Undoctored Advanced Topic, we first consider H. pylori and its consequences,
as well as how to identify and eradicate it, a project that you have the option of
tackling on your own without the doctor. We then consider hypochlorhydria, the
lack of stomach acid that can result from H. pylori infection or from
Helicobacter pylori—Disrupter of Stomach Health
Into the delicate balance of stomach acid production enters a microorganism
that first infected humans around the time that primitive humans first migrated
out of Africa, but became common somewhere around the advent of the industrial
age: Helicobacter pylori, or H. pylori.
H. pylori has an interesting history in the medical world. For centuries,
gastritis, heartburn, and stomach and duodenal ulcers were viewed as the
product of stress, consuming acidic foods, and myriad other explanations,
often treated with ineffective advice to avoid vinegar, tomato sauce, other
acidic foods and drink more milk. Then two Australian researchers, Barry
Marshall and Robin Warren, upended the entire gastroenterology world by
identifying H. pylori in the base of human ulcers, publishing their
observations in 1984. Infection by this organism
explained why people treated with only stomach acid-suppressing drugs
frequently experienced relapse or inadequate relief from symptoms.
Unfortunately, Marshall and Warren were ridiculed and ostracized from
medical circles (even prompting Marshall to infect himself with
H. pylori, then have biopsy-proven gastritis develop).
Subsequent work, however, proved them right, earning them a Nobel
Prize for Medicine 20 years later in 2005. It is now clear that
stomach and duodenal ulcers that are not caused by aspirin or
anti-inflammatory drugs (such as naproxen or ibuprofen) are
all caused by H. pylori.
It has since become clear that H. pylori is
ubiquitous, a parasite that can be found in about 15-35% of Americans
(variation due to age, geography, and other factors), 50% of people
around the world, with increasing likelihood of infection as we age.
While originally identified as the cause for ulcers, then gastric
cancer, it has become clear that H. pylori is responsible for
a lot more, including alterations in bowel flora composition further
down the gastrointestinal tract from the stomach.
H. pylori: More than ulcers
Among the health conditions that have been associated with H. pylori are:
- Increased stomach acid (hyperchlorhydria)—Particularly in
younger people in which H. pylori infects the antrum of
the stomach (towards the duodenum). This explains why acid reflux,
reflux esophagitis, and ulcers respond to stomach acid-blocking drugs,
the H2 blockers and PPIs, and why 80-95% of people positive for
H. pylori develop stomach or duodenal ulcers. In later
phases, hypo- or achlorhydria, i.e., low or absent stomach acid, can
develop, the situation that sets the stage for stomach cancer. (The
World Health Organization has classified H. pylori as
a class I carcinogen.) Note that acid-blocking drugs can also
provide relief from acid reflux and esophagitis, conditions separate
from H. pylori-based issues.
gastrin hormone levels—If hypo- or achlorhydria develop from
H. pylori, increased gastrin hormone secretion in response
to the lack of stomach acid can, over time, lead to stomach cancer, as
gastrin provokes proliferation of stomach lining. Stomach cancer is the
third most common form of cancer worldwide with H. pylori
as the leading cause.
- Skin rashes—A variety of skin rashes have been associated with
H. pylori, but persistent psoriasis
and rosacea are among the most common. In the case of rosacea,
eradication of H. pylori is more effective in
reversing the rash than modern rosacea treatments.
disease—Especially virulent varieties of H. pylori
(that express the CagA toxin) are more likely to be found in people who
develop heart disease.
thrombocytopenic purpura (ITP)—An uncommon condition in
which blood platelet counts dip dangerously low and bruising and
hemorrhage can occur.
conditions—The list of autoimmune conditions that accompany
H. pylori and recede with its eradication continue to
grow and includes ITP, Sjogren’s syndrome, Henoch-Schlonlein
purpura, some forms of autoimmune nephropathy (kidney disease) and
- A variety of lung diseases–Such as chronic
bronchitis and other
- Parkinson’s disease—People with Parkinsonism have greater
likelihood of having H. pylori with improvement in
Parkinson’s symptoms with eradication.
- Small intestinal bacterial overgrowth (SIBO)—may occur along with
H. pylori in as many as 50% of people diagnosed with either.
- Fatty liver, insulin resistance, inflammation—This combination of
abnormalities improve with H. pylori eradication.
