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Purpose of running this test:

This test examines your stool for the antigenic components of the bacteria H. pylori that may be detected when you have an active H. Pylori infection.

H.pylori has been associated with ulcers, acid reflux and cancer. My experience has been that there is a particularly high incidence of H. Pylori infection in children with autism, and that up to one third of the adult population may also be infected. If you have acid reflux, consistently low gut pH, high suberic acid on a MAP test, along with high arginine on a UAA, high level bismuth excretion on mineral tests in the absence of any bismuth support, then you should consider an H. Pylori Stool Antigen Test.

Wide swings in gut pH on either contemporaneously run or repeat CSA/GI Effects tests, such as a pH of 5 on one test and pH of 7.5 or 8 on another, may be an indirect indication of H. Pylori infection. While H. Pylori is initially attracted to low pH conditions in your GI tract, once it becomes firmly established, it produces the compound urease, which increases gut pH so it can thrive. This may cause wide swings in the pH of your GI tract on testing.

Pylori is able to sequester itself between the mucosal cells lining your stomach. There it is given additional protection by the thick layer of mucus that lines the inside of your stomach. As a result, the antigenic components of H. Pylori may not be detected. If active H. Pylori infection is present, it should be possible to identify these antigens with this test. Therefore, a positive antigen test is significant; however, a negative test does not rule out the presence of this organism.

A urease breath test can also be run through your doctor that indirectly indicates the presence of H.pylori. If H.pylori infection is established, and the organism is making urease in sufficient amounts, then the breath test will indicate its presence.

Ideally, a DNA probe test should also be run. This test would rule out the presence of H. Pylori that has not stimulated antigen formation by your immune system, but from which the DNA is able to be detected. I continue to search for a DNA test to be run in conjunction with this antigen test in order to offer you a comprehensive assessment of the H. Pylori that your body may harbor.

Result This table contains the rationale behind my suggestions. These suggestions are for your consideration. Defer your choices to your own health care practitioner, as always.
H.pylori positive antigen test The approach I suggest for consideration with your doctor is designed to interfere with a number of aspects of H. pylori function. This approach addresses the excess mucus that enables H. pylori to remain undetected in your GI tract, and makes the organism more accessible to anti-infective agents. It includes supplements that may limit H. pylori growth, those that generate a healthy level of inflammatory mediators, and balancing nutrients such as carnitine that H. pylori may compromise. Suggestions for consideration for supplementation with natural supports can include HELX nucleotide blend, Bowel Support nucleotide blend, cycling on and off Peptimycin, and Potassium Bicarbonate or sodium bicarbonate. The choice of sodium or potassium is dependent upon your levels of these minerals on a HMT and UEE. Consider low dose Hydroxy B12 and Adenosyl B12 once lithium is in balance, in addition to Potassium, Magnesium, and Biotin. Stomach pH Balancing nucleotide blend, Buffer pH, and VitaOrgan work to balance the gut pH. Also consider Carnitine, and low doses of both Ion Transport compound and Ion Transport nucleotide blend. Although the natural H.pylori approach presented above suggests the use of multiple supplements/herbs simultaneously, the same is true for a traditional medical approach to this organism. H.pylori is difficult to eradicate, so it requires a number of compounds over time, and a concerted effort to address this microbial imbalance. Standard medical approaches can be employed with the help of your doctor. These traditional approaches involve the use of multiple antibiotics and additional pharmaceuticals, including proton pump inhibitors and a source of bismuth and bicarbonate. For standard approaches see: http://www.globalrph.com/antibiotic/hpylori.htm and http://www.uptodate.com/contents/treatment-regimens-for-helicobacter-pyloriIt has been observed that the number of individuals with autism testing positive for the bacterium Helicobacter pylori is much higher than would be expected. One third of the adult population is reported to harbor H.pylori. In contrast, this number is generally not as high in the pediatric population. I have found that the autistic population is as high as 50 percent and that has been found by others to be in that range too. Changes in the mucous layer environment in children with autism may be a predisposing factor that accounts for this observed increase in H. pylori in that population.Helicobacter pylori is a Gram-negative, spiral-shaped bacterium that lives in the mucous layer of the stomach and duodenum. This ulcer-causing gastric pathogen is able to colonize the harsh acidic environment of the human stomach. Although the stomach is protected from its own gastric juice by a thick layer of mucus that covers the stomach lining, H. pylori takes advantage of this protection by living in the mucus lining itself. In the mucus lining, H. pylori survives the stomach’s acidic conditions by producing urease, an enzyme that catalyzes hydrolysis of urea into ammonia and bicarbonate. As strong bases, ammonia and bicarbonate produce a cloud of alkalinity around the bacterium, making it impossible for the body’s normal defenses such as T cells, natural killer cells, and other white blood cells, to get to it in the gastric mucus layer.

Because H. pylori burrows into the mucus layer of the stomach and is very persistent there, it is difficult to get a positive test for it even when it is present. In addition, H. pylori can remain for long periods of time and is extremely difficult to eradicate. Many factors that have been identified as playing a role in autism are related to H. pylori, including problems with gluten and casein, breakdown of glutathione, excess stomach acid, and the high norepinephrine seen in ADD and ADHD. H. pylori affects neurotransmitters and brain neurochemistry. H. pylori infection increases the incidence of food allergy by facilitating the passage of intact proteins across the gastric epithelial barrier. H. pylori depletes secretin, which has previously been reported to have positive impacts in some cases of speech delay.

Arginine makes urea to neutralize stomach acid, or, alternately, makes an intermediate such as nitric oxide that relaxes blood vessels. When H. pylori infection is present, it induces arginine to produce urea as opposed to nitric oxide because urea provides the alkalinity necessary for its survival. In this way, H. pylori depletes arginine through its overuse of the enzyme arginase. The depletion of arginine impacts the mitochondria, reducing mitochondrial energy production from glucose.

When H. pylori infection is present, it changes the way important phospholipids are positioned in the cell membrane. Phospholipid orientation has been described as playing a role in ADD/ADHD, as well as in immune system signaling. H. pylori also decreases levels of B12 in the body; decreases iron levels; increases ammonia and taurine; and can produce glaucoma in young individuals that resolves when the H. pylori is treated.

H. pylori infection is not just an immediate acute infection. Rather, it is a long-term, chronic problem that may take months or years to eradicate. Chronic H. pylori gastritis alters feeding behaviors, delays gastric emptying, alters gastric neuromuscular function, and impairs acetylcholine release. These effects can persist for months after the infection has been eradicated. Please watch the H. pylori DVDs to understand more fully the rationale behind this program and the magnitude of the impact H.pylori can have on your body.

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Related Tests to Run

While a positive antigen test is significant and indicative of H.pylori, since H.pylori can hide from the immune system a negative result on this antigen test is not totally conclusive. Ideally a DNA based molecular probe test would be run to check for H.pylori but at this time that form of testing is not available. Indirect indicators of H.pylori infection can be inferred from running a number of other tests including a CSA to look at gut pH, a GI effects test to look for a prevalence of anaerobic organisms, a MAP test which shows high suberic when noted in conjunction with a UAA showing high arginine in the absence of other elevated amino acids. Most telling is the presence of chronic gastic reflux from a clinical standpoint.

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