: In the article below we find what may be a clue: It would
: appear that they have let slip the fact that between 30-40%
: of the population of England is GENETICALLY DISPOSED to die
: of 'Mad Cow': "With perhaps 30% to 40% of the British
: population having the genetic make-up susceptible to vCJD
: infection, and so many contaminated meals eaten over the
: years, Professor DeArmond said one could have expected many
: more victims to have emerged by now."

There's been a recognized genetic predisposition (so they say) for Creutzfeld-Jacob Disease (Syndrome?) among Eastern European Jews - but it may have nothing whatsoever to do with 'Mad Cow' disease. Instead, Mad Cow may arise from chemical poisoning and its effect on prions:

Insecticide Causes Mad Cow Disease

by Fintan Dunne
Research by Kathy McMahon

Reprinted from eionews.com, email - news@eionews.com

Pharmaceutical interests in the UK are ignoring new scientific
research that shows the insecticide used in the UK government's
own warble-fly campaigns triggered the UK surge of 'Mad Cow'
disease.

Latest experiments by Cambridge University prion specialist,
David R. Brown, have shown that manganese bonds with prions.
Other researchers work shows that prions in the bovine spine
--along which insecticides are applied-- can be damaged by
ICI's Phosmet organophosphate(OP) insecticide -causing the
disease.

British scientists have led the current theory that
an infectious prion in bonemeal fed to cattle
causes bovine spongiform disease (BSE).

Infectious prions are also claimed to cause new variant
Creutzfeld-Jakob Disease (CJD) in humans -from ingesting
beef. But the infectious prion theory serves to obscure a tragic
chemical poisoning scandal behind the majority of BSE cases.

The new work proves that the prions can bond with manganese
in animal feeds or mineral licks. These manganese prions cause
the neurological degeneration seen in BSE. By a similar
process, prions in human brains are damaged by lice
lotions containing organophosphate. This can result in
neurological diseases like CJD and Alzheimers -later
in life.

Many might be surprised to hear that organophosphates were
developed by Nazi chemists during the course World War Two,
as a chemical weapon nerve agent. One formulation of the
insecticide --Maneb, or Mancozeb-- actually contains
manganese in addition to organophosphate.

The marginalized research has devestating financial
implications for ICI. It would provide a firm basis for litigants
-who could include CJD sufferers, farmers across the world and
families of the many British farmers who committed suicide
during this BSE debacle.

Phosmet organophosphate has been used at high doses in British
warble fly campaigns. In 1996, ICI subsidiary Zeneca sold the
phosmet patent to a PO Box company in Arizona called Gowan
-just one week before the UK government admitted to a link
between BSE and nvCJD.

The politically well-connected British pharmaceuticals group,
ICI has the financial and political clout to block research into
any cause other than the infective model. Indeed no substantive
alternative research has been done. British BSE disease
management and research bodies have taken decisions that do
not seem guided by spirited scientific enquiry. Mysterious prions
that jump species is the preferred research arena.

Scientist and organic farmer, Mark Purdey gave evidence to the
UK BSE inquiry, that warble fly insecticide was the cause of the
disease. The scientist wheeled out to rubbish Purdy's evidence
-Dr. David Ray, later turned out to have been receiving funding
from the insecticide manufacturer ICI.

A lobby group that includes Bayer, Monsanto, Novartis, Pfizer,
Roche and Schering-Plough was behind the effort to discredit
Purdey. In December 1999, the same David Ray was appointed to
the UK Veterinary Products Committee (VPC) -a government
body that licences animal medicines.

Purdey has been consistently denied even exploratory funding to
extend his privately supported research. Yet the Purdey/Brown
chemical poisoning model matches with the epidermiological
spread of CJD clusters in humans. It also predicts the incidence
of BSE-type diseases in animals. The accepted infectious model
fits neither.

The pharmaceutical industry is all the more
determined to hide the chemical source of BSE
and CJD, because a spotlight on chemicals would
expose the role the insecticides in Alzheimer's
--another neurodegenerative disease--that
might lead to claims which would dwarf those
from BSE and CJD litigants. In fact, two leading
brain researchers into CJD and Alzheimers have
died in suspicious circumstances in recent years.

In the United States, the Environmental Protection Agency is
already reviewing Phosmet's safety. The Centers for Disease
Control in the US has recently conducted experiments on mice
that confirm the organophosphate risk.

Not only is the EC beef slaughter campaign futile -because BSE
disease is mostly non-infectious, but unless the underlying
chemical cause is addressed, BSE will simply reappear from
chemical causes. A new warble fly campaign is already
underway in France using the organophosphate insecticide.

Of greater concern is that some lotions for scabies and head lice
are now priming children and adults, for CJD and Alzheimers
in later life.

Bonding The Prion

Cambridge University prion biochemist, David R. Brown is
dismissive of the science behind the infectious model of BSE. He
terms it "a very limited amount of science by a few assumed-
reputable scientists." He insists there is "no evidence an
infectious agent is present in either meat or milk."

"Simple tests on udder walls of cows --which
could easily detect an infectious prion-- have not
been done, why I don't understand."

A number of researchers have found that organophosphate(OP)
in systemic warble fly insecticide can deform the prion molecule,
rendering it ineffective at buffering free radical effects in the
body. Worse still, the prion is then partial to bond with
manganese and become a 'rogue' prion. A chain reaction
whereby rogue prions turn others to rogues also, can explain the
bovine spongiform disease mechanism.

Brown showed how prion protein bonds benignly with copper,
but lethally with manganese. Even natural variations in relative
environmental availability of manganese versus copper can
trigger prion degradation.

