Helicobacter pylori (stomach ulcer bacteria)

[Swarfmaker]

Someone on one of the Alz.org message boards alerted us to this
article about the stomach ulcer bacteria Helicobactor pylori:

"Eradication of Helicobacter pylori may be beneficial in the
management of Alzheimer's disease"
Abstract Infectious agents have been proposed as potential causes of
Alzheimer's disease (AD). Recently, we documented a high prevalence of
Helicobacter pylori (Hp) infection in patients with AD. We aim to
access the effect of Hp eradication on the AD cognitive (MMSE: Mini
Mental State Examination and CAMCOG: Cambridge Cognitive Examination
for the Elderly) and functional (FRSSD: Functional Rating Scale for
Symptoms of Dementia) status parameters. In the first part of the
study, a total of 50 consecutive patients with AD and 30 age-matched
anaemic controls underwent an upper gastrointestinal endoscopy, and
gastric mucosal biopsies were obtained to detect the presence of Hp
infection by histologic analysis and rapid urease test. Serum anti-Hp-
specific IgG level was analysed by enzyme-linked immunosorbent assay.
In the second part, Hp-positive AD patients received a triple
eradication regimen (omeprazole, clarithromycin and amoxicillin), and
all patients were followed up for 2 years, while under the same
treatment with cholinesterase inhibitors. Hp was detected in 88% of AD
patients and in 46.7% of controls (P < 0.001). Hp eradication was
successful in 84.8% of treated patients. At the 2-year clinical
endpoint, cognitive and functional status parameters improved in the
subgroup of patients where Hp eradication was successful (P < 0.001
and P = 0.049 for MMSE and CAMCOG, respectively; P < 0.001 for FRSSD),
but not in the other patients. Hp eradication may positively influence
AD manifestations, suggesting a possible common link between Hp and
AD.
http://www.springerlink.com/content/83147756538x7031/?p=4d07d65b60894df3bab4620921dcd1e6&pi=2

What caught my attention is this statement: "At the 2-year clinical
endpoint, cognitive and functional status parameters improved in the
subgroup of patients where Hp eradication was successful ..., but not
in the other patients. Hp eradication may positively influence AD
manifestations, suggesting a possible common link between Hp and AD."

I have to connect the links here to AD here.

We've recently read that corrupted tau proteins can have
characteristics similar to the prions of "mad cow disease", scrapie,
chronic wasting disease of deer, and CJD of humans:
"Rogue protein 'spreads in brain'"
BBC Sunday, 7 June 2009
Scientists have shown a rogue protein thought to cause Alzheimer's can
spread through the brain, turning healthy tissue bad. They believe the
tau protein may share characteristics with the prion proteins which
cause vCJD. When injected into the brains of healthy mice it triggered
formation of protein tangles linked to Alzheimer's. However, experts
stressed the Nature Cell Biology study did not mean tau could be
passed from person to person. Tau is a protein present in all nerve
cells, where it plays a key role in keeping them functioning properly.
But a rogue form of the protein can trigger the formation of protein
clumps within nerve cells known as neurofibrillary tangles. It is
thought that these tangles are likely to be a major cause of
Alzheimer's disease... Tau is a protein present in all nerve cells,
where it plays a key role in keeping them functioning properly. But a
rogue form of the protein can trigger the formation of protein clumps
within nerve cells known as neurofibrillary tangles. It is thought
that these tangles are likely to be a major cause of Alzheimer's
disease.
http://news.bbc.co.uk/2/hi/health/8084787.stm

But, can toxins produced by bacteria initiate the process?

"Profiling the culprit in Alzheimer's disease (AD): bacterial toxic
proteins - Will they be significant for the aetio-pathogenesis of AD
and the transmissible spongiform encephalopathies?" Schmitt HP.
Institute of Pathology, Department for Neuropathology, University of
Heidelberg, Germany
http://www.ncbi.nlm.nih.gov/pubmed/17337124?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Does a Hp infection explain the success some people have been
experiencing with the "perispinal Enbrel injections"? Enbrel is
thought to work by inhibiting the effects or the production (I don't
remember which right now) of "tumor necrosis factor", TNF-alpha. And
guess what substance a Helicobactor pylori infection in the stomach
causes the body to produce? Yep, TNF-alpha.

