On Sat, 3 Jan 2004 06:31:28 -0600, "Russ Thompson" >
wrote:

>
>> It IS true. Only meatheads and idiots who have made a business out of
>> killing animals will object to it.
>
>*** See the "uninformed and ignorant" part of my message. I retract the
>"well meaning".
> The message I replied to makes claims that are demonstratably false.
>
>Kala Thompson
>Farmer
>Richland Center, Wi

MAD COWS OR MAD SCIENTISTS?

THE SUPPRESSION OF ALTERNATIVE EXPLANATIONS

By David Crowe

The smoke and flames from funeral pyres for hundreds of thousands of
British cows are fading into distant memory, but the fear of this
disease affecting livestock or wildlife continues to circulate the
globe.

Most people do not realize that there is a non-infectious explanation
for Mad Cow disease and other spongiform encephalopathies and chronic
wasting diseases. This is due to the reluctance of scientists, health
and agriculture bureaucrats and most of the media to question a theory
that affects public health once it is active policy.

One man, Mark Purdey, has turned himself from organic dairy farmer
into an amateur scientist and globe-trotting epidemiologist to
doggedly continue building the major alternative theory.

The infectious theory of Mad Cow disease not only resulted in the
possibly unnecessary destruction of hundreds of thousands of cows, but
it diverted attention from other causes of health problems facing
livestock and wildlife. It created a fear of eating beef (perhaps not
entirely misplaced, but for the wrong reasons) and resulted in the
circulation of tons of toxic materials from the slaughtered cows into
the atmosphere. It also prevented investigations into alternative
solutions to the epidemic of disease, even though these might be
cheaper, more constructive and far less destructive.

The dominant belief is that Mad Cow disease (also known as Bovine
Spongiform Encephalopathy or BSE) and the related diseases Scrapie in
Sheep and vCJD (variant Creutzfeldt Jakob Disease) in humans are
caused by a prion, a mutant protein. These semi-living beings are
thought to be able to withstand temperatures that would kill the
hardiest bacteria, viruses and parasites. It is believed that this
allowed them to be transmitted from sheep to cows through the
rendering of sheep brains into MBM (Meat and Bone Meal) protein
supplements for cows.

An apparently unrelated health problem in cows that existed before Mad
Cow disease was warble fly infestation. These flies lay their eggs in
a cow’s skin, causing health problems and reducing the value of cow
hides. To combat this, in the early 1980’s the British government
mandated the use of heavy doses of organophosphate insecticides. These
were poured in an oil-based liquid along the spinal column of cows. It
was intended that they be systemic, absorbed into the cow’s body, as
it was believed that this was necessary to provide full and enduring
protection from warble flies.

Mark Purdey was one of a handful of farmers who refused to use
organophosphates (such as Phosmet) on their cows in 1982. He was
concerned that the high doses would damage the health of his cows
because the application was so close to the spinal column. He was also
concerned about the health of people who drank milk from his cows. In
1984, Purdey won his court fight, and gained the right to use less
toxic methods to combat warble fly.

When the first cases of neurological problems were reported in cows in
1985, Purdey felt that his avoidance of these pesticides had been
vindicated. However, researchers and the British Government had a
different idea, blaming the rapidly emerging disease on the recently
postulated prion, based on the detection of protein plaques in the
brains of sick cows.

Purdey started to publicly argue his theory that organophosphate
pesticides were actually the cause of neurological problems,
attracting some attention, and seriously annoying the British
scientific establishment and government who were starting to act as if
the infectious theory was fact.

Purdey noted many inconsistencies in the prion theory. Cows were
supposedly infected by feeding on supplements containing the brains of
sheep with Scrapie, yet Shetland Islanders had been eating potted
sheep brains for centuries without similar diseases occurring. He also
noted that British byproducts were exported around the world, yet the
170,000 British cases of BSE far outnumbered the total in the rest of
the world. Cases of BSE had been found on organic farms with cows
brought in from outside, but not on those raised from birth on the
organic farms, even though organic farming rules allow restricted
amounts of the suspect MBM feeds. Other ruminants, such as goats and
sheep, were not affected by Mad Cow-like diseases in England, even
though they were fed MBM supplements. Conversely, several antelopes at
the
London Zoo and cattle at the Liscombe experimental farm developed BSE,
but had never been fed MBM supplements.

When BSE was found in other countries it was in places like Bretagne
in northwest France where organophosphate pesticides were first
encouraged by the French government. As in the UK, BSE cases first
occurred a few years after the pesticide program was initiated. The
lower number of cases may be due to the lower doses used, the use of
annual treatments (as opposed to twice a year in the UK) and because
the program was not mandatory.

As further evidence, the decline in BSE cases in the UK began about
the same time the warble fly eradication program ended. British cases
of vCJD in humans also fit the environmental theory. The disease was
found in some long-term vegetarians and in humans who had never eaten
cow brains. There is no good explanation of why cows could only get
BSE from eating sheep brains, but humans could get it from eating only
other parts of cows.

Although there was a great deal of panic, there were actually few
cases in humans. Purdey noted that about 80% of the 82 cases were in
rural areas, even though more than 80% of Britons live in urban areas.
One cluster in the Weald district of Kent is in a hops growing area
where organophosphate pesticides are used at 100 times average levels
for all crops.

Purdey lobbied for government funding to test his research.
Eventually, he did get a small amount, and Dr. Stephen Whatley of the
University of London was able to show in a test tube that
organophosphates were found to produce 3 of the 4 protein
transformations required to create the mutant prion protein. A
victory, but also a major defeat. The UK BSE inquiry admitted that
"the door is not yet closed on the possibility that OPs
[organophosphates] played a role in rendering cattle susceptible to
BSE infectivity," but the infectious theory was still cast in the
primary role because of the inability of Whatley to show all four
transformations.

