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THE POLITICAL CONVENIENCE OF MAD COW DISEASE
by Steve Reed © January 2001

How is it that, uniquely in the world, the British herd has been decimated by BSE, over the last fifteen years, that the few cases which have occurred elsewhere are mostly traceable to cattle exported (a negligible proportion of the vast numbers of cattle exported) from Britain, since the outbreak began, and how was this convenient and for whom? First, I include a few paragraphs about the disease and its causative agent.

The Pathogen and its Effects

Bovine spongiform encephalopathy (BSE or Mad Cow Disease) is a new member of the group of diseases called transmissible (i.e. infectious) spongiform encephalopathies (TSE’s) which include scrapie, of sheep, the wasting diseases, of certain American deer, and kuru and Creutzfeld-Jakob’s disease (CJD) of humans. The TSE’s are a sub-group of the neuro-degenerative disorders, which include diseases not thought to be transmissible, such as Parkinson’s disease and Alzheimer’s Syndrome. The neuro-degenerative disorders are generally identified, before death, by co-ordination-loss and dementia, and, at autopsy, by neuronal atrophy (death of nerve-cells) vacuolation (sponginess) of the grey matter of the central nervous system (CNS) and accumulations of amyloid plaques and fibrils (patches and strands of a peculiar, proteinaceous material) in association with vacuolation.

This proteinaceous material, which, in sheep, is called scrapie prion-protein (PrPsc) is thought to be a mutant form of a normally-elaborated prion protein (PrP) Normally, PrP is produced, in any mammalian nerve-cell, for addition to the outside of the nerve-cell external membrane, where it is thought to serve a recognition function. i.e. PrP molecules are attached to the exterior of the cell to mediate between the surrounding fluids and the cytoplasm (interior of the cell) selecting or rejecting materials for intracellular use. If this is so, and if the classes of substances selected by PrP are vital for cell-function, then PrP is vital for cell-function.

The development of the neuro-degenerative disorders appears to be associated with a modification of the PrP molecule, which occurs after its amino-acid sequence (essential chemical composition) has been constructed. PrP, like all proteins, is a large, complex molecule exhibiting primary, secondary and tertiary etc. coiling of its constituent amino-acid chains. It has been established that the modification, which creates PrPsc from PrP, is a modification of the higher structure of the molecule (i.e.chemically, PrP and PrPsc appear to be identical)

In this modified form, PrP is not able to perform its normal function. Consequently, affected cells are stimulated, by an apparent lack of PrP, to make more PrP, and, when this too fails to work, yet more, and so on. The nerve-cell exhausts itself attempting to make good the functional PrP deficit, and quantities of the useless, modified form are re-envaginated in the cell, but, being resistant to proteolytic enzymes, such as protease, they are not re-absorbed and accumulate. This protease-resistance of PrPsc is crucial to understanding the transmission of the disease, as well as its pathology, and I shall return to it. Eventually the nerve-cell dies and breaks down, leaving a vacuole, in the grey matter, lined with the modified form of PrP.

In the non-transmissible, neuro-degenerative disorders, the foregoing procedure is initiated by the mammal’s own genome (either congenitally or after random mutation) apparently as part of the ageing process, and the PrP produced, after transfer to another host, has not been found to precipitate the procedure in that host. At this point, one begins to get some idea of the range of possibilities offered by any technique for altering the higher structure of the molecule.

In the TSE’s, however, after transfer to a conspecific, healthy host, the mutant PrP has been shown to be capable of inducing the same degenerative procedure in that host. This was an unprecedented finding, because PrP is not a self-replicating organism. It has no nucleic-acid component wherewith to effect - or, as in a virus, cause a host-cell to effect - its replication. Somehow, however, its presence in, or near, the host-cells causes the PrP they produce to be modified in similar fashion - and to become similarly infective. The best way to describe such an agent, I think, is to call it an organic poison which induces host-cells to produce the same, or a similar, organic poison. As we shall see, the poison produced by the poisoned host is not always identical, in the species-specificity of its infective power, to the poison with which the host was poisoned. Charting this process of modification-by-passage is crucial to tracking the poison from one host-species to another.

