Herpes Simplex Virus, lysine, curcumin, coconut oil (HSV-1, Cold Sore Virus)

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Swarfmaker

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Dec 10, 2010, 8:53:35 AM12/10/10
to Alzheimer's Medicines Supplements and Treatments
Lysine

See also Coconut oil (lauric acid may break down the lipid capsule of
HSV-1)
Infection
HSV-1

Could lysine supplementation prevent Alzheimer’s dementia? A novel
hypothesis
Neuropsychiatr Dis Treat. 2010 Oct 27;6:707-10.

Rubey RN.

Retired, Red Lodge, Montana, USA.
Abstract

There is a growing body of evidence that implicates the herpes simplex
type 1 virus (HSV-1) in the development of Alzheimer's dementia (AD).
HSV-1 has been found to be present in the cerebrum of the great
majority of older adults, and in many of the same areas of the brain
that are affected by AD. When active, the virus may contribute to the
formation of the neuro-fibrillary tangles and amyloid plaques
characteristic of AD. Like AD, HSV-1 encephalitis may cause long term
memory loss. HSV-1 replication is suppressed in lysine-rich/arginine -
poor environments, and population studies suggest that diets high in
lysine and low in arginine may be associated with lower rates of AD.
There are no prospective studies of the efficacy of lysine
supplementation to prevent or reduce the incidence of AD.
Supplementation with adequate doses of lysine could prevent the
development of AD.

PMID: 21127688 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/21127688
Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2987503/?tool=pubmed
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2987503/pdf/ndt-6-707.pdf

[NOTE: Jan. 17, 2009: Recently, some people have mentioned in posts
to some discussion forums that curcumin, resveratrol and lauric acid
(coconut oil!) may fight the HSV-1 virus. Need to find more info and
links to sources.]

********************************************************************************************
Herpes Simplex Virus (HSV-1)

See also Infection and the Immune System Response
Lysine
Curcumin


New Evidence Found Linking Herpes And Alzheimer’s
ScienceDaily (May 12, 2000)
"Could Lead to New Treatments Targeting the Herpes Virus"

"Researchers have long suspected a connection between the herpes virus
and Alzheimer’s disease. A new study provides a potential explanation
that could lead to development of a vaccine to prevent the disease or
new drugs to treat it, according to the researchers. The study appears
in the May 16 issue of Biochemistry, a peer-reviewed publication of
the American Chemical Society, the world’s largest scientific
society."

"Researchers at the University of California, Irvine, demonstrated
that a synthetic protein that resembles the herpes simplex 1 virus
(HSV-1) mimics the structure and function of a protein called beta-
amyloid, a toxic agent that accumulates in the brains of Alzheimer’s
patients."

"Genetic sequencing revealed that two-thirds of a portion of the viral
protein is identical to the beta-amyloid protein. The researchers
showed that, like beta-amyloid, it could kill brain neurons, a key
feature in the development of Alzheimer’s. Moreover, in laboratory
experiments, the viral protein formed abnormal twisted fibers like
those found in the brains of Alzheimer’s patients — the definitive
hallmark of the disease..."
http://www.sciencedaily.com/releases/2000/05/000512083302.htm

Another...

Cold Sore Virus Might Play Role In Alzheimer's
ScienceDaily (Jan. 3, 2007)
"A gene known to be a major risk factor for Alzheimer's disease puts
out the welcome mat for the virus that causes cold sores, allowing the
virus to be more active in the brain compared to other forms of the
gene..."
http://www.sciencedaily.com/releases/2007/01/070103110103.htm

From these articles (I suggest reading the full articles and others
you can find), it seems to be a reasonable theory that this HSV1 virus
invades the brain as one's immune system weakens with age, stress or
truma. Infected cells then expire, leaving behind amyloid beta (AB).
Some people's central nervous system (NS) are probably better than
other people's at removing this amyloid beta. So, most people develop
the classic characteristics of AD, which are loss of brain mass,
clumps of AB, and intracellular tau tangles. Others, whose CNS clears
out the AB still suffer the loss of brain mass as the disease ravages
the brain, and other proteins accumulate, such as just the tau tangles
or clumps of tau. Could this be behind CBD?

What this theory says to me is that there is a chance that many of
what today seem like separate neurodegenerative diseases may actually
be manifestations of the same root cause: A virus. But it also says
that most of the things we have been trying will ultimately fail.
Enbrel addresses inflammatory responses. Methylene blue and cinnamon
attack tau and maybe help neurons live longer. MCT's (coconut oil) and
cinnamon address sugar metabolism. Lithium fights tau corruption.
Curcumin is used in the hopes of reducing the AB load. Likewise with
all of the other the pharmaceuticals and supplements we have discussed
and had such hopes for.

