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Canada had just had its first mad cow discovery. The piece was written for the Calgary (known as Cowtown) alt-weekly. Knowing their readers are young and not easy to shock, the editor gave me the green light to open this very serious piece with a not very serious, but attention grabbing lead.

Mad cows, manganese and mystery:
Mark Purdey may know the real cause of BSE, so why isn’t anyone listening?

MARCH 25, 2004

Me and my friends, Hammer and Tigger, once won a girl infected with mad cow disease in a pool game. We were on our way from Vancouver to Nelson when Tigger decided it was time to start getting his drink on as we rolled into Grand Forks early on a Friday night. This was the third day of a bender and the three of us looked like some kind of alcoholic beasts from the Island of Dr. Moreau.

We walked into a bar on the main drag and made our way over to the pool tables, where a handful of young yokels were holding court and a slightly overweight, not-quite-homely girl with curly red hair and a million freckles was giggling like a gas-huffer.

Tigger, who grew up in the bars and pool halls of Ketchikan, Alaska, where he’d worked as a commercial fisherman since he was 12 years old, asked the yokels if they wanted to play for a little money. Alas, payday was next Friday. “How ’bout the girl?” I asked, nodding to the corner where Hammer was already pouring a fresh sleeve for the giggler.

“You wanna play us for Hanna?” asked a kid with a bad case of pizza face.

“Maybe? What’s her story?” said I.

“Doukhobor. Gone wild. Party girl. Crazy in the head. Got mad cow disease. Look at ‘er.”

“Mad cow disease, huh? Beautiful,” I said, laughing. “Hundred bucks if you beat us.”

Pizza Face explained the deal to Hanna, who was happy to go along with the idea of an all-expenses paid weekend in the hippie capital of B.C.

It was no contest. Tigger ran the table on the yokels and we were back on the road with a couple cases of Kokanee before anyone decided that maybe it wasn’t such a good idea after all.

Hammer, who grew up on a farm in Athabasca and fancies himself an amateur veterinarian, was in the cramped back seat of the truck with Hanna, subjecting her to all manner of testing to determine whether or not she really did have mad cow disease.

“No doubt about it,” Hammer told us with a grin, as we parked out front of the Heritage Inn, “she’s got mad cow disease, alright.”

We weren’t in Nelson for more than an hour before a woman known throughout the Kootenays as Ooglik the Terrible saddled up to our diseased Doukhobor darling. Eventually, Ooglik convinced Hanna that our intentions towards her were less than wholesome. Hammer feigned indignation until his pint glass ran dry and he had to top up at the bar. Hanna and Ooglik lumbered through the doors and, for all I know, the two of them are still involving themselves with all sorts of vile, unGodly biological experiments somewhere in the Slocan Valley.


That, boys and girls, is the closest I’ve ever come to mad cow disease and, being a vegetarian for the past 20 years, it’s the closest I will ever come. Or so I thought, until I stumbled upon the work of a Brit scientist named Mark Purdey.

Unlike myself, Purdey has spent a great deal of time around creatures afflicted with mad cow disease. In fact, Purdey is the only person on the planet to have travelled to every part of the world where mad cow and other similar diseases have broken out in significant numbers. And Purdey is convinced that the conventional wisdom about the cause of mad cow disease is all wrong.

First off, Purdey does not believe that cows become afflicted with what is officially known as bovine spongiform encephalopathy (BSE) by eating the remnants of other mad cows. The irrefutability of that theory is, to Purdey, “grossly exaggerated.” Secondly, Purdey does not necessarily believe that humans contract the human form of BSE – Creutzfeldt-Jakob Disease (CJD) – by eating the diseased flesh of mad cows.

Purdey points out that a lot of beef and feed was exported from the U.K. before countries banned the import of both. Why, then, asks Purdey, were there not large outbreaks of BSE and CJD in the creatures that ate those products, which surely had to have been infected?

The mad cow nightmare began in 1984 when a British rancher noticed one of his cows behaving strangely, very strangely – like, doing-the-Funky-Chicken strangely. Almost two years later, British scientists identified the cause of the bizarre symptoms as BSE. Two years after that, in 1988, a British government committee concluded that BSE was “probably” being spread through animal feed. Now, this is where you have to stop and ask, “What the hell were they thinkin’?”


It was common practice in the industry to grind up the parts of a slaughtered cow that were not marketable to humans – parts such as brains and spine, generally known as offal – and feed them to other cows. They’d do the same with the entire carcasses of cows that were visibly diseased, known as “downers.” Now, I’m willing to bet my left nut that if you were to put a dead cow in a field with a bunch of other cows, they will not mosey on over and start chowing down on their dead sister. What the Hell is that? It’s unnatural. Actually, it’s worse than unnatural. It’s some seriously ignorant shit to take a herbivore and force it into cannibalism, but greed will triumph over common sense almost every time.

Other than those in the cattle industry, nobody really gave a flying fuck about mad cow disease until 1995, when the two-legged meat munchers started dropping in the U.K. The first was a 19-year-old kid named Stephen Churchill. When they cut Churchill’s head open they noticed his brain was so full of holes it looked like Swiss cheese. A little light bulb went on over someone’s head that day and they said, “Hey! Wait a minute. I’ve seen this before, somewhere.” Of course they had – that’s what happens to a mad cow’s brain.

