The U.S. Department of Agriculture has been determined to keep mad cow a matter of government-to-government diplomacy. Now comes the payoff in the form of a recent agreement that has Japanese government inspectors descending on U.S. meatpacking plants, snapping photos and judging whether their output is fit for Japanese consumption.
This might seem, from the point of view of bureaucratic amour propre, to be ceding a precious piece of USDA's sovereignty to foreigners. But -- hooray! -- at least government bureaucrats remain in charge. The alternative, unbearable even to contemplate, would have been to leave it to private buyers and sellers to reach their own terms.
That was the terrible danger posed by Creekstone Farms. It had assayed the collective appetite of the Japanese and proposed testing each animal for mad cow before shipping beef to Japan. No, the expense is hardly justified by the risk. But Japan has instituted universal testing for its own beef and blocked imports of foreign beef that doesn't adhere to the same standard. Retail beef prices promptly blasted off in Japan, reaching an average of $27.80 per pound. Creekstone saw this and naturally would like to help itself to some of this money.
Let's stop here and note that markets are usually more adept than bureaucrats at catering to irrational tastes, fads and preferences. That's why our world is enriched with $700 perfumes, $10,000 wristwatches and Italian motorcycles. Japan's taste for beef subjected to mad cow testing falls into the same category -- an opportunity for somebody somewhere to make a lot of money selling overpriced beef.
Unfortunate for Creekstone was a preemptory decision by USDA to prohibit it from acquiring the necessary testing kits. The agency isn't just protecting its monopoly on testing: Its central planners have a "strategy." They want to use diplomacy and the power of government-to-government nagging to change Japanese preferences.
Toward this goal the machinery of trade negotiation has drudged away for three years, trying to get the Japanese to accept American beef without testing. Unwisely perhaps, the U.S. cattle industry has been supportive. Cattlemen, legislators and farm state radio commentators all flow freely with indignation about Japan's refusal to adopt "science-based" trade policies.
True enough. With each year, retrospect makes it clearer that the cycling up of a communicable epidemic of prion disease (for the misfolded protein widely believed to be the agent of infection) in the British cow was a fluky, one-of-a-kind phenomenon.
Nothing similar has been seen elsewhere, despite many of the same feeding practices. Though an odd case of mad cow turns up now and again, these increasingly are "atypical" -- they don't show the hallmarks of British-style mad cow and are most probably examples of a sporadic version that was there all along.
And without the now-banned feeding practices to turn one sick cow into a herd-wide epidemic, the danger to the public is virtually nil. Government's job is done. So far, exactly one Japanese has died from mad cow, and he lived in London in 1990. Japanese consumers continue to be in far greater danger from fugu, the toxic pufferfish eaten as a delicacy. One careful study showed that fugu was responsible for 179 deaths over a 10-year period.
And this is nothing compared to commoner forms of food poisoning. On the science alone, then, Japan would drop its own testing of every cow and its insistence that others do the same. On the science alone, the USDA would hastily retreat from worrying about mad cow. It would devote its resources instead to garden-variety bacterial poisonings that claim some 1,300 U.S. lives annually.
Then again, on the science alone, scientists like Stanley Prusiner, who won a Nobel Prize for identifying the prion, wouldn't be continuing to advise consumers not to eat beef that hasn't been tested for mad cow.
Here's a mixed blessing: Mad cow has unlimbered untold sums from governments, universities and drug companies for research into prion disease that wouldn't have been unlimbered otherwise. In the nature of things, prion disease has repaid the favor by continuing to yield mysteries to justify spending even more money. Scientific uncertainty is elastic -- it grows with the amount of funding available.
Scientists discovered that most of the human mad cow victims were young and all shared an identical genotype common to 40% of Britons. A review of tonsil and appendix tissue from otherwise healthy Britons of other genotypes was mounted. Sure enough, a few were found to contain the offending prions.
Researchers turned anew to a related disease, kuru, that raged among New Guinea cannibals half a century ago. Lo, aging survivors were found still to be contracting kuru 50 years after their mortuary feasts were banned.
Putting these facts together has led to a splurge of fearful new headlines. Hundreds of Britons once thought to be genetically immune may yet come down with mad cow decades after their exposure. Hundreds may be "symptomless carriers," capable of infecting fellow citizens of the vulnerable genotype through transfusions or surgical instruments. Or so scientists have not minded speculating.
Mad cow fears seem destined to be with us a while yet, and somebody will make a lot of money selling beef stamped "guaranteed mad cow free." But notice that USDA, its foreign counterparts and the beef industry are all fighting the last war. The vector of future troubles decidedly isn't from cows, but from human carriers.
USDA HANDBOOK addresses Farmers as Uneducated
ARAPA Statement to the Senate Ag Committee
2006 ARKANSAS COOPERATIVE AGREEMENT WITH USDA
2007 ARKANSAS COOPERATIVE AGREEMENT WITH USDA
ARKANSAS ANIMAL PRODUCERS ASSOCIATION
Organic & Grassfed Growers Also Affected
DATABASES - How Safe Are They?
CAPTIVE ANIMAL FACTORY FARMING
Ag Lawyer Responds to the NAIS
HORSE TIMELINE FOR NAIS INCLUSION
"CREATIVE" SIGN-UPS BY THE GOVERNMENT
Animal ID Problems in Other Countries
Retired Army Colonel Rebuts NAIS
Equine Species Working Group Contacts
INFO ON USDA'S NEW "USER'S GUIDE"
SCRAPIE ID for Goats/Sheep & the NAIS
Leon's Story - Chipped Dog Died From Cancer
Protection From Terrorist Livestock
Truth about FOOD CONTAMINATION
TRUTH about Foot & Mouth Vaccines
MICROCHIP PROBLEMS IN DUTCH HORSES
2005 ARKANSAS COOPERATIVE AGREEMENT WITH USDA/APHIS
| Mad Cow II: The Social Disease TESTING COWS FOR BSE AT SLAUGHTER IS THE *ONLY* SURE WAY TO KEEP IT OUT OF OUR FOOD SUPPLY - TAGS WILL NOT DO THAT! US to Meatpackers: Don't Do Mad Cow Test May 29, 2007 3:32 PM (ET) By MATT APUZZO WASHINGTON (AP) - The Bush administration said Tuesday it will fight to keep meatpackers from testing all their animals for mad cow disease. The Agriculture Department tests less than 1 percent of slaughtered cows for the disease, which can be fatal to humans who eat tainted beef. But Kansas-based Creekstone Farms Premium Beef wants to test all of its cows. Larger meat companies feared that move because, if Creekstone tested its meat and advertised it as safe, they might have to perform the expensive test, too. A federal judge ruled in March that such tests must be allowed. The ruling was to take effect June 1, but the Agriculture Department said Tuesday it would appeal - effectively delaying the testing until the court challenge plays out. Mad cow disease, or bovine spongiform encephalopathy, is linked to more than 150 human deaths worldwide, mostly in Britain. There have been three cases of mad cow disease in the U.S. The first, in December 2003 in Washington state, was in a cow that had been imported from Canada. The second, in 2005, was in a Texas-born cow. The third was confirmed last year in an Alabama cow. The Agriculture Department argued that widespread testing could lead to a false positive that would harm the meat industry. U.S. District Judge James Robertson noted that Creekstone sought to use the same test the government relies on and said the government didn't have the authority to restrict it. by: Holman W. Jenkins, Jr. The U.S. Department of Agriculture has been determined to keep mad cow a matter of government-to-government diplomacy. Now comes the payoff in the form of a recent agreement that has Japanese government inspectors descending on U.S. meatpacking plants, snapping photos and judging whether their output is fit for Japanese consumption. This might seem, from the point of view of bureaucratic amour propre, to be ceding a precious piece of USDA's sovereignty to foreigners. But -- hooray! -- at least government bureaucrats remain in charge. The alternative, unbearable even to contemplate, would have been to leave it to private buyers and sellers to reach their own terms. That was the terrible danger posed by Creekstone Farms. It had assayed the collective appetite of the Japanese and proposed testing each animal for mad cow before shipping beef to Japan. No, the expense is hardly justified by the risk. But Japan has instituted universal testing for its own beef and blocked imports of foreign beef that doesn't adhere to the same standard. Retail beef prices promptly blasted off in Japan, reaching an average of $27.80 per pound. Creekstone saw this and naturally would like to help itself to some of this money. Let's stop here and note that markets are usually more adept than bureaucrats at catering to irrational tastes, fads and preferences. That's why our world is enriched with $700 perfumes, $10,000 wristwatches and Italian motorcycles. Japan's taste for beef subjected to mad cow testing falls into