The environmental origins of TSEs: the ferrimagneto-prion theory

Townsend Letter for Doctors and Patients,  July, 2004  by Mark Purdey

• E-mail
• Print
• Link

The White Sands Missile Range is an extensive spread of US military controlled cacti country that spans the southernmost extremes of the San Andres mountain ridge. There is an eerie atmosphere to the place.

A Department of Natural Resources truck kicks up the dust across the dried out canyon, its engines reverberating in the quiet air. It stops at the main entrance gates along the perimeter fence. One of the wildlife officers gets out and walks to security, seemingly oblivious to the distant thump of a missile exploding across the range. He is clearly preoccupied with the more important task of slaughtering animals who have succumbed to a so-called "hyperinfectious" disease. The truck is soon on its way, disappearing within the thousands of acres of parched military compound.

They've come to investigate yet another new eruption of chronic wasting disease (CWD) in the USA--the deer equivalent of 'mad cow disease.' This outbreak is particularly significant, in that it represents the first cases of a transmissible spongiform encephalopathy (TSE) disease recorded in a deer herd within the state of New Mexico. Furthermore, the affected herd has been confined within the perimeters of this missile range for several decades.

This latest epidemiological aberration delivers a serious challenge to the viability of the conventional consensus on the origins of CWD. It has shaken the cornerstones of institutionalized 'expertise,' bringing into question those veterinarians who have opted for the assumption that some unknown "hyperinfectious" agent is spreading via body to body contact through the deer populations.

So how did the 'infectious agent' jump the 500 mile gap between the long standing CWD hotspot zone in Colorado and the CWD-free deer residing within the White Sands Missile Range? The 'experts' were baffled. But, true to form, this latest challenge to the official theory was conveniently obfuscated into oblivion; outcast as some illusory mirage that just happened one day in the New Mexico desert.

But the answer is only evident to those who care to scratch a bit deeper than the dust. For they cannot help but notice some overt environmental features that exclusively predominate this unique location. A package of factors which are invariably shared by every single TSE cluster location around the world.

Before the military came, White Sands was an industrial center for the mining of the manganese oxide and wulfenite ores (NB; wulfenite contains the copper chelating molybdenum metal). And since the military have occupied the range, the US authorities have been actively engaged in monitoring the unique intensity of infrasonic shock bursts that are radiated by the explosions of their missiles. The poor deer herd has played guinea pig to an unwitting experiment that has cracked the causal riddle of spongiform disease.

The BSE debacle

Since 1986, the infamous novel neurodegenerative syndrome, BSE and vCJD, has insidiously blighted the heartbeat of British rural life. The disease has annihilated thousands of cattle and a growing number of young people, as well as creating a fierce battleground between nations, vested interests, political parties, farmers, victim support groups and consumers. More recently, the shock waves of the BSE debacle have ricocheted around the entire world, reaching as far afield as Japan and North America.

Yet despite the severity of the mad cow legacy, little genuine attempt has been made to crack the causal riddle of these diseases; thereby leaving us devoid of insight into measures that would best cure, control and, better still, prevent this disease.

But hard scientific evidence is being amassed which indicates that vCJD and BSE could both result from separate exposure of bovines and humans to the same package of toxic environmental factors--ferrimagnetic metals and low frequency sonic shock--and not from the ingestion of the one species by the other. If such a polemic hypothesis continues to accumulate momentum, a radical upheaval of the status quo mindset can be expected.

As a working livestock farmer and TSE researcher with first hand experience of BSE erupting in cattle that had been purchased and brought into my organic farm, I was struck by the fact that no cases of BSE had ever emerged in cows that had been born and raised on fully converted organic farms, despite those cattle having been permitted access to the feed that contained the incriminated meat and bone meal (MBM) ingredient--as part of their 20% conventional feedingstuff allowance decreed in the organic standards at that time.

In this respect, I developed a hunch that the resistance of organic livestock farmers to comply with a UK compulsory livestock chemical treatment program using systemic organo dithiophosphorus (OP) insecticides--toxic chemicals derived from the OP military nerve agents--might offer an explanation for the total absence of BSE in 'home raised' organic cattle across the UK.

In 1982 measures were passed that enforced twice annual application of a uniquely concentrated dose (20 mg/kg bodyweight) of a systemic acting organodithiophosphate insecticide for the control of warbles on UK cattle. Amongst a myriad of toxicological effects, the systemic types of dithiophosphate can chelate copper and open up the blood brain barrier; thereby disturbing the overall crucial balance of metals in the brain. I was therefore not surprised to witness BSE rearing its ugly head in the UK cattle herd in 1986; which, in my opinion, was partly a direct legacy of the UK government's compulsory 'high dose' warble fly campaign. The few other European countries who instigated warble fly campaigns (eg; France, Switzerland, Ireland, etc.) used lower doses of insecticide, and, not surprisingly, developed proportionately fewer cases of BSE as a result.