Has any of the AD patients you are caring for been checked for
Helicobactor pylori infection? Have they been treated for it?

I started thinking, what substances inhibit or eliminate Hp bacteria?
I've heard that Pepto-Bismol will (the bismuth in it). And then I
remembered that in Chinese medicine, cinnamon had long been used to
treat stomach problems. A quick search of the Internet found that yes,
indeed, cinnamon has been and is being investigated for its anti-Hp
potential. But, which component of cinnamon is it? I don't know. This
may mean that using whole ground cinnamon may be more effective than
using extracts.

A couple more points...

The degeneration tends to follow the path of neural networks:

"Neuronal subpopulations and genetic background in tauopathies: a
catch 22 story?"
L. Bue´e*, A. Delacourte
Neurobiology of Aging 22 (2001) 115–118
"...these vulnerable neurons degenerate following precise pathways.
Regarding encephalopathy such as PEP, it is clear that a virus follows
neural networks for its propagation. It is now well established that
there is also a sequential degeneration of vulnerable networks of
neurons in AD and PSP. In AD, both biochemical and neuropathological
studies show that NFT formation starts in the hippocampal formation
(from transentorhinal to entorhinal and then hippocampus), progresses
sequentially as follows anterior, inferior and medium temporal cortex,
and then spreads into polymodal association areas, unimodal areas and
primary and/or sensory areas..."
http://www.alzheimer-adna.com/pdf/2001/2001Bueecatch22.pdf

With respect to the relationship between Enbrel and H-pylori
infection...

In the full text of the Heliobacter article, it says on page 8,
"However, Hp, an extracellular bacterium, could affect the brain and
other target organs, such as the heart, indirectly, through the
release of numerous cytokines, including TNF-[alpha] acting at a
distance." I hadn't read that before. My earlier post about the link
between TNF-alpha and Hp infection came from reading a paper about the
prevalence of Hp infection. I'm glad to see that my guess was already
proposed by a professional researcher.

To me, this gives a reason for why the perispinal injection of Enbrel
should work, why reports of its success are not merely wishful
thinking. It's the link to a cause that validates the idea. I think
that the success of Enbrel also supports the theory for the mechanism
by which Hp in the stomach affects the brain.

For those getting the Enbrel treatments, I think this says, check to
see if there is also an H-pylori infection present. (There may be
other bacteria or viruses involved, such as Herpes simplex virus type
1 (HSV1) and Chlamydophila (Chlamydia) pneumoniae.)

Here is the link to the full text of the paper. Even for us non-
professionals, it is understandable enough to undestand the ideas:
http://www.springerlink.com/content/83147756538x7031/fulltext.pdf

Wild speculation time:
If an Hp infection turns out to be the beginning of the AD disease
process, then for those currently suffering with the disease, I would
first stop the progression, then eradicate the infection(s). We appear
to have two ways to stop the progression: Enbrel or the MCT oil
regimen. They don't seem to conflict, targetting different steps of
the disease process, so it would probably be wise to use both.

There are probably several conditions that eventually lead to AD. This
particular one would not address genetic causes or exposure to a
toxin. If it worked for 3 out of 4 cases, that would be a good start!

I doubt that this is the end of the story. Never the less, I think
that the idea of Helicobacter pylori being involved should be
aggresively researched.

Obviously, if eliminating a chronic bacterial infection reduces the
body's production of TNF-alpha to normal levels, there will be no need
for TNF-alpha blocking drugs such as Enbrel. This news will not be
greeted with enthusiasm by the pro-Tobinick faction, nor the "there's
nothing we can do, we're powerless, everyone should just die now"
crowd.

Even more points...

