Chronic Wasting Disease Emergency!
In a study that could help develop cattle bred to resist mad cow disease, researchers showed in a laboratory experiment that a mutated protein may protect animals from the prion protein that causes the brain-destroying disorder.
Researchers at the University of California, San Francisco, reported that they genetically altered a strain of mice so the animals made a mutated form of prions which then prevented the animals from becoming ill when injected with a form of prion that usually causes the brain disease.
"We found that the (genetically engineered) mouse became completely resistant to the prion disease," said Dr. Jiri G. Safar, a co-author of the study appearing this week in the Proceedings of the National Academy of Sciences.
Safar said he and his colleagues now hope to develop a genetically engineered strain of cattle which is resistant to mad cow, known formally as bovine spongiform encephalopathy, or BSE.
Patrick W. Dunne, a veterinary scientist at Texas A&M and a BSE researcher, called the study by Safar and his colleagues "a breakthrough."
"This means that prion diseases in livestock could be at least inhibited, if not eliminated," said Dunne. "It is a very significant finding."
Prion diseases include BSE in cattle, scrapie in sheep and Creutzfeldt-Jakob Disease in humans. There is also a related wasting disease in deer and elk. The diseases are caused by an abnormal form of the prion protein that makes the normal form of prion change its shape and become infectious. The abnormal prion causes the progressive, irreversible destruction of brain cells. The disease is fatal in all species where it occurs.
An epidemic of mad cow disease developed in Britain in the 1980s after cattle there were given feed that included body parts from sheep with scrapie. Researchers later found that some people developed a form of prion disease, called new variant-Crutchfeld-Jacob Disease, after eating meat from infected cattle. The discovery caused a temporary ban on the import of British beef in many countries and the destruction of thousands of cattle in the United Kingdom.
More than 100 people in Europe have been diagnosed with new variant-CJD, but that form of prion disease has not been diagnosed in the United States. A type of CJD not related to eating meat, however, does occur in the United States.
In the new study, Safar and his co-authors, which includes Stanley B. Prusiner, who was awarded a Nobel Prize for discovering prion disease, found that by altering the genes of mice they could make the animals resistant to the brain-destroying disease.
Safar said earlier studies in Japan and elsewhere had suggested that some mutated forms of prion prevented the disease-causing form of the protein from causing disease.
To test this idea, researchers engineered a mouse strain with genes that caused key changes in the amino acids that make up the prion protein. When mature, the mice were injected with high doses of the disease-causing form of prion.
Although some of the test animals did form some pathogenic prions, none of them developed the full blown prion disease. Safar called this the "silent expression" of the diseased prion.
In contrast, mice with the normal type of prion developed a fatal brain disorder when they were injected with the disease-causing form of prion.
With selective genetic engineering, Safar said, "it is possible we could wipe out even the silent expression and transmission of the pathogenic prion."
Safar said that altering the prion gene to make it resistant to the disease is better than eliminating the gene altogether, as some have suggested. Taking out the gene altogether, he said, could cause subtle health changes in the animals since normal prions play a role in brain cell maintenance.
CWD is an always-fatal neurological disease, similar to mad cow disease in cattle. It is caused by a prion, a mutated protein. Although no one is certain what causes the mutation, it has been linked, in domestic stock at least, to animal feed containing animal parts (such as bone meal).
How CWD is passed between live animals, however, remains a mystery,
though it is assumed it's by close physical contact. But scientists have
no idea what agent -- saliva, urine, feces -- passes the disease, if
indeed, that is how it is transmitted.
Once thought to be contained out West, the discovery of CWD in Wisconsin
shocked biologists because the nearest known case of CWD was 600 miles
away in western South Dakota.
So what's the news? A post-season deer hunt to kill deer for testing has
turned up 10 more CWD-infected deer in Wisconsin so far, with more
testing coming. And in Colorado, where the disease was first identified,
three infected deer showed up west of the Continental Divide.
So geographical barriers -- the Mississippi River and the Rocky
Mountains, two reasonably imposing boundaries -- have failed to stop the
disease from spreading.