- Deficiencies of vitamin B12, vitamin D, and iron
cancers that include lung, liver, biliary, and pancreatic.
In other words, H. pylori is not just about stomach and
duodenal ulcers, but has wide implications for health across many health conditions.
Oddly, over the tens of thousands of years that this bacteria has coexisted
with humans, it may also have developed the ability to provide beneficial
effects such as modest reduction in
potential for asthma, some forms of allergy, inflammatory bowel disease,
and and cancer. On balance, however, the benefits of eradication of the
bacteria outweigh the modest potential for benefit.
H. pylori is therefore more like E. coli or
Staphylococcus aureus, i.e., species that can inhabit the human
body without harm but have potential to exert pathological effects when
circumstances permit, and less like, say, a Lactobacillus species
that provides benefits but poses almost no pathogenic potential. It is
therefore helpful to 1) identify whether you harbor this organism,
then 2) take steps to suppress or eradicate the organism. It is
a hotly-debated question whether people without symptoms or other
outward manifestations should pursue such a course, so it is a question
to decide on your own. But you will have Undoctored tools to do so on
your own, should you choose.
Identifying the presence of H. pylori
Unlike some issues in the Undoctored world such as SIBO in which identifying
the condition can be a bit tricky, identifying the presence of
H. pylori is straightforward. There are several choices.
The old way was to perform an endoscopy and examine a stomach biopsy
sample for the presence of the organism by culturing it; this is not
the best way as, besides involving an invasive procedure, it can often
fail to identify the organism even when it is present.
We therefore have access to several other methods that have advantages,
including being available directly to consumers, if necessary. Among the
methods available to you are:
- Blood testing—for presence of the IgG antibody against
H. pylori that has been shown to be a fairly reliable,
though not infallible, test, identifying around 85% of infections.
Downside: It cannot distinguish between active infection or prior
infection, a problem if trying to assess response to efforts to
eradicate H. pylori. The IgG test is therefore most
useful for initial identification, but not for follow-up. Several
direct-to-consumer labs make this available, including finger stick
test kits, though the number of labs offering it are diminishing as
breath testing and stool antigen testing have been proven to be
superior and useful for follow-up after treatment. One particularly
convenient test is the SELFCheck Stomach Ulcer Test that requires a
finger stick and yields results in 10 minutes and does not have
to be mailed to a laboratory.
- Urea breath test—Is relatively easy to perform, has high reliability
(sensitivity, specificity) for detecting the presence of
H. pylori, and can be used to both identify initial
presence and effects of eradication efforts. Downsides: It involves
drinking orange juice in (what we would regard as) an excessive quantity,
requires a pre-testing fasting period, and also requires radioactive
carbon, though the quantity of radiation is low. Urea breath testing
is also available via direct-to-consumer lab services in most states.
Note that taking a PPI drug such as Prilosec, Protonix or Aciphex reduces
the reliability of test results; for this reason, people are typically
advised to hold off taking a PPI for 2 weeks before conducting the
test. Also, urea breath test can yield a misleadingly positive result
for H. pylori if urease-containing species such as
Klebsiella and Streptococcus are present, an issue
when hypochlorhydria, autoimmune stomach inflammation, or SIBO are present.
- Stool antigen testing—Examining stool for evidence of the presence of
H. pylori has emerged as the preferred method of identification,
as it is the most accurate, less costly than urea breath testing, involves
no radioactivity, and no period of pre-test fasting is required. It is also
useful to monitor treatments effects. Note that a sample for stool antigen
testing should not be obtained if stool is unformed or watery as the
concentration of the H. pylori antigen is diluted; obtain
a sample when stool is solid. Several direct-to-consumer testing
services are available such as RequestATest and Verisana.
Interestingly, tongue color has been used in traditional Chinese medicine
as a means of identifying H. pylori that has proven to be
a fairly reliable sign when compared to conventional testing methods.
Yellow, red, and purple discoloration and/or a “greasy”
texture has proven to be highly suggestive of the presence of
H. pylori, though its absence cannot be used to prove
that the organism is not present.