the same category -- an opportunity for somebody somewhere to make a lot of money selling overpriced beef. Unfortunate for Creekstone was a preemptory decision by USDA to prohibit it from acquiring the necessary testing kits. The agency isn't just protecting its monopoly on testing: Its central planners have a "strategy." They want to use diplomacy and the power of government-to-government nagging to change Japanese preferences. Toward this goal the machinery of trade negotiation has drudged away for three years, trying to get the Japanese to accept American beef without testing. Unwisely perhaps, the U.S. cattle industry has been supportive. Cattlemen, legislators and farm state radio commentators all flow freely with indignation about Japan's refusal to adopt "science-based" trade policies. True enough. With each year, retrospect makes it clearer that the cycling up of a communicable epidemic of prion disease (for the misfolded protein widely believed to be the agent of infection) in the British cow was a fluky, one-of-a-kind phenomenon. Nothing similar has been seen elsewhere, despite many of the same feeding practices. Though an odd case of mad cow turns up now and again, these increasingly are "atypical" -- they don't show the hallmarks of British-style mad cow and are most probably examples of a sporadic version that was there all along. And without the now-banned feeding practices to turn one sick cow into a herd-wide epidemic, the danger to the public is virtually nil. Government's job is done. So far, exactly one Japanese has died from mad cow, and he lived in London in 1990. Japanese consumers continue to be in far greater danger from fugu, the toxic pufferfish eaten as a delicacy. One careful study showed that fugu was responsible for 179 deaths over a 10-year period. And this is nothing compared to commoner forms of food poisoning. On the science alone, then, Japan would drop its own testing of every cow and its insistence that others do the same. On the science alone, the USDA would hastily retreat from worrying about mad cow. It would devote its resources instead to garden-variety bacterial poisonings that claim some 1,300 U.S. lives annually. Then again, on the science alone, scientists like Stanley Prusiner, who won a Nobel Prize for identifying the prion, wouldn't be continuing to advise consumers not to eat beef that hasn't been tested for mad cow. Here's a mixed blessing: Mad cow has unlimbered untold sums from governments, universities and drug companies for research into prion disease that wouldn't have been unlimbered otherwise. In the nature of things, prion disease has repaid the favor by continuing to yield mysteries to justify spending even more money. Scientific uncertainty is elastic -- it grows with the amount of funding available. Scientists discovered that most of the human mad cow victims were young and all shared an identical genotype common to 40% of Britons. A review of tonsil and appendix tissue from otherwise healthy Britons of other genotypes was mounted. Sure enough, a few were found to contain the offending prions. Researchers turned anew to a related disease, kuru, that raged among New Guinea cannibals half a century ago. Lo, aging survivors were found still to be contracting kuru 50 years after their mortuary feasts were banned. Putting these facts together has led to a splurge of fearful new headlines. Hundreds of Britons once thought to be genetically immune may yet come down with mad cow decades after their exposure. Hundreds may be "symptomless carriers," capable of infecting fellow citizens of the vulnerable genotype through transfusions or surgical instruments. Or so scientists have not minded speculating. Mad cow fears seem destined to be with us a while yet, and somebody will make a lot of money selling beef stamped "guaranteed mad cow free." But notice that USDA, its foreign counterparts and the beef industry are all fighting the last war. The vector of future troubles decidedly isn't from cows, but from human carriers.
The U.S. Department of Agriculture has been determined to keep mad cow a matter of government-to-government diplomacy. Now comes the payoff in the form of a recent agreement that has Japanese government inspectors descending on U.S. meatpacking plants, snapping photos and judging whether their output is fit for Japanese consumption. This might seem, from the point of view of bureaucratic amour propre, to be ceding a precious piece of USDA's sovereignty to foreigners. But -- hooray! -- at least government bureaucrats remain in charge. The alternative, unbearable even to contemplate, would have been to leave it to private buyers and sellers to reach their own terms. That was the terrible danger posed by Creekstone Farms. It had assayed the collective appetite of the Japanese and proposed testing each animal for mad cow before shipping beef to Japan. No, the expense is hardly justified by the risk. But Japan has instituted universal testing for its own beef and blocked imports of foreign beef that doesn't adhere to the same standard. Retail beef prices promptly blasted off in Japan, reaching an average of $27.80 per pound. Creekstone saw this and naturally would like to help itself to some of this money. Let's stop here and note that markets are usually more adept than bureaucrats at catering to irrational tastes, fads and preferences. That's why our world is enriched with $700 perfumes, $10,000 wristwatches and Italian motorcycles. Japan's taste for beef subjected to mad cow testing falls into the same category -- an opportunity for somebody somewhere to make a lot of money selling overpriced beef. Unfortunate for Creekstone was a preemptory decision by USDA to prohibit it from acquiring the necessary testing kits. The agency isn't just protecting its monopoly on testing: Its central planners have a "strategy." They want to use diplomacy and the power of government-to-government nagging to change Japanese preferences. Toward this goal the machinery of trade negotiation has drudged away for three years, trying to get the Japanese to accept American beef without testing. Unwisely perhaps, the U.S. cattle industry has been supportive. Cattlemen, legislators and farm state radio commentators all flow freely with indignation about Japan's refusal to adopt "science-based" trade policies. True enough. With each year, retrospect makes it clearer that the cycling up of a communicable epidemic of prion disease (for the misfolded protein widely believed to be the agent of infection) in the British cow was a fluky, one-of-a-kind phenomenon. Nothing similar has been seen elsewhere, despite many of the same feeding practices. Though an odd case of mad cow turns up now and again, these increasingly are "atypical" -- they don't show the hallmarks of British-style mad cow and are most probably examples of a sporadic version that was there all along. And without the now-banned feeding practices to turn one sick cow into a herd-wide epidemic, the danger to the public is virtually nil. Government's job is done. So far, exactly one Japanese has died from mad cow, and he lived in London in 1990. Japanese consumers continue to be in far greater danger from fugu, the toxic pufferfish eaten as a delicacy. One careful study showed that fugu was responsible for 179 deaths over a 10-year period. And this is nothing compared to commoner forms of food poisoning. On the science alone, then, Japan would drop its own testing of every cow and its insistence that others do the same. On the science alone, the USDA would hastily retreat from worrying about mad cow. It would devote its resources instead to garden-variety bacterial poisonings that claim some 1,300 U.S. lives annually. Then again, on the science alone, scientists like Stanley Prusiner, who won a Nobel Prize for identifying the prion, wouldn't be continuing to advise consumers not to eat beef that hasn't been tested for mad cow. Here's a mixed blessing: Mad cow has unlimbered untold sums from governments, universities and drug companies for research into prion disease that wouldn't have been unlimbered otherwise. In the nature of things, prion disease has repaid the favor by continuing to yield mysteries to justify spending even more money. Scientific uncertainty is elastic -- it grows with the amount of funding available. Scientists discovered that most of the human mad cow victims were young and all shared an identical genotype common to 40% of Britons. A review of tonsil and appendix tissue from otherwise healthy Britons of other genotypes was mounted. Sure enough, a few were found to contain the offending prions. Researchers turned anew to a related disease, kuru, that raged among New Guinea cannibals half a century ago. Lo, aging survivors were found still to be contracting kuru 50 years after their mortuary feasts were banned. Putting these facts together has led to a splurge of fearful new headlines. Hundreds of Britons once thought to be genetically immune may yet come down with mad cow decades after their exposure. Hundreds may be "symptomless carriers," capable of infecting fellow citizens of the vulnerable genotype through transfusions or surgical instruments. Or so scientists have not minded speculating. Mad cow fears seem destined to be with us a while yet, and somebody will make a lot of money selling beef stamped "guaranteed mad cow free." But notice that USDA, its foreign counterparts and the beef industry are all fighting the last war. The vector of future troubles decidedly isn't from cows, but from human carriers.
