As considerably smaller outbreaks of BSE began to erupt across other European countries, and later Japan, my investigations revealed the voluntary usage of these same types of systemic insecticide in those countries, albeit at half the dose rates as applied in the UK. These European outbreaks seemed to follow an EU campaign, known as COST 811, that was aimed at purging the remaining bastions of warble infestation on the European mainland – countries where outbreaks had continued because their respective authorities had adopted a more laid back, voluntary approach towards the control of warbles.

In warble-free Japan, the BSE cases emerged in the specific herds which had imported breeding cattle from warble infested North America; and so the Japanese had taken preventative measures by blanket treating those herds with the same types systemic OP that had been used in Europe. It should be pointed out that the USA had wisely adopted a less toxic approach for dealing with their warbles. They employed lower doses of ‘non systemic’ acting insecticides – eg insecticides which were not designed to penetrate through the skin - whilst only treating the individual cattle that are warble infested .

I was a working dairy farmer with first hand experience of BSE erupting in cattle that had been purchased into my organic farm. But 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 feeding stuff allowance decreed in the organic standards at that time.

From then on, I became deeply sceptical of the conventional consensus on the origins of BSE and its human equivalent vCJD. There were just too many radical flaws blighting the hypothesis that bovine ingestion of micro doses of scrapie contaminated MBM lead to BSE. Equally flawed was the follow up theory that human ingestion of BSE contaminated beef caused vCJD.

The ‘hyperinfectious hysterics’ had based their hypothesis on the fact that TSEs could be transmitted via injections of TSE diseased brain tissues into misfortunate laboratory animals. Yet, various other neuro-degenerative diseases , such as familial alzheimer’s disease, have been transmitted in this way. So why is nobody freaking out about alzheimer’s disease?

Despite the myriad of epidemiological flaws and millions of pounds worth of research failing to ascertain any association between the origin of these diseases and the scrapie agent, the whole propaganda myth that BSE was caused by scrapie became impregnated as ‘gospel’ into mainstream public/professional mentality.

It is easy to see how the momentum of such a reductionist mindset took a hold; The media loved the theory because they could drum up a viral holocaust-horror scoop. The farming industry could get their beef sales back on the road by deluding consumers that the causal agent had been eliminated. The vegetarian lobby found themselves landed with a powerful propaganda weapon on their plate, whilst the scientific institutions could carry on drawing generous funding for their hyper-infectious witch hunt without the embarrassment of having to account for years of barking up the wrong tree. And the government could conveniently offload the blame onto the vagaries of some naturally occurring ‘nasty’ for which no vested interest or official directive could ever be held accountable.

In the early days, the world of TSE research had been confined to the rather cranky ranks of back street Institutions. Their researchers seemed more preoccupied with advancing acidic debate over the nature of the "infectious" agent than getting on with worthwhile research projects. It was these scientists who first fossilised the reductionist notion that TSEs stemmed from infectious origins.

But as soon as the positive evidence for the first case of BSE was back from the lab, a fast expanding clique of "expert" microbiologists swooped in, hijacking all the research grants and rapidly laying claim to full ownership and academic rights over this new strain of TSE. They coined the classy name ‘Prion disease’, and ran a host of sharp-suited symposiums set in expensive five star, Floridian hotels thousands of miles adrift from the English pasturelands – the hotbed of the real problem.

From then on, any investigations into the broader scientific perspectives surrounding TSEs were frozen out of the agendas of the funding bodies. Multidisciplinary research studies were forced to give way to research projects that conformed to the convergent assumption that the ‘prion’ would encapsulate all of the answers to this problem. The journals were soon bursting apart with a monotonous dirge of articles that bleated out yet another variation on the stereotype theme of the prion protein - prion protein genotypes, the biochemistry of the prion protein, along with a countless number of prion transmission live animal studies that had been duplicated by virtually every institution involved with TSE research – for no useful scientific purpose.

Once it became clear that the various feed bans had failed to halt BSE in the UK (eg; the 40,000 BSE cases in cattle born after the 1988 feed ban), the incestuous clique of ‘expert’ advisors were forced to come up with an ever increasing array of implausible reasons for explaining the continuation of BSE. And following on from their advice, an equally inept package of control measures were implemented whenever and wherever TSE reared its ugly head around the world.

Their final farcical solution entailed a wholesale annihilation programme of wild and domestic animal populations across specially designated TSE eradication zones. Despite the well publicised history of total failure of these control measures, this brave new wave of totalitarian overkill went ahead - gobbling up millions of healthy mammalian lives and millions of dollars of public funds.