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"Give with a free hand, but give only your own."
-- J.R.R. Tolkien The Children of Hurin
- Helicobacter pylori -
General Information:
Names:
Wikipedia entry:
Dr. Ray Shahelien entry:
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Observations:
Helicobacter
pylori (the stomach ulcer bacteria):
See also Infection and Immune System
Response
Broccoli Sprouts
Cinnamon
Enbrel
Methylene blue
Rember
Can a Helicobacter pylori bacterial infection be the root cause
of many (75%) cases of Alzheimer's disease cases? Genetic
or other factors would then comprise the root cause of the other
25%.
"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
It is interesting to note that 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
Alzheimer's Disease May Spread
by 'Jumping' from One Brain Region to Another
ScienceDaily (Feb. 1, 2012) — For decades, researchers have
debated whether Alzheimer's disease starts independently in
vulnerable brain regions at different times, or if it begins in
one region and then spreads to neuroanatomically connected
areas. A new study by Columbia University Medical Center (CUMC)
researchers strongly supports the latter, demonstrating that
abnormal tau protein, a key feature of the neurofibrillary
tangles seen in the brains of those with Alzheimer's, propagates
along linked brain circuits, "jumping" from neuron to neuron...
http://www.sciencedaily.com/releases/2012/02/120201173217.htm
Trans-Synaptic Spread of Tau
Pathology In Vivo.
Li
Liu, Valerie Drouet, Jessica W. Wu, Menno P. Witter, Scott A.
Small, Catherine Clelland, Karen Duff. PLoS ONE,
2012; 7 (2): e31302 DOI: 10.1371/journal.pone.0031302
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0031302
Vulnerable Brain Region May Be
Central to Progression of Alzheimer's Disease
ScienceDaily (Nov. 7, 2010)
New research is helping to unravel the events that underlie the
"spread" of Alzheimer's disease (AD) throughout the brain. The
research, published by Cell Press in the November 4th issue of
the journal Neuron, follows disease progression from a
vulnerable brain region that is affected early in the disease to
interconnected brain regions that are affected in later
stages... "Our findings directly support the hypothesis that
AD-related dysfunction is propagated through networks of
neurons, with the EC as an important hub region of early
vulnerability,"...
http://www.sciencedaily.com/releases/2010/11/101103135239.htm
[Note:
here seems to be a similar progression in Parkinson's
disease:
How
The Pathology Of Parkinson's Disease Spreads
ScienceDaily
(July
29, 2009) — Accumulation of the synaptic protein
alpha-synuclein, resulting in the formation of aggregates called
Lewy bodies in the brain, is a hallmark of Parkinson's and other
related neurodegenerative diseases. This pathology appears to
spread throughout the brain as the disease progresses. Now,
researchers at the University of California, San Diego School of
Medicine and Konkuk University in Seoul, South Korea, have
described how this mechanism works... "The discovery of
cell-to-cell transmission of this protein may explain how
alpha-synuclein aggregates can pass to new, healthy cells," said
first author Paula Desplats, project scientist in UC San Diego's
Department of Neurosciences. "We demonstrated how
alpha-synuclein is taken up by neighboring cells, including
grafted neuronal precursor cells, a mechanism that may cause
Lewy bodies to spread to different brain structures."... In
these studies, autopsies of deceased Parkinson's patients who
had received implants of therapeutic fetal neurons 11 to 16
years prior revealed that alpha-synuclein had propagated to the
transplanted neurons...
http://www.sciencedaily.com/releases/2009/07/090727191914.htm
How Disordered Proteins Spread
from Cell to Cell, Potentially Spreading Disease
ScienceDaily (Feb. 18, 2011) — ...Kopito found that the mutant
protein associated with Huntington's disease can leave one cell
and enter another one, stirring up trouble in each new cell as
it progresses down the line. The spread of the misfolded protein
may explain how Huntington's progresses through the brain.
This disease, like Parkinson's and Alzheimer's, starts in one
area of the brain and spreads to the rest of it. This is also
similar to the spread of prions, the self-replicating proteins
implicated in mad cow disease and, in humans, Creutzfeldt-Jakob
disease. As the misfolded protein reaches more parts of the
brain, it could be responsible for the progressive worsening of
these diseases...
http://www.sciencedaily.com/releases/2011/02/110218165254.htm]
Apparently, the amyloid beta plaques have prion-like properties
too:
Alzheimer's
has 'infectious' mechanism
Cosmos Online
Monday, 25 October 2010
by Gareth Barton
These misfolded proteins have properties similar to prions, the
researchers concluded. Prions are tiny, infectious protein
particles can cause disease, such as mad cow disease which
passes from infected cattle to humans through their meat.
In the
study, the researchers removed brain tissue from mice with
Alzheimer's-like symptoms, and injected into it into the stomach
cavity of healthy mice. Four months later, the previously
healthy mice showed symptoms similar to those of Alzheimer's
disease and their brains had similarly disease brain tissue.
http://www.cosmosmagazine.com/news/3824/alzheimers-disease-has-infectious-element
Peripheral
Induction of Alzheimer's-Like Brain Pathology in Mice
ScienceDaily
(Oct.