The U.S. Department of Agriculture has been determined to keep mad cow a matter of government-to-government diplomacy. Now comes the payoff in the form of a recent agreement that has Japanese government inspectors descending on U.S. meatpacking plants, snapping photos and judging whether their output is fit for Japanese consumption. This might seem, from the point of view of bureaucratic amour propre, to be ceding a precious piece of USDA's sovereignty to foreigners. But -- hooray! -- at least government bureaucrats remain in charge. The alternative, unbearable even to contemplate, would have been to leave it to private buyers and sellers to reach their own terms. That was the terrible danger posed by Creekstone Farms. It had assayed the collective appetite of the Japanese and proposed testing each animal for mad cow before shipping beef to Japan. No, the expense is hardly justified by the risk. But Japan has instituted universal testing for its own beef and blocked imports of foreign beef that doesn't adhere to the same standard. Retail beef prices promptly blasted off in Japan, reaching an average of $27.80 per pound. Creekstone saw this and naturally would like to help itself to some of this money. Let's stop here and note that markets are usually more adept than bureaucrats at catering to irrational tastes, fads and preferences. That's why our world is enriched with $700 perfumes, $10,000 wristwatches and Italian motorcycles. Japan's taste for beef subjected to mad cow testing falls into the same category -- an opportunity for somebody somewhere to make a lot of money selling overpriced beef. Unfortunate for Creekstone was a preemptory decision by USDA to prohibit it from acquiring the necessary testing kits. The agency isn't just protecting its monopoly on testing: Its central planners have a "strategy." They want to use diplomacy and the power of government-to-government nagging to change Japanese preferences. Toward this goal the machinery of trade negotiation has drudged away for three years, trying to get the Japanese to accept American beef without testing. Unwisely perhaps, the U.S. cattle industry has been supportive. Cattlemen, legislators and farm state radio commentators all flow freely with indignation about Japan's refusal to adopt "science-based" trade policies. True enough. With each year, retrospect makes it clearer that the cycling up of a communicable epidemic of prion disease (for the misfolded protein widely believed to be the agent of infection) in the British cow was a fluky, one-of-a-kind phenomenon. Nothing similar has been seen elsewhere, despite many of the same feeding practices. Though an odd case of mad cow turns up now and again, these increasingly are "atypical" -- they don't show the hallmarks of British-style mad cow and are most probably examples of a sporadic version that was there all along. And without the now-banned feeding practices to turn one sick cow into a herd-wide epidemic, the danger to the public is virtually nil. Government's job is done. So far, exactly one Japanese has died from mad cow, and he lived in London in 1990. Japanese consumers continue to be in far greater danger from fugu, the toxic pufferfish eaten as a delicacy. One careful study showed that fugu was responsible for 179 deaths over a 10-year period. And this is nothing compared to commoner forms of food poisoning. On the science alone, then, Japan would drop its own testing of every cow and its insistence that others do the same. On the science alone, the USDA would hastily retreat from worrying about mad cow. It would devote its resources instead to garden-variety bacterial poisonings that claim some 1,300 U.S. lives annually. Then again, on the science alone, scientists like Stanley Prusiner, who won a Nobel Prize for identifying the prion, wouldn't be continuing to advise consumers not to eat beef that hasn't been tested for mad cow. Here's a mixed blessing: Mad cow has unlimbered untold sums from governments, universities and drug companies for research into prion disease that wouldn't have been unlimbered otherwise. In the nature of things, prion disease has repaid the favor by continuing to yield mysteries to justify spending even more money. Scientific uncertainty is elastic -- it grows with the amount of funding available. Scientists discovered that most of the human mad cow victims were young and all shared an identical genotype common to 40% of Britons. A review of tonsil and appendix tissue from otherwise healthy Britons of other genotypes was mounted. Sure enough, a few were found to contain the offending prions. Researchers turned anew to a related disease, kuru, that raged among New Guinea cannibals half a century ago. Lo, aging survivors were found still to be contracting kuru 50 years after their mortuary feasts were banned. Putting these facts together has led to a splurge of fearful new headlines. Hundreds of Britons once thought to be genetically immune may yet come down with mad cow decades after their exposure. Hundreds may be "symptomless carriers," capable of infecting fellow citizens of the vulnerable genotype through transfusions or surgical instruments. Or so scientists have not minded speculating. Mad cow fears seem destined to be with us a while yet, and somebody will make a lot of money selling beef stamped "guaranteed mad cow free." But notice that USDA, its foreign counterparts and the beef industry are all fighting the last war. The vector of future troubles decidedly isn't from cows, but from human carriers.
The U.S. Department of Agriculture has been determined to keep mad cow a matter of government-to-government diplomacy. Now comes the payoff in the form of a recent agreement that has Japanese government inspectors descending on U.S. meatpacking plants, snapping photos and judging whether their output is fit for Japanese consumption. This might seem, from the point of view of bureaucratic amour propre, to be ceding a precious piece of USDA's sovereignty to foreigners. But -- hooray! -- at least government bureaucrats remain in charge. The alternative, unbearable even to contemplate, would have been to leave it to private buyers and sellers to reach their own terms. That was the terrible danger posed by Creekstone Farms. It had assayed the collective appetite of the Japanese and proposed testing each animal for mad cow before shipping beef to Japan. No, the expense is hardly justified by the risk. But Japan has instituted universal testing for its own beef and blocked imports of foreign beef that doesn't adhere to the same standard. Retail beef prices promptly blasted off in Japan, reaching an average of $27.80 per pound. Creekstone saw this and naturally would like to help itself to some of this money. Let's stop here and note that markets are usually more adept than bureaucrats at catering to irrational tastes, fads and preferences. That's why our world is enriched with $700 perfumes, $10,000 wristwatches and Italian motorcycles. Japan's taste for beef subjected to mad cow testing falls into the same category -- an opportunity for somebody somewhere to make a lot of money selling overpriced beef. Unfortunate for Creekstone was a preemptory decision by USDA to prohibit it from acquiring the necessary testing kits. The agency isn't just protecting its monopoly on testing: Its central planners have a "strategy." They want to use diplomacy and the power of government-to-government nagging to change Japanese preferences. Toward this goal the machinery of trade negotiation has drudged away for three years, trying to get the Japanese to accept American beef without testing. Unwisely perhaps, the U.S. cattle industry has been supportive. Cattlemen, legislators and farm state radio commentators all flow freely with indignation about Japan's refusal to adopt "science-based" trade policies. True enough. With each year, retrospect makes it clearer that the cycling up of a communicable epidemic of prion disease (for the misfolded protein widely believed to be the agent of infection) in the British cow was a fluky, one-of-a-kind phenomenon. Nothing similar has been seen elsewhere, despite many of the same feeding practices. Though an odd case of mad cow turns up now and again, these increasingly are "atypical" -- they don't show the hallmarks of British-style mad cow and are most probably examples of a sporadic version that was there all along. And without the now-banned feeding practices to turn one sick cow into a herd-wide epidemic, the danger to the public is virtually nil. Government's job is done. So far, exactly one Japanese has died from mad cow, and he lived in London in 1990. Japanese consumers continue to be in far greater danger from fugu, the toxic pufferfish eaten as a delicacy. One careful study showed that fugu was responsible for 179 deaths over a 10-year period. And this is nothing compared to commoner forms of food poisoning. On the science alone, then, Japan would drop its own testing of every cow and its insistence that others do the same. On the science alone, the USDA would hastily retreat from worrying about mad cow. It would devote its resources instead to garden-variety bacterial poisonings that claim some 1,300 U.S. lives annually. Then again, on the science alone, scientists like