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Dissenting voices.

Latest

"illogical, inconsistent and weirdly worded regulations"

"......the Regulations of 2002 were, in the first place, "based on the widespread assumption that a rogue isoform of a protein designated PrP - called prion protein by some - causes TSEs. That hypothesis is unsupported by rigorous analysis and substantial data contradict it." The transcript of the debate makes for deeply disturbing reading. The Countess of Mar politely and painstakingly dissects the illogical, inconsistent and weirdly worded regulations, concluding moreover that "I want the Minister to know that I am extremely concerned that all regulation in this field is based on a hypothesis - not even a theory - that none of the "establishment" scientific community can prove, despite millions of pounds of taxpayers' money being thrown at the subject.... . " Read in full

The link between vCJD...BSE....scrapie..... and calls for bigger research grants.

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The paper on TSEs in the Veterinary Times for Jan 27 2003 can be read in full here.

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November 3 2007 ~ Major investigation to find source of Donegal BSE case

The Minister for Agriculture in Ireland, Mary Coughlan, says that a major investigation is underway into a case of BSE in County Donegal. The five-year-old cow was born six years after tight controls were introduced. We not that the article in the Belfast Telegraph insists that BSE "can lead to variant CJD in humans".

June 15 2007 ~ The UK Government is still resisting the sensible amendments of the EU on BSE cohorts

Regulation (EC) No.1923/2006 allows Member States to permit the use of BSE cohorts until the end of their productive lives following such a request from a Member State. Permission is dependent upon a favourable risk assessment taking into account the control measures in that Member State. The TSE Roadmap http://ec.europa.eu/food/food/biosafety/bse/roadmap_en.pdf
Point 2.6 :
".... The derogation to defer the culling would be the Member States' decision. This relaxation would not endanger the current level of consumer protection. A relaxation would not only reduce the economical impact but also the social consequences following the complete destruction of the cohorts being often one of the main reasons to object to the culling policy.
The answer (Hansard) given yesterday by Ben Bradshaw does not answer the question from David Drew about the "scientific rationale" behind the culling of cohorts.
Mr. Drew: To ask the Secretary of State for Environment, Food and Rural Affairs what the scientific rationale is for continuing to cull bovine spongiform encephalopathy cohort cattle.
Mr. Bradshaw: A Veterinary Risk Assessment (VRA), published on 21 May 2007, concluded that culling cohorts of cattle affected with bovine spongiform encephalopathy (BSE) as soon as possible:
• supports the Government's challenging target of eradicating BSE in Great Britain by 2010;
• promotes consumer confidence in UK beef; and
• avoids the need for expensive additional control measures to monitor cohorts."
How much scientific rationale (as opposed to financial and political consideration) underpins the Veterinary Risk assessment (pdf new window) may be seen by reading the relevant pages. Indeed, the conclusions of the "risk assessment" seem to be driven more by considerations of "additional expense" and trying to prop up confidence in the government's policy (or "consumer confidence in UK beef") than on scientific veterinary risk assessment. One wonders if Ben Bradshaw has actually read any of the relevant documents in full or questioned the answers DEFRA gives him on such important issues.

January 31 2007 ~ " I think it's as likely to find infection with that protein as it is to find weapons of mass destruction in Iraq"

See report at science.monstersandcritics.com. Laura Manuelidis, professor and head of neuropathology at Yale University Medical School, has just published a paper supporting her theory that the most likely explanation for TSE diseases is a stealthy, slow-acting virus. Professor Manuelidis has been working on TSE's for decades. Back in 2004, she was quoted on JSonline.com at the end of a story about the researches of another scientist, Frank Bastian, a professor of neuropathology, who also challenged the prion theory.
"I don't believe protein is infectious," she said. "I think it's as likely to find infection with that protein as it is to find weapons of mass destruction in Iraq."

July-September, 2006 ~ " the human prion disease hypothesis is implausible..."

Journal of Postgraduate Medicine Vol. 52, No. 3, July-September, 2006, pp. 223-225http://www.bioline.org.br/request?jp06072 The human prion disease hypothesis is based on the authors' declaration that the large-scale import by UK of crushed/whole bones and carcass parts containing soft tissue of mammalian origin, from India, Pakistan and Bangladesh, in the 1960s, ended up under poor control and regulatory conditions as animal feed.[1] The authors declare that the half-burnt bodies of deceased Hindus that floated down the river Ganges were a source of human remains that were utilized together with animal bones by the processing mills for animal feed in the UK. According to Colchesters, these partly cremated bodies were infected with the human transmissible spongiform encephalopathy (TSE) called Creutzfeldt-Jacob disease (CJD), thereby becoming the root cause of the BSE epidemic in the UK.
The Colchester hypothesis is partly based on the book by Dr. Alley, a physical anthropologist, who has in the meanwhile disassociated himself with this hypothesis, categorically mentioning that the information in his book and some of the personal discussion Colchesters had with him had been misquoted.[2]
In our view, the human prion disease hypothesis is implausible since no cases of bovine spongiform encephalopathy (BSE) have been reported in India to date, this indicating a low level of TSE in the region.
Even suspecting that surveillance for BSE in India may not be perfect, BSE epidemics have only occurred in those countries where there has been intensive farming with recycling of waste cattle tissue back to cattle in meat and bone meal. Such a practice is uncommon in India, if it occurs at all. More

June 24 2006 ~ Latest vCJD scare-fest - " this iceberg is in a very shallow pond"

Close on the heels of the recent stories about "atypical" scrapie and the dramatic headlines of the 'Silent killer vCJD is more widespread than thought' variety back in March, we now have a fresh crop of vCJD scare stories featuring slow incubation and kuru ( Six years ago, a Telegraph article which was itself entitled: "After years of inquiry no-one knows how many lives nvCJD will claim" made many of the same points.)
The New York Times, however, does at least sound a note of scepticism over the latest report in the Lancet.
As yesterday's NYT said:
"Guesses as to how many people will eventually die of mad cow disease have varied wildly. In 2001, two groups of eminent British scientists argued over whether it would kill 136,000 Britons or only a few thousand. Recently some scientists have predicted that it will die out in a decade, while others have argued that it is still incubating in many people and will be transmitted by blood transfusions.
No one expects no more deaths, Dr. Major said, but to any suggestion that the 160 known now are merely the tip of an iceberg, he said, "I think this iceberg is in a very shallow pond."
The many unanswered questions about the nature of TSEs are less newsworthy - and much harder to write about - than doom scenarios written without scientific rigour. Mark Purdey, meanwhile - who, in pursuit of the real causes behind free radical based illnesses, shows that exposures to sonic shock waves will "activate the metal micro-crystallised piezoelectic prion contaminants in mammalian brain" (see his website) He has challenged the BSE orthodoxy for years with extraordinary results. He explains, for example, the Queniborough cluster. He remains not only unfunded and unsung but sneered at. A hero nonetheless.

June 9 2006 ~ USDA: Much Still Unknown About Two US BSE Cases

See cattlenetworkcom (Dow Jones) reports that USDA
"...now believes the only two native-born U.S. cows to contract mad-cow disease were infected with a little understood and rare "atypical" strain that throws into question how the animals were infected. .... abnormal, differing from the common form of the disease found in Canada and the U.K.
... Clifford also said USDA has no plans to change the way it safeguards the U.S. beef supply.
An internal USDA memo stated, "There is no evidence to justify any changes in surveillance methods, disease control, or public health measures already taken in the United States."
Clifford agreed, saying, "Until the science proves otherwise, we'll be treating all of these cases as BSE and the normal, typical BSE, and we still feel confident that the safeguards we have in place are effective." .......... this "atypical" form of bovine spongiform encephalopathy found in the U.S. might not be spread through feed. Clifford said he didn't know if the two U.S. cows were infected through contaminated feed - as most normal cases are - or whether they simply developed the disease spontaneously or by some other way. ..."
Read in full. It is interesting that the usual assertion that BSE is infected through "contaminated feed" is very rarely challenged.

June 9 2006 ~ A disease being termed "atypical BSE" is being found in older cattle in both USA and Europe

At an international conference on what are described as "prion diseases" in domestic livestock, French and Italian scientists have described how a TSE has been found in a small number of cattle ranging from 5 to 15 years old. One French researcher has revealed that the BSE cases in Texas last year 2005 and Alabama last spring 2006 were identical to "atypical" cases of BSE found in France. We read on ProMed's quoting of Farmers Weekly that "Marion Simmons of the Veterinary Laboratory Agency at Weybridge urged caution, saying there are not yet sufficient supporting data to suggest that the disease is a new strain of BSE."
A moderator comments, "It has long been debated whether this atypical form is sporadic or whether the sporadic appearance was an atypical form. There does not seem to be a good explanation, which simply highlights the need for more research and understanding of this disease. "
We have tried for some years to highlight the uncertainties. Although scientific reputations, massive regulation and huge amounts of money depend on certainties - those challenging the received wisdom seem to be considered contemptible by the establishment - there are indeed many more questions than answers about so-called Transmissible Spongiform Encephalopathies. See also previous ProMed posting