There's more. Colorado has found that the disease somehow remains in the
ground after decontamination procedures. Officials there now say they
believe it can persist for five years.
In Colorado, an infected captive elk herd was found on the western
slope, leading biologists to believe the deer contacted it from penned
animals. But Wisconsin is at a loss to explain where its CWD came from;
the two most likely guesses are from an infected captive animal or from
the carelessly disposed carcass of an infected Western animal brought
into the state by a hunter.
Although there is no evidence that CWD has found its way into Michigan
yet, we've been slow to adopt preventative measures. The Department of
Agriculture has banned the import of captive deer and elk from areas
known to have CWD, but sportsmen say that's not good enough. They are
Michigan United Conservation Clubs recently passed an emergency
resolution calling on the state to ban all imports of live deer and elk
and to prevent hunters from bringing in anything other than the antlers,
cape and boned meat of animals taken out of state. In addition, MUCC
wants no more captive deer or elk operations to be licensed and no
existing operations allowed to expand. Most importantly, MUCC wants
existing captive pens to be double-fenced to prevent close contact
between animals at the fences.
Department of Natural Resources officials agree, but they've been loathe
to demand double fencing because, I'm told, the guv wants his children
(DNR and Ag) to play nice.
Other states are way ahead of us. A number of them, including states as
far from the disease as New York and Florida, have closed their borders
to captive elk and deer imports.
We should, too. There's no definite way to know that a deer imported to
Michigan from, say, Arkansas, wasn't imported there from Colorado or
elsewhere. Why risk it?
As for double fencing, it's in the agriculture community's best interest
to adopt such a policy immediately. If the stuff can go one way through
a fence, it can go the other way, too. Should CWD find its way into the
wild herd, you can bet the captive operations will start screaming that
they want double fencing and that the sportsmen should pay for it. (It
always seems to come down to that, doesn't it?).
Wisconsin is contemplating some drastic measures, including reducing the
deer herd by 90 percent in the affected area. That's almost impossible
to accomplish through conventional hunting; it'll probably mean
year-round shooting, possibly from aircraft.
Do we want to see that here? There's no need to even ask that question.
So, do we have an appropriate cliche? How about this one: An ounce of
prevention is worth several tons of cure.
Contact Bob Gwizdz at (517) 487-8888 or e-mail him at
By Anita Manning, USA TODAY
Two young men, ages 26 and 28, died last fall in the same Michigan
hospital of a rare brain disease that occurs mainly in elderly people.
The incident, which raised fears that the human form of mad cow disease,
or something similar, had emerged in the USA, prompted a swift
investigation by federal health officials, but doctors familiar with the
cases say there is no evidence to support that fear. They say autopsies
and other tests indicate the victims died from so-called "classic" forms
of Creutzfeldt-Jakob disease (CJD).
While the cases are "highly unusual and disturbing," says University of
Michigan neurologist Norman Foster, the data show that the forms of CJD
suffered by the young men are ones seen previously in older individuals.
CJD occurs at the rate of about 1 person per million per year, almost
always in people over age 60. What doctors feared is that a new form of
CJD, possibly similar to a variant that emerged in the mid-1990s in the
United Kingdom and linked to consumption of mad-cow-infected beef, had
Unlike classic CJD, the new variant, vCJD, strikes mainly young adults.
It has killed more than 100 people. The only known case of vCJD in the
USA was diagnosed recently in a 22-year-old British woman living in
Florida, who is thought to have contracted the disease in England.
Mad cow disease has not been detected in cattle in the USA, but a
similar disease in deer and elk is spreading in the Midwest. Chronic
wasting disease (CWD) is fatal to deer and elk but is not known to cause
illness in humans.
Lawrence Schoenberger of the Centers for Disease Control and Prevention
in Atlanta says the agency sent investigators to Michigan in late
August, when the victims were still alive.
"The key thing here is the two were right together. We were worried that
there was maybe a common exposure, but our investigation revealed that
was not the case." The men lived in adjacent counties but did not know
each other, he says.
In the rare cases when CJD strikes before age 30, it is often caused by
a hereditary form of the disease, says Foster, and "tests are continuing
to see if that may be a factor in these cases."