Stanley Prusiner, who won a Nobel Prize for identifying the prion, wouldn't be continuing to advise consumers not to eat beef that hasn't been tested for mad cow. Here's a mixed blessing: Mad cow has unlimbered untold sums from governments, universities and drug companies for research into prion disease that wouldn't have been unlimbered otherwise. In the nature of things, prion disease has repaid the favor by continuing to yield mysteries to justify spending even more money. Scientific uncertainty is elastic -- it grows with the amount of funding available. Scientists discovered that most of the human mad cow victims were young and all shared an identical genotype common to 40% of Britons. A review of tonsil and appendix tissue from otherwise healthy Britons of other genotypes was mounted. Sure enough, a few were found to contain the offending prions. Researchers turned anew to a related disease, kuru, that raged among New Guinea cannibals half a century ago. Lo, aging survivors were found still to be contracting kuru 50 years after their mortuary feasts were banned. Putting these facts together has led to a splurge of fearful new headlines. Hundreds of Britons once thought to be genetically immune may yet come down with mad cow decades after their exposure. Hundreds may be "symptomless carriers," capable of infecting fellow citizens of the vulnerable genotype through transfusions or surgical instruments. Or so scientists have not minded speculating. Mad cow fears seem destined to be with us a while yet, and somebody will make a lot of money selling beef stamped "guaranteed mad cow free." But notice that USDA, its foreign counterparts and the beef industry are all fighting the last war. The vector of future troubles decidedly isn't from cows, but from human carriers. BSE TEST FOR LIVE CATTLE - HAVE YOU HEARD ABOUT THIS? NEW TEST MAY OFFER EASIER DETECTION OF BSE, vCJD by Ann Bagel on 7/10/2006 for Meatingplace.com A new test may be able to detect bovine spongiform encephalopathy in animals and variant Creutzfeldt-Jakob disease in humans before symptoms appear, according to research published in the journal Science. The study, conducted by scientists led by Claudio Soto of the University of Texas Medical Branch at Galveston, suggests that damaged brain cells may "leak" the prions that cause the diseases, offering a chance to detect the disease in blood. Current tests for BSE and vCJD require brain or other tissue samples. UTMB SPINS OFF FIRM TO DEVELOP MAD COW TEST By Greg Barr The Daily News Published July 7, 2006 GALVESTON — A breakthrough by a local research team could illuminate one of medicine’s darkest secrets by exposing how many people could unknowingly be infected with the human form of mad cow disease. The University of Texas Medical Branch team, headed by neurology professor Claudio Soto, has detected the malformed proteins that cause variant Creutzfeldt-Jakob disease, or vCJD, during the so-called silent phase of the infection. Previously, Soto’s team was only able to detect these diseased proteins — known as prions — in the blood of lab animals that were in advanced stages of the disease. This incubation phase of the disease in humans can stretch 20 to 40 years, Soto said. That fact raises fears in areas of the world hit hardest by mad cow disease, such as the United Kingdom, that thousands of apparently healthy people who ingested tainted meat — or received blood transfusions or organ donations from others carrying the brain-destroying disease — might be infected. +++ Thousands Exposed “That’s our biggest concern,” Soto said. “Potentially thousands of people could have been exposed in the early 1990s, but we would not expect the symptoms to appear until 2010 or 2020. “To many people, the epidemic of mad cow disease has gone away, but perhaps it hasn’t started yet.” Soto’s report was published today in Science magazine, in collaboration with assistant professor Joaquin Castilla and research assistant Paula Saá, formerly with the medical branch but now at Universidad Automnoma de Madrid in Spain. The research team was able to detect the mutated prions in hamsters infected with the disease used for testing using a technique that actually sped up the process by which the prions can convert normal proteins into the infectious version. +++ Biotech Spin-off To take his research into the next phase, Soto has taken an entrepreneurial tact by working with the medical branch to create a spin-off biotechnology company. The new company, Amprion, is in its formative stages while attorneys mull over the intellectual property — in this case the prion diagnostic test — before licensing and fundraising can begin. Russ Lebovitz, who has spent the past 10 years doing hands-on consulting work with start-up and mid-level biotech companies, has been named Amprion’s president and chief executive. Soto is the company’s chief scientific officer. Lebovitz said Thursday that Amprion’s commercial potential is not only in developing a diagnostic test for vCJD in humans, but also to detect mad cow disease — known as bovine spongiform encephalopathy — in cattle. “At this stage, all we’ve been able to do is look for animals in late stages of the disease and slaughter them, so no one really knows for sure how (prevalent) it is,” Lebovitz said. “And there hasn’t been any test yet for the world’s (human) blood supply (to detect vCJD).” +++ Testing Cattle The next phase of development would be to use the prion detection test on bovine and human blood samples. If that is successful, then full-scale human testing could begin as early as 2008 or 2009, pending approval by the federal Food & Drug Administration or its European equivalent. What this means, especially for areas of the world such as the United Kingdom, where a mad cow disease epidemic has infected some 200,000 cattle since the late 1980s, is a chance to find out how much of the human population might be exposed to the disease. Only three cases of mad cow disease have been reported in the United States since the first was detected in 2003. A sixth case was reported in the past week in Canada, out of an estimated national herd of 17 million cattle. Two human cases of vCJD have been reported in the U.S. since 2002. In the United Kingdom, the first onset of the human form of mad cow disease was in 1994, about a decade after the first appearance of the disease in animals. Seventy humans developed the disease in the U.K. between 1994 and 2000. “The worst-case scenario is that there could be 100,000 human cases (undetected) in people who will live normally for decades but don’t know of the infection,” Soto said. “To prevent the spread of the disease would be a major accomplishment for society.” FORMER EMPLOYEE EXPOSES BULL IN MOSES LAKE MAD COW! Insider's letter to editor exposes bull in mad cow coverage by Dave Louthan, Columbia Basin Herald [Moses Lake, WA] Jan. 22, 2004 My name is Dave and I work at Vern's Moses Lake Meats. I did until the day the mad cow test results on the Sunny Dene cow came back positive for BSE. That was Wednesday, Dec. 24. On Friday, Dec. 26, the KXLY news crew was at the end of Vern's driveway, locked out by a cable gate. The USDA had told the world that the mad cow had been slaughtered here, but it was not in the food chain. A blatant lie. It was one of many. I walked out with the news crew at lunch time because I can't stand a government cover-up. They asked me "was the cow in the food chain?" I told them of course it was, it's meat. Where else would it be? They asked me if the cow was a downer. I told them no, it was just an old cow. The USDA had us taking brain stem samples from downers and back door cripples only. Since we only had a few walkers on this trailer full of downers, we just killed her along with them. We took a brain sample from her head because the USDA gives up $10 per sample. If we would have unloaded her in the pens, we would have never caught the BSE. How many other walkers have BSE? We will never know. The USDA only tested the downers and cripples and only at our plant. We had only been taking brain samples for about a month when we found this one. When the USDA said no more downers would be slaughtered, they essentially said no more BSE testing would be done. Vern's and every other slaughterhouse kept right on killing and selling Holstein meat from the same area as the mad cow with no BSE testing whatsoever. This is true and easily verifiable. And just so the folks in Moses Lake don't feel left out, the beef head, tongue, liver, kidneys and tail were sold right here in the Columbia Basin. It's way past time for everybody to stop thinking with their bank accounts and start trying to find a way to stop the spread of BSE. The minute the USDA found the contaminated cow, they stopped the brain stem collection and testing. Why? Ka-ching! It's the money. Billions. If you want to be sure you and your family are eating safe meat, demand testing on every beef slaughter. It's quick and easy. Don't eat another piece of meat until you see a sticker that says tested and cleared for BSE on the package. BSE is 100 percent fatal -- if you or your kids get it, you die a very painful death. It's a slow, wasting disease. It's terrible. Right now, a lot of people are telling you how safe their