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The Prof. Gabriel Horne report on the origins of BSE and the research of Mark Purdey.
by Mark Purdey

Introduction

During 2001 a committee headed by Professor Gabriel Horne was commissioned by the Government to investigate the origins of BSE . They published their findings in the late summer of 2001. In my view this involved the government publishing outright bogus disinformation. Needless to say the treatment of my contribution to this committee was pathetic.

After receiving this publication last summer, I approached DEFRA over the bogus claims / misrepresentations which they had employed in their text to discredit the validity of my work, and informed them that if they did not amend their document immediately, then I would have no alternative but to sue them for publishing and circulating bogus claims throughout the international public/scientific domain.

In general, this DEFRA document employs a judicious selection of misrepresentation, innuendo, disinformation, half truths and outright bogus statements to discredit the overall validity of my work to the uninformed layreader. The bogus / misrepresentative nature of their statements are libellous and therefore serve as defamatory in relation to the credibility status of my work. This has personally prejudiced my professional integrity/ reputation as an international TSE disease researcher/lecturer as well as my capacity to generate grant funding for my research projects and to provide a personal income to maintain my family

The only reply that I have received from the DEFRA legal department to date, is a letter dated 1/11/2001 informing me that they are considering my comments and hope to be in a position to respond shortly. I have heard nothing since that date, nor have any of the amendments that I requested been applied to the DEFRA publication in question.

My rebuttal

In general the Professor Gabriel Horne committee publication written on behalf of DEFRA has sought to separate key synergistic facets of the overall multifactorial theory - such as the organo phosphate ( oxidant) and manganese factors - and then treat each tenet as entirely separate TSE causation theories. DEFRA therefore engineer themselves into an ideal position from which they can discredit the viability of my theory by operating a system of appraisal which only selectively considers half of the tenets proposed in the overall causal equation. eg by erroneously considering an "OP only" cause, or a "manganese only" cause , whilst failing to consider the synergistic outcome when both of these tenets are simultaneously combined within the causal interplay. The approach of this committee follows a more politically manipulative rather than scientifically based methodology.

Furthermore, the report betrays its unilateral , prejudiced perspective by employing unscientific methodology to stand up the conventional Establishment theory ( for instance, by repeated overuse of personal communications and unpublished papers as text references ), whereas any personal communications or unpublished papers that were presented as evidence in support of the dissident theories have been entirely discounted.

True to form, the dissident bodies find themselves in a no win situation, in which any presentation of their work to this committee needs to conform to a 200% "whiter than white" scientific approach to gain credence, whereas the Establishment bodies and chemical industry lobby groups who submitted to this committee find themselves able to get away with any old sloppy, unscientific style of presentation. A truly independent committee would have never permitted such a high degree of unilateral bias in their appraisal.

It is clear that this committee had no genuine intention to uncover the true origins of BSE, but were more concerned about cementing a firmer foothold on the conventional Establishment theory ( after the previous BSE Inquiry report (2000) had exposed so many flaws ).

  1. Section 4.8.3.1 (page 35)

"IT HAS BEEN SUGGESTED THAT ORGANO PHOSPHATE PESTICIDES (Ops) MAY HAVE BEEN THE PRIMARY CAUSE OF THE BSE EPIDEMIC IN THE UK. OPs HAVE BEEN USED WORLDWIDE FOR MANY YEARS FOR CONTROL OF ECTOPARASITES IN CATTLE"

This DEFRA statement is irrelevant to my published theory which clearly states that it is the SYSTEMIC types of OP formulation which penetrate into the brain/spinal cord of treated mammals and are involved in the pathogenesis of TSEs. Systemic OPs were used compulsorily at uniquely high concentrations/doses in the UK for the control of the endoparasitic warble fly larvae; eg; this being totally irrelevant to ectoparasitic control and the worldwide usage of all types of OPs as erroneously highlighted by DEFRA in their paragraph above

As my relevant published papers and oral evidence were presented to the DEFRA committee who authored this publication , these "experts" therefore have no excuse to misrepresent/muddle up the most fundamental tenet of my theory.