May 31 2006 ~ Telegraph article on challenges to Prusiner

"good work of others trashed by the traditional weapon of choice in scientific disputes - anonymous peer review" The Telegraph today, in an article by Roger Highfield, reports on the Jeffrey research see belowand says "almost a decade after Prusiner's Nobel prize, findings still challenge his hypothesis so that, at best, it seems incomplete and, at worst, it may even be wrong."
".....findings once again raise the possibility that the abnormal proteins are a consequence of the disease process, rather than a cause. (Interestingly, a similar argument is raging over the protein deposits linked with Alzheimer's disease.)
The most fundamental issue of all was raised by the Nobel prizewinner Prof Kurt Wuthrich of the Swiss Federal Institute of Technology, Zurich: he pointed out that researchers have failed to produce spongiform disease using laboratory-made prions, the only real way to eliminate the possibility that another agent might be responsible......
.... when ... Dr Jeffrey, looked at the effects of prion shape in sheep, he found that the shape can vary, depending on which sort of cell it inhabits, even though it produces the same strain of disease in mice.
Similar observations that prion shape changes do not alter the strain of the disease have also been reported by Prof Laura Manuelidis of Yale Medical School, who concluded that many facts "are discordant with the prion hypothesis" in a review in the journal Viral Immunology.
Prusiner's idea does not fulfil the classic criteria formulated by Robert Koch in 1884 to link an agent to a disease, says Prof Manuelidis. "Not a single one of Koch's proven postulates of infection are fulfilled by prion proteins." ....."It has also been obvious for a long time that abnormal prion protein is the consequence of infection, but not the causal agent," she says. "You might say that abnormal prion protein lacks the dynamite for weapons of mass destruction, though it certainly has a lot of rhetoric inside it. Those natural truths are not defined by popular vote or cabal."
She is also disturbed by the hostility faced by those who question the prion idea and says she has seen the good work of others trashed by the traditional weapon of choice in scientific disputes - anonymous peer review. "At issue, unfortunately, is public health."
(Read article in the Telegraph )

May 21 2006 ~ "no one really knows...." is Professor Hugh Pennington's view

on the latest wave of fear over vCJD raised by "British scientists" and Professor James Ironside in particular. Their pronouncements that blood transfusions and surgery could allow the disease to spread indefinitely is based on speculation about genotypes and whether dormant disease will ever take hold. But fear is a wonderfully golden goose for funding literally millions in research as we have seen recently. Meanwhile. other vital research establishments are starved of the funding necessary to enable us to use the latest technology in the area of animal health - which itself can affect human health. In Thursday's Lords debate, the Earl of Selborne :
"If you accept my thesis that the agricultural sector, above all, has to be seen to be embracing new technology, taking on the fundamentals of environmental considerations, nutrition, linkages with other biological sciences and contributing to some of the wider objectives of the National Health Service - all of which I believe the research councils are undertaking in a co-ordinated way - you will find that the old Research Council institutes, such as Rothamsted Research, the Institute of Grassland and Environmental Research at Aberystwyth and North Wyke in Devon and the Institute of Animal Health, are withering on the vine - and they are withering on the vine because Defra has withdrawn support..."

17 April 2006 ~ Michael Bateman, the food writer who died last month, is quoted in the Independent

".... In the midst of the 1996 BSE crisis he wrote a series of articles encouraging his readers to eat meat, but to eat better meat, pointing out that cheap prices entailed intensive farming practices such as cattle being fed the remains of other animals. He also pointed out that "you're as likely to choke on a cherry stone as contract CJD from eating beef"....Michael always did his homework. "

14 April 2006 ~ "Are prions the real cause of BSE and vCJD?"

Andy Coghlan in the New Scientist takes up the atory of the Jeffrey research (see below)
"Abnormal prions - misshapen versions of normal brain proteins - may not be infectious agents, but a consequence of "prion diseases" IT IS a finding that could turn the conventional wisdom of what causes diseases such as BSE and variant Creutzfeld-Jakob disease on its head. Experiments in sheep suggest that abnormal prions - misshapen versions of normal brain proteins - may not be infectious agents, but a consequence of "prion diseases".
Abnormal prions were thought to trigger disease by getting into the body through food or cuts and setting off a chain reaction that transforms native prions into harmful ones. These multiply and clog up the brain, and can be fatal. Prions eaten in contaminated food were thought to pass undigested through the gut wall into specialised lymphoid tissue called Peyer's patches, where they multiplied up before spreading to the central nervous system......."

April 14 2006 ~ vCJD death - open verdict

WMN ".......Details of Mrs Watts' case were sent to Prof James Ironside at the National CJD Surveillance Unit in Edinburgh, who said the rash Mrs Watts suffered in 2001 was unlikely to have any bearing on her condition.
Prof Ironside said: "Oral exposure to infection in the diet is the most likely cause of vCJD in this patient."
Exeter and Greater Devon Coroner Dr Elizabeth Earland said: "I am not satisfied that we have evidence that she contracted vCJD either from her food or some other exposure and accordingly I am bringing in an open verdict."...."

March 31 2006 ~ "a great deal of uncertainty about the origins of variant Creutzfeldt-Jakob disease and transmission risk in humans."

A review of the study by Dr Martin Jeffrey quoted below . Extract: Prion Theory of Mad Cow Disease Called Full of Holes at www.medpagetoday.com
"....Although people with a specific genetic mutation are thought to be less susceptible than others to infection with vCJD because their digestive systems degrade the infectious prion protein, experiments in sheep indicate that prion protein is taken up equally in the gut by animals with ostensibly protective, neutral, or susceptible mutations in the same gene. ...... "This clearly shows that resistance is not achieved by blocking uptake of abnormal proteins from the gut," said Dr. Jeffrey. "It must be achieved by some other mechanism."
In view of such new studies, one wonders what the widely detested National Scrapie Plan is achieving.
The Countess of Mar (see below) has often voiced concern about the "scientific" advice being given to the government. In the debate on March 7th she warned about both the unscientific nature and the over-prescription of the government's TSE regulations. The TSE Regulations of 2002 were, in the first place, "based on the widespread assumption that a rogue isoform of a protein designated PrP - called prion protein by some - causes TSEs. That hypothesis is unsupported by rigorous analysis and substantial data contradict it."
It looks as though the government will at last have to take note.

March 30 2006 ~ "scientists have struggled to make sense of how an abnormal variation of a normal protein can trigger an infectious disease..."

Journalists this week have rushed to copy headlines of the "Silent killer vCJD is more widespread than thought..." variety (see below). Scare stories about the "timebomb" disease rarely do much to emphasise the speculative nature of scientists' pronouncements. ( The Sun announced boldly "14,000 'infected' with CJD".)
Yet all sensational value would disappear were it not for the widespread - and unproved - assertion that eating BSE can cause vCJD because of an infectious " rogue prion".
New evidence publicised today is at least challenging the prion theory.
"Since the outbreak of BSE in cattle and vCJD in humans, scientists have struggled to make sense of how an abnormal variation of a normal protein can trigger an infectious disease. Some are questioning whether this simple relationship exists at all. This paper adds new evidence that can inform the debate..." More
Some heretics of the rogue prion theory consider that the very name "Transmissible" is absurd when so little hard evidence exists to suggest that Spongiform Encephalopathies are infectious at all. As Magnus Linklater says, "There is money to be lost and reputations to be damaged if the bottom drops out of the prion creed" Unfortunately, far more has been already lost because of it - swathes of regulation, trade wars costing billions, the infamous National Scrapie Plan - and the untimely deaths of millions of harmless animals. If "TSE" is shown to be a misnomer, the political fallout will be incalculable. For this reason, heretics tend to get their funding removed and their names discredited.

March 26 2006 ~ 'Silent killer vCJD is more widespread than thought' says the Independent - but no evidence given for this dramatic statement

'Silent killer vCJD is more widespread than thought' is the headline from the Independent's Health Editor, Jeremy Laurance as if frightening new evidence had been found - but there is no evidence offered from "researchers at the Institute for Animal Health in Edinburgh" - only speculation.
In a similar article in the Scotsman, Hugh Pennington, president of the Society of General Microbiology, is quoted:
"... there could be a second wave of fatalities if more genotypes are affected but not yet coming down with symptoms. You cannot rule out the possibility there may be some effect of BSE on people who have so far shown no effect. But, people with longer incubation periods are likely to be less susceptible to the disease."....... Prof Pennington thought a second wave would have begun to show."
As we say below, research grants are the life blood of science but the ever-dwindling number of deaths due to definite or probable vCJD in the UK during the 12 months of 2005 is 5. Scaremongering therefore seems mischievous.
The peak number of deaths was 28 in the year 2000, followed by 20 in 2001, 17 in 2002, 18 in 2003, 9 in 2004, 5 in 2005, and one so far in 2006. (Figures from ProMed.) (See also warmwell page on BSE/vCJD)

March 9 2006 ~ "Can the Minister please explain why, in a situation such as that surrounding scrapie, BSE, CJD or foot and mouth disease, the Government seem to turn to scientists who are not regarded by their peers as experts in the area while ignoring those who are?"