But extensive family interviews determined that neither man had a family
history of dementia, nor had they eaten venison or elk meat or visited
countries where mad cow disease has been detected.
"We feel as comfortable as anyone can that this is not related to either
CWD or (mad cow disease)," says Foster, who treated the patients at the
University of Michigan Medical Center in Ann Arbor.
Not everyone is comfortable. "I discount the statement that these two
young people, dying at the same time in the same hospital in southeast
Michigan, did not eat venison, after living their entire lives in that
state," says John Stauber of the Center for Media & Democracy and
co-author of Mad Cow USA.
He suspects a new American variant of CJD, perhaps related to chronic
wasting disease, may be emerging. "Any attempt to portray these CJD
deaths as some sort of 'normal' occurrence that has simply, to date,
gone unobserved is absurd," Stauber says.
Current estimates of only five cases per billion of CJD in people 30 and
younger may be incorrect, says Foster, who co-wrote a report on the
cases presented this month at a meeting of the American Academy of
"The fact that they both occurred at the same time in a relatively small
population suggests that (CJD in younger people) may be more common than
previously suspected," Foster says. Doctors don't expect to see it in
young people, so misdiagnosis may occur. "Any young individual with
progressive neurologic disease should be considered for CJD."
He says the cases also underscore the need for a national system to seek
out and report all cases of CJD. "There certainly is the possibility
that other cases have been seen and not diagnosed, or even if diagnosed,
5-4-02 Chicago (Reuters)
Like other hunters in Wisconsin this spring, David Peil is wondering whether the venison stowed in his freezer is safe to eat.
He has been contemplating the issue since the Wisconsin Department of Natural Resources said earlier this year that three deer shot by hunters last fall tested positive for chronic wasting disease (CWD), a fatal neurological illness related to mad cow disease.
The cases were the first ever found east of the Mississippi River.
A state-organized cull this spring of 516 deer from the same region of southwest Wisconsin turned up 11 more cases of CWD, prompting officials to plan a much larger de-population effort to halt the spread of the disease.
Starting next week, Wisconsin will call on farmers and other land owners to help shoot as many as 15,000 deer in the area.
Whatever the outcome, the disease outbreak has raised fears about the safety of meat left over from hunting season last fall.
"The deer that we've shot here didn't appear to be sick. But I really don't know if I'll eat more or not," said Peil, who owns Buffalo County Buck Connection, a hunting preserve in western Wisconsin, about 160 miles north of the area where the CWD-infected deer were found.
"You think about it -- is it really worth having a piece of venison?" Peil said in a telephone interview.
THREAT TO HUMANS UNLIKELY
Like mad cow disease, CWD is in the family of illnesses known as transmissible spongiform encephalopathies, or TSEs. About 100 people in Europe have died from a human version that scientists believe was caused by eating beef from cattle with mad cow disease.
There is no evidence that CWD, first identified in 1967, has ever spread to humans, cattle, or any species other than deer and elk. In one 2000 study, National Institutes of Health (news - web sites) researchers at Rocky Mountain Laboratories in Hamilton, Montana, determined that a molecular barrier appeared to help prevent CWD from jumping to other species.
However, the researchers were able to get a low quantity of diseased deer proteins, called prions, to convert healthy human prions to the diseased form, suggesting it might be possible for humans to get CWD.
Byron Caughey, one of the Rocky Mountain researchers behind the study, cautioned that it was difficult to draw any firm conclusions from the study about the human risk of CWD.
"This is a test tube reaction that is a poor surrogate for actual transmission studies in the real world (news - Y! TV), but no one wants to actually test whether chronic wasting disease can infect humans," he told Reuters.
"Our work suggests that while it may be possible for humans to get CWD, it's likely to be a low-efficiency process," he said.
Then again, would scientists even know how to recognize a human case of CWD?
"We don't know for sure," Caughey said. "Since no case of (a human TSE) has been documented to come from CWD, we don't know what such a case might look like."
EATING VENISON A PERSONAL DECISION
Wisconsin wildlife officials have responded to consumer queries by citing World Health Organization (news - web sites) guidelines, which recommend against eating any part of an animal showing signs of CWD. The WHO also says there is no evidence that CWD can infect humans.