Management of H. pylori
Conventional treatment of H. pylori involves so-called
triple or quadruple therapy that consist of the antibiotics clarithromycin
or amoxicillin, bismuth (e.g., PeptoBismol), a PPI drug such as omeprazole,
and the antibiotic metronidazole. The effectiveness of these combinations
has been declining in recent years, presumably due to
H. pylori’s ability to resist antibiotics with
eradication rates between 60 and 80%. This has sparked efforts to find
alternative agents, including supplements and nutritional agents.
Clarithromycin is also known to have substantial toxic effects.
The science on management of H. pylori has not progressed
to the point of allowing us to craft a specific Undoctored approach, but
here are some strategies to consider:
Probiotics—Probiotics alone have not been shown to eradicate
H. pylori but have been demonstrated to modestly improve
treatment efficacy when combined with conventional therapy, though the
species responsible for these effects are not clear. Because of this, it
is likely worth including a broad spectrum, high-potency probiotic as
part of your H. pylori eradication efforts. The
L. reuteri strains that we use in our yogurt have also
been shown to suppress (though not eradicate by itself)
H. pylori via production of antibacterial bacteriocins and
hydrogen peroxide. L. reuteri is also resistant to stomach
acid and bile and is able to colonize the stomach, effects that protect
against H. pylori overpopulation.
Lactobacillus rhamnosus GG has also been shown to
help suppress H. pylori.
Nigella sativa—The seeds of this plant have been used for
thousands of years in southern Europe, the Middle East, and Asia for
treatment of a variety of disorders, as well as food, used much like
poppy seeds to top baked products. It has come under study most recently
as a source for antibacterial compounds. A recent small clinical
trial demonstrated that 2 grams (approximately 1 level teaspoon)
of the ground seed eradicated H. pylori in 67% of people,
nearly as effective as conventional triple therapy. Nigella sativa seeds
are available from a number of online retailers.
Mastic gum—The oddly-named mastic gum is a traditional food
and folk treatment for stomach upset in Greece and the Mediterranean
dating back 2500 years, sourced from an evergreen shrub that grows
in that region. There is evidence that even one milligram per day taken
over two weeks can eradicate H. pylori and thereby heal
peptic ulcers, though higher doses were typically used in the few small
clinical trials. In one clinical trial, 350 mg three times per day
and 1050 mg three times per day over 14 days eradicated
H. pylori in one-third to one-half of participants.
(Also see below.)
Proton pump inhibitors (PPIs)—PPIs are widely overprescribed
for suppression of stomach acid and esophageal reflux, even when stomach
acid is deficient. Nonetheless, PPIs exert suppressive effects on
H. pylori by blocking the action of several bacterial enzymes,
as well as disrupting the acidic environment that is hospitable to
H. pylori. For these reasons, while PPIs alone are
ineffective for eradication, conventional triple or quadruple therapy
for eradication of H. pylori includes a PPI such as
omeprazole (Prilosec) to increase efficacy. Long-term PPI use has been
shown to disrupt intestinal flora, so this should be limited to a
Bismuth subsalicylate/subcitrate—Available over-the-counter
as Pepto Bismol, bismuth was the original treatment for H. pylori
in combination with H2 blocking agents. This antacid and antidiarrheal
was, in the early history of H. pylori eradication efforts,
nearly as effective as modern triple or quadruple therapy, but has become
less effective in recent years. However, it may still provide advantage
when used in combination with other efforts.
Vitamin C—Vitamin C 500 mg twice daily taken orally
has, in several studies, demonstrated an H. pylori-reducing or
eradicating effect, particularly when used along with other therapies. This
may be due to vitamin C’s ability to block the urease enzyme
expressed by H. pylori. There is some suspicion that
intravenous vitamin C may achieve blood levels that hold greater
potential for eradication.
N-acetyl cysteine (NAC)—NAC is a biofilm disrupter, i.e.,
it disrupts the mucous layer that H. pylori produces for its
own protection. Administration of NAC (in a variety of different dosing
regimens, e.g., 600 mg once or twice per day) has been shown to
substantially improve treatment efficacy in combination with conventional
therapies, including in people who have proven resistant to conventional
treatment, presumably by making the organism more susceptible to antibiotics.