The Countess of Mar has once again shown her deep concern about the "scientific" advice being given to the government. In Tuesday's debate she again warns about both the the unscientific nature and the over-prescription of the government's TSE regulations. Genuine experts such as Alan Dickinson warned 20 years ago that measures to reduce scrapie should avoid genetical extremes. The advice was ignored and the so-called "atypical scrapie" cases are now found in the very genotypes actually being selected by the National Scrapie Plan as being "resistant". Of even graver significance is the fact that the Regulations of 2002 were, in the first place, "based on the widespread assumption that a rogue isoform of a protein designated PrP - called prion protein by some - causes TSEs. That hypothesis is unsupported by rigorous analysis and substantial data contradict it."
The transcript of the debate makes for deeply disturbing reading. The Countess of Mar politely and painstakingly dissects the illogical, inconsistent and weirdly worded regulations, concluding moreover that
"I want the Minister to know that I am extremely concerned that all regulation in this field is based on a hypothesis - not even a theory - that none of the "establishment" scientific community can prove, despite millions of pounds of taxpayers' money being thrown at the subject.... . " Read in full

March 6 2006 ~ One certain thing is that we have been eating scrapied sheep for 200 years and nobody has come to any harm. Professor Hugh Pennington

We read in the Sunday Herald that "vCJD expert Dr Stephen Dealler" are once again raising the spectre of scrapie in sheep somehow masking BSE. An atypical form of scrapie has been found in 108 cases but there is no evidence that it is any more harmful to humans than scrapie itself. " The worry is, of course, that atypical scrapie will be infectious to humans, but we dont know, Dr Dealler is reported as saying, adding "..should we, in this wait-and-see period, be taking more aggressive action?"
While research grants are the life blood of science and "wait-and-see" periods may be rather lean, it seems nevertheless that the so-called "timebomb" disease of vCJD hardly merits all this scaremongering. The ever-dwindling number of deaths due to definite or probable vCJD in the UK during the 12 months of 2005 remains 5. The peak number of deaths was 28 in the year 2000, followed by 20 in 2001, 17 in 2002, 18 in 2003, 9 in 2004, 5 in 2005, and one so far in 2006. (Figures from ProMed.)

A European wide programme to eradicate sheep and goats susceptible to scrapie was given justification by fear of vCJD. Such public fear has been increased by speculation in the press of a "timebomb" disease - (whose numbers have in fact dwindled with 17 cases in 2002 and 18 last year and 142 deaths globally overall.) - by the death of one elderly patient who died of causes unrelated to vCJD but in whose spleen an abnormal prion protein was found; an incident publicised only five years later in August 2004.
BBC: Professor Ironside "I'm not in the business of scaremongering....."
Professor John Collinge : "There is considerable uncertainty over how this will unfold. ....."

21st October 2005 ~ Another "heresy" about rogue prions

The Daily Mail reports on US and Japanese research (led by Professor Laura Manuelidis, from Yale) in the journal Science suggesting that BSE, variant CJD in humans, and other kindred diseases are most probably caused by a virus. They also suggest that persistent infection by a "weak" CJD strain protected cells from infection by a more virulent and potentially lethal form of CJD. It also prevented infection by two versions of the sheep TSE disease, scrapie.
The government National Scrapie Plan carries on regardless of uncertainty.

20/21 February 2005 ~ Here and in Europe, the National Scrapie Plan rolls on - in spite of serious worries.

A symposium about TSEs to be held in Montana, co-sponsorored by the Rocky Mountain Laboratories, however, accepts that there are many more questions than answers. See Billingsgazette.com "....Much remains to be discovered about prion diseases. Scientists are investigating how and why normal prion protein molecules transform into abnormal forms that clump together and attack brain tissue, destroying portions of the brain and leaving "spongy" gaps. Scientists believe prion diseases might be linked to similar neurodegenerative diseases, such as Alzheimer's and Parkinson's."

October 29 - November 4 2004 ~ All farmers who report and have a confirmed case of the Scrapie in their flock will now have to cull the whole flock

or blood test the flock to determine its genetic profile.
Enforcement of the EU regulation requiring Member States to "take action on sheep flocks and goat herds that report scrapie" began on Monday. We can only repeat the words of Wales' top breeder of hardy Welsh Mountain sheep, Goronwy Edwards (he trades as JH Edwards & Sons):
"I have been breeding Welsh Mountain rams for 50 years and I have never seen this disease. I was up on the hills the other day and I was thinking how my flock was a picture of perfect health. So why do we need to start meddling and take something from our ewes simply to stop something I have never seen in my life? Often the best rams are not group 1 scrapie-resistant but group 2 or 3. I've bought a group 1 ram this year but I've also bought two group 2s. I see a lot of people buying inferior rams just because they're group 1, and that cannot be good for the future of a breed."
Once again, the bleak dogma of treating disease by killing healthy animals, with its roots in politics rather than veterinary science, and hedged about with unintelligible legislation, is threatening UK livestock farming. Notifiable disease is surely less likely to be "notified" when farmers are so wary of and weary of the reams of paper and rules and forms pouring out of the Ministry. Quiet burial of the evidence is far more likely. See also icnorthwales.co.uk. Warmwell has amassed many pages on the scrapie question since first becoming aware in 2001 that there was a serious intention drastically to reduce sheep numbers.

September 2005 "The fact that every cluster of TSE in the world is located around sites where piezoelectric micro-crystal contaminants {used as detonators} have leaked as a result of local activities with military munitions should not be ignored."

commenting on the recent much publicised view of Dr Colchester's "human remains" theory.(BBC) Mark Purdey wrote :

"....There has never been a case of BSE or vCJD in India .
Strangely back in the 1980s the 'incriminated' meat and bonemeal that was exported abroad widely and supposedly caused BSE in the UK in epidemic proportions was not causing BSE in countries to which it was exported.
All experiments to transmit TSEs by food products like meat and bone meal or beefburgers have failed. In this theory sporadic cjd has to cross the species barrier and cause BSE, a disease that resembles variant CJD not sporadic cjd.
Also remember that 18-20 years ago when British beef was highest in bse prion it was consumed by perhaps 50 million people in this country and also probably millions abroad, through both export (processed foods )and visits to the UK. Why, if eating this beef causes vCJD, have we (thankfully) only had about 160 cases of vCJD over twenty years and why is the incidence going down. ..."http://www.purdeyenvironment.com/

and here
"......the use of sound waves on living tissues will determine whether a person's prion protein is primed for BSE or not. Although widely aired on the BBC news, nobody had connected this lab observation to my 4x published field research studies carried out in every cluster zone of TSE across the world - which concluded that exposures to sonic shock waves will activate the metal micro-crystallised piezoelectic prion contaminants in mammalian brain.."
Read in full

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Metal microcrystal pollutants; the heat resistant, transmissible nucleating agents that initiate the pathogenesis of TSEs? Mark Purdey pdf file

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May 29 2005 ~ BSE he who does not remember the past is condemned to relive it in the future

Lawrence Broxmeyer MD offers a new approach ... .... 55% of mice injected with cattle BSE, and who came down with disease, had no detectable prions. Still, incredibly, prions, are held as existing TSE dogma and Heino Dringer, who did pioneer work on their nature, candidly predicts it will turn out that the prion concept is wrong....
Lawrence Broxmeyer MD sums up that there is no known disease which better fits into what is occurring in Mad Cow and the spongiform enchephalopathies than bovine tuberculosis and its bloodbrain barrier penetrating, virus-like, cell-wall-deficient forms. It is for these reasons that future research needs to be aimed in this direction.....Read in full
....Today, concluded Lawrence Broxmeyer MD, the greatest hindrance to finding a cure for TSEs lies in the very theory they have become embedded in. Santanas oft quoted he who does not remember the past is condemned to relive it in the future seems clear here.

December 18 - 25 2004 ~ the surprise development of clinical scrapie amongst a supposedly scrapie-resistant breed of sheep

Fear , as we see so often now, is used to make draconian legislation acceptable to those who believe the scare stories. Scrapie has been demonised by being constantly referred to in the press as "the sheep disease which is linked to BSE" and, (in the Scotsman at least) "and, by implication, variant CJD in humans"
EU wide attempts to wipe scrapie out using the methods of the Witch Finder General against sheep without the appropriate genotype look ever more disastrous as we hear of "new forms" of the disease. 83 "atypical" cases of scrapie have been found over the past three years. Twelve have been found in sheep with the genotype normally associated with the highest resistance to scrapie. Does this not make a mockery of the National Scrapie Plan - costing millions of pounds of taxpayers' money, untold numbers of healthy animals' lives, and traditional sheep flocks, diligently bred by countrymen who knew what they were doing?
Why is research not returning to the drawing board? Instead, in one emailer's effectively mixed metaphors;
" this kind of responsible lateral approach has never been taken. They merely choose to squeeze more blood out of the sinking stone, and move the goalposts - often to ridiculous extremes - as a last ditch attempt to keep their die hard, dumbo theory afloat.."

November 2004 ".. we have had 99 cases of BSE born since 1 August 1996..."

Defra news for Nov 23 is that "Professor William Hill FRS, Emeritus Professor at the Institute of Evolutionary Biology, School of Biological Sciences of the University of Edinburgh has been appointed by Defra to carry out an independent review of their work on BSE cases born since 1 August 1996 in the UK..." CVO Debby Reynolds: "The current advice, which has been considered by both SEAC and a European scientific advisory committee, is that feed contamination still remains the most plausible explanation, as the feed controls in some parts of Europe were not introduced until 2001. We have work in place to test this theory. However, there are also other possible explanations for at least some of these cases. We want to eradicate this disease and it is important for us to be sure that we are not overlooking any important factors and that the work we are doing is comprehensive and scientifically sound......."

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November 2004 ~ "...Scudamore can hardly deny that he did not know when warble fly treated ceased.."