Wisconsin DNR spokesman Bob Manwell conceded that the recommendations on venison were "a little bit vague."
"(But) It's similar to a lot of health advice that is given out, where it really comes down to a personal decision. There is a small risk, and it's the individual's decision as to how they feel about that," Manwell said.
Manwell said that for now, the state planned to go ahead this fall with a deer donation program that provided meat to food pantries and needy families. Hunters donated 3,921 deer to the program last year, resulting in about 176,000 pounds of venison.
"Even after the realization that we have this disease in the state, there has still been demand for the meat," Manwell said.
"It's really going to be up to individual food pantry organizations what they want to do about it."
STATE TO MONITOR HUNTER PARTICIPATION
One question is whether deer hunters will still hunt if they do not plan to eat what they kill.
"We're going to be watching our (hunting) license sales very closely," Manwell said, adding that sportsmen may see the task of reducing the state deer herd as a conservation duty.
"We have a chance right now, if we take this action, of possibly eradicating this disease and maintaining the health of the rest of the herd. While it's distasteful, it's one of those things that we feel the need to do."
Peil said his hunting customers were more interested in trophies than meat, but he expected his business would suffer eventually if CWD spread.
"In Wisconsin, deer hunting is a kind of religion," Peil said. "I think (hunters) will pitch in to see if they can slow the disease or stop it. But if they can't, and it spreads, I think it's going to be tough to hunt."
Animal Pharm by Mark Purdey
Note: As an organic farmer, Mark Purdey resisted the order to spray his cattle with organophosphates for warble fly and went to court for a judicial review; he won and was exempted from using the spray. No cows born in his herd developed BSE (mad cow disease). He has contributed numerous articles on the subject of BSE to scientific journals. He farms in Somerset, UK. This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Spring 2000
As the first snowstorm of winter hit the isolated hill where I farm, I pitched out the last forkfuls of hay to my cattle before nightfall. Much like the whirlwinds of snow surging all around me, my brain was turning over and over the catalogue of injustices that successive governments had levied onto the farming community over BSE. I felt paralysed and powerless in the encroaching snowstorm.
My confidence to carry on was battered to pieces by the recent ban on beef-on-the-bone. The announcement-based on the whims of a mere handful of government "experts"-renders my hard graft over the last twenty years in farming into pathetic insignificance. But how can there be any true "experts" from academia when the most basic facets of the Bovine Spongiform Encephalitis (BSE) disease process remain a total mystery? One would have thought that all of those farmers and independent vets living and working in the front line with BSE cattle would have been the first to be consulted. But strangely, their observations have been completely ignored by officialdom.
Cows frequently partake in the bizarre habit of eating their colleagues' afterbirths after calving, and I was particularly intrigued to watch my own home-reared, BSE-free cows positively relishing the delicacies of afterbirth tissues derived from a group of pedigree cows that I purchased into my farm in 1989. As the majority of these imported cows went on to develop BSE, it is interesting that BSE has not surfaced in my home-reared cows, despite their overzealous exposure to the allegedly "infectious" blood and lymph found in the afterbirths of the BSE cows. Other farmers sharing the same experience report the same outcome.
Another anecdote hails from the farming community of Shetland, where the island folk are free of Creutzfeld-Jakob disease (the human form of BSE), despite their ancient custom of eating "potted sheep's brain." Interestingly, the equivalent of BSE in sheep, called scrapie, has been rife in the sheep flock on Shetland for centuries.
The anecdotes are ever-flowing, and all point to a hypothesis based upon some environmental causal factor that falls a long way short of the current government's nightmare infectious "ingestion" scenario. If the spongiform agent is as infectious as the authorities would have us believe, why has chronic wasting disease (the BSE equivalent in deer) remained uniquely confined to a small cluster zone in the Rocky Mountains for thirty years now, without spreading across to the neighboring deer herds roaming the rest of the Rockies? Why has no spongiform developed in the various predators of those affected deer?