I should add that amyloidosis (PrP-poisoning) and vacuolation are often found in the brains of very old people who exhibited no signs of dementia before dying from some other cause (i.e., before amyloidosis was sufficiently advanced to cause dementia) It seems reasonable to suppose, therefore, that the non-transmissible, amyloidotic, neuro-degenerative disorders are naturally-selected, time-controlled, lethal mechanisms for eliminating obsolescent community-members, and that the transmissible forms are dysfunctional escapes from these mechanisms. The question I wish to ask is, did all of these TSE’s escape, without the intentional assistance of human agencies, or not - in particular, is BSE an intentional artefact, or not?

Biological Agents For Use Against Civilian Populations

The ways in which the BSE outbreak was convenient for certain agencies, I propose to discuss later; but I should like to affirm straight away that covert, biological aggression is a recognised tactic of the politico-commercial complex of the west, and has been for centuries, at least since the time, in the 17th century, when London prostitutes were shipped to the Americas in order to “pox the Indians”.

The United States Congressional Record shows that, in 1969, several millions of dollars per year were voted to a CIA-initiative “to develop an untraceable contagion for use against civil populations”. Some see this as the initiative which led to the development of human immuno-virus (HIV) the supposed agent of adult immune deficiency syndrome (AIDS) HIV remains undetectable in the host for long periods and, when it appears, only does so as the signs of secondary diseases. These characteristics, together with the elusive nature of the infective particle (whose identity some still question) fulfil the criteria for an “untraceable contagion”, which the CIA presented to Congress and which Congress approved.

Evidence, to the effect that researchers adapted immuno-virus of chimpanzees (CIV) to human hosts - by the action of mutagens on infected material and the injection of such material into human hosts - has been amassed by Robert Lederer (Covert Action Information Bulletin 28, 1987) Jon Rappoport (“AIDS Inc.: Scandal of the Century, 1988) and G.J. Krupey (“Aids: Act of God or of the Pentagon?”, 1992)

It is generally thought that HIV was introduced to the human population during the World Health Organisation’s smallpox-vaccination programme, in the Congo, in 1975, and by means of batches of “experimental hepatitis-B vaccine”, sent out to American volunteer-patients, by the US National Institutes of Health, in 1978.

Be this as it may - and, whether HIV is an intentional artefact or not - the fact remains that, in 1969, public money was voted for the purpose of acquiring the capacity to produce such an artefact. If one then baulks at the possibility of official agencies actually using such an artefact for purposes of political or socio-economic manipulation, one has only to look at the US Public Health Service’ “Tuskegee Syphilis Study” - in which 400 syphilitic, black men were denied treatment for syphilis, over a 40-year period, during which most of them died - or the Rockefeller Institute’s “Puerto Rico Cancer Experiment”, in which 13 human subjects were induced to develop fatal cancers - to see that official motivation for deploying diseases against the civilian population is not necessarily restrained by any considerations of conscience. Further examples of unethical procedures, which have actually come to light, within the purview of the controlling powers of the “western democracies” alone, could be cited, literally, ad nauseam. Almost everyone can think of an instance they have heard about. Particularly telling, in this context, however, is the use of anthrax by the Germans, during the First World War, mainly against cattle, and the findings of the International Scientific Commission (ISC) of 1952, “to examine the facts concerning bacterial warfare in Korea and China”, during the Korean War. The ISC found that numerous sites, in Korea and China, suffered outbreaks of bubonic plague and cholera after “bombs”, containing plague-infected fleas, or cholera-infected shellfish, were dropped, from American aircraft, over densely populated areas and reservoirs, respectively. According to Dr. Murray Sanders, a military physician in a position to know, weapons such as these were developed, using captured, Japanese, bio-warfare technology, at Fort Detrick, in Maryland, after WWII.

It might be argued, nevertheless, that the Tuskegee and Puerto Rico atrocities were purely scientific experiments, that anthrax, plague and cholera were only used in the context of international hostilities and that the Germans were anyway not living under democracy during the First World War. Indeed, if the BSE outbreak was caused by intentional human agency, in a so-called “democratic” country or countries, for the purposes of socio-economic manipulation, in peace-time, then, as far as is known, it is, in this respect also, almost unprecedented. Almost.