Dr. John Williams, Head of Bovine Genomics Program at The Roslin Institute in Edinburgh, recently visited Madcowtown to share his knowledge. During a very science-oriented, statistic-laden, almost-deathly-dull presentation (hey, we’re not talking monster trucks and go-go dancers), Williams estimated that the U.K. may have seen as many as 1.6 million cases of BSE in the past 20 years, with 183,000 confirmed cases. Between 1993 and 1994 Williams says 1,000 cows per week were being diagnosed as having contracted BSE. As horrifying as those numbers are, Williams trumped them by telling his crowd that in 2003 the U.K. recorded 147 new cases of mad cow.

“Wait a minute,” I hear you saying, “compared to 1,000 cases per week, 147 in a year is pretty damned good.” True, but there’s a problem, gentle reader: of the 147 confirmed cases of BSE in the U.K. last year, 75 were born after the European Union finally banned the practice of feeding animals to each other in 2001. So, if it’s true that mad cow disease is contracted by eating other mad cows, what the Hell caused these 75 new cases? Well, this is where we get back to Mark Purdey.


Purdey believes that cows that are deficient in copper are more likely to contract mad cow disease. When such cows also have an excess of manganese – another metallic element – their brains tend to turn into Swiss cheese. Or, at least that’s what Purdey told me.

When it was standard industry practice to feed animals to each other it was also – get this – standard practice to feed them each other’s shit. Prior to 1988, U.K. cattle were fed chicken manure. Chickens were fed high doses of manganese to strengthen their eggs but a high percentage of it passed right through the chickens.

Purdey has travelled to Slovakia, where incidences of CJD are drastically higher than the rest of the world. He was not surprised to find that most of the victims lived either downwind from one of two ferro-manganese factories, or in the shadow of a glass making plant where manganese is used. So maybe it’s these minerals that cause human mad cow disease as well, not eating infected beef.

The mere mention of Mark Purdey’s name brings derisive reactions from some BSE researchers. When I mentioned Purdey to Williams, it was all he could do to conceal his contempt. I wasn’t surprised.

Purdey has been the victim of a smear campaign, and most people who are not familiar with the scurrilous things that are done to destroy the credibility of individuals by professional character assassins are usually completely unaware that their opinions have been thoroughly and surgically manipulated. Also, Williams makes his living studying BSE. Purdey does not. Purdey is an organic farmer. Intellectual snobbery is nothing new. It is, in fact, still very common amongst academics who determine another’s credibility – and sometimes even their worth – by how much alphabet soup is attached to the end of their names.

Fortunately, not all scientists are gratuitously dismissive of others who lack institutional credentials but still dare to conduct research on their own and posit theories. Dr. David Brown, a respected biologist of the University of Bath, has conducted clinical tests that have validated Purdey’s field work and theories. When interviewed by the BBC, Brown said, “The work of Mark Purdey is of great interest.” Why? Because “he’s gone to various places in the world to look at regions where there is high incidence of (mad cow and similar diseases),” something nobody else has bothered to do.


There may, however, be more to explain the mainstream derision heaped on Purdey and his theory. When mad cow first blindsided British beef producers Purdey was very suspicious about the government’s conclusions about its cause. Purdey suspected that the use of organophosphates (OPs) might have played a role. At the time, most British cattle were being treated for infestations of parasitic warble flies with a highly toxic OP called phosmet, which was made by a subdivision of the British chemical giant ICI. The Brits used phosmet in doses that were twice as strong as other countries. Purdey does not think it’s a coincidence that BSE was far more prevalent in British cattle. And just how do OPs fit into Purdey’s copper-manganese theory? “These chemicals deprive the copper supplies in the brain of the treated cow,” Purdey says, which predisposes a cow’s brain to mad-cow infection. Purdey says that once the warble fly was eradicated in the U.K. and the use of OPs declined, BSE started to disappear.

If Purdey’s OP-copper-manganese theory is correct, ICI may find itself on the wrong end of one hell of a class-action suit.

Shortly after the British press picked up on Purdey’s theory, his farmhouse was burned to the ground, his science library was destroyed and his lawyer died in a mysterious car crash.

Purdey has never been given a research grant to further investigate his theories. Shortly after publishing his findings regarding copper-manganese that supported Purdey’s theory, Brown’s research funding was discontinued.


In Alberta, in the February 17 Throne Speech, the provincial government announced it would fund a new mad cow research program. Allan Hall, the man who will decide what, exactly, gets researched under the new program, says he has no intention of duplicating work that’s already been done and is not closing the door opened by Purdey and Brown.

For their part, Alberta cattle ranchers seem to also be interested in seeing this thread pulled a little more. Gary Sargent, general manager of the Alberta Beef Producers, says he is, “interested in getting to the bottom of these alternative theories.”

As for myself, I am going to stop being a smug, self-righteous vegetarian when it comes to mad cow disease – in researching this piece I discovered that two of the more than 150 people who have died from CJD were fellow veggies. And, in spite of Purdey’s assertion that neither BSE nor CJD is transferred from animal to animal, or animal to human, I’m going to make it a point to stay away from girls with mad cow disease – at least until it’s proven that the affliction can be neutralized with high volumes of alcohol.

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