Mad Cows Are Back


Published in BBC Wildlife

magazine April 2001


should have been dead and buried years ago. But somehow the spectre of BSE keeps

rising from the grave. In Britain, where billions of pounds have been spent and

millions of cattle slaughtered to stamp out the disease, new cases continue to

emerge. The German government, having congratulated itself for escaping the

crisis, had to sack two of its senior ministers after BSE roared into life there

at the end of last year. Beef from France, which claimed to possess the highest

safety standards in Europe, has now been banned by several European nations.


shouldn’t have been too difficult to eliminate BSE from the foodchain. If the

disease is simply the result of feeding mashed-up livestock to cows, infecting

them with mutated forms of brain proteins called prions, then banning the

practice should have brought it to an end. Similarly, if the human form of the

disease, new variant CJD, arises only from eating contaminated cows’ brains and

spinal cords, then their exclusion from the human diet should have eradicated

it. But still these horrors haunt us.

Indeed, the official explanation for the origination and spread of BSE and nvCJD

leaves a series of massive questions unanswered. Why, for example, has BSE only

just begun to emerge in Germany, eight years after meat and bonemeal were banned

from cattle feed there? Why have vegetarians succumbed to nvCJD? Why is this

disease clustered in certain places when contaminated beef has been so widely



one hypothesis appears to explain these anomalies. It is the work not of one of

the hundreds of scientists who have studied the disease, but of a small organic

farmer based in Somerset, who has never taken a degree. He could be about to

make a lot of important people look very silly indeed.


Purdey began his research into BSE after he noticed what seemed to be a

correlation between the use of a farm chemical and the spread of the disease. In

1982, the Ministry of Agriculture forced all cattle farmers to start treating

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 spine to kill warble fly maggots, which burrow into the animal’s hide. At

first, Purdey believed it was simply the phosmet, entering the nervous system

through the spinal cord, which caused BSE.


his research soon suggested that this explanation was inadequate. While the use

of organophosphates and the emergence of BSE did appear to overlap, the story

began to look more complicated. He decided to start again. He decided to visit

all the places in which BSE-like illnesses were clustered, to see if there might

be a common factor. His results were astonishing. Everywhere he went he found a

similar pattern: the humans or animals suffering from these diseases had been

exposed to both a surfeit of manganese and a deficiency of copper.


Iceland, he found that sheep reared in some volcanic valleys had a long history

of scrapie, which is the sheep equivalent of BSE. Though low in copper, the

vegetation in these places contained two and a half times the usual level of

manganese. In adjoining valleys where scrapie had never been reported, manganese

levels were normal. In Sardinia, he found that eleven flocks of sheep, grazing

on copper-deficient soils, had been treated with manganese oxide. All of them

had succumbed to scrapie, while no other sheep on the island had been affected.


Colorado, he found that BSE-like diseases suffered by deer and elk were reported

soon after their populations reached unsustainable levels. Overcrowding had

forced them to feed on pine needles, which had bio-accumulated manganese from

acid rain. In parts of the copper-deficient Orava Valley in Slovakia, Purdey

found, one in a thousand people have contracted CJD. They live downwind of two

huge ferro-manganese plants.


Purdey read about prion proteins, he found that they have two interesting

properties. The first is that they are unevenly distributed in the brain, being

heavily clustered just under the skull and, in particular, behind the retina.

Why should that be? Was it possible that they were defending the brain from some

damaging agent which might enter at these points? It is these parts of the

brain, Purdey realised, which are most exposed to ultraviolet light, whose

levels, in some parts of the world, have increased substantially over the past

few years.


second interesting property of prions, Purdey discovered, is that they bind to

copper. In the absence of copper, they would have to latch onto something else.

Manganese, if it were widely available, was the most likely candidate. Purdey

began to develop a new hypothesis. Prions, he suggested, help to protect the

brain by mopping up oxidising chemicals activated by agents such as ultraviolet

light. If they are exposed to too little copper and too much manganese, they

lose this function, with the result that either the brain is damaged directly by

the oxidising molecules, or the prions scramble, triggering further damaging

changes in the structure of the brain cells.


suddenly it all became horribly clear. One of the properties of phosmet, Purdey

knew, is that it captures copper, rendering it unavailable to biological

systems. If copper were removed from cows’ brains, the prions would grab another

mineral. Through most of the seventies and eighties, cattlefeed was

supplemented, disgustingly, with chicken manure. Chickens are fed manganese to

increase their production of eggs. Today, farmers add manganese to cattle feed

deliberately, as it encourages cows to absorb extra amino acids. Purdey had, he

believed, an explanation for BSE in Britain. But could his hypothesis account

for the emergence of nvCJD?


Britain has three main clusters of nvCJD: in the Weald Valley in Kent, Armthorpe

in Yorkshire and Queniborough in Leicestershire. At first Purdey thought he

would have to abandon his hypothesis, for he soon found that in all three places

the soil is deficient in manganese as well as copper. Then he discovered that in

1987 the official farming consultancy ADAS had started advising farmers in

manganese-poor areas to spray their crops with the mineral in both autumn and

spring, significantly increasing the dose. The Weald is also a major fruit and

hop growing area where farmers use organophosphate pesticides, which capture

copper, and manganese-based fungicides. Queniborough used to house a major

dyeworks. A few years ago, it caught fire, spraying chemicals over the village.

Dyeworks use loads of manganese.



might have imagined that a government confronting a multi-billion pound public

health disaster would be interested in findings like this. But Britain’s

Ministry of Agriculture has sought so far only to rubbish Mark Purdey. Other

people have taken an interest however: since he began publicising his

hypotheses, he has been shot at, his phone lines have been cut and his house has

been burnt down. But the man who, until recently, was ostracised by the

scientific community is suddenly enjoying a measure of credibility. Last year he

published his first scientific paper, in the respected journal Medical

Hypotheses. Now his ideas are beginning to be investigated, with fascinating



year biochemists at Cambridge, led by Dr David Brown, published a paper showing

that when copper was substituted by manganese in prion proteins, the prions

adopted precisely the distinguishing features which identify the infective agent

in BSE. Now both he and a team of French researchers have separately tested the

brains of CJD victims, and found that they contain around ten times as much

manganese as the brains of unaffected people. New research by Professor Michel

Bounias of the University of Avignon, which has yet to be peer reviewed,

suggests that there is a direct link between the spread of BSE across France and

the use of a pesticide to kill warble flies in cattle. In January, Purdey

submitted a new funding application to the Ministry of Agriculture, and this

time it seems prepared to give him serious consideration.


Purdey accepts that the horrible practice of feeding dead animals to cows has a

role in the development of the disease. But it cannot, he argues, explain its

origination, or that of similar illnesses all over the world. His evidence is,

of course, circumstantial: no causal link has yet been demonstrated. But at the

very least it is worthy of thorough investigation. Could it be possible that a

self-educated Somerset farmer has cracked one of the most important scientific

puzzles of our age?


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