The June issue of Discover magazine has an article on the insanity virus
and human endogenous retrovirus and bipolar, MS and Schizophrenia. Now we
have more evidence supporting the infection component of my FIGHT program.
This research about the "insanity" virus has not stopped, and in fact, the
more you read up on endogenous retrovirus the more you will see that this
all further reinforces my FIGHT4yourhealth concept. The June Discover
magazine on the newsstands brings this story up to date but the more you become
interested in the infection component of today's epidemic of impaired
health, the more you will see how this infection from endogenous retroviruses
found in what we used to call our JUNK DNA, helps explain Bipolar and MS as
well as Schizophrenia.
Maybe we all need to get toxins out so our immune system can handle these
inborn infections better, and more of us will need to lower the total body
burden of all infections fungal bacterial and viral using ACS 200 Silver
that is proven to efficiently lower even Borrelia and Candida.
This is worth really understanding, as this is real and when we begin to
understand how these virus that are in our DNA are kept under control, until
certain things happen, like a severe viral infection during pregnancy, and
then years later the child starts to hear voices
etc. I have covered on my website with 8 hours of webinars, the topics of
Food, Infection, Genetics, Hormones, Toxins, etc but this aspect of
infection was not covered. If we think about it, there could be some tie in here
to the live virus given children when they receive their MMR, and subsequent
development of Autism. There could be a HERV-W involved in that condition
too.
Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com
#1: http://discover.coverleaf.com/discovermagazine/201006/?pg=64#pg65
#2:
http://articles.sfgate.com/2002-08-05/news/17557040_1_mental-illness-mental-health-dr-e-fuller-torrey
Insanity virus -- a crazy idea? / Mainstream psychiatric outcast ponders
parasitic mental illness
August 05, 2002|By Keay Davidson, Chronicle Science Writer
#3: New Findings Boost Theory That Infection Causes Schizophrenia
Psychiatric News March 19, 2010
Volume 45 Number 6 Page 1
© American Psychiatric Association
1. Mark Moran
A review of studies of maternal exposure to infectious agents and
schizophrenia in their offspring suggests that eliminating certain infections could
prevent as many as 30 percent of schizophrenia cases.
Call it an instance of science being stranger than science fiction, and of
nature's unintended consequences.
In 2000, a team of British researchers published a remarkable paper in the
journal of the Royal Society titled "Fatal Attraction in Rats Affected
With Toxoplasma Gondii." It seems that rodents infected with Toxoplasmosis
gondi (T. gondii), a parasite that normally thrives in cats, become fatally
attracted to cat urine, causing them to shed their normal avoidant behavior
in the presence of a cat.
Naturally, cat catches rodent and devours it, with the result that the
parasite T. gondii is again where it belongs: in a feline host.
Observing this case of attraction gone fatally wrong, the researchers,
from the University of Oxford, postulated that T. gondii, one of nature's most
successful organisms, had developed an ingenious evolutionary mechanism
for manipulating the behavior of the rodent—in whom the parasite would have
reached a dead end—so that the rodent seeks out, suicidally, the feline host
in which the parasite can thrive and complete its life cycle.
Fast forward to 2009 when another group of researchers seeking to explore
the neurochemical mechanisms for the parasite's behavioral manipulation of
its host discover a likely culprit. In a paper published in the March 2009
PLoS One, Glenn McConkey, Ph.D., and colleagues at the University of Leeds
found that the genome of the T. gondii parasite encodes the enzyme tyrosine
hydroxylase, the central enzyme in dopamine synthesis.
"Intriguingly, dopamine is the most logical neurotransmitter candidate for
altering the avoidant behavior of the rodent," McConkey told Psychiatric
News. "So it would make sense for the parasite to increase dopamine. For the
parasite, this is an ideal way to manipulate the behavior of the host."
New Credibility for Infectious Etiology
And this strange cat-and-mouse story has yet another wrinkle.
For decades, an excess of dopamine has been implicated in schizophrenia.
And so last year's discovery that T. gondii synthesizes dopamine has lent
new credence to an intriguing, though not universally accepted, theory—that
at least some forms of schizophrenia may be caused by infection.
Among researchers inclined to the theory, T. gondii has been one, among
several, of the most prominent candidates.
"Humans infected with T. gondii will form the same cysts on the brain as
are found in infected rodents when high levels of the gene involved in
dopamine synthesis are expressed," McConkey said. "While production of dopamine
in the rodents could be an evolutionary mechanism devised by the parasite,
in humans it would be merely accidental. But now suddenly, this provides a
possible link to the observed correlation of T. gondii with some forms of
schizophrenia."
The theory of an infectious etiology for at least some forms of
schizophrenia has a long history, though it is still outside the mainstream. As far
back as the 1960s, British epidemiologist Edward Hare, Ph.D., documented a
marked increase in late-winter and early-spring births of people with
schizophrenia, a finding that pointed to an infection, possibly acquired during
winter months in utero.
Psychiatrist E. Fuller Torrey, M.D., a long-time proponent of the theory,
published a paper in the Lancet as early as July 1973 titled "Slow and
Latent Viruses in Schizophrenia."
