What if Mad Cow disease is being controlled by a agent being introduced into herds? Nothing unless someone knows it and has known it. Just a thought for now, something to keep in mind if a Hillary Clinton/Tyson food scam shows up on this matter.
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NICHOLAS REGUSH, ABC NEWS - What if it turns out that the human form of mad
cow disease is triggered by environmental factors - and not by infectious
beef products - as some ongoing British research at Cambridge University
suggests? What if much of the science to date, focusing on contaminated
meat, has been overly simplistic or even dead wrong? The immediate
implication would be that we would have to rethink everything already done
to fight the disease, both in Britain where it began, in Europe, where it
has spread, and in other nations, including the United States, where
concerns are mounting about its potential to be unleashed. . .

The viewpoint held by most scientists is that an infectious agent likely
moved from sheep to cows and gained enough strength in its cross-species
jump to ravage the nervous system and cause the bovine brain to appear
spongy and rife with holes like Swiss cheese. This brain-destroying "mad
cow" infection was further transmitted, according to this interpretation,
via the rendering of carcasses, to meat and bone meal in feed. . .

But not according to David Brown, a biochemist at Cambridge University, who
counters that "there is no conclusive proof that [mad cow disease] caused
vCJD." Next week at a scientific conference in Quebec City, he'll discuss
some of his most recent research, pointing to a possible environmental
explanation of both mad cow disease and vCJD. That conference is all about
manganese, a heavy metal, that is essential to life and is part of the daily
diet - for example, wheat, rice and tea provide the metal - but numerous
studies show that environmental overexposure to it can be dangerous to the
nervous system. . .

David Brown agrees with the conventional view that the key agent in the
disease is a protein called a "prion." These prions are thought to keep
nerve cells stable. The conventional view holds that prions can somehow
become malformed and that's when they become infectious and capable of
damaging the brain. The malformed prion, then, according to the conventional
view, is the infectious and transmissible agent in mad cow disease and vCJD.
The infection is neither a virus, nor a bacterium.

Brown parts company here with the conventional view, altogether dismissing
the notion of an "infectious" prion. He told me: "I have [published]
evidence from my cell culture experiments that shows manganese can change
the prion into its abnormal [and dangerous] form." This is especially the
case when the supply of copper to the cell is low. If David Brown's research
is on a correct path, then scientific and public concerns about infection
from beef could eventually be dwarfed by concerns about toxic effects in the
environment that cause copper levels to decrease and manganese levels to
rise. . .

Brown's research has given a boost to the controversial theories of Mark
Purdey, a farmer turned amateur scientist who has been challenging the
conventional view of mad cow disease and vCJD from the start. He has
provided detailed reports to the British government's hearings on mad cow
disease and has published several peer-reviewed scientific papers on the
subject, including data on how manganese in the environment may play a role
in both mad cow disease and vCJD.

BBC, MARCH 21, 20001 - The Phillips Inquiry into BSE confirmed that the
pesticides could make animals more susceptible to the disease. Not for the
first time, Mark Purdey had made a connection that the official scientists
had missed.

Edward Stourton The man from the Ministry had come with an order for the
treatment of Warble Fly - a parasite which lays its eggs under the skin of
cattle. Like all beef and dairy farmers in the area, Mark Purdey was told he
had to use an organophosphate pesticide on his livestock to eradicate the
infestation.

But he fought the order in court - and he won. When BSE was identified two
years later Mark Purdey noticed that the areas where the disease was
emerging more or less correlated with those where the organophosphates had
been used against Warble Fly. His conclusion that the pesticide caused BSE
turned out to be mistaken.

But nearly twenty years later the Phillips Inquiry into BSE confirmed that
it could make animals more susceptible to the disease. Not for the first
time, Mark Purdey had made a connection that the official scientists had
missed. . .
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