In 1972, the US-government officially renounced the use of biological weapons; but work on such weapons continued, all the more vigorously, at “independent” universities and “private” research institutes. In the 70’s, moreover, the science of genetic engineering came into its own, in the field of weapons-research, and, in 1986, the respected Wistar Institute of Philadelphia succeeded in (or “failed to avoid”) provoking an outbreak of disease, among cattle, in Argentina, using a genetically-modified form of the rabies-virus. This was also the year, in which BSE was first diagnosed in Britain.

If the US Congress openly voted funds, in 1969, “to develop an untraceable contagion for use against civil populations”, we may be sure that other governments and institutions - rather more discreetly, no doubt - have done likewise; and that, if they are capable of developing and deploying untraceable contagions against civilian populations, then they are certainly capable of developing and deploying them against livestock. It remains to be seen, of course, whether livestock are the ultimate target of BSE, or whether - through the possible transfer of BSE to humans, as CJD - the ultimate target is the civil population, after all.

There is another feature of both AIDS and BSE, besides the difficulty involved in detecting them - and the fact that they are invariably fatal - which should be noted in this context. Both appear to be derived from stable, endemic diseases (of chimpanzees and sheep, respectively) which never previously crossed the “species-barrier”. Although Africans hunted chimps - and must have been bitten and scratched by wounded quarry - and although sheep and cattle have shared pastures and dropped their young in shared pastures - for millennia, AIDS remained a disease of chimps and scrapie remained a disease of sheep, until the development of “an untraceable contagion” began. Now these diseases are running riot beyond the species barrier. Why, if sufficient motive, method and opportunity for their deployment can be demonstrated, should we not suspect that these diseases have been spread through the intentional intervention of some official or quasi-official, scientific agency or agencies? I think that such a motive, method and opportunity can be demonstrated - at least, in the case of BSE - and that suspicion should be directed towards certain agencies.

With this in mind, let us now consider the infectivity of PrPsc - since scrapie of sheep is generally supposed to be the direct precursor of BSE .

 

The Infectivity of PrPsc

The centuries, during which cattle and scrapie-infected sheep have shared grazing, and the fact that the practice of feeding meat-and-bone meal (MBM) to cattle dates back to 1926 (see Phillips Report, Vol.1, Oct. 2000) indicate that ovine TSE is not readily transmissible to cattle. Therefore, the hypothesis, that scrapie is the direct precursor of BSE, should have been rigorously examined, as a priority, from the outset (1986) with a view to eliminating PrPsc as a possible, immediate source of infection.

No work, on this essential question, was published, however, until April 1994, when Dr. R.C. Cutlip et al. showed, in the American “Journal of Infectious Diseases”, that the infective agent of scrapie did not cause BSE of cattle. On the contrary, the injection of homogenised, scrapie-infected tissues into the brains of calves, by Cutlip et al., was said to have produced signs of nervous degeneration typical of motor-neurone disease and none of the signs of BSE.

Also in April 1994, the Minister of Agriculture, when appraised of Cutlip’s results, in a Parliamentary Question, was asked to reveal what work had been done (by the numerous bodies engaged in investigating BSE on the government’s behalf) to substantiate the assumption that scrapie was the immediate source of the epidemic. In his Parliamentary Answer, the Minister replied to the effect that no experiments had been performed, in the UK, to examine the scrapie-as-immediate-BSE-source- hypothesis - the hypothesis, I should add, upon which the government’s entire BSE-policy had been, ostensibly, built and had been, for eight years, pursued.

The suspicion and unrest which this pronouncement provoked in a smitten farming community, in a devastated meat-industry and among concerned Members of Parliament was considerable, and, in June 1994, the Ministry of Agriculture Fisheries and Food (MAFF) saw fit to announce, after all, that experiments into the infectivity, to cattle, of scrapie-infected tissues, had been completed - in January 1992! - and that they had consisted of feeding scrapie-infected tissues to calves; but that they had resulted only (and not surprisingly) in traces of infectious material being recovered from the subjects’ guts.

I shall cite elsewhere further material, pointing to a government cover-up of the source of BSE. Suffice it, for the purpose of this section, to quote again from the Phillips Report on the BSE Inquiry, Oct 2000:

“BSE probably originated from a novel source early in the 1970’s, possibly a cow or other animal which developed disease as a consequence of gene-mutation.