Purdey was not about to give up. He felt that there must be a
co-factor that he had missed. To find it he went on a tour of places
in the world where spongiform encepalopathies had existed in animals
or humans for some time, collecting samples of soil and feed. In these
places, where organophosphates had little or no use, he found
extremely high Manganese levels and low Copper, Selenium, Zinc and
Iron. He did not find this in geographically similar areas where no
illness was found. The causes of this mineral imbalance varied,
including acid rain, volcanic emissions, lead-free gasoline
production, emissions from steel, glass, ceramic, dye and munitions
manufacturing and the take-off zones of major airports.

BSE-like diseases were found in Colorado among deer and elk in an area
of the front ranges where overpopulation often forced starving animals
to graze on pine needles. These showed very high levels of Manganese,
perhaps due to acid rain from upwind smelters. In Iceland, Purdey
found Scrapie associated with similar high Manganese/low Copper soil
conditions. In Slovakia the two clusters of CJD are close to
ferromanganese factories and glassworks (heavy users of Manganese).
These cases may well be related to the almost eradicated occupational
disease known as "Manganese Madness" which occurred among
miners exposed to poorly ventilated working conditions. Its symptoms
and brain pathology are similar to spongiform encephalopathies.

Purdey was not just randomly testing for mineral abnormalities. Copper
is a constituent of the normal prion protein, and Manganese could be a
replacement when Copper is deficient, or when Manganese is present at
high levels, such as in many mineral supplements for cattle. It is at
this point that Organophosphates re-enter the theory. They can remove
copper from the body, leaving the door open for Manganese (or other
similar metals) to replace it in the prion protein. This results in a
non-functional conformation of the molecule, particularly when
Manganese is from the 2+ form to the oxidative 3+ and 4+ forms.

Recently, Purdey traveled to Groote Eylandt, an island north-east of
Australia where 25% of the world’s Manganese is currently produced.
About one in thirty people in the largely aboriginal Agurugu village,
where the fine mine dust regularly settles most heavily, have Groote
Syndrome, a progressive neurological disease. Researchers supported by
the mining company hypothesize a genetic defect introduced by
Portuguese sailors 300 years ago, even though this theory does not
explain why some white mine workers also have this syndrome, nor does
it explain the emergence of this syndrome since open pit mining began
in the 1960s.

Purdey’s theory was now multi-factorial. Organophosphates were a major
factor, but the copper/manganese imbalance could be exacerbated by
animal feeds or mineral supplements. Similar situations could occur
where the soil is low in the antioxidant metals and high in Manganese.

After extending the theory, David Brown, a researcher at Cambridge
University performed experiments that incorporated high Manganese and
low Copper conditions and was able to reproduce all four protein
changes in vitro, thus providing full laboratory confirmation that
Purdey's theory is at least plausible.

At the height of the Mad Cow frenzy, the British government invited
Purdey to make a detailed proposal for research funding. Predictably,
after sitting on the proposal for more than a year, they rejected it,
and then funded two of its reviewers for some of the studies suggested
by it. A cynic might conclude that they had asked for a grant proposal
solely to have Purdey reveal his arguments and thoughts in full
detail, so that they could then fund some ‘reliable’ researchers to
debunk them, without giving Purdey resources that might strengthen his
arguments.

Interest in Purdey’s ideas is still growing in a grass roots fashion,
although slowly, and usually beneath the radar of major media outlets.
Purdey has a small grant from the US Fats and Protein Research
Foundation, supervised by Dr. Larry Berger of the Animal Science Lab
in Urbana, Illinois. Purdey recently gave 14 lectures in Japan, some
Slovakian researchers are studying the influence of Manganese and
Copper on familial and sporadic cases of CJD. Some British
universities are also quietly investigating in this area.

Purdey is attempting to obtain brain samples from Groote Eylandt to
test for manganese and copper levels, and has persuaded one local GP
there to see whether a chelating drug that removes Manganese will have
beneficial effects.

Purdey is now investigating whether ultra-violet light is an
additional factor in the development of SE diseases, perhaps in
concert with a haze of terpines from the pine trees that often grow at
these elevations. He hypothesizes that the eyes could act as a
trigger, because of their concentration of nerves
exposed to light.

Purdey and other researchers have turned up many potential factors
that could stimulate the development of spongiform encephalopathies
and chronic wasting diseases. If some or all components of this theory
prove to be valid, the solutions to these devastating diseases could
be incredibly simple. It may also open new avenues of research into
mental illness. Supplementation of cattle feeds with minute amounts of
copper and regulation of the manganese levels could work near
miracles, at minimal cost. Chelation could be used to reduce the
levels found in people or animals suffering from these illnesses. Yet,
it is likely that governments and the scientific establishment will
continue to concentrate their efforts almost exclusively on infectious
agents and genetic defects, suppressing anybody brave enough to argue
against them on this or other health issues.

_______________

Mark Purdey can be reached via his website:
http://www.markpurdey.com or by email to
.

Further Reading:

The Inquiry into BSE and variant CJD in the United
Kingdom: http://www.bse.org.uk.2000

Purdey M. Ecosystems supporting clusters of sporadic
TSEs demonstrate excesses of the radical-generating
divalent cation manganese and deficiencies of
antioxidant cofactors Cu, Se, Fe, Zn. Medical
Hypotheses, 2000; 54(2), 278-306

Brown DR et al. Consequences of Manganese replacement
of Copper for prion protein function and proteinase
resistance. EMBO J, 2000 Mar 15; 19(6): 1180-6.

Purdey M. The Purdey Environmental Home Page:
http://www.markpurdey.com



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