From the very beginning of the crisis, the farming community has been the unfortunate victim of the whole BSE campaign. Yet, ironically, the same presiding authorities who are responsible for foisting off the burden of BSE are, no doubt, totally oblivious to the fact that more farmers have committed suicide as a result of official BSE blunderings than people have died of new variant Creutzfeld-Jakob disease (nvCJD).
A body of government experts was quick to take exclusive control of BSE research, and very rapidly the cause of the disease was attributed to the feeding of scrapie-diseased sheep brains to cattle. In other words, scrapie was said to jump from sheep to cattle by virtue of some sort of infectious agent. And it naturally followed that this same assumption of disease cause was extrapolated into the human CJD context-the presumed "microorganism" had now jumped from cows into humans. But this was no more than unproven hypothesis, and it still remains that way today.
Not surprisingly, only a handful of folk had insight into the unsavory world of the meat and bone meal (MBM) rendering business. But for anyone who had scratched the mere surface of the global distribution of British MBM products, it became strikingly obvious that the very mainstay of the official hypothesis was radically flawed. For instance, during the 1980s thousands of tons of this very same incriminated MBM was exported to cattle farms in BSE-free countries such as the Middle East, Malta and South Africa. Officials have always brushed this challenge aside, arguing that the cattle in these countries did not receive sufficiently large doses of scrapie to contract BSE. But this contradicts their current official explanation for the 30,000-plus cases of BSE that have developed in cattle born after the 1988-ban on MBM, where government scientists conveniently claim that leakage of micro amounts of MBM (destined for pig and poultry feed) into the cattle rations, caused the 30,000 cases.
Furthermore, USA and Scandinavian rendering systems duplicated exactly the same prerequisites that were supposed to kick off BSE in Britain-scrapie affected brains being milled into feed-yet their livestock remained BSE-free.
Nor were we told of the numerous unsuccessful attempts by US scientists to induce BSE in cattle that had been experimentally fed or injected with massive amounts of scrapie brain material. Apparently, the cattle either just "got fat" or went down with a sickness more akin to motor neurons disease than BSE.
Despite millions of pounds worth of scientific research failing to ascertain a link between BSE and scrapie, the whole propaganda myth that BSE was caused by scrapie became gospel in mainstream public mentality.
The media loved the theory because they could drum up a viral holocaust-horror scoop. The vegetarian and green lobbies found themselves landed with a powerful propaganda weapon on their plate- turning cows into cannibals. And the UK scientific establishment could go on drawing generous grant funding for their viral witch-hunt without the embarrassment of having to account for years of barking up the wrong tree. And then the government could foist the blame of BSE onto a naturally occurring agent for which no significant vested interest or official body could be held accountable.
Whilst the maligned renderers and feed merchants got the full brunt of blame for BSE, it surprises me that neither were held accountable for the financial damages of the crisis. Instead, they all received generous compensation payments to the tune of millions.
Almost on a weekly basis we are now finding ourselves listening to the same experts regurgitating the same stereotype claims of how BSE has now jumped from cattle into humans. On Channel 4 Dispatches (last December), despite no reported cases of BSE in the British sheep flock, it was assumed that sheep must be affected with BSE because they had eaten meat and bone meal. We are now warned of the danger of eating sheep. Professor Blakemore summed up the programme by saying that we should all eat chicken and avoid beef and mutton. But as poultry received their fair share of meat and bone meal as well, should we not be cutting chicken out of our diet too, according the dictates of the official theory?
These spokespeople would do better to start questioning the entire foundation of their hypothesis, rather than squeezing the last drop of "infected" blood out of the sinking stone. What is more, the conventional consensus on BSE is ignoring that well-recognized academic yardstick, Koch's postulates, which is employed for assessing the cause of disease. The first postulate dictates that a theory begins to carry weight once the hypothetical causal agent can be identified in every victim of the disease in question. The conventional hypothesis on scrapie/BSE/CJD certainly fails to fulfil this basic postulate on several counts. In this respect it is particularly interesting that spongiform disease has been experimentally induced in animals after receiving injections of brain tissue derived from people who have died of Alzheimer's and Parkinson's Disease. Why is nobody freaking out about Alzheimer's disease?