“The origin of the disease will probably never be known with certainty.”

It is worth recalling, at this point, that no instance of a transmissible spongiform encephalopathy has ever been attributed to “gene-mutation”. The sporadic, or random, neuro-degenerative disorders, which arise from “gene-mutation”, have all been found to be non-infectious. As Richard Kimberlin, the government’s chief neuropathologist, said, in 1990 (by which time 20 000 cases had been recorded) “BSE is clearly not a disease of genetic origin - it has occurred, in all breeds and crosses, in the proportion corresponding with their representation in the national herd.”

Phillips continues through a further 15 volumes without advancing on his unsatisfactory statement or making any proposals for advancing on it. The origin of the plague which, by summer 2000, had killed 170 000 British cattle and led to the precautionary destruction of 4.7 million more, does not seem to concern Lord Phillips (or anyone else) very much. He has produced an alternative, lone aberrant-gene theory and left us with “the answer will (“probably”/“we hope!”?) “never be known with certainty”! We do know, however, that BSE was not caused by feeding scrapie-infected sheep-remains to cattle, that, even in the 2000 Report, Phillips can scarcely bring himself to admit this fact and that, even today, the public in Britain, in the newly affected parts of Europe (France and Germany) and in the USA are still under the impression - or being actively encouraged to believe - that scrapie-infected sheep-remains are the direct source of BSE! Let us begin where the Phillips Report seems to want us to stop - at the beginning!

Chronologically, scrapie comes first. Reliable records of it go back to 1730. All the other TSE’s appeared in the 20th century, starting with transmissible encephalopathy of mink (TME) of which the following account is drawn from a paper, presented by Williams and Young, in “La Revue Scientifique et Technique de l’Office International des Epizooties: Encephalopathies Spongiformes Transmissibles des Animaux, Vol. II, No.2”, June 1992 (OIE Revue, June 1992)

TME was first recorded, in 1947, from two sites simultaneously; a mink-ranch in Wisconsin, where the entire stock was wiped out, and another in Minnesota, where only 125 animals died, but all of which had been received, from the said Wisconsin ranch, seven months earlier. It is important to note that these data indicate an incubation period, for this outbreak, of at least seven months. I would also point out that, according to Murray Sanders, the USA’s first, serious research into bio-warfare techniques was progressing, at Fort Detrick, at this time, and that, according to the ISC findings (1952) biological attacks, by US-forces, on China and Korea, were soon to follow.

The next outbreak of TME occurred 14 years later, in 1961, ’62 and ’63, when five ranches, all of them in Wisconsin, lost between 10% and 30% of stock. In 1965, as Williams and Young (OIE Revue, June 1992) also note, TME wrought havoc in the mink-farms of the DDR and USSR.

No TME was reported thereafter for 22 years, until, in 1985 (when the first cases of BSE were recorded, retrospectively, in Britain) a severe outbreak occurred at a ranch near Stetsonville, Wisconsin. In contrast to the outbreaks of 1947 and 1961-3, the Stetsonville case was investigated publicly and with great thoroughness, and it was established that the pathogen required a longer incubation period (7 months) during passage of the first mink-host than during the passage of subsequent mink-hosts (“Passage”, here, is the period from infection, by means of feed contaminated with TME-infected material, to death of the host) In this way, four “generations” of pathogen were produced, each successive one capable of killing the host four weeks sooner than the generation before. The fourth generation, with an incubation-period of four months, could not be improved upon in this respect. It was said to have achieved complete adaptation to mink. The fact that such improvement was possible, however, indicates that the first generation was not well-adapted to mink and was only able to infect them at all because of some natural, partial affinity between its higher structure and that of the prion protein (PrP) of mink. Researchers concluded, therefore, that TME was a disease which, when it broke out in 1947 and 1985, at least, had just crossed the species-barrier, to mink, from its natural host.

The signs of TME are those of a typical spongiform encephalopathy, whose only known transmissible form, prior to the 20th century, was scrapie of sheep. Naturally (and with considerably more alacrity than MAFF investigated the aetiology of BSE - assuming MAFF ever really conducted such tests at all) the Stetsonville team attempted experimental transmission of scrapie, from British sheep, to mink, but without success. Then, and, for some reason, only then, did they try infecting mink with scrapie-contaminated tissues from American sheep, and they succeeded!

