Is Your Brain Slowly Rotting?

"I don't know how you were diverted
You were perverted too...
I don't know how you were inverted
No one alerted you.
Look at you all...
Still my guitar gently weeps."

-George Harrison, 1968

Are the cells of your brain slowly dying? Will
such cell death lead to the end of your life, or
compromise your joy in old age by subjecting you
to constant care by loved ones?

The latest link to rapid onset brain disease supports
that issue which I've been writing about for a more
than a decade. The study's abstract appears at the
end of this column. A simple summary:

In 1907, Dr. Alzheimer published a treatise about a
disease that would one day carry his name. He had two
young colleagues who worked with him, Dr. Creutzfeldt
and Dr. Jakob, and they too identified a similar
brain-wasting disease that now has the world in a panic.
The brains of cows turn into a sponge-like mass and
their behavior is called "mad." The human variant of
Mad Cow Disease has been named Creutzfeldt Jakob Disease,
or CJD. The protein causing CJD has no DNA, and has been
described as more like a crystal than cellular material.
That substance is called the Prion.

In labs, 1000 degree Fahrenheit heat does not destroy this
protein particle. Some scientists say that once infected,
the incubation period can last anywhere from one month to
thirty years. As the human brain turns into a sponge, this
spongioform encephalitic condition physically debilitates
those so infected.
____________________________________

"Mad cow disease or bovine spongiform encephalopathy (BSE)
is a fatal neurological disease of cattle first recognized
in the United Kingdom in 1986...a growing body of (still
largely circumstantial) evidence suggests that BSE may be
transmissible to humans."

J Public Health Policy, 1998, 19:2
____________________________________

"Transmission of prions from infected cattle to
humans by oral intake seems not only possible but
also very probable."

Annals of Italian Medicine, 1998 Oct, 13:4
____________________________________

"The outbreak of bovine spongiform encephalopathy
has had major impacts on the United Kingdom dairy
industry, including the loss of beef from dairy
markets, the culling of more than 900,000 dairy
bull calves, the removal of all cattle more than
30 months of age from the human food chain, and now
slaughter of cohort animals. Impacts on dairy
marketing have yet to be properly assessed."

Journal of Dairy Sci, 1998 Nov, 81:11
____________________________________

"Bovine spongiform encephalopathy and Creutzfeldt-Jakob
Disease belong to a group of degenerative neurological
disorders collectively known as the transmissible
spongiform encephalopathies. All the diseases have long
incubation periods which, depending on the host, may
range from many months to several decades. Death is
inevitable after a slow progressive illness."

British Med Bull, 1998, 54:3
____________________________________

"A 24-year-old vegetarian has been diagnosed with
Cruetzfeld-Jacob disease. Scientists fear that milk
and cheese may be the source of infection."

London Times, August 23, 1997 Michael Hornsby

Scientists' conclusion from latest research:

*********************************************
In view of a recent study showing evidence of prion
replication occurring in the mammary gland of scrapie
infected sheep suffering from mastitis, the appearance
of PrP(C) in milk implies the possibility that milk of
TSE-infected animals serves as source for PrP(Sc).
*********************************************
Medline Abstract Dated December 20, 2006:

1: PLoS ONE. 2006 Dec 20;1:e71. Links
Prion protein in milk.Franscini N, Gedaily AE, Matthey U, Franitza S,
Sy
MS, Burkle A, Groschup M, Braun U, Zahn R.
Alicon AG Schlieren, Switzerland.

BACKGROUND: Prions are known to cause transmissible
spongiform encephalopathies (TSE) after accumulation
in the central nervous system.

There is increasing evidence that prions are also
present in body fluids and that prion infection by
blood transmission is possible. The low concentration
of the proteinaceous agent in body fluids and its long
incubation time complicate epidemiologic analysis and
estimation of spreading and thus the risk of human
infection. This situation is particularly unsatisfactory
for food and pharmaceutical industries, given the lack
of sensitive tools for monitoring the infectious agent.

METHODOLOGY/PRINCIPAL FINDINGS: We have developed an
adsorption matrix, Alicon PrioTrap(R), which binds with
high affinity and specificity to prion proteins. Thus
we were able to identify prion protein (PrP(C))-the
precursor of prions (PrP(Sc))-in milk from humans, cows,
sheep, and goats. The absolute amount of PrP(C) differs
between the species (from microg/l range in sheep to
ng/l range in human milk). PrP(C) is also found in
homogenised and pasteurised off-the-shelf milk, and even
ultrahigh temperature treatment only partially diminishes
endogenous PrP(C)concentration.

CONCLUSIONS/SIGNIFICANCE: In view of a recent study
showing evidence of prion replication occurring in the
mammary gland of scrapie infected sheep suffering from
mastitis, the appearance of PrP(C) in milk implies the
possibility that milk of TSE-infected animals serves as
source for PrP(Sc).

PMID: 17183703

Robert Cohen
http://www.notmilk.com
i4crob@...