As an organic farmer, Mark Purdey resisted the order to spray his cattle with organophosphates for warble fly and went to court for a judicial review; he won and was exempted from using the spray. No cows born in his herd developed BSE (Mad Cow disease). He has contributed numerous articles on the subject of BSE to scientific journals. He farms in Somerset, UK.

Government experts have attributed the cause of BSE to the feeding of scrapie-diseased sheep brains to cattle. Scrapie was said to jump from sheep to cattle by virtue of some sort of infectious agent. This same assumption of disease cause was extrapolated into the human CJD—the presumed “microorganism” had now jumped from cows into humans. But this was no more than unproven hypothesis, and it still remains so today.

It is particularly interesting that spongiform disease has been experimentally induced in animals after receiving injections of brain tissue derived from people who have died of Alzheimer’s and Parkinson’s Disease.

The British government’s Spongiform Encephalitis Advisory Committee (SEAC), seems to have thrown aside one of its most relevant long standing observations on CJD epidemiology—people who are occupationally involved with pets and farm animals are at greater risk of developing CJD. And it is this observation that may well hold the key to the true cause of these diseases.

During the 1980s and early 1990s, cattle and cats (the species of animals that have developed BSE) were exclusively treated with systemically acting types of organophosphate (OP) insecticide which were designed to penetrate the entire physiological system of the animal, transforming the bloodstream into a toxic medium so as to kill off any unwanted parasites present. In the context of cattle, the use of these systemic OP’s was subject to a compulsory government order for the eradication of warble fly. The UK government was unique in compelling a substantially higher biannual dose of this OP in comparison with the few other countries around the world that were following similar, less intensive measures to control this fly. Interestingly, these other countries, including Switzerland, France and Ireland, comprise the few other countries that are suffering from very small epidemics of BSE in their home-reared cows.

The known toxic effects of OP’s lead me to wonder whether the use of systemic OP’s on British cattle have caused the malformation of another newly discovered brain protein called prion protein—the phenomenon that US scientists have proposed as the cause of spongiform encephalopathies. Whilst some types of spongiform disease have been attributed to genetically acquired damage to the shape of the prion protein, the underlying cause of protein damage in the BSE and new variant CJD strain of the disease remains a mystery. OP’s are known to generate a highly reactive type of “free radical” in the tissues that they intoxicate. And it is this free radical legacy of OP poisoning which is capable of instigating a chain reaction of lethal attacks on nerve membranes and proteins in the central nerves of susceptible individuals.

I still shudder each time I visit our local farm stores and see the canisters of systemic OP products up for sale. Although the warble fly is eradicated and BSE is on the wane, farmers can still apply these chemicals in a voluntary capacity for controlling lice and other pests. I shudder further when I see the bottles of OP head lice shampoo and OP systemics for pets and gardens still in the shops for human use.

The real madness of the Mad Cow fracas would seem to lie with the deadlock that has kept these products on the open market for a full year since experimental evidence first linked their use to the cause of BSE. Perhaps the government is so scared of compensation claims that it employs everything at its disposal to prevent any degree of acceptance of the idea that their compulsory warble fly program caused the biggest catastrophe in the history of British agriculture.

Further reading:
Purdey, Mark. Ecosystems supporting TSEs demonstrate excesses of the pro-oxidant manganese. Medical Hypotheses, 2000, 54 (2)
Brown, D.R. et al. Consequences of manganese replacement of copper for prion protein function and proteinase resistance. EMBO Journal. Vol.19, No.6, p1180-1186.
Mad Cowboy by Howard Lyman www.madcowboy.com