Here, I suggest, is the essential link between scrapie and BSE, because the American researchers went on to test the Stetsonville TME-strain on a large selection of other animals and succeeded in infecting, not only ferrets, hamsters, rhesus monkeys, macaques, squirrel monkeys, sheep and goats, but also cattle! Furthermore, the signs of the disease produced in cattle, by infection with TME, were indistinguishable from the signs of BSE. An infection pathway from sheep to cattle, via mink, was thus demonstrated. It is not a long, roundabout route (although a lot of work would have to have gone into finding it) nor is it an incredibly unprecedented, “infectious, spontaneous gene-mutation”; it is a means of conveying sheep-TSE to cattle via one intervening host - a host which can be farmed and harvested in large numbers.

Only one possible source of TME (scrapie of American sheep) had been found, and yet researchers were unable to substantiate the presence of material, infected from this source, in the feed supplied to the Stetsonville ranch. They therefore concluded that the cause of the 1985 outbreak was “an as yet unidentified, infectious ingredient of feed”. Thus, if American scrapie is the cause of TME, then scrapie-contaminated material has been introduced three times to Wisconsin mink-ranches, at three strategic moments in the history of biological warfare, either untraceably and by chance, or surreptitiously and untraceably, by design.

Another possible source of infection was discovered, however, not in Wisconsin, but 800 miles away, in Colorado. Here another TSE, chronic wasting disease (CWD) of deer, was identified, at an experimental centre, now known as the “Fort Collins Wildlife Research Facility”, in the 1960’s. Only mule- and black-tailed deer and elk were affected, and only animals in, or near, the facility, which, prior to 1974, carried out extensive work on sheep and goats for the purposes of disease-research and antibody-production. CWD has not been recorded anywhere else on Earth, excepting in, and around, another, similar research facility, in Wyoming.

Williams and Young state that activity at these facilities was particularly intense just before CWD broke out among the deer, but they add this intriguing sentence (referring to the experimental sheep and goats)

“None was noticed to have neurological disease, but it is unlikely that scrapie would have been recognised in these animals.”

But why not? Do not scientists researching diseases and culturing antibodies in live animals take an interest in the condition of their subjects? Are they not qualified to diagnose diseases or realise when a diagnosis is required? Or do we see, in the word “recognised” a euphemism for the word “admitted”?

However that may be, CWD, a TSE found only in association with these research facilities, originating during the darkest days of the Cold War - and at about the same time as the decimation of the farmed mink of Eastern Europe - was also found, by researchers in the 80’s, to be transmissible to mink. Moreover, the research facilities involved had the capacity to produce infective material in large quantities.

So we have two possible sources for the TME outbreaks of the 40’s, 60’s and 80’s - scrapie of American sheep and CWD of Rocky Mountain deer, neither of which could conceivably have reached Wisconsin’s mink-ranches except as a consequence of complex human intervention. Williams and Young do not tell us what became of the thousands (tens of thousands?) of TME-killed mink, which were removed from the Stetsonville ranch for testing, or in what numbers other mink - and individuals of other species - were infected and killed thereafter. Clearly, however, a large supply of material capable of infecting cattle with BSE became available, just before cattle in Britain began to contract BSE in large numbers.

The Progress of the BSE-Epidemic

Also in the OIE Revue of June 1992, there is a paper, presented by Dr. Richard H. Kimberlin and entitled “Bovine Spongiform Encephalopathy - a review-paper, commissioned by the Food and Agriculture Organisation [a Rome-based off-shoot of the United Nations Organisation] which kindly granted permission, to the OIE, to reproduce a similar version [here]”.

