By Fran Bach, Agri Digest staff

With two more BSE cases just confirmed in Canada, and one of them in an animal born after the ban on ruminant parts being used in concentrates fed back to cattle, the question foremost in the minds of cattle producers is, how do we figure out what is really going on? While testing and trace back programs have helped alleviate some consumer worries, neither approaches the cause or control of the disease. To increasing numbers of researchers ‹ and farmers ‹ "official" assumptions of the source of the disease and how it is transmitted just don't add up.

Transmissible Spongiform Encephalopathies, or TSEs, affect the central nervous system, and are characterized by development of a spongy consistency in the brain (soft tissue with unnatural holes forming in it), and are considered fatal. TSEs like bovine spongiform encephalopathy (BSE), or "mad cow disease", affects cattle; scrapie affects sheep and goats; and chronic wasting disease (CWD) affects deer and elk.

A rare form of TSE known as Creutzfeldt-Jakob Disease (CJD) affects humans and a recently recognized more aggressive form of it, called "variant Creutzfeldt-Jakob disease" (vCJD), first diagnosed in1996, has been tentatively linked to consuming meat products from BSE-infected cattle. The route of transmission between animals is widely believed to be through the use of blood and meat meal products from infected animals being fed back to other ruminants in concentrates. Since 1988, this practice has been banned in the UK, and 1997 banned in North America.

All this presupposes a hyperinfective system (like viruses and bacterial infections) of transmission from animal to animal or animal to person. Some well-informed individuals are looking for environmental factors that do a better job of explaining the sizable number of counter-indicators of the contaminated feed theory. An early proponent of the environmental theory and key contributor to this very heated discussion is that of farmer-turned-researcher Mark Purdey of Somerset, England.

The event that set Purdey on his search was a British government order in 1982 compelling all dairy farmers in the UK to use high concentrations of an organophosphate insecticide to treat warble flies on their cows. As an organic farmer, Purdey went to court and successfully challenged the ruling. Throughout the subsequent epidemic in Britain, he never had a case of BSE among his home-bred herd, though two cases appeared in animals he bought from a non-organic herd.

"There are many flaws in the standard explanation," says Purdey, for instance:

• There were 40,000 BSE cases in British cattle born AFTER the use of ruminant meat and blood meal in concentrates fed back to other ruminants was banned [in 1988].

• These animals were NOT the direct offspring of older infected cows.

• Customers in the Middle East, Africa and India were buying up boatloads of the same meat meal used in Britain to feed to their dairy cows [many of which had been purchased from the UK] during the time that the BSE epidemic was going on. Many of these areas were almost entirely dependent upon this type of concentrate feeding, as there is no grazing to speak of in their arid localities. Yet, instead of a worse mess than in Britain, as one would expect, there wasn't a single case of BSE in any of these countries.

• Sheep and goats fed the same meat and bone based formulations of feed in Britain didn't produce a single case of TSEs either.

• Antelope in the London Zoo developed it, but they never received feed containing the suspect meal.

• The Liscombe Experimental Station, which specializes in raising only grass-fed beef ‹ meaning the animals are fed no meal ‹ still had BSE.

• At the High Mowbray Experimental Farm, the meat meal concentrates were fed to 600 pregnant cows. The calves were reared and kept for a seven year period, yet none developed BSE.

All this, he says, proves the direct infection theory just plain doesn't work!

From work done since the mid 1980s by a number of highly recognized scientists in Britain and North America (John Collinge in the UK, Nobel Prize winner Stanley Prusiner, R.F. Marsh, and Paul Brown in the US), it is known that malformations in prion proteins are a specific feature of the brain tissue of animals that have died of TSE. This does not imply that the malformed prion proteins represent the causal agent, only that they are a recognizable feature in diseased animals when they are autopsied.

Paul Brown and others have shown that TSE diseased brain tissues that have been superheated (to 1000 degrees C) and ashed, will still induce TSE disease when injected into the brain of a healthy lab animal. This fact implied to Brown that the agent must be an INORGANIC component - and could not then be an organic protein-only prion.

With Brown's work in mind, Purdey travelled to areas around the world where animal and human forms of TSEs were known to have occurred in clusters. He tested soil, water, vegetation and air for 46 different metals, looking for common denominators shared by all of the TSE hotspots. What he found were high levels of four metals, each individually capable of "seeding" crystals once they had penetrated their way into brain tissue ‹ just as he theorizes that the phosphorus in the warble treatment did. Either strontium, barium, manganese or silver were all found at excessive levels in every type of TSE cluster environment visited ‹ scrapie, CWD, CJD or vCJD. Sometimes copper was present in normal concentrations but was "locked up" after binding with an organophosphate, or with other metal pollutants such as molybdenum.