Since then, Torrey has published a number of papers with Johns Hopkins
University pediatrician and virologist Robert Yolken, M.D., showing increased
antibodies to T. gondii—possibly acquired in utero or early childhood
through exposure to cat feces, undercooked meat, or contaminated water, dirt, or
sand—among people with schizophrenia.
Meanwhile, infectious agents have been implicated in other diseases—the
heliobacter pylori virus in peptic ulcers, the papilloma virus in cervical
cancer—that had been considered unlikely candidates for infection. "It's no
longer a theory from Mars," Torrey told Psychiatric News. "We've arrived on
planet Earth."
Epidemiologic Data Accumulate
Now, a report published online in AJP in Advance on February 1 by Alan
Brown, M.D., of Columbia University and colleagues, reviews more than 40
studies looking at seroepidemiologic findings, ecologic data, and maternal
reports on prenatal exposure to influenza and other infectious agents and the
development of schizophrenia.
They found that odds ratios for associations between schizophrenia in
offspring and serologically documented maternal influenza, elevated levels of
antibody to T. gondii, and other peri-conceptional genital or reproductive
infections ranged between 3.0 and 5.0.
The study, "Prenatal Infection and Schizophrenia: A Review of
Epidemiologic and Translational Studies," was done in collaboration with Catherine
Schaefer, Ph.D., director of the Kaiser Permanente Research Program on Genes,
Environment, and Health, and Barbara Cohn, Ph.D., director of the Child
Health and Development Studies, funded primarily by the National Institutes of
Health.
In a study published in the April 2005 American Journal of Psychiatry,
titled "Maternal Exposure to Toxoplasmosis and Risk of Schizophrenia in Adult
Offspring," Brown and colleagues conducted serological assays for
Toxoplasma antibody on maternal serum specimens from pregnancies giving rise to 63
cases of schizophrenia and other schizophrenia spectrum disorders and
compared them with assays from 123 matched healthy subjects.
They found that the adjusted odds ratio of schizophrenia/schizophrenia
spectrum disorders for subjects with high maternal Toxoplasma IgG antibody
titers was 2.61.
"The infectious theory has garnered more interest in the research
community," Brown told Psychiatric News. "This is being driven in part by
accumulating data from epidemiological studies of schizophrenia and translational
neuroscience in which offspring exposed prenatally to immune challenge and
infection show evidence of neurobiological abnormalities found in
schizophrenia."
A Gene-Environment Interaction
Still, the pathogenic theory of schizophrenia runs counter to years of
orthodox thinking that schizophrenia is a congenital, organic brain disorder.
Maternal and intrauterine infections are notably common, so one question is
that if schizophrenia is infectious in origin, why aren't more offspring
born with schizophrenia?
But proponents acknowledge that infection alone is unlikely to cause
schizophrenia. "Infections are almost certainly interacting with susceptibility
genes and other environmental factors," Brown explained. "So
gene-environment interactions likely play a very important role."
Nor do proponents of the pathogenic theory insist that infection is
necessarily the cause of all schizophrenia.
"While replication in independent samples is warranted, the data from our
sample suggest that up to approximately 30 percent of schizophrenia cases
could be prevented in the offspring of the pregnant population [in the
review appearing in AJP in Advance] if we were to completely eliminate three of
the infections we studied—influenza, elevated Toxoplasma antibody, and
peri-conceptional genital-reproductive infections," Brown told Psychiatric
News.
While complete eradication is highly unlikely, Brown says, the finding has
implications for prevention and treatment (see Can Infection-Related
Schizophrenia Be Prevented?).
More "orthodox" researchers acknowledge that infection may be a factor in
a more expansive research vision looking at "domains of psychosis" in
which schizophrenia-like symptoms stem from different gene-environment
interactions.
"Most people acknowledge today that schizophrenia is never going to be
found to have a single etiology," said psychiatric researcher and AJP deputy
editor Carol Tamminga, M.D., of the University of Texas Southwestern Medical
Center. "It's more likely a syndrome like congestive heart failure than a
disease like Parkinson's with a single molecular lesion. So we can assume
that schizophrenia is a diagnosis with multiple etiologies and overlapping
risk factors.
"We know genetics and environmental factors are risks," she continued. "
Keeping an open mind, I think we will find a list of risk genes and a list
of environmental factors, and we will have to see how both of those play out
in producing symptoms of a brain disease like schizophrenia."
An abstract of "Fatal Attraction in Rats Infected With Toxoplasma Gondii"
is posted at <www.ncbi.nlm.nih.gov/pubmed/11007336>. "A Unique Dual
Activity Amino Acid Hydroxylase in Toxoplasma Gondii" is posted at
<www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004801>. "Prenatal
Infection and Schizophrenia: A Review of Epidemiologic and Translational Studies"
is posted at
<http://ajp.psychiatryonline.org/cgi/reprint/appi.ajp.2009.09030361v1>. "Maternal Exposure to Toxoplasmosis and Risk of Schizophrenia in
Adult Offspring" is posted at
<http://ajp.psychiatryonline.org/cgi/content/full/162/4/767>.
http://pn.psychiatryonline.org/content/45/6/1.2.full
Related articles
Clinical & Research News: Can Infection-Related Schizophrenia be
Prevented? Psychiatr News March 19, 2010 45:19
[Non-text portions of this message have been removed]
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