The paper is illustrated with a graph and two maps (reproduced below) each accompanied by the legend, “courtesy of J.W.Wilesmith”. Kimberlin and Wilesmith were the government experts assigned to the Southwood Committee (June 1988 - Feb 1989) a body set up to determine the cause, extent and implications of the BSE epidemic and the remedy for it. As Prof. R.W.Lacey tells us, in his fascinating study of the epidemic, “Mad Cow Disease” (1994) Southwood and his group lacked expertise in epidemiology generally and in the science of TSE’s in particular. What’s more, they did not co-opt any experts from either of these disciplines. In his restrained way, Lacey refers to the “heavy burden of responsibility” which must have fallen upon the government experts - veterinary epidemiologist Wilesmith and neuropathologist Kimberlin - but the fact of the matter seems to be that the committee of inquiry was led by the nose, by Wilesmith and Kimberlin, through all the technical data about the origin and spread of BSE, to the erroneous conclusion the government wanted them to reach: i.e. “BSE was probably caused by feeding scrapie-infected sheep-remains to cattle”.

Like all government-sponsored material about the epidemic, Kimberlin’s paper in the OIE Revue of June 1992, is endlessly discursive, about the uncontroversial aspects of BSE, and perfunctory, when interpreting data about the origin and spread of the disease. The maps, however, tell their own, inconvenient story: one (Fig.1) indicates - with dates - the counties, where the earliest, “suspected” cases were reported, between April 1985 and November 1986, and the other (Fig.2) shows the proportion of dairy herds, per county, in which BSE had been reported by August 1990.

Since BSE was not formally described until late in 1986, “Fig.1” shows the cases which were identified retrospectively. However, the timing, distribution and frequency of their occurrence does not support either the initial, official line (that scrapie-infected sheep-remains were the origin of BSE) nor the later one (that BSE “possibly” originated from a “random mutation” in a single animal) There is thus no reason to believe that these data were doctored as part of any cover-up.

Geographical distribution of the first suspected cases of BSE

(April 1985 to December 1986)

Courtesy of J.W. Wilesmith

Three facts are immediately apparent: firstly, each case occurred in isolation from all the others (there is no point-source with a radiating frequency-gradient) secondly, all the counties affected, in 1985, are coastal, and, thirdly, half of the counties affected, by the end of 1986, are on the south coast (the others being dispersed in the Midlands, Wales and the North) so that all south-coast counties were affected, by that time.

The isolatedness of cases continued to be a feature of the epidemic throughout its history: even by 1992, as Kimberlin himself tells us, “over 47% of all affected herds had only one case, and another 18%, only two”, which (he goes on) “indicates a low, average exposure to a source of infection outside the cattle-population”. Since exhaustive experimentation has failed to demonstrate any sporadic, or Mendelian, genetic susceptibility to BSE, the incidence of cases must, as Kimberlin concedes, be due to the distribution-pattern of the infective agent. Clearly, therefore, the infective agent was distributed thinly and evenly over the affected areas.

It is “Fig.2” which really gives the game away, however. In this remarkable map, we see four well-defined bands of incidence, each showing a frequency of cases in direct proportion to its closeness to the curve of the southern and eastern coasts. The only anomalies in this pattern are the urban counties, and urbanised counties, of the south-east, the north Midlands and the north-east, where there are few or no cattle.

Cumulative proportion of dairy herds with BSE in home-bred cattle

(November 1986 to August 1990)

Courtesy of J.W.Wilesmith

Contrary to Kimberlin’s feeble explanation, of this beautifully defined pattern, to the effect that more efficient, feed-processing procedures, in Scotland and the north of England, were more likely to eliminate the infective agent from feed - which, anyway, we now know to be erroneous (because the infective agent has been shown to be indestructible by anything short of combustion) - there is no geographical pattern of feed-processing procedures or feed-distribution catchments which can account for this. The geology of Britain is aligned with the bands, as they appear on the map, but geology - and the resulting topography - would only affect feed-distribution, if it consisted of high mountains, with deep valleys, which permitted almost no communication between one valley and its neighbours to the south-east and north-west. This is not the case. Technically, indeed, there are no mountains, at all, in Britain, only hills, which present no effective barriers to the transport of goods along a south-east/north-west axis.