In the case of BSE where no viral cause has been identified, it is illogical to assume that one animal has to eat another in order to catch the same disease. Initially, the direction of any epidemiological research programme should follow elementary logic and investigate the most likely assumption that the various different species of mammals suffering from the same disease have all been exposed to the same causal factor in the environment. But it seems that nobody has investigated this route. Sheep did not cannibalize each other in order to catch scrapie, nor did wild deer in the Rocky Mountains cannibalize each other in order to catch their BSE-equivalent disease, chronic wasting disease.
The reductionist mindset of government scientists is betrayed by the narrow scope of questions that have been put to the relatives of the new variant Creutzfeld-Jakob disease victims. The questionnaire is almost entirely focused on the carnivorous perspective of the victims' diets, and therefore tailored to suit their own hypothesis from the outset. The Establishment's assessment of nvCJD etiology seem to have completely ignored the fact that adolescent CJD was recorded well before the 1980s. And why do they move the goal posts every time a new challenge confronts their theory-like extending nvCJD's incubation period to tally with the long term vegetarian victim from Kent? Take note that they have completely ignored the case of the lifelong vegetarian nvCJD victim from France.
The British government's Spongiform Encephalitis Advisory Committee (SEAC), seems to have thrown aside one of its most relevant long standing observations on CJD epidemiology-people who are occupationally involved with pets and farm animals are at greater risk of developing CJD. And it is this observation that may well hold the key to the true cause of these diseases.
During the 1980s and early 1990s, cattle and cats (the species of animals that have developed BSE) were exclusively treated with systemically acting types of Organophosphate (OP) insecticide which were designed to penetrate the entire physiological system of the animal, transforming the bloodstream into a toxic medium so as to kill off any unwanted parasites present. In the context of cattle, the use of these systemic OP's was subject to a compulsory government order for the eradication of warble fly. The UK government was unique in compelling a substantially higher biannual dose of this OP by comparison with the few other countries around the world that were following similar, less intensive measures to control this fly. Interestingly, these other countries, including Switzerland, France and Ireland, comprise the few other countries that are suffering from very small epidemics of BSE in their home-reared cows.
The National Farmers Union, the Meat and Livestock Commission and The British Veterinary Association formed a united front with MAFF (Ministry of Agriculture, Fish and Forestry) to ensure that all farmers complied with the law and treated their cattle. Systemic OP's are recognized as exerting their toxic effect by entering the central nervous system and deforming the molecular shape of various nerve proteins. These chemically-mutilated mutant proteins are subsequently rendered incapable of performing their proper function in the nerves.
The known toxic effects of OP's lead me to wonder whether the use of systemic OP's on British cattle have caused the malformation of another newly discovered brain protein called prion protein-the phenomenon that US scientists have proposed as the cause of spongiform encephalopathies. Whilst some types of spongiform disease have been attributed to genetically acquired damage to the shape of the prion protein, the underlying cause of protein damage in the BSE and new variant CJD strain of the disease remains a mystery-amongst "open-minded" scientific circles, at any rate.
OP's are known to generate a highly reactive type of "free radical" in the tissues that they intoxicate. And it is this free radical legacy of OP poisoning which is capable of instigating a chain reaction of lethal attacks on nerve membranes and proteins in the central nerves of susceptible individuals.
Once tissues become 'infected' with free radical chain reactions, the introduction of freezing, heat or radioactive conditions to the affected cells does not arrest such an 'infection.' In fact, irradiation, heating and homogenizing of such tissue (brain tissue from spongiform affected animals is homogenized before it is inoculated into healthy animals in transmission trials) actually proliferates the free radical phenomena. This suggests that these free radicals may constitute the as yet unidentified "infectious" transmissible agent of these diseases.
Concerned members of the public helped me to fund a £14,000 experimental research project at the Department of Neuroscience, Institute of Psychiatry in London, where living tissue culture cells which express the prion protein were exposed to low doses of the OP chemical; so as to stimulate the context of a living cow undergoing OP treatment. Significantly some of the recognized changes of the prion protein which appear in the early stages of spongiform disease were induced in these OP-treated cells.