Given the growing resistance of H. pylori to conventional
therapies, there have been increasing efforts to identify additional
alternative or additive treatments. There are preliminary data to suggest
that key lime, the juice of the bergamot fruit, polyphenols from almonds,
the traditional Chinese treatment Chenopodium ambrosioides L,
extracts of the Mallotus philippinensis plant from Pakistan, and
some traditional yogurts and kefirs containing various Lactobacilli and
yeasts may also provide suppressive or eradicative effects.
A combination of natural agents was used in a small study of 39 participants
that yielded successful eradication of H. pylori by stool
antigen testing in 29 (74.3%), on a par with conventional three- or
four-drug treatment. The regimen used was:
- Mastic gum (Jarrow Formulas, Los Angeles, California ):
500 mg, 1 capsule 3 times daily
- Emulsified oil of oregano as A.D.P. 50 mg (Biotics Research
Corporation): 1 tablet 3 times daily
- Pepto-Bismol: 4 to 6 tablets daily in divided doses between meals
In addition, a probiotic containing 5 billion CFUs of 10 species
taken twice daily (Vital 10, Klaire Laboratories) and a prebiotic
fiber supplement were included.
The composition of bowel flora changes with eradication of
H. pylori, though it is not clear whether these changes are
favorable or not. While bacterial species diversity is unchanged, the
relative percent of Firmicutes species increases while Bacterioidetes
decreases and (potentially pathogenic) Proteobacteria also increases.
The meaning and consequences of these shifts in bacterial populations
are of uncertain significance, but suggest that purposeful efforts to
restore presumably healthy bacterial species may be in order.
The Undoctored Approach to H. pylori
In the Undoctored experience, 80% of people with symptoms of gastroesophageal
reflux respond to the elimination of wheat and grains, freeing them of the
need for long-term acid-suppressing medications and the health-complicating
issues they introduce. The remainder who have persistent symptoms typically
have small intestinal bacterial overgrowth, SIBO, that requires specific
efforts to confirm, then correct and manage. (See the Undoctored
Protocol for SIBO in this Inner Circle.)
However, this does not address the presence of H. pylori. If
there is a history of stomach or duodenal ulcers, persistent acid reflux
symptoms despite the above efforts, or SIBO is present, efforts should be
made to determine whether H. pylori is part of the picture.
On balance, eradication of H. pylori yields advantages in
long-term health and strong consideration should be given to confirming
with a IgG blood test, stool antigen or urea breath testing. The
combination of mastic gum, oil of oregano, Pepto Bismol, with a probiotic
and prebiotic fibers, perhaps with efficacy enhanced with the
biofilm-disrupting properties of N-acetyl cysteine, would be a reasonable
regimen to start, treatment that appears to not hold the same bowel
flora-disrupting effects of standard antibiotic treatments.
In addition, because H. pylori can interfere with nutrient
absorption, it would also be helpful to assess the status of iron,
vitamin B12, and vitamin D.
The production of stomach acid is a basic requirement for human digestion, as well
as protection from foreign microorganisms contained in food and water that
humans ingest and microorganisms that ascend up from the lower reaches of the
bowels. The acidic environment of the human stomach is so powerful that, if you
were to insert your finger into stomach contents, you wouldn’t have much
left besides bone within a few minutes. The stomach lining therefore maintains
a complex protective mechanism that allows it to produce the acidic material
that breaks down food yet protects itself from this potentially toxic mix, a
fascinating and delicate balance.
Along with production of hydrochloric acid, the stomach maintains a continuous
mucous lining, or biofilm, that coats the stomach for its protection. The
parietal cells of the stomach lining produce acid, while other cells produce mucous.
Disorders of stomach acid production, despite being common, yield a confusing
array of symptoms since, for example, excessive stomach acid causes similar
symptoms to inadequate stomach acid.