90% of the people with an Helicobacter pylori (Hp) infection do NOT
have stomach trouble or ulcers. Or, only 10% of people with an Hp
infection have stomach trouble.

I'm sure that the percentage of people with an Hp infection that will
develop AD is similarly small.

From what I've read, this bug is particularly hard to treat. They seem
to be using a cocktail of three drugs for something like 14 days. The
antibiotics can have side effects, making the treatment unpleasant.

I looked up the statistics for Aricept. It is only effective for 50%
of the people who take it, and then, it is only effective for about 6
to 12 months. If I were in charge of an insurance company, I think I
would consider the cost of treating an Hp infection followed by the
stabilization of the patient as a discount when compared to six months
worth of Aricept, followed by the cost of a nursing home.

If the statistics of this research hold true, then one could expect
the eradication of an Hp infection to be effective for about 75% of
those treated, and the effect should last at least 2 years (which was
the limit of how long they tracked the test participants).

There are some interesting charts in the full text .pdf file of the
paper:
http://www.springerlink.com/content/83147756538x7031/fulltext.pdf

"H. pylori gastritis produces no symptoms in 90 percent of infected
persons. The prevalence of H. pylori infection varies geographically
and has been demonstrated to be as high as 52 percent in the United
States. Factors associated with higher infection rates are increasing
age, African-American or Hispanic race, lower levels of education, and
birth in a developing country."
http://www.aafp.org/afp/20020401/1327.html

sulforaphane from broccoli sprouts seems to help...

"Broccoli Sprouts Good for the Gut"
Compound in Broccoli Sprouts May Protect Against Ulcers, Stomach
Cancer
By Jennifer Warner
WebMD Health April 6, 2009
http://www.webmd.com/digestive-disorders/news/20090406/broccoli-sprouts-good-for-the-gut

The original article was from researchers in Greece.

Another thought I had was that the treatment for Hp is a two or three
week course of multiple antibiotics. This probably knocks out a whole
bunch of other bacteria in all parts of the body. What if the culprit
is NOT Hp, but gets killed off by the Hp antibiotics?

Whatever the case, I think there are some simple tests such as a blood
test for Hp antibodies, or this "breath test" that could be done
relatively easily. I think it's worth asking the phsyicians about.

And finally, this concept may also apply to the other rare
neurodegenerative diseases such as PSP, CBD, the FTD, etc.

With regard to prescription antibiotics, you might find this
intesting...

I started thinking about other antibiotics. I read that methylene blue
is used
as an antibiotic to treat urinary tract infections, malaria, and even
bacteria
"infections" in fish aquariums. Does it also eliminate Hp? Could that
be why it
has helped people with AD (Rember study)? Well, maybe. I found this
article, but
I don't have the whole text. It is intriguing.

"Evaluation of methylene blue and triple therapy for eradication of
Helicobacter
pylori infection in the nude mouse model"
KARITA M. (1) ; TADA M. (1) ; OKITA K. (1) ; TSUDA M. ; NAKAZAWA T.
International symposium on Helicobacter pylori and its diseases No5,
Tokyo ,
JAPON (04/04/1992)
1993, vol. 5, SUP1 (6 ref.), pp. S79-S83
European journal of gastroenterology & hepatology

Abstract: "Objective: To determine how far Helicobacter pylori
infection can be eradicated with methylene blue and triple therapy
(amoxicillin, metronidazole, bismuth subnitrate), using a nude mouse
model. Methods: Four weeks after inoculation of H. pylori into the
stomach, two groups of nude mice were administered methylene blue or
triple therapy via the stomach for 1 week. A control group of nude
mice was given culture fluid alone after the inoculation. The number
of H. pylori and histological changes in the stomach were determined
weekly for 5 weeks, starting from the completion of drug
administration. Results: In the methylene blue treatment group, the
concentration of H. pylori was significantly reduced for 1-3 weeks
after treatment compared with the control group..."

Some more on broccoli sprouts...
Posted by BeckyP August 09, 2009 on the Alz.org message board:

Just got this in one of my newsletters.

