Originally from: mark purdey
                        
Hi folks,

I got a reply from Hugh McDonald who actually cites a point in the BSE Inquiry where they had claimed that the OP theory was not viable, although this statement relates to the OP theories which exclude a role of the prion protein in the theoretical mechanism. Since my own theory has always included a role of the prion protein, then I guess that this means that my theory is not considered to be non viable by the BSE Inquiry !!

My reply letter to Hugh follows;

Dear Hugh,

Thank you for your reply which I appreciate.

Firstly, I would like to stress that my research into the origins of TSE has consistently considered a role for the involvement of systemic OP warblecides in the multifactorial aetiology of BSE. It is even cited in my Med Hyp paper of this year; to which you refer and incorrectly state that OPs are not included. See Figure 3, bottom corner of page 219 of that article , where I merely mention the role of OP warblecides in chelating copper availability to the prion protein / increasing permeability of the blood / brain / barrier to the uptake of the rogue metal microcrystals in BSE. I did not reiterate a full exposition of this prerequisite in greater detail, because, as you well know, I have covered this aspect in depth in previous papers.

Like all working hypotheses, my work has needed to evolve over the years as new evidence has come to light surrounding the pathogenesis of TSEs, or as aspects of my work have been disproven or proven due to follow up lab challenge. This is the healthy evolution of scientific ideas in practice, and makes life exciting, as opposed to remaining confined to the rigid, entrenched reductionist approach that resists change and only survives through a denial of the fresh evidence that has come to light.

In this respect, I take your point that DEFRA takes a more impartial, open view these days towards the origins of TSEs, as opposed to your early days of rigid subscription to the scrapie-in-the-feed hypothesis of BSE origins.

And secondly I should make it clear that my postulations on the pathogenic involvement of OPs in BSE do firmly integrate the well established role of prion protein in that theory, thereby categorising my theory as one that should be considered under the recommendations of the BSE Inquiry – You quoted these lines.

My criticism of these official reports on the origins of BSE ( G Horne, etc
) is also aimed at their failure to grasp the multifactorial concept that undeniably exists within the aetiology of any disease – genetic, environmental, microbiological factors which invariably seem to interact to cause a disease to emerge within a given individual. Yet, the G Horne committee took my theory and split it into two theories – the mineral theory and OP theories of BSE causation, despite their reviewing of my papers and having me up to deliver oral evidence where the multifactorial perspectives of my work were clearly presented. This mode of appraisal clearly missed the relevance of the crucial cornerstones of the pathogenci mechanisms that i have been proposing all along
– eg; the free sulphurs in the organo dithiophosphate molecules acting as copper chelators. In this respect, one did not need the prerequisite of a soil copper deficiency in BSE ( as is required in scrapie; in accord with my theory ), since the exposure to the Cu chelating OP was bypassing that requirement. But Horne et al, got this totally muddled and ended up misrepresenting my work on several counts.

I hardly think that DEFRA are in a position to distance themselves from the contents of the G Horne report, since they have been avidly promoting it on the DEFRA website, in press conferences at a five star hotel at Hyde Park Corner, etc. In respect of the disinformation in this report, I am sure that my opponents would understandably hit the roof if I were to publish, as if undeniable 'fact', that meat and bone meal consumption first started in 1988 !! I would rightly be discredited for life !!
So perhaps you can see how infuriating it is for me and the development of my work, if the kind of disinformation on the finish date of OP warble fly treatment is persistently presented as fact due to the publication of this erroneous statement in the G Horne report.

You work on a fixed salary, but my income ( currently generated from lectures / meagre research grant ) is controlled by various precarious influences – such as the public perception of the credibility of my work. Recent proliferation of the contents of the Horne Report in various reports / papers published in the US / Canada has lead to a massive downturn in my income from lecturing / researching in these countries to near zero. Had the critique of the Horne report towards my work been valid, then i could accept that fact. But since the relevant bits of the report portray a misrepresented and innaccurate version of my work, then I am very angry about the extreme difficulties that this document is creating for the viable continuation of my work – which I still view as important..

Obviously you are not prepared to budge from your current policy of promoting the unamended original version of the Horne report around the world. This leaves me with no alternative but to deviate from my positive global field research studies that i have been involved with for the last two years , and channel my energies into relaunching a campaign through the politicians and media to expose these inaccuracies and injustices – both in the UK and North America.

Best Wishes,

Mark Purdey.