Whilst it is well established that the key pathological hallmark of the spongiform diseased brain is represented by a malformed version of the prion protein, known as a prion, there is no actual evidence in support of the assumption that the protein portion of the prion represents the TSE infectious agent. Nor is there any evidence that TSEs are infectious diseases that can be spread via body to body contact. And furthermore, nobody has offered a credible explanation as to how these abnormally shaped ‘prions’ are initially created in the mammalian brain, nor have they explained how these prions are capable of inducing a cascade of self-replication in the TSE diseased brain.

I became interested in the possibility that the use of systemic organo phosphate (OP) warble fly insecticides may have triggered off this protein malformation in some way; thereby serving as one of the primary causes of the modern BSE/vCJD strains of this disease. For these oil based chemicals were designed to penetrate through the skin and metamorphose the internal environment of the cow into a poisonous medium so as to exterminate internal parasites. Farmers were forced to pour the chemical along the head/backline of the cow just millimeters from where the prion protein is manufactured in the cell lines of the spinal cord.

It was well recognised that OP insecticides exert their toxic effects in mammals by deforming the molecular shape of various nerve proteins like acetyl-cholinesterase; whereupon these malformed proteins cease to perform their proper function in the brain. But nobody had ever considered that a similar style molecular interaction may occur between OPs and the prion protein. Since the prion protein has been shown to bond up with copper in the healthy brain, I felt that the ability of these dithio insecticides to lock up copper in the treated animal may play some role in deforming the prion protein.

After many abortive attempts to coerce the Establishment into running the correct laboratory test, I eventually raised funds from well wishers and personal loans to finance Dr Stephen Whatley of the Institute of Psychiatry in London to challenge brain cell cultures with the OP phosmet - the actual OP used at uniquely high doses on UK farms.

Amazingly, these trials demonstrated that the OP altered the cellular metabolism of prion protein in some of the ways observed in the early stages of spongiform disease - suggesting that phosmet exposure may render mammals more susceptible to the disease. Unfortunately, these experiments did not produce the key deformation of the prion protein that is seen in TSEs. I returned to square one, assuming that OPs in combination with a further factor X, could fulfill the final missing link in the causal jigsaw. Or perhaps OPs weren’t involved at all!

Caught in the midst of a minefield of multinational interests, medical spin doctors and political propagandists, I grew exhausted by the vortex of professionals that had successfully hijacked and cul-de-sac’ed all UK scientific research into TSEs. Furthermore, I’d found myself frozen out into the cold, operating much like an underground scientist, tramping a covert journey around the rustic out-backs of the UK’s dairy lands to nail down the true cause of BSE.

So I expanded my horizons and embarked upon a refreshing eco-detective trek to analyse the unique environments around the world where traditional TSEs had erupted as high incidence clusters for many years. By scanning the overall characteristics of each cluster location, I attempted to pinpoint the common causal factors – the aetiological needles in the causal haystack

Set against a backdrop of flamboyant and sometimes threatening scientific scenery, I embarked on a lone journey to the ends of the earth, sampling exotic corners of Colorado, Iceland, Slovakia, Calabria, Sardinia, Japan, etc; areas where an assortment of animals and humans had demonstrated a high incidence rate of TSE. My analytical results displayed abnormally high levels of the metal manganese, and rock bottom levels of copper, selenium and zinc in all of these food chains in common. Levels of manganese returned to normal in adjoining disease-free areas.

I was also fascinated to discover these TSE affected populations living in areas that were enduring ‘front line’ exposure to intensive shock bursts of low frequency infrasound – military and quarry explosions, volcanic and earthquake shocks, low flying supersonic jets, Concorde over-flights, etc. It took many further miles of investigation before the full relevance of this additional environmental facet could be integrated into the causal equation. But the role of the high manganese/low copper finding seemed very clear from the outset.

A specific environmental source of manganese could be pinpointed in every TSE cluster zone that I had investigated to date; where each TSE affected ecosystem could be directly connected to the atmospheric fall out of some naturally occurring or industrial source of combusted manganese oxide; eg stemming from volcanic, acid rain, steel/glass/ceramic/dye/munitions factories, lead-free petrol refineries, the take off airspace beyond airports, etc. In this respect, it should be born in mind that atmospheric manganese, much like silver and aluminium, can be absorbed directly into the brain via the nasal-olfactory inhalatory route of intake (eg; the infamous cocaine snorter’s route). Perhaps this highly efficient mode of uptake enables sufficient concentrations of manganese to accumulate in the brain and initiate TSE?

Furthermore, many of the mammalian populations involved in the outbreaks of both traditional and new strain TSE could be linked to the consumption of high concentration manganese supplements for bone growth, etc. For instance, the clusters of chronic wasting disease in deer could all be linked to the areas where a ‘spiced up’ manganese mineral lick had been put down by the deer hunters for addicting deer to their shooting territories. The manganese is added for promoting antler growth. In fact all species connected with TSEs – deer, humans, cows, goats, mink, sheep, zoo animals, cats, etc – are fed artificial manganese supplements in their feeds.

Disturbingly, manganese is also added to artificial milk substitute powders for calves (and human infants) at levels up to 1000 times those found in normal cow’s milk respectively. This practice has been widespread in all countries affected with BSE to date.

Excess intakes of dietary manganese pose a great risk when fed to the immature mammal since the regulatory mechanisms of the blood brain barrier are underdeveloped at this stage; thereby permitting an excessive uptake of manganese and other metals into the brain.

The addition of manganese to artificial milk powders explains why European dairy cattle (who were invariably reared on this powder) suffered such high incidence rates of BSE in relation to the negligible rates of BSE encountered in beef suckler or organically reared cattle (who were invariably reared on natural cow’s milk). The more extensively reared BSE-free cattle herds of Australasia have also never fed these mineral boosted milk powders.