But, none of these attack what might be the root cause, HSV1; and if
they don't, then their positive effects are all doomed to eventually
be overwhelmed by the virus' insatiable hunger for brain cells. It is
every bit as horrific as the plot from some "B" science fiction movie.
Here is the link to a study Michigan State University about curcumin
and HSV-1:

Curcumin inhibits herpes simplex virus immediate-early gene expression
by a mechanism independent of p300/CBP histone acetyltransferase
activity.
Virology. 2008 Apr 10;373(2):239-47. Epub 2008 Jan 14.
Kutluay SB, Doroghazi J, Roemer ME, Triezenberg SJ.

Graduate Program in Cell and Molecular Biology, Michigan State
University, East Lansing, MI 48824, USA.
Abstract

Curcumin, a phenolic compound from the curry spice turmeric, exhibits
a wide range of activities in eukaryotic cells, including antiviral
effects that are at present incompletely characterized. Curcumin is
known to inhibit the histone acetyltransferase activity of the
transcriptional coactivator proteins p300 and CBP, which are recruited
to the immediate early (IE) gene promoters of herpes simplex virus
type 1 (HSV-1) by the viral transactivator protein VP16. We tested the
hypothesis that curcumin, by inhibiting these coactivators, would
block viral infection and gene expression. In cell culture assays,
curcumin significantly decreased HSV-1 infectivity and IE gene
expression. Entry of viral DNA to the host cell nucleus and binding of
VP16 to IE gene promoters was not affected by curcumin, but
recruitment of RNA polymerase II to those promoters was significantly
diminished. However, these effects were observed using lower curcumin
concentrations than those required to substantially inhibit global H3
acetylation. No changes were observed in histone H3 occupancy or
acetylation at viral IE gene promoters. Furthermore, p300 and CBP
recruitment to IE gene promoters was not affected by the presence of
curcumin. Finally, disruption of p300 expression using a short hairpin
RNA did not affect viral IE gene expression. These results suggest
that curcumin affects VP16-mediated recruitment of RNA polymerase II
to IE gene promoters by a mechanism independent of p300/CBP histone
acetyltransferase activity.

PMID: 18191976 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/18191976
Free full Text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2668156/?tool=pubmed

The Pathogen Hypothesis (Live Discussion on www.alzforum.org)
Moderator’s summary: Pathogens as a cause of Alzheimer’s disease
By June Kinoshita

The notion that microbes such as herpes simplex virus 1 (HSV1) and
Chlamydophila pneumoniae (Cp) could be a causal factor in Alzheimer’s
diseases would probably be viewed by the main stream of AD researchers
as being beyond the pale. Although a small body of recent findings has
reported strikingly strong associations between these pathogens and AD
[1,7], subsequent attempts to replicate the findings have met with
mixed results (discussed in [10]). At this juncture, it might be
convenient to dismiss the hypothesis, but as both sides of this debate
session agreed, there are plausible reasons for these discrepancies
that deserve to be resolved through further research. While opinions
diverged on the strength of evidence for and against the hypothesis,
there was a consensus that the possibility of common infectious agents
causing such a widespread scourge of old age is one that is too
important to ignore.
http://www.alzforum.org/res/for/journal/balin/default.asp


Lauric Acid:

Apparently the nerves to the face originate deep in the brain. It is
very conceivable that a cold sore outbreak on the skin could travel
along the nerve path and back deep into the brain. The neurons have
thousands of connections to other neurons and the virus could spread
that way to other cells. See Dr. Ruth Itzhaki's research. It has
shown the presence of DNA of the herpes virus in beta-amyloid plaques
in people with APOE4 gene. For people without the APOE4 gene, it could
be another infection or toxin that results in AD or other
neurodegenerative diseases. The lauric acid in coconut oil also kills
helicobacter pylori, candida and other fungi, and other viruses with
lipid capsules, such as HIV and other members of the herpes virus
family.

See refs at: http://www.coconutketones.com

Other things to research w.r.t. HSV-1: Lithium

Swarfmaker

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Dec 10, 2010, 10:56:29 AM12/10/10
to Alzheimer's Medicines Supplements and Treatments
However, we have a report that lysine is ineffective against HSV...

http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/6984024187?r=8324044187#8324044187
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