"What I believe is that the prion protein binds up with the rogue metal pollutant in place of its normal copper co-partner. The 'substitute' metal then deforms the shape of the prion protein and 'seeds' the growth of quite substantial metal-protein crystals which hallmark the TSE diseased brain, " says Purdey. Healthy brain tissue has a supply of 'free' copper in it: diseased tissue has none.

He thinks the source of these metal microcrystals is naturally occurring (volcanoes ) and man-made (munitions plants, etc.) pollutants, and that the high levels of these metals in these cluster environments almost invariably derive from the activities of adjoining military facilities where munitions (particularly chemical weapons) have been manufactured, tested, stored, dumped or incinerated.

The UK cattle industry has been reliant on fish meal protein derived from those specific fishing areas off the coast of England which have become heavily contaminated with phosphorus, barium and strontium - probably due to the dumping of thousands of tons of munitions on the seabed, says Purdey. UK organic standards prevent the fish meal being fed to organically-raised cattle. Perhaps this factor, in combination with the reluctance of organic farmers to use the organophosphate-based warble fly insecticide, explains why this exclusive sector of the farming community has been spared the fate of BSE.

His lack of a university degree is often held against him by detractors, but that should not blind anyone to the inherent value of the theory of environmental factors being the root cause of the physiological changes in the brains of TSE-susceptible animals and humans. It makes far more sense than the contaminated feed theory. Why aren't we hearing from the scientists? Why is it left to one farmer to carry the banner? And most of all, why does officialdom insist on supporting theories that obviously don't hold water, that criminally malign the practices of an entire industry and leave them vulnerable to billion-dollar losses at the hands of political expediency and fear-mongering?

Lead on, Mr. Purdey.

(Editor's note: In Canada, government regulations have also called for mandatory warble treatments for the past 20 years and more. A number of different formulations have been used, all except the ivermectin class (Ivomec, Eprinex etc.) are organophosphates, though the dosages used in Canada were/are much lower than those used in Britain.)

There are hundreds of articles on BSE on the internet -- far too many to list here as resources. Do your own search.

Preventive and control measures:

• Test soil and provide it with balanced mineral supplementation where necessary.

• And/or supplement minerals in feedstuffs to assure a proper balance, especially adequate copper and sulfur (which can be locked up by the rogue metals)

• Test feeds for the levels of these rogue ' seeding' metals that lock up/displace copper or sulphur ‹ eg; strontium, barium, manganese, silver, molybdenum

• Blood or hoof/horn/antler/hair testing of animals can be undertaken but is too expensive for the individual, though could be used in a testing program by governments.

TSE outbreaks and corresponding adjacent military facilities

• Colorado - CWD in deer and elk - Rocky Flats Nuclear Weapons factory, which leaked radioactive metals in the 1960s and the Rocky Mountain Arsenal which incinerated 11 million gallons of organophosphate nerve gas munitions.

• Wisconsin - CWD in deer discovered in 2000 - Badger Ammunitions Plant, after they started incinerating munitions to clean up the site in1998/99.

• New Mexico - CWD in deer discovered in 2000 - White Sands Missile Ranch, where massive missile/munitions testing has gone on for years.

• Arizona - CJD outbreak in staff at a missile factory in Tucson in the late 1970s.

• Britain - The most severe outbreak of vCJD (5 people out of a population of 1800) were in the vicinity of the Queniborough Ordnance Factory, where shells were filled with chemicals and transported to military airfields down the east coast. When not needed in WWII they were dumped into the North and Irish Seas (around Beaufort's Dyke) where the canisters that contained them are now corroding and washing up on the UK's beaches.

• Papua-New Guinea - 1950s epidemic of Kuru disease, almost identical to vCJD - The Fore tribe in the highlands found downed WWII bombers, and exploded bombs whilst scavenging the aircraft for metal, etc, killing some and contaminating the survivors.

• Sask/Alta, Canada - TSEs in all species - NATO testing and disposal of waste munitions at Cold Lake and Camp Wainwright. Areas where CWD is common, and the Canadian cases of BSE originated, are areas with high silver as well as high barium and strontium concentrations. (Silver is used in detonators and as a cloud seeding agent.)