beef is, but they don't know if it is or is not without testing. That's their checkbook talking. Tat rendering plant in Canada wasn't feeding 81 cows, it was feeding thousands of cows. Every second that goes by, more untested beef goes on the dinner plate. If you eat mad cow, you are going to get sick and you are going to die. Stand up and demand safe meat. Dave Louthan Moses Lake, WA ***************************************************************************** The small scientific world of prion researchers -- the scientists who investigate "transmissible spongiform encephalopathies" (TSE) such as mad cow disease in cattle and Creutzfeldt-Jakob Disease (CJD) in humans -- is abuzz. That's because the two confirmed cases of US mad cow disease in Texas and Alabama are an "atypical" strain different from the British strain but identical to an atypical strain found so far in a small number of cattle in France, Germany, Poland and Sweden. The discovery of "atypical" mad cow disease in the US should not be surprising. Sheldon Rampton and I reported way back in 1997 that very strong evidence of an "atypical" TSE disease infecting US cattle was established by the work of Dr. Richard Marsh, the researcher to whom we dedicated our book Mad Cow USA [1]. Even before Britain confirmed its first case of mad cow, Dr. Marsh of the University of Wisconsin was investigating a similar disease in Stetsonville, Wisconsin, a 1985 outbreak in mink that he traced to Wisconsin dairy cattle. Marsh's published research confirmed suspicions among US scientists since the mid 1960s that the rare but deadly TSE disease in US mink -- transmissible mink encephalopathy or TME -- resulted from their having eaten TSE-infected US cattle. DID THE US INFECT EUROPE WITH ATYPICAL MAD COW DISEASE? The discovery that the Texas and Alabama BSE cases are a variant strain identical to EU cases begs the question of whether the atypical EU cases resulted from European cattle being fed infected US feed made from rendered by-products and sold in Europe. After all, the US has been the biggest creator, user and exporter of by-product feed made from slaughterhouse waste. Also, scientists need to examine the TSE isolated by Richard Marsh in mink and traced to Wisconsin cattle, and compare it to the atypical BSE strain found in Texas, Alabama, France, Poland, Germany and Sweden. Is the Stetsonville TSE strain discovered by Richard Marsh the same strain as the US and EU atypical BSE cases, or is it another atypical strain? Here below is our report on Marsh's discovery in 1985 of an atypical strain of BSE in US cattle from our 1997 book Mad Cow USA [2]. (You can order the book for free from your favorite library and it is for sale in the usual places.) ### MAD COW USA (The following excerpt is from Mad Cow USA [3], by Sheldon Rampton and John Stauber, pages 154-156:) The common denominator in all of these [transmissible mink encephalopathy - TME] outbreaks was either "cattle" or "unknown." It was possible, of course, to imagine other scenarios, but Marsh believed he had at least strong circumstantial evidence that a TSE similar to mad cow disease already existed in U.S. cattle. "You can trace it back to feed real easy in mink," Marsh said. "And then you're left with the question, what was it in the feed that affected them? And what we find is it's these downer cows that are the common link. You don't have to be a genius to figure it out." Within the field of veterinary medicine, "downer cow syndrome" was a "garbage can" category, used indiscriminately as the official diagnosis for any animal that died or had to be put down after failing to stand on its own legs for 24 hours or more. These included cows suffering from paralysis, arthritis, grass tetany, ketosis, bone fractures, and a form of calcium deficiency known as "milk fever." Most downer cows died from causes unrelated to the spongi- form encephalopathies, but it was possible that the generic nature of the clas- sification enabled some TSE-infected cows to slip into the mix. It was impossible in practice to absolutely prove the link between downer cows and transmissible mink encephalopathy. By the time the disease appeared in mink, any cow that might have been the source would be long gone, its tissues unavailable for testing. To test his theory, therefore, Marsh did the next best thing—a series of experiments using brain matter from one of the mink that had died in the Stetsonville outbreak. He puréed the brain in a blender and used hypodermic syringes to inject the homogenized liquid into test animals: fourteen healthy mink, eight ferrets, two squirrel monkeys, twelve hamsters, forty-five mice and two Holstein bull calves. The mice, remarkably, all stayed healthy, but every other species proved susceptible. The mink went down first, four months after inoculation. The two monkeys were the next to show neurological signs, at months nine and thirteen respectively. Two of the twelve hamsters survived, but the other ten succumbed in the fifteenth and sixteenth months. The two calves went down in months eighteen and nineteen. The ferrets lasted longest, but eventually the disease emerged in all but one of them, with incubation periods ranging between twenty-eight and thirty-eight months. These species barrier effects corresponded closely to the results from experiments with previous mink outbreaks. Cattle are expensive test animals, and Marsh's experiments marked the first time that cattle had been tested for susceptibility to transmissible mink encephalopathy. His results proved that cattle could get the mink disease, and in turn led to unexpected new questions. "The real surprise of this experiment is that the clinical signs were quite different from what we've seen in Great Britain," he said. "This is what's changed our perspective on a surveillance of BSE in the United States. We thought BSE in the U.S. would look like BSE in Great Britain—a mad cow type of disease where the animal would have behav- ioral changes, become aggressive and look very much like a rabies infection does in cows." Marsh's bull calves showed none of the unusual "mad" behavior that emerged as early warning signs in British cattle. "Eighteen months after inoculation, one animal simply collapsed in its holding room and could not be returned to a standing position," he reported. "This animal had shown no previous signs of behavioral change or loss of body condition. . . . The second animal was normal until nineteen months after inoculation when it too sud- denly collapsed." Indeed, the test bulls behaved exactly like downer cows—the type of ani- mals which the Stetsonville rancher had been feeding to his mink. "The most disturbing finding of all is that they have very minimal spongiform lesions in their brains," Marsh said. In previous experiments with mink, he had shown that the spongy holes in brains were a secondary effect of the disease which did not always appear in noticeable quantities. Some mink breeds infected with TME would develop all of the usual clinical symptoms, but upon autopsy their brains showed a marked lack of spongiform degeneration. Now it appeared that cattle could also develop a form of TSE without the telltale lesions to aid in diagnosis. Their symptoms would look like downer cow syndrome, and even a brain autopsy might find nothing out of the ordinary. "Without the brain lesions, the best way to diagnose the infection is a protein in the brain," Marsh said. "But there are only a few labs in the country that can look for this protein. This is not something that can be done by the local veterinarian or even most state diagnostic laboratories. You need to have pretty sophisticated means of testing. This is going to complicate our efforts at surveillance and testing for BSE in thiscountry." Histopathology and immunohistochemistry tests confirmed that Marsh's bulls had died of a spongiform encephalopathy, but it was a different strain of spongiform encephalopathy than the one that was killing cows in England. Its behavior in test animals showed significant differences also. In England, mice succumbed when exposed to brain tissue from mad cows, but hamsters seemed immune. In Marsh's experiments with the Stetsonville isolate of TME, the pattern was exactly the opposite: mice lived, but hamsters died. FROM MAD COWS TO MAD MINK AND BACK To test whether passage through cattle altered the characteristics of the Stetsonville isolate, Marsh injected another 45 mice with brain tissue from his two test bulls. They also stayed healthy, just like the mice he had previously injected with mink brains. By itself, the fact that mink encephalopathy could infect cows was not terribly significant or surprising. After all, scientists had previously shown that TME could be transmitted to a wide variety of other test animals. What was significant was the result when Marsh took the brains of the dead bulls and used them on further tests with healthy mink. When backpassaged into mink, the bull brains behaved exactly the way mink brains behaved, causing symptoms of TME to emerge within four months after exposure by inoculation, or within seven months after oral exposure. "There was no evidence for any deadaptation of the bovine agent for mink compared to . . . non-bovine-passaged