From an email sent to the farmtalking forum. November 13 2004 Mark Purdey writes: ". ....bogus disinformation ... in the Gabriel Horne Report on the origins of BSE.
The worst innaccuracy involved the claim that warble fly treatment with OPs had ceased in 1982, when , in truth, the twice annual compulsory OP warble fly treatment programme was actually first instigated in 1982 .... . it is clearly politically convenient for them to have a finish date in 1982, since they have been arguing that "since all cases of BSE were largely born after 1982, then how could OP warble fly treatments be linked with the cause of BSE when these treatments were ceased in 1982 "
.... the former Chief Veterinary Officer, Jim Scudamore,... argued against my work using these same bogus paragraphs from the Gabriel Horne Report .... I pointed out that Jim Scudamore himself had actually been sent out to my farm near Taunton in 1985 - in the days when he was acting as a divisional vet Officer for the Taunton area - to force me to comply with the compulsory OP warble fly treatment campaign. This clash lead to my refusal and victory in the high court that debarred MAFF from forcibly treating my cows. What with all of this , and the compulsory use of the chemical right up to the end of the 1990s, Scudamore can hardly deny that he did not know when warble fly treated ceased ...
So what is going on with our democracy, where we have officials and gov / quango scientists knowingly pumping out pure disinformation under the guise of sound science, and then criminalising and ridiculing those of us who are trying to work within the confines of the truth? Read in full

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September 2004 ~ "... if you or your animals thrive off ecosystems which carry the higher levels of natural radioactive metals (NORM)

- as in Iceland where NORM is high downwind of some of the volcanoes - then you have to be careful that you are nourished with ample antioxidant co factors such as copper, selenium / vitamin E, zinc, vitamin C. These arrest the free radical mediated chain reactions which are initiated by the radioactive decay around the crystals in the contaminated brain. In this respect, these antioxidants will therefore act as a preventative against diseases like TSEs, explaining why the sheep farmers in Iceland fail to contract CJD because they consume ample seafood which contains all of these antioxidants, whereas their scrapie riddled sheep remain confined to the copper / selenium / zinc deficient pastures ..." Read in full

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July 10 - 16 2004 ~ " US officials really have missed the true cause of mad cow disease..."

Mark Purdey's theories about the real cause of TSEs in cattle are persuasive. Here he argues that he now has:
"... sufficient analytical data that conclusively indicates that exposure to certain environmental metal microcrystal pollutants is responsible for the true cause of these diseases.
.... barium, strontium 90, silver or manganese and are released into the environment from various naturally occurring ( volcanoes, etc ) and man made ( military, industrial, etc ) sources.
Exposure to each different metal species dictates which specific 'strain' of the disease will emerge.
Once implanted in the brain, these crystals seed the multireplication / growth of significant sized metal-protein crystal arrays ( the heat resistant fibrils which hallmark the BSE diseased brain) , which behave much like the piezoelectric crystals found in microphones , thereby screwing up the ability of the organism to deal with incoming sonic pressure waves. The sound energy is converted into electrical shock bursts which, in turn, initiate free radical mediated neuro degeneration and mad cow disease.
It was the release of strontium 90 into the atmosphere from the April 1986 Chernobyl nuclear plant blow out that rained down over North western Europe and contaminated their pastures. This radioactive metal microcrystal was able to penetrate the brains of cattle because of the simultaneous use of a high dose systemic acting pesticide used uniquely for warble fly eradication here in the UK. ...."Read in full.
The scientific establishment remains resolutely unimpressed, preferring apparently to ignore rather than attempt seriously to refute his work - but what if Mark Purdey is right? The unthinkable. A mountain of legislation, regulation, and panicky trade restrictions, at a cost of billions, revealed as mere hot air for the support of inflated political and scientific reputations. As Mr Purdey himself wryly remarks, "governments remain totally negligent... ..for obvious reasons."

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June 29 2004 ~ ".. If the animal tests positive, it would be the second case of mad cow discovered in the United States. In December 2003, a single Holstein on a Washington state farm was found to have the disease, prompting more than 50 countries to ban imports of U.S. beef. Japan and South Korea, 2 of the biggest export markets for U.S. beef, still have their bans in effect despite the efforts of American officials to get them lifted..." Daily News Jun 27 2004
The madness of BSE (and the billion pounds worth of lost trade and gained research that follows in its wake ) is set to continue. Alternative research that questions the current dogma about the disease itself and its assumed link with vCJD continues to be ignored and unfunded. Warmwell understands that the British government view - sent to a farmer by a DEFRA official concluded with the extraordinary point "Moreover, when presenting the report to the House of Commons on 26 October 2000, the Minister of Agriculture, Nick Brown, accepted that there was a link between BSE and vCJD."

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May 1 2004 ~ "I just find it odd that everybody who writes something different is ridiculed," she said. "That's what they do in this field. It's stingy, small and graceless."

(Milwaukie Journal) "In recent years, a small but growing number of scientists have raised questions about the prion theory, said Bruce Chesebro, a leading TSE researcher with the National Institutes of Health. Chesebro said he believes that eventually the real infectious agent will be found to have DNA. Spiroplasma is a "tantalizing idea," but Bastian has not published enough research to be convincing, Chesebro said. ....... "In the past 25 years, I haven't seen anything that has dissuaded me from this," Bastian said. "I'll work on this until I die or until we solve it.
I'm having fun."
Read in full

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The paper on TSEs in the Veterinary Times for Jan 27 2003 can be read in full here.

 

Jan 23 ~"Injecting human brain material into animals is considered "unethical"....

.... yet "the experiments that are the main support for the hypothesis that vCJD and BSE are the same disease also require that vCJD be injected into the brain of the putative source 'host' animal. Until this is performed, hypotheses of the causal relationship of BSE and other TSE's, including vCJD, remain conjectural and the role of other, possibly environmental, factors must be reconsidered..."
A new paper on Transmissable Spongiform Encephalopathies by Susan Haywood BVSc, PhD, MRCVS and David R. Brown M.Sc, Ph.D. is published in the Veterinary Times on January 27th The authors "discuss a re-evaluation of the TSE enigma and explore the role of environmental factors in prion diseases."
Extract: ".....does not conclude that vCJD is caused by BSE, as Phillips implies.
Circumstantial evidence linking the consumption of beefburgers by young people in support of the transinfection theory, whilst persuasive, has never been proven, in that the putative 'infectious' burgers have never been identified, nor indeed fed, to experimental animals.
Groups supposedly more at risk such as farmers, vets, abattoir workers and butchers have not shown an increased risk of vCJD.
It is quite surprising that the one experiment that would confirm a link between BSE and vCJD has not been carried out. If BSE and vCJD are the same strain of disease and take on different characteristics dependent on the host organism, then infecting cows with vCJD should lead to the cows developing BSE.
This would prove BSE and vCJD to be the same disease. However, those who could have carried out the experiments have classed them as "unethical" because of the need to inject human brain into an animal. It is incontrovertible that, the experiments that are the main support for the hypothesis that vCJD and BSE are the same disease also require that vCJD be injected into the brain of the putative source 'host' animal.
Until this is performed, hypotheses of the causal relationship of BSE and other TSE's, including vCJD, remain conjectural and the role of other, possibly environmental, factors must be reconsidered.. ...." Read paper

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Jan 23 ~" even if manganese is just a risk factor, it is important that this factor be kept in the equation, because it might just be the key that unlocks the truth about these diseases. "

A new paper on Transmissable Spongiform Encephalopathies by Susan Haywood BVSc, PhD, MRCVS and David R. Brown M.Sc, Ph.D
.....there is a solid and expanding amount of literature showing that metal imbalance and TSEs are linked....Mark Purdey, a farmer from Somerset, has published evidence that hotspots of TSEs exist in regions of the world where there is environmental imbalance between copper and manganese.
Farms in Iceland prone to scrapie have soils with dramatically increased manganese levels. A similar situation exists in Colorado where deer develop chronic wasting disease (9). These findings led both Mark Purdey and David Brown to hypothesise that sporadic TSEs might be a result of animals becoming exposed to conditions where manganese in their diets is elevated and copper is deficient.....The Horn report "failed to note that comparing maps of BSE incidence to a map of manganese hotspots across the UK when the epidemic was well established was inappropriate, since BSE was clearly spread at this stage by recycling infected offal.
A more detailed analysis, looking at the location of the very first cases of where BSE were reported (as viewed on the DEFRA web page,) and the map provided in the Horn report, indicates that the original BSE farms lie directly in a manganese hot spot!
Others, however, have not allowed themselves to be side tracked in this way but concentrated on the scientific evidence. In particular, authorities in the Environmental Protection Agency in Colorado have begun investigating the link between manganese, copper and chronic wasting disease incidence in deer. This disease was originally thought to be a copper deficiency disease before the prion hypothesis came to be recognised and CWD was recognised as a TSE. Although manganese might not be 'the cause' it is clear from the biochemical studies that have been carried out that metals do play a role in the pathogenesis of TSEs. Therefore, even if manganese is just a risk factor, it is important that this factor be kept in the equation, because it might just be the key that unlocks the truth about these diseases. ....(Read full paper)

September 2003 "Does an infrasonic acoustic shock wave resonance of the manganese 3+ loaded/copper depleted prion protein initiate the pathogenesis of TSE?"

From Abstract " Intensive exposures to natural and artificial sources of infrasonic acoustic shock (tectonic disturbances, supersonic aeroplanes, etc.) have been observed in ecosystems supporting mammalian populations that are blighted by clusters of traditional and new variant strains of transmissible spongiform encephalopathy (TSE). But TSEs will only emerge in those 'infrasound-rich' environments which are simultaneously influenced by eco-factors that induce a high manganese (Mn)/low copper (Cu)-zinc (Zn) ratio in brains of local mammalian populations. Since cellular prion protein (PrPc) is a cupro-protein expressed throughout the circadian mediated pathways of the body, it is proposed that PrP's Cu component performs a role in the conduction and distribution of endogenous electromagnetic energy; energy that has been transduced from incoming ultraviolet, acoustic, geomagnetic radiations. .."