(2) Section 4.8.3.1 ( page 36 ).

"THERE IS NO DIRECT EXPERIMENTAL EVIDENCE TO SUPPORT OR REFUTE THE PROPOSED MECHANISMS OF ACTION " ( eg the biochemical mechanisms proposed in my theory ).

Whilst this Inquiry team did consider the published findings of the experimental work by Gordon et al ,1998, carried out at the Institute of Psychiatry ( funded by private individuals ) which DOES support my theory, their publication deliberately omits to report one half of the positive results of this study which confirms the increased period of retention of the prion protein onto the cell membrane in the phosmet treated cells – a well known hallmark of the prion diseased cell. This phosmet –mediated effect on the prion protein was hypothesised in my publications of 1994/1996 ( enshrined into the actual wording of the title of one of them !) which were supplied to this Inquiry committee .

  1. Section 4.8.3.1. (page 36).

"THIS REQUIRED TREATMENT OF ALL INFESTED ANIMALS WITH OPs ( SPECIFICALLY PHOSMET WHICH IS DESCRIBED BY HUMPHREYS AS A NON SYSTEMIC INSECTICIDE )

To state that phosmet is a"non systemic" insecticide is irrelevant in the context of its use as a warble fly treatment. All warble fly insecticides HAD to be formulated as a "systemic" oil based liquid "pour on" to enable them to act as a SYSTEMIC poison so that they could penetrate through the skin of the cow to kill off the warble larvae living inside . A non systemic formulation of phosmet would simply fail to kill the warble fly and therefore fail to fulfil its intended insecticidal function.

(4) Section 4.8.3.1. ( page 36 )

"NEARLY ALL COWS WHICH DEVELOPED BSE WERE BORN AFTER 1982 SO WERE NEVER TREATED WITH PHOSMET TO ERADICATE WARBLE FLY"

This is the most blatantly bogus statement in the whole document. Ironically, warble eradication first became compulsory in 1982 and, subsequent to this, MAFF were compelling phosmet treatment in the warble infested areas of the UK as well as consistently urging annual prophylactic phosmet treatment of all herds in the UK ( whether residing in infested or non-infested areas ) up until 1995. I hold copies of pamphlets which were circulated to all UK livestock farmers up until 1995, urging them to treat all cattle with the approved treatment ,phosmet.

Furthermore, my own high court case had to be mounted in 1985 to prevent MAFF’s forced treatment of my dairy herd with phosmet. If , as MAFF now say, warble treatment ceased in 1982, did I need to challenge their enforced phosmet treatment programme through the courts, three years after that date !!

Furthermore, data supplied by the chemical industry to the first BSE Inquiry demonstrates that the toxic concentration of the phosmet brands on the market had gradually increased from the days of 1972 when a 5% concentrated solution was first licensed to December 1978 when a 20% concentrated solution was first approved. It is perhaps no surprise that BSE first broke out in the mid 1980s as a legacy of the first field applications of the high concentatrion 20% phosmet in the early 1980s.

(5) Section; 4.8.3.1 ( page 36)

"GUERNSEY, WHICH HAD NO OFFICIAL CAMPAIGN AGAINST WARBLE FLY HAD 669 CASES OF BSE; JERSEY WHICH DID OFFICIALLY TREAT CATTLE FOR WARBLES HAD ONLY 138 CASES (NOAH REPORT TO THE INQUIRY)..

Again, this statement employs bogus disinformation to discredit my theory. Jersey NEVER officially treated cattle for warbles - confirmed by the jersey government’s chief vet officer, Noel Martin, in letters that he wrote to the farming press when NOAH ( the veterinary insecticide industry’s lobby group ) first employed this false statement to discredit my theory.