mink brain," Marsh observed. "This suggests that there are no species barrier effects between mink and cattle in relation to the Stetsonville source of TME" — more evidence pointing to cattle as the source of the infection. "If mink on the Stetsonville ranch were exposed to TME by feeding them infected cattle, there must be an unrecognized scrapie- like disease of cattle in the United States," Marsh concluded. "If this is true, the disease is rare. The low incidencerate of TME and the fact that the Stetsonville mink rancher had fed products from fallen or sick cattle to his animals for the past 35 years suggests a very low prevalence of this disease." The rarity of the disease, however, did not mean that it posed no danger. In fact, it could mean the very opposite. Mad cow disease had also been rare once in England. The very fact that it was rare, combined with its slow incubation period, were the factors that prevented the British from recognizing its dangers until it had already infected tens of thousands of animals. Moreover, the British had an advantage that U.S. farmers might not enjoy. Their strain of bovine spongiform encephalopathy was picked up fairly soon once cattle started behaving strangely. If a different strain of BSE existed in U.S. cattle— a strain where the animals didn't act deranged but simply fell over, like thecows in Marsh's tests—the disease could conceivably go unrecognized for a long time, invisible within the larger population of U.S. downer cows. Every year, some 100,000 U.S. cows get classified as downers. Marsh was not suggesting that all 100,000 were carriers of a spongiform encephalopathy. What concerned him was the possibility that downer cow syndrome could mask the emergence of a TSE in the cattle population, allowing the disease to invisibly spread until it reached dangerous levels. It could multiply the same way it had multiplied in England, as rendering plants recycled the infection by converting sick animals into meat and bone meal which was then fed back to other cattle. The only certain way to prevent a cattle epidemic, therefore, would be to adopt the same policy that the British had already been forced to adopt: ban the practice of feeding rendered cows and other ruminant ani- mals back to members of their own species. ### (End of excerpt) HOW TO HIDE A MAD COW Today the ability to test cattle for mad cow disease has greatly advanced, and so-called rapid tests are used on all cattle before they are allowed into the human food chain in Japan, for example. I describe the situation in the United States as a cover-up of the extent of mad cow disease because the US needs to test millions of cattle a year, and in a transparent and verifiable way, before we can know with accuracy how much disease is present in the US herd. Currently the US is testing less than 1% of its cattle a year, and the procedures are shrouded in secrecy. The US forbids anyone but the government to conduct tests in the United States making it impossible for Americans to purchase meat that has been tested and found free of the disease. In addition, despite the false PR assurances from government and the livestock industry, there is no "firewall feed ban" in the United States to completely stop the spread of mad cow disease. Today it is legal and widespread to feed US cattle on cattle fat contaminated with cattle protein, on cattle blood, and on poultry shit and litter contaminated with cattle protein. In addition, slaughterhouse waste from cattle is fed to pigs, and in turn the slaughterhouse waste from pigs is fed back to cattle. We now know we have "atypical" mad cow disease in the US and even the USDA admits that it has probably been spreading for at least a decade through feeding cattle to cattle. Yet, the cannibal feeding practices continue and the US's mad cow testng program is a farce. Dick Marsh died in 1997 before our book Mad Cow USA [4] was published. He was a careful scientist who undersood the precautionary principle and who worked tirelessly and was terribly and personally attacked for his prescient warnings that a unique strain of mad cow disease already existed in the US, and that unless the dangerous feeding practices of cow cannibalism were stopped, it would spread through cattle and threaten human health. Perhaps if cancer had not silenced Dick Marsh a decade ago, his strong voice would have helped change the current dangerous policies of the United States Department of Agriculture (USDA) and the Food and Drug Administration (FDA). Currently these federal agencies are threatening animal and human safety in the US simply so the US government can protect and preserve the livestock industry's deadly but lucrative practice of animal cannibalism, turning slaughterhouse waste into cheap feed for cattle and other livestock. ****************************************************************************************** MAD COW DISEASE MORE QUESTIONS THAN ANSWERS By Jane Williams (Reprint from American Family Voice Feb. 2004) On December 23, 2003, many ranchers let out a sigh of despair as major media announced mad cow disease in the United States. A Holstein cow, tripping, stumbling, falling and shaking appeared on most TV news broadcasts across the country. This film clip was immediately followed with a clip of a robust feedlot black Angus which left in the viewer’s mind the impression that the Holstein was from a herd near Mabton, Washington, and the black Angus calf could possibly put mad cow disease on their table. About 25% of the polled U.S. population indicated they would no longer consume beef, cattle prices began to fall, 30 countries banned the importation of US beef while stocks dropped for fast food corporations and meat packers. Major media neglected to tell viewers that some countries had already banned the importation of US beef cuts from along the spinal column, like T-bone steaks, long before the Washington incident. Everyone had seen the Holstein clip before when mad cow broke out in the United Kingdom, since the clip was made in England in the 90s, but major media neglected to inform viewers where and when the clip had been made. They could have explained that the dairy farm was owned by a veterinarian and that the cow became a downer as a result of birthing problems and had shown no signs of mad cow. Have any cattle other than Holstein developed mad cow? The answer to that question is illusive. Possibly one Angus was identified in Canada with the disease, but most reports have indicated only the Holstein breed involved in mad cow, so why was the Angus calf shown? Was it a subliminal message to deaden one’s taste buds? Most people have accepted the theory presented to them by major media that mad cow disease is a result of feeding mad cow diseased animal products to ruminants. Ruminants are animals that have 3 or 4 stomach chambers, evenly divided hoofs and who chew a cud of undigested stomach matter. Basically ruminants sold in the U.S. for food consist of cattle, sheep and goats. In order to sell livestock in Arkansas, producers must sign an affidavit that the ruminants they are selling have not been fed ruminant products. Ingredient labels are placed on sacked feed so purchasers can know what they are buying. There are no regulations prohibiting the sale of feeds containing ruminant products in pet, chicken, hog or other animal feed, and there is no restriction on feeding these processed animals to ruminants. If accepting the feed theory, does it make any sense that it is ok to feed animals who have eaten ruminants to ruminants? As an example, an infected cow can be fed to a chicken but not to another cow. The chicken that ate the infected cow can then be fed to a cow. It is also ok to use animal parts in vaccines, pharmaceuticals, gel caps and in surgery. Nothing has been done to prevent envelopes from having glue made from ruminant products on them. It seems logical that BSE would also be in blood, urine, all cuts of meat and saliva, but we are being told we do not need to worry about such a possibility or sewer water from packing houses going into our streams. It also seems logical that animals other than ruminants could contract the disorder. How bright are the people making the rules or is there no connection between the meat product the animal has eaten and mad cow disease? According to the big boys, a protein called a prion causes mad cow and the disease is spread from one animal to another through consumption of a particular prion, that has no DNA, causes pitting of the animal’s brain. Supposedly eating the animal brain and spinal nerves can cause the disease in man known as Creutzfeldt-Jakob disease (CJD). [In 1907 Dr. Alzheimer, Dr. Creutzfeldt and Dr. Jakob identified brain- wasting diseases] It is reported that the prion can not be destroyed by any chemical and temperatures required for destruction are so high that saws, dental instruments, knives and medical instruments would be melted by using such temperatures to sterilize them. From this we would presume that the prion remains dangerous on grass and soil too and could be found in any part of a ruminant or its products. Yet, we are being told that only the brain and spinal cord are dangerous for consumption. What we are being told just doesn’t add