The two most common causes for low stomach acid, hypochlorhydria, are
H. pylori infection of the stomach and autoimmune gastritis.
While H. pylori can cause hyperchlorhydria (increased stomach
acid) early in the infectious process, hypochlorhydria (low stomach acid
later) is a common late manifestation. Because the symptoms of hyperchlorhydria,
hypochlorhydria, and esophageal acid reflux are similar, it is not uncommon
to see people taking stomach acid-suppressing medications for years for the
For instance, if H. pylori leads to hypochlorhydria, taking a
proton pump inhibiting drug like Prilosec or Aciphex provides no benefit
and may add to complications such as cultivating small
intestinal bacterial overgrowth, SIBO. Likewise, if esophageal acid
reflux was really SIBO all along—as it often is—it will not
respond to acid-suppressing drug, or respond only partially, while SIBO
(and all its long-term consequences) is unaddressed.
Stress is also a cause for increased stomach acid and can manifest as
symptoms of acid reflux or as ulcers when H. pylori is
present. (Ulcers in the absence of H. pylori is uncommon
and largely confined to people experiencing extreme physical stress
during hospitalization in intensive care units.)
It is, no doubt, a tangle, but a tangle that is most commonly not
disentangled by the cursory approach that dominates in most healthcare
settings, from the primary care doctor’s office who reflexively
prescribes stomach acid-suppressing drugs to the gastroenterologist
most interested in scheduling more endoscopies.
A pivotal decision-making issue is to therefore distinguish
hyperchlorhydria from hypochlorhydria.
Gastroesophageal reflux vs. ulcer: An important distinction
Even more common than stomach/duodenal ulcers are gastroesophageal reflux
and esophagitis, i.e., feelings of heartburn associated with reflux of
stomach contents, including stomach acid, up past the gastroesophageal
sphincter and into the esophagus. Relief provided by acid-suppressing
drugs is felt to be diagnostic of this condition, as is abnormal acid
measured with a pH meter or inflammation seen with endoscopy.
Problem: PPIs and H2-blockers are often prescribed to provide relief but
no effort is made to determine whether H. pylori is the
driver of excess stomach acid. You can imagine that the difficulty is
that H. pylori remains unidentified and its long-term
consequences unsuppressed, even if symptoms are relieved.
Should gastroesphageal reflux be identified as the cause of symptoms and
H. pylori is ruled out, then the question of small
intestinal bacterial overgrowth, SIBO, should be pursued, as many, if
not most, cases of acid reflux are really just reflections of undesirable
bacterial species that have ascended up the gastrointestinal tract.
While the prevalence of H. pylori in the U.S. has been
decreasing, the incidence of autoimmune gastritis is increasing. Of the
two common causes of hypochlorhydria, i.e., lack of stomach acid,
H. pylori and autoimmune gastritis, H. pylori
has been gradually decreasing due to efforts to eradicate this
microoganism, while the incidence of autoimmune gastritis has been increasing.
Autoimmune gastritis involves an autoimmune attack against the stomach
lining’s parietal cells. Loss of stomach parietal cells results in
hypochlorhydria that, in turn, leads to iron and vitamin B12
deficiencies. Iron deficiency results because stomach acid is required
to extract iron from food, while B12 deficiency develops because the
parietal cells no longer produce the so-called “intrinsic factor”
necessary for B12 absorption when it reaches the ileum further down
the intestinal tract. If uncorrected, iron deficiency can lead to a form
of anemia, microcytic (meaning small red blood cells), while
B12 deficiency can lead to a macrocytic (large red blood cells)
anemia. In advanced stages, the stomach lining becomes atrophied
(“atrophic gastritis”) and stops producing stomach acid
altogether. Identification of vitamin B12 or iron deficiency
should therefore prompt an investigation into whether hypochlohydria
is to blame.
Atrophy of the stomach lining, whether triggered by H. pylori
or autoimmune gastritis, results in reduction in stomach acid that, in turn,
causes levels of the hormone gastrin to rise in the bloodstream as a response
to try to increase stomach acid. An abnormally high gastrin blood level is
therefore a reliable sign that there is insufficient stomach acid present.
The high gastrin level also stimulates abnormal growth of the stomach
lining, a process that can lead to stomach cancer.
Autoimmune gastritis is closely associated with Hashimoto’s thyroiditis,
with over 50% of people carrying anti-thyroperoxidase
antibodies. It is also commonly associated with vitiligo, alopecia,
myasthenia gravis, autoimmune hepatitis, type 1 diabetes, and celiac
disease–conditions that are also all closely associated with wheat/grain
consumption. Up to 10% of people with type 1 diabetes, for instance,
develop autoimmune gastritis. A direct connection between wheat/grain
consumption and autoimmune gastritis has not yet been made, but many arrows
point in that direction. Autoimmune gastritis can also occur
in tandem with H. pylori infection, though it is not
clear whether H. pylori is a causal factor.