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Sept 21 - 27 2003 ~ "the banning of Canadian beef might have had a lot more to do with protectionism than health concerns"

writes the journalist Peter Foster of the National Post in Canada "...vCJD. This disease, which hits young people, has been assumed to be linked to eating infected meat; indeed, it is regularly referred to in the media as the "human version of mad cow disease." This is the stated opinion of the British government, which has been most affected by both BSE and the vCJD scare. Concern over BSE led to the slaughter of some five million British cattle and cost the industry billions. However, there have not merely been doubts cast on the BSE/vCJD link, but suggestions the British government doesn't want to hear them because it is so locked into the molecular "prion" theory attributed to Nobel prize winner Stanley Prusiner. However, not merely have vegetarians come down with the disease, but the number of cases of vCJD in the U.K. is not escalating, as "experts" suggested, but declining. A fascinating recent article in the Times of London noted that an Australian scientist named Alan Ebringer had posited an alternative theory that vCJD is in fact a microbe-based autoimmune disease somewhat like multiple sclerosis. However, the British government withdrew his research grant...."

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Extract from Mark Purdey's article: The WASTING LANDS

......why has such a deeply flawed and scientifically inept theoretical consensus been permitted 'gospel' status for such an unusually protracted period of time? The launch of any new theory into the notoriously sceptical scientific establishment invariably attracts a fair degree of healthy challenge. But strangely enough with TSEs, there has been an exception to this rule. This is largely because the UK government has been actively engaged in tailoring or outright suppressing, any publicity surrounding dissident scientific studies that invalidate or even begin to threaten any aspect of the official hypothesis. Furthermore, it is strange to witness the same old 'masters of complacency' in the higher echelons of UK officialdom, suddenly adopting a high degree of hypersensitivity over the way that they deal with their affairs. Such an incongruous style of official behaviour has betrayed a deep level of insecurity over anything that they are telling us on BSE. .....

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June 12 -16 ~If Professor Alan Ebringer's theory that BSE and MS are autoimmune diseases which are linked to the microbe Acinetobacter were to be confirmed, the implications are of huge importance - but his department is forced to close.

As has been mentioned below, the respected scientist Professor Alan Ebringer, Professor of Immunology, School of Health and Life Sciences, Kings College, University of London, has had all funding withdrawn, so that the next stage of his research (to investigate whether vCJD patients also exhibit antibodies to Acinetobacter) cannot now be undertaken. His entire department at Kings College is to close down and all the expertise that has been built up will be lost.
His findings were not consistent with the official infectious prion theory. However, if Professor Ebringer's theory can be confirmed that BSE and MS are autoimmune diseases which are linked to the microbe Acinetobacter, the implications are of huge importance and are far reaching. The following conclusions arise:
1. There will be no vCJD epidemic and the panic measures currently costing Canada so much will be shown to have been groundless.
2. A cure for vCJD, based on treatment for Acinetobacter, could be set in motion.
3. BSE cannot be passed on by eating infected meat. The meat from BSE cows is safe to eat and has always been safe to eat.
4. The massive cattle cull in the UK was unnecessary.
5. The devastating blow dealt to the UK livestock industry, and elsewhere, was unnecessary.
6. The financial outlay for the BSE disaster of £5 billion of taxpayers money could have been spent on other socially more relevant needs.
7. The massive European and wider research programmes on TSEs in sheep, with potentially disastrous implications for the sheep industry in the UK, are flawed and therefore worthless.
8. A possible cure for MS may be found.
9. The extremely costly tonsil screening programme plus associated costs was unnecessary.
10. Reputations will be damaged.
11. It may pave the way to improving the reputation/perception of science/scientists in the eyes of the public, by allowing scientific research to be open to rigorous peer group scrutiny, by showing that alternative views are encouraged rather than suppressed, and most importantly that funding is not linked to producing politically acceptable results.

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There is a lot in the news recently regarding the "epidemic that never was", and scientists are hastily revising estimates of future cases of vCJD. Surely, scientists should be re-examining the original prion theory, Nobel prize winner or not"

"....The persistence by DEFRA in funding research connected with the prion theory is all the more surprising in view of the recent funding fiasco in the same area regarding a long term TSE research project supposedly examining sheep brains. In error, cattle brains had been used in the research...." A letter from Anne Lambourn deploring the axing of the work of Professor Ebringer' Professor of Immunology, School of Health and Life Sciences, Kings College, University of London - and of his department.

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Professor Ebringer was given 25 minutes

to present his autoimmune theory of BSE to SEAC. ( Article by warmwell.)
The auto-immune theory of BSE implies that the cull of cattle was unnecessary and the disease can be prevented by simply removing the relevant microbes from the normal flora and the animal feeds.

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warmwell note : on the very day that Prince Charles announced that he was backing Dr David Brown (see below), the British press resurrected the story of Prince Harry's "pot smoking" from the previous summer and all attention switched to that.

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The origins of hyper infectious hysteria

See http://www.markpurdey.com/articles_thewastingland.htm
".... This whole hyper infectious myth has been based on the fact that TSEs can be transmitted in the laboratory; whereby TSE affected brain tissue is injected into misfortunate laboratory animals that subsequently contract TSE. The fact that classes of Alzheimer's and other neurodegenerative diseases can be transmitted in this way is completely ignored. But these transmission experiments prove nothing in terms of demonstrating whether TSEs are caused by a microbiological infectious agent or not. After all TSEs do not fulfil Koch's postulates; the conventional yardstick for assessing whether a given disease stems from infectious origins.
The 'all important' success of these 'trumped up' transmission experiments could have equally easily represented the fact that a highly toxic chemical or metal species which had originally contaminated and killed the initial TSE diseased animal was then being transmitted into a secondary host. Once again, this equally feasible alternative explanation has been ignored.
But one of the first lines of epidemiological inquiry aimed at investigating the origins of CWD ought to have addressed the question why the disease has not spread like wildfire..."

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May 18 ~ Britain's most expensive myth

Sunday Telegraph Booker's Notebook
"Everyone knows that the claimed link between BSE and the singularly unpleasant disease "new variant CJD" set off the greatest and most expensive food scare in history. In the days that followed the health minister Stephen Dorrell's fateful announcement in March 1996, predictions of deaths from eating beef ranged from 500,000 by the government's chief BSE scientist, John Patteson, to many millions (The Observer).
With very few exceptions (this column being one), the media unquestioningly accepted thatthere was such a link. As one result, £3 billion of public money was spent on incinerating elderly cows. The costs to industry and the UK economy, not least from a consequent thicket of further regulations, have been many times that, and are still continuing.
The chief reason for doubting a link between beef and CJD lay in the epidemiological evidence, which even in 1996 suggested that the promised epidemic was a fantasy. Over the past seven years, as the incidence curve has begun a steady fall, that has seemed ever more certain. Now, after reviewing the evidence, Professor Roy Anderson and his Imperial College team have published a revised estimate of the total number of victims likely to die of vCJD in the future (link available through www.warmwell.com). Their figure? Not 400,000, or 40,000, just 40.
As Britain's farming and food industry grapples with the latest regulatory insanity inspired by the BSE scare, the EU Animal By-Products Regulation that is predicted to drain billions more pounds from the UK economy, it is clearer than ever that Mr Dorrell's monumentally foolish statement in 1996 was the most costly blunder ever perpetrated by a British minister."

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May 8 2003~ The primary vCJD epidemic in the known susceptible genotype in the UK appears to be in decline

http://www.biomedcentral.com/1471-2334/3/4/abstract Azra C Ghani , Christl A Donnelly , Neil M Ferguson and Roy M Anderson

"....Our results show a substantial decrease in the uncertainty of the future course of the primary epidemic in the susceptible genotype (MM-homozygous at codon 129 of the prion protein gene), with a best estimate of 40 future deaths (95% prediction interval 9-540) based on fitting to the vCJD case data alone. Additional fitting of the appendix data increases these estimates (best estimate 100, 95% prediction interval 10-2,600) but remains lower than previous projections. ..."

How many restrictive laws, regulations and directives (rules on fallen stock, waste disposal, tagging, abattoir rules etc. etc) use as their rationale the fear of vCJD - a fear based on the former predictions ( and initial estimates were as high as 100,000 ) of the Imperial College team? When is independent research into TSEs going to be properly funded? The pharmaceutical industry in particular seems determined that the source of BSE and CJD should be assumed to be that favoured by current SEAC thinking. A spotlight on chemicals could expose the role of insecticides in other neurodegenerative diseases. That might lead to claims which would dwarf those from BSE and CJD litigants.