The above paragraph of the report then goes on to mention aspects of my own alternative explanation for the difference of BSE cases between Guernsey and Jersey lying in the variation of the soil mineral content of the two islands. It employs yet another personal communication from a PJ Loveland to state that "evidence of such differences has proved difficult to find ". Once again this biased committee clearly didn’t see the need to collect evidence to support the pesticide industry’s claims of an official warble fly eradication campaign existing on Jersey. Had they looked for the evidence to back my opponent’s claims – in the proper impartial scientific way – then they would have realised the bogus nature of NOAH’s claim

(6) Section 4.8.3.2. (page 36)

"WHILE SOME IMBALANCES OF TRACE ELEMENT NUTRITION MAY HAVE BECOME MORE PRONOUNCED IN RECENT YEARS, NONE ARE UNIQUE TO THE UK"

By separating the trace element tenet of my multifactorial theory from the organo-phosphate ( oxidative ) tenet, DEFRA have been able to demolish my explanation for the unique association of the BSE epidemic to the UK; eg, by erasing the high dose/high concentration usage of systemic organo phosphate warblecide tenet from the equation – a facet that is unique to the UK - , and treating it as an entirely separate causal theory.

My published theory clearly states that the oxidizing impact in the CNS following systemic OP exposure will transform CNS accumulations of manganese 2+ into highly lethal, proxidant manganese 3+ form – which triggers off the free radical mediated chain reaction of neurodegeneration that leads to TSE. Such an oxidative conversion will be greatly favoured and accelerated in metabolic systems that are already deficient in the antioxidant minerals selenium, zinc and copper, etc.

(7) Section 4.8.3.2. (page 36)

"IN ADDITION THE SPATIAL DISTRIBUTION OF AREAS OF LOW COPPER AND HIGH MANGANESE IN TOPSOILS DO NOT COINCIDE WITH THE BSE INCIDENCE DISTRIBUTION IN ENGLAND ( SEE FIGURE 2)" P>

Firstly, the publications depicting my theory - which were supplied to the Gabriel Horne committee – clearly propose that BSE was caused by the recent increased artificial supplementation of feeds / replacement calf milk powders / fertilisers with excessive doses of manganese etc, and is NOT fundamentally related to local soil levels of the mineral.

Indeed ,the local environments in which agricultural soils demonstrate low manganese levels may actually be exposed to higher levels of available manganese; due to the modern requirement for spraying on liquid manganese fertiliser several times a year to make good the deficiency !

Secondly, the maps employed on page36/37 to substantiate this irrelevant line of DEFRA’s rebuttal draw a comparison between a map of the high manganese/low copper regions in the UK and three maps of BSE incidence distribution in the UK - which only covers a mere three separate year periods of the total 15 year UK BSE epidemic.

However, if you study the further 12 maps ( from MAFF’s own BSE publications ) that cover the remaining 12 years of the BSE epidemic - which the Gabriel Horne committee document has conveniently omitted - then you do in fact see an actual overall correlation between the 15 maps of BSE incidence distribution in the UK and the high Mn/Low Cu UK soil map.

(8) Section 4.8.3.2 ( page 36)

"FURTHERMORE, BEEF COWS WHICH OBTAIN MOST OF THEIR FOOD FROM PASTURE , ARE MORE LIKELY THAN DAIRY COWS TO EXPERIENCE AN ABNORMAL IMBALANCE IN DIETARY INTAKE OF THE TRACE ELEMENTS COPPER, MOLYBDENUM, SELENIUM AND MANGANESE, SINCE COMPOUND FEEDS FOR DAIRY COWS ARE SUPPLEMENTED WITH THESE TRACE ELEMENTS AS NECESSARY TO MEET NUTRIENT REQUIREMENTS. ACCORDINGLY, A HIGHER INCIDENCE OF BSE WOULD BE EXPECTED IN BEEF COWS RATHER THAN IN DAIRY COWS. THE REVERSE IS TRUE."

Once again, The DEFRA committee miss the whole point of my theory- that it IS the feeding of mineral supplements ( via compound feeds, mineral licks, artificial calf milk powder, etc ) containing high levels of manganese which I have proposed as the central cause of BSE .

Whilst DEFRA correctly point out the differential; that Dairy as opposed to Beef suckler cattle are the class of cow who are largely receiving these supplements, then surely this explains, according to my theory, why dairy cows are going down with a far higher incidence rate of BSE than beef suckler cattle.

Mark Purdey. Dec 2001