The conventional medical “solutions” to autoimmune gastritis, high
gastrin levels, and stomach atrophy are—no surprise—generally
unsatisfactory, solutions such as removal of the stomach or blocking the
action of the hormone gastrin with the drug, netazepide.
Identification of autoimmune gastritis therefore typically involves:
- Suspecting the presence of autoimmune gastritis if symptoms of acid
reflux, esophagitis, heartburn, or unexplained abdominal discomfort
are present, or feeling full with a modest quantity of food or the
feeling that food remains in the stomach for extended periods
- If symptoms of acid reflux fail to respond to stomach acid-blocking
drugs, PPIs and H2-blockers
- Identifying increased blood levels of anti-parietal cell antibodies
and anti-intrinsic factor antibodies
- Suspecting the presence of autoimmune gastritis if H. pylori
has been ruled out as a cause of hypochlorhydria or if symptoms of
esophageal reflux/esophagitis persist despite eradication of
- If iron deficiency or vitamin B12 deficiency are present and without
- If there is poor response to vitamin D supplementation
- If SIBO is recurrent and without other explanation (e.g., stress,
PPI drugs, course of antibiotics, etc.)
Because most autoimmune inflammation recedes with adoption of the Undoctored
Wild, Naked, Unwashed strategies, the same efforts should be made to subdue
or reverse autoimmune gastritis if identified, namely wheat/grain/sugar
elimination, vitamin D, magnesium, EPA + DHA from fish oil, iodine and
thyroid optimization, and basic efforts to cultivate healthy bowel flora.
As with hypochlorhydria from H. pylori, the status of iron
and vitamins B12 and D should be assessed.
Unfortunately, however, once autoimmune gastritis damages the parietal cells
of the stomach, the parietal cells do not regenerate and you can be left
with persistent hypochlorhydria, nutrient deficiencies, symptoms such as
reflux, and increased risk for SIBO. While unproven, acidification of the
stomach appears to relieve symptoms of reflux, heartburn, and intolerance
to protein digestion. It is not clear, however, whether stomach acidification
reduces levels of gastrin, has any impact on risk for stomach cancer,
impacts the likelihood of SIBO, or can improve nutrient status.
Among the choices in methods to acidify stomach contents are:
Carbonated beverages—Consumption of a carbonated beverage
before or during meals that acidifies the stomach contents may partially
replace the functions of stomach acid such as breakdown of dietary proteins.
The level of acidity achieved is modest with a pH of 2.5 typically
achieved, not the pH of 1-2 of natural stomach acid production.
It is not clear how much such a practice will restore effects such as
vitamin B12 and iron absorption. However, be aware that repeated
contact of highly acidic beverages with teeth may add to dental decay.
Vinegars—Vinegar, e.g., 1-2 tablespoons before or during meals,
as with carbonated beverages, helps acidify stomach contents. Apple cider
vinegar is the most popular for this purpose, since it also contains probiotic
bacterial and fungal species, but other vinegars work, as well. Vinegars
suffer the same dental hazards as carbonated beverages.
Betaine HCL—Betaine HCL dissociates in the stomach into
betaine (a naturally occurring compound found in food) and hydrochloric
acid and is the most effective means of acidifying the stomach contents,
recreating the very acidic pH of normal stomach acid
production (0.6-2.0). Effective doses range from 750 to 1500 mg
prior to or during a meal that yields an acidic pH within 2-12 minutes
of ingestion and maintains an acid pH for about 75 minutes after
consumption (though can be as brief as 30 minutes or as long as
120 minutes in some individuals). Because of the more effective
acidification achieved with betaine HCl, along with the absence of
dental issues, betaine HCl is the preferred method of acidifying the
stomach when hypochlorhydria is present.
Due to the uncertainties with efforts at stomach acidification, it is worth
tracking blood levels of iron and vitamins B12 and D over
time, as well as being alert to the signs of SIBO.
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