The CJD and BSE symptoms mirror 'manganese
madness', an irreversible fatal neuro-psychiatric
degenerative syndrome that plagued manganese miners in the
first half of the last century

Shining a Light on Spongiform

Organic dairy farmer and peer-review-published independent
scientist, Mark Purdey, says the accepted theory of transmission
from BSE-infected cattle to human CJD -by bonemeal or meat, is
dependent on a mutant prion that has never been isolated under
the scientific protocol called Koch's postulates.

Purdey's insistence on sticking to the letter of this scientific law
earned him the condemnation of UK officialdom when he first
mooted his theory. But Purdey pointed to CJD clusters downwind
of a British Phosmet production plant to back his case.

He gave evidence to the UK Government BSE inquiry and was
supported by Conservative MP, Thessa Gorman. His views were
discounted, but his subsequent research and the new Cambridge
prion work have confirmed the alternative theory. Despite this,
and the backing of a British peer, he is denied even exploratory
funding.

Speaking from his rural English Somerset farm yesterday -as
plans forge ahead for the European cattle cull, he asks:

"Why does CJD degeneration in humans begin in
the retina, and why are CJD disease clusters
found in high altitude locations?"

The question is rhetorical, and Purdey has an eye-opening
answer. He argues that the prion molecule has a known
natural role as a shock adsorber of damaging
energy from ultraviolet rays and other oxidizing
agents.

Once this prion defence system is rendered ineffective by
organophosphates - for example in human head lice lotions,
these oxidizing effects have an unmediated impact on tissues.
Eventually, UV radiation damages the retina and oxidative
stress destroys the brain tissues of CJD patients. This theory
would expect to find higher CJD incidence in mountain regions
-where UV radiation levels are elevated. That prediction holds
true.

A similar but accelerated mechanism could be driving BSE.
ICI's Phosmet organophosphate warble fly insecticide -applied
on the backs of animals along the spinal column, similarly
degrades prions. "Systemic versions of the insecticide are
designed to make the entire cow carcass toxic to warble fly,"
explains Purdey. "Unfortunately it's toxic to prions too
-especially those prions located just millimeters from the point
of application."

The damaged prions are then ready to react with manganese in
animal feed, or manganese sprayed on land or in mineral licks
-to become the driving force of BSE neurodegeneration. Purdey
says manganese-tipped prions set off lethal chain reactions that
neurologically burn through the animal.

Chickens notoriously excrete most of the supplements fed to
them -including manganese. And their manganese-rich
excreta have been blended into cattle feed in the UK. Natural
variations in the relative environmental availability of copper
and manganese can also spur prion degeneration says Purdey.

From this research, any prudent person would conclude there is
a significant risk attaching to the use of organophosphate in
humans. Preparations for head lice and scabies
are known to be overused in practice and might
be priming users for CJ disease.

Purdey believes his bias for field work is the key to his success.
He bemoans the "reductionism" of much lab-centered science.
"I have traveled the world to investigate known clusters of
spongiform disease -something mainstream researchers don't
seem remotely interested in doing."

Since first postulating an environmental -rather than
infectious- theory of spongiform diseases, Purdey has built
evidence from around the world that explains and predicts the
incidence in humans and animals: a cluster of CJD in Slovakia,
Eastern Europe -around a manganese plant; Rocky Mountain
deer with Chronic Wasting Disease (CWD), who were found to be
eating pine needles rich in manganese; the futile slaughter of
sheep in Cyprus -only for BSE to reemerge within years.

"The reappearance of BSE in Cyprus obviously points to an
environmental cause," says Purdey, who is sanguine when
reflecting on the condemnation of him by mainstream scientists.

"I suppose they have mortgages and kids who need to go to
university," he muses. "Privately, some were agreeing with me,
but then they would denounce me publicly. It was quite strange
really."

The Money Trail

Critical scientists like Purdey are unlikely to prevail. The
pharmaceutical industry holds most research purse strings,
and would hardly energetically explore an avenue of research
that could expose them to litigation for causing BSE. The official
theory is lavishly funded, alternative theories rarely, if at all.

There are more explosive implications to his -and other's latest
research. Purdey says similar organophosphate-induced
protein deformation could also underlie Alzheimer's disease. If
that were true, the litigation fallout would destroy some
pharmaceutical giants, and a lot of very influential noses would
be out of joint.

Disturbingly, Purdey and other brain researchers seem to have
had an undue share of unfortunate accidents. Purdey's house
was burned down and his lawyer who was working with him on
Mad Cow Disease was driven off the road by another vehicle and
subsequently died. The veterinarian on the case also died in a car
crash -locally reported as: 'Mystery Vet Death Riddle.'

Dr. C. Bruton, a CJD specialist --who had just produced a paper
on a new strain of CJD-- was killed in a car crash before his
work was announced to the public. Purdey speculates that
Bruton might have known more than what was revealed in his
last scientific paper.

In 1996, leading Alzheimer's researcher Tsunao Saitoh, 46 and
his 13 -year-old daughter were killed in La Jolla, California, in
what a Reuters report described as a "very professionally done"
shooting.

What Alzheimer's Disease, Mad Cow Disease, and CJ Disease
have in common, is abnormal brain proteins and a putative link
to organophosphates. Even Gulf War syndrome among
returning veterans has been attributed, in part to the insecticide.
But the sidelined scientists' suspicions are still largely ignored.

In their favour at the moment, is a growing unease on the part of
the public. As BSE forges on and Governments panic, Science
may be out to lunch on BSE, compromised by bovine
spongythinking myopathy.

{snip}

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