When any kind of drug might be questionable, I look for healthy
alternatives. This might be one of them. Can't hurt, right?

Just for added info.

Better than Antibiotics in H. Pylori Battle: Broccoli Sprouts

Helicobacter pylori (H. pylori) bacteria presents a medical conundrum
-- while the gut bacteria has been implicated in ulcers and stomach
cancer, it also seems to confer protection against other health
problems, including esophageal cancer. What's a person to do? One
helpful strategy might be to eat broccoli sprouts. It seems they are a
natural way to help maintain H. pylori at a level that is helpful, not
harmful.

Sitting right next to the much more popular alfalfa sprouts in
groceries and health-food stores, these "baby broccoli plants" are
even better for you than in their grown-up form. New research from
Tokyo University of Science and Johns Hopkins University School of
Medicine investigated how regular consumption of broccoli sprouts
affected people with H. pylori infection, the frequent cause of peptic
ulcers and stomach cancer. The study included 48 H. pylori-infected
adults who were randomly assigned to consume 70 grams a day (about two
and one-half ounces) of either broccoli sprouts or alfalfa sprouts.
Researchers found that after eating broccoli sprouts for eight weeks,
participants significantly lowered biomarkers for H. pylori while
those who ate alfalfa sprouts did not show this benefit.

Jed W. Fahey, ScD, a faculty research associate in the department of
pharmacology and molecular sciences, was a study coauthor. He told me
that the active component against the bacterium is a phytochemical
called sulforaphane. This natural substance induces and boosts some of
the body's protective anti-inflammatory enzymes and also has
antibiotic properties particularly effective against some strains of
H. pylori. Broccoli sprouts are a much more potent source of
sulforaphane than is even the freshest broccoli, Dr. Fahey said.

A dietary source to combat H. pylori is excellent news for many
people. Estimates are that as many as 50% of Americans harbor the
bacteria, though they don't always have symptoms. However, when the H.
pylori runs rampant and causes infection, treatment can be tough --
typically it involves taking two different antibiotics simultaneously,
often in addition to a bismuth preparation or an acid-suppressing
protein-pump inhibitor. The end result of all this is, quite often,
yet another ulcer -- and, in about 20% of patients, it doesn't even
solve the problem.

Broccoli sprouts offer a natural alternative and an easy and tasty way
to combat H. pylori. Note, however, that the protective effect fades
if you stop eating the sprouts, so you should eat broccoli sprouts
regularly (two to three times a week). Dr. Fahey points out that they
keep for several days in the refrigerator and are wonderful in salads,
sandwiches and wraps.

Source(s):

Jed W. Fahey, ScD, faculty research associate, department of
pharmacology and molecular sciences, Johns Hopkins University School
of Medicine, Baltimore, Maryland.
http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/503105341?r=71710057\
1#717100571

Here's even more info for those interested:
http://www.raysahelian.com/sulforaphane.html

Let me go through my line of thinking about this again. Many people
with AD getting Dr. Tobinick's perispinal Enbrel treatments experience
benefits. Enbrel blocks TNF-alpha. Helicobacter pylori infections of
the stomach induce the body to produce TNF-alpha in its fight against
the bacteria. A study of 50 AD patients in Greece found that for 3 out
of 4, the treatment of H.pylori infection resulted in improved mental
abilities over the 2 years of the study. Therefore, treating an AD
sufferer for H.pylori has a good chance, 3 out of 4, of arresting the
disease. Broccoli sprouts contain sulphoraphane. H.pylori is inhibited
by sulphoraphane. Therefore, there is a chance that merely adding
broccoli sprouts to the diet of an AD sufferer will slow, halt, or
even reverse their decline.

If nothing else, it's a hell of a lot cheaper than Enbrel shots.

