Mad cow researcher attacked (fwd)

[Guest guest]

" 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. "

from:

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0012 & L=sanet-mg & F= & S= &

P=8854

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From: <keith@...>

Reply- Sustainable Agriculture Network Discussion Group

<SANET-MG@...>

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 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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