Mark Purdey’s hypothesis is the only one which explains the spread of BSE
By George Monbiot. Published in the Guardian 23rd November 2000
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, disgracefully, we continued sending it to the Third World until 1996). In most other EU countries, cases have already, as expected, peaked and declined. But in France, the number of infected animals has doubled in the past year. It’s impossible to see how this pattern could result from the export of British bonemeal.
The simple fact is that the transmission of BSE has never been satisfactorily explained by the prevailing theory. While the consumption of meat and bone meal from infected cows doubtless has had an important role to play, this explanation alone fails to account for the huge numbers of cattle in Britain which continued to become infected after most of it had been removed from the food chain. The latest research on the human form of the disease, nvCJD, published three weeks ago, failed to find any link with the consumption of infected beef.
You might have imagined that when its theory isn’t working, a government would wish to test the alternatives. But the British administration has, so far, sought only to attack a hypothesis which does appear to fit the facts. Since 1988, a Somerset farmer called Mark Purdey has been arguing that scientists have overlooked the root causes of BSE. Self-taught and self-financed, he has mastered the brain’s complex biochemical pathways to the extent that this year he was able to publish a groundbreaking paper in a respected medical journal. His sole reward is to have been reviled, misrepresented and physically attacked.
Prions, the brain proteins whose alteration seems to be responsible for BSE, are, Purdey argues, designed to protect the brain from the oxidising properties of chemicals activated by dangerous agents such as ultraviolet light. When, he suggests, the prion proteins are exposed to too little copper and too much manganese, the manganese takes the place of the copper the prion normally binds to, with the result that the protein becomes distorted and loses its function.
BSE arose in British herds during the 1980s, Mark 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, disgustingly, 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 the country’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 in Britain, one, in Kent, is in the middle of a fruit and hop growing area where huge quantities of both 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, he alleges, to dump some of their residues into the sewage system. The sewage was spread over the fields. Dyeworks use shedloads of manganese.
Purdey has tested his theory in BSE and CJD clusters in Iceland, Colorado, Slovakia and Sardinia. In every case 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 this year. They found that when copper was substituted by manganese in prion proteins, the prions adopted precisely the distinguishing features which 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 burnt down. The Ministry of Agriculture, which for past 50 years has enjoyed 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 Somerset dairy farmer could be about to overturn the entire body of scientific research on the biggest public health scandal of modern times.