Put the following article together with the article I posted earlier
about Helicobacter pylori being a source for increased levels of TNF-
alpha, that the mental abilities of those AD patients successfully
treated by the researchers in Greece for Hp infection IMPROVED, and
that 2.5oz of broccoli sprouts 3 or 4 times per week will inhibit
certain strains of Hp, and... well, will there be an article some day
proclaiming that "Broccoli sprouts arrest Alzheimer's disease"?

(Read my previous posts online about this for more information.)

Infections May Lead To Faster Memory Loss In Alzheimer's Disease
ScienceDaily (Sep. 8, 2009)

"Getting a cold, stomach bug or other infection may lead to increased
memory loss in people with Alzheimer's disease, according to research
published in the September 8, 2009, print issue of Neurology®, the
medical journal of the American Academy of Neurology. The study found
that people who had respiratory, gastrointestinal or other infections
or even bumps and bruises from a fall were more likely to have high
blood levels of tumor necrosis factor-á, a protein involved in the
inflammatory process, and were also more likely to experience memory
loss or other types of cognitive decline than people who did not have
infections and who had low levels of the protein..."
http://www.sciencedaily.com/releases/2009/09/090907162306.htm

[Swarfmaker]

I was reading a thread on another message board about the effects of a
urinary tract infection (UTI) on someone with Alzheimer's disease or
other dementia. For those who don't know, a UTI is ofen the cause of
a sudden worsening of symptoms.

A question came to my mind. If a helicobacter pylori infection affects
the brain by way of TNF that the body produces to fight the infection,
what about a UTI? So, I did a quick Internet search on these two
phrases: "tumor necrosis factor" "urinary tract infection" OK, so I
think it is pretty clear that TNF levels increase when a UTI is
present. If "perispinal Enbrel injections" can reverse AD symptoms in
a matter of minutes by blocking the effects of TNF, then increased
levels of TNF due to a UTI should have the opposite effect.

Is it possible that common "toenail fungus" infection could be a
source for TNF-alpha???

Stimulation, inhibition and death of macrophages infected with
Trichophyton rubrum.
Campos MR, Russo M, Gomes E, Almeida SR.
Departamento de Análises Clínicas e Toxicológicas, Faculdade de
Ciências Farmacêuticas, Universidade de São Paulo, Avenida Prof. Lineu
Prestes, 580,
Bloco 17, CEP 05508-900, São Paulo, Brazil.

Trichophyton rubrum is the most common pathogen causing
dermatophytosis, accounting for approximately 80% of the reported
cases of onychomycosis. Since 90% of the chronic dermatophyte
infections are caused by T. rubrum, it is likely that this pathogen
must have evolved mechanisms that evade or suppress cell-mediated
immunity. Several reports have highlighted the participation of
phagocytes in the immune defense against fungi; however, few studies
have addressed the role of these cells in dermatophytosis. In this
study, we investigated the interactions of resident and peritoneal
macrophages with T. rubrum. We show here that the interaction of T.
rubrum conidia with resident macrophages results in the production of
TNF-alpha and IL-10 but not IL-12 and nitric oxide...
PMID: 16293438

This study says lauric acid has "bactericidal activity" against
Helicobacter pylori. Maybe some folks taking coconut oil are
benefiting from lauric acid it in this manner.

Susceptibility of Helicobacter pylori to bactericidal properties of
medium-chain monoglycerides and free fatty acids
http://aac.asm.org/cgi/content/abstract/40/2/302

Very interesting. Maybe the coconut oil does both. It has several oils
in it. Caprylic fatty acid may provide the brain with ketones while
the lauric acid may be fighting the H.pylori. This would mean that
those who do not have an H.pylori infection, such as someone with a
genetic cause for their illness, would not benefit as much from
coconut oil.

I found that cinnamon may also inhibit H.pylori, so the benefits
people are seeing from taking cinnamon may also be do to a reduction
in H.pylori. I originally attributed the effect to the so-called
"cinnamon proanthocyanidins". Later I started wondering if the
chemical in cinnamon that has been used by diabetics to improve
insulin useage should be credited. Perhaps all three effects are
helping.