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Jan 23 ~ More about the Horn Report

It is interesting to see what Mark Purdey, mentioned in the paper above as having researched the link between metal imbalance and TSEs, had to say about the Horn Report in this article in the Ecologist: "....Since the BSE inquiry had rejected the official scrapie-BSE hypothesis and found in favour of some aspects of my own theory, the UK government responded by setting up a further mini-inquiry to re-examine the origins of BSE. The resulting publication, known as the 'Gabriel Horn Report', employed a mix of misrepresentation and outright bogus disinformation in order to discredit the validity of my theory. When I attempted to sue the government for libel, it pleaded ‘qualified privilege' of the expert committee and then spun out the legal communications beyond the one-year post-publication mark - thereby exempting itself from my claim. See article in the Ecologist by Mark Purdey and the Mark Purdey page on warmwell

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Alan Dickinson, who provided the material used by Prusiner but who did not share the Nobel Prize with him,

wrote to the Agricultural Select Committee in January 2001, gently pointing out some truths.
Extracts: ".... You may be assuming that the molecular nature of TSE agents has been "proved" to be, simply, a modified form of this protein (a so- called "rogue protein"), but the number of those who doubt this is steadily growing, if only for the reason that this hypothesis has never been able to explain the facts.."
"...What has been well established is that if any scrapie strain has passed from sheep to humans, this must be such a rare event that it has not been detected as a component of the 1:50,000 rate of incidence of CJD in humans. It seems reasonable to conclude that the scale of exposure of humans to scrapie strains during the 20th century will have been vastly less than that to the BSE strain during the epidemic. The simple observation that humans and several other species have become infected with BSE proves nothing about whether it transmits more easily to other species when the same doses of different strains of infective agent are compared. The cases seen in other species can be explained either by the massive scale of exposure to BSE agent afforded by the epidemic, or by the BSE strain having "higher infectiousness" for other species, or both. Its known greater thermal stability than other strains may well be an important aspect of this. The Phillips Report, unfortunately, jumps to a premature conclusion on this whole question, but that is not their only lapse....

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The Purdey pages on warmwell

The Phillips Report into BSE and variant CJD in the United Kingdom

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News from Mark Purdey

..

..now I have found myself so severely criminalized by the Establishment that my voice carries no weight whatsoever.

This is ridiculous since the hard evidence that has accumulated in support of my work over the last years greatly exceeds the total lack of evidence supporting the hyperinfectious theory. .... - all politics and nothing to do with good science ..(See article from Mark Purdey received May 15th 2002)

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Mark later reported: "The research is going amazing here. I think I have confirmed the lethal link between sales of high grade manganese dioxide off this island to UK animal feed firms in the early 1980s. ...The aboriginees did not used to behave in this way until they stopped their nomadic life and came to live fulltime on top of this bedrock of manganese and work in the mines.

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A report from the SDC Network 1998 - extract:"BSE was certainly around earlier than 1986, and it did not 'suddenly' appear. Slides taken from cattle postmortems in 1985 by MAFF in 1985, and known as 'Pitsham Farm Syndrome ' were subsequently identified as BSE. ... we have first hand knowledge of cattle displaying symptoms, which had they been notifiable at the time, would have required reporting to SVS as BSE suspects,
.....* New or previously Unrecognised? Although 'new' has now been quietly dropped from the description nvCJD, and it is now known as vCJD, the first person ever to suffer from CJD was just 20 years old. ...... the Corsellis collection, housed at Wickford Essex, some of which appear to show lesions compatible with the so called 'new' type of CJD, but dating back to the early part of the 20th century."

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April 4 2002 _ Lancet report backs sheep dip campaign

Fordyce Maxwell Rural Affairs Editor
A REPORT published in the Lancet last month concluded: "Our results support the hypothesis that organophosphates contribute to the reported ill health of people who dip sheep." Some campaigners against OP dips, such as Brenda Sutcliffe and Brian Anderson, have never doubted that. They have argued for years against what they see as a medical, veterinary and health and safety establishment agog with apathy. ......
Sutcliffe, from the 70 acre family farm of Sheep Bank, Littleborough, Lancashire, saw the Lancet report as a possible step forward in a very personal, very expensive, campaign against OPs used in any connection by humans. That now includes the OP malathion, used in a medically prescribed shampoo to kill nits on children's hair, and her belief that an OP called cruformate caused BSE in cattle. (more)

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Insecticide Causes Mad Cow Disease

by Fintan Dunne Research by Kathy McMahonReprinted from eionews.com, email - news@eionews.com -------------------------------------------------------------------------------- Pharmaceutical interests in the UK are ignoring new scientific research that shows the insecticide used in the UK government's own warble-fly campaigns triggered the UK surge of 'Mad Cow' disease.

Latest experiments by Cambridge University prion specialist, David R. Brown, have shown that manganese bonds with prions. Other researchers work shows that prions in the bovine spine --along which insecticides are applied-- can be damaged by ICI's Phosmet organophosphate(OP) insecticide -causing the disease.

British scientists have led the current theory that an infectious prion in bonemeal fed to cattle causes bovine spongiform disease (BSE).

Infectious prions are also claimed to cause new variant Creutzfeld-Jakob Disease (CJD) in humans -from ingesting beef. But the infectious prion theory serves to obscure a tragic chemical poisoning scandal behind the majority of BSE cases.

The new work proves that the prions can bond with manganese in animal feeds or mineral licks. These manganese prions cause the neurological degeneration seen in BSE.

By a similar process, prions in human brains are damaged by lice lotions containing organophosphate. This can result in neurological diseases like CJD and Alzheimers -later in life.

Many might be surprised to hear that organophosphates were developed by Nazi chemists during the course World War Two,as a chemical weapon nerve agent. One formulation of the insecticide --Maneb, or Mancozeb-- actually contains manganese in addition to organophosphate.

The marginalized research has devestating financial implications for ICI. It would provide a firm basis for litigants -who could include CJD sufferers, farmers across the world and families of the many British farmers who committed suicide during this BSE debacle.

Phosmet organophosphate has been used at high doses in British warble fly campaigns. In 1996, ICI subsidiary Zeneca sold the phosmet patent to a PO Box company in Arizona called Gowan -just one week before the UK government admitted to a link between BSE and nvCJD.

The politically well-connected British pharmaceuticals group, ICI has the financial and political clout to block research into any cause other than the infective model. Indeed no substantive alternative research has been done. British BSE disease management and research bodies have taken decisions that do not seem guided by spirited scientific enquiry. Mysterious prions that jump species is the preferred research arena.

Scientist and organic farmer, Mark Purdey gave evidence to the UK BSE inquiry, that warble fly insecticide was the cause of the disease. The scientist wheeled out to rubbish Purdy's evidence -Dr. David Ray, later turned out to have been receiving funding from the insecticide manufacturer ICI.

A lobby group that includes Bayer, Monsanto, Novartis, Pfizer, Roche and Schering-Plough was behind the effort to discredit Purdey. In December 1999, the same David Ray was appointed to the UK Veterinary Products Committee (VPC) -a government body that licences animal medicines.

Purdey has been consistently denied even exploratory funding to extend his privately supported research. Yet the Purdey/Brown chemical poisoning model matches with the epidermiological spread of CJD clusters in humans. It also predicts the incidence of BSE-type diseases in animals. The accepted infectious model fits neither.

The pharmaceutical industry is all the more determined to hide the chemical source of BSE and CJD, because a spotlight on chemicals would expose the role the insecticides in Alzheimer's --another neurodegenerative disease--that might lead to claims which would dwarf those from BSE and CJD litigants. In fact, two leading brain researchers into CJD and Alzheimers have died in suspicious circumstances in recent years.

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March 28 2002 Search for BSE in muscle meat draws blank

17:05 27 March 02

NewScientist.com news service

Tests by government scientists in France have allayed renewed fears that eating beef can cause variant Creutzfeldt Jakob Disease, the human form of BSE. The fears were heightened on 18 March when scientists unexpectedly reported finding traces of infective material in the muscles of mice.

The findings carried extra weight because they came from the lab of Stanley Prusiner, the scientist at the University of California in San Francisco who won a Nobel Prize for discovering mutated "prions". These are the defective proteins believed to cause brain-wasting diseases like BSE, vCJD and scrapie..........
The new twist in the story came on Wednesday, when French government scientists announced that they had drawn a complete blank when they looked for prions in muscles from several BSE or scrapie-infected animals including mice, sheep, goats and cows.

"The tests proved negative in the search for pathological prions in the set of samples, including those taken from the hind limb muscles," says the AFSSA, France's food safety watchdog. Read more

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Article:THE MONEY TRAIL

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Critical scientists like Purdey are unlikely to prevail. The pharmaceutical industry holds most research purse strings, and would hardly energetically explore an avenue of research that could expose them to litigation for causing BSE. The official theory is lavishly funded, alternative theories rarely, if at all. ...See article

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Charles backs controversial CJD research
Telegraph - Jan 13 2002

By Lorraine Fraser, Medical Correspondent
THE PRINCE OF WALES has given his support to a British scientist who believes that the human equivalent of mad cow disease may be caused by pollution rather than by eating BSE-infected beef.
Prince Charles has asked friends in the medical community to lobby for research funds for Dr David Brown, whose findings suggest that contamination with the metal manganese may be to blame for the fatal brain illness, vCJD (variant Creutzfeldt-Jakob disease).
Dr Brown, who is an expert on prions, the proteins thought to be central to vCJD and BSE (bovine spongiform encephalopathy), was invited to the Prince's Highgrove home last year to discuss the findings. Also in attendance was Mark Purdey, a former organic farmer from Taunton, Somerset, who was the first to propose that high levels of manganese in the environment may be causing BSE and vCJD.......