up. Is the reported theory about mad cow being caused by eating infected animals correct, or could something else be causing mad cow? Major media reports bovine spongiform encephalopathy (BSE), mad cow disease, is an off shoot of scrapie, a disease found in sheep and goats. If the theories put forth to us about BSE are correct, then the same theories should be true for scrapie and all transmissible spongiform encephalopathy (TSE), but that is not the case as reported by www.animalagriculture.org when one compares their reports of scrapie with current reports of BSE. Scrapie, like BSE, chronic wasting disease (CWD) found in deer and elk, feline spongiform encephalopathy (FSE) in cats, mink encephalopathy, kuru, classical and variant CJD, Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia and 5 rare diseases in humans is classified in the family of TSE. Scrapie was diagnosed as a disorder in sheep over 250 years ago. Australia and New Zealand are the only countries recognized today as being scrapie free. In the U.S., about 1000 flocks had been diagnosed with the disorder from the first occurrence through July 2001. The Suffolk breed is the primary victim, although scrapie has been diagnosed in 12 other breeds and in crossbreeds. Through August 2001, about 1,600 diagnoses had been made in sheep and 7 diagnoses in goats. An active eradication program is in effect in the U.S. Scrapie is considered a degenerative disease which affects the central nervous system of the sheep or goat. It is believed to be spread to susceptible animals via a tiny virus from the ewe to her offspring and other lambs through contact with the placenta and placental fluids. There is no scientific evidence linking scrapie transmission to humans or other animals by any natural means—including consumption of brains and spinal columns. Scrapie has been transmitted in the laboratory to other animals. Although valid tests are being developed for testing live animals, we are being told diagnosis can only be made presently from microscopic examination of the brain. It is believed that condons 136, 154 and 171 of the prion protein play the largest role in susceptibility. It is therefore believed that genetic selection is the key to controlling and eliminating scrapie within flocks. This information was provided by the National Institute for Animal Agriculture. The USDA, through the Animal and Plant Health Inspection Service (APHIS), is using genetic testing to eradicate scrapie, which is not considered a human health hazard, but an economic detriment for sheep producers because the sheep die. This information about scrapie makes one wonder if the public is being feed a line about mad cow disease transmission. Injections into the brains of cows with sheep brains infected with scrapie have not produced BSE, mad cow disease. Could a chemical agent be allowing animals to develop TSE? Many researchers in the United Kingdom believe that the government’s warble-fly eradication campaigns using organophosphates triggered the outbreak of mad cow in England. Organophosphates were developed by Nazi scientists during WW II to be used as a chemical nerve agent weapon. Could pouring organophosphates along the spinal column of cattle to eradicate warble-flies have damaged prions and thus caused mad cow? Could injections designed to control parasites be causing neurological damage in animals? Can using lice shampoos and other products containing organophosphates damage prions in human brains? Some scientists believe that the use of organophosphates combined with other factors can result in neurological disorders such as TSE, CJD and Alzheimers later in life. An organophosphate is an insecticide containing phosphorus which inhibits cholinesterase. Cholinesterase is an enzyme that hydrolyzes choline esters that is found especially in blood plasma. Said in laymen’s terms, organophosphates prevent choline esters from being split and hydrated. Malathion is probably the most well known organophosphate currently in use, since our “public servants” frequently order spraying millions of acres of America with it to prevent fruit flies and mosquitoes. Many livestock producers use it to control external parasites on their livestock and fruit growers use it to spray fruit trees. Few people are aware of the extreme neurological damage that malathion and other organophosphates can cause. Chemical companies with unlimited funds and political clout control research, its outcome and the spin that major media puts out about TSE. Their preferred pitch is mysterious prions that jump species when consumed. It has been reported that Bayer, Monsanto, Novartis, Pfizer, Roche and Schering-Plough have been behind the efforts to discredit researchers, like Mark Purdey, who have attempted to scientifically confirm and announce the chemical source they believe is responsible for BSE and CJD. Two leading brain researchers connecting the same dots have died in recent years under mysterious circumstances. Veterinary labs have been burned where research into insecticides causing BSE were being conducted, one veterinarian working in such a lab was shot and another died in a very questionable car crash. If Purdey’s research is correct and word got out to the general public, it would cost the big chemical companies billions of dollars as civil suits were won by plaintiffs damaged by organophosphates. It is much cheaper to buy off politicians and major media as they keep selling their poisons. According to Purdey and others, the prion molecule buffers free radical effects in the body. Organophosphates can damage or deform the prion molecule which makes it ineffective in its buffering role. Prion protein bonds benignly with copper, but bonds lethally with manganese. Organosphophates prevent copper bonding with proteins and actually chelate them. If one is high in manganese and then comes into contact with an organophosphate, get ready for what was once called “manganese madness” which plagued manganese miners. The symptoms of CJD and BSE are identical to “manganese madness”. Some chemical companies are actually adding manganese to their organophosphate products which intensifies the problem. TSE regions world-wide all share common denominators of low frequency sonic shock, high levels of manganese, strontium, uranium and barium as well as low levels of copper. These factors create a mineral imbalance which in turn prevents the body from protecting the brain from the neuro-toxic effects of incoming sonic shocks produced by jets, explosions, tectonic rifts, thunder, electric storms, cell phones, UV, radar, sound waves and HAARP. The chemtrails which people have been observing world wide since the mid 90s contain barium. Wonder why? The use of depleted uranium by our military and the melt down of a nuclear power plant in Russia has caused radio active particles to have been spread world wide. Could these factors be involved in TSE? The process of brain destruction is far more complicated than the above explanation and more depth can be found by visiting www.markpurdey.com. Thirty percent of information in the United Kingdom relating to mad cow is veiled under the UK’s Official Secret’s Act. Why? The USDA has supposedly tested more than 20,000 cattle for BSE, but the results of those tests have not been made public. Why? FOIA requests have been made for the test results by United Press International, but they have received no data as of January 1st. If the USDA has been doing all these tests, why was it necessary for them to have the Washington cow tested in England? Other countries test all food animals. Why is this not done in the U.S.? Why was the meat of a suspected mad cow allowed into the food chain before tests were conducted? The U.S. Senate voted to outlaw the processing of downer cattle for food. The U.S. Congress was unable to pass such a law. Since the Washington mad cow identification, the USDA has issued regulations to prevent downer cows from going into the human food chain. The thousands of other ruminant products we use daily are not included in these regulations. Why? U.K. officials knew about cases of BSE in the early 1980s but did nothing about them until 95. Killing animals and not allowing repopulation on certain farms has been that government’s response as well as holding thousands of tons of stinky ground beef parts in warehouses awaiting burning while rodents and insects crawl in and out continues today. Many cattle were buried and have now decomposed. If BSE is not destroyable, is it leaching into the aquifers? If eating BSE infected meat causes TSE, why are coyotes, dogs, vultures and other wild life that eat carrion not being identified with TSE? When eagles began dying of a brain defect some years ago, what was the cause? If deer can develop CWD, why do antelope not develop it? Why was Prince Charles’s livestock exempt from eradication? Reports are surfacing that the U.S. plans on animal eradication on farms and surrounding farms where BSE is identified. Since they plan on following the U.K. plan, will Rockefeller livestock be exempt? Undoubtedly mad cow is present in the U.S., but it is doubtful that without pressure by citizens, the extent or the true cause will ever be reported. WE NEED TESTED CATTLE, NOT TAGGED!
