[pf] BSE - mad cow disease, and organophosphate pesticides. And Manganese.

by David MacClement

08 December 2000 03:20 UTC

· Most of you will have no interest in this, but I can't predict who will.
Sorry.

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Date: Fri, 08 Dec 2000 15:26:39 +1300
To: David MacClement <davd@ihug.co.nz>
From: Bera MacClement <b.macclement@auckland.ac.nz>
Subject: Re: mad cow disease.

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.

The Guardian Weekly 30-11-2000, page 19

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sent on to Pos Fut by David.
(David MacClement) davd@ihug.co.nz 
http://www.geocities.com/davdd.geo/index.html#top
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