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Organophosphates, BSE, CJD, Scrapie, Prions, Chronic Fatigue Syndrome, Pesticides, Industrial Pollutants, Metals, Soils, Diet

Alan Ebringer, professor of immunology at King's College, London believes that BSE is caused by the acinetobactor calcoaceticus bacterium - i.e. that it is an auto-immune disease. SEAC maintains that the cause is rogue prions and has suppressed findings by another researcher, the independent Mark Purdey (see below) that suggests otherwise. Now, Professor Ebringer's funding runs out on 31 December and SEAC has postponed the consultation they were due to have with him until next February. " There is still a lot we need to discover about TSEs provided it fits in with our own way of looking at this" would have been a more accurate statement from DEFRA and SEAC than the bland DEFRA statement "There is still a lot we need to discover about TSEs". Prof Ebringer believes that if BSE is an auto-immune disease it would mean that British beef is safe, and that the mass slaughter of cattle over 30 months of age and other measures costing the taxpayer several billion pounds, were unnecessary. Why is SEAC so keen to test for BSE in sheep (and, one would be forgiven for assuming, to find it) and why does it turn away from any independent research that suggests that there is nothing for humans to fear from TSEs in farm animals? Why does the threat of a national sheep cull always seem to lead back to SEAC and the FSA? Why are the major figures involves all connected by the Royal Society or their link to Imperial College? Why are they so dismissive of Professor Ebringer's work that his funding is running out in spite of its evident usefulness in providing the country with a live test? Why do all "Animal Health" policies appear to be aimed at slaughtering British livestock? Professor Ebinger's test would lift the threat of a national sheep cull.

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See Mark Purdey's website

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His theory summarised

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And especially his LATEST NEWS 21/10/01 BSE in sheep Here we go again. Extraordinary to spend so many years researching such a damp squib of a project - not one case of clinical BSE in sheep nearly 20 years on from when the causal factors (whatever you think they might be) were at their height and precipitated the BSE epidemic.The cock up on the homogenate - well, yes, more money wasted but not surprising. Cull the whole of the national flock - I'm going to pause now to find a brick wall to bang my head against.What next ?- BSE has crossed into warble fly and the flies have reinfected cattle and other animals- 5 year research project. half million research grant ! Why not treat a scrapie sheep with EDTA?.......

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Doubt cast on BSE-CJD link

Scientists step on the toes of biotech companies at their peril...

BSE bacteria test could save livestock

By Sandra Barwick
(Filed: 13/10/2001)
A TEST for BSE in live animals, which could eradicate the need to slaughteryoungcattle and lift the threat of a national sheep cull, has been proposed by agovernment funded study.Alan Ebringer: needs further funding to validate testThe full report, which has only recently been sent to the Department ofEnvironment, supports the theory that BSE is an auto-immune disease causedbya common bacteria.The theory, first proposed by Alan Ebringer, professor of immunology atKing'sCollege, London, and his colleague the late Prof John Pirt, opposes theacceptedidea that rogue prions are responsible. ( read full article here)

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Spinning Science into GOLD.(management of research and product development by biotechnology industry)
Sierra

Author/s: Karen CharmanIssue: July, 2001When research scientist Arpad Pusztai appeared on British television in August 1998 to talk about his studies of genetically engineered potatoes, he was suspended and later fired from his job at the Rowett Research Institute in Scotland. After a distinguished 36-year career there, his research was terminated, his data seized, and a contract clause was invoked that put his pension in jeopardy. At that point, the contract became a gag order forbidding him to discuss his work or defend himself in the ensuing six months--during which his scientific reputation was trashed by a fierce cadre of pro-biotech scientists in Britain and around the globe.What had Pusztai done? With the prior approval of his boss, this world authority on a class of plant compounds called lectins had made the case for food safety testing for all genetically engineered crops. At the time, Pusztai's team was conducting the only independent scientific research in the world designed to test the safety of genetically engineered foods. Originally an enthusiastic supporter of genetic engineering, Pusztai had not expected to find any negative results. Biotech researchers were interested in lectins because of their pesticidal properties and the possibility of inserting genes from the compounds into food crops. So Pusztai was both surprised and alarmed to find that rats fed potatoes genetically engineered with a specific lectin developed disturbing changes in the size and weight of some of their vital organs. He also found evidence of weakened immune systems. ....

Cover-up: Insecticide causes Mad Cows & vCJD
CJD alert investigates organophosphates

If Mark Purdey is right we are in big trouble. We are destroying our brains with insecticides.His groundbreaking research into the cause of BSE in cattle and new variant CJD in humans, has been sidelined by United Kingdom officials. They attribute both diseases to ingestion of prion protien found in contaminated beef. But Purdey has evidence the government's anti-parasite campaigns unleashed a chemical holocaust for cattle -resulting in BSE, and that human CJD is accelerated by the same chemical effects.

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Scientist and organic farmer, Mark Purdey gave evidence to the UK BSE inquiry, that warble fly insecticide was the cause of the disease. The scientist wheeled out to rubbish Purdy's evidence -Dr. David Ray, later turned out to have been receiving funding from the insecticide manufacturer ICI.

A lobby group that includes Bayer, Monsanto, Novartis, Pfizer, Roche and Schering-Plough was behind the effort to discredit Purdey. In December 1999, the same Dr. David Ray was appointed to the UK Veterinary Products Committee (VPC) -a government body that licences animal medicines.

Purdey has been consistently denied even exploratory funding to extend his privately supported research. Yet the Purdey chemical poisoning model matches with the epidemiological spread of CJD clusters in humans. It also predicts the incidence of BSE-type diseases in animals. The accepted infectious model fits neither. See Mark Purdey's evidence to the BSE inquiry in 1999

Purdey believes his bias for field work is the key to his success. He bemoans the "reductionism" of much lab-centered science. "I have travelled the world to investigate known clusters of spongiform disease - -- something mainstream researchers don't seem remotely interested in doing."

"I suppose they have mortgages and kids who need to go to university," he muses. "Privately, some were agreeing with me, but then they would denounce me publicly. It was quite strange really."

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Pesticide linked to Britain's Mad Cow epidemic

ENN Daily News -- April 8, 1996

.......Purdey said farmers were forced to use phosnet -- a blend of organo-phosphates and base of the drug thalidomide -- in the 1980s to combat warble fly infestation. Massaging it into a beast's rump to ensure it penetrated hide, flesh and muscle and reached deep-burrowing larvae meant OP toxins affected the animal's nervous system. Purdey successfully defended himself against an Agriculture Ministry prosecution for refusing to use phosnet. He then began to study organic chemistry to back his practical experience with scientific knowledge.

In the process he lost his farm, was shot at, blockaded in his home to prevent him giving a lecture, and saw a new farmhouse go up in flames the day he was due to move in. Purdey says it was significant that Switzerland, the only other European country to insist on the use of phosnet is the only other European country with large-scale BSE (bovine spongiform encephalopathy) outbreaks. OPs readily cross body barriers and bind with crucial nerve enzymes, disrupting pathways of the central, peripheral and autonomic nervous systems, Purdey said.

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Organophoshates (OPs) and TSEs: The OP Phosmet used at 4 times the ecommended max dose on cows in Britain in the 80s to control warble fly is a di thiophosphate systemic OP.The 2 sulphurs bind to copper forming a mercaptide ring. The Institute of Psychiatry conducted trials adding this OP to living cell cultures at very low dose. Off the record we were told that phosmet had created conformational change in prion protein.

This part of the work was suppressed by SEAC and not published or presented to the BSE inqiry.

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Bovine Spongythinking Myopathy. .....In view of the fiasco of the ill-fated soup of mixed brains (October 18) , described by Peter Smith as a fairly disastrous error....we feel that more notice than ever should be paid to Dr Venters'demand for a public inquiry into the supposed link between BSE and vCJD.

BSE-related sites

Spongiform Encephalopathy Advisory Committee (SEAC)www.defra.gov.uk BSE Inquiry Institutute of Food Science and Technology (UK) World Health Organisation Human BSE Foundationwww.humanbse.org.uk UK CJD Surveillance Unitwww.cjd.ed.ac.uk USA Federal Government website BSE documentswww.foodsafety.gov/~fsg/bse.html Which? Online information on BSEwww.which.net/campaigns/bse/bsecontents.html EU Food Communications Information Service BSE

(We find it interesting that SEAC has, on its panel of twelve members, Professor Roy Anderson, chief architect of the "cull by computer" FMD policy. The body it advises, the Food Standards Agency, is chaired by Anderson's friend Sir John Krebs. The spectre of CJD being spread by infected sheep seems soley the result of "reassuring" pronouncements by the FSA and SEAC. The threat of a cull of all sheep, "should even one be found to be infected with BSE" has been given by our Chief Vet, Jim Scudamore. The researcher whose findings linked BSE with organo-phosphates was leant on heavily. His reports were unaccountably destroyed. When BSE is "found" in sheep grazing in another wild place such as Exmoor, it needs to be remembered that while we are unable to move a sheep without jumping through hoops, such a restriction could easily be overcome by the men in white - who have artificially infected sheep in the laboratory by injecting them with BSE infected brain tissue.)

During the BSE inquiry, of 111 projects commissioned by the agriculture ministry, only 12 were awarded after open competition, "none were properly peer-reviewed, most produced no published papers and none produced final reports": Malcolm Ferguson-Smith, a veterinary pathologist from the University of Cambridge.
Ferguson-Smith was the only scientist on the three-strong panel that wrote the report of the official inquiry into BSE. The human form, vCJD, disease has now killed 106 people.

source: New Scientist Sept 2001

Dr George Venters wants a public debate on the evidence supporting a link between the two diseases

The brain of a CJD patient
(from BBC page http://news.bbc.co.uk/hi/english/health/newsid_1590000/1590863.stm)

Part of Today programme - Transcript by http://www.warmwell.com

Sue McGregor: What leads you to think there isn't a connection between BSE and nvCJD?