The pattern shown in Fig.2 does not correspond with the prevailing isotherms or isohyets (patterns of temperature and rainfall) but it does correspond with the falling speed of the wind, when it blows from the south-east, encountering, first the south and east coasts, the Downs and the south-western moors (herds affected, up to 36%) then the Mendip, Salisbury Plain, the Chilterns and the Wolds (herds affected, up to 21%) then the Pennines, Cambrians and Grampians (herds affected, up to 14%) and, finally, the north-western seaboard (herds affected, up to 7%)

Kimberlin directs us to an incredible explanation of this SE-NW pattern, which he misleadingly calls “The North-South gradient”, based entirely on erroneous assumptions about variations in the quality of feed-processing procedures. His despairing, parting shot, on this matter, is to assert that there might have been more scrapied sheep in the catchment-areas of the feed-plants which supplied the regions worst-affected by BSE! Yet we only have to look at the distribution of sheep, in Britain, to see that it grades from a high in the north-west to a low in the south-east, in direct contradiction of this idea - unless we imagine that the incidence of scrapie is more than inversely proportional to the incidence of sheep, which is obvious nonsense. I suggest that Kimberlin and Wilesmith deceived the Southwood Committee, and that Kimberlin (in OIE Revue, June 1992) is lying to us.

Of course, Wilesmith and Kimberlin were not in this on their own; they were acting on behalf of highly-placed, British bureaucrats and politicians who, as I shall outline later, are part of a close-knit, supranational, politico-commercial complex, linking Washington and Brussels with all the capitals of the western world. Thus, the suspected deception - being the cover-up of an operation tantamount to an act of war - is a deception designed by supranational forces and deployed by the British government on behalf of those forces; but what exactly are Wilesmith and Kimberlin, and all those they represent, covering up?

In Volume II of his 16-volume morass of a report (October 2000) Lord Phillips describes recent experiments, carried out by the government’s Central Veterinary Laboratories, which “demonstrated that 1 gram of homogenised brain, from BSE-infected cattle, is sufficient to transmit the disease orally to cattle” (my italics) This quantity of material - about the size of a peppercorn - furthermore, is certainly not the minimum, infective quantity, because the quantity of the active agent (mutant PrP) in the 1-gram mass of homogenised brain, was not determined. Clearly, the mass of the infective prion-protein, necessary to cause infection, when isolated from, or concentrated within, homogenised, infected tissues, could be very tiny indeed: small enough, in fact, to be borne on a light south-easterly breeze, from a line-source above the English Channel, and distributed thinly and uniformly, within each of a series of well-defined, fall-out zones, right across mainland Britain.

This, I suggest, indicates the truth which, according to Phillips, “will probably never be known with certainty”, because all the official investigators and their masters, and their masters’ associates, have no interest in making it known at all. Quite the reverse.

Kimberlin’s paper in OIE Revue, June 1992, presents us with yet another piece of solid data: this too is a Wilesmith-contribution, which, like the maps, conveys rather more to the alert observer than it was, in my opinion, intended to convey.

Month/Year of onset of clinical signs

Fig. 3

Number of cases of BSE by the month and year of onset of clinical signs

(April 1985 to April 1991)

Courtesy of J.W.Wilesmith

The feature to note, besides the sustained, overall increase in the incidence of BSE, is the regular surge in the onset of signs, which occurred during the winter of each year shown. As far as I am aware, it has never been argued that general loss of condition, in the cattle-population, such as might be expected during the winter-months, could expedite the onset of the clinical signs of BSE, and Kimberlin does not argue this. In fact, he ignores the seasonal factor completely. From his point of view, I imagine, this was a prudent choice, because BSE is not a disease which would be enhanced by loss of condition, or any factor which would retard metabolic processes: it is a disease which is aggravated by the efficiency of metabolic processes! The more efficient they are, the more rapidly they produce mutant PrP and the more rapidly they operate to destroy the nervous system.

I further suggest, therefore, that the winter-surges, in the onset of the clinical signs of BSE, are due to the timing of the distribution of the infective agent. Moreover, since the incubation-period, in cattle, of orally-ingested, mutant PrP is considered to be about three years in length, each of these winter-surges probably represents a distribution of the infective agent, which occurred during one or more of the long, dark nights of the corresponding winter, three years before.

In his book, “Mad Cow Disease” (1994) Professor of Clinical Microbiology, Richard Lacey tells us, “re-feeding of the same species of animal with its own material […] could well increase the incidence of BSE; but does this really account for the sudden and widespread occurrence of BSE in 1987 [or, indeed, I would add, its periodically surging, almost exponential spread thereafter]?