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The U.S. Department of Agriculture — invoking an obscure 1913 law intended to thwart con artists from peddling bogus hog cholera serum to pig farmers — is blocking companies from selling the testing kits to Creekstone. USDA is doing the bidding of large cattle barons afraid that Creekstone's marketing will force them to do the same tests to stay competitive. It's true that the incidence of mad cow disease is quite low. But there's little logic in stopping a company from exceeding regulations to meet the demands of its customers, or protecting its rivals from legitimate competition. Not only is USDA blocking Creekstone, the department said last month that it's reducing its mad cow testing program by 90%. The industry and its sympathetic regulators seem to believe that the problem isn't mad cow disease. It's tests that find mad cow. The department tests only 1% of the roughly 100,000 cattle slaughtered daily. The new plan will test only 110 cows a day. By cutting back on testing, USDA will save about $35 million a year. That's a pittance compared with the devastation the cattle industry could face if just one human case of mad cow disease is linked to domestic beef. The brain-wasting disease — known formally as bovine spongiform encephalopathy, or BSE — is extremely rare but extremely deadly. Since 1986, it has killed more than 150 people worldwide, mostly in Britain, who ate infected meat. Scientists don't know the exact cause of BSE but think it's spread when cows are fed ground-up parts of cattle and other cud-chewing animals. The government has tightened cattle-feed rules, but loopholes still permit cattle blood as a milk substitute and chicken waste as a protein supplement. Canada has found four cows with BSE this year, and at least one was born after similar cattle feed rules were imposed that should have prevented the animal from being infected. Acting out of an abundance of caution, U.S. plans to increase Canadian beef and cattle imports have been put on hold until the new cases are investigated. That makes sense, but it's hard to justify cutbacks on U.S. testing at the same time we demand other nations provide greater assurances. Sixty-five nations have full or partial restrictions on importing U.S. beef products because of fears that the testing isn't rigorous enough. As a result, U.S. beef product exports declined from $3.8 billion in 2003, before the first mad cow was detected in the USA, to $1.4 billion last year. Foreign buyers are demanding that USDA do more. "In a nation dedicated to free market competition," says John Stewart, CEO of Creekstone, which is suing USDA, "a company that wants to do more than is required to ensure the quality of its product and to satisfy customer demand should be allowed to do so." When regulators disagree with reasoning like that, you know the game is rigged. http://www.usatoday.com/news/opinion/editorials/2006-08-03-our-view_x.htm **************************************************************************************************************************************** UPDATE ON CREEKSTONE LAWSUITE AGAINST THE USDA FOR BSE TESTS! QUESTION: IF PACKERS CAN TEST EVERY ANIMAL AT SLAUGHTER FOR BSE, *WHY* DO WE NEED THE NAIS? ANSWER: WE DON'T! WE NEED *TESTED* COWS, NOT TAGGED! MANUFACTURER TO REV UP MARKETING FOR BSE TEST KITS As justification for reopening the Canadian border to cattle imports, USDA/APHIS released a report totaling more than 500 pages, of which over 100 pages is an economic analysis. Secretary Veneman, claims “We got it right” with our “comprehensive and exhaustive” analysis. Secretary Johanns says that the USDA decision to reopen the border was “based on sound science.” Meat industry executives and other packer apologists claim that the study shows that consumers would benefit from reopening the border and that the consumer benefits would outweigh “modest” producer losses. Senator Mark Dayton’s (MN), however, claims that the economic analysis is “something out of Mad Magazine.” Who is right? Senator Dayton goes to the head of the class! There are so many fatal technical flaws in their economic analysis that it would take a 100 page report with many charts and equations to begin to fully explain the flaws. Since OCM allows me only 750 words and since OCM members not interested in academic mumbo-jumbo, my comments in this column will focus on what the economic analysis actually showed, which is completely opposite the USDA and meat industry spin! Table I of the Executive Summary of the USDA report shows a 5-year cumulative “consumer” impact of $2.982 million, a “producer” impact of negative $2.907 million, and a “net” impact of $75 million (3% discount rate and 2005 dollars). To begin with, their use of the words consumer and producer are deceptive and misleading. Most of us think consumers are those who eat steaks, and producers are ranchers, feeders and perhaps packers. Not to the USDA: to them the “consumer” who benefits is in truth the packer! Who are producers and consumers in their analysis? One has to be familiar with highly technical economic jargon, and flip over about 100 pages from Table I to Appendix Tables H and J to uncover the deception. Their detailed analysis presents impacts on consumers and producers of feeder cattle, consumers and producers of fed cattle, and consumers and producers of beef. Something they fail to point out is that a producer at one market level is a consumer at the upstream market level. Thus, the feeder cattle consumer is the feedlot operator who purchased feeder cattle. The fed cattle consumer is none other than the producer of wholesale beef—the packer. USDA’s combined impacts on “consumers” were the sum of what they labeled “consumer” effects at the three market levels, beef, fed cattle and feeder cattle. In fact, this is a meaningless mix of impacts on producers and consumers. Similarly, combined impacts on “producers” were the sum of producer effects at the three market levels, which, in fact, is a meaningless mix of impacts. The following Table shows the USDA estimates, along with my designation of to whom the benefits or costs actually accrue. USDA/APHIS Estimates of Economic Impacts, 5-Year Cumulative Effects, 3% Discount Rate, 2005 Dollars Sector USDA/APHIS Label Actual Group USDA/APHIS Estimated Impact (Thousand Dollars) Beef (wholesale) Consumers Mix of Meat Retailers and Meat Consumers -$76,356 Producers Meat Packers & Processors $76,082 Fed Cattle Consumers Meat Packers $2,473,205 Producers Feedlot Operators -$2,426,966 Feeder Cattle Consumers Feedlot Operators $585,240 Producers Cow-Calf Operators -$556,578 Combined Consumers Meaningless Mix $2,982,088 Producers -$2,907,462 Net $74,626 There are two serious theoretical flaws with their analysis. First, the measures of economic effects are valid only in competitive markets and then only under restrictive assumptions. To the extent that cattle markets are not competitive, the USDA results may be invalid. Second, Economic effects in vertically related markets are not additive, unless proper measures of supply and demand are used. It is not evident that the economic analysts used theoretically appropriate measures. In summary, the USDA/APHIS labeling of benefits and costs is incredibly deceptive. Moreover, their lumping together of upstream and downstream benefits and costs is meaningless. Nevertheless, their estimates of impacts shown in the table above may be reasonable, recognizing who is actually impacted. What the USDA/SPHIS analysis actually shows is that packers would gain substantially and that their gain would be roughly equal to losses to cow-calf and feedlot operators. Although the spin given to the border reopening is that it would benefit consumers, their analysis actually indicates that meat consumers would lose by $76 million. The net impact on society—ignoring to whom benefits and costs accrue—would be quite small. To the extent that USDA/APHIS estimates are valid, the net economic impact of reopening the border amounts to a whopping 5 cents per person per year. Additional health risks from reopening the border should be weighed against the 5 cent per person impact. Links to the USDA/APHIS reports: http://www.aphis.usda.gov/lpa/issues/bse/risk_assessment/03-080-3_econ_analysis.pdf http://www.aphis.usda.gov/lpa/issues/bse/risk_assessment/03-080-3_appendices.pdf Footnote for Academic Economists: Interpretation of consumer and producer surplus in vertically related markets is clearly laid out in the article by Richard Just and Darrell Hueth, “Welfare Measures in a Multimarket Framework,” American Economic Review, December 1979. They show “that the area behind a general equilibrium demand curve in an intermediate market does not measure benefits to buyers in that market alone, but rather measures the sum of rents to producers selling in all higher markets plus final consumer’s surplus. Symmetrically, the area behind the general equilibrium supply curve in an intermediate market measures not only rents for producers selling in that market, but also rents for all producers selling in more basic markets plus initial resource supplier’s surplus.”
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