Dr Venters: When you apply epidemiological criteria that are testing the strength of the causal hypothesis there are gaps in the evidence; there are loose ends when we apply these to the link between Bovine Spongiform Encephalopathy and the nvCJD

Sue McGregor: Loose ends in the fact - or including the fact - that more people would have nvCJD in your opinion if it did come from eating infected meat?

Dr Venters: That's correct.

Sue McGregor: And what are some of the other loose ends?

Dr Venters: The fact is that you can never actually prove that the BSE prion causes these diseases in human beings because human beings can only ever produce human prion. Therefore isolating BSE prion from a human brain is not possible.

Sue McGregor: And you think it's a coincidental connection that people have made?

Dr Venters : Yes. If you look at the surveillance enterprise in the UK, it's far superior, it's the best anywhere in the world. We collect cases more comprehensively and process them more systematically than anywhere else in the world. As a result of that, in CJD surveillance, manage to increase the detection rate of sporadic CJD threefold and the sampling process by which we recruit ..cases for study by that you know also changed qualitatively in the 1980s because of concerns about Spongiform Encephalopathy. So what happens is that we had younger people being interviewed... (interrupted)

(questions for Prof Peter Smith of SEAC)Prof Smith : I think the concerns that Dr Venters is raising were reasonable concerns to raise in 1996 when the link between vCJD and BSE were first postulated - and indeed they were raised and this was something to be very concerned about; was it a new disease and was it linked to BSE? I think the evidence that's accumulated in the subsequent time has done much more to firm up the link than Dr Venters suggests. I think we haven't found the disease before 1994. Had we found it before the BSE epidemic that would have questioned the link. We haven't found it significantly outside the UK - four cases in France and one in Ireland. We know we exported a lot of meat products to France and to Ireland. Interesting that there's been one case in Hong Kong but that was in a person who had actually spent much of their life living in the UK

Sue McGregor: So you believe there is a traceable connection?

Prof Smith: I think that the strongest evidence is really the work that was done in the year following the link which has shown that biological properties of the agent that is infecting humans with vCJD were to all intents and purposes identical to the BSE agent. I think that was really the evidence that established beyond reasonable doubt that these are caused by the same agent.

Sue McGregor: Dr Venters, your theory seems to be very much a minority one. Do you think that what Prof Smith has said holds no water at all?

prof Venters: As I've said, the similarities of what we call strain typing strengthen the association but we can never ever produce anything other than human prion as human beings and therefore to assert that prions that have got the same shape and physical and chemical properties are necessarily the same is not the case....(interrupted)

Sue McGregor: Dr Philip Monk said that if you cast doubt on what seems to be the received opinion of the majority of scientists at the moment then effectively you are asking them to take their eye off the ball and we will never find a cure for it

Dr Venters: No. Entirely the reverse! What I am saying is that I would like government policies to be applied on the basis of a more realistic appraisal of risk, addressing what is likely to happen rather than what is frightening but increasingly a less likely possibility.

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From the BBC

The link between "mad cow disease" and vCJD - commonly thought to be its human equivalent - has been disputed by an expert. Dr George Venters, a consultant in Public Health Medicine in Lanarkshire, Scotland, claims evidence linking the two conditions is weak.

The variant form of CJD may simply be a rare type which existed long before the BSE epidemic in cows - but was simply not diagnosed and catalogued properly until the 1990s. If his theory is correct it would mean victims of the condition did not get it by eating infected meat.

I believe the evidence now available casts serious doubts on the case for a causal link

But other CJD experts say the evidence is strong enough to firmly suggest humans contract vCJD by eating meat from cattle with BSE containing infectious "prion" proteins. Dr Venters bases his opinion on the fact that the rate of growth in the number of confirmed cases is much less than might be expected from a food-borne source.

He suggests the rate of growth in the number of vCJD cases is more consistent with a previously misdiagnosed but extremely rare disease being found.

Advances in the detection and reporting of suspected cases through the CJD Surveillance Unit in Edinburgh could account for an apparent rise in the number of cases, none of which would have been officially recorded previously. He wants a public debate on the evidence supporting a link between the two diseases.

Dr George Venters put forward the controversial theory

Speaking on BBC Radio 4's Today programme, Dr Venters said government policy should focus on "a more realistic appraisal of risk, addressing what is likely to happen rather than what is a frightening but increasingly less likely possibility".

He said: "Without doubt, general anxiety about so dreadful a possibility as BSE causing a similar disease in humans resulted in many workers involved with BSE and CJD having to reach precipitate conclusions in which public safety was rightly the prime consideration.

"I believe the evidence now available casts serious doubts on the case for a causal link between bovine spongiform encephalopathy and 'new' variant Creutzfeldt-Jakob disease.

"A particular problem is that when you have a food-born infection you expect the rate at which cases occur to run parallel to the rate at which the population is exposed to infection - That doesn't seem to be happening."

vCJD cases don't occur in those countries that have not got BSE

Dr Phillip Monk But Dr Phillip Monk, a consultant in communicable diseases who investigated a vCJD cluster in Queniborough, Leicester, dismissed the theory.

He told Today: "You only have to realise that vCJD occurs in countries like ours that have had high problems with BSE.

"vCJD cases don't occur in those countries that have not got BSE. "The moment we relax our guard we put people at risk again." (warmwell note: where have we heard that before?)Professor James Ironside, from the CJD Surveillance Unit, also disagreed with Dr Venters' theory.

Professor Peter Smith said the link was beyond reasonable doubt

He said: "I think it is an interesting paper and it is always important to consider a range of arguments on this subject because there are huge numbers of uncertainties. "But we do know from a number of studies done both here and in the States that the transmissible agent that causes BSE is the same as that which causes CJD and has also transmitted to other species including cats, wild cats and antelope in zoos.

"The most probable hypotheses for linking the numbers of species together is by food-borne exposure as was the case with BSE."

Professor Ironside added that the incubation period of the disease was significant and there had been a slight rise in the number of cases over the past 12 months.

Professor Peter Smith, chairman of SEAC, the scientific body that advises the government on CJD, said the only way to prove the link between BSE and CJD would be to inject BSE-infected material directly into a human. (warmwell note: Extraordinary! And this is precisely what they have done to sheep. Does that therefore prove that sheep have vCJD? Or does it prove rather that if you inject brain-diseased tissue directly into a healthy animal you get a very unhealthy one as a result?)

But he said: "The circumstantial evidence is beyond reasonable doubt now that BSE and vCJD are caused by the same infectious agent."

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The Purdy hypothesis in summary:

In prion disease there is an error in the manufacture of the prion protein caused by an abnormal configuration and or binding of two key metals Copper (Cu) and Manganese (Mn). Mn substitutes for Cu when the latter is low or fails to bind to the histadine sites of the octapeptide repeat region of the protein.

This substitution results in eventual conformational change/ protease resistance . In addition the host would be exposed to a free radical trigger that generates excessive oxidative stress and up regulates the prion protein as a defense

The most important function of the Prion is to resist oxidative stress by acting as a Super Oxide Dismutase (SOD).

On conformational change the prion cannot function as a SOD and protect cells, and consequently a pro oxidative status quo is established at a location in the host.

This pathology spreads through the host during the incubation period, with neurones eventually being destroyed by the build up of toxic by products such as hydrogen peroxide, quinones or peroxynitrite.

Finally the metal species bound by the prion is more highly oxidised ie Mn 3+ or 4+ and this may explain strain difference and difference in incubation times.

Environmental factors that affect the levels of metals ,their species and protein "sinks"cause the disease.

Oral infectivity via food products is secondary and we think is rare in vivo.

The often quoted transmission experiments are not reliable predictors of the situation in life - even oral homogenate studies are unreliable because reactive metals are freed from protein sinks in the process.

Further reading:

Mark Purdey Ecosystems supporting TSEs demonstrate excesses of the pro-oxidant Manganese Medical Hypotheses (2000) 54 (2)(Coming on eionews)

D.R Brown et al Consequences of Manganese replacement of Copper for prion protein function and proteinase resistance. EMBO journal vol 19 no.6 p 1180 - 1186

Useful background

New Scientist 26 august 2000 article "Metal Heads" by Jonathan Knight

FAQ ;Organophoshates (OPs) and TSEs: The OP Phosmet used at 4 times the ecommended max dose on cows in Britain in the 80s to control warble fly is a di thiophosphate systemic OP.

The 2 sulphurs bind to copper forming a mercaptide ring. The Institute of Psychiatry conducted trials adding this OP to living cell cultures at very low dose.

Off the record we were told that phosmet had created conformational change in prion protein.

This part of the work was suppressed by SEAC and not published or presented to the BSE inqiry.

Some OPs contain Mn - Mancozeb, Maneb. Mn is often sprayed on farmland where Mn levels are low. OP residues increased in Mbm in the early 80s.

Our current studies:

Scrapie in Sardinia , TSEs in Calabria , vCJD (Kent, Queniborough, Armthorpe ) - We receive no funding for these.

Past studies:

Rida in Iceland,CWD in Colorado , CJD in Slovakia , Scrapie in Somerset/ N.Devon

Urgently neededstraightforward, Lab research :

Identify what is bound to the histadine sites of the octapeptide repeat in BSE, CJD and Scrapie prion material.

Phosmet + live cell culture, transmit the result

Maneb + live cell culture, transmit result.

High Mn and low cu in transgenic mice. Transmit Trial

therapeutic strategies:

1)Desferrioxamine

2) Porphyrins

3) Atropine/ oxime.