“I think not,” continues Lacey, “nor did the UK government or its advisers.”

Thus, not only has the initial cause of the outbreak never been established - the mechanism by which it spread has never been properly elucidated either. I suggest that the initial cause and the mechanism of spread are, in fact, one and the same. I suggest that periodic distribution of infective material, in a north-westerly direction, accounts both for the initiation of the outbreak and, in the main, for its disastrous continuation.

 

The Political Convenience of BSE

Any reader of Volume I of the Phillips Report will be astounded by the catalogue of apparent incompetence, on the part of the Ministry of Agriculture, Fisheries and Food and the Department of Health, which are chronicled there. Each item of “failure of communication”, inexcusable delay, laying-off of essential staff, unwarranted secrecy and misinformation is described, by a seemingly puzzled Phillips, with the ubiquitous codicil, “this should not have happened”. Indeed, it should not. Neither should Phillips wring his hands impotently while those responsible for these crimes continue in their posts, or, as is more frequently the case, continue in the posts to which they were promoted, and with the honours they were awarded, shortly after committing them. It has not even been found necessary to pillory a few innocent and low-ranking scapegoats. What an operation!

In his Report, Phillips describes, also in loving detail, the efficiency with which British agriculture once supplied the home market and exported abundantly, under a sage regime of self-sufficiency, thus securing Britain against the blackmail of embargo and siege, and contributing handsomely to the national balance of payments. He goes on to mention the network of small abattoirs, feed-plants and food-factories, which still existed entire, in the early 80’s, and which was able to supply each locality, without transporting beasts-for-slaughter, or their products, long, gruelling or expensive distances.

It was this admirable system of small-to-medium-sized farms and firms which protected us against famine, against the threat of foreign domination and against take-over by international big-business. It was this admirable system which BSE appears to have been designed, and certainly did, very largely, destroy.

Britain is now heavily dependent on an uninterrupted flood of food-imports. The EU-Directorates could now take measures which would declare, in effect, “comply with our decrees, or starve!” Meanwhile, mighty supranational combines (of the ilk which support the endless extension of the borders and powers of the EU) have bought out great swaths of our food-producing capacity, on the cheap, to do with as it suits their global policies. This is an important source of our much-vaunted “record inward investment” of recent years!

All of this has happened - largely as a result of BSE - and under the cloak, I suggest, of government complicity and cover-up, not just to bring the British to the globalist, EU heel, but to break down the socio-economic structure of all western capitalism’s captive states. The same tactics, I suggest, are now being used to undermine the similarly self-sufficient, food-supply systems of Germany, France and the USA.

In order to destroy the nation-state, which is such an inconvenient obstacle to maximising the profits of untrammelled, global commerce (or “free trade”, as it is euphemistically called) you must first break the backbone of the nation (which consists of small business, in general, and small farming, in particular) and threaten to empty the nation’s belly.

This is what the creators of superstates, in cahoots with the moguls of big business and the proponents of (necessarily undemocratic) global governance, are doing. We know that, in pursuit of this aim, they sanction a vast arms-for-drugs trade, in order to destabilise recalcitrant states elsewhere (and not so far away) in the world, swell the covert budgets of the secret services and channel vast, untaxable profits into so-called “legitimate” businesses. Anyone can see that the “war on drugs” is a sham, intended only to suppress competitors and raise prices - hence its apparent, dismal failure! In this new, cold war, waged by a plutocracy against the rest of humanity, the suffering wrought, both by the weapons (in the hands of western-sponsored insurgents, in dozens of second- and third-world target nations) and by the drugs (in the veins of the ever-increasing numbers of the disillusioned and the dispossessed in western society) dwarfs the misery caused by all the hot wars in history.

Why should we not imagine that such people are incapable of unleashing BSE upon us - and seeding new-variant CJD here and there - as part of their global plan? Motive, method and opportunity can all be demonstrated; but is such an idea just too Machiavellian to impute to the Rockefellers, Rothschilds, Warburgs, Lehmanns et al., of the Council on Foreign Relations’ Corporate Program, and the politicians they select, and persuade us to elect, by means of blanket mass-media control?

I regret to say that I do not believe it is.

Steve Reed