25, 2010)
Pathological
protein
deposits linked to Alzheimer's disease and cerebral amyloid
angiopathy can be triggered not only by the administration of
pathogenic misfolded protein fragments directly into the brain
but also by peripheral administration outside the brain...
http://www.sciencedaily.com/releases/2010/10/101021141453.htm
Peripherally Applied
Aβ-Containing Inoculates Induce Cerebral β-Amyloidosis
Yvonne
S. Eisele
Science
DOI: 10.1126/science.1194516
Published
Online
October 21, 2010
The
intracerebral injection of β-amyloid–containing brain extracts
can induce cerebral β-amyloidosis and associated pathologies in
susceptible hosts. Here, we found that intraperitoneal
inoculation with β-amyloid–rich extracts induced β-amyloidosis
in the brains of β-amyloid precursor protein transgenic mice
after prolonged incubation times
http://www.sciencemag.org/cgi/content/abstract/science.1194516
Could A-beta plaques from animal tissue in our food be a
problem? I'm not a vegetarian, but (pardon the pun) it is
food for thought.
Can toxins produced by bacteria initiate the process?
Can 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 of "tumor necrosis
factor alpha", (TNF-alpha). And guess what substance a
Helicobactor pylori infection in the stomach causes the body to
produce? Yep, TNF-alpha. 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."
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 experiencing improvements from Enbrel
treatments, I think this says, check to see if there is also an
H-pylori infection present. If so, treating the H.pylori infection
may increase the time needed between treatments, or may even
eliminate the need for Enbrel treatments entirely. (There
may be other bacteria or viruses that could cause the body to
produce TNF-alpha, 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 those
like me, still in the process of learning language of
biochemistry, it is understandable enough for one to grasp the
ideas. (It is rarely necessary to know the intimate details
of how a computer works in order to be effective in using a
computer.):
http://www.springerlink.com/content/83147756538x7031/fulltext.pdf
Wild speculation time:
If an Hp infection turns out to be the initiating factor in many cases
of
AD, then for those currently suffering with the disease, I would
first stop the progression, then eradicate the infection(s). We
appear to have at least two ways to stop the progression at this
time: 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 may also be some benefit
to suing the tau busters, as this may attack even another
step in the disease process.
Obviously, if eliminating a chronic bacterial infection reduces
the body's production of TNF-alpha to normal levels, there would
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 will it make the "there's nothing we can do,
we're powerless, everyone should just die now and get it over
with" crowd happy.
In the Greek study, Hp was detected in 88% of AD patients. Hp
eradication was successful in 84.8% of treated patients, which is
about normal for all cases of Hp infection. If you multiply
88% by 84.8%, you get ~75%... which, coincidently, seems to be
about the percentage of people that are helped by MCT/coconut
oil.
I'm sure people are thinking, my loved one never had a stomach
ulcer, yet now she has AD. Well, one does not need to have
an ulcer to have an Hp infection. I don' t know where they got
this statistic, but I found...
90% of the
people with an Helicobacter pylori (Hp) infection do not
have stomach trouble or ulcers. Or, to put it another way, only
10% of people with an Hp infection have stomach trouble.
"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
I'm sure that not everyone with an Hp infection will develop AD.
However, one of the greatest risk factors for developing AD is
age. Perhaps the cumulative effects of a chronic H.pylori
infection explains this.
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
the statistics of the Greek study holds true, then one could
expect the eradication of an Hp infection to be effective for
about 75% of those treated, and that the effect should last at
least 2 years (which was the limit of how long they tracked the
test participants).
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.
There
are some interesting charts in the full text .pdf file of the
paper:
http://www.springerlink.com/content/83147756538x7031/fulltext.pdf
The original article was from researchers in Greece, so the
statistics given for the prevalence of Hp infection may be
different in your country.
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.
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
started thinking, what substances, other than prescription
antibiotics, 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.
Some
foods or spices may also reduce the Hp infection, but I haven't
found anything yet, other than prescription antibiotics, that will
eliminate it. Broccoli sprouts, dill, and cinnamon
may be good candidates. "Probiotics", or "good bacteria" may
help by crowding out the H-pylori. Others will have to be
explored.
For broccoli sprouts, it's the sulforaphane in them that
seems to help.
Of
course, if you can get a physician to test for Hp, and then
prescribe antibiotics, go for it!
There
are probably several conditions that eventually lead to AD. This
particular one would not address genetic causes or exposure to a
toxin.
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. If eliminating a Helicobacter pylori
infection worked for 3 out of 4 cases, that would be a good
start! How much needless suffering could be avoided if
people only knew this?
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..."
http://cat.inist.fr/?aModele=afficheN&cpsidt=4893514
It is interesting to
note in this article about the experimental drug Rember,
ICAD: Tau-Targeted Therapy Slows
Alzheimer's Progression for 19 Months it says,
"In the trial reported here, 321 patients were randomized
to 30 mg, 50 mg, 100 mg or placebo. The drug, Dr. Wischik said,
was effective when it dissolved in the stomach, but was not
effective when the drug was absorbed through the intestines.
This was an issue for the 100-mg dose, which had 'absolutely no
activity because it didn't dissolve in the stomach.'"
http://www.medpagetoday.com/MeetingCoverage/ICAD/10320
As I wrote above, the
Helicobacter pylori bacteria finds methylene blue to be rather
toxic. This tends to support the idea that the dominant effect of
Rember may not have been as a "Tau aggregation inhibitor (TAI)",
but rather as an antibiotic. This would explain why the 100mg dose
was not effective when it dissolved in the intestines, whereas the
30 and 60mg doses, which disolved in the stomach, were effective.
The antibiotic effect of the rember (which is basically
methylene blue) reduced the H.pylori infection, thereby reducing
the TNF levels. It seems to me that anyone getting Enbrel
injections to reduce TNF levels should take a hard look at this.
A final thought on this topic, this concept may also apply to the
other rare neurodegenerative diseases such as PSP, CBD, the FTD,
etc.
Other things to research: Lauric acid in coconut oil kills
H.pylori?
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Known sources:
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Natural sources:
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References:
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Updated: July 2, 2012
Inception: July 2, 2012