Forwarding this from another list.
Judith.

" If Purdey is right, he deserves a Nobel Prize for medicine.
Instead he has been shot at, his phone lines have been cut,
and his house has been burned down. "

Sustainable Agriculture Network Discussion Group
<[email protected]>
Date:         Mon, 4 Dec 2000 23:29:29 +0900
Subject:      Copper-bottomed answer to mad cow disease?


The Guardian Weekly 30-11-2000

Copper-bottomed answer to mad cow disease?

There may be a simple explanation for BSE, argues George Monbiot

The most interesting aspect of France's BSE scandal is that it makes
no sense at all. Britain stopped exporting contaminated cattle feed
to Europe in 1991 (though it continued sending it to the third world
until 1996). In most other European Union countries cases have
already peaked and declined, as expected. But in France the number of
infected animals has doubled in the past year. It is impossible to
see how this pattern could result from the export of British bone
meal.

The transmission of BSE has never been satisfactorily explained by
the prevailing theory. The consumption of meat and bone meal from
infected cows has doubtless played an important role. Yet this alone
fails to account for the huge numbers ofcattle in Britain that
continued to become infected after most contaminated feed had been
removed from the food chain. The latest research on the human form of
the disease, vCJD, published four weeks ago, failed to find any link
with the consumption of infected beef.

You might imagine that when its theory isn't working, a government
would wish to test the alternatives. But the British government has
so far sought only to attack a hypothesis that does appear to fit the
facts. Since 1988 a Somerset farmer, Mark Purdey, has been arguing
that scientists have overlooked the root causes of BSE. Self-taught
and self-financed, he has studied the brain's complex biochemical
pathways, and this year published a groundbreaking paper in a
respected medical journal. His reward is to have been reviled,
misrepresented and physically attacked.

Prions, the brain proteins whose alteration seems to be responsible
for BSE, are designed to protect the brain from the oxidising
properties of chemicals activated by dangerous agents such as
ultraviolet light, Purdey argues. When, he suggests, the prion
proteins are exposed to too little copper and too much manganese, the
manganese takes the place of the copper that the prion normally binds
to. The protein becomes distorted and loses its function.

BSE arose in British herds in the 80s, Purdey asserts, because the
Ministry of Agriculture started forcing all cattle farmers to treat
their animals with an organophosphate pesticide called phosmet, at
far higher doses than are used elsewhere in the world. The pesticide
had to be poured along the line of the spinal cord. Phosmet, Purdey
has shown, captures copper. At the same time cattle feed was being
supplemented with chicken manure, from birds dosed with manganese to
increase their egg yield. The prion proteins in the cows' brains were
both deprived of copper and dosed with manganese. In France the use
of phosmet first became mandatory in Brittany. Twenty of France's
initial 28 cases of BSE emerged there. BSE's subsequent spread,
Purdey maintains, mirrors the use of the pesticide.

Poisoning by similar means may explain the distribution of the human
form of the disease. Of the two main clusters of vCJD in Britain one,
in Kent, is in the middle of a fruit- and hop-growing area where huge
quantities of organophosphates and manganese-based fungicides are
used. The other is in Queniborough in Leicestershire, whose dyeworks
(until they caught fire a few years ago, spraying chemicals over the
village) used to dump some of their residues into the sewerage
system, Purdey alleges. The sewage was spread over the fields.
Dyeworks use shedloads of manganese.

Purdey has tested his theory on BSE and CJD clusters in Iceland, the
United States, Slovakia and Sardinia. He found that people and
animals had been exposed to deficiencies of copper and surfeits of
manganese. Most of the clusters, intriguingly, are in mountainous
areas, where levels of ultraviolet light are high.

But the most compelling evidence in support of his hypothesis comes
from a paper published by a team of biochemists at Cambridge
University this year. They found that when copper was substituted by
manganese in prion proteins, the prions adopted precisely the
distinguishing features that identify the infective agent in BSE.

If Purdey is right, he deserves a Nobel Prize for medicine. Instead
he has been shot at, his phone lines have been cut, and his house has
been burned down. The Ministry of Agriculture, which for 50 years has
had a dangerously close relationship with the agrochemical industry,
has repeatedly sought to discredit him. Suddenly, however, its tone
has changed, and it has now promised to start funding his research.
The families of the French victims of CJD are threatening to sue the
British government, and it desperately needs an alternative
transmission theory.

With funding on its way, and new evidence accumulating every month, a
self-educated dairy farmer may be about to overturn the entire body
of scientific research on the biggest public health scandal of modern
times.






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