drug-resistant, especially to clarithromycin. Medically there is just no real good explanation for this, especially in such a short period of time. Energetically speaking, 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 the same result. Also, there are many, random people, contacting me to let me know that they have undergone triple and quadruple therapies to no avail. This proves in my mind, that biofilm itself and/or the bacteria that create them, are learning to defend themselves more effectively. They are adapting and mutating, genetically and energetically, 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. All treatment are merely substances and at their core, energy. This self-treating is not killing the H. pylori or eliminating the biofilm but to the contrary, making them both stronger by building up their innate 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 are effective treatment options still available, it may just take a little more time and/or more products, allopathic (Prevpac or Pylera) combined with specific nutraceuticals and biofilm disruptors 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 is not one of them. This is just my opinion.
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.
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, 1011, Update – Helicobacter pylori infection have 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.