Clearly, these results go some way towards proving that OP's represent a primary or partial cause of BSE. Yet it was this very same simple test that the government had always assured me was too expensive for the tax payer to fund and, besides, impossible to set up anyway, even with the most updated lab technology.
In December 1996 Lord Lucas, MAFF's spokesman in the House of Lords, gave a written answer stating that the government had asked the SEAC committee to revisit the OP-BSE theory as a result of the recent research findings conducted at the Institute of Psychiatry.
After being invited to deliver my thesis to a SEAC meeting in April, 1997, I was disturbed that at no stage during the protracted enquiry that followed was the experimental evidence of the Institute's work addressed-the prime purpose behind this hearing. The committee dismissed the evidence that I presented, which had been drawn from independent peer-reviewed, published science literature. I was not surprised to learn that the outcome of this enquiry-the proceedings of which were described as "confidential" to any enquiring journalist-was a recommendation to government that any applications for funding research into the OP-BSE theory should not be supported.
I still shudder each time I visit our local farm stores and see the canisters of systemic OP products up for sale. Although the warble fly is eradicated and BSE is on the wane, farmers can still apply these chemicals in a voluntary capacity for controlling lice and other pests. I shudder further when I see the bottles of OP head lice shampoo and OP systemics for pets and gardens still in the shops for human use.
The real madness of the mad cow fracas would seem to lie with the deadlock that has kept these products on the open market for a full year since experimental evidence first linked their use to the cause of BSE. Perhaps the government is so scared of compensation claims that it employs everything at its disposal to prevent any degree of acceptance of the idea that their compulsory warble fly programme caused the biggest catastrophe in the history of British agriculture.
The brave new SEAC committee appears to be totally preoccupied with "effect" rather than "cause." Such a back-to-front approach betrays their sensitivity with anything to do with "cause." But how can any government programme seriously hope to eradicate BSE or nvCJD if it has failed to eradicate, let alone recognize, the disease's true cause?
Mad Cow Update
Those in charge of public health policy in the US do not really understand what I am demonstrating about bovine spongiform encephalopathy (BSA) and Creutzfeld-Jakob Disease (CJD). They get the main linchpin of the work wrong by stating "manganese deficiency" instead of "manganese excess." Then they seem to marginalize my position in the BSE debate by falsely suggesting that I am at odds with Stanley Prisiner's prion concept that has now been accepted as mainstream.
Ironically, both my own studies and those of Dr. David Brown largely open up the final door of evidence in support of Prisiner's concept. We have shown what causes the prion protein to transform into its protease-resistant form (the disease-associated form). Prisiner first identified the abnormal prion as the hallmark of the BSE-diseased brain and he hypothesized that his abnormal protein somehow caused the disease. Where I do differ from the Prisiner brigade is only in one point-I don't believe that the "prion" is highly infectious as they are suggesting; that is, I don't believe that it can infect those who eat prion-contaminated meat. I believe that it is the manganese 3+ attached to the prion that is the infectious agent and only when it is transmitted by injection, etc., into susceptible genotypes. Prisiner himself is skeptical of "the-BSE-feed-caused-new-variant-CJD" hypotheses. He was the only person (apart from myself) who suggested this to the BSE inquiry!
I just hope that the beef industry in America realizes that we're not as "way out" as has been suggested. The industry is shooting itself in the foot by rejecting the link to toxic mineral excess and organophosphate pesticides. We have accumulated so much hard evidence now-more than all other theories.
I have been to Calabria in Southern Italy looking at the case of 20 CJD victims in a hamlet of 150 population since 1995. Intriguing stuff! But I was warned that the Mafia controls the property market and meat market in this part of Italy and would be hostile to me. So I was unable to get soil samples at that time.
Things are so desperate in farming in Europe at present. We are so concerned by the totalitarian, global control that is molding the direction of agriculture into complete ecological and economic crisis. The "arable aid payments scheme" has caused acres of former livestock grassland to be ploughed up. The global warming flash flood storms have caused an unprecedented degree of soil erosion, with its attendant self-perpetuating drain on human reserves.
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